tag:blogger.com,1999:blog-87965900648746676052024-03-06T22:03:09.967+02:00Cardiology: A modern free online cardiology ebook and cardiology casesA free (open access) Cardiology ebook online,(Cardiology website) Content is added continuously. Author: Georgios Chatziathanasiou MD, PhD Cardiologist (Copyright).E mail ghatziathan@gmail.com.
CLICK ON THE TABLE OF CONTENTS TO SEE THE LIST OF CHAPTERS (IN THE FORM OF LINKS)
FOR BETTER VIEW OF THE WEBSITE PLEASE INACTIVATE AD-BLOCK PROGRAMS FOR THIS SITE Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.comBlogger26125tag:blogger.com,1999:blog-8796590064874667605.post-67660231956727161472019-12-26T00:05:00.002+02:002020-09-27T02:32:36.498+03:00Cardiology free book TABLE OF CONTENTS ( Click on the title of each chapter to see the selected chapter<div dir="ltr" trbidi="on">
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<b><span style="font-family: inherit; font-size: large;">Cardiology free e-book online </span></b></h2>
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<i><span face=""arial" , "helvetica" , sans-serif" style="color: #cc0000; font-size: large;">TABLE OF CONTENTS ( Click on the title of each chapter to see the selected chapter)</span></i></h3>
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<span face=""arial" , "helvetica" , sans-serif" style="font-size: large;"><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/06/the-electrocardiogram-ecg-adult-and-pediatric-ecg-interpretation.html">The Electrocardiogram -ECG (adult and pediatric)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2018/02/left-ventricle-systolic-and-diastolic-function-echocardiography.html">Assessment of left and right ventricular systolic and diastolic function with echocardiography</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/07/arterial-hypertension-hypertensive-emergencies-hypertension-in-pregnancy.html">Arterial hypertension-hypertensive crisis-hypertension in pregnancy</a><br /><br /><a href="https://cardiologybookandcases.blogspot.gr/2016/05/coronary-artery-disease-stable-unstable.html">Coronary artery disease stable and unstable-Cases and Notes</a><br /><br /> <a href="https://cardiologybookandcases.blogspot.com/p/computed-tomography-ct-is-based-on-x.html">CT coronary angiography-CTA (or multidetector computed tomography - MDCT )</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/05/congestive-heart-failure-diagnosis-and-treatment-a-case-of-ischemic-cardiomyopathy.html">Congestive heart failure diagnosis and treatment and a case of heart failure (video)</a><br /> <br /><a href="https://cardiologybookandcases.blogspot.com/p/heart-failure-and-heart-disorders-due.html">Heart failure and heart disorders caused by cancer treatment (cardio-oncology)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/12/cardiomyopathies-cardiomyopathy-diagnosis-treatment-cardiologyfreebook.html">The Cardiomyopathies</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/06/acute-pericarditis-pericardial-effusion.html">Pericarditis -pericardial effusion</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/05/a-cardiology-video-constrictive.html">Constrictive pericarditis: Pathophysiology, diagnosis, echocardiography and treatment</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/05/a-cardiology-case-video-male-patient-82.html">Aortic stenosis -A case of stenosis of the aortic valve</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/07/aortic-regurgitation.html">Aortic regurgitation (AR)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/08/mitral-regurgitation-diagnosis-assessment-of-severity-treatment.html">Mitral regurgitation. Diagnosis, echocardiography and management. / A clinical case (VIDEO)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/09/mitral-stenosis-free-cardiology-book-valvular-heart-disease.html">Mitral stenosis</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/09/tricuspid-valve-regurgitation-free-cardiology-book-valvular-heart-disease.html">Tricuspid regurgitation</a><br /><br /><a href="https://cardiologybookandcases.blogspot.gr/2017/07/stenosis-of-right-cardiac-valves-pulmonic-stenosis-tricuspid-stenosis.html">Stenosis of the right cardiac valves: Pulmonic stenosis, Tricuspid Stenosis</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2017/09/prosthetic-heart-valves-cardiology-book.html">Prosthetic heart valves</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2017/01/infective-endocarditis-diagnosis-management-cardiology-book.html">Infective Endocarditis ( Diagnosis, treatment and a case)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/08/tachyarrhythmias-cardiac-arrhythmias-supraventricular-and-ventricular-tachycardia-atrial-fibrillation.html">Tachyarrhythmias-supraventricular and ventricular tachycardia</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2016/09/bradyarrhythmias-bradycardia-sick-sinus-syndrome-atrioventricular-block.html">Bradycardia-Bradyarrhythias. Diagnosis,treatment and clinical cases</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2017/03/pulmonary-hypertension-pulmonary-arterial-hypertension-cardiology-books.html">Pulmonary Hypertension and pulmonary arterial hypertension</a><br /><br /><a href="http://cardiologybookandcases.blogspot.com/2018/10/acute-pulmonary-embolism-cardiology.html">Pulmonary embolism</a></span><br />
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<span face=""arial" , "helvetica" , sans-serif" style="font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/2019/12/diseases-of-thoracic-and-abdominal-aorta-aneurysm-dissection-cardiology-book.html">Diseases of the thoracic and abdominal aorta (aneurysm-dissection)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2017/10/congenital-heart-disease-cardiology.html">Congenital heart disease. A concise introduction (overview)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2017/10/atrial-septal-defects-ASD-atrial-septum-ventricular-septal-defect-VSD-cardiology.html">Common congenital cardiac anomalies with a left to right shunt: Atrial septal defects (ASDs), Partial anomalous pulmonary venous return, Ventricular septum defects (VSDs), and Patent ductus arteriosus (PDA)</a><br /><br /><a href="https://cardiologybookandcases.blogspot.com/2018/07/cyanotic-congenital-heart-disease.html">Cyanotic congenital heart disease (the most common types)</a><br /><br /><a href="http://cardiologybookandcases.blogspot.gr/2018/04/cardiac-tumors-cardiac-neoplasms-myxoma.html">Cardiac tumors (cardiac neoplasms)</a></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><span style="background-color: cyan; color: red;"><span style="color: black;"><br /></span></span></b></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><span style="background-color: cyan; color: red;"><span style="color: black;"><br /></span></span></b></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b style="color: red;"><i style="background-color: cyan;">USEFUL LINKS ...</i></b></span><br />
<span style="color: #cc0000; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /><b style="background-color: #ffe599;">My free emergency medicine book online: <a href="http://emergencymedicinefirstaidfreebook.blogspot.com/">Emergency Medicine and First Aid. A free ebook online.</a></b></span><span style="color: red; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i style="background-color: cyan;"><br /></i></b></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i><br /></i></b></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i>A useful link for a free Cardiology journal (Continuing Cardiology Education, a journal with review articles):</i></b></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i><a href="http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2059-1594" target="_blank">CONTINUING CARDIOLOGY EDUCATION</a></i></b></span><br />
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<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b>A link for a website about mobile echocardiography devices (echo-stethoscope) and transthoracic echocardiography (TTE) <a href="https://echoscope.org/" target="_blank">https://echoscope.org/</a></b></span><br />
<b style="color: #0b5394; font-family: georgia, "times new roman", serif; font-size: x-large;"><i><br /></i></b><b style="color: #0b5394; font-family: georgia, "times new roman", serif; font-size: x-large;"><i>A Useful and interesting website about Cardiovascular Research</i></b><br />
<b style="color: #0b5394; font-family: georgia, "times new roman", serif; font-size: x-large;"><i><a href="http://careinstitute.gr/index.html#header6-0" target="_blank">Cardiovascular Research Institute</a></i></b><b style="color: #0b5394; font-family: georgia, "times new roman", serif; font-size: x-large;"><i><br /></i></b><br />
<b style="color: #0b5394; font-family: georgia, "times new roman", serif; font-size: x-large;"><i><br /></i></b><b style="color: #0b5394; font-family: georgia, "times new roman", serif; font-size: x-large;"><i>Useful links for drug information :</i></b><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i><a href="https://www.medicines.org.uk/emc/" target="_blank">medicines.org- emc</a></i></b></span></div><div dir="ltr" trbidi="on"><span style="color: #0b5394; font-family: georgia, times new roman, serif; font-size: large;"><b><i><a href="https://www.drugs.com/" target="_blank">https://www.drugs.com/</a> ( Drugs.com : Find drugs and conditions)<br /></i></b></span>
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><br /></b></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b>LINKS TO MEDICAL CALCULATORS</b></span><br />
<span face=""arial" , "helvetica" , sans-serif"><b>These are sites that contain easy-to-use medical calculators, to calculate for example body surface area (BSA), body mass index (BMI), estimated glomerular filtration rate (eGFR), CHA₂DS₂-VASc Score for Atrial Fibrillation Stroke Risk, </b></span></div>
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<b style="font-family: Arial, Helvetica, sans-serif;"> 10 -year cardiovascular risk scores,</b><b style="font-family: Arial, Helvetica, sans-serif;">TIMI and GRACE risk scores for acute coronary syndromes, Duke criteria for infective endocarditis, Cardiac index and systemic vascular resistance calculators, Calorie calculators/ Drug dosage calculators, etc</b></div>
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<span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><a href="https://www.mdcalc.com/#all" target="_blank">MDCalc</a></b></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://medicineworld.org/online-medical-calculators.html" target="_blank">Online Medical Calculators-Medicine World org</a></span><br />
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<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://reference.medscape.com/guide/medical-calculators" target="_blank">Medscape-Medical Calculators</a></span><br />
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<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://clincalc.com/" target="_blank">ClinCalc.com-calculators for medical professionals</a></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><br /></b></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b>LINKS TO OTHER FREE SOURCES OF MEDICAL INFORMATION (About Cardiology, emergency medicine, internal medicine, and other clinical fields)</b></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="https://www.youtube.com/channel/UCRoOCgmBNnj1kjaemu8dhWw/videos" target="_blank">Cardiology cases-videos by Dr Chatziathanasiou </a> </span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;">(This is my own channel ! It contains cardiology cases. It is under development -more videos are being continuously added).</span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><a href="http://www.clinicaladvisor.com/decision-support-in-medicine/section/7069/" target="_blank">Clinical Advisor - Decision Support in Medicine</a></b></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://www.msdmanuals.com/professional/cardiovascular-disorders" target="_blank">The Merck Manual - MSD Manual Professional Edition-Cardiovascular Disease</a></span><br />
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<a href="https://www.radcliffecardiology.com/topics" target="_blank"><span style="font-size: large;">Radcliffe Cardiology - Information for Cardiology Professionals</span></a><br />
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<a href="https://www.evidence.nhs.uk/Search?q=cardiology" target="_blank"><span style="font-size: large;">NICE Evidence search: Cardiology</span></a><br />
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<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: medium;"><b><i>Continuing Cardiology Education, a journal with review articles):</i></b></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: medium;"></span><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i><a href="http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2059-1594" target="_blank">CONTINUING CARDIOLOGY EDUCATION</a></i></b></span><br />
<span style="font-size: large;"><br /></span><span style="font-size: large;"><a href="http://emedicine.medscape.com/cardiology" target="_blank">E medicine-Medscape-Cardiology</a></span><br />
<span style="font-size: large;"><br /></span><span style="font-size: large;"><a href="http://echojournal.com/" target="_blank">The Echo-Journal-Echocardiography videos and Tutorials</a></span><br />
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<span style="font-size: large;">123 sonography you tube channel (by Professor of Cardiology and echocardiography Thomas Binder) Link <a href="https://www.youtube.com/user/123sonography/videos" target="_blank">https://www.youtube.com/user/123sonography/videos</a></span><br />
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<br />
<ins class="adsbygoogle" data-ad-client="ca-pub-3897630395074540" data-ad-format="fluid" data-ad-layout-key="-fg+5q+6u-gv+5y" data-ad-layout="image-side" data-ad-slot="5455865416" style="display: block;"></ins><span style="color: red; font-size: large;"><a href="https://lifeinthefastlane.com/ecg-library/" target="_blank">ECG Library-Life in the fast lane medical blog</a></span><br />
<span style="color: red; font-size: large;"><br /></span><span style="color: red; font-size: large;"><a href="http://hqmeded-ecg.blogspot.gr/" target="_blank">Dr. Smith's ECG blog</a></span><br />
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<a href="http://www.metealpaslan.com/enindex.htm" target="_blank"><span style="font-size: large;">Doktor EKG com (by Prof. Mete Alpaslan)</span></a><br />
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<span style="font-size: large;"><a href="http://www.cardioserv.net/echocardiography/" target="_blank">Cardioserv blog-Echocardiography</a></span><br />
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<a href="http://ccclivecases.org/new/" target="_blank"><span style="font-size: large;">CCC Live Cases (Interventional cardiology cases and videos)</span></a><br />
<span style="font-size: large;"><br /></span><span style="font-size: large;"><a href="http://www.mdedge.com/ecardiologynews" target="_blank">Cardiology News</a> (site for physicians about cardiology news and new developments in cardiovascular medicine)</span><br />
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<a href="https://www.ecrjournal.com/" style="font-size: x-large;" target="_blank">European cardiology review (ECR)</a><span face=""arial" , "helvetica" , sans-serif"> This is a free journal, but to view all contents you need to register online to the webpage (Registration is free -Takes about 5 minutes)</span><br />
<b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: medium;"><br /></span></b><b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: medium;"><span face=""arial" , "helvetica" , sans-serif"><a href="https://www.youtube.com/channel/UCgTkVi5RFXNRH9uR6gdq0QQ" target="_blank">Prof N Kumar Cardiology lectures (videos about interventional cardiology -electrophysiology-ECG etc)</a></span></span></b><br />
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<b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="https://www.youtube.com/channel/UCb8PGmJ6SILfyOvOWJvHZIg/videos" target="_blank">DeBakey Institute For Cardiovascular Education and Training-videos-cardiology lectures</a></span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif"><br /></span></b><b><br /></b><b><span face=""arial" , "helvetica" , sans-serif"><a href="http://uofl%20internal%20medicine%20lecture%20series/" target="_blank">UofL Internal Medicine Lecture Series-cardiology lectures</a> (videos)</span></b><br />
<b><br /></b><b><br /></b><b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://www.drjohnm.org/" target="_blank">Dr. John M ( a medical-cardiology blog)</a></span></b><br />
<b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span></b><b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://blogs.bmj.com/heart/" target="_blank">BMJ-Heart-Blog</a></span></b><br />
<b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><br /></span></b><b><span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><a href="http://blogs.nejm.org/now?s=cardiology&x=0&y=0" target="_blank">NEJM blog-cardiology posts</a></span><span style="font-size: large;"><span style="color: #b45f06;"><br /></span></span></b><br />
<b><span style="font-size: large;"><span style="color: #b45f06;">LINKS TO FIND FREE BOOKS</span>:</span></b><br />
<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"></span><br />
<span style="font-size: large;"><a href="http://www.freebookcentre.net/" target="_blank" title="Free computer books download">FREE BOOKS DOWNLOAD</a> (freebookcentre net)</span><br />
<span style="font-size: large;"><br /></span><a href="http://www.freebooks4doctors.com/" target="_blank"><span style="font-size: large;">freebooks4doctors</span></a><br />
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<span style="color: #0b5394; font-family: "georgia" , "times new roman" , serif; font-size: large;"><b><i>Cardiology free ebook online</i></b></span><br />
<span face=""arial" , "helvetica" , sans-serif" style="color: #0b5394; font-size: large;"><b>IMPORTANT NOTE: THE SITE IS UNDER CONTINUOUS DEVELOPMENT AND CONTENTS GRADUALLY INCREASE</b></span><br />
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<ins class="adsbygoogle" data-ad-client="ca-pub-3897630395074540" data-ad-slot="7008941317" style="display: inline-block; height: 250px; width: 300px;"></ins>Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-43455368235874849532019-12-25T23:12:00.017+02:002020-08-23T13:21:45.764+03:00Diseases of the thoracic and abdominal aorta (aneurysm-dissection)<h2 style="text-align: left;"><span style="font-family: times;">Diseases of the thoracic and abdominal aorta (aneurysm-dissection-aortic intramural hematoma / penetrating aortic ulcer)</span></h2><div><span style="font-family: times;"><br /></span></div><div><span style="font-family: times;"><br /></span></div><div><span style="font-family: times;"><br /></span></div><div style="text-align: left;"><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span></div><div style="text-align: left;"><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="font-family: "times new roman"; margin-left: auto; margin-right: auto; text-align: center;"><tbody><tr><td><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhb7Ti2zIa_k8Q4IZCKJol4hTwjhQnFCR5OT2eMSlPJt4YeLwHPqpYvqvh0s0hFPoZNXFDVH9XgIGESH79KAc9c1jJ_3wNCo4R-j3Jy_Mb1HbLH6rZi_UHX_j_pxavgwNq3Q78mz5r-1Ssm/s1600/%25CE%25B4%25CE%25B9%25CE%25B1%25CF%2587%25CF%2589%25CF%2581%25CE%25B9%25CF%2583%25CE%25BC%25CF%258C%25CF%2582+5+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB%25CF%258C%25CF%2584%25CE%25B7%25CF%2584%25CE%25B5%25CF%2582.png" style="margin-left: auto; margin-right: auto;"><span face="" style="font-family: arial, helvetica, sans-serif;"><b><img border="0" data-original-height="595" data-original-width="873" height="340" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhb7Ti2zIa_k8Q4IZCKJol4hTwjhQnFCR5OT2eMSlPJt4YeLwHPqpYvqvh0s0hFPoZNXFDVH9XgIGESH79KAc9c1jJ_3wNCo4R-j3Jy_Mb1HbLH6rZi_UHX_j_pxavgwNq3Q78mz5r-1Ssm/w500-h340/%25CE%25B4%25CE%25B9%25CE%25B1%25CF%2587%25CF%2589%25CF%2581%25CE%25B9%25CF%2583%25CE%25BC%25CF%258C%25CF%2582+5+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB%25CF%258C%25CF%2584%25CE%25B7%25CF%2584%25CE%25B5%25CF%2582.png" width="500" /></b></span></a></td></tr><tr><td class="tr-caption" style="text-align: left;"><span face="" style="font-family: arial, helvetica, sans-serif; font-size: small;"><b><br /></b></span></td></tr></tbody></table></span></div><div style="text-align: left;"><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span></div><div style="text-align: left;"><i>Acute aortic dissection (type A), transesophageal echocardiographic 5 chamber midesophageal view. The image shows: The intimal flap inside the significantly dilated ascending aorta (Ao) Ao valve aortic valve, LV left ventricle, LA left atrium, RV right ventricle). Courtesy of Dr. Ioannis Dernellis cardiologist.)</i></div><div style="text-align: left;"><i><br /></i></div><div style="text-align: left;"><i><br /></i></div><h3><span face="" style="font-family: times, "times new roman", serif; font-size: large;">Anatomy of the aorta</span></h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The aorta is the largest artery of the body and is divided into two parts: the thoracic and the abdominal aorta. The wall of the aorta consists of three layers: the intima, media, and adventitia. The intima is the inner layer, the media is the middle layer, and the adventitia is the outer layer<span style="background-color: white; color: #545454;">.</span> </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The thoracic aorta arises from the left ventricle at the level of the third sternocostal joint and it consists of the ascending aorta, the aortic arch, and the descending thoracic aorta, which extends down to the diaphragm.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> The ascending aorta extends from the aortic valve to the origin of the innominate (brachiocephalic) artery. The aortic root consists of the aortic annulus (the "ring" of the aortic valve) and the three sinuses of Valsalva (aortic sinuses) with the two coronary arteries originating from the left and right sinus. Normally, the widest portion of the aorta is at the sinuses of Valsalva. The aortic root ends at the sinotubular junction, which is the point where the tubular ascending aorta begins. The tubular ascending aorta is the distal part of the ascending aorta.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The aortic arch is defined as the segment of the aorta from which the large blood vessels of the head and upper limbs originate. It gives three branches, the innominate (brachiocephalic) artery, which divides into the right subclavian artery and the right common carotid artery, the left common carotid artery, and the left subclavian artery.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Immediately adjacent to the left subclavian artery is the arterial ligament (ligamentum arteriosum), in the place of the closed arterial duct (ductus arteriosus) that existed in fetal life. The aortic isthmus is a short segment of the aorta located between the left subclavian artery and the ligamentum arteriosum. The aortic isthmus is the most common site of the aorta where diseases occur. Such disorders and diseases are coarctation of the aorta, persistent ductus arteriosus, and aortic dissection of traumatic etiology, e.g., due to chest injury or injury to the aorta, such as the deceleration injury that occurs in traffic accidents.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The descending thoracic aorta begins just distal to the origin of the left subclavian artery and penetrates the diaphragm at the level of the 12th thoracic vertebra, where it continues down into the abdominal aorta. The descending thoracic aorta gives the following branches: the bronchial arteries, the esophageal arteries, and the third to twelfth intercostal arteries. (The first 2 intercostal arteries are branches of the subclavian arteries).</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> The abdominal aorta is smaller in diameter than the thoracic aorta. It begins from the aortic hiatus of the diaphragm and courses downward, giving branches that deliver blood to the abdominal viscera, and ends at the lower level of the 4th lumbar vertebra (L4) dividing into the two common iliac arteries. The iliac arteries supply with blood the pelvis and lower extremities. The abdominal aorta gives the following three groups of branches a) unpaired visceral arteries to the gastrointestinal tract,</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">spleen, pancreas, gallbladder, and liver b) paired arteries to the kidneys, adrenal glands, and gonads. c) parietal branches to the structures of the abdominal wall.</span><br />
<div>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span></div>
<b><span face="" style="font-family: times, "times new roman", serif; font-size: large;">Thoracic aortic aneurysm</span></b><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Definition: It is a segment of the thoracic aorta with an abnormally increased diameter which is > 1.5 times the expected mean normal diameter. (Thus for the ascending aorta, an aneurysm will have a diameter > 2.75 cm /<span lang="" style="line-height: 107%;">m<sup>2</sup> </span>of body surface area). True aneurysms have a wall that consists of all three layers of the arterial wall, whereas in pseudoaneurysms there is a rupture of the inner and middle layers, and the aneurysm is surrounded only by the outer layer of the arterial wall and sometimes by a clot.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The most common thoracic aortic aneurysms are those of the ascending aorta, followed by the aneurysms of the descending aorta. Aneurysms of the aortic arch are rare.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Morphologically, aneurysms are classified as: </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> <span lang="">♦</span> fusiform aneurysms (most commonly), in which there is a uniform dilation of the entire periphery of the vessel in its affected segment, and </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> <span lang="">♦</span> saccular aneurysms where the dilation involves only a portion of the periphery of the vessel. These aneurysms often contain thrombus due to the slow flow of blood in the area of the aneurysmal sac.</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Pathogenesis of thoracic aortic aneurysms</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Aneurysms are due to abnormal production or progressive degeneration of aortic wall structural proteins (collagen and elastin). The most common cause of ascending aortic aneurysms is cystic medial necrosis, a form of degeneration of the aortic media (the middle layer of the aortic wall), with a reduced content of collagen and elastin fibers. This lesion is observed in some hereditary syndromes such as Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta, and polycystic kidney disease.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Cystic degeneration of the middle layer of the aortic wall (media) is also present in the case of annuloaortic ectasia (more common in males). In annuloaortic ectasia, there is an aneurysm of the proximal ascending aorta which involves the aortic root and there is also accompanying aortic regurgitation. Other manifestations and features of a particular genetic syndrome are not present, although a defective gene is implicated.</span><br />
<span face="" style="font-family: times, "times new roman", serif;"><span face="" style="font-family: times, "times new roman", serif; font-size: large;">The most usual cause for aneurysms of the aortic arch and descending aorta is atherosclerosis, which causes degenerative changes in the vascular wall. Risk factors are hypertension (a major cause of dilatation in any part of the aorta), smoking, hypercholesterolemia, diabetes mellitus and advanced age. </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">Other causes of aortic aneurysms: </span></span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Poststenotic dilatation of the aorta (e.g. in aortic valve stenosis, or in the aortic segment which is located just distally from the position of aortic coarctation), </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">infectious etiology (microbial or mycotic aneurysms due to septic emboli in ischemic endocarditis),</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> in the context of autoimmune or rheumatic disease (Takayasu arteritis, giant cell arteritis, ankylosing spondylitis, systemic lupus erythematosus, rheumatoid arthritis, Adamantiadis-Behcet disease, Reiter syndrome).</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Aneurysms of the aortic sinuses of Valsalva present a separate category and are congenital. These aneurysms most commonly involve the right sinus (70%), less frequently the noncoronary sinus (25%).</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Clinical manifestations and diagnosis of thoracic aortic aneurysms. </span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Thoracic aortic aneurysms are most often asymptomatic, and the diagnosis is often made by the finding of a widened mediastinum on a chest X-ray. A shift of the trachea or the left main bronchus due to pressure from the aneurysm may also be present.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> Some patients may have symptoms of adjacent organ pressure: Dyspnea, cough (due to pressure on the trachea), hoarseness (due to pressure on the left recurrent laryngeal nerve), dysphagia (pressure on the esophagus), chronic mild deep chest pain (when this pain becomes more intense there is a suspicion of impending rupture). Manifestations of congestive heart failure can occur in the case of severe aortic valve regurgitation (due to large ascending aortic aneurysm). </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In some patients, the first manifestation is aneurysm rupture, presenting with acute thoracic pain, hemorrhagic shock with a sudden decrease in blood pressure and death. In the case of hemorrhage into the pericardium, due to the rupture of an aneurysm of the ascending aorta, cardiac tamponade occurs. </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Diagnostic tests for thoracic aortic aneurysms are the following: echocardiography (transthoracic and transesophageal), chest CT scan with intravenous radiographic contrast, magnetic resonance imaging, and aortography.</span><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span></div><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><i>Transthoracic echocardiogram left parasternal long-axis view (PLAX view) in a 38-year-old woman with Marfan syndrome. What is the pathological finding shown in this image?</i></span></div><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><i><br /></i></span></div><div><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgV-G9bjh_jfwdz6gDFGMsgTLNCe8wA6eunCbnS5hhuMBsxcGWLLNSpIGYyF_vi4lblDwuwx5PGA6y5B1PniJGXKPqHUsAk0-wEs3khII-QePZjR3H9oLCowWKMSSoOjzmSn0_bU6CnC96l/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25B1%25CE%25BD%25CE%25B5%25CF%258D%25CF%2581%25CF%2585%25CF%2583%25CE%25BC%25CE%25B1+%25CE%25B1%25CE%25BF%25CF%2581%25CF%2584%25CE%25AE%25CF%2582+%25CF%2583%25CE%25B5+%25CF%2583%25CF%258D%25CE%25BD%25CE%25B4%25CF%2581%25CE%25BF%25CE%25BC%25CE%25BF+Marfan.JPG" /></div><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><i><br /></i></span></div><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><i>Aneurysm of the aortic root at the level of the Valsalva sinuses, maximum diameter 4.7 cm (Ao aorta, AoV aortic valve, RVOT right ventricular outflow tract, LA left atrium, LV left ventricle)</i></span></div><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span></div><div><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span>
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Treatment of thoracic aortic aneurysms and indications for surgery: </span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Long-term administration of beta-blockers is indicated in patients with thoracic aortic aneurysms (this treatment may delay aneurysm progression). Treatment with additional antihypertensive medications is indicated in hypertensive patients (strict control of hypertension is important). Surgical treatment with prosthetic graft placement is indicated: </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">1) In patients with symptoms such as thoracic pain indicative of rupture or of threatened rupture of the aneurysm, if the symptoms are not explained by another cause </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">2) In patients with manifestations due to compression of adjacent organs such as the esophagus, trachea, or left main bronchus, or</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> 3) In asymptomatic patients with an ascending aortic aneurysm with a maximum diameter > 5.5 cm or when there is evidence of a rapid increase in the aneurysm diameter (> 1 cm in one year). </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The general diameter threshold of 5.5 cm for ascending aortic aneurysm surgery is also applicable to patients with a bicuspid aortic valve, whereas in Marfan syndrome the threshold is lower (5 cm).</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> Patients with an ascending aortic aneurysm and a bicuspid aortic valve may receive surgical treatment at a lower aneurysm diameter of 5 cm if they also have an additional risk factor for dissection, such as a family history of aortic dissection, an increasing diameter of the aneurysm > 3 mm / year, coarctation of the aorta, or small body size. Arterial hypertension is also considered a risk factor if it has not been adequately controlled. An indication for surgery in the case of an ascending aortic aneurysm is the coexistence of severe aortic regurgitation. </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In patients with Marfan syndrome, there is an indication for surgical correction when the ascending aortic aneurysm diameter is > 5 cm. Moreover, in patients with Marfan syndrome, the decision for surgery can be made at a smaller threshold of aortic diameter, (at 45 mm) if they have any additional risk factors, such as</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">- a family history of aortic dissection</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">-an increase in aneurysm diameter> 3mm / year (using the same imaging technique)</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">- severe aortic regurgitation or</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">- a desire for pregnancy (because pregnancy is associated with an increased risk for a rapid increase in diameter and for the occurrence of complications of the aneurysm). Patients with manifestations of a connective tissue disorder similar to Marfan syndrome who do not completely meet the criteria of Marfan syndrome should receive the same treatment for the aneurysm and with the same diameter thresholds as patients diagnosed with Marfan syndrome. </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In patients with an aneurysm confined to the aortic arch, surgical treatment should be considered if the maximal diameter of the aortic arch ≥ 55 mm (a class IIa indication in the guidelines). <br />For aneurysms of the descending thoracic aorta when there is an indication of surgery (see below for the diameter threshold ) Thoracic Endo-Vascular Aortic Repair (TEVAR) should be considered since it is preferable to surgery if the anatomy is appropriate. When repair with a stent-graft (TEVAR) is technically feasible, then this treatment (class IIa indication based on the ESC guidelines) should be seriously considered for patients with an aneurysm of the descending aorta with a diameter ≥ 55 mm. (5,5 cm). Endovascular repair is performed by the introduction of the guidewire and the stent delivery system, through the common femoral or iliac artery (following surgical exposure of the artery). The stent delivery system is advanced by sliding over the guidewire. In this manner, the guidewire and intraluminal stent-graft system are advanced to the descending thoracic aorta. The system is introduced from the iliac artery when the diameter of the femoral artery is not sufficient to allow this artery to be used as the entry site. In patients with an aneurysm of the descending aorta, when TEVAR is not technically feasible, surgical treatment should be considered if the aneurysm diameter ≥ 6 cm. Surgical intervention at a smaller descending aortic diameter threshold (5.5 cm) should be considered in patients with Marfan syndrome. When intervention is indicated for an aneurysm of the descending thoracic aorta in cases of Marfan syndrome or other connective tissue disorders, surgery should be preferred instead of endovascular repair with a stent (TEVAR).</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Dilatation of the ascending aorta and pregnancy </span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Women with a dilated aortic root or ascending aorta with a diameter > 4.5 cm are at increased risk during pregnancy for a progressive increase in diameter, dissection, or rupture of the aorta. This risk is present for all women with ascending aortic aneurysms but is even higher in women with Marfan syndrome. In Marfan syndrome, there is an increased risk in pregnancy at a lower limit of aortic diameter (when the ascending aorta > 4 cm in diameter).</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The increased risk of complications of aneurysms in pregnancy is attributable to the increased stroke volume in pregnancy, but possibly also hormonal changes adversely affect pre-existing histological lesions of the aortic wall.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> In patients with aortic root or ascending aortic dilation who desire pregnancy, surgery in the ascending aorta (replacement of the aortic root and ascending aorta with a graft) before pregnancy is recommended in the following cases: </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">1. In patients without a genetic syndrome that increases the risk for aortic dissection (see below) when the ascending aorta has a maximum diameter of ≥ 50 mm (5 cm). </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">2. In patients with Marfan syndrome or other high-risk genetic syndromes, such as Loeys-Dietz syndrome, Ehlers-Danlos syndrome, or Smad-3 gene mutation, when the ascending aorta is ≥45 mm.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><span lang="" style="line-height: 115%;">Body surface area should probably be taken into
account in women with small body size. An ascending aorta diameter index>2.7
cm / m<sup>2</sup> body surface area is associated with a high risk
of dissection, therefore pre-pregnancy prophylactic surgery should be
considered. Patients with aortic root or ascending aortic dilation are usually
on treatment with beta-blockers to slow and limit the progression of aortic
dilation. </span><span style="line-height: 115%;">These medications should be continued during pregnancy.</span></span><br />
<h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Abdominal aortic aneurysm</span></h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The descending thoracic aorta passes through the aortic hiatus of the diaphragm and continues into the abdominal aorta. (The aortic hiatus is a hole in the diaphragm through which the aorta, the azygos vein, and the thoracic duct enter the abdomen). The abdominal aorta is located in the retroperitoneal space, descends in front of the spine (in close proximity to the spine), slightly to the left of the midline. The abdominal aorta from top to bottom supplies the following branches: The celiac artery or celiac axis, the superior mesenteric artery (which runs immediately above the left renal vein, which is a branch of the inferior vena cava), the renal arteries (right and left-renal artery), and the inferior mesenteric artery. The abdominal aorta, at the level of the fourth lumbar vertebra, divides into the right and left common iliac arteries.<br /> The inferior vena cava (IVC) is located to the right of the aorta. On ultrasound, the IVC is easily distinguished from the aorta since it has a more ellipsoid (oval) shape in transverse section and also a thinner wall than the abdominal aorta, which has a more round shape.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">An aneurysm is a focal dilatation of an artery with diameter increased by at least 50% of the normal diameter. The wall of this dilated portion of the artery contains all three layers of the arterial wall. (If the wall of the aneurysm does not consist of all three layers of the arterial wall then it is called a pseudoaneurysm).</span><br />
<span face="" style="font-family: times, "times new roman", serif;"><span style="font-size: large; text-align: justify;">The most common aneurysms of the aorta are the abdominal aortic aneurysms (frequency> 3% in people > 50 years of age), while the aneurysms of the thoracic aorta are less common. The most common thoracic aortic aneurysms are those of the ascending aorta followed by the aneurysms of the descending aorta. Aortic arch aneurysms are rare. </span><span style="color: #222222; font-size: large; text-align: justify;"><span style="background-color: white;">In the abdominal aorta, an aneurysm is a part of the artery with diameter ≥ 3 cm. The normal diameter of the abdominal aorta is 1.5 - 2.5 cm. When the diameter is 2.6-2.9 cm, this is considered as a mild or marginal dilation of the artery. About 90% of abdominal aortic aneurysms lie below the level of the renal arteries.</span></span></span><br />
<h4 style="text-align: justify;">
<span face="" style="background-color: white; color: #222222; font-family: times, "times new roman", serif; font-size: large;">Causes and pathogenesis of abdominal aortic aneurysms</span></h4>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">There is a degeneration of the aortic media (the middle layer of the aortic wall), resulting in a decrease in wall strength and a slow progressive dilation of the vessel. The most common underlying cause is atherosclerosis. Rarer causes are arteritis, injury, hereditary diseases of the connective tissue that cause cystic degeneration of the media, and damage to the vascular wall at sites of previous surgical anastomosis. </span></span></div>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;"><b>Risk Factors: </b></span></span></div>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">Smoking (Smoking is the risk factor most strongly associated with abdominal aortic aneurysms), </span></span></div>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">Old age, </span></span></div>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">Hypertension, </span></span></div>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">Male gender (abdominal aortic aneurysms are more common in men than in women),</span></span></div>
<div style="text-align: justify;">
<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">Family history (a family history is present in about 15-20% of patients, indicating a genetic predisposition) and</span></span></div>
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<span face="" style="color: #222222; font-family: times, "times new roman", serif; font-size: small;"><span face="" style="background-color: white; font-family: times, "times new roman", serif; font-size: large;">Chronic obstructive pulmonary disease (COPD). </span></span></div>
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<span style="font-size: large;">Men > 65 years of age, smokers </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><span style="background-color: white; color: #222222;"><span style="background-color: white;">are at higher risk for an abdominal aortic aneurysm, </span></span><span style="background-color: white; color: #222222;">and especially so if they also have peripheral arterial disease. It has also been observed that in p</span><span style="background-color: white; color: #222222;">atients with aneurysms of the popliteal artery, </span><span style="background-color: white; color: #222222;">commonly an</span><span style="background-color: white; color: #222222;"> aneurysm of the abdominal aorta is also present.</span></span></div>
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<span face="" style="background-color: white; color: #222222; font-family: times, "times new roman", serif; font-size: large;"><b>Preventive screening</b> with abdominal aortic ultrasound is recommended for men ≥ 65 years of age, especially if they have a history of smoking or hypertension. </span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Clinical findings and diagnosis of abdominal aortic aneurysms</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Most abdominal aortic aneurysms are asymptomatic and diagnosed as an incidental finding in imaging tests of the abdomen, usually performed for another reason. When symptoms are present, this is often an indication of aneurysm expansion. In some cases, mild pain may be present in the back, abdomen, or groin area. Pain limited within the groin area is a manifestation that is due to the retroperitoneal expansion of the aneurysm, with pressure on the femoral nerve. Some patients may have a feeling of palpitations in the abdomen, a feeling of abdominal fullness, a feeling of fast satiety with meals, nausea, or manifestations of peripheral embolism in the toes. A sudden expansion of the aneurysm causes severe and constant pain in the lumbar area, abdomen, or groin. In some cases, renal colic is misdiagnosed.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In cases of rupture of the aneurysm, in addition to pain, the clinical manifestations of circulatory shock predominate, with hypotension, tachycardia, pallor or cyanosis, an altered mental status (e.g. confusion, disorientation), or syncope. In > 50% of cases of ruptured abdominal aortic aneurysm, the patient dies of circulatory shock before arriving at the hospital. However, there are cases where the only manifestation is sudden severe pain in the lumbar area or abdomen. This is the case when the retroperitoneal tissues contain the hematoma preventing a massive hemorrhage and resulting in a relatively localized retroperitoneal hematoma.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><span face="" style="font-family: times, "times new roman", serif;">Rupture of an abdominal aortic aneurysm should be suspected in all patients over 50 with acute abdominal or back pain and hypotension, or a palpable pulsatile mass in the abdomen. (This the classic diagnostic triad presentation). The mass may be obscured in patients with a large abdominal circumference. An episode of syncope can be indicative of orthostatic hypotension. I</span><span face="" style="font-family: times, "times new roman", serif;">n such patients, a</span><span face="" style="font-family: times, "times new roman", serif;">n emergency Doppler ultrasound should be performed to confirm the diagnosis. The patient should be transferred to the nearest high-volume hospital where a vascular/endovascular surgical team is available. </span></span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><span face="" style="font-family: times, "times new roman", serif;"><b>Physical examination</b>: In most (but not all) cases of a clinically significant abdominal aortic aneurysm, a palpable pulsatile abdominal mass is detected on physical examination. However, it is often difficult </span><span face="" style="font-family: times, "times new roman", serif;">or impossible to detect a pulsatile abdominal mass in obese patients.</span></span><br />
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Diagnosis of abdominal aortic aneurysms-Imaging</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Ultrasound is the most widely used imaging test, with very high sensitivity and specificity for aneurysms below the level of the renal artery. It may also detect the presence of blood in the peritoneal cavity in the event of aneurysm rupture. A complete examination of the abdominal aorta can sometimes be difficult in obese patients, or when a large amount of bowel gas is present. Usually, no special preparation is required for the patient who is lying supine with a pillow under the head. Sometimes we need to place the patient in a lateral decubitus position in order to move gas-containing bowel segments that prevent clear imaging. A low ultrasound frequency is used. The transverse image plane is initially obtained, i.e. a plane perpendicular to the longitudinal axis of the body, with the transducer 3-4 cm above the navel and the marker of the transducer pointing towards the patient's right side, perpendicular to the longitudinal axis of the body. Then, by slowly dragging the transducer upwards and downwards, the abdominal aorta is visualized along its entire length, from the level of the celiac and upper mesenteric artery down to its bifurcation into the two common iliac arteries. If an aneurysm is present, a dilation of the aorta in the affected area is identified.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> The aorta is then visualized along its longitudinal axis at the sagittal plane (with the transducer placed on the midline of the abdomen, above the aorta and its marker pointing towards the head of the patient). In this way, it is possible to visualize the abdominal aorta throughout its length. (Note: A sagittal plane is one directed from the front to the back and divides the body into a left and a right part). The transducer is then positioned more laterally in the abdomen and the aorta is again visualized along its longitudinal axis, but at a coronal plane (see figure). (A coronal plane is one that divides the body into an anterior and posterior portion, i.e a plane parallel to the anterior surface of the body.] This view allows for the measurement of the lateral diameter of the aorta. The iliac arteries should also be examined, in a longitudinal and transverse view, to check for an iliac artery aneurysm, or to determine if an abdominal aortic aneurysm extends to the iliac arteries.</span><br />
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<span face="" style="font-family: arial, helvetica, sans-serif; font-size: small;"><b><b>Transducer positions for abdominal aortic ultrasound. The abdominal aorta is depicted in the figure in red color whereas the inferior vena cava in blue.</b></b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif; font-size: small;"><b><b> 1 transverse view, 2 saggital view, 3 frontal view, 4 position for examination of the proximal segment , 5 position for examination of the bifurcation of the abdominal aorta. </b></b></span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Other imaging tests for the diagnosis of abdominal aortic aneurysms </span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Other diagnostic methods that provide more detailed images and are not affected by obesity or the presence of gas in the bowel, are computed tomography (CT) and magnetic resonance imaging (MRI). These tests accurately depict the location of the aortic branches relative to the aneurysmal segment of the aorta. Such information is useful in the event of an invasive procedure.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> CT with intravenous contrast provides excellent image quality, and it is especially superior to ultrasound in the visualization of an aneurysm located above the renal arteries. It also depicts the posterior peritoneum. It has the disadvantage of exposing the patient to ionizing radiation and the use of iodine contrast agent (which may cause deterioration of renal function, especially in patients with a degree of renal impairment). MRI does not have these two disadvantages. </span><br />
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A man 65 years old asymptomatic, smoker with a history of mild hypercholesterolemia (cholesterol 240, LDL 175). Physical examination: pulses 80 / min without arrhythmia, blood pressure 155/80 mmHg. This is an image from his abdominal ultrasound (Click on the image for a larger view). What is the proposed management ?</b></span><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>The answer:</b></span><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>An abdominal aortic aneurysm up to 3.8 cm in diameter is depicted. Management: Administration of antihypertensive medication and statin (The patient is considered to have a high cardiovascular risk because he has an arterial disorder. Therefore, a reasonable target should be for arterial pressure ≤ 130/80 and LDL <70 mg / dl). The inclusion of a beta-blocker in his antihypertensive regimen should be strongly considered because this drug-class has a favorable effect on reducing the rate of expansion of the aortic aneurysms. The patient should also be advised on smoking cessation. At this diameter, surgery or any interventional procedure is not indicated, but ultrasound monitoring of the abdominal aortic aneurysm is required annually (once every year). When the diameter of the aneurysm reaches 4 cm or more, then ultrasound monitoring is recommended every 6 months.</b></span><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b><br /></b></span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">Interventional treatment of abdominal aortic aneurysm</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In case of a ruptured aortic aneurysm, emergency surgery must be performed immediately.<br /><br />Other indications for invasive (surgical or interventional) </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">treatment of an </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">abdominal aortic aneurysm :</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Surgery is required if symptoms arise due to expansion of the aneurysm, compression of adjacent structures, or vascular complications.<br />In case of an asymptomatic abdominal aortic aneurysm when there is a rapid increase in diameter (> 1 cm / year), or when the maximum diameter of the aneurysm is ≥ 5.5 cm in men or ≥ 5.2 cm women, the patient should be referred to a vascular surgeon, because invasive treatment is indicated.<br />There are two methods of invasive treatment of an abdominal aortic aneurysm: 1) open surgery with an abdominal or posterior peritoneal access and 2) endovascular (interventional) treatment.</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Follow-up of patients diagnosed with an abdominal aortic aneurysm</span></h4>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Patients with an abdominal aorta </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">diameter </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">< 3 cm require no further monitoring for the abdominal aorta, only cardiovascular risk factors should be addressed. Asymptomatic aneurysms of maximal diameter 3-4 cm, annual monitoring with ultrasound is required. An asymptomatic aneurysm of </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">diameter</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">4-4.5 cm in requires examination with ultrasound every six months, and when the maximal diameter is > 4.5 cm the patient should also be followed by a vascular surgeon. If the diameter is </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">≥</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> 5.5 cm or larger, or if symptoms occur, there is an indication for surgical treatment.</span></div>
<h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The acute aortic syndromes</span></h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The term "acute aortic syndromes" refers to </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">severe and potentially life-threatening</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> disease of the aortic wall, which usually presents with severe </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">pain of s</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">udden onset, often described as "stabbing or tearing" and other acute manifestations, depending on the location of the lesion and associated complications. The location of the pain may be in the anterior thorax, the posterior thorax, or the lumbar region (waist) and the abdomen, depending on the location of the aortic disease. The acute aortic syndromes include three pathological conditions, the most important of which is <u>aortic dissection</u>. The other two less common and more localized pathological conditions (they usually involve a smaller area of the aorta than aortic dissection) are the <u>aortic intramural hematoma (IMH)</u> and the <u>penetrating aortic ulcer (PAU)</u>. The presence of pain, which is usually intense and of sudden onset (most often in the chest or back), is a common feature of all the above types of acute aortic syndromes. Therefore, there is an overlap in their clinical picture. </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">An acute aortic syndrome is suspected in the event of such persistent sudden pain in a patient with a history of either hypertension or an aortic aneurysm. The usual differential diagnosis includes an acute coronary syndrome.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The most common and important <b>risk factor</b> for an acute aortic syndrome is moderate to severe hypertension. However, other risk factors associated with atherosclerotic arterial disease (e.g. smoking, age, chronic kidney disease) also play an important role, while an important but less common risk factor is the presence of an inherited, connective tissue disease </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">associated with </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">risk of aortic dissection.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The <b>diagnosis</b> of acute aortic syndromes is based on three imaging techniques: ultrasound (transthoracic or transesophageal echocardiography for the thoracic aorta, with the latter having greater sensitivity and specificity, or abdominal ultrasound for the abdominal aorta), computed tomography (CT) or magnetic resonance imaging (MRI).</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">The <b>classification of the acute aortic syndromes </b>and its importance for the choice of the appropriate therapeutic strategy:</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">The acute aortic syndromes are classified into:</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> <u>Type A </u>when the ascending aorta is involved. In type A the lesion of the aortic wall may be limited to a part of the ascending aorta or it may extend from the ascending aorta also to other parts of the aorta. Type A acute aortic syndromes have a higher risk of early (in-hospital) mortality and usually require prompt surgical treatment.</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><u>Type B</u>: When there is no involvement of the ascending aorta. The lesion may be located in the descending thoracic or abdominal aorta or in the aortic arch. In type B, initial treatment usually includes only conservative medical treatment (pain management, beta-blockers, prompt treatment of hypertension with appropriate medications). In the case of a complicated clinical course, invasive treatment is indicated, preferably endovascular repair with placement of an intravascular stent-graft</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">. Surgical treatment can be performed when endovascular treatment is not technically feasible.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The topic of aortic dissection is discussed below, while the description of the other two acute aortic syndromes follows immediately after the aortic dissection chapter.</span><br />
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Aortic dissection</span></h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> Aortic dissection is one of the most severe causes of acute thoracic pain. It is the entry of blood from a rupture in the intima (inner layer) of the aorta into the aortic wall, forming a false lumen. An aortic dissection is more common in people </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">of age</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> 50-70 years, but it can also occur in younger people with aortic disease due to a connective tissue disorder, such as Marfan syndrome. The ratio of men to women with aortic dissection is 2: 1.</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The site where the blood enters the aortic wall (the intimal tear) is located, in order of frequency, in the ascending aorta in 65% of cases (the most frequent location), in the descending thoracic aorta in 20% (the second most frequent location), in the aortic arch (10%) and in the abdominal aorta in 5% of cases.</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Classification of aortic dissection</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Classification based on the location of aortic dissection<br /><b>According to the Stanford Classification</b> : </span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><b>Type A</b>: any dissection involving the ascending aorta. An acute type A aortic dissection requires prompt surgical treatment (it is a surgical emergency).<br /><b>Type B</b>: any dissection that does not include the ascending aorta. The treatment is conservative (medical) unless there are indications of complications or propagation of the dissection.<br /><b>According to the Debakey Classification:</b></span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> <b>Type I</b>: The intimal tear (the site of blood entry) is in the ascending aorta, but the dissection extends more distally than the ascending aorta, into the aortic arch or even more distally into the descending aorta.<br /><b>Type II</b>: The dissection is confined to the ascending aorta.<br /><b>Type III:</b> The site of blood entry is in the descending aorta, thus the dissection is confined in the descending aorta, distally to the origin of the left subclavian artery.<br />Classification based on time:<br /><b>Acute aortic dissection</b>: one that occurred less than 2 weeks ago.<br /><b> Chronic aortic dissection</b>: when more than 2 weeks have elapsed from the time of occurrence of the dissection.<br />This distinction is important because the mortality curve increases sharply within the first 2 weeks, whereas after this time interval the mortality is significantly lower.</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> Clinical manifestations of aortic dissection</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The pain is sudden, usually intense, tearing (like a tear or a knife), and excruciating (high-intensity unrelenting pain with sudden onset and lasting for hours). Although the pain is usually severe, in rare cases it can be mild or absent (in about 10% of cases). Pain location: in the sternal area or in the back. The pain may often gradually extend to the abdomen or hip or to the neck, depending on the propagation of the dissection. There is no referred pain of the upper extremities (a feature present in some cases of acute myocardial infarction, which is another cause of acute chest discomfort, always to be considered in the differential diagnosis). The pain of acute aortic dissection has its highest intensity from the beginning, in contrast to the pain of acute myocardial infarction.<br />The location of pain may indicate the site of the dissection. Anterior thoracic pain suggests a dissection located in the ascending aorta, while pain in the central region of the back, between the scapulae, is suggestive of dissection involving the descending aorta and abdominal pain occurs when the dissection is extending into the abdominal aorta. Neck and jaw pain may occur with dissection extending into the aortic arch and involving its branch vessels, whereas flank pain may occur when the dissection extends to a renal artery.<br />Aortic dissection usually affects people who have some predisposing factors (hypertension, atherosclerosis, Marfan syndrome, pregnancy in women with pre-existing aortic root dilation).<br />In addition to the pain, which is the most common manifestation, other manifestations may also be present or even predominate in the clinical picture, depending on the location and the extent of the dissection and its associated complications. Such manifestations include symptoms and signs of acute heart failure (due to acute severe aortic regurgitation), hypotension, syncope, or even cardiac arrest (due to a rupture of the aorta into the pericardial space causing tamponade), stroke, paraplegia. The last two (neurologic) manifestations are due to an obstruction of arteries involved in the perfusion of the brain, or the spinal cord, respectively. Rarely (in 1–2% of proximal aortic dissections) an acute myocardial infarction occurs, resulting from the </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">occlusion of a </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">coronary artery (more commonly the right coronary artery is involved). The patient with acute aortic dissection may present with elevated, normal or low blood pressure.</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> Many patients present findings similar to the manifestations of an internal hemorrhage: pallor, perspiration (sweating), tachycardia, a low blood pressure of a previously hypertensive patient, and a decrease in the values of the hematocrit and hemoglobin. In case of a proximal aortic dissection, cardiac auscultation may reveal a high pitched decrescendo early-diastolic murmur of aortic regurgitation.</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">As already mentioned, blood flow to arteries arising from the area of the dissection is often interrupted and this can result in weak or absent pulses of the arteries of an upper or lower limb or an unpalpable pulse of a carotid artery or in the development of stroke symptoms (eg hemiparesis or hemianesthesia), hematuria, oliguria or anuria resulting from an obstruction of the renal arteries.</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Imaging tests and the diagnosis of aortic dissection</span></h4>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The chest X-ray often shows a widened mediastinum due to aortic dilation. In some cases a pleural effusion (hemothorax) is also present.</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br />Echocardiography (transthoracic and transesophageal), with the latter being much more useful) displays important findings: The aorta is usually appears dilated. </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">The most characteristic finding of an aortic dissection is the intimal flap, a linear structure with a pulsatile motion in the aorta, which separates two spaces filled with blood, the two lumens: </span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">a) The false lumen consists of blood which has entered the aortic wall. It often demonstrates slower blood flow (an appearance of spontaneous contrast which resembles "smoke" may be present in the false lumen) or occasionally a blood clot may form in the false lumen</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">b) The true lumen, i.e, blood that flows inside the aorta. </span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The true lumen is distinguished from the false by the different flow characteristics. The true lumen appears with color Doppler examination to fill with blood that flows with a higher velocity in systole than the blood velocity in the false lumen. In the false lumen, varying flow at slower velocities is demonstrated and/or areas with partial or complete thrombosis.</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> The point of entry of blood from the true lumen into the false lumen (the site of the intimal tear) may appear as a small area of turbulent flow with color Doppler examination. The false lumen is usually larger than the true lumen in diastole, whereas the true lumen expands during the phase of cardiac systole. The intimal flap in systole usually moves toward the false lumen. The one-dimensional M-mode echocardiography can be used to demonstrate more clearly the motion of the intimal flap: The intimal flap moves in the opposite direction than the aortic wall during the cardiac cycle. .<br />Transesophageal echocardiography (TEE) has the advantage of excellent sensitivity and specificity for the diagnosis of a dissection of the thoracic aorta, whereas transthoracic echocardiography is less sensitive and less specific than TEE.<br />Other imaging tests which can clearly depict with excellent sensitivity and specificity the false and the true lumen and the intimal flap, thus making the diagnosis of aortic dissection are the following: 1) Computed tomography with intravenous contrast (which is the imaging modality most often used for the diagnosis of aortic dissection) It is usually the modality of choice for hemodynamically stable patients, but TEE is usually preferred for unstable patients. 2) Magnetic resonance imaging (MRI), 3) Aortography (although previously considered as the gold standard, currently it has been largely replaced by the newer noninvasive imaging techniques). </span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Note: D-dimers (which are degradation products of plasma fibrin and fibrinogen) can also be considered as a useful but nonspecific test. This blood test can</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> be a part of the initial workup when aortic dissection is suspected, because a negative result makes the presence of aortic dissection less likely.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><span style="background-color: orange;"><br /></span></span>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><span style="background-color: orange;">Video</span>: </span><span face="" style="font-family: arial, helvetica, sans-serif; font-size: medium;"><b>The following video is an overview of acute aortic dissection with a presentation of cases and findings on imaging tests ( transesophageal echocardiography, transthoracic echocardiography, chest X-ray, CT scan of the aorta, magnetic resonance imaging-MRI). After the case presentation, a summary of the etiology, diagnosis, and treatment of aortic dissection follows. I would like to thank my colleagues Ioannis Dernellis and Lambros Lakkas who have contributed images for this video. If you want to view the video in a large size, after you start it, you can click on the [] symbol at the bottom right of the video. (whereas you can return to a small size by pressing the esc key).</b></span><br />
<span face="" style="font-family: arial, helvetica, sans-serif; font-size: medium;"><b><br /></b></span>
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<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Prognosis</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In acute type A aortic dissection, without treatment mortality in the first 48 hours is 1% per hour. In general, death in aortic dissection is due to (a) </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">cardiac tamponade from hemorrhage into the pericardium.</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">(b) aortic rupture, or (c) </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">propagation of the dissection, leading to occlusion of arterial branches of the aorta.</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">The prognosis can be improved by prompt and appropriate treatment.</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><br /></span>
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<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Treatment of aortic dissection:</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large; font-weight: normal;">In acute type A dissection: Surgery is required promptly. </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">In acute type B dissection, if the patient is stable, with no complications or evidence of propagation of the dissection, only conservative (medical) treatment is provided. </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">In a chronic dissection if the patient is stable, without complications and without signs of propagation, conservative treatment is also administered.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"> Conservative (drug) treatment is also provided to patients who have an indication for surgery, as the initial treatment until they are transferred to the operating room as soon as possible, and it is also administered as the only treatment to patients who have no indication for surgery.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">The goal of drug therapy is to avoid propagation of the dissection, by reducing contractility of the left ventricle (so that it does not propel blood with a great force into the aorta), as well as by controlling blood pressure, if hypertension is present. In cases with hypertension, systolic pressure should be reduced to 100–120 mmHg. Analgesic treatment (morphine sulfate intravenously) is also given. I</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">n acute aortic dissection, a</span><span face="" style="font-family: times, "times new roman", serif; font-size: large;"> beta-blocker is initially administered intravenously, whereas in chronic aortic dissection a beta-blocker is administered orally. Α beta-blocker is administered not only when blood pressure is elevated, but also when it is normal. The reason is that beta-adrenergic receptor blockade reduces myocardial contractility, thereby reducing the rate of pressure rise (dP / dt) within the aorta. This action limits the expansion of the dissection, provided that there is no significant contraindication to the administration of a beta-blocker. The dose of the beta-blocker should be adjusted so that the heart rate is maintained at approximately 60-65 beats/ min. If blood pressure remains elevated after the administration of a beta-blocker, a vasodilator drug is added. In acute dissection of the aorta with a blood pressure above the desired target, the vasodilator drug sodium nitroprusside is administered intravenously. </span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">To patients with acute heart failure due to acute aortic valve regurgitation (caused by the dissection), drugs that reduce contractility (such as beta-blockers) are not administered. In this case, only vasodilators (sodium nitroprusside) are indicated for the treatment of hypertension. In chronic aortic dissection, other antihypertensive drugs, such as an ACE-inhibitor, or a calcium channel antagonist are added to the treatment with a beta-blocker, when needed to control blood pressure. In patients with an aortic dissection, the arterial blood pressure must be strictly controlled.</span><br />
<h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Drug dosages:</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Beta-blockers:<br />Atenolol 5–10 mg in slow intravenous injection. After 15 minutes 50 mg orally (PO) , after 12 hours 25-50 mg PO and then treatment is continued with 50-100 mg PO daily. Alternatively: <br />Propanolol intravenously 0.5-1 mg every 2–5 min until heart rate is reduced to 60-70 beats/ min (maximal dose 10 mg). Then usually 1 mg every 3-6 hours is administered intravenously. When oral medication is started, the dose is 10–40 mg PO x 3–4 times/day.<br /><br />Sodium Nitroprusside: It is administered by intravenous infusion of 0.25–10 µg / kg body weight / min.</span></div>
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<span face="" style="font-family: times, "times new roman", serif; font-size: large;">(mg = milligram / μg = microgram).</span><br />
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<h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Other acute aortic syndromes</span></h3>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Patients with these syndromes (aortic intramural haematoma and penetrating aortic ulcer) have the same risk factors and several similarities in the clinical picture with patients with acute aortic dissection. However, these patients tend to be older (regarding their mean age) compared to those with aortic dissection. While the pain occurring in these two acute aortic syndromes is similar to the pain of acute aortic dissection, clinical manifestations of arterial occlusion are less common, because these syndromes are typically characterized by a more localized aortic lesion. </span></div><div dir="ltr" trbidi="on"><h4 style="text-align: left;"><span face="" style="font-family: times, "times new roman", serif; font-size: large;">Aortic intramural hematoma</span></h4>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Aortic intramural hematoma is characterized by the presence of blood inside the aortic media (the middle layer of the aortic wall). This is thrombosed blood without flow. Imaging techniques do not demonstrate a visible site of rupture of the inner layer of the aortic wall (intimal tear) in contrast to aortic dissection. Also in contrast to aortic dissection, there is no intimal flap and one or more sites of return of blood from the aortic wall back to the true aortic lumen are not present. Pain may occur due to the dilatation of the outer layer (adventitia) of the aortic wall.</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">Intramural hematoma (IMH) is etiologically attributed to:</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">-Rupture of vessels of the aortic wall (small arteries that supply blood to the aortic wall- vasa vasorum) or</span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"></span><br />
<span face="" style="font-family: times, "times new roman", serif; font-size: large;">-In a few patients, an intimal tear may be present, which </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">is not detectable, </span><span face="" style="font-family: times, "times new roman", serif; font-size: large;">due to its small size, with blood entering the aortic wall and subsequent thrombosis of this intramural blood.</span><br />
<span style="font-size: large;"><div dir="ltr" style="font-size: large;" trbidi="on">
<span style="font-size: large;"><br /></span></div></span></div><br /><span style="font-size: 14pt;">A CT
angiography of the aorta depicts a thickening of the aortic wall with a
crescentic shape and relatively high density. It is not enhanced by the
contrast medium and involves a short or long segment of the aorta. On magnetic
resonance imaging (MRI) the intramural hematoma in the acute phase (within the
first 24-72 hours) in the T1 sequences appears as a crescentic (semilunar) or
circular thickening of the arterial wall of approximately the same density
(signal strength) as the aortic wall, while in T2 sequences it is depicted as a
signal of increased intensity (white). After the first 24-72 hours, it appears
as a signal of increased intensity within the wall also in T1 sequences due to
the change in hemoglobin from oxyhemoglobin to meta-hemoglobin</span>.<br /><div dir="ltr" trbidi="on"><span style="font-size: large;"><br /></span><i>Aortic CT angiography: What do the arrows show? </i><span style="font-size: large;"><div dir="ltr" style="font-size: large;" trbidi="on"><i><br /></i></div><div dir="ltr" style="font-size: large;" trbidi="on"><i><br /></i></div><div dir="ltr" style="font-size: large;" trbidi="on"><img height="426" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKPh97HaTsKQLvyAjQSzpVcri5logrO4CeNQ22p49SY4vzj60tcJxkdt9aLmakTMr2sXQHQP938xJd6s83KKvEZVeJ3moBbXTaTTX_Z_ctXuTYsHsK6FxlKJ2T-RkRehEtxTs2ZRqBOM27/w380-h426/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25B1%25CE%25BF%25CF%2581%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C+%25CE%25B5%25CE%25BD%25CE%25B4%25CE%25BF%25CF%2584%25CE%25BF%25CE%25B9%25CF%2587%25CF%2589%25CE%25BC%25CE%25B1%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C+%25CE%25B1%25CE%25B9%25CE%25BC%25CE%25AC%25CF%2584%25CF%2589%25CE%25BC%25CE%25B1+CT.png" style="font-size: medium; text-align: center;" width="380" /></div><div dir="ltr" style="font-size: large;" trbidi="on"><i><br /></i></div></span><i>1. intramural hematoma in the ascending aorta 2. intramural hematoma in the descending thoracic aorta 3. sternum, 4. ascending aortic lumen (shown white due to the intravenous contrast), 5. right pulmonary artery, 6. left atrium, 7.body of thoracic vertebra, 8. right lung, 9. left lung, 10. lumen of the descending thoracic aorta</i><span style="font-size: large;"><div dir="ltr" style="font-size: large;" trbidi="on"><i><br /></i></div><div dir="ltr" style="font-size: large;" trbidi="on"><i><br /></i></div><p><span lang="EN-US" style="color: #222222; font-size: 14.0pt; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">A penetrating aortic ulcer (PAU) is an erosion
of an atherosclerotic plaque that penetrates the inner layer of the aortic wall
(intima) and reaches deeper into the middle layer (media). It is often
accompanied by the formation of an intramural hematoma. Often aortic ulcers can
be multiple and their depth may vary from 4 to 30 mm. Typical patients are
elderly (> 70 years) and often have diffuse and extensive atherosclerotic
disease of both the aorta and the coronary arteries. In transesophageal
echocardiography, a penetrating ulcer of the aorta is imaged as a focal
outpouching of the aortic lumen, which resembles a crater entering into the
vessel wall. This is located at the site of an atherosclerotic plaque. Color
Doppler shows that blood enters this crater. It can often be accompanied by an
intramural hematoma. <o:p></o:p></span></p>
<p><span lang="EN-US" style="color: #222222; font-size: 14.0pt; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">MRI also shows a penetrating ulcer of the
aorta as a crater-like wall lesion that penetrates into the media. Magnetic
angiography (MRI with intravenous administration of contrast) shows that the
lumen of the artery forms in that position an outpouching that enters the
vascular wall. <o:p></o:p></span></p>
<p><span lang="EN-US" style="color: #222222; font-size: 14.0pt; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">The diagnostic imaging technique of choice is
computed tomography with intravenous contrast (CT angiography of the aorta). In
this imaging test, a penetrating aortic ulcer appears as a focal outpouching of
the aortic lumen. The contrast medium enters this lesion and gives the
appearance of a crater-shaped protrusion of the lumen into the vascular wall.
When this crater increases in size on consecutive imaging, then there is a
clear indication that the lesion is unstable, with a risk of dissection or
rupture of the aorta, and requires invasive treatment. Treatment is most often
endovascular with the placement of an endovascular stent-graft.<o:p></o:p></span></p></span></div><div dir="ltr" trbidi="on"><div dir="ltr" trbidi="on"><div dir="ltr" trbidi="on"><span style="font-size: large;"><div dir="ltr" style="font-size: large;" trbidi="on"><br /></div><div dir="ltr" style="font-size: large;" trbidi="on"><img height="229" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh-pAIjI70HOt4Hz-XZKXQOgUs2CDusSsOeSRvXtAw5VjERnPnjmj0fCk-v4k9H4JRbbaEzlDcNuJM4O_he18zNnpwksNXA3sHGx-CllXv2AdeJv6X2NsiPRxFl7I6zh6ujEyA6k1K0C9Vs/w345-h229/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BB%25CE%25B5%25CF%2580%25CF%2584%25CE%25BF%25CE%25BC%25CE%25AD%25CF%2581%25CE%25B5%25CE%25B9%25CE%25B1+%25CE%25B1%25CF%2580%25CF%258C+%25CE%25B1%25CE%25BE%25CE%25BF%25CE%25BD%25CE%25B9%25CE%25BA%25CE%25AE+%25CF%2584%25CE%25BF%25CE%25BC%25CE%25BF%25CE%25B3%25CF%2581%25CE%25B1%25CF%2586%25CE%25AF%25CE%25B1+%25CE%25BC%25CE%25B5+%25CE%25B4%25CE%25B9%25CE%25B1%25CF%2584%25CE%25B9%25CF%2584%25CF%2581%25CE%25B1%25CE%25AF%25CE%25BD%25CE%25BF%25CE%25BD+%25CE%25B1%25CE%25BF%25CF%2581%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C+%25CE%25AD%25CE%25BB%25CE%25BA%25CE%25BF%25CF%2582.png" width="345" /></div></span><i><br /><br />Detail from a CT aortic angiography. The descending thoracic aorta (1) is atherosclerotic and aneurysmal with the presence of a penetrating ulcer (2) and intramural hematoma. (3. thoracic vertebral body)</i></div><div dir="ltr" trbidi="on"><i><br /></i><span style="font-size: large;"><div dir="ltr" style="font-size: large;" trbidi="on"><p><span lang="EN-US" style="color: #222222; font-size: 14.0pt; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">The symptoms (pain) of a penetrating aortic
ulcer are similar to those of aortic dissection, except that the penetrating
ulcer usually does not cause aortic valve insufficiency or occlusion of
arterial branches of the aorta. In some cases, an asymptomatic penetrating ulcer
of the aorta may be found as an incidental finding on imaging performed for
another indication. A penetrating aortic ulcer may develop complications such
as intramural hematoma of the aorta, aortic dissection, pseudoaneurysm, or
rupture of the aortic wall. Patients with penetrating ulcers have a higher risk
of aortic rupture compared to patients with aortic dissection.<o:p></o:p></span></p>
<p><span lang="EN-US" style="color: #222222; font-size: 14.0pt; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">Regarding treatment, the same principles
mentioned above also apply for an aortic intramural hematoma. That is, in type
A penetrating ulcer, as a rule, surgical treatment is required, whereas for
type B, medical treatment with clinical and imaging follow-up. In type B
lesions with a complicated course (with signs of threatened rupture of the
aorta) invasive treatment is performed (endovascular treatment with the
placement of a stent-graft), whereas surgical treatment is performed when this
is not technically possible.<o:p></o:p></span></p></div></span></div></div><div><br /></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b style="background-color: #ea9999; color: rgba(0, 0, 0, 0.87); font-family: times, "times new roman", serif; font-size: x-large; line-height: 28px; text-align: center; white-space: pre-wrap;">Bibliography </b></span><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>Apostolakis E, Papakonstantinou NA, Baikoussis NG, Petrou A, Goudevenos J.Imaging of acute aortic syndrome: advantages, disadvantages and pitfalls. (Hellenic J Cardiol. 2015 ;56:169-80. </b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b style="font-family: arial, helvetica, sans-serif; text-align: start;">LINK </b><b> <a href="http://www.hellenicjcardiol.org/archive/full_text/2015/2/2015_2_169.pdf" target="_blank">http://www.hellenicjcardiol.org/archive/full_text/2015/2/2015_2_169.pdf</a></b></span><span face="" style="font-family: arial, helvetica, sans-serif; font-size: medium;"><b><br /></b></span><b><span face="" style="font-family: arial, helvetica, sans-serif;"><br /></span></b><br />
<b><span face="" style="font-family: arial, helvetica, sans-serif;">Goldfinger JZ1, Halperin JL1, Marin ML, et al. </span></b><b><span face="" style="font-family: arial, helvetica, sans-serif;">Thoracic aortic aneurysm and dissection.</span></b><b><span face="" style="font-family: arial, helvetica, sans-serif;"><a href="https://www.ncbi.nlm.nih.gov/pubmed/25323262#">J Am Coll Cardiol.</a> 2014 Oct 21;64:1725-39. doi: 10.1016/j.jacc.2014.08.025. </span></b><span face="" style="font-family: arial, helvetica, sans-serif;"><b style="font-family: arial, helvetica, sans-serif; text-align: start;">LINK </b><b> <a href="https://www.clinicalkey.com/#!/content/playContent/1-s2.0-S0735109714060082?returnurl=http:%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0735109714060082%3Fshowall%3Dtrue&referrer=https:%2F%2Fwww.ncbi.nlm.nih.gov%2F" target="_blank">https://www.clinicalkey.com/#!/content/playContent/1-s2.0-S0735109714060082?returnurl=http:%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0735109714060082%3Fshowall%3Dtrue&referrer=https:%2F%2Fwww.ncbi.nlm.nih.gov%2F</a></b></span><br />
<span face="" style="font-family: arial, helvetica, sans-serif; font-size: medium;"><b><br /></b></span><span face="" style="font-family: arial, helvetica, sans-serif; font-size: medium;"><b>Coulon C. Thoracic aortic aneurysms and pregnancy. Presse Med. (2015), http://dx.doi.org/10.1016/j</b></span><br />
<span face="" style="font-family: arial, helvetica, sans-serif; font-size: medium;"><b><br /></b></span>
<b><span face="" style="font-family: arial, helvetica, sans-serif;">Mussa FF, Horton JD, Moridzadeh R, et al. Acute Aortic Dissection and Intramural Hematoma: A Systematic Review.<a href="https://www.ncbi.nlm.nih.gov/pubmed/27533160#">JAMA.</a>2016;316:754-63.doi:10.1001/jama.2016.10026.</span></b></div>
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<b style="font-family: arial, helvetica, sans-serif; text-align: start;">LINK</b><b><span face="" style="font-family: arial, helvetica, sans-serif;"><a href="https://air.unimi.it/retrieve/handle/2434/450334/782315/2016-JAMA%20Trimarchi_AAD_IMH_Review.pdf" target="_blank">https://air.unimi.it/retrieve/handle/2434/450334/782315/2016 JAMA%20Trimarchi_AAD_IMH_Review.pdf</a></span></b></div>
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<a href="https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/eurheartj/35/41/10.1093_eurheartj_ehu281/1/ehu281.pdf?Expires=1502065686&Signature=eamsf05xpB7OO0v6LTf2vByFTalJCaPqhuvj8qOjG5zYd0GHrUYALlNQB4YCT8BNGtcYa4zn4u1cPSV2P50J83YwvKA-QMzyEoKUA8KaryNjdetYLwLqqhiiBRZ3mQ~hWRXZA0L~JqwTAU97cfZBk-MKsVtr-NRYahXPvGzQh63mhP6IwN2ctdWqsjEFJOkT78Rm-VYFEE-~jdOiwvawsW4VebkWSlZHKQLzmwixURAsgoG0S8H9p0tUEMZYvsDcC7n6o74ZXO-wPfxwSPzO-BPzu0F4rx~z~kt5kuycTGA2~29OdJ7CXgODxQCSg958UdMeWZ4KoNBsyX4yMD-0zA__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q" target="_blank"><br /></a></div>
<span face="" style="font-family: arial, helvetica, sans-serif;"><b>2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult.The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC), European Heart Journal 2014;35: 2873 -2926, <a href="https://doi.org/10.1093/eurheartj/ehu281">https://doi.org/10.1093/eurheartj/ehu281</a></b></span><br />
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<b style="font-family: arial, helvetica, sans-serif;">LINK </b><b><span face="" style="font-family: arial, helvetica, sans-serif;"> <a href="https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/eurheartj/35/41/10.1093_eurheartj_ehu281/1/ehu281.pdf?Expires=1502065686&Signature=eamsf05xpB7OO0v6LTf2vByFTalJCaPqhuvj8qOjG5zYd0GHrUYALlNQB4YCT8BNGtcYa4zn4u1cPSV2P50J83YwvKA-QMzyEoKUA8KaryNjdetYLwLqqhiiBRZ3mQ~hWRXZA0L~JqwTAU97cfZBk-MKsVtr-NRYahXPvGzQh63mhP6IwN2ctdWqsjEFJOkT78Rm-VYFEE-~jdOiwvawsW4VebkWSlZHKQLzmwixURAsgoG0S8H9p0tUEMZYvsDcC7n6o74ZXO-wPfxwSPzO-BPzu0F4rx~z~kt5kuycTGA2~29OdJ7CXgODxQCSg958UdMeWZ4KoNBsyX4yMD-0zA__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q" target="_blank">2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC)</a></span></b><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. Circulation. 2010;121:e266-e369</b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b style="font-family: arial, helvetica, sans-serif;">LINK </b><b> <a href="http://circ.ahajournals.org/content/121/13/e266" target="_blank">Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. Circulation. 2010</a></b></span></div>
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<b><span face="" style="font-family: arial, helvetica, sans-serif;">Clough RE, Nienaber CA. Management of acute aortic syndrome.<a href="https://www.ncbi.nlm.nih.gov/pubmed/25511084#">Nat Rev Cardiol.</a> 2015:103-14. </span></b><br />
<b><span face="" style="font-family: arial, helvetica, sans-serif;"><br /></span></b>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"><b style="font-family: "times new roman"; font-size: medium;"><span face="" style="font-family: arial, helvetica, sans-serif;">Weinreich M, Yu P, Trost B. Sinus of Valsalva Aneurysms: Review of the Literature and an Update on Management. Clin Cardiol 2015; 38:185-189.</span></b></span><br />
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<b style="font-family: arial, helvetica, sans-serif;">LINK </b><span face="" style="font-family: arial, helvetica, sans-serif;"><b> <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/clc.22359#" target="_blank">Sinus of Valsalva Aneurysms</a></b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b><br /></b></span></div>
<span face="" style="font-family: times, "times new roman", serif; font-size: large;"></span><br />
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<b><span face="" style="font-family: arial, helvetica, sans-serif;">Weinreich M, Yu P, Trost B. Sinus of Valsalva Aneurysms: Review of the Literature and an Update on Management. Clin Cardiol 2015; 38:185-189.</span></b><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>LINK <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/clc.22359#" target="_blank">Sinus of Valsalva Aneurysms</a></b></span><br />
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b><br /> Antonello M.Ruptured Abdominal Aortic Aneurysms Intechopen DOI: 10.5772/19740</b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>LINK<a href="https://www.intechopen.com/books/diagnosis-screening-and-treatment-of-abdominal-thoracoabdominal-and-thoracic-aortic-aneurysms/ruptured-abdominal-aortic-aneurysms" target="_blank">https://www.intechopen.com/books/diagnosis-screening-and-treatment-of-abdominal-thoracoabdominal-and-thoracic-aortic-aneurysms/ruptured-abdominal-aortic-aneurysms</a></b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>Abdominal aortic aneurysm Medscape-emedicine </b></span></div>
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<span face="" style="font-family: arial, helvetica, sans-serif;"><b>LINK<a href="https://emedicine.medscape.com/article/1979501-overview#showall" target="_blank">https://emedicine.medscape.com/article/1979501-overview#showall</a></b></span><span face="" style="font-family: arial, helvetica, sans-serif;"><br /></span></div>
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</div>Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-58146459796981986822018-10-07T19:53:00.000+03:002018-10-07T20:16:22.983+03:00Acute pulmonary embolism<h2>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Acute pulmonary embolism</span></h2>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">This is an obstruction of a branch of the pulmonary artery by thrombus originating in the systemic venous system (most commonly in the lower extremity or deep pelvic veins). The thrombus travels through the venous system into the right heart chambers and from there it lodges in the pulmonary artery.</span><br />
<span style="font-size: large;">Chest pain of sudden onset, accompanied by dyspnea, cough, and in some cases hemoptysis, developing </span><span style="font-size: large;">in a patient who has been immobilized or bedridden or has a recent history of surgery, pelvic or lower extremity injury or cancer is suggestive of pulmonary embolism.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In patients with acute pulmonary embolism, the most common symptom is dyspnea of sudden onset, followed by chest pain.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Risk factors that may predispose to the development of pulmonary embolism are the following :</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A recent history of abdominal, pelvic or lower extremity surgery</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Low extremity or pelvic trauma</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A patient with a previous history of thromboembolism, or family history of thromboembolism</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Paralysis, immobility, lower extremity casting or immobility</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cancer and some chemotherapeutic agents</span></div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Estrogen use (hormone replacement/ oral contraceptives)</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pregnanc</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">y</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Indwelling central venous catheters, p</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">acemaker or implantable cardiac defibrillator leads</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Congestive heart failure</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Chronic kidney disease including nephrotic syndrome</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Long distance air travel</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Advancing age</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Symptoms and clinical findings of pulmonary embolism</span></h3>
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<span style="font-size: large;">Chest pain of sudden onset, accompanied by dyspnea, cough, and in some cases hemoptysis developing </span><span style="font-size: large;">in a patient who has been immobilized or bedridden is suggestive of pulmonary embolism</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In patients with acute pulmonary embolism, the most common symptom is dyspnea of sudden onset. Depending on the severity of the pulmonary embolism and the patient's condition, dyspnea (shortness of breath) may be prominent at rest or it may be minimal at rest but worsening during activity. Chest pain (often -but not always-pleuritic) and cough are also common. Low-grade fever occurs in some patients. Hemoptysis also occurs in some cases. In a massive pulmonary embolism, there is severe dyspnea, cyanosis, or syncope and the patient commonly is hypotensive.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The most common clinical findings are tachypnea and tachycardia.<br />A massive pulmonary embolism manifests with hypotension and cardiogenic shock. A large but submassive pulmonary embolism will not manifest hypotension but it will exhibit signs of right ventricular failure (tachycardia, jugular venous distension, tricuspid<br />regurgitation) or of elevated pulmonary arterial pressure (an accentuated pulmonic component of the second heart sound-P2). These patients also have an increased risk of early mortality, although the risk is less than in a massive pulmonary embolism. An acute pulmonary embolism with normal systemic blood pressure and no evidence of right ventricular dysfunction when managed with standard therapeutic anticoagulation, generally will demonstrate a benign hospital course.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pulse oxymetry and arterial blood gases: A </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">low arterial oxygen saturation, either from pulse oximetry </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">or arterial blood gases in the absence of an adequate explanation ( e.g. acute left sided </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">heart failure, chronic obstuctive pulmonary disease or pneumonia) should raise </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">suspicion for pulmonary embolism. A normal oxygen saturation cannot exclude pulmonary embolism.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">ECG </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The most common (but nonspecific) finding in the electrocardiogram (ECG) </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">is sinus tachycardia.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Other findings that may be present in acute pulmonary embolism include right ventricular strain (</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> a right bundle branch block and T-wave inver-</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">sions in the precordial leads, especially the right ones) or the classic, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">but less com</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">mon, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">S1Q3T3 pattern (deep S</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> wave in lead I, Q wave in lead III, and T-wave </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">inversion in lead III ). </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The chest X-ray in pulmonary embolism in many cases does not demonstrate significant findings, in some cases it shows nonspecific findings such as </span><span style="font-size: large;">atelectasis, an </span><span style="font-size: large;">elevated hemidiaphragm, or a pleural </span><span style="font-size: large;">effusion, and in some patients it demonstrates classical signs of pulmonary embolism such as the </span><span style="font-size: large;">Westermark's sign or a </span><span style="font-size: large;">pleural-based wedge-shaped consolidation. </span></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Diagnosis:</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> In patients with a moderate or high index of clinical suspicion CT pulmonary angiography or a ventilation perfusion scan ( V/Q) scan will establish the diagnosis or exclude it. Note that</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> in many cases a V/Q scan can provide diagnosis, but it has the disadvantage of a high number </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">of indeterminant studies, where </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">subsequent imaging (usually CT -pulmonary angiography) will be required. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The most accurate test is pulmonary angiography, but it is an invasive test. </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In patients with a low probability of pulmonary embolism a negative sensitive D-Dimers test excludes the diagnosis of pulmonary embolism, whereas if the test is positive, a CT pulmonary angiography ( or a V/Q scan) will be required. The reason for this is that elevated D-dimers are sensitive but have a low specificity.</span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">A patient complaining of chest pain, worse with deep respiration, cough, and mild dyspnea. Recent surgery for a femoral fracture. What are the findings in this chest X ray?</span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj-7y2OVJXw7v5FRW-wFhkIBzQh5taN58fsRseTSKyJk1F4AajQo9AxvR85VW5ZLPwxkb22lGGI9OYZ5sX6ftPxlu81P4QEvy0qa_G9Y8g65hl9D1jWak_TqEBDFB_XVNBinaTTNaIhmL4/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2580%25CE%25BD%25CE%25B5%25CF%2585%25CE%25BC%25CE%25BF%25CE%25BD%25CE%25B9%25CE%25BA%25CE%25AE+%25CE%25B5%25CE%25BC%25CE%25B2%25CE%25BF%25CE%25BB%25CE%25AE+%25CE%25AD%25CE%25BC%25CF%2586%25CF%2581%25CE%25B1%25CE%25BA%25CF%2584%25CE%25BF+%25CE%25B1%25CF%2580%25CF%258C+%25CF%2580%25CE%25B1%25CF%2581%25CE%25BF%25CF%2585%25CF%2583%25CE%25AF%25CE%25B1%25CF%2583%25CE%25B7+%25CE%2586%25CE%25BD%25CE%25B8%25CE%25B7.png" style="clear: left; margin-bottom: 1em; margin-right: 1em;"><img alt="" border="0" height="317" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj-7y2OVJXw7v5FRW-wFhkIBzQh5taN58fsRseTSKyJk1F4AajQo9AxvR85VW5ZLPwxkb22lGGI9OYZ5sX6ftPxlu81P4QEvy0qa_G9Y8g65hl9D1jWak_TqEBDFB_XVNBinaTTNaIhmL4/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2580%25CE%25BD%25CE%25B5%25CF%2585%25CE%25BC%25CE%25BF%25CE%25BD%25CE%25B9%25CE%25BA%25CE%25AE+%25CE%25B5%25CE%25BC%25CE%25B2%25CE%25BF%25CE%25BB%25CE%25AE+%25CE%25AD%25CE%25BC%25CF%2586%25CF%2581%25CE%25B1%25CE%25BA%25CF%2584%25CE%25BF+%25CE%25B1%25CF%2580%25CF%258C+%25CF%2580%25CE%25B1%25CF%2581%25CE%25BF%25CF%2585%25CF%2583%25CE%25AF%25CE%25B1%25CF%2583%25CE%25B7+%25CE%2586%25CE%25BD%25CE%25B8%25CE%25B7.png" title="Quiz chest X-ray-chest pain-emergency medicine book" width="400" /></a><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /><br /><br />In the lower right lung, there is a wedge-shaped consolidation with its base against the pleural surface. This radiographic sign and also the patient's history is highly suggestive of a pulmonary embolism.</span></b><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment of pulmonary embolism</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Therapeutic anticoagulation is needed promptly because it reduces mortality in acute symptomatic pulmonary embolism. This anticoagulant treatment is the same as in acute deep venous thrombosis. Some usual treatment options are presented here:</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Low-molecular-weight heparin (LMWH) 100 U /kg</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">every 12 hours (e.g. enoxaparin) or 200 U/kg once per day. Another choice of LMWH is tinzaparin 175 U /Kg SC x 1 time/day.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">LMWH does not require any blood test for treatment monitoring (in contrast to unfractionated heparin). It is contraindicated in severe renal failure</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> or</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Unfractionated heparin 80 U/kg IV bolus, followed by</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> 18 U/kg/hour IV infusion. The dose of the IV infusion is adjusted to achieve activated partial thromboplastin </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">time (aPTT) 1.5 to 2.5 times the control value</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> or</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Unfractionated heparin 17,500 U SC x 2 times/day ( </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">17,500 U SC </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">every 12 hours). The dose is adjusted to achieve the above target aPTT. </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A vitamin K antagonist (VKA), warfarin or acenocoumarol can be started on the first or second day of treatment and must be overlapped with </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">heparin for 4-5 days, and until target international normalized ratio </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">(INR) 2 - 3 is reached. Then the parenteral anticoagulant is discontinued and treatment continuous only with the VKA.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">When a VKA is started in an acute thrombotic state, there is a decline of antithrombotic proteins C and S before the decline in coagulation factors. This causes a transient increase in thrombogenic potential, until the anticoagulant effect of the VKA starts to develop. The concomitant administration of he</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">parin (unfractionated or LMWH) during the first 5 days of treatment counteracts this transient procoagu</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">lant effect.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">For the chronic anticoagulant treatment of patients with pulmonary embolism (usually for 3-6 months) instead of a VKA, one of the newer PO anticoagulants (NOACs= non-vitamin K antagonist oral anticoagulants) can be given. In fact NOACs (dabigatran, rivaroxaban, apixaban, edoxaban are preferred over VKAs.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br />In stable patients with acute pulmonary embolism, NOACs (such as rivaroxaban, apixaban, edoxaban, and dabigatran) can now be administered as initial treatment without the need for parenteral or subcutaneous medications. NOACS should be avoided in patients with severe renal failure. Choices of |NOACs for pulmonary embolism or deep venous thrombosis include:<br />Oral rivaroxaban, a factor Xa inhibitor 15 mg x2 times/day for 3 weeks, followed by 20 mg x1/day<br />Oral dabigatran, a direct thrombin inhibitor 150<br />mg x 2 times/ day)<br />Oral apixaban, a factor Xa inhibitor, 10 mg x2/day for a week, followed by 5 mg x2/day).<br />Thrombolytic therapy in pulmonary embolism is indicated only in massive pulmonary embolism with hypotension or a pulmonary embolism with severe compromise in oxygenation (when there is a deterioration in the clinical course despite anticoagulation), in the absence of contraindications to thrombolysis. Thrombolysis provides rapid resolution of thrombus. A possible complication of thrombolytics is major bleeding ( the incidence of intracranial hemorrhage is up to 3%).<br />The usual option for thrombolysis in a massive pulmonary embolism is alteplase (t-PA= tissue plasminogen activator) 100 mg IV infusion over 2 hours. (Other choices include streptokinase and urokinase).<br />Thrombolysis is also indicated in extensive iliofemoral deep venous thrombosis.<br />In submassive pulmonary embolism, thrombolysis is controversial because it has not been proven to offer a decrease in mortality in such cases.</span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Contraindications to thrombolytic treatment include:<br />Absolute contraindications: Active bleeding, intracranial or intraspinal disorders, trauma or surgery in the preceding 2 months<br />Relative contraindications: organ biopsy, large-vessel puncture, cardiopulmonary resuscitation, within 10 days postpartum.<br />In patients with a massive pulmonary embolism, when thrombolysis is contraindicated, an alternative treatment is surgical or catheter embolectomy.<br />The placement of a filter in the inferior vena cava (IVC filter) is indicated in patients with pulmonary embolism who have a contraindication to anticoagulation, or when pulmonary embolism or deep venous thrombosis recurs despite treatment with therapeutic anticoagulation.<br />The usual duration of anticoagulation for pulmonary embolism or deep venous thrombosis is 3-6 months (most authorities generally recommend 6 months) but in cases of pulmonary embolism without a transient (reversible) predisposing factor, anticoagulation should be continued for a longer time interval, probably indefinitely.<br />For the long-term treatment for pulmonary embolism not associated with malignancy a vitamin K antagonist (warfarin or acenocoumarol) or a NOAC (e.g. rivaroxaban) is used, but generally, for the long-term treatment of pulmonary embolism associated with malignancy, a LMWH is the recommended choice.</span></span><br />
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-64511583902878788432018-07-21T13:51:00.000+03:002018-08-12T00:09:55.731+03:00Cyanotic congenital heart disease<h2>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cyanotic congenital heart disease (the most common types)</span></h2>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Generally, cyanosis is defined as a bluish discoloration of the skin and mucous </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">membranes as a result of the increased content of deoxygenated (reduced) hemoglobin in the blood. Cyanosis can be due to a reduced oxygen saturation (desaturation) of arterial blood </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">or increased extraction of oxygen from the blood. Both mechanisms lead to an </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">increased concentration of reduced hemoglobin. In general, desaturation </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">of arterial blood can be the result of decreased oxygenation of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">blood due to a pulmonary disease reducing the ability of the lungs to effectively oxygenate blood or a central nervous system </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">disease causing a reduction in ventilation. However, desaturation of arterial blood can also result from situations where mixing of oxygenated and deoxygenated blood occurs. This is the mechanism responsible for cyanosis in cyanotic congenital heart disease.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cyanotic congenital heart disease is charac</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">terized by a right to left shunt causing deoxygenated blood to enter</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> the oxygenated limb of the circulatory system. In other words,</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> systemic venous blood </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">gets shunted into the left side of the heart or into the aorta, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">bypassing the pulmonary circulation. The result is systemic arterial desaturation, i.e., a lower than normal oxygen saturation of the arterial blood causing cyanosis. </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Several types of congenital defects cause a right-to-left shunt:</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Obstruction to pulmonary blood flow in combination with a ventricular septal defect (as in tetralogy of Fallot),<br />Complete admixture of pulmonary and systemic venous returns (as in total anomalous pulmonary venous return and in double-inlet left ventricle) and</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The presence of two parallel rather than in-series circulations (as in transposition of the great arteries)<br />The most important cyanotic congenital heart defects are called the “5 Ts”</span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"> Tetralogy of Fallot </span></span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Transposition of the great arteries </span></span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Tricuspid atresia </span></span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Total anomalous pulmonary venous connection</span></span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Truncus arteriosus</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tetralogy of Fallot (</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">TOF) is the most common cyanotic congenital heart disease. The second most common is dextro-transposition of the great arteries (d-TGA).</span><br />
<h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tetralogy of Fallot (TOF)</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tetralogy of Fallot (TOF) accounts for approximately 10% of all complex congenital heart disease and it is usually diagnosed during infancy.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The four features of TOF are : </span></div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A nonrestrictive (large) ventricular septal defect (VSD) located in the membranous septum in the subaortic region.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Subpulmonic stenosis resulting in right ventricular outflow tract obstruction</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Overriding aorta, and </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Right ventricular hypertrophy (RVH).<br />The clinical manifestations (signs and symptoms) depend on the severity of the narrowing (obstruction) of the right ventricular outflow tract (RVOT) because this determines the degree of right to left shunting and the severity of cyanosis. In other words, the ratio of flows to the pulmonary and the systemic circulation (Qp/Qs) depends on the ratio of the resistance caused by the RVOTstenosis to the systemic vascular resistance (the resistance of the systemic circulation). In the usual form of TOF the RVOT stenosis is severe enough to cause cyanosis. However, there is also an acyanotic form of TOF, where the stenosis is mild and so the shunt is left to right and the clinical picture resembles that of a large ventricular septal defect (VSD).</span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> In infancy, signs and symptoms include tachypnea, dyspnea (during feeding or crying), and cyanosis. Infants and children with |TOF also demonstrate</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">poor somatic growth.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cyanosis is caused by right-to-left shunting through the VSD. This occurs because the obstruction (stenosis) of the RVOT results in an increased right ventricular pressure which favors shunting of blood from the right to the left ventricle.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tetralogy spells "Tet spells" or hypoxic spells are common. These are episodes of increased cyanosis that usually occur in events that suddenly decrease the systemic vascular resistance (SVR) such as increased physical activity, crying, defecation, or when the infant or child is in agitation, or in hypovolemia which increases RVOT stenosis. The decrease in SVR causes an increase of the right-to-left shunt. Hypoxic spells are characterized by tachypnea, hyperpnea, a decrease in the intensity of the heart murmur, and increased cyanosis. In some cases, this can be followed by loss of consciousness, seizure, and even a cerebrovascular accident or death. Older children with hypoxic spells usually have learned to find a relief in squatting. This position increases systemic vascular resistance, thus increasing left ventricular pressure and decreasing right to left shunting of blood, leading to decreased hypoxemia. Untreated adults with TOF manifest dyspnea, cyanosis, and decreased exercise tolerance or dyspnea on exertion. Cyanosis results in secondary erythrocytosis, hyperviscosity, abnormal hemostasis and predisposes to stroke. Other complications that can occur in patients with TOF are infective endocarditis and aortic regurgitation.</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Physical examination in TOF shows cyanosis, often with clubbing of the fingers. </span><span style="font-size: large;">Auscultation reveals a harsh systolic ejection murmur at the left mid and upper sternal border due to the pulmonary stenosis. The VSD produces no murmur because it is large and does not have a pressure gradient. In TOF the second heart sound (S2) is usually single because the pulmonary component is markedly reduced (due to the reduced pulmonary arterial pressure as a result of the RVOT stenosis). A prominent right ventricular impulse along the left sternal border and a systolic thrill at the upper and mid left sternal border may be present.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In TOF, the ECG shows r</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">ight ventricular hypertrophy with right QRS axis deviation and may also demonstrate right atrial hypertrophy. These findings are consequences of the RVOT obstruction. After surgical correction, a right bundle branch block (RBBB) appears on the ECG. When the QRS is markedly prolonged (> 180 ms) there is an increased risk of ventricular tachycardia and sudden cardiac death.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Chest X-ray shows a concave main pulmonary artery segment (because the RVOT obstruction results in a small pulmonary artery) and an upturned apex (due to right ventricular hypertrophy). This results in a boot-shaped heart (coeur en sabot) with diminished pulmonary vascular markings. A right aortic arch is present in 25% of the cases.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Echocardiography in TOF shows a large perimembranous VSD, an overriding aorta, the presence and the degree of RVOT obstruction and right ventricular hypertrophy.</span><br />
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<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Parasternal long axis echocardiographic view of a patient with cyanosis due to tetralogy of Fallot.<br />1 left ventricle, 2 right ventricle (It is enlarged with hypertrophied wall, 3 ventricular septal defect (VSD), 4 aorta ( the aorta is overriding the ventricular septum), 5 aortic valve, 6 mitral valve</b></span></td></tr>
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<tr><td class="tr-caption" style="text-align: left;"><b style="font-family: Arial, Helvetica, sans-serif; font-size: medium;">Parasternal long axis echocardiographic view with color Doppler of a patient with cyanosis due to tetralogy of Fallot.<br />1 right ventricle, 2 left ventricle, 3 overriding aorta, 4 left atrium. The arrow points at the flow (right to left shunt) at the VSD</b></td></tr>
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<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment of TOF </span></h4>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Neonates with severe cyanosis usually are treated with an IV infusion of prostaglandin E1 (0.01 to 0.1 mcg/kg/min ) to open the ductus arteriosus. This causes an increase in pulmonary blood flow.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">For hypoxic spells the infant is held in a knee-chest position and oxygen is usually administered, although it has a small effect. Morphine sulfate 0.1-0.2 mg/kg subcutaneously or intramuscularly can be administered to reduce hyperpnea. Intravenous propranolol 0.05 mg/kg also has a beneficial effect because it stabilizes peripheral vascular reactivity, and thus it prevents a sudden reduction of the SVR. To prevent hypoxic spells oral propranolol 2-4 mg/kg/day can be used.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Complete surgical repair of TOF generally is undertaken at the age of 4 to 12 months. Complete surgical repair, when feasible (when there is a favorable anatomy of the RVOT) generally is the treatment of choice. The ventricular septal defect (VSD) is closed with a patch, and the right ventricular outflow tract (RVOT) obstruction is relieved by resecting the obstructing hypertrophied infundibular muscle, when necessary with the additional placement of a patch at the main pulmonary artery or the pulmonic annulus and by repairing the pulmonic valve. Surgical mortality rate is 2-3%. After total repair of TOF the 25-year survival rate is 94%.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Shunt procedures may be needed in cases of pulmonary atresia, hypoplastic pulmonary annulus, hypoplastic pulmonary arteries and in infants < 3 months with severe cyanosis.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In such cases two shunt procedures </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">can be used in </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">order to increase blood flow to the lungs and hence blood oxygenation</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">:</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The Blalock Taussig shunt is the creation if an anastomosis between the subclavian artery and the ipsilateral pulmonary artery </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The Gore-Tex shunt or modified Blalock Taussig shunt is the connection of these two arteries with a tube (graft). This is the shunt procedure usually employed.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Instead of a shunt procedure, an alternative procedure to increase blood flow to the lungs is balloon dilatation of the RVOT and pulmonary arteries with or without stenting.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Most patients that have undergone a shunt procedure or balloon dilatation of the RVOT, will later need complete surgical repair unless they have developed irreversible pulmonary hypertension.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">After surgical repair, patients need regular follow up every 6-12 months.</span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Complications of TOF </span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pulmonary regurgitation (PR) can occur following transannular patch repair. Other possible complications include distal pulmonary artery stenosis or rarely pulmonary arterial hypertension (PAH). When chronic severe pulmonary regurgitation develops it results in right ventricular (RV) dilatation and dysfunction. Severe PR may warrant intervention when it is associated with substantial RV dilation, right ventricular EF < 45%, or exercise intolerance. Severe PR is treated with surgical or percutaneous replacement of the pulmonary valve.<br />Residual stenosis may occur either at the RVOT or at the pulmonary valve. Intervention is required if the RV systolic pressure is ≥ 2/3 of the arterial systolic pressure. <br />Another possible complication of surgically corrected TOF is the development of an RVOT aneurysm.<br />Some patients have a residual VSD. If it is large, it can lead to left ventricular (LV) volume overload. The cause is either incomplete closure at the time of surgery or partial dehiscence of the patch. A residual VSD with a shunt > 1.5 : 1 will probably need surgical intervention.<br />Aortic root dilatation with aortic regurgitation (AR) is another possible complication of TOF. Surgical treatment will be needed if there is severe symptomatic AR, or severe AR with progressive left ventricular dilatation, or an aortic root diameter ≥ 5.5 cm.<br />Left ventricular (LV) dysfunction can occur as a result of LV volume overload. It may be due to a delayed repair of the tetralogy, a longstanding palliative shunt, a residual VSD, or severe aortic regurgitation.<br />Patients with corrected TOF may develop arrhythmias, such as atrial fibrillation or ventricular tachycardia (VT). The development of arrhythmias is often a sequela of hemodynamic deterioration.<br />Endocarditis may complicate TOF, although it rarely occurs.</span><span style="font-size: large;"><br /></span>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Complete transposition of the Great Arteries (d-TGA)</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br />Transposition of the great arteries (TGA) is defined by a discordant ventriculoarterial connection, i.e. the great arteries arise from the wrong ventricle. </span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">In the complete (d-) transposition the aorta originates from the right ventricle with a position in front and to the right of the pulmonary artery and the pulmonary artery arises from the left ventricle. </span><span style="font-size: large;">This results in two parallel circulations in contrast to the normal anatomy and physiology, where the s</span><span style="font-size: large;">ystemic and pulmonary circulation are in series.</span><span style="font-size: large;"> In d-TGA, the desaturated systemic venous blood enters </span><span style="font-size: large;">the right atrium, then through the tricuspid valve the right ventricle </span><span style="font-size: large;">and then the aorta, and flows into the arterial system. Thus unoxygenated blood enters the systemic arteries. It passes through the capillaries of the tissues and then it returns through the venous system to the right atrium</span><span style="font-size: large;">. </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the other circuit, the oxygenated pulmonary venous blood passes through the left atrium, the mitral valve and the left ventricle to the pulmonary artery. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Through the pulmonary artery it enters the pulmonary circulation </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">and then back to the pulmonary </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">veins and to the left atrium. These two parallel circulations would not permit the flow of oxygenated blood through the systemic arteries to the tissues without the presence of a communication between the two circulations. Thus, f</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">or life to be possible, some communication between the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">two circulations must exist after </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">birth. In many patients, the only communication between the two parallel circulations, which allows mixing of oxygenated and unoxygenated blood, is a patent foramen ovale or a patent ductus arteriosus, without any other associated defects (simple transposition). A patent ductus arteriosus</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> (PDA) is present in 2/3 of the patients with d-TGA, and a ventricular septum defect is present in 1/3 of the patients</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Another abnormality that may be present in up to 25% of patients with d-TGA is a left ventricular outflow tract obstruction in the form of pulmonary or subpulmonary stenosis.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In d-TGA deoxygenated blood returning from the tissues and passing through the right heart chambers, enters the aorta together with a quantity of oxygenated blood that has returned from the pulmonary veins and passes through a communication. The portion of deoxygenated venous blood in the aorta is large, resulting in a low oxygen saturation of the arterial blood with cyanosis and reduced tissue oxygenation, which leads to an increase in anaerobic glycolysis. This results in metabolic acidosis. Hypoxia and metabolic acidosis have detrimental effects on myocardial function and in association with volume overload of the right ventricle, which plays the role of the systemic ventricle, they cause congestive heart failure in the first weeks of life.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Dextro-transposition of the great arteries (d-TGA) is the second most common cyanotic congenital heart disease.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Symptoms and signs of d-TGA</span></h4>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Severe cyanosis usually occurs within hours of birth. The most remarkable finding in physical examination is generalized cyanosis. On auscultation of the heart, the second heart sound (S2) is single (because its pulmonary component is inaudible, due to the posterior location of the pulmonary valve). S2 apart from being single, is also loud, due to the anterior location of the aorta. H</span><span style="font-size: large;">eart murmurs may be absent unless there are associated anomalies, such as pulmonic stenosis.</span><span style="font-size: large;"> S</span><span style="font-size: large;">ymptoms and signs of heart failure such as tachypnea, dyspnea, tachycardia, diaphoresis (sweating), inability to gain weight may develop in the first weeks of life. In the presence of a large VSD cyanosis can be relatively mild and congestive heart failure dominates the clinical picture in the first weeks of life.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Patients with a VSD also have a higher risk of early development of obstructive changes of the pulmonary arterioles leading to pulmonary arterial hypertension (PAH)</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">In general, early surgical correction of d-TGA during infancy is required because otherwise many patients develop progressive cyanosis and acidosis leading to death, while others develop pulmonary arterial hypertension (PAH), a complication that often appears very early in d-TGA patients.</span></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cyanosis in a neonate should be treated as an emergency.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Diagnosis and investigations in complete transposition of the great arteries (d-TGA)</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The diagnostic modality of choice is echocardiography. The parasternal long axis view characteristically demonstrates a parallel course of the proximal segments of the aorta and the pulmonary artery. By small changes in the position and angulation of the transducer, if </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">one can follow the course of the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">vessel arising from the left ventricle and demonstrate its </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">bifurcation then it is identified as a pulmonary artery.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The parasternal short axis view at the base of the heart shows both arteries in short axis as two circular structures with the aorta usually having an anterior position. (This is strikingly different from the normal appearance of this short axis view, which shows the aorta as a circular structure and the pulmonary artery viewed along its long axis with a "sausage appearance").</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>A case of a female infant, age 3 months, with cyanosis. The top echocardiographic image (A) is a parasternal basal short axis view and the bottom image (B) is a parasternal long axis. What are the findings that will make you suspect the cause of the cyanosis? After making the diagnosis, can you name the numbered structures? ( The case is courtesy of <b>Dr. Ahmed Said</b> and the cardiologic facebook group <b><a href="https://www.facebook.com/groups/578271242304737/?fref=nf" target="_blank">Cardiology CME @ Shebin Elkoum Teaching Hospital</a> )</b></i></span><br />
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<b>A</b></div>
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<b>B</b></div>
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>The main diagnostic feature in both images is the parallel course of the two great arteries. In the top image (A) which is a short axis at the base of the heart both arteries are shown in short axis and have the appearance of two circular structures. This is strikingly different from the expected normal appearance of this short axis view, which would demontrate the aorta as a circular structure and the pulmonary artery viewed along its long axis with a "sausage-like" appearance. In the botom image (B) which is a parasternal long axis, two ventricles are seen separated by the interventricular septum and the two great arteries, each originating from a ventricle, are shown in long axis. The proximal segments of the great arteries have an abnormal <u>parallel course</u>, which never occurs in a normal heart. These findings in a cyanotic infant suggest the diagnosis of complete transposition of the great arteries (d-TGA), which is characterized by a parallel course of the great arteries with aorta anterior to the pulmonary artery. D-TGA is a cyanotic congenital heart disease (the second most common cyanotic congenital heart anomaly), therefore it explains why this infant is cyanotic. In d-TGA the ventricles have their normal posιtion with the anatomic left ventricle located posterior and to the left and the anatomic right ventricle anterior, but the aorta originates from the right ventricle and the pulmonary artery from the left ventricle (transposed great arteries). With these thoughts in mind, we can now name the structures: In the top image (A) 1 is the aorta (having an anterior position, as it usually occurs in d-TGA) and 2 the pulmonary artery.</i></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>In the botom image (B) 1 is the posterior ventricle, thus the left ventricle in d-tGA which is connected to the pulmonary artery (5)</i></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>In front of the pulmonary artery, with a course parallel to it, is the aorta (6), with its valve (the aortic valve-7), originating from a ventricle, which is the right ventricle (3). Note that the right ventricle, in this case, is severely dilated. (2 is the interventricular septum and 4 the left atrium.)</i></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span></h3>
<h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment of d-TGA</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The treatment of choice </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">for d-TGA is the arterial switch operation because it offers a complete surgical correction of the anomaly (see below). Till the neonate is transferred </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">to the suitable center for surgical correction of the anomaly an intravenous prostaglandin E1 (PGE1) infusion </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">(0.01 - 0.1 mcg/kg/min </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">should be started to keep </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the ductus arteriosus patent, except in cases where</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the atrial communication is adequate and </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">arterial oxygen saturation is only mildly decreased. PGE1infusion by opening and maintaining patency of the ductus arteriosus increases pulmonary blood flow, which may increase the return of oxygenated blood to the left atrium and promote left-to-right atrial shunting of oxygenated blood. This oxygenated blood will enter the right heart chambers and from there it will flow into the aorta leading to improved systemic oxygenation. However, the use of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">PGE1 requires caution and close patient monitoring, because it can reduce systemic blood flow. Caution is also required in cases where </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the patent foramen ovale has a small opening. In some patients with a small patent foramen ovale PGE1 may have the opposite effect if the increased blood return to the left atrium closes the flap of the foramen ovale. Severely hypoxemic neonates who do not respond promptly to PGE1 or who have a very small and restrictive foramen ovale can be managed with the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Rashkind procedure which can improve arterial oxygen saturation. This procedure involves </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">cardiac catheterization and balloon atrial septostomy which increases the interatrial communication through the patent foramen ovale and hence the flow of oxygenated blood from the left atrium to the right atrium. This oxygenated blood will enter the right ventricle and the aorta, which in d-TGA arises from the right ventricle.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b>The arterial switch or Jatene operation</b> </span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b>The arterial switch or Jatene operation</b> is the operation of choice for most patients with dextro- trasposition of the great arteries (d-TGA).</span><span style="color: #2a2a2a; font-family: "proxima_nova_rgregular" , "arial" , sans-serif; font-size: 18px; line-height: 22px;"> </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">This procedure has the advantage of restoring the left ventricle as the systemic ventricle (supporting the systemic circulation) and also the advantage that it provides the potential for long-term maintenance of sinus rhythm. The arterial switch procedure should be performed at an age < 4weeks. Otherwise, the left ventricle may not be able to handle systemic pressure postoperatively if it is left too long to support the low-pressure, low-resistance pulmonary circulation. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the arterial switch operation, the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">arterial trunks of the two great arteries are transected and </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">reanastomosed to the contralateral arterial </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">root. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The coronary arteries are transplanted to the proximal pulmonary artery which originates from the left ventricle and will be anastomosed to the aorta. The aorta and the pulmonary artery are excised from their original position. Then the excised aorta is connected to the proximal pulmonary artery which arises from the left ventricle, while the excised pulmonary artery is connected to the proximal part of the aorta which arises from the right ventricle. In this way, the left ventricle becomes the ventricle supporting the systemic circulation because the aorta is connected to it, and the right ventricle will support the pulmonary circulation since the pulmonary artery is connected to that ventricle. The surgeon repairs the defects created by the excision of the coronary ostia from the aorta with portions of the pericardium prepared at the beginning of the operation. Atrial septal defects and ventricular septal defects are corrected by primary closure or patch closure. T</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">he arterial switch operation has a surgical mortality of about 2% or less and most patients have good results with good left ventricular function and normal exercise capacity. Patients need regular follow- up for the detection and treatment of the infrequent potential </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">complications such as :</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Supravalvular pulmonary stenosis (which may be treated by either reoperation or balloon angioplasty)</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">S</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">upravalvular aortic </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">stenosis</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">An aneurysm of the ascending aorta</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Neoaortic regurgitation (regurgitation of the patient's original pulmonary valve which after the operation has the role of an aortic valve). If it is significant, valve replacement will be required.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Coronary artery obstruction that may lead to myocardial ischemia or infarction and may require by-pass surgery</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Complete heart block (requiring pacemaker insertion)</span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The atrial switch operations (Mustard /Senning procedures)</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Although the arterial switch is the procedure of choice there are still some adult patients who have undergone in infancy an atrial switch procedure. Moreover, an atrial switch procedure is still used in the rare cases where the arterial switch is very difficult or not feasible to perform due to anatomical reasons (when coronary artery translocation is not feasible, e.g. in case of an intramural coronary artery). There are two atrial switch procedures, the Mustard and the Senning operation. The Mustard procedure was </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">originally described in 1964. Both atrial switch operations </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">involve</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> re</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">directing the systemic and pulmonary venous returns </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">by means of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">a baffle made of Dacron or pericardium (Mustard operation) or atrial septal flaps (Senning operation). </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">This will direct the systemic venous return through the mitral valve to the left ventricle, so that it will enter the pulmonary artery (since the pulmonary artery in d-TGA originates from the left ventricle). The pulmonary venous return will be directed through the tricuspid valve to the right ventricle. From there,it will enter to the aorta, since the aorta arises from the right ventricle in d-TGA. In the Mustard procedure, the</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> use of a pericardial baffle (instead of Dacron </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">baffle) is preferred. The patients need close follow up. </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Complications that may develop in patients having undergone an atrial switch procedure include:</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Obstruction to the pulmonary or systemic venous return (treated with balloon dilatation and stenting) </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Residual baffle shunt (Transcatheter or surgical closure is needed if there is a left to right shunt exceeding 1.5:1, or if a right to left shunt is present)</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Supraventricular arrhythmia (treated with drugs or ablation)</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tricuspid valve regurgitation (this is the atrioventricular valve of the systemic circulation). If significant regurgitation is present, valve replacement or repair will be necessary.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Failure of the systemic ventricle (the right ventricle which must support the systemic circulation). This may be treated with a two stage-arterial switch operation.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tricuspid atresia (TA)</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tricuspid atresia (TA) is a cyanotic, congenital heart disease characterized by the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">congenital absence (agenesis) of the tricuspid valve. It is the third </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">most common cyanotic congenital cardiac anomaly. Two of its main characteristic features are cyanosis with left ventricular </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">hypertrophy in the ECG.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The lack of formation of the tricuspid valve results in the absence of a direct connection between the right atrium and right ventricle</span><span style="color: #2a2a2a; font-family: "proxima_nova_rgregular" , "arial" , sans-serif; font-size: 18px; line-height: 22px;">. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">There is</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> a fibrous thickening </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">in the floor of the right atrium at the expected position of the tricuspid valve. Associated defects, such as an atrial septum defect (ASD) or a widely patent foramen ovale, a ventricular septal defect (VSD) or a patent ductus arteriosus (PDA) are necessary for survival. There is usually an enlarged right atrium and an</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> inter-atrial communication</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> is invariably present, because it is required for survival. This interatrial communication usually is a dilated patent foramen ovale. The left atrium </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">is always enlarged and the mitral valve </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">is morphologically a mitral valve, usually with two leaflets, but with a large orifice.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The left ventricle is </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">enlarged and hypertrophied. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">A ventricular septal defect (VSD) most commonly muscular, of a large or small size is often present, or even multiple VSDs, but in some cases, there is an intact ventricular septum) with no VSD. In patients with tricuspid atresia, the right ventricle is small and hypoplastic. The position of the great vessels is variable and has been the basis for classification of' this congenital heart disease as:</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In type I, the great arteries are related normally to the appropriate ventricle</span><br />
<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">In type II there is a d-transposition of the great arteries . <br />In type III, the great arteries are l-transposed.<br />In type IV there is a truncus arteriosus (the two great arteries originate from a common arterial trunk</span>)</span><br />
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<span style="font-size: large;">Pathophysiology of tricuspid atresia</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Desaturated </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">venous blood returning via the systemic veins to the right atrium,</span><span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"> due to t</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">he absence of any continuity between the right atrium and right ventricle, can exit only by an intra-atrial communication. This results in a right-to-left shunt at the level of the atria. (For a right to left shunt in the atrial level to occur, the right atrial pressure must be elevated over the left atrial pressure. The elevated right atrial pressure is the cause of the right atrial dilatation). Thus, due to the obligatory interatrial shunt, the systemic and coronary venous blood mixes with the pulmonary venous return in the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">left atrium, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">leading to a diminished saturation of the left atrial blood and hence to cyanosis. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The mixed left atrial blood flows through the mitral valve into the left ventricle.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> In the most usual type of tricuspid atresia, from the left ventricle, blood flows to the aorta and the systemic circulation and also through the VSD to the small (hypoplastic) right ventricle and from there to the pulmonary artery.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The small and hypoplastic right ventricle and the enlarged and hypertrophied left ventricle are features of tricuspid atresia that can be explained as follows: The</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> left ventricle receives all the venous return and this leads to a small right ventricle and a dilated left ventricle due to volume overload. As a consequence of volume overload and persistent hypoxemia, left ventricular function will commonly become impaired. This results in decreased ejection fraction (EF), mitral annular dilatation, and mitral regurgitation. Most patients with tricuspid atresia have a VSD</span><span style="color: #2a2a2a; font-family: "proxima_nova_rgregular" , "arial" , sans-serif; font-size: 18px; line-height: 22px;"><br /></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">An important anatomic factor, further determining the pathophysiology of tricuspid atresia is the presence or absence of accompanying pulmonary arterial pathology. In the absence of pulmonary stenosis, the volume of blood to the lungs may be normal and this normal blood oxygenation results in milder cyanosis. In contrast, when pulmonary artery or valve stenosis is also present, this leads to a reduced pulmonary blood flow, resulting in increased cyanosis.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Symptoms, signs, and diagnosis of tricuspid atresia</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Tricuspid atresia is usually diagnosed in infancy. Patients present with cyanosis, congestive heart failure, and growth retardation (due to inadequate feeding because of dyspnea, pauses during feeding and/or anorexia). Dyspnea is a common manifestation and in an infant, it may manifest with tachypnea and/or by nasal flaring or intercostal muscle retractions. Cardiac auscultation reveals a single second heart sound (S2) and usually the murmur due to the VSD, which is a 2-3/6 pansystolic murmur at the lower left sternal border. Hepatomegaly caused by congestion of the liver may be present if there is an interatrial communication of inadequate size, (resulting in elevated right atrial and central venous pressure), or if there is congestive heart failure. <br />The ECG in tricuspid atresia usually will demonstrate left ventricular hypertrophy, left QRS axis and signs of right atrial enlargement or of biatrial enlargement.<br />In the chest X-ray usually the cardiac silhouette will be normal or slightly enlarged. The reason for this is that although there is an enlarged left ventricle and right atrium, there is also a small-hypoplastic-right ventricle. The pulmonary vascularity in most patients is decreased and occasionally due to an underdeveloped pulmonary artery, there is a concave pulmonary artery segment resulting in a boot-shaped cardiac silhouette, which is similar to the radiographic findings of TOF. It can be increased in some patients with accompanying TGA because then the pulmonary artery arises for the left ventricle.<br />Echocardiography is the diagnostic test of choice because it reveals the absence of the tricuspid valve and its orifice, a right ventricle of a small size and an enlarged right atrium and left ventricle. At the site where the tricuspid valve should be, usually a dense band of echoes is seen and the anterior leaflet of the single detectable atrioventricular valve (mitral valve) is attached to the left side of the atrial septum. An interatrial communication is also seen. The size of the interatrial communication and the size of the VSD should be assessed, as well as the presence or absence of pulmonary stenosis and the relationship of the great arteries. The great arteries can be identified as the pulmonary artery or the aorta by tilting the transducer to follow the great vessel until the bifurcation of the pulmonary artery or arch of the aorta is visible. This will help decide if each of the great arteries is related to the appropriate ventricle or if there is associated transposition of the great arteries (TGA).</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment of tricuspid atresia</span></h4>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The most effective treatment for tricuspid atresia is the Fontan operation. Thus, the main goal of management is to achieve a successful Fontan operation. A problem is that the Fontan</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> operation is not tolerated well in early infancy, therefore it is best to perform this intervention at about the age of 2 years if the clinical condition of the child permits this delay. Thus, the surgical treatment of patients with tricuspid atresia typically consists of palliative procedures performed in three stages. The first stage of surgery is performed in the neonatal period and it depends on the anatomical variants. When there is a reduced pulmonary blood flow (which is the most usual problem) the initial operation is a modified Blalock-Taussig shunt (a shunt created between the innominate artery and the central pulmonary artery). This will increase pulmonary blood flow. In the rare cases with an increased pulmonary blood flow, a pulmonary band may be placed to reduce pulmonary blood flow, protecting the pulmonary circulation from the effects of elevated pressure. In cases of tricuspid atresia with transposition of the great arteries, subaortic obstruction and a restrictive (small) VSD another type of initial palliative surgery will be needed, such as the creation of a shunt between the main pulmonary artery and the ascending aorta.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The second palliative surgical procedure for tricuspid atresia without TGA but also for tricuspid atresia with TGA is a Glenn shunt (cavopulmonary anastomosis) performed at the age of 3-6 months. The Glenn procedure involves removing the original shunt and creating a shunt from the superior vena cava (SVC) to the pulmonary artery, with the goal to establish passive flow from the superior vena cava to the pulmonary artery. This measure will increase pulmonary blood flow and hence blood oxygenation.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The third stage consists of a final palliative surgery, the Fontan procedure or one of its modifications. This involves the creation of a connection between the right atrium and the pulmonary artery. With this procedure, the two circulations (pulmonary and systemic) are finally fully separated, with the deoxygenated systemic venous blood entering the right atrium and then passing through the shunt to the pulmonary artery. The oxygenated blood returning to the left atrium passes through the mitral valve to the left ventricle (which in these patients, is the only ventricle providing the pumping force to the circulation) and then to the systemic circulation. The Fontan procedure usually is performed at 2-3 years of age. In general, the Fontan operation is performed not only for the treatment of patients with tricuspid atresia but also for other congenital malformations with univentricular circulation, such as the hypoplastic left heart syndrome, pulmonary atresia with an intact ventricular septum, and double inlet left ventricle. The goal of the Fontan operation is to divert systemic venous blood to the pulmonary circulation in patients with a single effective ventricle.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Long-term complications associated with the Fontan procedure include dilatation of the right atrium, persistent atrial arrhythmias (refractory to treatment), congestive heart failure as a result of the failure of the single functioning ventricle (the left ventricle) and protein-losing enteropathy.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Truncus arteriosus or Persistent truncus arteriosus</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">This is a rare congenital cardiac anomaly, in which the aorta, the coronary arteries, and the pulmonary artery arise from a common arterial trunk (the truncus arteriosus). This single arterial trunk is positioned above the ventricular septum and has one valve (the truncal valve). The truncal valve can be bicuspid, tricuspid or quadricuspid (i.e., it may have 2, 3, or 4 cusps) and it is often incompetent (with regurgitation) but occasionally it can be stenotic. A large perimembranous ventricular septal defect (VSD) is present below the single arterial trunk.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Patients with truncus arteriosus commonly have anomalies of the aortic arch, such as a right, an interrupted or a hypoplastic aortic arch (with or without coarctation). In patients with interrupted or hypoplastic aortic arch, a patent ductus arteriosus is very important and necessary, because it provides blood flow to the descending aorta and relieves heart failure. The truncus arteriosus also leads to heart failure because of the large left to right shunt (with a mechanism similar to the left ventricular failure due to a large VSD, caused by volume overload of the left ventricle resulting from the increased pulmonary venous return of blood). At birth, pulmonary vascular resistance (PVR) is high, therefore the left to right shunt is relatively small in the newborn. However, the shunt and pulmonary arterial flow increase in the next weeks, as PVR falls.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In truncus arteriosus the single arterial trunk receives blood from both ventricles, therefore it receives mixed oxygenated and deoxygenated blood. This mixing of blood results in cyanosis. </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Patients present in the neonatal period with progressive cyanosis. </span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Clinical picture and diagnostic investigations</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cyanosis often is present immediately after birth. Congestive heart failure (with poor feeding, diaphoresis, and tachypnea) usually develops days to weeks after birth. Sudden shock may develop if the ductus arteriosus closes. </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Adults with unrepaired truncus arteriosus develop Eisenmenger syndrome.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The ECG is not very helpful in the diagnosis of this condition. It usually shows biventricular hypertrophy.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The chest radiograph shows an enlarged cardiac silhouette, increased pulmonary vascular markings and it may also show fullness in the region of the truncal root.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The best diagnostic investigation is with echocardiography, by demonstrating a single overriding great artery. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Parasternal long-axis and subcostal coronal (long axis) views demonstrate the single arterial trunk arising from the ventricles. The arterial trunk overrides the ventricular septum.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> The suprasternal and the high parasternal views demonstrate the aortic arch and the anatomy of the central pulmonary arteries.</span><span style="color: #2a2a2a; font-family: "proxima_nova_rgregular" , "arial" , sans-serif; font-size: 22.5px;"> </span><br />
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<span style="color: #2a2a2a; font-family: "proxima_nova_rgregular" , "arial" , sans-serif; font-size: 22.5px;"><span style="color: black; font-family: "times" , "times new roman" , serif; font-size: large;">Treatment and follow up of patients with persistent truncus arteriosus</span></span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment is initially with medical stabilization of congestive heart failure, with diuretics, ACE-inhibitors and digoxin. If there is an interruption of the aortic arch or coarctation, PGE1 (intravenous infusion) is administered, to keep the ductus arteriosus patent.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In patients with truncus arteriosus, corrective surgery must be performed as soon as possible (in the neonatal period, i.e in the first 30 days of life).</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Surgical treatment involves the excision of the pulmonary arteries from the common arterial trunk. The pulmonary arteries are connected to a prosthetic conduit which contains a valve or to an aortic homograft with a valve. The conduit or the homograft is connected to the right ventricle and to the pulmonary arteries. The ventricular septal defect is closed leaving the aorta arising from the left ventricle. In cases with significant regurgitation of the truncal valve, which will have the role of the aortic valve, the valve is repaired or replaced with a prosthetic valve.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Follow up</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Patients with repaired </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">truncus arteriosus need clinical and echocardiographic follow up. Possible complications that may develop and need recognition and treatment :</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Regurgitation through the conduit which has been placed between the right ventricle and the pulmonary arteries or obstruction of the conduit, or the need to replace it because, as the patient grows, it will become small for the circulatory needs.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Regurgitation of the truncal valve</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pulmonary arterial hypertension</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In patients with associated interrupted aortic arch, there is a risk of recurrent arch stenosis, after surgical correction.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Total anomalous pulmonary venous return or total anomalous pulmonary venous connection (TAPVC)</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">TAPVC is a cyanotic congenital heart disease characterized by the return of all four pulmonary veins directly or indirectly to the right atrium and not to the left atrium. In other words, all the pulmonary veins drain into the systemic venous circulation. There are anatomic variants depending on the site of the anomalous connection of the pulmonary veins. </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the supracardiac type, all the pulmonary veins return to a</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> common pulmonary vein behind the left atrium. The common pulmonary vein usually courses</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> upward </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">in front of the pulmonary artery, and it drains into the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">left innominate vein. Rarely this pulmonary venous confluent chamber or common pulmonary vein drains to the superior vena cava or to the azygos vein.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the cardiac type of TAPVC the pulmonary veins drain to the posterior aspect of the coronary sinus or directly to the right atrium.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the infracardiac type of TAPVC the pulmonary veins connect to a common vertical vein which has an inferior course and ususally passes through the esophageal hiatus of the diaphragm and drains to the portal vein or the hepatic vein. Another site where this common vertical vein may drain, is the inferior vena cava below or above the diaphragm.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the mixed type of TAPVC any combination of pulmonary venous connections at two or more different sites of the systemic venous system may be present. In the mixed type most commonly three pulmonary veins connect to form a common pulmonary venous confluence while the fourth drains separately.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;">A consequence of the anomalous drainage of the entire pulmonary venous return into the systemic venous system is the mixing of the oxygenated pulmonary venous blood with the deoxygenated systemic venous blood. A portion of this mixed blood enters the systemic circulation usually through a shunt at the atrial level and from the left heart chambers, this mixed oxygenated and deoxygenated blood will pass to the aorta, resulting in cyanosis. Because the right atrium receives an increased volume of blood (both the systemic and the pulmonary venous return) another feature of TAPVC is a dilated right atrium and right ventricle.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The pathophysiology and the clinical picture of</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">total anomalous pulmonary venous connection (TAPVC) is influenced by the degree of obstruction to the pulmonary venous flow. The obstruction can be caused by compression of the pulmonary veins by neighboring structures. Other causes of obstruction are tortuous or stenotic pulmonary veins or common pulmonary veins. An obstruction to pulmonary venous flow causes a significantly elevated pulmonary venous pressure. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">This elevated pressure is transmitted backward to the pulmonary vasculature resulting in pulmonary edema (interstitial or alveolar) and pulmonary hypertension. Neonates with significant obstruction of the pulmonary venous return present with respiratory distress, tachypnea, marked cyanosis and they often develop pulmonary edema. Cardiac auscultation usually reveals a single, loud second heart sound (S2) and no murmur. Hepatomegaly can be present because of venous congestion.<br />When there is no obstruction of the pulmonary venous flow there is an increased flow in the pulmonary arterial circulation (because the right atrium and right ventricle receive an increased amount of blood). Thus, these patients without surgical correction will develop pulmonary hypertension and progressive obstructive changes of the pulmonary vasculature due to the pulmonary overcirculation.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">This can lead to pulmonary arterial hypertension and right ventricular hypertrophy or failure. Patients with severe obstruction of the pulmonary venous flow have an earlier and much more severe clinical presentation than patients without significant obstruction. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The infradiaphragmatic type of TAPVC is always associated with severe obstruction of pulmonary venous return, leading to pulmonary edema and cyanosis unresponsive to supplemental oxygen. </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The other two types (supracardiac and cardiac) usually do not involve significant obstruction and lead to </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">mild or moderate cyanosis and</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> may also demonstrate mild signs of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">heart failure in</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> the first month of life. Generally in infants without significant pulmonary venous obstruction p</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">hysical examination, apart from variable degrees of cyanosis, also detects signs that are similar to those of an atrial septal defect. Such signs are caused by the volume overload of the right heart chambers and usually include a widely split S2, occasionally with a loud pulmonary component, a grade 2 -3/ 6 systolic ejection murmur audible along the upper to mid-left sternal border (due to the increased flow through the pulmonary valve)). Also due to increased transvalvular flow in the right heart, a mid-diastolic tricuspid flow murmur </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">at the lower left sternal border</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> may be audible.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="color: #333333;"><span style="background-color: white;">The </span></span>ECG in TAPVC shows right axis deviation, right ventricular hypertrophy, and in some cases also right atrial enlargement.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In echocardiography, the right atrium and the right ventricle are dilated in all types of total anomalous venous connection (TAPVC or TAPVR) and there is an inability to demonstrate the expected normal connections of the pulmonary veins to the left atrium (this should raise the examiner's suspicion of this diagnosis). Color Doppler will demonstrate a right to left shunt through the atrial septum. Moreover depending on the type of TAPVC a common collecting vein or venous confluence can be seen near the left atrium, a dilated superior vena cava or a dilated inferior vena cava, due to the increased flow (this depends on the site of the anomalous pulmonary venous connection), or the pulmonary venous connection to the coronary sinus or to the right atrium may be visible.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Surgical correction at the time that the diagnosis is made and the patient has been stabilized is required in all cases of TAPVC regardless of the degree of obstruction. TAPVC without surgical treatment generally has a poor prognosis. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Surgical repair involves creating a wide connection between the pulmonary venous confluence and the posterior wall of the left atrium. The surgical technique for repair of cases with pulmonary venous return to the coronary sinus is different. Then the coronary sinus is unroofed into the left atrium so that it drains to the left atrium and its opening to the right atrium is closed.</span><br />
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<span style="background-color: orange; font-family: "times" , "times new roman" , serif; font-size: large;"><b>Bibliography</b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <span style="background-color: white;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Rao PS. Diagnosis and management of cyanotic congenital heart disease: Part I. </span></b></span><br />
<span style="background-color: white;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;">2009 Indian J Pediatr ;76(1):57-0. </span></b></span><span style="background-color: white; font-family: "meta serif pro" , "georgia" , , "simsun" , , "microsoft yahei new" , "microsoft yahei" , , serif; font-size: 14px;">http://dx.doi.org/10.1007/s12098-009-0030-4</span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br />Syamasundar Rao P. Diagnosis and management of cyanotic congenital heart disease: Part II. Indian J Pediatr. 2009;76(3):297-308. doi: 10.1007/s12098-009-0056-7</span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="https://www.msdmanuals.com/professional/pediatrics/congenital-cardiovascular-anomalies/total-anomalous-pulmonary-venous-return-tapvr" target="_blank">The MSD manual-Total Anomalous Pulmonary Venous Return (TAPVR)</a></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="https://www.msdmanuals.com/professional/pediatrics/congenital-cardiovascular-anomalies/tricuspid-atresia" target="_blank">The MSD manual-Tricuspid Atresia</a></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <a href="https://emedicine.medscape.com/article/900574-overview" target="_blank"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Transposition of the Great Arteries - Medscape eMedicine</b></span></a><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b><span style="font-family: "arial" , "helvetica" , sans-serif;">Natraj Setty HSS, Gouda Patil SS, Ramegowda RT, V V, Vijayalakshmi IB. Comprehensive Approach to Congenital Heart Defects. Journal of Cardiovascular Disease Research 2017;8:1-5. </span></b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK: <a href="https://www.jcdronline.org/sites/default/files/10.5530jcdr.2017.1.1.pdf">https://www.jcdronline.org/sites/default/files/10.5530jcdr.2017.1.1.pdf</a></b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Bhat V. Illustrated Imaging Essay on Congenital Heart Diseases: Multimodality Approach Part III: Cyanotic Heart Diseases and Complex Congenital Anomalies. J Clin Diagn Res. 2016;10(7):TE01-10 http://dx.doi.org/10.7860/jcdr/2016/21443.8210</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5020285/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5020285/</a></b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b><span style="font-family: "arial" , "helvetica" , sans-serif;">Kang S-L, Benson L. Recent advances in cardiac catheterization for congenital heart disease. </span><span style="font-family: "arial" , "helvetica" , sans-serif;">F1000Res. 2018; </span><span style="font-family: "arial" , "helvetica" , sans-serif;">7:370. Available from: http://dx.doi.org/10.12688/f1000research.13021.1</span></b><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5871969/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5871969/</a></b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br />Blonshine SK. Transposition of the Great Arteries. The Jatene procedure. <br /><a href="https://www.sciencedirect.com/science/journal/00012092">AORN Journal</a> 1989 ;49(4):973-87. http://dx.doi.org/10.1016/s0001-2092(07)66805-7</span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span><span style="background-color: orange; font-size: large;"><br /></span><span style="background-color: orange; font-family: "times" , "times new roman" , serif; font-size: large;">Videos</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://www.youtube.com/watch?v=C4Kz5cG3VUI" target="_blank">TETRALOGY OF FALLOT (TOF) - ECHOCARDIOGRAPHY Dr Ankur Chaudhari</a></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://www.youtube.com/watch?v=Zrj7AKdAxz0" target="_blank">Surgery of Cyanotic CHDs - CRASH! Medical Review Series Paul Bolin, M.D. </a></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://www.youtube.com/watch?v=N6pvBSQMz-g" target="_blank">"Cyanotic Congenital Cardiac Defects: Diagnosis & Treatment," by Tom Kulik, MD, f- OPENPediatrics</a></span></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-63149505204506777672018-04-06T03:02:00.001+03:002018-11-12T01:17:13.739+02:00Cardiac tumors (cardiac neoplasms)<h2>
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</script> <span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac tumors (cardiac neoplasms)</span></h2>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac tumors may be primary (benign or malignant) or metastatic (these are always malignant and are far more common than primary tumors). Signs and symptoms are nonspecific and highly variable depending on the localization, size, and composition of the cardiac neoplasm. The first imaging modality alerting the clinician to the presence of a cardiac mass usually is echocardiography, most often performed for another indication.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Primary tumors of the heart</span></h3>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Primary cardiac tumors are rare. They are much rarer than metastatic ones. Most primary cardiac tumors are benign (75-80%). The most common type of primary benign cardiac tumor is myxoma (followed by lipoma and fibroelastoma).<br />Primary malignant cardiac tumors are extremely rare and they are almost all sarcomas, with angiosarcoma being the most common among them (Lymphomas and malignant paragangliomas are even more rare types of primary cardiac malignancies). Sarcomas</span><span style="font-size: large;"><span style="background-color: white;"> can occur in any chamber of the heart </span><span style="background-color: white;">but they are more frequently located in the right or left atrium. </span></span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Malignant cardiac tumors have</span><span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"> </span>a poor<span style="font-family: "times" , "times new roman" , serif;"> </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">prognosis.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">In childhood, primary cardiac tumors are extremely rare and mainly include rhabdomyoma and fibroma. Rhabdomyomas are the most common cardiac tumors in childhood. Cardiac r</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">habdomyomas are benign tumors that</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> originate from cardiac myocytes. Some cases are </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">sporadic and isolated, but in 50% of cases, they </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">are associated with tuberous sclerosis. The </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">most common malignant cardiac tumor in childhood </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">is rhabdomyosarcoma. Cardiac tumors in children are often associated with genetic syndromes.</span></span><br />
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Primary cardiac tumors should be totally resected (in a cardiac operation performed on cardiopulmonary by-pass) whenever possible. For benign cardiac tumors, this is almost always possible.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The perioperative mortality is about 8% overall </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">but </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">for myxoma, which is the most common cardiac tumor resected, the perioperative mortality is much lower, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">approximately 1% .</span></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Metastatic cardiac tumors</span></span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Metastatic cardiac tumors are far more frequent (approximately 30- 40 times more frequent) than primary tumors of the heart. Neoplasms that may involve the heart are mainly melanomas, lymphomas, lung, breast, and renal cancer. <br />Metastases to the heart can occur by the following three mechanisms:</span></div>
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<ul>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Direct extension of a neoplasm via adjacent tissues</span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Dissemination of cancer cells in the blood or the lymphatic system</span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Propagation through the superior or the inferior vena cava to the right atrium.</span></li>
</ul>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The site of the heart most commonly affected by metastatic malignant disease is the pericardium. Pericardial involvement results in a pericardial effusion which is often </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">large and</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">hemorrhagic and may contain masses comprising of cancer cells or blood clots and fibrin. Thus, echocardiography apart from the echolucent pericardial effusion may demonstrate distinct regions </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">of thickening of the visceral pericardium. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Generally, pericardial</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> metastases are common and they result in persistent pericardial effusions, also posing the risk of tamponade. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The differential diag</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">nosis in a patient with known malignant neoplasm and a pericardial effusion includes</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> malignant pericardial effusion (metastasis to the pericardium), radiation-induced peri</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">carditis, drug-induced pericarditis, and idiopathic pericarditis. In many cases, a histologic diagnosis can be made by pericardial fluid aspiration or pericardial biopsy. Treatment with a pericardial window and/ or fibrosing agents lessen the need for repeated pericardiocentesis.</span></span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Less often metastatic tumors may affect the myocardium or the endocardium (causing manifestations of heart failure or arrhythmias), or the venae cavae (causing manifestations due to obstruction of venous flow). Generally, possible presentations of a </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> myocardial metastasis include </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">nonspecific </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">ST-T wave changes, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">cardiac arrhythmias, heart block, or myocardial dysfunction. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Echocardiography is the most commonly used imaging method </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">in suspected cardiac metastatic disease, but magnetic resonance </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">imaging and computed tomography are also </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">valuable. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Metastatic tumors affecting</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> the myocardium, usually appear as distinct,</span><span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;"> </span><span style="font-size: large;">brightly echogenic masses. Rarely, metastatic tumors may</span><span style="font-size: large;"> </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">seed the endocardium and echocardiographically appear as intracavitary masses.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac metastases are clinically apparent only in 10% of the cases, and usually, they are not the cause of the patient's presenting symptom, although in some cases they cause symptoms (dyspnea due to heart failure, or due to a large pericardial effusion, chest pain due to pericarditis, signs of cardiac tamponade, arrhythmias, syncope due to atrioventricular block, etc). They usually occur in the setting of a previously diagnosed malignant neoplasm ( almost always a widespread primary neoplasm). The differential diagnosis of a cardiac manifestation in a patient with cancer includes cardiotoxicity because of chemotherapy or occurrence of cardiac metastases.</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The general prognosis of patients with cardiac metastases is poor. For patients with intramyocar</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">dial metastasis, survival generally </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">is limited to a few months at most. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Survival is longer for intracavitary tumors. Occasional </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">patients have survived several years.</span></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Symptoms and clinical findings of cardiac neoplasmatic disease</span></h3>
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<span style="font-family: Times, Times New Roman, serif; font-size: large;">Symptoms and signs of cardiac tumors are related to obstruction of blood flow, embolic phenomena, pericardial involvement, cardiac failure, arrhythmias and elaboration of substances causing constitutional symptoms. Since embolic and obstructive phenomena are common, the presenting symptoms of cardiac tumors are generally more related to their location in the heart and their size and less to the tumor type.<br />Myxomas, as well as other primary cardiac tumors, may present with one or more of a classic triad of manifestations which includes sequelae of valvular obstruction, embolic phenomena and constitutional symptoms.<br />Manifestations of heart failure are common in case of large intracavitary tumors causing obstruction to blood flow. Depending on the heart chamber involved, the resulting manifestations may be of :</span></div>
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<ul>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">congestive (backward) heart failure, such as dyspnea, peripheral edema, or </span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> low cardiac output (forward) heart failure, such as fatigue, or hypotension. </span></li>
</ul>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;">Intracardiac (intracavitary) tumors, if they are large enough, cause clinical manifestations due to the obstruction of blood flow. Myxomas of the left atrium may prolapse via the mitral valve, causing symptoms of mitral obstruction (dyspnea, syncope depending on a change of patient's position, etc.). Tumors of the right heart chambers may manifest with signs and symptoms of right-sided heart failure<span style="background-color: white;">.</span> Primary malignant cardiac tumors can also cause congestive heart failure when there is extensive myocardial involvement.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Constitutional symptoms (fever, chills, fatigue, malaise, weight loss, Raynaud phenomenon), as well as some laboratory findings (elevated erythrocyte sedimentation rate, anemia, polycythemia, leucocytosis, thrombocytosis, thrombocytopenia), result from substances secreted by the tumor or released due to tumor necrosis.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The constitutional symptoms, signs and laboratory findings may resemble the findings of vasculitis or autoimmune connective tissue disease.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Embolism due to a cardiac tumor can in many cases be the first manifestation. An embolism can manifest as a pulmonary embolism or more commonly as a peripheral embolism (e.g a stroke or acute ischemia of an extremity or a digit), depending on the location of the tumor in a right or left heart chamber, respectively.<span style="font-family: "times" , "times new roman" , serif; font-size: medium;"><span style="background-color: white;"> </span></span>The embolus consists either of tumor cells or of thrombi formed on the tumor surface.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Atrial or ventricular arrhythmias or atrioventricular block can occur as a result of tumor infiltration of the myocardium or the conductive pathways of the heart. This is particularly true for fibromas<span style="background-color: white;"> </span>(these are intramural tumors, located in the left ventricle, mainly in the interventricular septum). In some cases, sudden cardiac death is the first manifestation of a cardiac tumor.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The clinical examination is nonspecific in cardiac tumors. However, cardiac symptoms and signs in a patient who has had no previous cardiac disease, in association with general symptoms and embolic events, should initiate cardiac investigations.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Diagnosis of cardiac tumors</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Whenever a cardiac mass is encountered on echocardiography, the differential diagnosis includes a thrombus, a vegetation or a tumor, with the first two being much more common in comparison with a tumor. To reach a conclusion the physician should focus on: </span><br />
<ul>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the clinical context and presentation </span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the location </span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the imaging characteristics </span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the findings of additional imaging tests (when necessary), such as CT or MRI</span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">in case of a tumor the definitive diagnosis is by biopsy (histological examination), although imaging is in many cases suggestive of the correct diagnosis.</span></li>
</ul>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Generally, echocardiography (transthoracic followed in some cases by transesophageal) is the first diagnostic procedure. </span></span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Cardiac tumors may be intra</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">cavitary or intramural</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">. Echocardiography depicts intracavitary tumors as sessile or mobile </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">echo densities attached to the endocardium, whereas intramural </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">tumors as a localized thickening of the left ventricular wall. Cardiac tumors may also involve the pericardium</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">, with or without a</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> concomitant pericardial effusion.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Differential diagnosis of an intracavitary cardiac tumor includes an intracavitary thrombus.</span></span><span style="font-size: large;"> Contrast injection can be helpful in the differential diagnosis because it will </span><span style="font-size: large;">intensify the signals from tumors, but not from thrombi.</span><span style="font-size: large;"> </span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">If echocardiographic findings cannot suggest the diagnosis, further imaging procedures such as computed tomography (CT) or magnetic resonance imaging are employed. </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Magnetic resonance imaging (MRI)</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> provides the best spatial resolution and allows </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">exact localization of the tumor. It may also </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">differentiate fat from a thrombus or </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">tumor. It provides particularly valuable information for intramyocardial and </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">malignant tumors.</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;"> I</span><span style="font-size: large;">n differentiating between benign and malignant neoplasms, a useful test is</span><span style="font-size: large;">18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT). If there is a decision to proceed with </span><span style="font-size: large;">cardiac tumor surgery (surgical excision of the tumor under cardiopulmonary by-pass), i</span><span style="font-size: large;">n the presence of risk factors for coronary heart disease, coronary angiography or CT coronary angiography should be performed, so that coronary stenoses can be bypassed during surgery for the tumor. Note that primary cardiac tumors should be totally resected whenever possible.</span></span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A woman 55 years old with a history of diabetes and hypertension. The ECG showed sinus rhythm with mild nonspecific T wave inversion. Recently she suffered an ischemic stroke with mild left hemiparesis. A 5-chamber apical echocardiographic view of this patient is shown below. Please name the structures 1-5. What has probably caused the ischemic stroke and which is the proposed management ?</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEioTyXEKZE-ClHfPZJfWZNoFKkKjYisOoOqusZARVxvdfIbVnaQamaYEeD2NQBvw02AaA2aTkfGFxRYuc1K4E6Iqbvfhrbrc0nS6HA4YK28aj9w2k0dF6SY7enILn9yW_wHG-ZK7Vt-mWo/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2586%25CE%25B1%25CF%2583%25CE%25B9%25CE%25AC+%25CF%2583%25CE%25BF%25CF%2586%25CE%25AF%25CE%25B1-%25CE%25BC%25CF%258D%25CE%25BE%25CF%2589%25CE%25BC%25CE%25B1-2+.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><span style="font-family: "times" , "times new roman" , serif;"><img alt="" border="0" data-original-height="375" data-original-width="474" height="253" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEioTyXEKZE-ClHfPZJfWZNoFKkKjYisOoOqusZARVxvdfIbVnaQamaYEeD2NQBvw02AaA2aTkfGFxRYuc1K4E6Iqbvfhrbrc0nS6HA4YK28aj9w2k0dF6SY7enILn9yW_wHG-ZK7Vt-mWo/s320/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2586%25CE%25B1%25CF%2583%25CE%25B9%25CE%25AC+%25CF%2583%25CE%25BF%25CF%2586%25CE%25AF%25CE%25B1-%25CE%25BC%25CF%258D%25CE%25BE%25CF%2589%25CE%25BC%25CE%25B1-2+.jpg" title="echocardiogram -quiz-intracardiac mass-possible cardiac tumor-cardiology book" width="320" /></span></a></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1Ws_Dcea5wNMcYOvEDX6UF2MQ7PcW2BU3h0R2jKPFu-nQNQZusZBNV68BHsznLAGUELM_9zjuzkIm9KTd0-WfXX7utofnbIrer0XU5cfc-6k3tSHlvMQuAYNnYE1SRzub35NNaPYi5HM/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2586%25CE%25B1%25CF%2583%25CE%25B9%25CE%25AC+%25CF%2583%25CE%25BF%25CF%2586%25CE%25AF%25CE%25B1-%25CE%25BC%25CF%258D%25CE%25BE%25CF%2589%25CE%25BC%25CE%25B1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><span style="font-family: "times" , "times new roman" , serif;"><img alt="" border="0" data-original-height="405" data-original-width="426" height="304" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg1Ws_Dcea5wNMcYOvEDX6UF2MQ7PcW2BU3h0R2jKPFu-nQNQZusZBNV68BHsznLAGUELM_9zjuzkIm9KTd0-WfXX7utofnbIrer0XU5cfc-6k3tSHlvMQuAYNnYE1SRzub35NNaPYi5HM/s320/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2586%25CE%25B1%25CF%2583%25CE%25B9%25CE%25AC+%25CF%2583%25CE%25BF%25CF%2586%25CE%25AF%25CE%25B1-%25CE%25BC%25CF%258D%25CE%25BE%25CF%2589%25CE%25BC%25CE%25B1.jpg" title="echocardiogram -quiz-intracardiac mass-cardiac tumor-cardiology book" width="320" /></span></a></div>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>1. Left ventricle 2. Mitral valve 3 A mass in the left atrium, with an appearance which is highly suggestive of a tumor (with a myxoma being by far the most probable diagnosis). A thrombus could be considered in the differential diagnosis, but in this case, it is not likely since there is a left atrium of normal size, and there was no history of atrial fibrillation or of mitral stenosis (conditions that can lead to the formation of a left atrial thrombus). Also, the position and size of the mass are clearly more suggestive of a tumor than of a thrombus. 4. Left atrium 5. Aorta.</b></span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>The patient was managed with a successful surgical resection of the tumor. Biopsy has proven that it was a myxoma.</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Is there any abnormality in this image of cardiac magnetic resonance imaging (MRI)?</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Name the structures shown in the image.</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>There is a large intracavitary mass in the left ventricle in contact with the apical part of its lateral wall which has a morphology suggestive of a cardiac tumor. The mass is homogeneous, broad-based and well circumscribed. 1. left ventricle 2 interventricular septum 3 right ventricle 4 tumor in the left ventricle 5 left atrium 6 mitral valve 7 right atrium. 8 intratrial septum 9 left lung 10 right lung. 11 descending aorta. The mass was surgically excised and histologic examination showed that it was a lipoma (left ventricular lipoma) Note that transverse sections in MRI or CT are displayed as if the viewer looks at the patient from the patient's feet, so that the left-sided structures are seen on the right side of the image , the right-sided structures on the left side of the image, the anterior structures are seen on the top of the image and the posterior structures on the bottom. Courtesy of Dr. Ketikoglou Dimitrios, Cardiologist <span lang="EN-US">MD</span><span lang="EN-US"> </span><span lang="EN-US">PhD</span><span lang="EN-US"> </span><span lang="EN-US">FESC</span></b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A patient with hepatic cancer. What kind of view is this, how is it obtained, which are the structures 1-6 and what is the probable diagnosis for this patient ?</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhTtTIdWD9dtCs7p90RorsdmkR6R6mjS1BwFOaj-JlkaxQpnsc-WAqnl9XVHDAPh7Jk7VtUyYByQMucA9Qgj0HmGt1BUbwu6yOcX5_lzItBraynnSK2ZTL3uBbt9skq4tXP4qmaAgCnxrk/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BC%25CE%25B5%25CF%2584%25CE%25B1%25CF%2583%25CF%2584%25CE%25B1%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C%25CF%2582+%25CF%258C%25CE%25B3%25CE%25BA%25CE%25BF%25CF%2582+%25CE%25B4%25CE%25B5%25CE%25BE+%25CE%25BA%25CF%258C%25CE%25BB%25CF%2580%25CE%25BF%25CF%2585+%25CE%25B1%25CF%2580%25CF%258C+%25CE%25AE%25CF%2580%25CE%25B1%25CF%2581+%25CE%25B4%25CE%25B9%25CE%25BF%25CE%25B9%25CF%2583%25CE%25BF%25CF%2586+%25CE%25BA%25CE%25B5%25CF%2584%25CE%25AF%25CE%25BA%25CE%25BF%25CE%25B3%25CE%25BB%25CE%25BF%25CF%2585.jpg.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="495" data-original-width="542" height="365" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhTtTIdWD9dtCs7p90RorsdmkR6R6mjS1BwFOaj-JlkaxQpnsc-WAqnl9XVHDAPh7Jk7VtUyYByQMucA9Qgj0HmGt1BUbwu6yOcX5_lzItBraynnSK2ZTL3uBbt9skq4tXP4qmaAgCnxrk/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BC%25CE%25B5%25CF%2584%25CE%25B1%25CF%2583%25CF%2584%25CE%25B1%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C%25CF%2582+%25CF%258C%25CE%25B3%25CE%25BA%25CE%25BF%25CF%2582+%25CE%25B4%25CE%25B5%25CE%25BE+%25CE%25BA%25CF%258C%25CE%25BB%25CF%2580%25CE%25BF%25CF%2585+%25CE%25B1%25CF%2580%25CF%258C+%25CE%25AE%25CF%2580%25CE%25B1%25CF%2581+%25CE%25B4%25CE%25B9%25CE%25BF%25CE%25B9%25CF%2583%25CE%25BF%25CF%2586+%25CE%25BA%25CE%25B5%25CF%2584%25CE%25AF%25CE%25BA%25CE%25BF%25CE%25B3%25CE%25BB%25CE%25BF%25CF%2585.jpg.png" title="transesophageal echocardiography (TOE)-cardiology free book-cardiac tumors" width="400" /></a></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>This is a transesophageal echocardiographic (TEE) bicaval view (a long axis view of the right atrium obtained from the middle esophageal position with a plane angle of about 90-10</b></span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>0</b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><sup>o</sup></b></span><b style="font-family: Arial, Helvetica, sans-serif;">and clockwise rotation of the transducer shaft). 1 left atrium 2 interatrial septum 3 entrance of the superior vena cava, 4 right atrium 5 entrance of the inferior vena cava 6 a large non-homogeneous mass in the right atrium with a morphology suggestive of a tumor. It is a metastatic tumor from the liver (as suggested by the patient's history which has metastasized through a hepatic vein and then through the inferior vena cava into the right atrial cavity. Courtesy of </b><b style="font-family: arial, helvetica, sans-serif;"> Dr. Ketikoglou Dimitrios, Cardiologist <span lang="EN-US">MD</span><span lang="EN-US"> </span><span lang="EN-US">PhD</span><span lang="EN-US"> </span><span lang="EN-US">FESC</span></b><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A 3-D echocardiographic image. Which view is this and where is the abnormality ? Name possible symptoms that may result from such a pathology.</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjyBzaMUa_LU3LbS925_F0ID9hDMlpgrSfn9mw5fWmO_uTkSrsuGeJS00f1hMpAM3Zwsncugymi867qLhxQtweiGLhRHNJDAU5ib-T-P6aD57kh79r1eisFBypeSf7yd5tYfWuExd1KHrI/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BA%25CE%25B5%25CF%2584%25CE%25AF%25CE%25BA%25CE%25BF%25CE%25B3%25CE%25BB%25CE%25BF%25CF%2585+%25CE%25BC%25CE%25B5%25CF%2584%25CE%25B1%25CF%2583%25CF%2584%25CE%25B1%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C%25CF%2582+%25CF%258C%25CE%25B3%25CE%25BA%25CE%25BF%25CF%2582+%25CE%25BB%25CE%25B5%25CF%2580+%25CE%25B5%25CE%25BD%25CF%2584%25CE%25AD%25CF%2581%25CE%25BF%25CF%2585+%25CF%2583%25CF%2584%25CE%25BF%25CE%25BD+LA+-3D.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="454" data-original-width="698" height="416" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjyBzaMUa_LU3LbS925_F0ID9hDMlpgrSfn9mw5fWmO_uTkSrsuGeJS00f1hMpAM3Zwsncugymi867qLhxQtweiGLhRHNJDAU5ib-T-P6aD57kh79r1eisFBypeSf7yd5tYfWuExd1KHrI/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BA%25CE%25B5%25CF%2584%25CE%25AF%25CE%25BA%25CE%25BF%25CE%25B3%25CE%25BB%25CE%25BF%25CF%2585+%25CE%25BC%25CE%25B5%25CF%2584%25CE%25B1%25CF%2583%25CF%2584%25CE%25B1%25CF%2584%25CE%25B9%25CE%25BA%25CF%258C%25CF%2582+%25CF%258C%25CE%25B3%25CE%25BA%25CE%25BF%25CF%2582+%25CE%25BB%25CE%25B5%25CF%2580+%25CE%25B5%25CE%25BD%25CF%2584%25CE%25AD%25CF%2581%25CE%25BF%25CF%2585+%25CF%2583%25CF%2584%25CE%25BF%25CE%25BD+LA+-3D.jpg" title="3 D echocardiography - a rare cardiac tumor -cardiology book" width="640" /></a></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>An apical 4-chamber 3-dimensional echocardiographic view showing a mass (tumor) in the left atrium. This was a rare case of metastasis of a tumor of the small intestine. A tumor in the left atrium can cause dyspnea (due to elevated left atrial and pulmonary venous pressure), syncope, arterial embolism (e.g. a stroke) and constitutional symptoms (e.g. malaise, fatigue, weight loss) 1. left ventricle 2. interventricular septum 3. right atrium 4 left atrium 5 interatrial septum 6 tumor in the left atrium 2 </b></span><b style="font-family: Arial, Helvetica, sans-serif;">Courtesy of </b><b style="font-family: arial, helvetica, sans-serif;"> Dr. Ketikoglou Dimitrios, Cardiologist <span lang="EN-US">MD</span><span lang="EN-US"> </span><span lang="EN-US">PhD</span><span lang="EN-US"> </span><span lang="EN-US">FESC</span></b></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac myxoma</span></h3>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Myxomas are the most common benign cardiac tumors </span><span style="font-size: large;">in adults. A myxoma is an intracavitary mass, usually</span><span style="font-size: large;"> 4 -8 cm in diameter. In most cases, </span><span style="font-size: large;">it is located in the left atrium (75%), attached to the interatrial septum, over </span><span style="font-size: large;">the foramen ovale. More rarely, it is found in the right </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">atrium and even less commonly in the ventricles. </span><span style="background-color: white;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Most myxomas are sporadic (>90%) and seldom reoccur after complete resection. </span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Multiple myxomas (synchronous, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">successive, or recurrent) are a feature of the myxoma syn</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">dromes (which account for 7% of cardiac myxoma cases). These cases are</span><span style="background-color: white; font-size: large;"> familial, as part of the rare Carney syndrome, which is a combination of cardiac and cutaneous myxomas, endocrine disorders </span><span style="background-color: white; font-size: large;">(</span><span style="background-color: white; font-size: large;">pituitary adenomas, adrenocortical disease, </span><span style="background-color: white; font-size: large;">or testicular tumors</span></span><span style="background-color: white;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">), and cutaneous lentiginosis.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> </span></span><span style="font-family: "arial" , "helvetica" , sans-serif;">(Lentiginosis is the presence of multple lentigines, i.e. small pigmented spots on the skin with a clearly defined edge, due to a benign hyperplasia of melanocytes which is linear in its spread) </span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="background-color: white;">W</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">hen a familial myxoma syndrome is identified or suspected, s</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">creening first-degree relatives with echocardiography is mandatory.</span></span></div>
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<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;">Large myxomas are often mobile. They may move back and forth into the mitral valve annulus during a cardiac cycle.</span></span></div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Histologically, myxomas are neoplasms of multipotent mesenchymal cells in the subendocardial tissue. These are polygonal, occasionally multinucleate cells surrounded by a myxoid stroma. </span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">A cardiac myxoma may induce constitutional symptoms (fever and weight loss) due to the production of interleukin-6, embolic phenomena, that can mimic systemic vasculitis or infective endocarditis and symptoms due to valvular obstruction (often mimicking mitral stenosis). Presenting symptoms of left-sided myxomas are dyspnea on exertion, paroxysmal nocturnal dyspnea, fever, and syncope. Sudden death may also occur. The most common physical finding with a myxoma of the left atrium is a mitral diastolic murmur (similar to mitral stenosis but without the opening snap) or an apical systolic murmur due to mitral incompetence. Occasionally there is an additional heart sound called tumor plop. This is an early diastolic sound. Raynaud phenomenon or clubbing of the fingers may occasionally occur.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"></span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">On echocardiography, a myxoma has the appearance of a heterogeneous mobile mass, often globular, usually with a smooth or lobulated surface, 4-8 cm in diameter, attached to the endocardial surface (usually the interatrial septum) with a narrow base (stalk or pedicle). Occasionally it is attached with a wide base. Their echogenicity is not homogeneous and they may include areas of echolucensy and in some cases calcifications. Polypoid myxomas are larger with a smooth surface and they include lucencies and cystic areas due to hemorrhage and necrosis. Papillary myxomas tend to be smaller and have multiple villi. This subtype is associated with embolic phenomena,</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The treatment of a cardiac myxoma is surgical resection of the tumor.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A transesophageal echocardiographic (TEE) image of a patient with exertional dyspnea and an episode of syncope. What kind of a TEE section is shown here, how is it obtained, which are the structures 1-9 and what is the diagnosis?</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgyei6NDH5MFJHdlBUr8owl4fJ04cyFkojW2R73SaEC9Np-InWS91V2DPFweByjd5H106wwpe6Micbgt8-5XICPkVkalTiCdZRx1sltmg5fBj0k1pHko4-MMnKNR9ceJEVH_rcktz5kYjg/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BC%25CF%258D%25CE%25BE%25CF%2589%25CE%25BC%25CE%25B1+%25CE%25B1%25CF%2581%25CE%25B9%25CF%2583%25CF%2584+%25CE%25BA%25CF%258C%25CE%25BB%25CF%2580%25CE%25BF%25CF%2585+-%25CF%2584%25CE%25BF%25CE%25BC%25CE%25AE+5+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB%25CE%25BF%25CF%2584+%25CE%25BC%25CE%25AD%25CF%2583%25CE%25BF%25CF%2582+%25CE%25BF%25CE%25B9%25CF%2583%25CE%25BF%25CF%2586+%25CE%25BA%25CE%25B5%25CF%2584%25CE%25AF%25CE%25BA%25CE%25BF%25CE%25B3%25CE%25BB%25CE%25BF%25CF%2585.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="212" data-original-width="272" height="498" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgyei6NDH5MFJHdlBUr8owl4fJ04cyFkojW2R73SaEC9Np-InWS91V2DPFweByjd5H106wwpe6Micbgt8-5XICPkVkalTiCdZRx1sltmg5fBj0k1pHko4-MMnKNR9ceJEVH_rcktz5kYjg/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25BC%25CF%258D%25CE%25BE%25CF%2589%25CE%25BC%25CE%25B1+%25CE%25B1%25CF%2581%25CE%25B9%25CF%2583%25CF%2584+%25CE%25BA%25CF%258C%25CE%25BB%25CF%2580%25CE%25BF%25CF%2585+-%25CF%2584%25CE%25BF%25CE%25BC%25CE%25AE+5+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB%25CE%25BF%25CF%2584+%25CE%25BC%25CE%25AD%25CF%2583%25CE%25BF%25CF%2582+%25CE%25BF%25CE%25B9%25CF%2583%25CE%25BF%25CF%2586+%25CE%25BA%25CE%25B5%25CF%2584%25CE%25AF%25CE%25BA%25CE%25BF%25CE%25B3%25CE%25BB%25CE%25BF%25CF%2585.png" title="transesophageal echocardiography (TOE)-cardiology free book-cardiac tumor" width="640" /></a></div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>It is a TEE 5 chamber view obtained from the middle part of the esophagus (midesophageal 5 chamber view) with the image plane at 0</b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><sup>o</sup></b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>1 a large mass in the left atrium which is non-homogeneous and well circumscribed with a morphology suggestive of a tumor (myxoma). 2 mitral valve 3 left ventricular outflow tract 4 aortic valve 5 left ventricle 6 interventricular septum 7 right ventricle 8 right atrium 9 interatrial septum. The tumor was resected surgically and histology confirmed the diagnosis of a myxoma. </b></span><b style="font-family: arial, helvetica, sans-serif;"> Courtesy of Dr. Ketikoglou Dimitrios, Cardiologist <span lang="EN-US">MD</span><span lang="EN-US"> </span><span lang="EN-US">PhD</span><span lang="EN-US"> </span><span lang="EN-US">FESC.</span></b><br />
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</script> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><strong style="background-color: white;">Other benign cardiac tumors: Lipoma / Papillary fibroelastoma (endocardial papilloma)</strong></span></h3>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b>Lipomas</b> result from a benign neoplastic proliferation of mature adipocytes and they </span></span><span style="background-color: white; font-size: large;">are usually enclosed in a capsule in contrast to </span><span style="background-color: white; font-size: large;">lipomatous hypertrophy (which is a condition that affects the interatrial septum). The majority of cardiac lipomas </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">arise in the subepicardium, but occasionally they can be located in the pericardium, in the subendocardium, in the myocardium (intramural) or on the cardiac valves. Their size usually ranges from a few to several centimeters. On echocardiography, they appear </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">homogenous,</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> broad-based, immobile and well circumscribed. Usually, lipomas are asymptomatic, but occasionally they cause arrhythmias, atrioventricular block, or valvular dysfunction. A subepicardial lipoma may compress a coronary artery resulting in ischemic chest pain.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Excision may be required because of</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> the progressive growth of lipomas, as well as the above potential manifestations, </span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b>Lipomatous hypertrophy</b></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; font-size: large;"><span style="background-color: white;"> of the interatrial septum is a prominent thickening of the septum due to the accumulation of adipose tissue. </span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; font-size: large;">T</span><span style="background-color: white;"><span style="font-size: large;">he proximal and distal portions of the atrial septum appear thickened, generally with sparing of the fossa ovalis.</span></span></span><span style="background-color: white; font-size: large;"> Lipomatous hypertrophy of the interatrial septum is not a true tumor. It is more common in obese elderly women. It may be associated with supraventricular arrhythmias.</span></span></span></div>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjCcr5t7HKVXA4asDasrjwwSRcqxn083pq82xkAl2llU0I_WrwqUOG_iKN2M4ouV2UY4rUck8xeXUCXf_UlIVHIZFsWbG9Th4fASbytHO48oLt09bmf1kcsWQg12uVGcfet-nN5NpsxY4s/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+papillary+fibroelastoma+of+the+AV.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><span style="font-family: "times" , "times new roman" , serif;"><img alt="" border="0" data-original-height="179" data-original-width="142" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjCcr5t7HKVXA4asDasrjwwSRcqxn083pq82xkAl2llU0I_WrwqUOG_iKN2M4ouV2UY4rUck8xeXUCXf_UlIVHIZFsWbG9Th4fASbytHO48oLt09bmf1kcsWQg12uVGcfet-nN5NpsxY4s/s320/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+papillary+fibroelastoma+of+the+AV.png" title="Papillary fibroelastoma of the aortic valve-cardiac tumor-cardiology book" width="253" /></span></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><b><span style="font-family: "times" , "times new roman" , serif; font-size: small;">Papillary fibroelastoma of the aortic valve</span></b></td></tr>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="background-color: white; font-family: "times" , "times new roman" , serif;"><br /></span></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="background-color: white; font-family: "times" , "times new roman" , serif;"><b><br /></b></span></span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;"><span style="background-color: white;"><b>Papillary fibroelastoma</b> is a benign tumor arising from the cardiac valves. It is the most common tumor of the cardiac valves. The average patient age is 60 years. Its diameter is often < 1 cm, but it may reach 1-2 cm, it has a small stalk and a shape resembling</span><span style="background-color: white;"> a sea anemone, floating in the blood. On echocardiography, these benign tumors have a</span></span><span style="font-size: large;"> small size, with independent motion and attachment to an endocardial surface (of a valve) via a central pedicle. The tumor typically has</span><span style="font-size: large;"> </span><span style="font-size: large;">frond-like arms (small </span><span style="font-size: large;">finger-like projections) and its</span><span style="font-size: large;"> borders appear shimmering, due to the vibration at the tumor-blood interface. The most common location is the aortic valve, followed by the mitral valve and rarely the right-sided valves or even the mural, nonvalvular endocardium. </span><span style="background-color: white; font-size: 15.9991px;">,</span><span style="font-size: large;">Papillary fibroelastomas </span><span style="font-size: large;">may cause valvular incompe</span><span style="font-size: large;">tence and thromboembolic complications.</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Thromboembolic complications may manifest as a transient ischaemic attack, a stroke, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">myocardial infarction, sudden death, syncope, blindness, or pulmonary embolism.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> If the tumor is located on the arterial side of the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">aortic valve, it may cause coronary obstruction.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Surgical excision of the tumor is curative and it is a reasonable decisio</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">n in symptomatic patients or when the tumor has been diagnosed incidentally in a </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">preoperative evaluation before </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">cardiac surgery for another reason.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><br /></span> <span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> </span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="color: #111111; white-space: pre-wrap;"><b style="background-color: orange;">A Video</b><span style="background-color: white;"> Papillary fibroelastoma in 2D (modified short- and long-axis views) and 3D-transesophageal echocardiography. by the You Tube channel </span></span><yt-formatted-string class="style-scope ytd-video-owner-renderer" id="owner-name" style="background-color: white; line-height: 1.6rem;"><a class="yt-simple-endpoint style-scope yt-formatted-string" href="https://www.youtube.com/channel/UC40suIYE3RDE90v1zLwT3Hg" style="cursor: pointer; display: inline-block; font-weight: var(--yt-formatted-string-endpoint_-_font-weight); line-height: var(--yt-formatted-string-endpoint_-_line-height); text-decoration-line: none;">CDT</a></yt-formatted-string></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">LINK <a href="https://www.youtube.com/watch?v=nwDKIFGLnMo" target="_blank">Papillary fibroelastoma of the aortic valve</a></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac sarcoma</span></h3>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Sarcomas are the most common malignant primary cardiac tumors. Typical age of presentation is between 40 and 50 years. On echocardiography, they appear as a broad-based mass with</span><span style="font-size: large;"> </span><span style="font-size: large;">heterogeneous echogenicity, usually in the right atrium. They may also appear in any cardiac chamber and they also often affect the pericardium, resulting in a pericardial effusion and pericardial chest pain. When located in a right cardiac chamber they can affect tricuspid valve function, produce clinical manifestations of right-sided heart failure and /or metastasize to the lungs. Hypoechogenic areas may indicate tumor necrosis. D</span><span style="font-size: large;">ifferential diagnosis is with a myxoma. In contrast to a myxoma, sarcomas do not have a stalk. Sarcomas tend to have a rapid growth, obstructing blood flow. Treatment with surgical debulking of the tumor is occasionally performed.</span></span></div>
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<span style="font-size: large;"><span style="color: #111111; font-family: "roboto" , "arial" , sans-serif; white-space: pre-wrap;"><b style="background-color: orange;"><br /></b></span></span></div>
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<span style="font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span><span style="color: #990000;">:</span></b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<span style="background-color: orange; font-size: large;"><b>Bibliography and links </b></span></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b></span></b></div>
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"> Paraskevaidis IA, Michalakeas CA, Papadopoulos CH, Anastasiou-Nana M. Cardiac Tumors. ISRN Oncology 2011:1-5.</span> http://dx.doi.org/10.5402/2011/208929</b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195386/" target="_blank">Cardiac Tumors</a></span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Hoffmeier, A, Sindermann, JR, Scheld H, Martens, S. Cardiac Tumors-Diagnosis and Surgical Treatment. Deutsches Ärzteblatt International 2014; 111: 205-211. http://doi.org/10.3238/arztebl.2014.0205</span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3983698/" target="_blank">Cardiac Tumors-Diagnosis and Surgical Treatment</a></b></span></div>
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /><br />Takahashi A, Otsuka H, Harada M. Multimodal Cardiovascular Imaging of Cardiac Tumors. 2015;2(1):61-67. http://dx.doi.org/10.17996/anc.02.01.61</span></b><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.jstage.jst.go.jp/article/anc/2/1/2_61/_pdf" target="_blank">Multimodal Cardiovascular Imaging of Cardiac Tumors</a></b></span></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /><br />Mankad R, Herrmann J. Cardiac tumors: echo assessment. Echo Res Pract 2015;3(4):R65-R77. http://dx.doi.org/10.1530/erp-16-0035</b></span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5292983/" target="_blank">Cardiac tumors: echo assessment</a></span></b><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Yuan S-M, Shinfeld A, Lavee J, et al. Imaging morphology of cardiac </b></span><b style="font-family: arial, helvetica, sans-serif;">tumours. Cardiol J 2009; 16:26-35.</b></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-5872482856596602762018-02-04T22:02:00.000+02:002020-02-15T17:05:32.425+02:00Assessment of left and right ventricular systolic and diastolic function with echocardiography<script async="" src="//pagead2.googlesyndication.com/pagead/js/adsbygoogle.js"></script> <script>
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<b style="font-size: x-large;">Echocardiography: Useful indices of left ventricular systolic function</b></h4>
<span style="font-size: large;">The most frequently used methods for the assessment of left ventricular (LV) systolic function are LV ejection fraction (EF) and regional wall motion analysis. Two dimensional (and also M-mode) echocardiography is the most common technique used but other tests that can examine LV systolic function are </span><span style="font-size: large;">tissue Doppler imaging (TDI), speckle tracking imaging, three-dimensional (3D) echocardiography, </span><span style="font-size: large;">computed tomography (CT), and cardiac magnetic resonance imaging </span><span style="font-size: large;">(CMR).</span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;"><u>M-mode echocardiography</u>, which records the motion of cardiac structures in one dimension, can be used to obtain some indices of left ventricular (LV) systolic function. Measurements of LV dimensions are made </span><span style="font-size: large;">in the parasternal long-axis view </span><span style="font-size: large;">by positioning the cursor through the LV minor axis at the level of the tips of the mitral leaflets. Then fractional shortening (FS) </span><span style="font-size: large;">can be calcu</span><span style="font-size: large;">lated </span><span style="font-size: large;">and even ejection fraction (EF) can be calculated with geometric assumptions (that are not accurate, if there are significant differences in regional contractile function, between various segments of the LV walls).</span><br />
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<span style="font-size: large;"><u>Fractional shortening (FS)</u> is calculated from linear measurements</span></div>
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<span style="font-size: large;">of LV dimensions from M-mode or 2D images:</span></div>
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<span style="font-size: large;">FS = 100% × (LVDd – LVDs)/LVDd </span></div>
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<span style="font-size: large;">where LVDd and LVDs are the LV end-diastolic dimension and</span></div>
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<span style="font-size: large;">end-systolic dimension, respectively. FS normal values: 25-45 %</span><br />
<span style="font-size: large;">FS as an index of global LV function can be problematic when there is a marked difference in regional function, in patients with a previous myocardial infarction.</span></div>
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<span style="font-size: large;">Two-dimensional (2D) echocardiography for the evaluation of LV systolic function</span></h4>
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<span style="font-size: large;">This is the primary mode for evaluation of LV systolic function. Endocardial border </span><span style="font-size: large;">motion and wall thickening can be visualized and an experienced examiner can assess regional and global contractile function and roughly estimate the ejection fraction (EF) just by visualizing the LV in various echocardiographic views ("eyeball approach"). Quantitative measurements are obtained by tracing the endocardial border in end diastole and end systole in the apical 4- and 2-chamber views using the method of discs (modified Simpson rule). The machine software divides the LV along its long axis into a series of </span><span style="font-size: large;">discs of equal height. Individual disc volume is calculated as </span><span style="font-size: large;">height x disc area. LV volume is then calculated as the sum of disc volumes.</span></div>
<span style="font-size: large;"></span><span style="font-size: large;"><b>The ejection fraction (EF)</b>= stroke volume/end diastolic volume.<br />Stroke volume= the volume of blood ejected by a ventricle in systole= EDV-ESV. </span><br />
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<span style="font-size: large;">(EDV= end diastolic volume, ESV= end systolic volume). </span><br />
<span style="font-size: large;">Thus, </span><span style="font-size: large;">EF= </span><span style="font-size: large;"> (</span><span style="font-size: large;">EDV-ESV)/ EDV. </span></div>
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<span style="font-size: large;">The left ventricular EF generally has a normal value </span><span style="font-family: "times new roman" , serif; line-height: 18.4px;"><span style="font-size: large;">≥</span></span><span style="font-size: large;"> 55%.</span><br />
<span style="font-size: large;"> It is a measure of global LV systolic function, with established prognostic significance (the lower the EF, the worse the prognosis), but it is also influenced by preload, afterload, heart rate, and valvular function. (In patients with severe aortic or mitral regurgitation, conditions causing volume overload of the left ventricle, the normal value for the EF is </span><span style="font-family: "times new roman" , serif; font-size: large; line-height: 25.68px;">≥ 60%.) </span><span style="font-size: large;"> Systolic function of the left ventricle (LV) is considered as mildly reduced when EF is between 45 and 55 %, moderately reduced with EF between 30 and 45 % and severely reduced with EF< 30%.</span><br />
<span style="font-size: large;"> Left ventricular </span><span style="font-size: large;">EF is a strong predictor of clinical outcome </span><span style="font-size: large;">and is widely used to make clinical decisions.</span><br />
<span style="font-size: large;">EF should be calculated from volumetric measurements</span><br />
<span style="font-size: large;">by 2D echocardiography. Even more accurate measurements of left ventricular volumes and EF are obtained with three dimensional (3D) echocardiography, or magnetic resonance imaging (MRI). The latter two techniques have similar accuracy.</span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">(The answers are given at the end of the video). To see it larger after starting the video click on the symbol [] on the lower right corner.</span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;">Parasternal long axis echocardiogram of a patient with dilated cardiomyopathy</span></h1>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;">A male patient (age 40 ) with symptoms of heart failure (nocturnal and exertional dyspnea). He was diagnosed with dilated cardiomyopathy. Parasternal long axis echocardiographic view: The left ventricle and the left atrium are dilated. The anteroseptal and the posterior left ventricular wall are severely hypokinetic. There is also a very small pericardial effusion.The coronary arteriography was normal. He was treated with ramipril (ACE inhibitor), carvedilol (beta-blocker), furosemide (loop diuretic) and eplerenone (aldosterone antagonist). On re-examination symptoms and left ventricular function showed improvement.</span></h4>
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<span style="font-size: large;">Doppler Echocardiography derived systolic indices (stroke volume)</span></h4>
<span style="font-size: large;">Doppler echocardiography also provides some indices of LV systolic function, such as the stroke volume </span><span style="font-size: large;">(SV), i.e. the </span><span style="font-size: large;">blood volume ejected per beat. For this measurement one obtains from the apical 5 chamber view the pulse wave doppler signal of the velocity in the left ventricular outflow tract (LVOT) and also measures the diameter of the LVOT (in the parasternal long axis view at the base of the aortic valve leaflets or immediately proximal to the aortic valve). </span><br />
<span style="font-size: large;">SV= VTI</span> (LVOT) <span style="font-size: large;">x area </span>(LVOT)<br />
<span style="font-size: large;">VTI is the </span><span style="font-size: large;">velocity time </span><span style="font-size: large;">integral (also named time velocity integral-TVI) of blood flow through the LVOT during systole. </span><br />
<span style="font-size: large;">This formula is explained as follows: VTI is calculated as the area under the curve of the Doppler velocity signal (which displays velocity on the vertical axis and time on the horizontal axis). This area of the Doppler signal is automatically calculated by the machine software, after the examiner manually traces the doppler velocity signal. It mathematically represents a velocity time integral, i.e. the sum of many products of velocity x time, each corresponding to every small time interval in systole. Since in every small time interval the column of blood moves by a distance given by the product of blood velocity x time interval, the VTI as a sum represents the total distance the column of blood has "traveled" in systole. This distance multiplied by the area of the orifice through which blood has passed, is the volume of blood which passed through the orifice in systole= the stroke volume (SV). </span><span style="font-size: large;"> <span style="font-family: "times" , "times new roman" , serif;">A</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-size: medium;">ssuming a circular </span><span style="font-family: inherit; font-size: medium;">LVOT with radius r and diameter D (=2r) :</span><span style="font-weight: bold;"> </span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">LVOT area = <span style="text-align: justify;">πr<sup>2</sup>=3,14r<sup>2</sup>=3,14(D/2)</span><sup style="text-align: justify;"><span lang="EN-US">2</span></sup><span style="text-align: justify;"> </span><span style="text-align: justify;">=</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="text-align: justify;"> (3,14 D</span><sup style="text-align: justify;"><span lang="EN-US">2</span></sup><span style="text-align: justify;">)/4=<span style="font-size: medium;"> <span style="font-family: inherit;">0,785D</span></span></span><sup style="text-align: justify;"><span lang="EN-US">2</span></sup> </span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-size: medium;">In the absence of aortic</span> <span style="font-size: medium;">regurgitation, SV reflects the forward effective blood flow in a cardiac beat and multiplied by heart rate (beats per minute) it gives the cardiac output (= the volume of blood passing through the circulation per minute). Strictly speaking, the SV is the hemodynamic result of LV function and not a true index of systolic function. Normal values of SV: 55-80 mL.</span></span><br />
<span style="font-family: inherit; font-size: large;">It is better to express the normal values of stroke volume per </span><span style="font-size: large;">m</span><sup style="text-align: justify;"><span lang="EN-US" style="font-family: inherit; font-size: 14pt;">2 </span></sup><span style="font-size: large;">of body surface area: </span><br />
<span style="font-size: large;">Normal values of </span><span style="font-family: inherit; font-size: large;">SV(ml/m</span><sup style="font-family: inherit; text-align: justify;"><span lang="EN-US" style="font-family: inherit; font-size: 14pt;">2</span></sup><span style="font-size: large;">): </span><span style="font-size: large;">26-54</span><br />
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<span style="font-size: large;">Tissue Doppler Imaging (TDI)</span></h4>
<span style="font-size: large;">Measurement of mitral ring velocities or myocardial velocities of the basal segments (velocity of the movement of these tissues along the longitudinal axis of the heart) is a simple and sensitive method for the assessment of the left ventricular systolic and diastolic function. Both peak systolic (Sm) and early diastolic (Em) mitral annular or left ventricular basal velocities are nearly always reduced in patients presenting with the clinical syndrome of systolic heart failure.</span><br />
<span style="font-size: large;">The systolic annular velocity of the mitral valve (<b>Sm</b>) is a measure of left ventricular longitudinal contraction (contraction of the long axis oft the ventricle). It generally correlates well with the left ventricular EF. Normally Sm of the septal mitral annulus is > 6.5 cm/sec, and Sm of the lateral mitral annulus </span><span style="font-size: large;">≥ 8 cm/sec</span><span style="font-size: large;">, when measured with pulse wave tissue doppler (PW-TDI). It is better to assess the mean Sm of the septal and lateral mitral annulus (normal value > 7.5 cm/sec). Note that myocardial velocities measured by the color TDI method are lower than velocities by pulsed Doppler (typically about 25% lower).</span><br />
<span style="font-size: large;">Early myocardial damage often involves the subendocardial fibres, with impairment in long-axis contraction occuring before changes in short-axis function. Thus, the Sm is a sensitive marker of mildly impaired left ventricular systolic function, even in people with apparently preserved systolic function and a normal EF, for example in those with diastolic heart failure, or in some diabetic patients without overt heart disease. Reduced annular TDI velocities are also present in subjects with hypertrophic cardiomyopathy, (even in people having the related gene mutations, who are at the stage of subclinical disease, with no cardiac hypertrophy).</span><br />
<span style="font-size: large;">Note that whereas the Sm velocity is an index of left ventricular systolic function, the Em or E΄velocity (the peak early diastolic mitral annular velocity, which is a negative wave) is an index of LV diastolic function and the Am or A΄velocity (an end-diastolic negative wave) is an index of the systolic function of the left atrium.</span><br />
<span style="font-size: large;"><br /></span><span style="font-size: large;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small; font-weight: 700;">Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and Limitations.Heart, Lung and Circulation 2015;24:224-233</span></span><br />
<span style="font-size: large;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small; font-weight: 700;"> LINK </span><a href="http://www.heartlungcirc.org/article/S1443-9506(14)00733-1/pdf" style="font-family: Arial, Helvetica, sans-serif; font-size: medium; font-weight: 700;" target="_blank">Tissue Doppler Imaging in Echocardiography</a></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b>Myocardial strain and strain rate</b> imaging</span></h4>
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<span style="color: #222222; font-size: large;">In general, in myocardial segments with diminished systolic function, systolic velocities are typically reduced and there are also reductions in systolic strain and strain rate.<span style="font-family: "times" , "times new roman" , serif;"> </span><b style="font-family: Times, "Times New Roman", serif;">Strain</b><span style="font-family: "times" , "times new roman" , serif;"> </span><span style="font-family: "times" , "times new roman" , serif;">is the proportion (percentage) of change in length of the myocardium (units %) and it is negative in systole, since there is a negative change in length (shortening), and positive in diastole (because in diastole the length increases).</span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;"> Strain = L-Lo /Lo, where L is the current length and Lo is the original length of a myocardial segment. </span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;">Strain describes deformation (change in length) of the myocardium which occurs in three different directions, therefore there are three different types of strain, longitudinal (which is most often measured), circumferential and radial. Deformation in these three directions results from the different orientation of subepicardial and epicardial myofibers, that also generate a counterclockwise twist at the apex of the left ventricle and a clockwise twist at the base. </span></span></span><span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;">During systole the left ventricle undergoes </span><span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;">longitudinal and circumferential shortening,</span><span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;">(denoted by a negative value of longitudinal and circumferential strain) and radial</span><br />
<span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;">thickening (positive value of radial strain in systole).</span><br />
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<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;"><b><br /></b></span></span></span></div>
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<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;"><b></b><b></b></span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;"><b>Strain rate (SR)</b> is the rate of change of the strain value= the proportional change in length per unit of time. SR units are </span><span style="background-color: white; color: #222222;">s<sup>-1</sup></span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;">SR is negative in systole (because it represents the rate of proportional decrease in myocardial length) and positive in diastole (because it represents the rate of increase in length). LV longitudinal velocities measured from an apical window increase progressively from the apical toward the basal myocardial segments. Longitudinal strain and strain rate, however, are essentially similar between apical and basal segments.</span></span></span></div>
<span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;"> Global longitu</span><span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;">dinal strain (GLS) is derived from averaging multiple </span><span style="color: #222222; font-family: "times" , "times new roman" , serif; font-size: large;">regions. It is a useful and sensitive marker of systolic function. It has a negative value (shortening). Normal GLS has a value between 18-20%. Borderline values are between 16-18 %, whereas abnormal (reduced) GLS is < 16% and severely reduced below 12%. </span><br />
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<span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;">The normal value of the peak systolic strain (percentage of shortening) of the left ventricle during systole in the longitudinal axis is greater than 15%. To be more accurate, let us mention that normal peak systolic strain has a value more negative than -15%, usually between -15 and -25%. (The negative sign indicates a decrease in the length of the myocardium, i.e. shortening).</span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;">Peak systolic strain is influenced by preload (like the ejection fraction which is also influenced by the ventricular loading conditions) and can be used as an indicator of the total, and of the regional systolic function (when measured at a segment of the left ventricle). </span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;">The normal value for the peak systolic strain rate of the left ventricular myocardium is between - 1.2 and - 2 </span><span style="background-color: white; color: #222222;"> </span><span style="background-color: white; color: #222222;">s<sup>-1 </sup></span><span style="background-color: white; color: #222222;">(sec</span><sup style="background-color: white; color: #222222;">-1</sup><span style="background-color: white; color: #222222;">=1/s).</span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;"> In normal hearts the value of strain rate and strain is about the same in all myocardial segments from the base to the apex of the heart, (showing no significant difference). Conversely, myocardial velocity recorded by the tissue Doppler (in cm/s), and the displacement (change in position) of a given point of the myocardium (in mm) is greater in the basal portions and is getting smaller towards the apex. </span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="background-color: white; color: #222222;">An advantage of the percentage of myocardial deformation (strain) and of the rate of the proportional change in deformation (strain rate) is the following: Strain and strain rate is not affected by the translational motion of the heart ("bouncing" movements in the chest during systole). In contrast, the myocardial velocities recorded with tissue Doppler (TDI) are affected by the translational motion of the heart within the chest and not only by the motion of myocardial shortening in systole or lengthening in diastole.</span></span></span></div>
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<span lang="EN-US"><sup><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><o:p></o:p></span></sup></span></div>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: inherit; font-size: large;"><span style="background-color: white; color: #222222;">A diminished peak systolic strain or strain rate is a sensitive marker of an impairment in systolic function. </span>Need more information about these modern echocardiographic techniques? In that case, here is a link </span><span style="font-size: large;">for you to click on</span><span style="font-family: inherit; font-size: large;"> (free review article with the option to download PDF) ...</span></span><br />
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805816/" target="_blank"><span style="font-size: large;">Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability</span></a><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Dandel Μ ,Lehmkuhl H, et al. Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability. Current Cardiology Reviews, 2009, 5, 133-148.</b></span><span style="font-family: inherit; font-size: large;"> </span></div>
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<span style="font-size: large;">Assessment of left ventricular diastolic function (a summary)</span></h4>
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<span style="font-size: large;">Diastolic dysfunction can occur in many kinds of heart disease such as hypertensive heart disease, diabetes, hypertrophic cardiomyopathy, aortic stenosis with left ventricular hypertrophy, ischemic heart disease, restrictive cardiomyopathy, constrictive pericarditis, etc.</span></div>
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<span style="font-size: large;">Assessment of left ventricular (LV) diastolic function with echocardiography is a part of the routine evaluation of patients presenting with symptoms of dyspnea or heart failure. </span><br />
<span style="font-size: large;">There are four key variables for a quick assessment of LV diastolic function. LV diastolic dysfunction is present if more than half of these parameters meet the abnormal cutoff values. These key parameters are:</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b>The peak early diastolic velocity of the mitral annulus </span><span style="font-size: large;">e΄</span><span style="font-size: large;">, obtained from the pulse wave tissue Doppler velocity tracing of the septal and lateral mitral annulus, in the apical 4 chamber view. The velocity </span><span style="font-size: large;">e΄is a marker of myocardial relaxation and it is reduced in all stages of diastolic dysfunction. A normal </span><span style="font-size: large;">e΄ is a strong indication that the diastolic function is normal, except in patients with constrictive pericarditis or significant mitral regurgitation.</span><br />
<span style="font-size: large;">The normal septal </span><span style="font-size: large;">e΄ </span><span style="font-family: "times new roman" , serif; font-size: 18pt;">≥ 8 cm/ s (centimeters per second). The lateral </span><span style="font-size: large;">e΄ is normally higher than the septal (> 10 cm/s). Abnormal values suggestive of diastolic dysfunction: a septal </span><span style="font-size: large;">e΄< 7 and a lateral </span><span style="font-size: large;">e΄< 10 cm/s.</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The average E/</span><span style="font-size: large;">e΄ ratio. This is the ratio of the peak early diastolic mitral inflow velocity E to the average of the </span><span style="font-size: large;">e΄ velocities of the septal and lateral mitral annulus. Abnormal is a ratio E/</span><span style="font-size: large;">e΄>14. The ratio E/</span><span style="font-size: large;">e΄ is less age-dependent than other indices of LV diastolic function. A ratio > 14, regardless of the patient's age, is almost always abnormal, suggesting elevated LV diastolic pressures (and thus, an elevated mean left atrial pressure and pulmonary capillary wedge pressure)</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The LA volume index is the maximum volume of the left atrium (LA), measured at the end of ventricular systole, divided by the patient's body surface area (BSA). </span><span style="font-size: large;">LA volume index > 34 ml/</span><span style="font-family: inherit; font-size: large;">m<sup>2 </sup></span><span style="font-size: large;">is considered abnormal, indicating left atrial dilation. LA dilation in the absence of a chronic atrial arrhythmia (e.g. atrial fibrillation), or mitral valve disease, is an indication of increased LV filling pressures, resulting in chronically elevated left atrial pressures.</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The peak tricuspid regurgitation (TR) velocity measured with the continuous wave Doppler. A peak TR velocity > 2.8 m/s is suggestive of an elevated pulmonary arterial systolic pressure (with the exception of pulmonary stenosis). This can often result from elevated pulmonary venous pressures due to the elevated left atrial pressure caused by LV diastolic dysfunction (provided that there are no indications suggestive of another cause of pulmonary hypertension e.g. pulmonary arterial hypertension, lung disease, valvular heart disease, LV systolic dysfunction).</span><br />
<span style="font-size: large;">A more detailed discussion follows:</span><br />
<span style="font-size: large;">Evaluation of left ventricular (LV) diastolic function begins with M-mode and 2D echocardiography : </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> Assessment of </span><span style="font-size: large;"> LV size, and wall thickness and </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b>Assessment of left atrial (LA) </span><span style="font-size: large;">volume and anteroposterior dimension. </span><br />
<span style="font-size: large;">In patients with LV diastolic dysfunction, concentric or</span><br />
<span style="font-size: large;">eccentric LV hypertrophy can be found. Pathologic LV hypertrophy is usually associated with an increased left ventricular stiffness which results in diastolic dysfunction. </span><br />
<span style="font-size: large;">Increased LA volume reflects the effects of the </span><span style="font-size: large;">increased LV filling pressures over time. </span><span style="font-size: large;"> Elevated left ventricular filling pressures can occur in patients with diastolic or systolic dysfunction. LA dilation can also occur in patients with mitral stenosis or regurgitation and in patients with chronic permanent atrial fibrillation. LA volume is measured at end-systole in the apical 4 chamber view with the same method (Simpson's method of summation of disks) used for the measurement of left ventricular volume.</span><span style="font-size: large;"></span></div>
<span style="font-size: large;">Doppler assessment: To assess the mitral inflow a</span><span style="font-size: large;">lign the Doppler beam with the inflow direction and p</span><span style="font-size: large;">lace a 1-3 mm pulse wave (PW) Doppler sample volume between the </span><span style="font-size: large;">tips of the </span><span style="font-size: large;">mitral leaflets. If the </span><span style="font-size: large;"> PW sample volume position is not at the valve tips, but </span><span style="font-size: large;">towards the mitral annulus or towards the </span><span style="font-size: large;">apex, this can alter significantly the mitral flow </span><span style="font-size: large;">velocities.</span><br />
<span style="font-size: large;">E is the peak early diastolic velocity of transmitral flow and A is the peak late diastolic velocity at the time of atrial contraction. In adults with normal diastolic function E/A has a value between 0.8 and 2, but less than 2 (In younger people E>A and in middle-aged or older people E wave normally becomes lower and A increases and can be higher than A).<br /> In adults with <b>normal diastolic function (normal pattern)</b> the E > A but is less than 2A (except in very young persons), or E may be a little smaller than A, but more than 0.8 A (the E wave can be lower than the A wave by less than 20 %). The deceleration time (DT) of the E wave (time from the peak of the E wave to its end at the baseline) is </span><span style="font-size: large;">150-200 ms (milliseconds). Isovolumic relaxation time (the time from the end of aortic flow to the beginning of mitral flow) is IVRT = 50-100 ms. </span><span style="font-size: large;">Measure isovolumic relaxation time (IVRT) by placing </span><span style="font-size: large;">the PW Doppler sample volume in- between LV inflow and </span><span style="font-size: large;">outflow to simultaneously display the end of aortic flow </span><span style="font-size: large;">and the onset of mitral E-wave velocity. </span><br />
<span style="font-size: large;">In very young people with normal diastolic function E/A can be >2, but this is not due to an increased LA pressure as in the restrictive pattern. This pattern in young people is normal and is due to a more active relaxation of the left ventricle (LV) in early diastole so that early diastolic flow velocity is increased. It is easy to distinguish this from the restrictive pattern because these are very young individuals with no heart disease, no symptoms of effort dyspnea, normal left atrial size and normal tissue Doppler velocities of the mitral annulus.</span></div>
<div>
<span style="font-size: large;">Pulse wave Doppler of pulmonary venous flow (obtained in the apical 4 chamber view) in adults with normal diastolic function and also in those with mildly impaired diastolic function (delayed relaxation) shows S ≥ D. S is the peak velocity of the systolic wave and D the peak velocity of the early diastolic wave of pulmonary venous flow. </span><br />
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<span style="font-size: large;">In people with normal diastolic function and also in those with mild diastolic dysfunction (impaired relaxation) </span><span style="font-size: large;">the ratio E/e΄ is <10. E is the peak velocity of the early transmitral flow and e'</span><span style="font-size: large;"> (or </span><span style="font-size: large;">Ea) is the peak early diastolic velocity of the mitral annulus measured by pulse wave tissue Doppler.</span></div>
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<span style="font-size: large;">In more advanced forms of diastolic dysfunction (moderate or grade- 2 diastolic dysfunction with a pseudonormal pattern of transmitral flow-see below, or severe diastolic dysfunction with the restrictive pattern), the pulmonary venous flow shows S<D and tissue Doppler of the mitral annulus shows an elevated ratio E/</span><span style="font-size: large;">e΄</span><span style="font-size: large;"> and a reduced velocity </span><span style="font-size: large;">e΄</span><span style="font-size: large;">. According to the recent ASE (American Society of Echocardiography) and EACVI (European Association for Cardiovascular Imaging) recommendations, abnormal values indicating left ventricular (LV) diastolic dysfunction are the following: Peak early diastolic velocity (</span><span style="font-size: large;">e΄) of the septal mitral annulus< 7 cm/s, </span><span style="font-size: large;">e΄ of the lateral mitral annulus < 10 cm/s and an average ratio E/</span><span style="font-size: large;">e΄> 14. </span><br />
<span style="font-size: large;"><b>Mild (grade 1) diastolic dysfunction</b> is characterized by the impaired relaxation (or delayed relaxation) mitral inflow pattern with E/A<0.8, </span><span style="font-size: large; text-align: justify;">E </span><span style="font-family: "times new roman" , serif; font-size: 18pt; text-align: justify;">≤ </span><span style="font-size: large; text-align: justify;">50 cm/s </span><span style="font-size: large;">and a prolonged deceleration time DT of the mitral flow E wave ( DT> 200 ms). DT is the time from the peak to the end </span><span style="font-size: large;">of the E wave</span><span style="font-size: large;">. There is also prolongation of isovolumic relaxation time, </span><span style="font-size: medium;"><span style="font-size: large;">IVRT ≥ 100 ms. </span><span style="font-family: "arial" , "helvetica" , sans-serif;">The IVRT is the time from the closure of the aortic valve (end of left ventricular ejection) to the opening of the mitral valve (onset of ventricular filling). In this time interval, left ventricular dimensions are constant and the mitral annulus does not move. So, the IVRT can be measured on the pulse wave tissue Doppler tracing of the mitral annulus as the time from the end of the systolic S wave to the onset of the </span></span><span style="font-family: "arial" , "helvetica" , sans-serif;">e΄ (Ea) wave.</span><br />
<span style="font-size: large;">In grade 1 diastolic dysfunction the pulse wave Doppler of pulmonary venous flow shows S>D, where S is the peak velocity of the systolic flow in the pulmonary vein and D the peak velocity of the early diastolic flow.</span><br />
<span style="font-size: large;">In grade 1 diastolic dysfunction mean left atrial pressure and left ventricular filling pressure is not elevated.</span><br />
<span style="font-size: large;">An important point is that <b>age </b>should be taken into account when evaluating LV diastolic function since the LV filling pattern in healthy elderly individuals resembles that of younger people (e.g. 40-60 years old) with mild (grade 1) diastolic dysfunction. Indeed, healthy sedentary elderly people usually have a mild degree of diastolic dysfunction (grade 1) as a result of an increased left ventricular stiffness and a slower myocardial relaxation in comparison to younger individuals.</span><br />
<span style="font-size: large;"><b>Moderate (grade 2) diastolic dysfunction </b>shows the same transmitral flow pattern (</span><span style="font-size: large;">0.8 < E/A <2), as that observed in people with normal diastolic function. It is called <b>pseudonormal pattern</b>.</span><br />
<span style="font-size: large;">In the pseudonormal pattern (as well as in the normal pattern),</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">150 <DT <200 ms and </span><span style="font-size: large;">IVRT is <100 msec (range 60-100 msec).</span><br />
<span style="font-size: large;">This pattern can be distinguished from the normal pattern of diastolic inflow because at the peak of the Valsalva maneuver (which causes a reduction of preload = a reduction of ventricular filling) in people with grade-2 diastolic dysfunction, the pattern of mitral inflow takes the morphology of impaired relaxation (E< A). Other features of the pseudonormal pattern which allow its differentiation from the normal pattern are the following:</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> A reduced mitral annular e΄ velocity (this is a simple way to distinguish it from normal diastolic function, which is characterized by a normal </span><span style="font-size: large;">e΄).</span><span style="font-size: large;"> </span><span style="font-size: large;">The normal and pseudonormal filling pattern have the same pattern of transmitral flow (generally E>A), but </span><span style="font-size: large;">in case</span><span style="font-family: inherit; font-size: large;"> of a pseudonormal pattern,</span> <span style="font-size: large;">the </span><span style="font-size: large;">e΄</span><span style="font-size: large;"> velocity is reduced. </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The increased E/e΄ </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The pulse wave Doppler signal of the pulmonary venous flow showing S<D (S/D <1). </span><span style="font-size: large;">The peak velocity of the end-systolic pulmonary vein reverse flow wave at atrial systole </span><span style="font-size: large;">(AR)</span><span style="font-size: large;"> is elevated ( > 35 cm/s) and the duration of AR wave is increased: </span><br />
<span style="font-size: large;">AR wave duration-mitral<span style="font-family: inherit;"> A wave duration </span></span><span style="font-family: inherit;"><span style="font-size: large;"><span style="background-color: white; color: #222222; text-align: justify;">≥</span> </span><span style="font-size: large;">30 msec.</span></span><br />
<span style="font-size: large;">The pseudonormal mitral inflow pattern can change to a delayed relaxation pattern by reducing preload with diuretic treatment.</span><br />
<span style="font-size: large;"></span><br />
<b><span style="font-size: large;">Severe diastolic dysfunction is characterized by the </span><span style="font-size: large;">restrictive left ventricular </span></b><span style="font-size: large;"><b>filling pattern</b>, where the markedly elevated left atrial pressure causes an increased early transmitral pressure gradient (pressure difference between the left atrium and the left ventricle) in early diastole. This causes the following findings: </span><br />
<span style="font-size: large;"> E/A ratio >2, a short deceleration time (DT </span><span style="font-size: large;"><150 ms) and also a short IVRT < 60 ms. Due to the severe impairment of diastolic function, </span><span style="font-size: large;">mitral annular e΄ velocity is usually severely reduced, the ratio E/e΄ is increased and </span><span style="font-size: large;">pulmonary venous flow shows S<<D (the peak velocity of the S wave is much lower than the peak velocity of the D wave). </span><span style="font-size: large;">The peak velocity of the end-systolic pulmonary vein reverse flow wave at atrial systole </span><span style="font-size: large;">(AR)</span><span style="font-size: large;"> is elevated ( > 35 cm/s) and </span><span style="font-size: large;">AR wave duration-mitral<span style="font-family: inherit;"> A wave duration </span></span><span style="font-family: inherit;"><span style="font-size: large;"><span style="background-color: white; color: #222222; text-align: justify;">≥</span> </span><span style="font-size: large;">30 msec.</span></span><br />
<span style="font-size: large;">The restrictive pattern </span><span style="font-size: large;">is called <b>stage 3 diastolic dysfunction</b></span><span style="font-size: large;"> if it can change, by reducing preload with diuretic treatment, </span><span style="font-size: large;">to a pattern of stage 1 or 2 diastolic dysfunction. If treatment cannot change the restrictive pattern of left ventricular filling, then there is <b>stage-4 diastolic dysfunction </b>which carries a severe prognosis.</span><br />
<span style="font-size: large;">Regarding the tissue Doppler examination of the velocities of the mitral annulus, the early diastolic peak velocity of the mitral annulus (</span><span style="font-size: large;">e΄ or </span><span style="font-size: large;">Ea) is generally a good index of diastolic function. It is </span><span style="font-size: large;">higher at the lateral mitral annulus than at the septal </span><span style="font-size: large;">annulus. An indication of diastolic dysfunction is </span><span style="font-size: large;">an e΄ < 7 cm/s at the septal annulus,</span><span style="font-size: large;"> </span><span style="font-size: large;">or <10 cm/sec at the lateral annulus. Moreover, </span><span style="font-size: large;">e΄</span><span style="font-size: large;"> has a </span><span style="font-size: large;">reasonable accuracy in</span><span style="font-size: large;"> identifying patients with diastolic dysfunction </span><span style="font-size: large;">and pseudonormal LV filling. </span><br />
<span style="font-size: large;">In people with cardiac disease, an increased E/e΄ ratio can provide an indication of the presence of an elevated left ventricular filling pressure and pulmonary capillary wedge pressure, </span></div>
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<span style="font-size: large;">if the ratio is > 15 for the septal mitral annulus or > 13 for the lateral mitral annulus. For the septal mitral annulus, an E/e΄ between 10 and 15 is borderline, and cannot predict if the left ventricular diastolic pressures are elevated or normal. </span><span style="font-size: large;">When an average (septal, and lateral) e΄ velocity is available, a cutoff value of 14 should be considered for the E/e΄ ratio.</span><span style="font-size: large;"><br /></span><br />
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<h3>
<span style="font-size: large;">Assessment of the dimensions and function of the right ventricle with echocardiography</span></h3>
<span style="font-size: large;">Evaluation of right ventricular (RV) function is important because RV dysfunction has been associated with increased morbidity and mortality in patients with </span><span style="font-size: large;">valvular heart disease, </span><span style="font-size: large;">congenital heart disease, </span><span style="font-size: large;">pulmonary hypertension, </span><span style="font-size: large;">heart failure and</span><span style="font-size: large;"> coronary artery disease.</span></div>
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<span style="font-size: large;">Assessment of the size and function of the right ventricle (RV) is complex because it has a </span><span style="font-size: large;"> unique</span><span style="font-size: large;"> crescentic </span><span style="font-size: large;">geometry, and also because changes in its shape and orientation occur under </span><span style="font-size: large;">conditions of increased volume or resistance loading. Generally, the con</span><span style="font-size: large;">tractile pattern of the RV involves longitudinal </span><span style="font-size: large;">muscle fibers more than those in the transverse plane. Visual assessment of the motion of the RV free wall, although useful in the assessment of RV function, should not be the sole method for the evaluation of right ventricular systolic function, especially in cases where there are reasons to suspect that it may be abnormal.</span><br />
<span style="font-size: large; font-weight: normal;">.</span><span style="font-size: large;">Normally the right ventricular wall is thinner and more compliant than the left ventricular wall. Right ventricular wall thickness in diastole can be measured in the subxiphoid echocardiographic view. Normally it is < 5 mm.</span><br />
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<span style="font-size: large;"><span style="font-weight: normal;">A practical assessment of the right ventricular size is obtained by its comparison </span></span><span style="font-size: large; font-weight: normal;">with the size of the left ventricle in the apical four-chamber view. Normally the right ventricle (RV) </span><span style="font-size: large; font-weight: normal;">should be less than two-thirds of the </span><span style="font-size: large; font-weight: normal;">size of the left ventricle (LV). However, this may be misleading </span><span style="font-size: large; font-weight: normal;">when LV dilation coexists.</span></div>
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<span style="font-size: large;"><span style="font-weight: 400;">Moreover, it can be roughly estimated that the right ventricle is enlarged when on the apical 4 chamber view, the size of the right ventricle is equal to or greater than the left ventricle and when the distal part of the right ventricle contributes together with the left ventricle in the formation of the heart apex. Normally the heart apex is formed solely by the left ventricle. Also, in the case of right ventricular dilatation, the interventricular septum is shifted towards the left ventricle, thus reducing the dimensions of the left ventricle. This has an adverse effect on left ventricular diastolic filling.</span></span></div>
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<span style="font-size: large;">The most useful echocardiographic view for the assessment of right ventricular dimensions is the apical 4 chamber view and preferably the RV-focused apical view. This is an apical 4 chamber view obtained by tilting the transducer to point more towards the right side of the patient's body, allowing in most cases better </span><span style="font-size: large;">visualization of the entire right ventricular (RV) free wall than in a standard four-chamber view which is centered on the left ventricle.</span><span style="font-size: large;"> It is useful to have the transducer approximately at the position of the cardiac apex. If it is medially from the apex, then the view may represent a larger part of the right ventricle and a smaller part of the left one. This can sometimes give a false impression of a dilated right ventricle</span><span style="font-size: large; font-weight: normal;"><span style="font-size: 18.72px;">. </span></span><br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhVeTdYjaaUhdVyV4evwBlhOJ_GJkhElGzK3lfQCdwxRkvY2b_8GMiiT9uk80fq_3jIMuPMcbhtfSJozwBBsVmB48kPk5SKG3PubH7SZNVoQ7M2W81yNE4E6KOXd1WCde1j7AdxMuGBNdQ/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+RV+focused+apical+4+chamber+view.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="" border="0" data-original-height="254" data-original-width="342" height="296" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhVeTdYjaaUhdVyV4evwBlhOJ_GJkhElGzK3lfQCdwxRkvY2b_8GMiiT9uk80fq_3jIMuPMcbhtfSJozwBBsVmB48kPk5SKG3PubH7SZNVoQ7M2W81yNE4E6KOXd1WCde1j7AdxMuGBNdQ/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+RV+focused+apical+4+chamber+view.png" title=" Echocardiography: An RV- focused apical 4 chamber view-cardiology book" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: small;"><b> An RV-focused apical 4 chamber view. </b></span></td></tr>
</tbody></table>
<span style="font-size: large; font-weight: normal;"><span style="font-size: 18.72px;"><br /></span></span>
<span style="font-size: large; font-weight: normal;"><span style="font-size: 18.72px;"><br /></span></span>
<span style="font-size: large;">It is recommended to measure the RV dimensions in the RV focused apical 4 chamber view. </span><br />
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<span style="font-size: large; font-weight: normal;">In this view, the short axis (width) of the right ventricular cavity is normally at the base < 4.1 and at the mid-ventricular level ≤ 3.5 cm (normal values 2-3.5 cm).</span></div>
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<span style="font-size: large;"><span style="font-weight: 400;">In the apical </span></span><span style="font-size: large; font-weight: 400;">4 chamber </span><span style="font-size: large;"><span style="font-weight: 400;">view, the right ventricle can be planimetered, that is, it's area can be measured. The right ventricular area at end-diastole with respect to the body surface area (BSA) normally is 5-12.6 c</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="line-height: 27.6px;"> </span><span style="font-weight: 400;">/ </span><span style="font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span></span><span style="font-size: large;"><span style="font-weight: 400;">. </span></span></div>
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<span style="font-size: large;"><span style="font-weight: 400;">The area of the right ventricle normally is less than 2/3 of the left ventricular area. When the ratio of the right ventricular area to the left ventricular area is between 1 and 1.5 then there is a moderate dilatation of the right ventricle while when it is > 1.5 then the dilatation of the right ventricle is severe. (In mild enlargement of the right ventricle, the ratio is between 0.6 and 1).</span></span></div>
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<span style="font-size: large; font-weight: 400;"> I</span><span style="font-size: large; font-weight: 400;">n the apical 4-chamber view, t</span><span style="font-size: large; font-weight: 400;">he end-systolic area of the right ventricle divided by the BSA normally is in men ≤ 7.4 c</span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: 400;">/ </span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="font-size: large; font-weight: 400;"> and in women ≤ 6.4 c</span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: 400;">/ </span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span></div>
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<span style="font-size: large; font-weight: normal;">In the parasternal long-axis view, an index of the size of the right ventricle is the end-diastolic width of the right ventricular outflow tract RVOT). This is the width of the RVOT measured from the junction of the interventricular septum and the aorta to the free wall of the RVOT in end-diastole. It should normally be <3 cm.</span></div>
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<span style="font-size: large;"><span style="font-size: large;">(Watch this <span style="background-color: #e06666;">video</span> from 123sonography, which demonstrates these echocardiographic findings Link:</span><span class="video-thumb yt-thumb yt-thumb-48 g-hovercard" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" style="background: rgb(241 , 241 , 241); border: 0px; color: #167ac6; cursor: pointer; display: inline-block; font-family: "roboto" , "arial" , sans-serif; font-size: 0px; margin: 0px; overflow: hidden; padding: 0px; position: relative; vertical-align: middle; width: 48px;"><span class="yt-thumb-square" style="background: transparent; border: 0px; display: inline !important; height: auto; margin: 0px; padding: 0px 0px 48px;"><span class="yt-thumb-clip" style="background: transparent; border: 0px; bottom: -100px; display: inline !important; left: -100px; margin: 0px; padding: 0px; position: absolute; right: -100px; text-align: center; top: -100px; white-space: nowrap; word-break: normal;"><a class="yt-user-photo g-hovercard yt-uix-sessionlink spf-link " data-sessionlink="itct=CDAQ4TkiEwiY8p3issDSAhXOWxYKHUbjDiYo-B0" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" href="https://www.youtube.com/user/123sonography" style="background: rgb(255, 255, 255); border: 0px; color: #167ac6; display: inline; font-size: 13px; margin: 0px; padding: 0px; text-decoration-line: none;"> </a><a class="yt-user-photo g-hovercard yt-uix-sessionlink spf-link " data-sessionlink="itct=CDAQ4TkiEwiY8p3issDSAhXOWxYKHUbjDiYo-B0" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" href="https://www.youtube.com/user/123sonography" style="background: rgb(255, 255, 255); border: 0px; color: #167ac6; display: inline; font-size: 13px; margin: 0px; padding: 0px; text-decoration-line: none;"><span class="video-thumb yt-thumb yt-thumb-48 g-hovercard" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" style="background: rgb(241, 241, 241); border: 0px; display: inline-block; font-size: 0px; margin: 0px; overflow: hidden; padding: 0px; position: relative; vertical-align: middle; width: 48px;"><span class="yt-thumb-square" style="background: transparent; border: 0px; display: inline !important; height: auto; margin: 0px; padding: 0px 0px 48px;"><span class="yt-thumb-clip" style="background: transparent; border: 0px; bottom: -100px; display: inline !important; left: -100px; margin: 0px; padding: 0px; position: absolute; right: -100px; top: -100px; word-break: normal;"><span class="vertical-align" style="background: transparent; border: 0px; display: inline-block; height: 248px; margin: 0px; padding: 0px; vertical-align: middle;"><span style="background-color: transparent;">123sonography</span></span></span></span></span></a></span></span></span></span></div>
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<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=jpEXFf2tRL4" target="_blank">https://www.youtube.com/watch?v=jpEXFf2tRL4</a>)</span></div>
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<span style="font-size: large; font-weight: 400;">For the assessment of right ventricular contractile function, it is useful to examine the M-mode of the movement of the lateral annulus of the tricuspid valve in the apical 4-chamber view. The maximum displacement of the lateral tricuspid annulus in the direction of the cardiac apex during systole (TAPSE) is measured. After the M mode function is selected, the cursor is positioned along the right side wall of the right ventricle in the apical 4-chamber view. The displacement of the lateral tricuspid annulus from end-diastole to end-systole is measured. This index provides a reliable estimate of right ventricular systolic function and has a good association with the right ventricular ejection fraction. (Exception: in case of severe tricuspid regurgitation, the association of TAPSE with the right ventricular ejection fraction is weaker.) TAPSE in normal subjects is on average 2.2-2.3 cm, while the lower normal limit is 1.8 cm. In the international guidelines for the echocardiographic assessment of the cardiac chambers, a TAPSE <17 mm is considered as a strong indication of right ventricular systolic dysfunction. TAPSE <1.5 cm indicates severe systolic dysfunction of the right ventricle. Prognostic significance: A low TAPSE indicates worse prognosis in pulmonary hypertension, heart failure, or chronic obstructive pulmonary disease.</span></div>
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<span style="font-size: large; font-weight: 400;">Right ventricular fractional area change (FAC) is calculated from the end-diastolic and the end-systolic surface of the right ventricle (RV), in an apical 4-chamber view. FAC provides an estimate of global right ventricular systolic function. When tracing the right ventricular cavity with the cursor, the entire RV must be contained in the imaging sector, including the apex and the free wall, during both diastole and systole. Also, care must be taken to include myocardial trabeculae and the moderator band as part of the RV cavity. The fractional area change (FAC) is calculated as follows:</span></div>
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<span style="font-size: large; font-weight: 400;">FAC = (EDA-ESA) / EDA (%).</span></div>
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<span style="font-size: large; font-weight: 400;">Where EDA is the end-diastolic and ESA the end-systolic area of the right ventricle. Right ventricular systolic dysfunction is indicated by FAC <35%.</span></div>
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<span style="font-size: large; font-weight: 400;">Another index of global right ventricular (RV) contractility is the peak systolic velocity S' of the lateral tricuspid annulus. This is obtained with pulse wave tissue Doppler imaging (TDI), by aligning the Doppler cursor with the lateral annulus and the basal segment of the right ventricular free wall, in the apical 4-chamber view. Suggestive of RV systolic dysfunction is S'< 9.5 cm/s. </span></div>
<span style="font-size: large;">Another </span><span style="font-size: large;">technique </span><span style="font-size: large;">used for the assessment of RV function</span><span style="font-size: large;"> is the myocardial performance index (MPI)</span><span style="font-size: large;">. It has the unique feature of incorporating </span><span style="font-size: large;">both systolic and diastolic function</span><span style="font-size: large;">. Isovolumic relaxation time (IVRT), isovolumic contraction </span><span style="font-size: large;">time (IVCT), and RV ejection time (RVET) are measured. These time intervals are better measured with </span><span style="font-size: large;">the tissue Doppler technique, by using the tissue Doppler velocity signal of the lateral tricuspid annulus. In </span><span style="font-size: large;">this way, measurements are obtained from the same heartbeat.</span><span style="font-size: large;"> </span><span style="font-size: large;">(Alternatively, MPI can be obtained with pulsed wave Doppler, with the RVET measured from the pulmonic outflow tract and the IVRT and IVCT at the tricuspid valve. When using the pulsed wave Doppler technique, since two different, not simultaneous measurements are required, these measurements should be always obtained at comparable R-R intervals.)</span><br />
<span style="font-size: large;">Myocardial performance index MPI= (IVRT + IVCT) / RVET</span><br />
<span style="font-size: large;">An elevated (abnormal) MPI indicates reduced right ventricular global function (either diminished right ventricular diastolic or diminished right ventricular systolic function or more commonly both) and is associated with a worse prognosis.</span><br />
<span style="font-size: large;">Abnormal tissue Doppler MPI </span><span style="font-size: large;">≥ 0.54</span><br />
<span style="font-size: large;">Abnormal pulsed Doppler MPI </span><span style="font-size: large;"> ≥ 0.43</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>For a better understanding of these time intervals and of the method used to calculate the MPI see below:</i></span></div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i> The isovolumic contraction time (IVCT) is a short time interval at the beginning of the ventricular systole in which the intraventricular pressure increases without a change in ventricular volume. This is the time from the closure of the tricuspid to the opening of the pulmonary valve. Since there is no blood flow at this time and the ventricular volume remains constant, there is also no displacement of the tricuspid annulus. </i></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>The ejection time (ET) lasts as long as the pulmonary valve is open when the ventricle ejects blood, ventricular volume decreases, and the tricuspid annulus moves towards the apex of the heart. </i></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>The isovolumic relaxation time (IVRT) is the initial part of diastole when the intraventricular pressure diminishes without any change in ventricular volume and therefore without any blood flow through the tricuspid valve and with no displacement of the tricuspid annulus. It is the time interval between the closure of the pulmonary valve and the opening of the tricuspid valve.</i></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i> From the above definitions, the following can be understood: The time interval between the closure of the tricuspid valve and its next opening (tricuspid valve closure to opening time-TCOT) is the sum of isovolumic contraction time (IVCT), the ejection time (ET) and the isovolumic relaxation time (IVRT). That is, TCOT = IVCT + ET + IVRT,</i></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>therefore IVCT + IVRT = TCOT-ET and </i></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>MPI = (IVCT + IVRT) / ET = (TCOT-ET) / ET</i></span></div>
<span style="font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<span style="color: #660000; font-family: "arial" , "helvetica" , sans-serif; font-size: large;"><b>Bibliography and links </b></span><br />
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<a href="http://asecho.org/wordpress/wp-content/uploads/2016/03/2016_LVDiastolicFunction.pdf" target="_blank"><span style="color: red; font-size: large;">Guideline ASE -2016 : Echocardiographic evaluation of diastolic function</span></a><br />
<i style="font-family: 'Helvetica Neue', Arial, Helvetica, sans-serif;">Cardiology free e-book online</i><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Lang, R. M., Badano, L. P., Mor-Avi, et al. Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015; 16 (3 ), 233-271. https://doi.org/10.1093/ehjci/jev014</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://academic.oup.com/ehjcimaging/article/16/3/233/2400086" target="_blank">https://academic.oup.com/ehjcimaging/article/16/3/233/2400086</a></b></span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Jones N, Burns AT, Prior DL Echocardiographic Assessment of the Right Ventricle–State of the Art. Heart Lung and Circulation 2019;28(9): 1339–1350 </span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="https://www.heartlungcirc.org/article/S1443-9506(19)30366-X/fulltext" target="_blank">Echocardiographic Assessment of the Right Ventricle–State of the Art</a></span></b><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br />Horton, K. D., Meece, R. W., & Hill, J. C. (2009). Assessment of the Right Ventricle by Echocardiography: A Primer for Cardiac Sonographers. Journal of the American Society of Echocardiography 2009;22: 776-792. https://doi.org/10.1016/j.echo.2009.04.027</span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="http://www.precisdanesthesiecardiaque.ch/Pdf/AnnECardiol/VD%20Examen%20%C3%A9cho.pdf" target="_blank">Assessment of right ventricular function with echocardiography-ASE 2009</a></span></b></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-44851335901191290712017-10-15T21:35:00.006+03:002021-08-28T20:36:33.501+03:00Common congenital cardiac anomalies with a L-R shunt Atrial septal defects (ASDs),Partial anomalous pulmonary venous return, Ventricular septal defects (VSDs), and Patent ductus arteriosus (PDA)<div>
<h2>
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</script> <span style="font-size: large;"><br /></span><span style="font-size: large;">Common congenital anomalies with a left to right shunt: Atrial septal defects (ASDs), Partial anomalous pulmonary venous return, Ventricular septal defects (VSDs), and Patent ductus arteriosus (PDA)</span></h2>
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<span style="font-size: large;"><br /></span></h3>
<h3>
<span style="font-size: large;">Atrial septum defect (ASD)</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /><span style="font-family: "times" , "times new roman" , serif;">An atrial septal defect (ASD) is a congenital defect in the interatrial septum allowing a direct communication between the atria. It is common, about 10% of all congenital heart disease cases, more common in females. (male to female ratio of 1:2).<br />There are three main types of ASDs:<br />Secundum ASD, the most common type (70-75% of ASDs) is located in the central portion of the interatrial septum.<br />Primum ASD, about 20% of all ASDs, (or partial endocardial cushion defect ) is in the lower part of the septum, near the atrioventricular valves. This is the second most common type. </span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Primum ASDs are a part of the spectrum of endocardial cushion defects. They are often accompanied by a c</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">left in the anterior leaflet of the mitral valve, causing mitral regurgitation. A complete endocardial cushion defect (complete atrioventricular canal defect) is a more complex congenital anomaly consisting of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">a primum ASD, a ventricular septal defect of the inlet type, and anomalies of the atrioventricular valves (a common atrioventricular valve). Endocardial cushion defects are commonly seen in patients with trisomy 21 (Down syndrome).</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Sinus venosus defect is located near the entrance of the superior vena cava (SVC) or the inferior vena cava IVC to the right atrium and is a less common type (about 5-10% of all ASDs), commonly associated with a partial anomalous pulmonary venous return.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pathophysiology of atrial septal defects ( ASDs)</span></h4>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">An ASD causes an abnormal flow between the atria, called a left to right (L-R) shunt, i.e. flow of blood through the defect with a direction towards the right heart chambers. This results in a volume overload to the right atrium and right ventricle and an increase in blood flow through the pulmonary arterial circulation. The magnitude of the L-R shunt depends upon the size of the defect and also the relative pressures on the left and right sides of the heart.</span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Clinical, electrocardiographic and echocardiographic findings in atrial septal defects </span></h4>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The patients are asymptomatic in the majority of cases but large defects can be associated with recurrent respiratory infections, shortness of breath on exertion (dyspnea), easy fatiguability, or atrial arrhythmias (palpitations). Patients with large defects, late in the course can develop complications, such as right heart failure, or pulmonary arterial hypertension PAH (see also chapter <a href="http://cardiologybookandcases.blogspot.gr/2017/03/pulmonary-hypertension-pulmonary-arterial-hypertension-cardiology-books.html" target="_blank">Pulmonary Hypertension</a>). Another rare complication of an ASD is a stroke due to paradoxical embolism (caused by a thrombus reaching the right atrium from the venous circulation and then crossing the ASD and entering the left cardiac chambers and the arterial circulation).</span></div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In a moderate or large ASD, physical examination findings usually include a widely and fixed split second heart sound (S2) and a systolic ejection murmur of low intensity, (grade 2 to 3/6) at the upper left sternal border (at the area of the pulmonary artery due to the increased blood flow through the right heart and the pulmonary artery).<br />In case of a large ASD with a large L-R shunt, a mid-diastolic rumble may be audible at the left lower sternal border, i.e. at the tricuspid area due to the increased flow through the valve.<br />The typical auscultatory findings often are not present in infants and toddlers, even with a large defect, because at this age the right ventricle often is not compliant enough to allow a large L-R shunt.<br />The ECG usually shows a RBBB, or an incomplete RBBB with an rsR′ pattern in V1 (also see chapter <a href="http://cardiologybookandcases.blogspot.gr/2016/06/the-electrocardiogram-ecg-adult-and-pediatric-ecg-interpretation.html">The Electrocardiogram -ECG</a> . In case of a moderate to large ASD, right QRS axis deviation (frontal axis between +90 to +180°) and/or other indications of right ventricular hypertrophy may be present, but in the case of an ostium primum defect, there is an RBBB pattern with a left QRS axis.<br />Chest radiographs if the shunt is moderate or large, show cardiomegaly (with right atrial and right ventricular enlargement), increased vascular markings in the lungs and a prominent main pulmonary artery (at the mid-left heart border).<br />Echocardiography in a patient with an atrial septal defect (ASD) shows the position and the size of the defect and the abnormal flow (shunt) through the interatrial septum. If the defect is moderate to large, echocardiography also shows a dilated right atrium, right ventricle, and pulmonary artery. The finding of dilated right heart chambers proves that the ASD is hemodynamically significant and is in favor of ASD closure.<br />Cardiac catheterization is not necessary for the diagnosis of an ASD, but it can be necessary in the case of significant pulmonary hypertension to decide if the defect should be closed.</span><br />
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<span face=""arial" , "helvetica" , sans-serif"><b>An asymptomatic female 14 years old with a low -intensity systolic ejection murmur at the upper left sternal border This is a modified apical 4 chamber view. Are there any abnormalities? What do the numbers 1-5 show? What treatment do you propose? (ALSO SEE THE VIDEO (two paragraphs below).</b></span><span face=""arial" , "helvetica" , sans-serif" style="font-size: medium;"><b><br /></b></span> <span face=""arial" , "helvetica" , sans-serif" style="font-size: medium;"><b><br /></b></span>
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<span face=""arial" , "helvetica" , sans-serif"><b>1. Right atrium (enlarged -compare with the left one)<br />2. Right ventricle (enlarged-compare with the left one)<br />3.Left atrium<br />4.Left ventricle<br />5. A color jet passing through the midportion of the atrial septum with a direction from left to right. It is a left to right shunt of blood at the midportion of the atrial septum due to a secundum ASD. Closure of the defect is indicated because the L-R shunt is significant enough to result in right heart chamber enlargement. In this case, transcatheter device closure was successfully performed.</b></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Natural history of atrial septal defects (ASDs)</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Spontaneous closure of an ASD often occurs in patients with secundum ASDs with a diameter < 8mm before the age of 1.5 years, but an ASD >8 mm rarely closes spontaneously.<br />After the age of 4 years, spontaneous closure is not likely to occur.<br />Spontaneous closure may occur only in secundum defects. It does not occur in primum or sinus venosus ASDs. If a large ASD is left without closure, pulmonary hypertension and signs of right heart failure can develop in the third or fourth decade of life.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Management of atrial septal defects</span></h3>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> In a patient with an ASD exercise restriction is not required unless the patient has symptoms.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Children with a secundum atrial septal defect are usually observed without intervention for at least the first 3 years of life, due to the possibility of spontaneous closure.</span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Closure of an ASD in children or adults, is indicated when there is evidence of right ventricular volume overload (a dilated right ventricle) in the presence of an atrial septal defect with size > 5 mm and in the absence of irreversible pulmonary arterial hypertension. In this case measurement of the ratio of pulmonary to systemic flow (Qp/Qs) is not necessary to confirm that the ASD is hemodynamically significant. If the ratio Qp/Qs is used, then the defect is considered hemodynamically significant and closure is decided if Qp/Qs ≥ 1.5:1, in the absence of irreversible pulmonary arterial hypertension. Closure of an ASD can be surgical or with a catheter device. Device closure is the preferred method when feasible, but it is only feasible in patients with a secundun ASD with a diameter ≥5 mm but < 32 mm for Amplatzer device and <18 mm for Helex device, provided there is enough rim ( at least 4 mm) of septal tissue around the defect ( for the appropriate placement of the device). The rim around the ASD is measured with 2-D echocardiography in 4 directions. After device closure of an ASD antiplatelet treatment is given, with aspirin 80-100 mg per day for 6 months. In children, device closure can be performed preferably if they weigh >15 kg.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">In the rare case of an ASD with pulmonary hypertension, closure of the ASD is indicated if systolic pulmonary arterial pressure is <2/3 of systemic systolic blood pressure and pulmonary vascular resistance <2/3 of systemic vascular resistance. If systolic pulmonary artery pressure and pulmonary vascular resistance exceed the above limits, ASD closure can be decided only when there is a L-R shunt with a ratio of pulmonary to systemic flow Qp / Qs of at least 1.5: 1, provided that pulmonary hypertension is reversible.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-family: "times new roman"; font-size: medium;"><b><i><u><br /></u></i></b></span> <span style="font-family: "times new roman"; font-size: medium;"><b><i><u><span style="background-color: #e06666;">A case (Video)</span> showing the ECG and echocardiographic features of a secundum atrial septum defect</u></i></b></span></span><br />
<span style="font-family: "times new roman"; font-size: large;"><b><i><u><br /></u></i></b></span> <span style="font-family: "times new roman"; font-size: large;"><b><i><u><br /></u></i></b></span>
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<iframe allowfullscreen="" class="YOUTUBE-iframe-video" data-thumbnail-src="https://i.ytimg.com/vi/IWqnmDnCAJk/0.jpg" frameborder="0" height="266" src="https://www.youtube.com/embed/IWqnmDnCAJk?feature=player_embedded" width="320"></iframe></div>
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<br /></div><div class="separator" style="clear: both; text-align: center;"><span style="font-size: medium;"><br /></span></div><div class="separator" style="clear: both; text-align: left;"><span style="background-color: white; color: #050505; white-space: pre-wrap;"><b><span style="font-family: arial; font-size: medium;">SECOND VIDEO: A case of a secundum atrial septal defect (ASD) In this patient there was a very late diagnosis in advanced age. The findings in the ECG, chest X-ray, transthoracic echocardiography (TTE), 2-D and 3-D transesophageal echocardiography (TEE) are shown and explained in this cardiology video. The diagnosis of ASD is often missed and one should consider it in cases with right atrial and right ventricular enlargement without any other cause. </span></b></span></div><div class="separator" style="clear: both; text-align: left;"><span style="background-color: white; color: #050505; white-space: pre-wrap;"><b><span style="font-family: arial;"><br /></span></b></span></div><div class="separator" style="clear: both; text-align: left;"><span style="background-color: white; color: #050505; white-space: pre-wrap;"><b><div class="separator" style="clear: both; text-align: center;"><iframe allowfullscreen="" class="BLOG_video_class" height="341" src="https://www.youtube.com/embed/lBwzv-nnbHo" width="410" youtube-src-id="lBwzv-nnbHo"></iframe></div><br /><span style="font-family: arial;"><br /></span></b></span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">Partial anomalous pulmonary venous </span><span style="font-size: large;">return </span></span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">This is a congenital anomaly, causing a L-R shunt. One or more (but not all) pulmonary veins drain into the right atrium directly or indirectly by draining into a systemic vein (e.g. into the superior vena cava , inferior vena cava, left innominate vein). The right pulmonary veins are more often involved. They may drain into the right atrium, or into the superior vena cava (in this case, often there is also an associated ASD of the sinus venosus type), or into the inferior vena cava in association with an intact atrial septum.<br />When the left pulmonary veins are involved, they drain into the left innominate vein or into the coronary sinus. Partial anomalous pulmonary venous return has many of the physiologic characteristics of an atrial defect (ASD) and it is also often associated with an ASD. Therefore, this condition is usually discussed in the same chapter with the ASD. Most often, there is an associated ASD, but in some cases, partial anomalous pulmonary venous return is present without an ASD.<br />The hemodynamics are those of an atrial defect, i.e. this condition also causes volume overload of the right atrium and the right ventricle and increases flow through the pulmonary circulation. <br />On clinical examination, a difference of an isolated partial anomalous pulmonary venous return from an ASD is the following: In the absence of a concomitant ASD, although the second heart sound (S2) can be widely split, this wide split of S2 is not fixed relative to respiration. <br />Similar to an ASD, often a midsystolic murmur (grade 2/6-3/6) is heard at the upper left sternal border, due to the increased flow through the pulmonary artery. Occasionally, a mid-diastolic rumble may also be present, resulting from increased flow through the tricuspid valve. <br />When there is an isolated partial anomalous pulmonary venous return without an ASD, this condition only rarely causes symptoms and the development of pulmonary hypertension is extremely rare.<br />ECG and radiographic findings are similar to those of an ASD: The ECG is normal or with RBBB or indications of right ventricular hypertrophy. The chest X-ray may demonstrate mild to moderate cardiomegaly due to the enlargement of the right heart chambers, prominence of the main pulmonary artery and increased vascular markings in the lungs.<br />Echocardiography should lead to the suspicion of partial anomalous pulmonary venous return when there is an enlargement of the right ventricle and atrium, without any other obvious cause and inability to visualize all four pulmonary veins. In normal infants and children, the suprasternal coronal "crab" view typically demonstrates the connection of the four pulmonary veins to the left atrium. The absence of any normal pulmonary venous connection to the left atrium should raise a suspicion of an anomalous pulmonary venous return. Transthoracic echocardiography (TTE) can demonstrate the dilated right ventricle and right atrium and it can often also demonstrate anomalous cardiac connections, but extracardiac connections may be difficult to identify on TTE. The demonstration of anomalous pulmonary venous return with extracardiac connections typically requires magnetic resonance imaging (MRI) or computed tomography (CT). <br />Partial anomalous pulmonary venous return is often found in patients with an ASD. The ASD can be of any type, although a sinus venosus ASD is most commonly associated with anomalous pulmonary venous return. A sinus venosus ASD often is associated with abnormal drainage of the right upper pulmonary vein. In the presence of diagnostic difficulties, cardiac MRI can establish the diagnosis of partial anomalous pulmonary venous return.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">of partial anomalous pulmonary venous return.</span></h4>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Surgery is indicated if there is a significant left-to-right shunt with a Qp/Qs ratio ></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> 2:1. Surgery is also indicated i</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">f patients demonstrate </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">evidence </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">of right heart volume overload (dilated right heart chambers on echocardiography) </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">or symptoms. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Surgery, when needed, is performed at an age of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">2 -5 years. When there is only an anomaly of one pulmonary vein, without an ASD, surgery is not undertaken.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Ventricular septal defects (VSDs)</span></h2>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">There are four anatomic types depending on the location of the defect.<br />Perimembranous or membranous VSD is the most common type (70%) and it involves the membranous septum, a small part of the septum immediately beneath the aortic valve. These defects usually also have an accompanying defect of the adjacent muscular septum and depending on the location of this defect they are further classified as perimembranous trabecular, perimembranous inlet or perimembranous outlet.<br />Another type of VSDs are inlet defects, which are located beneath the septal leaflet of the tricuspid valve.<br />Outlet VSDs, also called conal or supracristal, are located in close proximity to the annulus of the aortic valve and of the pulmonary valve. These two valve annuli form part of the defect's rim. A common complication of this defect involves herniation of the right coronary cusp of the aortic valve through the defect. This can cause a reduction of the shunt, but also it often causes progressive aortic regurgitation. It may also result in a degree of obstruction of the right ventricular outflow tract.<br />Trabecular (muscular) VSDs may be central or apical, depending on their location in the muscular interventricular septum.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pathophysiology of ventricular septal defects (VSDs)</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The main pathophysiologic feature of a VSD is a left to right (L-R) shunt. The magnitude of the shunt depends on the size of the defect and the pressure difference between the two ventricles, which in turn depends on the pulmonary arterial pressure and thus, on the level of the pulmonary arterial resistance. The larger the size of the defect and the lower the pulmonary vascular resistance, the larger the L-R shunt. </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A small defect does not cause any ventricular dilation or hypertrophy, a moderate-sized defect usually can cause left ventricular hypertrophy or dilation and a large defect can cause hypertrophy or dilation of both ventricles. Moreover, a small VSD, also called a restrictive VSD, has a large resistance and results in a significant pressure gradient between the two ventricles and a small shunt with Qp/Qs<1.5 :1 and pulmonary systolic pressure/systemic systolic pressure<0.3. </span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">On the contrary, a large nonrestrictive defect will cause a large shunt with Qp/Qs >2.2 and a small pressure gradient between the two ventricles. Pulmonary arterial systolic pressure/systemic systolic arterial pressure will be > 0.6. With a VSD of a moderate size these values will be intermediate, with a Qp/Qs between 1.5 and 2.2.<br />A large VSD if left untreated will cause over the years a progressive rise of the pulmonary vascular resistance, due to progressive obstructive changes of the pulmonary arterioles. This leads to an elevated pulmonary arterial and right ventricular systolic pressure resulting in a reduction in the magnitude of the L-R shunt. This condition has also effects on the ventricles with the left ventricle decreasing in dimensions, whereas the size of the right ventricle increases. When the obstructive changes in the pulmonary vasculature become serious and irreversible, bidirectional shunt develops across the VSD (or even net right to left R-L shunt) and this leads to the development of cyanosis because unoxygenated venous blood from the right ventricle enters the left ventricle and the systemic circulation.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Symptoms and signs of a VSD</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In infants and children, a small restrictive defect does not cause any symptoms and is diagnosed because of the auscultation of a murmur. A large non-restrictive VSD can cause dyspnea, failure to thrive and signs of congestive heart failure early, even at the age of 2-3 months, or later. In adults a small restrictive defect will be asymptomatic (and the only sign will be the murmur), a defect of a moderate size may cause dyspnea on exertion and palpitations due to the development of atrial fibrillation, whereas a large non-restrictive VSD can cause symptoms and signs of right heart failure and central cyanosis (Eisenmenger syndrome). Apart from cyanosis patients with Eisenmenger syndrome often have edema (due to the right-sided heart failure) and clubbing.<br />The murmur of a VSD is pansystolic (holosystolic, i.e. it is present during the whole duration of systole), grade 2/6-5/6, best heard at the lower left sternal border. The murmur can be accompanied by a palpable systolic thrill (also at the lower sternal border). The murmur occasionally can be early systolic in patients with small muscular VSDs.<br />Murmurs of increased flow may be audible if the shunt is moderate to large, such as a systolic murmur due to increased flow through the pulmonary valve, or an apical diastolic rumble due to increased flow through the mitral valve (The L-R shunt causes not only increased flow through the pulmonary valve and the pulmonary circulation, but also an increased flow through the mitral valve which also leads to volume overload of the left ventricle. This happens because as a result of the increased flow through the pulmonary circulation, there is also an increased pulmonary venous return of blood to the left atrium).<br />If pulmonary hypertension develops, the pulmonic component (P2) of the second heart sound becomes loud (generally a loud P2 is a sign indicative of pulmonary hypertension, regardless of the etiology). With the development of pulmonary hypertension the systolic murmur of a VSD becomes less prominent and if severe pulmonary hypertension develops the murmur usually disappears. This happens because in the presence of pulmonary hypertension there is a smaller pressure difference between the left and right ventricle resulting in a reduction in the flow of blood through the defect from the left into the right ventricle.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The ECG and the chest X-ray in patients with a VSD</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In patients with a small restrictive VSD both the ECG and the chest X-ray are usually normal. In patients with a defect of moderate size the ECG will usually show features of left ventricular and left atrial hypertrophy and enlargement respectively and in a large non-restrictive defect left atrial enlargement with combined ECG features of left and right ventricular hypertrophy. In the case of pulmonary vascular obstructive disease with pulmonary hypertension the ECG usually shows features of isolated right ventricular hypertrophy.<br />The chest X-ray in the case of a VSD with a moderate or large shunt will show enlargement of the cardiac silhouette (due to dilation of the left atrium and ventricle and occasionally also the right ventricle). A moderate to large shunt will also result in increased pulmonary vascular markings (to a degree that is in direct proportion to the magnitude of the L-R shunt). If pulmonary vascular obstructive disease with significant pulmonary arterial hypertension has developed, the main pulmonary artery and its main branches at the hila of the lungs are dilated, while there are markedly reduced pulmonary vascular markings at the lung fields (this is a typical chest X-ray pattern of pulmonary arterial hypertension of any cause).</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Echocardiography in a patient with a ventricular septal defect</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Transthoracic echocardiography can identify the presence of a VSD, from the turbulent jet of flow across the interventricular septum, and it can also demonstrate the location and size of the defect and it can provide information about its hemodynamic significance. An increased left ventricular and left atrial size (and also a Qp/Qs>1.5) indicates the presence of a significant (moderate or large) L-R shunt.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"> With the exception of the trabecular VSDs, a useful marker for the identification of the type of the VSD is its location relative to the valves. A membranous defect is near the aortic valve, an infudibular defect near both the pulmonic and the aortic valve and an inlet defect near the tricuspid valve. </span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;">From the peak gradient across a VSD measured with continuous wave Doppler, by subtracting this gradient from the systolic arterial pressure, the right ventricular systolic pressure (RVSP) can be calculated. RVSP is equal to PASP (pulmonary artery systolic pressure) if there is no coexisting stenosis of the right ventricular outflow tract or the pulmonary valve.</span></h4>
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<b><span face=""arial" , "helvetica" , sans-serif"><span style="background-color: yellow;"><br /></span></span></b>
<b><span face=""arial" , "helvetica" , sans-serif"><span style="background-color: yellow;">VIDEO </span>A restrictive (small) muscular ventricular septum defect located at the apical interventricular septum in a 15-years-old-boy with a holosystolic murmur</span></b><br />
<b style="font-family: arial, helvetica, sans-serif;">( ECHO- apical 4 chamber view). </b><span face="arial, helvetica, sans-serif" style="background-color: #f9cb9c;"><b>The case is </b><u><b>courtesy of Dr. </b><span style="font-size: large;">Kazi Ferdous </span></u></span></div>
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<b><span face=""arial" , "helvetica" , sans-serif" style="background-color: #f9cb9c;">(From the facebook group <a href="https://www.facebook.com/groups/340969856787445/" target="_blank">Cardiology</a>) </span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif">To view the video on a large screen, you can start it and click the symbol [] on the lower right corner. To return to the small screen press Esc</span></b></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;">Link in you tube: <a href="https://www.youtube.com/watch?v=1cYqcORTtFg&feature=youtu.be" target="_blank">Video- Small apical muscular VSD</a></span></div>
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<span face=""arial" , "helvetica" , sans-serif">A young woman with a harsh holosystolic murmur best heard at the mid-to lower left sternal border. Echocardiogram left parasternal long axis view. What is the cause of the patient's cardiac murmur ?</span></h4>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiuX4Vz6mJeB03jb_uHjKRay3mKCKYGMA0qq_2zfisY03Jnspoem65K5OKAgN8iZeFz80xHPC-QXrL2h1tAvxbE2JFXo8e7mMVqx5KdGiFjTmn3ACO3Mz3s4WIdpflYRNOeGxDMgmn6z4s/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+perimembranous+VSDr.png" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="334" data-original-width="477" height="280" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiuX4Vz6mJeB03jb_uHjKRay3mKCKYGMA0qq_2zfisY03Jnspoem65K5OKAgN8iZeFz80xHPC-QXrL2h1tAvxbE2JFXo8e7mMVqx5KdGiFjTmn3ACO3Mz3s4WIdpflYRNOeGxDMgmn6z4s/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+perimembranous+VSDr.png" title="congenital heart disease-cardiology book" width="400" /></a></div>
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<b style="font-family: arial, helvetica, sans-serif;">The cause of the murmur is a small perimebranous VSD.</b><br />
<b style="font-family: arial, helvetica, sans-serif;">1. The jet of turbulent high velocity flow originating from the left ventricle just proximal to the aortic valve and entering the right ventricle is shown (with color flow Doppler) 2. left ventricle, 3. aorta, 4. left atrium.</b><br />
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<span style="font-size: large;"> </span></h4>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac catheterization</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac catheterization is not needed for the diagnosis of a VSD, but only if there is pulmonary hypertension to calculate the pulmonary vascular resistance and in some cases where echocardiography does not fully clarify the anatomic diagnosis, or if there is a significant possibility of coronary artery disease. In a VSD with a L-R shunt cardiac catheterization will reveal an elevated oxygen saturation in the pulmonary artery, and this is also an indication that there is no severe pulmonary hypertension. In case that severe pulmonary hypertension has developed this will result in a significant reduction in the L-R shunt and so, much less oxygenated blood from the left ventricle will enter the right ventricle and the pulmonary artery. Therefore, in this case, the oxygen saturation in the pulmonary arterial blood will be low. In these cases, simultaneous comparison of the pulmonary arterial and systemic blood pressures is mandatory, as well as calculation of the pulmonary vascular resistance and assessment of its response to vasodilators. This assessment is necessary to demonstrate if pulmonary arterial hypertension is reversible or irreversible. </span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The natural history of ventricular septal defects (VSDs) </span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Membranous and muscular VSDs can decrease in size with time, or close spontaneously. Until the age of 6 months spontaneous closure occurs in about 30-40% of these defects. On the contrary, inlet or infudibular defects do not decrease in size and thus they also do not demonstrate spontaneous closure. <br />In infants with large VSDs congestive heart failure can occur but usually after the first 6-8 weeks of life, because at that time the pulmonary vascular resistance has fallen enough to allow a large L-R shunt which can cause severe volume overload of the left heart chambers due to the increased pulmonary venous return.<br />Large VSDs can cause a slowly progressive elevation of the pulmonary arterial pressure. This is the result of progressive obstructive changes in the pulmonary arterioles as a reaction of the pulmonary arterial circulation to the chronically increased blood flow. Although pulmonary vascular changes may begin early, even at an age of 6-12 months, severe pulmonary arterial hypertension leading to a R-L shunt and the appearance of cyanosis usually does not occur before the second decade of life. <br />Another complication that can develop in some infants with a large VSD is infudibular stenosis, i.e. stenosis of the right ventricular outflow tract just below the pulmonary valve. This reduces the L-R shunt and in some cases it may even cause the development of a R-L shunt with cyanosis, a condition similar to the tetralogy of Fallot.</span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment of the patient with a VSD </span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In infants with large defects usually medical treatment is given initially (furosemide, ACE inhibitor) to control heart failure, while waiting for the gradual spontaneous decrease in the size of the defect, but if this does not happen or if there is inadequate control of the manifestations of congestive heart failure then closure of the defect is decided. <br />In children and adults indications for VSD closure are the following: A VSD of a hemodynamically significant size, i.e a defect causing symptoms or dilation of the left ventricle, or a gradual worsening in left ventricular function, or Qp/Qs> 1.5:1 or an elevation in pulmonary arterial pressure > 50 mmHg but in the last case with a pulmonary vascular resistance <7 Wood Units. If the pulmonary vascular resistance > 7 Woods then the defect is closed if there is a shunt with a Qp/Qs> 1.5 : 1 or reactivity of the pulmonary circulation to vasodilators has been demonstrated (a fall in pulmonary vascular resistance and pulmonary arterial pressure with vasodilators). If there is irreversible pulmonary arterial hypertension and Eisenmenger syndrome then closure of any pathologic communication between the left and right circulation (such as a VSD or an ASD) is contraindicated. <br />Another indication for the closure of a VSD is related to the development of aortic regurgitation as a complication of an outlet VSD, which can be progressive. There is an indication for closure if such a VSD causes more than mild AR.</span><br />
<span style="font-size: large;"><br /></span> <span face=""arial" , "helvetica" , sans-serif"><b style="background-color: #ffd966;">A video. Echocardiogram of a woman (age 22) with a small perimebranous ventricular septal defect. From the you tube channel </b></span><br />
<yt-formatted-string class="style-scope ytd-video-owner-renderer" id="owner-name" style="--yt-endpoint-hover-color: var(--yt-channel-owner); line-height: 1.6rem;"><span face=""arial" , "helvetica" , sans-serif" style="cursor: pointer; display: inline-block;"><b><span style="background-color: #ffd966;"><a class="yt-simple-endpoint style-scope yt-formatted-string" href="https://www.youtube.com/channel/UCOkL3t3eT-uIhYMUQofOXUg" spellcheck="false" style="cursor: pointer; display: inline-block; text-decoration-line: none;">Julián Vega Adauy</a> </span><span style="background-color: white;"> LINK to the Video: </span></b></span></yt-formatted-string><span face=""arial" , "helvetica" , sans-serif"><b><a href="https://www.youtube.com/watch?v=K7OFrdxRVBc" target="_blank">perimembranous ventricular septal defect-echocardiogram</a></b></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Patent ductus arteriosus (PDA)</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The ductus arteriosus is a vessel of the fetal circulation which forms a communication between the proximal descending aorta, just distal to the origin of the left subclavian artery and the bifurcation of the pulmonary artery. This vessel is open in the fetus, but it normally closes immediately after birth. The closed ductus after birth will normally form the ligamentum arteriosum.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A patent ductus arteriosus (PDA) is a congenital anomaly occurring when the ductus fails to close after birth, occurring in 1:2000 live births. It is more common in females. Factors increasing the risk for a PDA are premature birth, maternal rubella, birth at a high altitude and genetic factors.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A PDA causes a left to right ( L-R) shunt with a direction from the aorta to the pulmonary artery, because the pressure in the aorta is higher than that of the pulmonary artery. </span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">A PDA (patent ductus arteriosus) is classified based on its </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">size and the magnitude of the L-R shunt. A measure of the magnitude of the shunt is </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Qp/Qs (</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">the ratio of pulmonary to systemic flow).</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">• A silent PDA: very small duct, no murmur on clinical examination, usually detected </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">only on echocardiography</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">• A small PDA : A continuous murmur is present. Qp/Qs <1.5</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">• A moderate PDA: </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">A continuous murmur is present.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Qp/Qs between 1.5 and 2.2</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">• A large PDA: </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">A continuous murmur is present.</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Qp/Qs > 2.2</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">• PDA with Eisenmenger syndrome: Significant pulmonary hypertension with reversal of the shunt direction (R-L, i.e., from the pulmonary artery to the aorta). This causes differential</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> cyanosis (cyanosis </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">in toes and not fingers). In this case, the murmur is only </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">systolic or inaudible (not heard).</span></span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pathophysiology of patent ductus arteriosus</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">A patent ductus arteriosus (PDA), when it is of a moderate or large size, pathophysiologically causes:</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">1) Increased flow in the pulmonary circulation. This happens because, in addition to the normal flow of blood from the right ventricle through the pulmonary artery to the lungs to get oxygenated, an additional amount of blood enters the pulmonary circulation through the ductus.</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;">2) Left ventricular volume overload. This is an important consequence and occurs in a PDA of a large or at least moderate size. The left ventricle (LV) is forced to accommodate and pump a larger volume of blood. This happens because the blood returning to the LV through the pulmonary veins and the left atrium, includes not only the cardiac output of the systemic circulation, that is, the amount of blood returning from the tissues to the right heart cavities and then to the pulmonary circulation, but also blood shunted into the pulmonary circulation through the PDA, which has bypassed the systemic circulation. Therefore, the LV needs to pump more blood (both the amount of blood that will pass into the systemic circulation plus the shunt that bypasses the systemic circulation through the PDA.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;">LV volume overload, when large, may cause left heart failure. Increased blood flow through the pulmonary circulation, when there is a large shunt, can cause gradual changes in the pulmonary arterioles resulting in an elevated pulmonary vascular resistance and the occurrence of pulmonary arterial hypertension after some years.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">If pulmonary arterial pressure increases to levels equal to or greater than the systemic blood pressure, then the shunt will reverse. That is, the shunt will have an opposite direction, from the pulmonary artery to the aorta (Eisenmenger syndrome). In case of a PDA, if Eisenmenger syndrome occurs, the murmur is only systolic or inaudible (the amount and velocity of the shunting blood</span><span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif;"> </span>is </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">reduced due to a smaller pressure difference between the two communicating arteries). Moreover, the leakage of non-oxygenated blood from the pulmonary artery through the PDA to the descending aorta causes differential hypoxemia and differential cyanosis. This means that a low hemoglobin oxygen saturation and cyanosis are present in the lower extremities, but not in the face, nor in the upper extremities. The reason is that non-oxygenated blood enters the pulmonary artery into the aorta at the site of the PDA, i.e. distal to the origins of the arteries of the head and the upper limbs.</span></span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Clinical manifestations of a patent ductus arteriosus (PDA) </span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Patients with a small PDA with an audible continuous murmur, do not have any clinical manifestations except from rare cases of infectious endarteritis (infective endocarditis at the site of the abnormal arterial communication). In a moderate or large-sized PDA, patients may have dyspnea (due to left ventricular volume overload and failure or due to pulmonary hypertension) or palpitations, resulting from atrial fibrillation or flutter (the left atrial dilation resulting from the increased pulmonary venous return is a predisposing factor for these arrhythmias).</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span> </span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Physical examination</span></h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Cardiac auscultation reveals a continuous murmur best heard on the first or second intercostal space at the left sternal border, with its maximum intensity at end-systole.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">In cases of a PDA of large or moderate size:</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><br /></span>
<br />
<ul>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">There are bounding peripheral arterial pulses and wide pulse pressure (an elevated<span style="font-family: "times" , "times new roman" , serif;"> difference between the systolic and the diastolic pressure), due to runoff of blood into the pulmonary artery during diastole. </span></span></li>
<li><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The apical impulse of the left ventricle (LV) can be prominent and laterally displaced (due to LV enlargement/ LV volume overload). </span></li>
</ul>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">When moderate pulmonary hypertension occurs, the diastolic component of the murmur disappears and only a systolic murmur remains. In severe pulmonary hypertension with a shunt reversal (Eisenmenger's syndrome), differential cyanosis is observed. (Cyanosis of the lower extremities, but not the upper part of the body). </span><br />
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Diagnostic testing</span></h4>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"></span><br /></span> <span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">The ECG in PDA if the L-R shunt is small is normal. If the ductus</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> is large, the ECG shows left ventricular or biventricular hypertrophy .</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">The chest X-ray in a large PDA shows a prominent </span><span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">pulmonary artery with increased pulmonary vascular markings. When the shunt is large the chest X-ray usually shows an enlargement of the</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> left atrium and left ventricle. </span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Εchocardiography in PDA will show in the basal parasternal short-axis view, a jet of </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">systolic and diastolic (usually both) retrograde turbulent flow in the </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">pulmonary artery. L</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">eft atrial and left ventricular</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">enlargement will be present only if the shunt is large.</span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: #c27ba0;"><br /></b></span> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: #c27ba0;">A video</b> ( ECG and echocardiography of a woman with a patent ductus arteriosus)</span></span><br />
<span face=""arial" , "helvetica" , sans-serif" style="font-size: medium;"><span style="background-color: white; color: #111111; white-space: pre-wrap;"><b>A 30-year-old woman, who presented for cardiac evaluation, because of a continuous cardiac murmur (grade 3/6, best heard at the second left intercostal space). She was asymptomatic. Physical examination also revealed a wide pulse pressure. Echo showed patent ductus arteriosus of small to moderate size, and normal estimated pulmonary arterial pressure. The PDA was closed with a transcatheter closure device in a specialized center.</b></span></span><br />
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<h4><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span></h4><h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Treatment of PDA</span></h4>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Duct closure is usually recommended, irrespective of the patient's age, if a duct is clinically detectable, i.e. there is a continuous murmur in the left subclavicular area. The reason is to avoid long-term </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">complications, such as endarteritis (which is also possible with a small ductus), or if the </span></span><span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">ductus is of a moderate to large size, arrhythmias, left ventricular failure, or pulmonary hypertension. T</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">ranscatheter device closure is usually preferred and feasible for ducts with a diameter</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> up to 14 mm. If transcatheter closure is not feasible, then surgical closure is undertaken. B</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">efore repair of large </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">ducts, the presence of severe p</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">ulmonary vascular disease should be excluded</span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">. </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Pulmonary hypertension is not a contraindication to surgical or transcatheter PDA closure at any age if cardiac catheterization demonstrates that shunt flow is still predominantly left to right and that severe pulmonary vascular disease is not present.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<b><span face=""arial" , "helvetica" , sans-serif" style="background-color: #93c47d; font-size: large;">Bibliography and links </span></b><br />
<h2 style="box-sizing: border-box; font-family: "Meta Serif Pro", Georgia, serif; font-size: 1em; margin: 0px 0px 1em;">
</h2>
</div><div><span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span></div><div><span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span></div><div><span style="font-family: arial;"><span style="font-weight: 700;">Puri K, Allen HD, Qureshi AM. Congenital Heart Disease. Pediatrics in Review 2017;38(10):471–486. Available from: </span><a href="https://doi.org/10.1542/pir.2017-0032" style="font-weight: 700;" target="_blank">10.1542/pir.2017-0032</a></span></div><div><span face=""arial" , "helvetica" , sans-serif"><div><span lang="EN-US" style="line-height: 17.12px;"><b><span style="font-family: arial;"><br /></span></b></span></div><div><span lang="EN-US" style="line-height: 17.12px;"><b><span style="font-family: arial;"><br /></span></b></span></div><div><span lang="EN-US" style="line-height: 17.12px;"><b><span style="font-family: arial;">Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(14):e698-e800. </span></b></span></div><div><span style="font-family: arial;"><b>LINK <a href="https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603" target="_blank">https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603</a></b></span></div></span></div><div><span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span></div><div><span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span></div><div><span face=""arial" , "helvetica" , sans-serif"><b>Deri A, English K. EDUCATIONAL SERIES IN CONGENITAL HEART DISEASE: Echocardiographic assessment of left to right shunts: atrial septal defect, ventricular septal defect, atrioventricular septal defect, patent arterial duct. Echo research and practice 2018;5(1):R1-R16. http://dx.doi.org/10.1530/erp-17-0062</b></span></div>
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<span face=""arial" , "helvetica" , sans-serif"><b>LINK <a href="http://www.echorespract.com/content/5/1/R1.long" target="_blank">http://www.echorespract.com/content/5/1/R1.long</a></b></span><b><span face=""arial" , "helvetica" , sans-serif" style="font-size: large;"><br /></span></b>
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<span face=""arial" , "helvetica" , sans-serif"><br /></span> <span face=""arial" , "helvetica" , sans-serif"><span color="rgba(0 , 0 , 0 , 0.9)" style="background-color: white;"><b>Rao PS, Harris AD. Recent advances in managing septal defects: ventricular septal defects and atrioventricular septal defects </b></span></span><span face=""arial" , "helvetica" , sans-serif"><b> F1000Res </b></span><b style="color: rgba(0, 0, 0, 0.9); font-family: Arial, Helvetica, sans-serif;">2018;7:498. http://dx.doi.org/10.12688/f1000research.14102.1</b><br />
<b style="color: rgba(0, 0, 0, 0.9); font-family: Arial, Helvetica, sans-serif;">LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5931264/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5931264/</a></b><br />
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<span color="rgba(0 , 0 , 0 , 0.9)" style="background-color: white;"><span face=""arial" , "helvetica" , sans-serif"><b>Savis A, Simpson J. Echocardiographic approach to catheter closure of atrial septal defects: patient selection, procedural guidance and post-procedural checks.</b></span></span><br />
<span color="rgba(0 , 0 , 0 , 0.9)" style="background-color: white;"><span face=""arial" , "helvetica" , sans-serif"><b> </b></span></span><b style="background-color: white; border-bottom: 0px; color: #660066; outline: 0px;"><span face=""arial" , "helvetica" , sans-serif"><a abstractlink="yes" alsec="jour" alterm="Echo Res Pract." aria-expanded="false" aria-haspopup="true" href="https://www.ncbi.nlm.nih.gov/pubmed/29588310#" role="menuitem" style="background-color: white; border-bottom: 0px; color: #660066; outline: 0px;" title="Echo research and practice.">Echo Res Pract</a> </span></b><b style="background-color: white; color: rgba(0, 0, 0, 0.9); font-family: Arial, Helvetica, sans-serif;">2018;5(2):R49-R64. http://dx.doi.org/10.1530/erp-18-0007</b><br />
<b style="background-color: white; color: rgba(0, 0, 0, 0.9); font-family: Arial, Helvetica, sans-serif;">LINK<a href="https://www.ncbi.nlm.nih.gov/pubmed/29588310" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/29588310</a></b><br />
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<span face=""arial" , "helvetica" , sans-serif"><b>Lam JY, Lopushinsky SR, Ma IW, Dicke F, Brindle ME. Treatment Options for Pediatric Patent Ductus Arteriosus. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25835756#">Chest.</a> 2015;148(3):784-793</b></span></div>
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<span face=""arial" , "helvetica" , sans-serif"><b>LINK <a href="https://linkinghub.elsevier.com/retrieve/pii/S0012-3692(15)50658-2" target="_blank">https://linkinghub.elsevier.com/retrieve/pii/S0012-3692(15)50658-2</a></b></span><br />
<span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span> <span face=""arial" , "helvetica" , sans-serif"><b><a href="file:///C:/Users/admin/Desktop/Acyanotic%20congenital%20heart%20disease%20Congenital%20Heart%20Surgery%20handout.pdf" target="_blank">Acyanotic congenital heart defects</a></b></span> <span face=""arial" , "helvetica" , sans-serif"><br /></span> <span face=""arial" , "helvetica" , sans-serif"><br /></span></div>
Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-27823615753780176622017-10-15T21:31:00.004+03:002021-08-28T20:28:38.755+03:00Congenital heart disease. A concise introduction (overview)<h2>
Congenital heart disease. A concise overview</h2>
<span style="font-size: large;">This chapter is a brief, general introduction to congenital heart disease. The diagnosis and treatment of specific congenital heart defects will be discussed in other chapters.</span><br />
<h3>
<span style="font-size: large;">Definition and causes of congenital heart disease</span></h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-size: medium;">Congenital heart disease includes cardiac lesions that are present from birth. They are </span>anatomic malformations of the heart or great vessels which occur during intrauterine development, irrespective of the age at presentation. The most common congenital defects in humans are congenital heart defects. The overall incidence of congenital heart disease is about 1 in 100 infants (live births). The incidence of moderate to severe congenital heart disease is approximately 6/1000 infants.</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-size: medium;">Congenital heart defects are usually classified into acyanotic and cyanotic depending whether the patients clinically exhibit cyanosis. The acyanotic defects are further classified into </span>left-to right shunt lesions and obstructive lesions. In contrast to the acyanotic defects, in cyanotic heart defects unoxygenated systemic venous blood bypasses the pulmonary circulation and gets shunted into the left side of the heart.</span><br />
<span style="font-size: large;">Remarkable improvement in outcomes for patients with congenital heart disease </span><span style="font-size: large;">has occurred over the last 50 years, because of the progress in the early diagnosis and in the development of surgical or catheter-based treatment</span><span style="font-size: large;">. This has resulted in a growing population of adults with congenital heart disease (approximately 85% of all newborns with congenital heart </span><span style="font-size: large;">disease will reach adulthood). As a result, the </span><span style="font-size: large;">number of adults with congenital heart disease is larger than the number of children with such disease.</span><br />
<span style="font-size: large;">Congenital heart disease usually results from the abnormal embryonic development of a normal cardiac structure or failure of a structure to progress beyond a certain stage of embryonic development.</span><span style="font-size: large;">The causes of congenital heart disease are multiple, genetic and environmental factors affecting cardiac development in the uterus. Genetic causes include gene mutations and chromosomal anomalies. Environmental factors include viral infections in pregnancy (such as rubella), alcohol abuse during pregnancy, effects of certain drugs during pregnancy. In most cases, the cause of a congenital heart defect in a given patient is not known.</span><br />
<span face=""arial" , "helvetica" , sans-serif"><b>[The term " syndrome" will often be encountered in this chapter, and notably, although every doctor understands its meaning, some cannot give its exact definition. A definition of "syndrome" is a combination of symptoms, or abnormal clinical or laboratory findings that constitute a distinct clinical picture because they result from a single cause or because they very commonly occur together and have a linked etiology or pathophysiology.]</b></span><br />
<h4>
<span style="font-size: large;">Some known causes of congenital heart disease include:</span></h4>
<span style="font-size: large;">Fetal alcohol syndrome (resulting from alcohol abuse by a pregnant woman, it is associated with cardiac defects, but also non-cardiac defects, such as microcephaly, micrognathia, and growth retardation).<br />Maternal rubella [it can cause patent ductus arteriosus (PDA) and pulmonary stenosis and also non-cardiac lesions such as microcephaly, cataracts, and deafness]<br />Maternal systemic lupus erythematosus (it can cause fetal complete heart block).<br />Many genetic defects are associated with congenital heart disease, including:<br />Marfan syndrome caused by a gene mutation (it is associated with aortic dilatation and aortic regurgitation, mitral valve prolapse and regurgitation). </span><br />
<span style="font-size: large;">Holt-Oram syndrome, also caused by a gene mutation (autosomal dominant), which is characterized by an atrial septal defect combined with skeletal anomalies of the upper extremities, such as a short thumb, or a thumb with 3 phalanges or a short antebrachium.<br />William's syndrome, a genetic disorder characterized by distinctive facial features ("elfin facies"), cardiovascular defects such as supravalvar aortic stenosis and other features such as neonatal hypocalcemia and later in life mild mental retardation is evident, usually with a friendly talkative personality. The inheritance is autosomal dominant.</span><br />
<div>
<div>
<span style="font-size: large;">Examples of chromosomal anomalies associated with congenital heart disease are:</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Turner syndrome (XO) </span><span style="font-size: large;">is the condition in which a female is partly or completely missing an X chromosome. It</span> <span style="font-size: large;">is associated with coarctation of the aorta, congenital aortic stenosis and atrial septum defect (ASD).</span><br />
<span style="font-size: large;">Trisomy 21, also called Down syndrome (it is associated with endocardial cushion defects, atrial septal defect of the ostium primum type, ventricular septal defect).</span><br />
<span style="font-size: large;"><br /></span>
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<h3>
<span style="font-size: large;">General classification of congenital heart defects</span></h3>
<span style="font-size: large;">Congenital heart </span><span style="font-size: large;">lesions can be classified as acyanotic (defects that do not cause cyanosis) or cyanotic (defects that cause central cyanosis due to a right- to- left shunt). Cyanosis is a blue discoloration of the mucous membranes or the skin caused by an increased amount of reduced hemoglobin (hemoglobin not combined with oxygen).</span><span style="font-size: large;"> Central cyanosis occurs when the circulation is </span><span style="font-size: large;">mixed as a result of a right-to-left shunt (pathologic flow of unoxygenated blood from a right-sided cardiac chamber to a left-sided one). </span><br />
<h4>
<span style="font-size: large;">Acyanotic congenital heart defects include:</span></h4>
<span style="font-size: large;">Ventricular or atrial, or other cardiac communications with left-to-right shunting such as: ventricular septal defect [</span><span face=""arial" , "helvetica" , sans-serif"><b> An opening in the ventricular septum. The most common type of congenital heart disease encountered in children]</b></span><br />
<span style="font-family: inherit; font-size: large;">atrial septal defect </span><span face=""arial" , "helvetica" , sans-serif"><b>[An opening in the atrial septum.The most common congenital heart defect encountered in adults, excluding mitral valve prolapse and bicuspid aortic valve]</b></span><br />
<span style="font-size: large;">partial </span><span style="font-size: large;">anomalous pulmonary venous return,</span><span face=""arial" , "helvetica" , sans-serif"><b><span style="font-size: medium;"> </span></b></span><span face=""arial" , "helvetica" , sans-serif"><b>[ One or more of the pulmonary veins connect to the superior vena cava or to the right atrium.This condition has many of the physiologic characteristics of an atrial defect and it is also often associated with such a defect (in 80-90% of cases).]</b></span><br />
<span style="font-size: large;">patent ductus arteriosus (PDA) </span><span face=""arial" , "helvetica" , sans-serif"><b>[PDA is the second most common congenital heart defect encountered in adults (after ASD) It is a persistent communication between the descending aorta and the left pulmonary artery at the level of the left subclavian artery. A characteristic sign usually present is a continuous murmur (heard in both systole and diastole) which is best heard on the area under the left clavicle]</b></span><br />
<span style="font-size: large;"></span><br />
<div>
<span style="font-size: large;">Congenital abnormalities of the heart valves and great vessels, e.g:</span><span style="font-size: large;">congenital aortic stenosis due to a congenital bicuspid aortic valve</span></div>
<b><span face=""arial" , "helvetica" , sans-serif">[An aortic valve with two cusps instead of three. Studies have reported an incidence of about 0.5-2 % in the general population. In many- but not all- cases the valve may have a dysfunction, stenosis or regurgitation]</span></b><span style="font-size: medium;"><span style="font-size: large;">coarctation of the aorta,</span></span><b><span face=""arial" , "helvetica" , sans-serif"> [This is usually a narrowing of the descending aorta just distal to the origin of the left subclavian artery, caused by an indentation protruding in its lumen opposite to the entry of the ductus arteriosus, so-called juxtaductal aortic coarctation. Much less commonly there is an elongated, narrowed segment of the proximal descending thoracic aorta that can also involve the arch. Aortic coarctation is often associated with a bicuspid aortic valve and usually it is diagnosed in childhood because of hypertension or a heart murmur.]</span></b><br />
<span style="font-size: large;">congenital subvalvular aortic stenosis</span><span face=""arial" , "helvetica" , sans-serif"><b> [This is a stenosis of the left ventricular outflow tract caused by a discrete fibrous or fibromuscular membrane, or a diffuse, fibromuscular, narrowing of the left ventricular outflow tract (like a narrow tunnel), or rarely accessory tissue on the basal anterior mitral leaflet, or an anomalous chordal attachment of the mitral valve]</b></span><br />
<span style="font-size: large;"> or supravalvular aortic stenosis </span><span face=""proxima_nova_rgregular" , "arial" , sans-serif" style="color: #2a2a2a; font-size: 18px;"> </span><span face=""arial" , "helvetica" , sans-serif"><b>[A localized or diffuse narrowing of the ascending aorta distally to the superior margin of the sinuses of Valsalva, which may occur sporadically, as a manifestation of elastin arteriopathy, or as a manifestation of Williams syndrome]</b></span><br />
<span style="font-size: large;">pulmonary stenosis </span><span face=""arial" , "helvetica" , sans-serif"><b>[This term is used for an obstruction (narrowing) to the right ventricular outflow, that may be located at the valvular, subvalvular, or supravalvular level. The most common form is valvular pulmonary stenosis]</b></span><br />
<span style="font-size: large;">congenital mitral stenosis </span><span face=""arial" , "helvetica" , sans-serif"><b>[due to a parachute mitral valve where all chordae tendinae are connected to a single papillary muscle, congenitally dysplastic mitral valve with fused commissures, hypoplastic (small) mitral annulus or a double orifice mitral valve, or mitral stenosis due to the presence of a supravalvular ring].</b></span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">Other lesions such as </span><br />
<span style="font-size: large;">Congenital abnormalities of the coronary arteries.</span><br />
<span style="font-size: large;">Congenitally corrected transposition of the great arteries<b> </b></span><span face=""arial" , "helvetica" , sans-serif"><b>[A rare congenital disorder, where the ventricles are in a reversed position, i.e. the right ventricle is in the position of the left ventricle, receiving blood from the left atrium and ejecting blood into the aorta, whereas the left ventricle is receiving blood from the right atrium and ejecting it into the pulmonary artery. This condition is usually diagnosed late in childhood or in early adult life, with the patient presenting with complete heart block or heart failure due to the decompensation of the right ventricle which is the systemic ventricle in this condition, supporting the systemic circulation]</b></span><br />
<h4>
<span style="font-size: large;">Cyanotic congenital heart defects include :</span></h4>
<span style="font-size: large;">The two most common in order of frequency are </span><br />
<span style="font-size: large;">Tetralogy of Fallot (</span><span style="font-size: large;">TOF) </span><span face=""arial" , "helvetica" , sans-serif"><b>[ It is the constellation of four findings: right ventricular outflow obstruction, a large subaortic ventricular septal defect, an overriding aorta, and right ventricular hypertrophy. Frequently an atrial septum defect may coexist and then the condition is called pentalogy." Common manifestations of TOF include cyanosis, clubbing, dyspnea on exertion, hypoxic spells and squatting ]</b></span><br />
<span style="font-size: large;">and </span><br />
<span style="font-size: large;">Complete transposition of the great arteries (TGA) </span><span face=""arial" , "helvetica" , sans-serif"><b>[ The reversal of the relation of the aorta and pulmonary artery to the ventricles, i.e the aorta arises from the right ventricle and the pulmonary artery from the left ventricle. The common classic type of complete TGA is called d -transposition, with the aorta located anteriorly and to the right of the pulmonary artery. In cases of TGA where the aorta lies to the left of the pulmonary artery, the condition is called l -transposition.) Because in complete TGA the systemic and the pulmonary circulation are two separate circuits, defects that permit a communication of the two circulations always coexist, such as an atrial septum defect, a patent foramen ovale, a ventricular septum defect or a patent ductus arteriosus). The presence of such a communication is necessary for survival. ]</b></span><br />
<span style="font-size: large;">Less common malformations such as: </span><br />
<span style="font-size: large;">Pulmonary atresia, </span><br />
<span style="font-size: large;">Hypoplastic left heart, </span><br />
<span style="font-size: large;">Ebstein anomaly with an ASD </span><b><span face=""arial" , "helvetica" , sans-serif"> [In Ebstein anomaly there is an inferior apical displacement of the septal and posterior leaflets of the tricuspid valve into the right ventricle. This results in an "atrialized" part of the right ventricle, i.e. a part of the ventricle which has become a portion of the right atrium because of the apical displacement of the tricuspid valve. The remaining right ventricle below that part is small and often dysplastic. The anterior leaflet of the tricuspid valve is large and has a sail-like appearance. Among the patients with Ebstein anomaly, 50% have a communication between the atria, i.e. a patent foramen ovale or a secundum atrial septal defect. Another abnormality that can coexist in patients with Ebstein's anomaly is Wolff-Parkinson-White syndrome since 25% of these patients have one or more accessory pathways of atrioventricular conduction].</span></b><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">Patients with congenital heart defects are divided into three categories according to the surgical status:</span><br />
<span style="font-size: large;">unoperated, surgically palliated (patients that have undergone operations that partially improve their condition without complete correction of their defect) or physiologically repaired (complete or near-complete surgical repair of the defect). </span><br />
<h4>
<span style="font-size: large;">General problems and complications in patients with congenital heart disease</span></h4>
<span style="font-size: large;">Patients with congenital heart disease can develop various symptoms and complications. In adults with congenital heart disease, there are certain symptoms, particularly </span><span style="font-size: large;">progressive dyspnea on exertion and </span><span style="font-size: large;">syncope, that should prompt a thorough evaluation.</span></div>
<span style="font-size: large;">Arrhythmias present a common problem in adults with congenital heart disease. Arrhythmias in these patients often originate near the myocardial scars of previous surgical operations. The most common arrhythmias that occur, are supraventricular arrhythmias, such as atrial flutter or atrial fibrillation. </span></div>
<div>
<span style="font-size: large;">Ventricular tachycardia (VT) may occur in adults with congenital heart disease as a late complication of prior ventriculotomy or patching of a ventricular septal defect. VT is an important arrhythmia because it can cause sudden death. In adults with corrected tetralogy of Fallot (TOF) the incidence of ventricular arrhythmias is 0.5% -5 %. Risk factors for the occurrence of ventricular arrhythmias in such patients include an </span><span style="font-size: large;">older age at the </span><span style="font-size: large;">time of surgical repair, </span><span style="font-size: large;"> a significantly prolonged QRS interval (>180 ms) and </span><span style="font-size: large;">significant dilation of the right ventricle.</span><br />
<span style="font-size: large;">Pulmonary hypertension is a common complication of </span><span style="font-size: large;">certain congenital heart defects. There are two possible causes of pulmonary hypertension, depending on the type of congenital heart disease:</span><br />
<span style="font-size: large;">1. Pulmonary hypertension as a result of pulmonary venous</span><br />
<span style="font-size: large;">hypertension due to elevated left-sided filling pressures, </span><br />
<span style="font-size: large;">or</span><br />
<span style="font-size: large;">2. Pulmonary hypertension as the result of a left to right shunt, i.e an abnormal communication between the left and right heart chambers with blood flow from a left heart chamber towards a right heart chamber. This increases flow in the pulmonary arterial circulation and can result over the years in pulmonary arterial hypertension (PAH).<br />Shunts proximal to the tricuspid valve such as atrial septal defects or partial anomalous pulmonary venous return uncommonly result in pulmonary hypertension ( about 15 % of cases), whereas shunts distal to the tricuspid valve, for example a large ventricular septal defect, more commonly cause pulmonary hypertension</span><span style="font-size: large;">. </span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">Left to right (L-R) shunt lesions are common types of congenital heart disease. As a general rule, a significant L-R shunt is characterized by a</span><span style="font-size: large;"> ratio of pulmonary flow to systemic flow </span><br />
<span style="font-size: large;"> ≥</span><span style="font-size: large;">1.5 : 1, but this rule may not </span><span style="font-size: large;">apply to adults if pulmonary hypertension has developed.</span><span style="font-size: large;"> In such a case, the elevated pressures on the right side and the reduced right ventricular compliance gradually cause the reduction of the L-R shunt flow. When pulmonary arterial hypertension becomes severe, the L-R shunt may reverse, resulting in the development of a right to left (R-L) shunt, i.e. an abnormal flow of desaturated blood from a right heart chamber to a left heart chamber. This causes a reduction in the hemoglobin-oxygen saturation of the arterial blood (arterial desaturation) with the development of cyanosis, a condition called Eisenmenger syndrome. </span><br />
<span style="font-size: large;">Cyanosis in congenital heart disease occurs when persistent mixing of desaturated blood to arterial blood, due to a R-L shunt, results in </span><span style="font-size: large;">hypoxemia (reduced oxygen content of the arterial blood and a fall in hemoglobin saturation with oxygen).</span><span style="font-size: large;"> In such cases, the body has some adaptive mechanisms to increase oxygen delivery to the tissues, such as a rightward shift in the oxyhemoglobin dissociation curve, a rise of the hematocrit (secondary erythrocytosis), and a rise in cardiac output. C</span><span style="font-size: large;">hronic hypoxemia and erythrocytosis in patients with cyanotic congenital heart disease can cause the development of various complications, such as: </span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">hematologic </span><span face=""arial" , "helvetica" , sans-serif"><b>(hyperviscosity, iron deficiency, and bleeding diathesis)</b></span><br />
<span style="font-size: large;"> neurologic </span><span face=""arial" , "helvetica" , sans-serif"><b>(possible complications include cerebral hemorrhage or paradoxical cerebral embolization from a venous thrombus entering the systemic circulation through a congenital heart defect)</b></span><span style="font-size: large;">, </span><br />
<span style="font-size: large;">renal </span><span face=""arial" , "helvetica" , sans-serif"><b>(proteinuria, hyperuricemia, or renal failure)</b></span><br />
<span style="font-size: large;">pulmonary </span><span face=""arial" , "helvetica" , sans-serif"><b>(pulmonary in </b></span><b style="font-family: Arial, Helvetica, sans-serif;">situ arterial thrombosis, or pulmonary hemorrhage)</b><br />
<span style="font-size: large;">and rheumatologic complications </span><b><span face=""arial" , "helvetica" , sans-serif">(gout and hypertrophic osteoarthropathy causing arthralgias. Another musculoskeletal manifestation of cyanotic congenital heart disease is digital clubbing, which is an enlargement of the distal segments of the fingers. Clubbing is usually an indication of an underlying disease such as a cyanotic congenital heart disease, a chronic pulmonary disease or lung cancer, infective endocarditis, inflammatory bowel disease, cirrhosis of the liver. But there are also cases where clubbing is idiopathic or hereditary without any underlying disease.</span></b><b><span face=""arial" , "helvetica" , sans-serif">)</span></b></div>
<div>
<span style="font-size: large;">Symptoms of hyperviscosity include head</span><span style="font-size: large;">aches, dizziness, </span><span style="font-size: large;">visual disturbances, </span><span style="font-size: large;">altered mentation, </span><span style="font-size: large;">fatigue and paresthesias.</span><br />
<span style="font-size: large;">Another important issue related to congenital heart disease, is pregnancy in a woman with congenital heart disease. The presence of congenital heart disease is associated with an increased risk for </span><span style="font-size: large;">peripartum complications. However, maternal congenital heart disease is </span><span style="font-size: large;">not a contraindication to pregnancy unless certain</span><span style="font-size: large;"> high-risk features are present, such </span><span style="font-size: large;">as pulmonary hypertension, cyanosis, decompensated heart failure, aortic aneurysm, severe valve disease.</span><br />
<span style="font-size: large;"><br /></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span></div>
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</h3>
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<span style="background-color: #e06666; font-size: large;"><b>Bibliography and links </b></span><br />
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<span style="font-family: arial;"><b><span face=""arial" , "helvetica" , sans-serif">Triedman JK, Newburger JW. Trends in Congenital Heart Disease.The Next Decade. Circulation. 2016;133:2716-2733</span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif"><a href="http://circ.ahajournals.org/content/133/25/2716.long" target="_blank">http://circ.ahajournals.org/content/133/25/2716.long</a></span></b><br />
<b><br /></b></span><span lang="EN-US" style="line-height: 107%;"><b><span style="font-family: arial;"><br /></span></b></span></div><div><span lang="EN-US" style="line-height: 107%;"><b><span style="font-family: arial;">Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018
AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A
Report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines. Circulation. 2019;139(14):e698-e800. </span></b></span></div><div><span style="font-family: arial;"><b>LINK <a href="https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603" target="_blank">https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603</a><br /><br /><br /></b><span style="font-weight: 700;">Puri K, Allen HD, Qureshi AM. Congenital Heart Disease. Pediatrics in Review 2017;38(10):471–486. Available from: </span><a href="https://doi.org/10.1542/pir.2017-0032" style="font-weight: 700;" target="_blank">10.1542/pir.2017-0032</a><b><br /><br /></b> <b><br /></b> <b><span face=""arial" , "helvetica" , sans-serif"> </span></b><span face=""arial" , "helvetica" , sans-serif"><b><a href="https://watermark.silverchair.com/ehq249.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAeMwggHfBgkqhkiG9w0BBwagggHQMIIBzAIBADCCAcUGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMtzlJ7Sv4s0Naso1XAgEQgIIBliQuDs8_9VpLp7Vn9zC8Y0fE2hoqt-O_qQyR2nJXpAEvGRg1USSrbu5dyztlgFRtAMa4Xp9Y0EZ2IwLPYaChy4RtP_Zzy6b9W_WsVAv1pWujC_-TtGe2X2b3uvo-ojzDI1CMRtplU1aJR2bflx91mf2Q8yLoOud5jNThUa8cDGy2egssZHZD5NYjm89zGB6onFkO2L2c0JvqfTX5fh9sGry7SOGGFYeBBdTEt7OTlEpBtBtou1xuIyFtuSEV8XyXGzvlY_GAC5lZfSiVyW8A9AozUatm0E--oe3a7AtG3TCMiA_yuMRWIB2dpiS98cS4yEE3VIzFTP4YlVv2X4K5ORo_mQbtrKhgX5TlH4tBQmHsvIeAAnmsWRTnuiE8PtRAk1Ar7IAAvzw1T0kA4VEBh47AfWEM545CPrvFjSxjDkgrWwbkI2aL90U_XWM7yVS-diS09TpbPG20iS2BlpLaW6730rWQz2XD6ieFWpaRnsl56UYtCPAbMMV0nVjO8goVEWNAQDf_Ao9g3FFlPWsz9vzTRG29tdU" target="_blank">ESC Guidelines for the management of grown-up congenital heart disease (new version 2010)</a> </b></span><b><span face=""arial" , "helvetica" , sans-serif">European Heart Journal (2010) 31, 2915–2957</span></b><br />
<b><br /></b> <span face=""arial" , "helvetica" , sans-serif"><b>Congenital Heart Disease in Children <a href="https://patient.info/doctor/congenital-heart-disease-in-children#" target="_blank">https://patient.info/doctor/congenital-heart-disease-in-children#</a></b></span><b><br /></b> <b><span face=""arial" , "helvetica" , sans-serif"><br /></span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif">Guidelines for Evaluation and Management of Common Congenital Cardiac Problems in Infants, Children, and Adolescents<br />A Statement for Healthcare Professionals From the Committee on Congenital Cardiac Defects of the Council on Cardiovascular Disease in the Young, American Heart Association</span></b><b><span face=""arial" , "helvetica" , sans-serif"><a href="http://www.besancon-cardio.org/recommandations/cacon_aha.htm" target="_blank">http://www.besancon-cardio.org/recommandations/cacon_aha.htm</a></span></b><br />
<b><br /><br /></b> <span face=""arial" , "helvetica" , sans-serif"><b>Canadian cardiovascular society guidelines on the management of adult congenital heart disease 2009 <a href="http://www.cachnet.org/res_intlguide.shtml" target="_blank">http://www.cachnet.org/res_intlguide.shtml</a></b></span><b><br /></b></span> <b><br /></b> <b><br /></b> <b><br /></b> <b><br /></b></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-71570158855848644182017-09-10T18:29:00.000+03:002018-08-12T00:44:44.225+03:00Prosthetic heart valves ( a concise overview)<h2>
Prosthetic heart valves</h2>
<br />
<span style="font-size: large;">There are two main types of prosthetic heart valves, mechanical valves which are durable but require chronic anticoagulation<br />because of thrombogenicity and biological valves which are less durable, but also less thrombogenic. Biological valves do not require lifelong anticoagulation (unless there are other reasons for anticoagulation, such as atrial fibrillation).</span><br />
<div>
<span style="font-size: large;">The hemodynamic characteristics of a prosthetic heart valve (flow velocity, peak pressure gradient, mean pressure gradient) are influenced by the type of the valve and the </span><span style="font-size: large;">diameter of the valve </span><span style="font-size: large;">ring (smaller diameter entails a higher peak flow velocity and pressure gradient). An echocardiogram should be performed after the implantation of a prosthetic valve so that the findings can be used for future comparison.</span></div>
<div>
<span style="font-size: large;"></span><br />
<h3>
<span style="font-size: large;"> Mechanical heart valves</span></h3>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;">Mechanical heart valves consist of a sewing ring and the occluder (the moving part of the valve which moves from the opening to the closing position at the appropriate phases of the cardiac cycle). Bileaflet mechanical valves, the type of mechanical valves currently used, have two occluders (leaflets), while single tilting disk and cage-ball valves have one occluder ( a disk, or a ball) respectively.</span><br />
<span style="font-size: large;"><b>Tilting disk valves</b>: They are classified in single and double tilting disk (bileaflet) valves. Nowadays mainly double disk (bileaflet) valves are used.</span></div>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;"><b>Single tilting disk valves</b> (Medtronic-Hall, Omniscience, Bjork-Shiley, </span><br />
<span style="font-family: inherit; font-size: large;">Lillehei-Kaster</span><span style="font-size: large;">) consist of a ring and a disk, that shifts between the opening position and the closing position, supported by metal struts. In the opening position the disc forms with the plane of the ring an angle of 60-80 degrees.</span></div>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;">For a single tilting disk mechanical valve at the aortic position, the peak blood velocity is usually in the range of 1.6-3.3 m /sec. At the mitral position, the peak velocity is usually 1.4-1.7 m /sec.</span></div>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;"><b>The bileaflet (double disk) valves</b> (e.g. St Jude Medical, Carbomedics, </span><span style="font-size: large;">Sorin Bicarbon, </span><span style="font-size: large;">Medtronic Open Pivot, ATS valve, </span><span style="font-size: large;">On-X</span><span style="font-size: large;">) consist of two semi-circular pyrolytic carbon disks attached to the ring of the valve with special hinges. At the opening position, each disc forms an angle of 75-90 degrees. (This is a general description, but there are some differences in certain technical details between valve types).</span></div>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;">The bileaflet valves are the mechanical valves currently used because they have better hemodynamic characteristics ( lower transvalvular gradients) and low thrombogenicity in comparison to other types of mechanical cardiac valves, such as cage ball or tilting single disk valves</span></div>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;"> For a double disk mechanical valve in the aortic position the peak blood velocity is usually 2-3 m /sec (up to 3.3 m /sec for valves with a smaller diameter) and the peak pressure gradient 16-45 mm Hg.(Higher values apply to a small diameter valve ring: 19 or 21 mm). Of course, these limits are approximate and not absolute.</span></div>
<span style="font-size: large;"> </span><br />
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<span style="font-size: large;">For a double-disk mechanical valve at the mitral position, the mean pressure gradient is usually 2.5-7 mm Hg and the peak velocity is 1.1-2 m /sec.</span></div>
<span style="font-size: large;"> </span><br />
<div>
<span style="font-size: large;">Small deviations may be observed from the above flow velocity measurements and pressure gradients. An echocardiogram should be performed after the implantation of a prosthetic valve so that the measurements can be used for future comparison.</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>What do these two images show?</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjc9QHJYICIgdcZzUflHcXzfnMMEnghnzUvfJ86ShPXy4mdlgBo_rQ98umMjA8mL9bR4845bSXlPGSbJAGhJvsVH3aO6NbdOTzSC14zvXTYFZl5WVpQ8reqyUchj1m96IsRk4hIhyphenhyphens3D8I/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2580%25CF%2581%25CE%25BF%25CF%2583%25CE%25B8%25CE%25B5%25CF%2584%25CE%25B9%25CE%25BA%25CE%25AE+%25CE%25BC%25CE%25B7%25CF%2587%25CE%25B1%25CE%25BD%25CE%25B9%25CE%25BA%25CE%25AE+%25CE%25B4%25CE%25AF%25CF%2586%25CF%2585%25CE%25BB%25CE%25BB%25CE%25B7+%25CE%25BC%25CE%25B9%25CF%2584%25CF%2581%25CE%25BF%25CE%25B5%25CE%25B9%25CE%25B4%25CE%25AE%25CF%2582+3+D+%25CF%2585%25CF%2580%25CE%25B5%25CF%2581%25CE%25B7%25CF%2587%25CE%25BF%25CE%25B3%25CF%2581+%25CE%25BA%25CE%25BB%25CE%25B5%25CE%25B9%25CF%2583%25CF%2584%25CE%25AE.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="348" data-original-width="375" height="296" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjc9QHJYICIgdcZzUflHcXzfnMMEnghnzUvfJ86ShPXy4mdlgBo_rQ98umMjA8mL9bR4845bSXlPGSbJAGhJvsVH3aO6NbdOTzSC14zvXTYFZl5WVpQ8reqyUchj1m96IsRk4hIhyphenhyphens3D8I/s320/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2580%25CF%2581%25CE%25BF%25CF%2583%25CE%25B8%25CE%25B5%25CF%2584%25CE%25B9%25CE%25BA%25CE%25AE+%25CE%25BC%25CE%25B7%25CF%2587%25CE%25B1%25CE%25BD%25CE%25B9%25CE%25BA%25CE%25AE+%25CE%25B4%25CE%25AF%25CF%2586%25CF%2585%25CE%25BB%25CE%25BB%25CE%25B7+%25CE%25BC%25CE%25B9%25CF%2584%25CF%2581%25CE%25BF%25CE%25B5%25CE%25B9%25CE%25B4%25CE%25AE%25CF%2582+3+D+%25CF%2585%25CF%2580%25CE%25B5%25CF%2581%25CE%25B7%25CF%2587%25CE%25BF%25CE%25B3%25CF%2581+%25CE%25BA%25CE%25BB%25CE%25B5%25CE%25B9%25CF%2583%25CF%2584%25CE%25AE.jpg" title="mechanical bileaflet prosthetic heart valve in the mitral position (closed)-cardiology book" width="320" /></a></div>
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>The top image shows a 3 dimensional (3D) echocardiogram of a mechanical bileaflet prosthetic valve in the mitral position viewed from the left atrial side in diastole with the leaflets in the open position. Normal opening of the valve can be seen. The lower image shows the same valve in systole (closed position). 1. sewing ring of the prosthesis/ 2. leaflets</b></span><br />
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<span style="font-size: large;">The <b>Cage-Ball Valve</b> (Starr-Edwards) is an old valve type, which had been in use for twenty-five years, but nowadays it is not being implanted. It consists of a ball of silicone, swinging in a cage of metal alloy (cobalt-chromium). On the valve base, there is a sewing ring that serves to secure the valve to its position. When the valve opens, the ball moves away from the ring and blood flows around it, while on closing the ball fits onto the ring, preventing blood regurgitation. This valve is bulky (unsuitable for patients with a small aortic annulus or small left ventricle). Turbulent flow also occurs around the sphere. Due to the above, a higher pressure gradient is generated compared to other valves. In addition, turbulent flow causes endothelial injury, so this valve is more thrombogenic. On auscultation of the patient, multiple opening sounds are heard due to the impact of the ball on the cage supports. There is also a metallic closing sound.</span></div>
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<h3>
<span style="font-size: large;"> Bioprosthetic heart valves (</span><span style="font-size: large;">Biological tissue valves or bioprostheses)</span><span style="font-size: large;"> </span></h3>
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<span style="font-size: large;">Bioprosthetic valves (bioprostheses) can be heterografts or xenografts (valves made of animal tissue), which are composed of</span><br />
<span style="font-size: large;">porcine, bovine, or equine tissue (valvular or pericardial), or homografts, which are preserved </span><span style="font-size: large;">human aortic valves. In cardiac auscultation, normally functioning bioprosthetic (biological) valves do not differ from normal native valves. There are several types of bioprosthetic valves: </span><span style="font-size: large;">.</span></div>
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<span style="font-size: large;"><b>Heterografts or Xenografts</b>: </span><span style="font-size: large;">Heterografts include stented and stentless biological valves. </span><span style="font-size: large;">In stented valves, the biological valve tissue is mounted on a rigid </span><span style="font-size: large;">stent (plastic or metallic), also called sewing ring, covered with fabric. Conversely, stentless bioprostheses do not include a stent, thus they use the </span><span style="font-size: large;">patient’s native aortic root as the valve stent. </span><br />
<span style="font-size: large;"> Heterografts </span><span style="font-size: large;">are: 1) Porcine valves properly suited to a suture ring made of synthetic material. Such valves are: Carpentier-Edwards, Hancock II and Mosaic (Medtronic). With echocardiography, for the Carpentier-Edwards valve at the mitral position, the expected peak velocity is about 1.5-2 m /sec and the expected mean pressure gradient of 5-9 mmHg. In the aortic position, the expected peak velocity is 2-3 m /sec and the expected mean pressure gradient 8-20 mmHg.</span></div>
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<span style="font-size: large;">A more recent development is the introduction of stentless porcine valves. </span><span style="font-size: large;">The absence of a stent enables</span><span style="font-size: large;"> implantation of a larger </span><span style="font-size: large;">valve for a given native annulus size, resulting in a larger effective orifice area (EOA) and a lower transvalvular pressure gradient, which is an advantage of these valves.</span><span style="font-size: large;"> Such are: Edwards Prima Plus, Medtronic Freestyle, and Toronto SPV (St. Jude Medical.)</span><br />
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<span style="font-size: large;"> 2) </span><span style="font-size: large;">Valves made of <b>bovine pericardium</b>. These include the following: Perimount series valves (Edwards LifeSciences). and Ionescu-Shiley, which is no longer produced.<br />Pericardial valves are also two<u> valve types used in transcatheter aortic valve implantation (TAVI)</u>: SAPIEN XT (Edwards LifeSciences) made of bovine pericardium and CoreValve (Medtronic) made of porcine pericardium. The valves used for TAVI are trileaflet bioprosthetic valves mounted in a wire mesh stent. Delivery of the valve is performed over a catheter and the stent is expanded in the position of the aortic valve. TAVI can be performed with a catheter advanced from the femoral artery in retrograde fashion across the aortic valve, or from a small thoracotomy with the catheter passed through the apex of the left ventricle and advanced across the aortic valve. This procedure is used for calcific aortic stenosis with the native valve being compressed but remaining in place. TAVI is indicated in patients with severe symptomatic aortic stenosis who have a high risk of adverse surgical outcomes due to comorbidities. Possible complications include stroke, vascular complications (at the entrance site at the femoral artery), and paravalvular regurgitation</span></div>
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<span style="font-size: large;"><b>Homografts or allografts</b></span></div>
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<span style="font-size: large;">Preserved aortic valves from human cadavers.</span><br />
<span style="font-size: large;">Usually taken 24 hours after the donor's death, they are sterilized by antibiotics and maintained at a temperature of -196 ° C. The recorded Doppler velocities are approximately the same as those of native aortic valves.</span><br />
<span style="font-size: large;"><b>Autograft (Ross operation)</b></span><br />
<span style="font-size: large;">Pulmonary autograft is the patient's own pulmonary valve implanted to replace a pathologic aortic valve, during a Ross operation. The pulmonary autograft consists of the pulmonary valve with its ring and a small part of the main pulmonary artery. The aortic valve and the aortic root are replaced with the autograft, to which the coronary arteries are then implanted. Subsequently, a pulmonary allograft (cadaveric graft) is implanted in place of the pulmonary valve. Advantages of this operation are that the autograft placed in the aortic position has a very good hemodynamic behavior and better durability than other biological valves. The disadvantage is that it is a technically difficult procedure that requires a long duration of extracorporeal circulation and is only performed in a few cardio-surgical centers with experience.</span><br />
<h3>
<span style="font-size: large;">Stentless prosthetic valves</span></h3>
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<span style="font-size: large;">These are prostheses that do not contain a prosthetic ring and include stentless heterografts (e.g stentless porcine valves), aortic homografts, and the pulmonary autografts. These have lower transvalvular gradients that the other types of prosthetic heart valves.</span></div>
<h3>
<span style="font-size: large;">Selection of the type of prosthetic heart valve</span></h3>
<span style="font-size: large;">The patient should be informed about the advantages and disadvantages of each option and the desires of the well-informed patient are also taken into consideration, as well as the following important factors. Mechanical valves have greater durability, but need lifelong anticoagulation, whereas bioprostheses are less durable, but have the advantage of a lower thrombogenic potential and do not need lifelong anticoagulation.</span><br />
<span style="font-size: large;"><u>In favor of a mechanical prosthetic valve are the following:</u></span><br />
<span style="font-size: large;">Age< 65 with a long life expectancy (> 10 years on the basis of age and the presence or absence of serious comorbidities), </span><br />
<span style="font-size: large;">No contraindications for anticoagulation, or a patient already receiving anticoagulation treatment (a patient that already has a mechanical prosthesis and needs a second prosthetic heart valve).</span><br />
<span style="font-size: large;"><u>In favor of a biological prosthetic valve are the following:</u></span><br />
<span style="font-size: large;">Age </span><span style="font-family: "times new roman" , serif; font-size: 24px;">></span><span style="font-size: large;">65, (more specifically for a valve in the aortic position age> 65 and for a valve in the mitral position age > 70) or a limited life expectancy,</span><br />
<span style="font-size: large;"> a contraindication for anticoagulation, </span><br />
<span style="font-size: large;">or a woman of childbearing age who desires pregnancy.</span><br />
<span style="font-size: large;"><u>Age limits</u> are <u>not absolute </u>and they can be further refined, depending on the position if the prosthetic valve:</span><br />
<span style="font-size: large;"><u>In the mitral position,</u> a mechanical valve should be generally preferred in patients of age <65, and both valve types (mechanical or bioprosthetic) are acceptable in patients between 65-70 years.</span><br />
<span style="font-size: large;"><u>In the aortic position</u>, </span><span style="font-size: large;">a mechanical valve should be generally preferred in patients of age <60, and both valve types (mechanical or bioprosthetic) are acceptable in patients between 60-65 years.</span><br />
<h3>
<span style="font-size: large;"><br /></span><span style="font-size: large;">Antithrombotic treatment in patients with prosthetic heart valves</span></h3>
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<span style="font-size: large;"> Bioprosthetic valves:</span></h4>
<span style="font-size: large;"> Bioprosthetic (biological) valves are clearly less thrombogenic than mechanical ones, so they do not necessarily need anticoagulation. However, there is a risk of embolism during the initial postoperative period (mechanism: thrombus production on the prosthetic valve support ring). According to the guidelines in patients with a bioprosthetic valve in the mitral or tricuspid position, it is a good practice (with a category IIa-not absolute- indication) to administer anticoagulation with a vitamin K antagonist (acenocoumarol or warfarin) for the first 3 months after valve implantation. Postoperatively heparin (unfractionated or low molecular weight) is initially administered and treatment with a vitamin K antagonist (VKA) is also initiated. When the INR reaches therapeutic levels (2-3) heparin is discontinued and oral anticoagulant treatment is continued (with INR 2-3) for 3 months After 3 months, the risk of thromboembolism is much lower. (INR = international normalized ratio). Therefore, anticoagulation with VKA is discontinued, and permanent antithrombotic treatment with aspirin 80-100 mg (or clopidogrel 75 mg) per day is initiated.<br />Oral anticoagulation using a VKA should also be considered for the first 3 months after surgical mitral or tricuspid valve repair (a class IIa indication)<br /> After surgical implantation of a bioprosthetic valve at the aortic position, because at this position there are higher blood flow velocities resulting in less risk of thrombosis, guidelines recommend administering only low dose aspirin (eg 80-100 mg daily) for the first 3 months after surgery. This has a Class IIa indication.<br />However, guidelines allow the option to give these patients (with an aortic bioprosthesis) in the first 3 months a VKA instead of aspirin but with a class IIb indication ( a "weak" indication).<br />
<b>Exception</b>: In patients with a bioprosthetic valve that also have other risk factors for thromboembolism (such as: a previous embolic episode, atrial fibrillation, or severe left ventricular systolic dysfunction with an ejection fraction <span style="font-size: 14pt;">≤</span> 35% or a hypercoagulable state), anticoagulation with INR 2-3 is administered lifelong (and not just for the first 3 months). This is an absolute (class I) indication for permanent anticoagulation.<br />After transcatheter aortic valve implantation (TAVI), dual antiplatelet therapy is administered for the first 3-6 months. This is followed by lifelong single antiplatelet therapy in patients who do not need oral anticoagulation for other reasons. In case of TAVI, where an additional thromboembolic risk factor (atrial fibrillation, left ventricular systolic dysfunction, hypercoagulability) is also present, a vitamin K antagonist (VKA) is permanently administered with target INR 2-3, while aspirin 80-100 mg, or clopidogrel 75 mg daily is given during the first year and then it is discontinued</span></div>
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<h4>
<span style="font-size: large;">Mechanical prosthetic heart valves</span></h4>
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<span style="font-size: large;">Lifelong oral anticoagulation with a vitamin K antagonist (VKA) is recommended for all patients with mechanical prosthetic valves (this is an absolute-class I-recommendation). Note that the new oral anticoagulants (NOACs) are <u>not used </u>in patients with mechanical cardiac valves. The target INR depends on the thrombogenicity of the type of the mechanical valve prosthesis and patient risk factors (such as mitral or tricuspid valve replacement, previous thromboembolism, atrial fibrillation, mitral stenosis of any degree, severe left ventricular systolic dysfunction with EF <35%).</span><br />
<span style="font-size: large;">Thrombosis and </span><span style="font-size: large;">thromboembolism risks are greater with a mechanical valve in the </span><span style="font-size: large;">mitral than in the aortic position.</span></div>
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<span style="font-size: large;">If the patient has <b>a mechanical valve prosthesis of low thrombogenicity</b> and no other risk factors for thromboembolism the target INR is around 2.5, but if 1 or more of the other risk factors are present, then the target INR is around 3.</span></div>
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<span style="font-size: large;">Mechanical heart valves with a low thrombogenicity are most bileaflet valves: St Jude Medical, Carbomedics, Sorin Bicarbon, </span><span style="font-size: large;">Medtronic Open-Pivot, ATS, </span><span style="font-size: large;">On-X </span><span style="font-size: large;">(all these are mechanical bileaflet valves), and also</span><span style="font-size: large;"> Medtronic Hall </span><span style="font-size: large;">(a single disk valve).</span></div>
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<span style="font-size: large;">If the patient has <b>a mechanical valve prosthesis of medium thrombogenicity</b> and no other risk factors for thromboembolism the target INR is around 3, but in the presence of 1 or more of the other risk factors the target INR is around 3.5</span><br />
<span style="font-size: large;">Mechanical valves of medium thrombogenicity are some other bileaflet valves with insufficient data.</span></div>
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<span style="font-size: large;">If the patient has <b>a mechanical valve prosthesis of high thrombogenicity</b> and no other risk factors for thromboembolism the target INR is around 3.5, but in the presence of 1 or more of the other risk factors, the target INR is around 4.</span><br />
<span style="font-size: large;">Mechanical valves of high thrombogenicity are: the ball-cage valve (Starr-Edwards) and most single disk valves (with the exception of Medtronic Hall) such as Lillehei-Kaster, Omniscience, Bjork-Shiley and other single tilting-disc valves.</span><br />
<span style="font-size: large;">Good management of anticoagulation is important since a high variability of the INR is a strong independent predictor of</span><br />
<span style="font-size: large;">reduced survival after heart valve replacement with a mechanical prosthesis.</span></div>
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<span style="font-size: large;">The addition of low-dose aspirin (75-100mg/day) to VKA should be considered if thromboembolism occurs, despite an adequate INR (IIa C)</span></div>
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<span style="font-size: large;"> In cases when VKA treatment should be interrupted, bridging with therapeutic doses of unfractionated heparin (UFH) or low molecular weight heparin (LMWH) is recommended.</span><br />
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<h4>
<span style="font-size: large;"> Patients with mechanical heart valves undergoing a percutaneous coronary intervention (PCI) </span></h4>
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<span style="font-size: large;">In patients with mechanical heart valves undergoing a percutaneous coronary intervention (PCI) with stenting, there is a need for a temporary combination of anticoagulant (VKA) and antiplatelet drugs( aspirin, clopidogrel), a situation that increases the risk of bleeding. Guideline recommendations for these patients can be summarized as follows:<br />Initially triple antithrombotic treatment (VKA+aspirin+clopidogrel) is administered for 1 month (it may be given for up to a maximum duration of 6 months if the patient is considered to have a high thrombotic risk and a low bleeding risk). After the period of triple antithrombotic treatment, dual therapy (VKA+clopidogrel, or VKA+aspirin) follows until up to 12 months after coronary stent implantation. Then antiplatelet treatment is discontinued and the patient continues only VKA (anticoagulation). </span><span style="font-size: large;">In patients with a high bleeding risk (when bleeding risk is considered as more important than ischemic risk), triple antithrombotic treatment is not given. Then treatment after PCI includes only a period of dual antithrombotic therapy (VKA+ clopidogrel) which can last up to 12 months. After that antithrombotic therapy continues only with the VKA. A high ischemic risk ( a high risk for a subsequent myocardial infarction) is considered to be present in patients presenting with an acute coronary syndrome or having certain characteristics of the coronary lesion (e.g. presence of thrombus, a complex lesion), whereas the bleeding risk is estimated by using the HAS-BLED score.</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><i><b>HAS-BLED stands for:</b><br /><b>Hypertension (</b>systolic >160 mmHg<b>) or</b><br /><b>Abnormal renal function </b>(creatinine >2.2 or dialysis or renal transplant)</i></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><i>Abnormal liver function (</i></b></span><span style="background-color: #f8f9fa; font-family: sans-serif; font-size: 14px;">Cirrhosis or Bilirubin >2x Normal or AST/ALT/ALP >3x Normal)</span><span style="font-family: "arial" , "helvetica" , sans-serif;"><i><br /><b>Stroke </b>(history of previous stroke)<br /><b>Bleeding (</b></i></span><span style="background-color: #f8f9fa; font-family: sans-serif; font-size: 14px;">Prior major bleeding or predisposition to bleeding</span><span style="font-family: "arial" , "helvetica" , sans-serif;"><i><br /><b>Labile INR </b>(unstable or high, remains in the therapeutic range for < 60% of the time)<br /><b>Elderly </b>(> 65 years)<br /><b>Drugs </b>(medication usage that predisposes to bleeding, such as NSAIDs or antiplatelet drugs) <b>or</b></i></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><i> alcohol</i></b></span><span style="background-color: #f8f9fa; font-family: sans-serif; font-size: 14px;">(≥ 8 drinks/week)</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><i>The presence of each of the above adds 1 point to the score.</i></b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">A HAS-BLED score of ≥3 indicates high risk for major bleeding ( defined as intracranial hemorrhage, or bleeding requiring hospitalization, or hemoglobin decrease > 2 g/dL, and/or transfusion) </span></b></div>
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<h3>
<span style="font-size: large;"><br /></span></h3>
<h3>
<span style="font-size: large;">Clinical and echocardiographic follow-up of a patient with a prosthetic heart valve</span></h3>
<span style="font-size: large;">In general, emphasis should be placed on informing the patient about proper adherence to anticoagulation and endocarditis prophylaxis.<br />According to the guidelines of the European Society of Cardiology (ESC) a patient who undergoes a valve replacement requires after 6-12 weeks a complete follow-up examination, including clinical examination (history of possible symptoms, cardiac auscultation to check for the expected auscultatory findings for the type of prosthetic valve and also to check for a possible new cardiac murmur), ECG, chest X-ray, transthoracic echocardiography (TTE) and blood tests. </span><br />
<h4>
<span style="font-size: large;">Physical examination and cardiac auscultation of a patient with a prosthetic heart valve</span></h4>
<span style="font-size: large;">Significant abnormal findings from the physical examination of a patient with a prosthetic heart valve may include a new or changed murmur, muffled valve sounds, or signs indicative of an embolic event (e.g. a neurological deficit in a case of an embolic stroke).</span><br />
<span style="font-size: large;">The expected auscultatory findings in patients with a prosthetic valve depend on the type of the valve prosthesis. Normally functioning biological prosthetic valves have the same auscultatory findings as normal native valves. Among the mechanical valves, the bileaflet mechanical valves, which are the type of mechanical valves currently implanted, do not produce an opening sound but only a metallic closing sound. Single-tilting disc mechanical valves produce an opening sound and a closing sound, while the cage-ball valves produce multiple opening sounds, due to the impact of the ball on the cage. On auscultation of the heart, the absence of the expected sounds produced by the prosthetic valves is a pathological finding indicative of limited valve mobility due to thrombosis or tissue hyperplasia.</span><br />
<span style="font-size: large;">All mechanical valves in the aortic position additionally produce a characteristic mild systolic ejection murmur. In contrast, the small normal regurgitation of blood (small physiological insufficiency) present in the mechanical valves does not produce a murmur. Therefore, in a patient with a mechanical aortic valve, the finding of a diastolic murmur is a pathological finding, indicating a paravalvular leak (paravalvular regurgitation).</span><br />
<h4>
<span style="font-size: large;">Echocardiography of prosthetic heart valves</span></h4>
<span style="font-size: large;"></span> <span style="font-size: large;">The echocardiogram should include measurement of the transvalvular pressure gradient, color Doppler examination to search for a paravalvular regurgitation and assessment of ventricular function.</span><br />
<span style="font-size: large;">Echocardiographic findings and measurements within the first few weeks after surgery will serve as a reference for comparison with future findings. </span><span style="font-size: large;">A basic parameter is the pressure gradient (pressure difference) across the valve when it is open. The measurement of the peak velocity and the calculation of the peak and mean transvalvular pressure gradient is performed with the continuous wave Doppler. All prosthetic valves have a peak transvalvular velocity which is higher than that of a normal, native valve. They also create a greater pressure gradient than a normal natural valve, given that the latter creates a negligible pressure gradient. As mentioned, depending on the type of prosthetic valve, there are some expected limits for the pressure gradient (some approximate limits have been given above).</span><br />
<span style="font-size: large;">Elevated transvalvular velocity and pressure gradient in a prosthetic valve, as compared to the expected values, is observed in cases of: 1) Valve malfunction causing stenosis (thrombus or pannus development, mechanical degeneration and stenosis due to degeneration and calcification of a bioprosthetic valve), </span><br />
<span style="font-size: large;">2) In cases of increased flow through of the valve with no narrowing of the valve (conditions with an increased cardiac output such as hyperthyroidism, anemia or a significant valvular or paravalvular regurgitation). </span><span style="font-size: large;">In the case of significant regurgitation at the valve, there is a volume overload of the ventricular cavity located proximally to the valve, resulting in a larger volume of blood passing through the valve when it opens and thus</span><span style="font-size: large;"> in </span><span style="font-size: large;">a higher velocity and pressure gradient.</span><br />
<span style="font-size: large;">3) In prosthesis-patient mismatch (PPM), where there is no valve dysfunction, but the valve is small for the patient's body size and circulatory needs. </span><br />
<h4>
<span style="font-size: large;">Echocardiographic indications of prosthetic valve stenosis</span></h4>
<span style="font-size: large;">In a prosthetic aortic valve (bioprosthetic or mechanical), indications of a significant stenosis are a peak flow velocity> 4 m / sec, a mean pressure gradient> 35 mmHg, an effective valve orifice <0.8 <span style="font-family: "times new roman" , serif; font-size: 24px;">cm</span><sup style="font-family: "times new roman", serif;">2</sup>, and an acceleration time > 100 msec. An indication for a possible stenosis or a moderate stenosis is a peak velocity between 3 and 4, a mean pressure gradient between 20 and 35, an effective orifice between 0.8 and 1.2 and an acceleration time between 80 and 100. The acceleration time is the time interval between the onset of blood flow through the valve and the peak flow velocity. Apart from the adequacy of valve opening, it is also affected by the heart rate and contractility of the left ventricle. When the shape of the flow signal obtained with the continuous Doppler is triangular with the peak velocity occurring early, this is a sign of normal flow, whereas when it is symmetrical and rounded, this is indicative of stenosis.</span><br />
<span style="font-size: large;">In a prosthetic mitral valve (biological or mechanical), a sign of significant stenosis is a peak flow velocity> 2.5 m / sec, a mean pressure gradient ≥ 10 mmHg, </span><br />
<span style="font-size: large;">an effective valve orifice<1 </span><span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 18pt; line-height: 115%;">cm<sup>2</sup> </span><span style="font-size: large;">and a pressure half time (PHT) > 200 msec.</span><br />
<span style="font-size: large;"> An indication of a possible stenosis, or moderate stenosis of a prosthetic mitral valve is a peak velocity is between 1.9 and 2.5 / a mean pressure gradient between 6 and 10 / an effective orifice area between 1 and 2 and a PHT between 130 and 200. Apart from valvular function, the PHT is also influenced by left ventricular diastolic function (compliance).</span><br />
<h4>
<span style="font-size: large;">Calculation of the functional orifice area or effective orifice area (EOA) of prosthetic valves </span></h4>
<span style="font-size: large;">The functional orifice area or effective orifice area (EOA) of prosthetic valves is calculated with the continuity equation, which is based on the principle that flow in a heartbeat is the same through all areas of the circulation. </span></div>
<div>
<span style="font-size: large;">The EOA of a prosthetic aortic valve is calculated </span><span style="font-size: large;">with the continuity equation as</span></div>
<div>
<span style="font-size: large;"> EOA= (CSA LVOT x VTI LVOT )/VTI </span><span class="" style="font-size: large;">PrAV</span> .<span style="font-size: large;"> </span></div>
<div>
<span style="font-size: large;">CSA LVOT is the cross-sectional area of the LVOT, VTI LVOT the velocity-time integral measured by using pulse wave Doppler in the LVOT, VTI PrAV the velocity-time integral obtained by continuous wave (CW) Doppler through the prosthetic aortic valve. The cross-sectional area of the LVOT is obtained from diameter measurement just proximally to the prosthesis from the parasternal long-axis view. CSA LVOT = π</span><span style="font-size: 24px;">r</span><sup style="font-family: "times new roman", serif; text-align: justify;">2 </sup><span style="font-size: large;">= 3.14 x (</span><span style="font-size: 24px;">d/2)</span><sup style="font-family: "times new roman", serif; text-align: justify;">2</sup><span style="font-size: large;">= 0.785 </span><span style="font-size: 24px;">d</span><sup style="font-family: "times new roman", serif; text-align: justify;">2</sup><span style="font-size: large;">, where r is the radius and d is the diameter of the LVOT measured in the parasternal long axis echocardiographic view. Instead of measuring d, the diameter of the sewing ring of the prosthetic aortic valve can be used in this equation as the diameter of the LVOT.</span><br />
<span style="font-size: large;">The EOA of a prosthetic valve in the mitral position is calculated as EOA = (CSA LVOT </span><span style="font-size: large;">xVTI </span><span style="font-size: large;">LVOT )/VTI</span><span style="font-size: large;"> PrMV,</span></div>
</div>
<div>
<span style="font-size: large;">where VTIPrMV is the velocity-time integral obtained by CW Doppler through the prosthetic mitral valve. </span><br />
<span style="font-size: large;">CSA LVOT </span><span style="font-size: large;">= 0.785 </span><span style="font-size: 24px;">d</span><sup style="font-family: "times new roman", serif; text-align: justify;">2</sup><span style="font-size: large;">, where d is the diameter of the LVOT measured in the parasternal long axis echocardiographic view, just proximal to the aortic valve.</span><br />
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<h3>
<span style="font-size: large;">Prosthetic valve regurgitation</span></h3>
<span style="font-size: large;">For the detection and grading of prosthesis regurgitation, the echocardiographic methods and measured parameters used are similar to those used for native cardiac valves.</span><br />
<span style="font-size: large;">It is important to distinguish p</span><span style="font-size: large;">athologic prosthesis regurgitation </span><span style="font-size: large;">from the small physiologic regurgitation usually present in prosthetic valves. </span><span style="font-size: large;">Mechanical prosthetic valves have a normal small amount of regurgitation called</span><span style="font-size: large;"> leakage backflow which has </span><span style="font-size: large;">a washing effect against</span><span style="font-size: large;"> blood stasis and thrombus formation</span><span style="font-size: large;">. In contrast to the jets of pathologic regurgitation</span><span style="font-size: large;">, the normal leakage backflow jets are </span><span style="font-size: large;">short in duration, narrow, symmetric and have a small size. Also in bioprosthetic heart </span><span style="font-size: large;">valves</span><span style="font-size: large;">, </span><span style="font-size: large;">a minor degree of central transvalvular </span><span style="font-size: large;">regurgitation is often present</span><span style="font-size: large;">. </span><br />
<span style="font-size: large;">In the case of pathologic regurgitation, </span><span style="font-size: large;">the origin of the regurgitant jet should be located to distinguish </span><span style="font-size: large;">paravalvular from transvalvular regurgitation. </span><br />
<span style="font-size: large;">Causes of pathologic prosthesis regurgitation include paravalvular regurgitation </span><span style="font-size: large;">or pannus both in mechanical and biological valves, calcific degeneration and tear of valve leaflets in bioprosthetic valves, thrombus in mechanical valves. P</span><span style="font-size: large;">aravalvular regurgitation is caused by infective </span><span style="font-size: large;">endocarditis, calcification or fibrosis of the native valve annulus with poor contact with the suture ring, or suture detachment.</span><span style="font-size: large;">Thrombus and pannus can also cause valve stenosis (this is their most usual presentation). The stentless prosthetic valve substitutes can also develop functional central aortic regurgitation as a result of continued dilation of the aortic root.</span><br />
<span style="font-size: large;">For the evaluation of prosthetic valve regurgita</span><span style="font-size: large;">tion, with transthoracic echocardiography (TTE) as well as with transesophageal echocardiography (TEE), </span><span style="font-size: large;">obtaining color Doppler images in multiple views and multiple </span><span style="font-size: large;">planes is essential.</span><br />
<span style="font-size: large;">Acoustic shadowing can obscure </span><span style="font-size: large;">regurgitant jets and this is more an issue for prosthetic valves in the mitral than for those in th</span><span style="font-size: large;">e aortic position.</span><br />
<h4>
<span style="font-size: large;">Grading of a mechanical or bioprosthetic aortic valve regurgitation (central or paravalvular)</span></h4>
<span style="font-size: large;">An indirect sign is left ventricular (LV) size which in the case of mild aortic regurgitation (AR) is expected to be normal, in moderate AR it will be either normal or mildly increased but in severe AR prominent LV dilation will be present.</span><br />
<span style="font-size: large;">Regurgitant </span><span style="font-size: large;">color Doppler </span><span style="font-size: large;">jet width at its origin expressed as % of the left ventricular outflow tract (LVOT) diameter: the wider the jet the more severe the regurgitation: Mild regurgitation ≤30 %, moderate between 30 and 60%, severe regurgitation >60%.</span><br />
<span style="font-size: large;">Vena contracta is another useful echocardiographic parameter used to grade valve regurgitation severity. Vena contracta is defined as the narrowest region of a flow jet that occurs at, or just downstream to, the regurgitant orifice </span><span style="font-size: large;">(the orifice at the valve where regurgitation occurs).</span><br />
<span style="font-size: large;">Vena contracta width in mm: </span><br />
<span style="font-size: large;">mild regurgitation <4, moderate 4-6, severe regurgitation >6</span><br />
<span style="font-size: large;">Vena contracta area (measured with </span><span style="font-size: large;">3D color Doppler in </span><span style="font-size: large;">m<span style="text-align: justify;">m</span><sup style="text-align: justify;">2</sup></span><span style="font-size: large;">): </span><br />
<span style="font-size: large;">mild regurgitation </span><span style="font-size: large;"><20</span><span style="font-size: large;"> moderate </span><span style="font-size: large;">20-40</span><span style="font-size: large;">, severe regurgitation</span><span style="font-size: large;"> >40</span><br />
<span style="font-size: large;">The density of the regurgitant jet examined with continuous wave (CW) Doppler: in mild regurgitation, the jet is incomplete or faint, whereas in moderate or severe regurgitation it appears dense.</span><br />
<span style="font-size: large;">The pressure half time </span><span style="font-size: large;">(PHT measured in ms) </span><span style="font-size: large;">of the regurgitant jet This is the time from the onset of the regurgitant flow to the point the pressure gradient (=4x</span><span style="font-size: large;">velocity<sup style="text-align: justify;">2</sup>) </span><span style="font-size: large;">between the aorta and the left ventricle becomes half of its initial value. It is calculated by the machine from the CW Doppler signal of the regurgitant flow when you trace the slope of the signal. The more severe the regurgitation the quicker the decline of the pressure difference (pressure gradient) between the two communicating cavities (aorta and left ventricle) and thus the smaller the value of the PHT: </span><span style="font-size: large;">mild regurgitation PHT</span><span style="font-size: large;"> >500 ms, </span><span style="font-size: large;">moderate</span><span style="font-size: large;"> regurgitation 200-500 ms, </span><span style="font-size: large;">severe regurgitation </span><span style="font-size: large;"><200 ms.</span><br />
<span style="font-size: large;">Another useful index is the diastolic flow reversal in the descending aorta, assessed with PW Doppler from the suprasternal echocardiographic view: </span><span style="font-size: large;">In a mild regurgitation, this is absent or brief early-diastolic, whereas in severe regurgitation there is a prominent holodiastolic flow reversal with an end-diastolic velocity >20 cm/s. In moderate regurgitation, the findings are intermediate between those two situations.</span><br />
<span style="font-size: large;">Left ventricular outflow to right ventricular outflow ratio. This is calculated by obtaining the PW Doppler signal of the systolic flow in the left ventricular and right ventricular outflow tract and expressed as the ratio of the respective stroke </span><span style="font-size: large;">volumes or velocity-time integrals. The greater the aortic regurgitation (AR), the greater the ratio of LV outflow/RV outflow. This happens because AR causes an increased stroke volume of the left ventricle due to volume overload of the ventricle, which has to eject not only the effective forward flow of blood that will reach the systemic circulation but also the volume of blood that regurgitates during diastole.</span><br />
<span style="font-size: large;">Thus in severe AR this ratio is increased (>1.8).</span><br />
<span style="font-size: large;"></span><br />
<h4>
<span style="font-size: large;">Grading of a mechanical or bioprosthetic mitral valve regurgitation (central or paravalvular)</span></h4>
<div>
<span style="font-size: large;">Vena contracta width in mm (for the definition of vena contracta see above): mild regurgitation < 3, moderate with a vena contracta width between 3 and 6 and severe regurgitation ≥ 6 mm.</span><br />
<span style="font-size: large;">The color flow jet area can also provide an indication but it underestimates regurgitation severity when the jet is not central but eccentric, impringing on the interatrial septum or the wall of the left atrium. When we are dealing with a relatively central jet, mild regurgitation is characterized by a small jet size (usually < 4 c<span style="text-align: justify;">m</span><sup style="text-align: justify;">2</sup> or</span><br />
<span style="font-size: large;"><20% of left atrial area), whereas severe mitral regurgitation (MR) is characterized by a large jet</span><span style="font-size: large;"> (usually >8</span><span style="font-size: large;"> c<span style="text-align: justify;">m</span><sup style="text-align: justify;">2</sup></span><span style="font-size: large;"> or </span><span style="font-size: large;">>40% of left atrial area) </span><br />
<span style="font-size: large;">The size of the zone of flow convergence, which is viewed with color Doppler as a hemispheric area of blood at the left ventricular side, accelerating towards the regurgitant orifice: mild MR is characterized by a nonvisible or minimal zone of flow convergence, whereas severe MR is characterized by a large flow convergence zone.</span><br />
<span style="font-size: large;">MR jet density assessed with CW Doppler: </span><span style="font-size: large;">mild MR is characterized by an i</span><span style="font-size: large;">ncomplete or faint CW signal of the regurgitant jet</span><span style="font-size: large;">, whereas severe MR by a d</span><span style="font-size: large;">ense CW signal.</span><br />
<span style="font-size: large;">MR Doppler signal contour assessed with CW Doppler: in mild MR it has a parabolic shape, whereas in severe MR the CW signal is triangular and early peaking.</span><br />
<span style="font-size: large;">The PW Doppler signal of pulmonary venous flow in mild MR demonstrates </span><span style="font-size: large;">dominance of the systolic wave (versus the diastolic wave), in moderate MR there is systolic blunting (the height of the systolic wave is reduced), and in severe MR there is systolic flow reversal (a negative systolic flow wave).</span><br />
<span style="font-size: large;">A quantitative parameter is the effective regurgitant orifice area</span><span style="font-size: large;"> EROA (m</span><span style="font-size: large;"><span style="text-align: justify;">m</span><sup style="text-align: justify;">2</sup> </span><span style="font-size: large;">), which in moderate MR is between 20 and 40 and in severe MR ≥40 </span><span style="font-size: large;">m</span><span style="font-size: large;"><span style="text-align: justify;">m</span><sup style="text-align: justify;">2</sup></span><span style="font-size: large;"> (0.4 c</span><span style="font-size: large;"><span style="text-align: justify;">m</span><sup style="text-align: justify;">2</sup></span><span style="font-size: large;">)</span><br />
<span style="font-size: large;">Another quantitative parameter is the r</span><span style="font-size: large;">egurgitant volume RV (mL/beat) which in moderate MR is between 30 and 60 and in severe MR >60. These two quantitative parameters of MR severity are calculated by using the proximal isovelocity surface area (PISA) method (see chapter on mitral regurgitation, link </span><b><span style="font-size: large;"><a href="http://cardiologybookandcases.blogspot.gr/2016/08/mitral-regurgitation-diagnosis-assessment-of-severity-treatment.html">Mitral regurgitation. Diagnosis, echocardiography and management.</a></span></b><span style="font-size: large;">)</span><br />
<span style="font-size: large;">The regurgitant fraction= regugitant volume/stroke volume in moderate MR is 30-50 % and in severe MR >50 %</span><br />
<span style="font-size: large;">Indirect signs of the severity of MR that should not be neglected:</span><br />
<span style="font-size: large;">LV size : In mild MR it is expected to be normal, in moderate MR the LV is expected to be normal or mildly dilated and in severe MR it should be clearly dilated.</span><br />
<span style="font-size: large;">Left atrial (LA) size: in moderate MR it is usually normal or mildly dilated and in severe chronic MR left atrial dilation is prominent (but in cases of acute severe MR the LA size can be normal, because it did not have the time to enlarge).</span><br />
<span style="font-size: large;">Pulmonary hypertension is generally present in cases of severe MR </span><br />
<span style="font-size: large;">( systolic pulmonary arterial pressure SPAP ≥50 mm Hg at rest and ≥60 mm Hg at exercise).</span></div>
<span style="font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="background-color: yellow;">Useful videos !! (LINKS) </span><br /><a href="https://www.youtube.com/watch?v=3ftvT-lCdw8">Assessment of Prostheses in Echocardiography 123sonography</a> (Prof Thomas Binder)<br /><br />Prosthetic Valve Assessment (William A. Zoghbi, MD) <a href="https://www.youtube.com/channel/UCb8PGmJ6SILfyOvOWJvHZIg">DeBakey Institute For Cardiovascular Education & Training</a><br />LINK <a href="https://www.youtube.com/watch?v=e0ERw33Irdg">https://www.youtube.com/watch?v=e0ERw33Irdg</a><br /><br />Prosthetic valve echocardiography </b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>(Dr. John Chambers, Youtube channel <a href="https://www.youtube.com/channel/UCuju134ZgbHJFFdyOnCcXgQ">MEDICAL IMAGING</a>)<br />LINK <a href="https://www.youtube.com/watch?v=XZwE_KBxCeo">https://www.youtube.com/watch?v=XZwE_KBxCeo</a></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A normally functioning bileaflet mechanical prosthetic valve in the mitral position (3D echo)</b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-family: "arial" , "helvetica" , sans-serif;">From you tube channel </span><a class="yt-simple-endpoint style-scope yt-formatted-string" href="https://www.youtube.com/channel/UCCrVaRNq6hQ7WZu108lFZjA" style="cursor: pointer; display: inline-block; text-decoration-line: none;">LondonCardioClinic</a></span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="https://www.youtube.com/watch?v=ahkKZQBzss8" target="_blank">https://www.youtube.com/watch?v=ahkKZQBzss8</a></span></b></div>
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<span style="font-size: large;"><br /></span>
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<h3>
<span style="font-size: large;">Prosthetic valve complications</span></h3>
</div>
</div>
<div>
<div>
<div>
<h4>
<span style="font-size: large;">Prosthetic valve thrombosis</span></h4>
<span style="font-size: large;">There is an increased risk in case of inadequate anticoagulation in a patient with a mechanical prosthetic valve (INR significantly lower than target value) and mechanical prosthetic valves in the mitral position, or the older types of mechanical prosthetic valves (cage-ball, single leaflet). Clinical presentation can be with embolization, e.g. an embolic stroke, or acute limb ischemia, or acute valvular dysfunction causing acute pulmonary edema, or sudden death.<br />On physical examination diminished intensity of valve sounds may be present. On echocardiography or fluoroscopy, there is a reduced movement of the valve leaflets. There is also an increased transvalvular gradient on echocardiography.<br />Treatment: Anticoagulation with heparin. If the thrombus is <5 mm on echocardiography, then anticoagulation may suffice. If the thrombus is > 5 mm then apart from heparin, thrombolysis, thrombectomy or valve replacement will be required. Generally, for thrombosis of left-sided prosthetic heart valves, surgical treatment with valve replacement is indicated, unless there is a prohibitive surgical risk or a small thrombus. For thrombosis of a right-sided prosthetic valve, the treatment of choice is thrombolysis (fibrinolysis). Surgery is indicated if thrombolysis is unsuccessful 24 hours after discontinuation of the infusion.</span><br />
<h4>
<span style="font-size: large;">Embolization</span></h4>
</div>
<div>
<span style="font-size: large;">An embolization in a patient with a prosthetic heart valve more commonly manifests as an ischemic stroke (cerebral infarction).<br />In patients with prosthetic valves presenting with peripheral embolization, endocarditis should also be considered.<br />Risk factors include: atrial fibrillation, left ventricular systolic dysfunction, age > 70 years, mitral prostheses, cage-ball valves, the presence of more than 1 prosthetic heart valve. If there are clinical findings suggesting a stroke, a brain computed tomography (CT) should be performed immediately to exclude an intracranial hemorrhage ( in case of an intracranial hemorrhage anticoagulation is withheld and specialist help from a neurologist or neurosurgeon is also needed).</span><br />
<h4>
<span style="font-size: large;">Patient-prosthesis mismatch (PPM)</span></h4>
<span style="font-family: inherit; font-size: large;">PPM is a situation where the problem is not prosthetic valve dysfunction, but a small prosthetic valve for patient needs. The effective orifice area (EOA) of the valve is indexed to body surface area (BSA), i.e. it is divided by the BSA. In a prosthetic valve in the aortic position when EOA / BSA</span><span style="font-family: inherit; font-size: large;"><span style="font-size: medium;">> </span><span style="text-align: justify;"><span style="text-align: start;">0.85 </span>cm</span><sup style="text-align: justify;">2</sup><span style="text-align: justify;">/m</span><sup style="text-align: justify;">2</sup><span style="font-size: medium;">,</span></span><span style="font-size: large;"> </span><span style="font-size: large;">then there is only mild or no PPM. On the contrary, when EOA / BSA ≤ </span><span style="font-family: inherit; font-size: large;"><span style="font-size: medium;"><span style="font-size: large;">0.65</span> </span><span style="text-align: justify;">cm</span><sup style="text-align: justify;">2</sup><span style="text-align: justify;">/m</span><sup style="text-align: justify;">2 </sup></span><span style="font-size: large;">then there is considerable PPM and significant stenotic phenomena. Intermediate values below 0.85 but over 0.65 </span><span style="font-size: large; text-align: justify;">cm</span><sup style="text-align: justify;">2</sup><span style="font-size: large; text-align: justify;">/m</span><sup style="text-align: justify;">2</sup><span style="font-size: large;"> suggest a moderate degree of patient-prosthesis mismatch (PPM).</span><br />
<span style="font-family: inherit;"><span style="font-size: large;">In a case of a prosthetic valve at the mitral position, when </span></span><br />
<span style="font-family: inherit;"><span style="font-size: large;">EOA / BSA ></span></span><span style="font-family: inherit; font-size: large;"><span style="font-size: medium;"><span style="font-size: large;">1.2</span> </span><span style="text-align: justify;">cm</span><sup style="text-align: justify;">2</sup><span style="text-align: justify;">/m</span><sup style="text-align: justify;">2</sup><span style="font-size: medium;">,</span></span><span style="font-size: large;"> </span><span style="font-size: large;">there is only mild or no mismatch between prosthetic valve and patient. Conversely, when EOA / BSA ≤ </span><span style="font-family: inherit; font-size: large;"><span style="font-size: medium;"><span style="font-size: large;">0.9</span> </span><span style="text-align: justify;">cm</span><sup style="text-align: justify;">2</sup><span style="text-align: justify;">/m</span><sup style="text-align: justify;">2</sup><span style="font-size: medium;">,</span></span><span style="font-size: large;"> </span><span style="font-size: large;">then there is considerable PPM and significant stenosis. Intermediate values, below 1.2 but over 0.9 </span><span style="font-size: large; text-align: justify;">cm</span><sup style="text-align: justify;">2</sup><span style="font-size: large; text-align: justify;">/m</span><sup style="text-align: justify;">2</sup><span style="font-size: large;"> indicate a moderate degree of PPM.</span><br />
<span style="font-size: large;">Several studies link PPM with a decreased postoperative cardiac index, a worse New York Heart Association (NYHA) functional class, a higher likelihood of late adverse events and shorter mean patient survival.</span><br />
<h4>
<span style="font-size: large;">Haemolysis in patients with prosthetic heart valves</span></h4>
<span style="font-size: large;">A mild haemolysis is common in patients with mechanical prostheses (even with normal prosthetic valve function). Severe haemolysis is not common and is usually a result of prosthetic valve dysfunction (regurgitation, dehiscence, infection).<br />Blood tests in case of haemolysis show anemia (decreased hemoglobin and hematocrit), increased levels of lactate dehydrogenase (LDH) and reticulocytosis.<br />Treatment: Administration of folic acid and ferrous sulphate may be needed to increase production of erythrocytes. In severe cases, blood transfusions will be required and identification and treatment of the underlying problem (including valve replacement for cases requiring frequent blood transfusions).</span><span style="font-size: large;"><br /></span></div>
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<span style="font-size: large;">Prosthetic valve endocarditis</span></h4>
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<span style="font-size: large;">Early prosthetic heart valve endocarditis (≤ 2 months after implantation) is usually caused by staphylococcus epidermidis and often presents as acute endocarditis with a fulminant clinical course and high mortality rates (>20%). Late prosthetic valve endocarditis is usually caused by microorganisms that are the usual pathogens in native valve endocarditis, such as streptococci which are the most common causative agents, followed by gram negative bacteria and enterococci. <br />The imaging modality of choice is transesophageal echocardiography (TEE) which can detect vegetations, or complications of prosthetic valve endocarditis, such as valve dehiscence or an abscess.</span><br />
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<span style="font-size: large;">Paravalvular leak or paravalvular regurgitation of prosthetic heart valves</span></h3>
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<span style="font-size: large;">It is the regurgitation of blood in an area just next to the sewing ring of the valve, due to a poor contact of the valve with adjacent tissues to which it has been sutured. Possible causes include an infection (endocarditis), calcification or fibrosis of the native valve annulus, resulting in poor contact with the suture ring, or suture detachment. In patients with a mild (small) paravalvular leak, the prognosis is good and only periodic follow-up is required. In a severe paravalvular leak that causes symptoms, significant hemolysis, or left ventricular dilation due to volume overload, surgical or transcatheter management is required. A paravalvular leak is more common with transcatheter aortic valve implantation (TAVI) than with surgical implantation of a prosthetic valve.</span></div>
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<span style="font-size: large;">Prosthetic valve dehiscence</span></h4>
<span style="font-size: large;">Dehiscence (detachment) of the prosthetic valve suture ring from the valve annulus may occur in the early postoperative period due to surgical errors, the presence of extensive calcification of the valve annulus, infection (endocarditis), fragile valve annular tissue due to previous surgery, or chronic corticosteroid use. Late dehiscence of a prosthetic valve is due to infectious endocarditis. An indication of valve dehiscence is an abnormal rocking motion of the prosthetic valve in echocardiography or fluoroscopic examination. Dehiscence is an indication for emergency surgery.</span><br />
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<span style="font-size: large;"><br /></span><span style="font-size: large;">Prosthetic heart valve structural degeneration</span></h4>
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<span style="font-size: large;">Bioprosthetic valves, as opposed to mechanical valves, have the advantage of being less thrombogenic, but they also have the disadvantage that they develop degenerative lesions over the years (thickening and/or calcification with progressive stenosis or regurgitation). Factors associated with increased risk for a patient to develop degenerative lesions in a bioprosthetic valve are young, age, a bioprosthetic valve in the mitral position, renal failure, and hyperparathyroidism. The most common cause of malfunction of a bioprosthetic valve is the structural degeneration of the valve causing valve stenosis or regurgitation.</span><br />
<span style="font-size: large;">Reoperation is required once symptoms develop (class I), or even in asymptomatic patients with severe regurgitation, or severe stenosis of the bioprosthesis because reoperation at a stable stage reduces the risk of this second operation and thus may be justified. The risk associated with reoperation in a stable patient is only slightly higher than the risk of the first operation. Bioprosthetic aortic valve failure in patients with a high surgical risk can be treated by transcatheter valve‐in‐valve implantation.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;"><br /></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<span style="font-size: large;"><span style="background-color: #93c47d;"><br />BIBLIOGRAPHY AND LINKS</span></span></div>
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<span style="font-size: large;"><br />
</span><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Zoghbi, WA, et al. Recommendations for Evaluation of Prosthetic Valves With Echocardiography and Doppler Ultrasound. <span style="font-size: medium;">Journal of the American Society of Echocardiography 2009;22: 075-1014.</span></span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK<a href="http://www.onlinejase.com/article/S0894-7317(09)00676-2/pdf" target="_blank"> http://www.onlinejase.com/article/S0894-7317(09)00676-2/pdf</a></span></b><br />
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<b style="font-family: arial, helvetica, sans-serif; font-size: large;"><span style="background-color: white; color: #2a2a2a;">Baumgartner H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease: The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), </span><em style="background-color: white; border: 0px; box-sizing: border-box; color: #2a2a2a; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">European Heart Journal</em><span style="background-color: white; color: #2a2a2a;">, ehx391, </span><a href="https://doi.org/10.1093/eurheartj/ehx391" style="background-color: white; border: 0px; box-sizing: border-box; color: #006fb7; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">https://doi.org/10.1093/eurheartj/ehx391</a></b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK<a href="https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data"> https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data</a></b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span></b></span></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b> Chambers JB. Prosthetic heart valves. The International Journal of Clinical Practice 2014; 68:1227-1230 LINK <a href="http://onlinelibrary.wiley.com/doi/10.1111/ijcp.12309/pdf" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/ijcp.12309/pdf</a></b></span></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Bajaj R<span style="background-color: white;">, </span>Karthikeyan G<span style="background-color: white;">, et al.</span>CSI consensus statement on prosthetic valve follow up. Indian Heart Journal 2012; 64: S3 -S11 LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244813/pdf/main.pdf" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244813/pdf/main.pdf</a></b></span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Habets, J. et al. Diagnostic evaluation of left-sided prosthetic heart valve dysfunction Nat. Rev. Cardiol 2011;8: 466-478.</span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b style="font-family: Arial, Helvetica, sans-serif;">Huang G1, Schaff HV, et al. </b><b style="font-family: Arial, Helvetica, sans-serif;">Treatment of obstructive thrombosed prosthetic heart valve.</b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="https://www.ncbi.nlm.nih.gov/pubmed/23994405#">J Am Coll Cardiol.</a> 2013 ;62:1731-1736.</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://www.sciencedirect.com/science/article/pii/S0735109713038898?via%3Dihub" target="_blank">http://www.sciencedirect.com/science/article/pii/S0735109713038898?via%3Dihub</a></b></span><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-63783210232006481102017-07-23T18:49:00.004+03:002018-08-16T23:32:51.758+03:00Stenosis of the right cardiac valves: Pulmonary stenosis, Tricuspid Stenosis<h2>
Stenosis of the right cardiac valves: Pulmonary stenosis, Tricuspid Stenosis</h2>
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<h3>
<span style="font-size: large;">Pulmonic stenosis</span></h3>
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<span style="font-size: large;">Etiology of pulmonic stenosis (narrowing) is usually congenital (in 95 % of cases).</span><span style="font-size: large;"> An acquired form of pulmonic stenosis can occur with carcinoid heart disease (it can cause both pulmonic stenosis and pulmonic regurgitation). Rheumatic heart disease is a rare cause of pulmonic stenosis and, when present, it is accompanied by multiple valve disease. Large vegetations on a pulmonic valve infected by endocarditis can be a very rare cause of pulmonary stenosis (or regurgitation).</span><br />
<span style="font-size: large;"> Children with pulmonic stenosis are most often asymptomatic and the diagnosis is made by auscultation of the systolic murmur at the region of the pulmonary artery by the pediatrician. (See below) Over the years in patients with a significant degree of pulmonic valve stenosis syncopal episodes, angina-like discomfort in physical effort, effort dyspnea or fatigue may occur. </span></div>
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<span style="font-size: large;">In neonates with severe narrowing of the pulmonary valve, cyanosis is often observed due to shunting of blood with a direction from right to left through a patent foramen ovale. This shunt is the result of an elevated pressure in the right atrium. The latter is a consequence of increased pressure in the right ventricle, due to the pulmonary stenosis, which imposes an increased load on right ventricular function. Differential diagnosis of cyanosis in the neonate includes, in addition to severe pulmonary stenosis, with a shunt at the level of the atrial septum, some other congenital anomalies such as transposition of the great arteries or pulmonary atresia.</span></div>
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<span style="font-size: large;">The systolic murmur of pulmonary stenosis is heard louder parasternally at the second left intercostal space. The murmur has a maximum intensity at the middle of systole. The murmur often is preceded by an ejection click heard at the beginning of systole. The click often is better heard lower parasternally, or at the cardiac apex and not at the position of the maximum intensity of the systolic murmur. Usually, the click is not heard in case of a severe stenosis. There is often a wide splitting of the second heart sound, due to the slower ejection of blood by the right ventricle as a result of pulmonary stenosis.</span></div>
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<span style="font-size: large;">Indications of severity of pulmonic valve stenosis are the following: a murmur with its maximum intensity occurring late in systole, the longer the duration of the murmur, the greater the splitting of the second heart sound and the lower the intensity of the pulmonic component of the second heart sound, which in some cases of severe stenosis of the pulmonary valve may not be audible.</span></div>
<h4>
<span style="font-size: large;"> ECG and echocardiographic findings in pulmonic stenosis</span></h4>
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<span style="font-size: large;">ECG: In moderate to severe pulmonic stenosis, a right QRS axis and ECG findings of right ventricular hypertrophy are observed. In severe stenosis, there may also be an indication of right atrial abnormality or dilatation (tall P waves > 2.5 mm in the inferior leads)</span></div>
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<span style="font-size: large;">Echocardiography in pulmonic stenosis:</span></div>
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<span style="font-size: large;">It detects the position of the stenosis. In particular, the stenosis (narrowing) can be valvular, subvalvular, or supravalvular (stenosis of the pulmonary artery).</span></div>
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<span style="font-size: large;">When the stenosis is valvular, in the left parasternal short axis view at the base of the heart, there is thickening, reduced mobility and a dome-shaped opening of the valve leaflets. When a subvalvular stenosis is present, there is a narrowing caused by excess muscle tissue in the right ventricular outflow tract, and when it is supravalvular, a narrowing of the main pulmonary artery or of one of its main branches is observed (a pathologic narrowing of the arterial lumen causing turbulent flow at the site of the stenosis, detected with color flow doppler).</span></div>
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<span style="font-size: large;"> </span><br />
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<span style="font-size: large;">In general, in pulmonic stenosis with the color doppler, turbulent blood flow is observed with aliasing, i.e. an abrupt change in color with a mosaic color pattern in the area of stenosis, due to increased blood flow velocity.</span></div>
<span style="font-size: large;"> </span><br />
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<span style="font-size: large;"> The severity of the stenosis is determined by examining blood velocity through the stenosis with continuous wave doppler, which provides the maximum pressure gradient. A pressure gradient is the pressure difference that develops between the two sides of a stenotic valve, i.e. the pressure immediately proximal minus the pressure immediately distal to the stenosis. The patient during the examination should be in a relaxed state, in order to avoid an overestimation of the severity of the stenosis.</span></div>
<span style="font-size: large;"> </span><br />
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<span style="font-size: large;"> Pulmonary artery magnetic resonance imaging (MRI) or helical CT scan can be used to depict a stenosis of the pulmonary artery or its branches.</span></div>
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<h4>
<span style="font-size: large;"> Treatment of pulmonary valve stenosis</span></h4>
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<span style="font-size: large;"> The decision for treatment (with transcutaneous balloon valvuloplasty being preferred over surgical treatment) is made when the peak pressure gradient is > 40 mmHg.</span><span style="font-size: large;"><br />Patients with dysplastic valves may not be suitable for balloon valvuloplasty and may require pulmonary valve replacement with a bioprosthetic valve. Percutaneous stented pulmonary valve<br />implantation is an alternative to surgical replacement of the pulmonary valve </span><span style="font-size: large;"> </span><span style="font-size: large;">in selected </span><span style="font-size: large;">patients with pulmonic </span><span style="font-size: large;">stenosis and regurgitation.</span><br />
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<span style="font-size: large;"><span style="background-color: orange;">A video</span> of valvular pulmonary stenosis (echocardiogram) by Dr Ramachandra Barik</span></div>
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<span style="font-size: large;">See Link <a href="https://www.youtube.com/watch?v=gmCRZskZYf8" target="_blank">https://www.youtube.com/watch?v=gmCRZskZYf8</a></span><span style="font-size: large;"><br /></span><span style="font-size: large;">An <span style="background-color: orange;">echo case:</span> A patient with severe pulmonary stenosis, right ventricular hypertrophy and right to left shunt through a small ventricular septum defect by Dr. Maged Al Ali</span></div>
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<span style="font-size: large;">See <span style="background-color: orange;">Video,</span> Link: <a href="https://www.youtube.com/watch?v=s-tfOTR11r0" target="_blank">https://www.youtube.com/watch?v=s-tfOTR11r0</a></span></div>
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<h3>
<span style="font-size: large;">Tricuspid valve stenosis (Tricuspid stenosis)</span></h3>
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<span style="font-size: large;"> It is much rarer than mitral stenosis. It is more frequent in women than in men, but overall it is a very rare condition. Tricuspid valve stenosis is usually due to rheumatic fever. Then it does not occur as a single valve disease but it usually coexists with mitral stenosis and it is often accompanied by some degree of tricuspid regurgitation. Among patients with severe mitral stenosis, hemodynamically significant tricuspid stenosis is present in 5-10%.<br />Tricuspid stenosis of non-rheumatic etiology is even rarer than stenosis due to rheumatic valve disease.<br />Such rare causes of tricuspid valve stenosis are carcinoid syndrome (which more often causes tricuspid regurgitation), congenital tricuspid atresia, intramyocardial fibrosis and vegetations on the tricuspid valve due to endocarditis (these usually cause valvular regurgitation and rarely valvular stenosis).<br />
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<h4>
<span style="font-size: large;"> Pathophysiology, symptoms and clinical findings in tricuspid valve stenosis</span></h4>
<span style="font-size: large;"> Tricuspid stenosis causes a diastolic pressure gradient (pressure difference) between the right atrium and the right ventricle, resulting in an elevated pressure in the right atrium and in the systemic veins (systemic venous congestion). The pressure gradient depends on the severity of the stenosis and on the blood flow. It increases on inspiration, in which venous return to the large intrathoracic systemic veins increases and therefore the tricuspid transvalvular blood flow increases. The opposite occurs on expiration. A mean diastolic pressure gradient in the tricuspid valve of <span style="font-family: inherit;">≥ </span>4 mmHg is usually sufficient to result in an increase in mean right atrial pressure to levels that can cause a degree of systemic venous congestion, but this can be reduced by salt intake limitation and the administration of a diuretic.<br /> Systemic venous congestion causes peripheral edema (swelling at the lower parts of the body, usually the ankles), hepatomegaly (liver enlargement) and ascites (accumulation of fluid in the abdominal cavity). These are the main manifestations of tricuspid stenosis along with fatigue due to the decreased cardiac output.<br />However, because mitral stenosis usually precedes the development of tricuspid stenosis, many patients have initial symptoms of effort dyspnea and nocturnal dyspnea, as a result of mitral valve stenosis. Typically, when severe tricuspid stenosis develops, dyspnea decreases and is relatively mild compared to the severity of symptoms and signs of systemic venous congestion (edema, ascites, and hepatomegaly).<br />In tricuspid stenosis, the jugular veins are distended (jugular venous distention on the neck) and if heart rhythm is sinus ( thus if atrial contraction occurs), very tall a- waves are observed in the jugular pulse. This is the result of an elevated pressure in the right atrium at atrial systole, because the stenotic valve creates an obstacle to blood flow into the right ventricle. Also in the jugular pulse, there is a slow y -descent (negative wave), because emptying of blood from the right atrium to the right ventricle is delayed by the stenotic valve. In severe tricuspid valve stenosis, severe hepatic congestion may result in some cases in the development of cirrhosis of the liver, with jaundice, muscle wasting, large ascites, and splenomegaly.<br />The diastolic murmur (diastolic rumble) of tricuspid stenosis has some similarities to the diastolic murmur of mitral stenosis. Because mitral valve stenosis usually coexists, the murmur of tricuspid stenosis may not be detected by the examining physician. The diastolic murmur of tricuspid stenosis is usually heard better on the left lower sternal border and on the xiphoid area. Its intensity increases during inspiration. In expiration and during the stress phase of the Valsalva maneuver its intensity decreases (because then the venous blood return to the right atrium and flow through the tricuspid valve decreases).<br />
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<h4>
<span style="font-size: large;"> The ECG and the echocardiogram in tricuspid stenosis </span></h4>
<span style="font-size: large;"> The ECG in tricuspid stenosis shows right atrial enlargement (increased P wave amplitude in leads II, and V1-see ECG section). In a patient with clinical manifestations of right heart failure, the presence of ECG signs of right atrial enlargement in the absence of ECG signs indicative of right ventricular dilatation or hypertrophy should raise a suspicion of tricuspid valve disease.<br />The echocardiogram in tricuspid valve stenosis<br />Echocardiography shows thickening of the leaflets of the tricuspid valve with a dome-shaped valve in diastole (this is similar to the dome-shaped appearance of the mitral valve in diastole observed in mitral stenosis). There is a large dilatation of the right atrium and the superior vena cava (right atrial enlargement is also seen in the postero-anterior chest x-ray).<br />The area of the functional tricuspid valve orifice can be calculated by using continuous wave doppler in the same way as in mitral stenosis with a calculation of the PHT-pressure half time. A severe narrowing of the tricuspid valve is indicated by PHT ≥190 ms and an orifice area ≤1 c<span lang="EN-US" style="font-family: "times new roman" , serif; line-height: 107%;">m</span><sup><span style="font-family: "times new roman" , serif; line-height: 107%;">2</span></sup>. Continuous wave doppler also calculates the mean transvalvular pressure gradient, which according to the European guidelines (by ESC-2012) in severe tricuspid stenosis is ≥ 5 mmHg. In addition, echocardiography indicates whether there is also tricuspid regurgitation, as well as other valvular diseases (often rheumatic mitral disease).<br />Treatment of tricuspid valve stenosis<br />Systemic venous congestion is treated by the limitation of salt consumption and administration of a diuretic drug. This treatment of venous congestion may reduce hepatic congestion and improve liver function, thereby reducing the risk of surgery (especially the increased risk of bleeding associated with hepatic dysfunction, since the blood coagulation factors are synthesized in the liver).<br />In patients with moderate or severe tricuspid stenosis (with a mean transvalvular diastolic pressure gradient o> 4 mmHg and a calculated valve orifice area <1.5-2 c<span lang="EN-US" style="font-family: "times new roman" , serif; line-height: 25.68px;">m</span><sup><span style="font-family: "times new roman" , serif; line-height: 21.4px;">2</span></sup>), surgical treatment with surgical repair of the tricuspid valve is recommended or, if the repair is not feasible, tricuspid valve replacement with a bioprosthetic valve. Preferably, surgery for tricuspid valve disease is performed along with the operative treatment of commonly coexisting mitral valve disease. Because tricuspid stenosis is very rarely an isolated disorder and is usually accompanied by moderate to severe tricuspid regurgitation and rheumatic mitral valve disease, balloon tricuspid valvuloplasty is very rarely applicable. This is true, since this procedure is contraindicated when there is a significant tricuspid regurgitation, and of course, it does not treat mitral valve disease, which often coexists.</span><span style="font-size: large;"></span><br />
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<span style="font-size: large;"><span style="font-size: large;"><br /></span></span></div>
<span style="font-size: large;"> <span style="background-color: orange;">A video</span> (echocardiogram) of Rheumatic tricuspid stenosis and regurgitation<br />by Dr Venkatesan Sangareddi</span></div>
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<span style="font-size: large;">Link <a href="https://www.youtube.com/watch?v=WZVOLSj-e04" target="_blank">https://www.youtube.com/watch?v=WZVOLSj-e04</a><br /><span style="background-color: orange;"><br /></span></span></div>
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<span style="font-size: large;"><span style="background-color: orange;">A Video</span> Echo of a patient with tricuspid valve stenosis (with tricuspid regurgitation also) and mitral valve stenosis</span></div>
<span style="font-size: large;">by Dr. Maged Al Ali</span></div>
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<span style="font-size: large;">Link <a href="https://www.youtube.com/watch?v=jO-VwlLt1lA" target="_blank">https://www.youtube.com/watch?v=jO-VwlLt1lA</a></span><br />
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<span style="font-size: large;"><br /></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<span style="font-size: large;"> <b style="background-color: #e06666;"><br /></b> <b style="background-color: #e06666;">Bibliography and links </b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><span style="background-color: white; color: #2a2a2a;">Baumgarther H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease: The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), </span><em style="background-color: white; border: 0px; box-sizing: border-box; color: #2a2a2a; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">European Heart Journal</em><span style="background-color: white; color: #2a2a2a;">, , ehx391, </span><a href="https://doi.org/10.1093/eurheartj/ehx391" style="background-color: white; border: 0px; box-sizing: border-box; color: #006fb7; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">https://doi.org/10.1093/eurheartj/ehx391</a></b></span></div>
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK<a href="https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data"> https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data</a></span></b><span style="font-size: large;"></span><br />
<span style="font-size: large;"><b><br /></b> <a href="https://www.escardio.org/static_file/Escardio/Subspecialty/EACVI/position-papers/Echocardiographic-assessment-valve-stenosis-slides.pdf" target="_blank">EAE/ASE: Echocardiographic assessment of stenotic heart valves (A very useful guideline in slides)</a><br />
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<a href="http://www.wikiecho.org/wiki/Pulmonary_stenosis" target="_blank">Wickiecho: Pulmonary stenosis</a><br />
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<span style="font-size: large;"><span style="font-size: large;"><span style="font-family: inherit;"><br /></span></span></span></div>
<span style="font-size: large;"> <b><a href="http://emedicine.medscape.com/article/759890-overview" target="_blank"><span style="font-family: inherit;">Pulmonic Valvular Stenosis-emedicine/medscape</span></a></b></span><br />
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<span style="font-size: large;"><b><span style="font-family: inherit;"><span class="fontstyle0">Holzer RJ, et al. Transcatheter pulmonary valve replacement: state of the art. </span><span class="fontstyle2">Catheter Cardiovasc Interv</span><span class="fontstyle0">. 2016;87(1):117–128. [PMID: 26423185]</span> </span><span style="font-family: "arial" , "helvetica" , sans-serif;"> </span></b></span></div>
<span style="font-size: large;"><b> </b><a href="http://www.acc.org/latest-in-cardiology/ten-points-to-remember/2016/04/19/14/23/diagnosis-and-treatment-of-tricuspid-valve-disease" target="_blank">American College of Cardiology: Tricuspid valve disease: 10 points to remember </a></span></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Rodés-Cabau J, Taramasso M, O’Gara PT. Diagnosis and Treatment of Tricuspid Valve Disease: Current and Future Perspectives. Lancet 2016;Apr 2</span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-family: "times new roman"; font-size: large;"><br /></span><br /><b>B Phillips. Tricuspid Valve Disease: A Few Points Regarding Right-Sided Heart Failure. The Internet Journal of Thoracic and Cardiovascular Surgery. 2004 Volume 7 Number 1.</b></span><span style="font-size: large;"> </span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://ispub.com/IJTCVS/7/1/10907" target="_blank">http://ispub.com/IJTCVS/7/1/10907</a></b></span></div>
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</script>Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-31727913672410526882017-03-06T00:26:00.001+02:002019-03-25T01:27:48.829+02:00Pulmonary Hypertension<script async="" src="//pagead2.googlesyndication.com/pagead/js/adsbygoogle.js"></script> <script>
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<h2>
Pulmonary Hypertension</h2>
<span style="font-size: large;">It is defined as a mean pulmonary arterial pressure <span style="color: #222222; font-family: "times new roman" , serif;">≥ </span>25 mmHg measured by right cardiac catheterization. The normal limits of the mean pulmonary arterial pressure are 11-20 mmHg. A borderline level between 20 and 24 is of unknown clinical significance. These patients should be carefully followed especially when they have conditions predisposing to the development of PH (eg connective tissue disease).</span><br />
<span style="font-size: large;"> By echocardiography, an indication of pulmonary hypertension (PH) is a peak velocity of the jet of tricuspid regurgitation > 2.8 m/s (in the absence of pulmonary valve stenosis), or an estimated pulmonary artery systolic pressure <span style="color: #222222; font-family: "times new roman" , serif;">≥</span> 40 mmHg.</span><br />
<span style="font-size: large;">Although pulmonary hypertension is often first suspected or discovered by echocardiography, for confirming the diagnosis a right heart catheterization (RHC) demonstrating mean pulmonary arterial pressure ≥ 25 mm Hg is required.</span><br />
<span style="font-size: large;"> Another information from the RHC that is central to the diagnosis is the pulmonary arterial occlusion or pulmonary capillary wedge pressure (PCWP</span><span style="background-color: white; color: #333333; font-family: "arial" , "helvetica" , sans-serif; font-size: 15px;">).</span><br />
<span style="font-size: large;">A hemodynamic classification of pulmonary hypertension (PH) includes</span><br />
<span style="font-size: large;">- Precapillary PH, where the pulmonary capillary wedge pressure PCWP is normal ( ≤ 15 mmHg). This applies to PH due to</span><span style="font-size: large;"> lung disease or chronic thromboembolic lung disease or pulmonary arterial hypertension (PAH)</span><span style="font-size: large;"> and </span><br />
<span style="font-size: large;">-Postcapillary PH, where the PCWP is elevated (>15 mmHg). This is the case </span><span style="font-size: large;">in the most common group of PH, classified under WHO group II ( in this group, PH is due to pulmonary venous hypertension as a result of left heart disease).</span><br />
<span style="font-size: large;">PH is a</span><span style="font-size: large;"> disorder that may develop in multiple clinical conditions and can complicate the majority of cardiovascular and respiratory diseases (especially diseases at a severe stage).</span><br />
<span style="font-size: large;">From the preceding discussion, it is clear that for the accurate diagnosis and classification of pulmonary hypertension (especially when the cause is not obvious or when PAH is suspected) right heart catheterization is necessary. </span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhYkWsDu9QA53X2bYmMP4HexCfVMFSSXvAWq68CoWGaBNcBVsltWNPQbMAIh-SHUj_wEVvJrM73S9uMJErEjgX_a56s38-ElcWJDlrSpEZG98pFUB8B57oED27TgwodsY3-TyRHMds3Jk0/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+700px-RightHeart_Waveforms_Fig1.svg+%25CE%25B1%25CF%2580%25CF%258C+PCIpedia+-CC+licence-2.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="387" data-original-width="700" height="352" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhYkWsDu9QA53X2bYmMP4HexCfVMFSSXvAWq68CoWGaBNcBVsltWNPQbMAIh-SHUj_wEVvJrM73S9uMJErEjgX_a56s38-ElcWJDlrSpEZG98pFUB8B57oED27TgwodsY3-TyRHMds3Jk0/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+700px-RightHeart_Waveforms_Fig1.svg+%25CE%25B1%25CF%2580%25CF%258C+PCIpedia+-CC+licence-2.png" width="640" /></a></div>
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>This is an image showing right cardiac catheterization and the normal pressure curves obtained. The image depicts the successive positions of the Swan-Ganz catheter tip during the process of right heart catheterization and below the corresponding pressure curves of the right atrial (RA), right ventricular (RV), pulmonary arterial (PA) ) and pulmonary capillary wedge pressure (PCWP)</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b> Figure by PCIpedia Link: </b></span><span style="background-color: white; color: #222222; text-align: justify;"><a href="https://www.pcipedia.org/wiki/Right_heart_catheterization" style="color: #ee0044; text-align: left;" target="_blank"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>PCIpredia-The right heart catheterization</b></span></a></span><br />
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<h4>
<span style="font-size: large;"> Classification of severity of pulmonary hypertension.</span></h4>
<span style="font-size: large;">Mild pulmonary hypertension (PH) is characterized by systolic pulmonary arterial (PA) pressure 35–50 mmHg and mean PA pressure 25–35 mmHg. </span><br />
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<span style="font-size: large;">Moderate PH is characterized by systolic PA pressure 50–70 mmHg and mean PA pressure 35–45 mmHg.</span><br />
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<span style="font-size: large;">Severe PH is characterized by systolic PA pressure >70 mmHg and mean PA pressure >45 mmHg, or pulmonary vascular resistance (PVR) >6-7 Wood units.</span></div>
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<span style="font-size: large;">In chronic severe PH, although the PA pressure initially is severely elevated, later it may start declining into the moderate to mild range as right ventricular failure progressively worsens. When there is a severe right ventricular failure, the right ventricle cannot generate a high PA pressure. On the other hand, PVR remains severely elevated.</span></div>
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<span style="font-size: large;">Pathophysiology of pulmonary hypertension</span></h3>
<span style="font-size: large;">The pulmonary and systemic circulations are in series with each other and normally the total pulmonary and systemic blood flows are virtually identical.</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">Despite the same rate of blood </span><span style="font-size: large;">flow, the anatomic, hemodynamic, and physiological </span><span style="font-size: large;">characteristics of these two sections of the cardiovas</span><span style="font-size: large;">cular system have substantial differences. </span><span style="font-size: large;">The main difference is in vascular resistance: The pulmonary circulation is a low-resistance </span><span style="font-size: large;">network of highly distensible vessels.</span><br />
<span style="font-size: large;">An elevated pulmonary arterial pressure can be caused by:</span><br />
<span style="font-size: large;">An elevated pulmonary arterial resistance (normally pulmonary arterial resistance is about 10 times less than systemic vascular resistance)</span><br />
<span style="font-size: large;">An increased blood flow in the pulmonary circulation</span><br />
<span style="font-size: large;">An increased pulmonary venous pressure </span><br />
<span style="font-size: large;">Pulmonary hypertension can lead to right ventricular failure. The ability of the right ventricle to adapt to pulmonary hypertension depends not only on the level of pulmonary arterial pressure, but also on the rapidity of the development of PH and on other factors such as the age of the patient, hypoxemia due to a pulmonary disease or concomitant coronary artery disease (these factors can impair the ability of the right ventricle to compensate). The onset of clinical symptoms and signs of right ventricular failure indicates a poor prognosis.</span><br />
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<span style="font-size: large;">Symptoms of pulmonary hypertension </span></h3>
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<span style="font-size: large;">The most common symptom is exertional dyspnea, which may progressively worsen. Other manifestations include fatigue (also a very common manifestation), angina (right ventricular hypertrophy and the increased workload of the right ventricle due to the elevated pulmonary arterial pressure can cause right ventricular ischemia), presyncope or syncope, peripheral edema (due to right ventricular failure) and in some cases hemoptysis (in cases of mitral stenosis, or pulmonary thromboembolic disease).</span></div>
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<span style="font-size: large;">Physical examination in pulmonary hypertension (PH)</span></h4>
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<span style="font-size: large;">An accentuated pulmonic component of the second heart sound (P2) is common. There may be evidence of right ventricular failure with elevated jugular venous pressure (a common finding), a </span><span style="font-size: large;">right-sided S3 or S4 and a holosystolic murmur of secondary tricuspid regurgitation, </span><span style="font-size: large;">lower </span><span style="font-size: large;">extremity edema (this is common), hepatomegaly (enlargement of the liver) and/or ascites. </span></div>
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<span style="font-size: large;">Symptoms and signs of the disease that has caused the </span><span style="font-size: large;">PH are often present, e.g. paroxysmal nocturnal dyspnea, hypertension, or crackles at the lung bases can be clues to </span><span style="font-size: large;">left-sided systolic </span><span style="font-size: large;">or diastolic heart failure, a murmur can be a clue to left sided valvular heart disease,</span><span style="font-size: large;"> </span><span style="font-size: large;">rhonchi indicate obstruction of medium sized airways of the bronchial tree, as in chronic obstructive pulmonary disease,</span><span style="font-size: large;"> clubbing may be seen in some chronic lung diseases, </span><span style="font-size: large;">sclerodactyly and telangiectasia can be present in scleroderma, etc.</span><br />
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<span style="font-size: large;">The ECG in pulmonary hypertension</span></h3>
<span style="font-size: large;">An electrocardiogram (ECG) may show evidence supportive of PH, but a normal ECG does not exclude the diagnosis. ECG abnormalities can be suggestive of the diagnosis but they are neither specific nor sensitive. ECG abnormalities in cases of moderate to severe PH may include right ventricular </span><span style="font-size: large;">strain (inverted T waves in the right precordial leads-this is a relatively sensitive, but not specific sign), </span><span style="font-size: large;">P pulmonale, right axis deviation, right ventricular hypertrophy, right bundle branch block, and QTc prolongation. In cases of PH due to a left heart disease, the ECG usually shows evidence consistent with this disease, e.g a P mitrale in mitral valve disease, evidence of a previous myocardial infarction in cases of ischemic cardiomyopathy, left ventricular hypertrophy in hypertensive heart disease or in aortic valve stenosis, etc.</span></div>
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<h3>
<span style="font-size: large;">Chest radiography in pulmonary hypertension (PH)</span></h3>
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<span style="font-size: large;"><div style="font-size: medium; font-weight: normal;">
<span style="font-size: large;">Chest X-ray in pulmonary arterial hypertension (PAH) shows enlarged central pulmonary arteries with rapid </span><span style="font-size: large;">tapering of vessels toward the periphery of the lungs </span><span style="font-size: large;">(a “pruned tree” appearance) and reduced vascular markings in the periphery of the lungs. The chest X-ray may </span><span style="font-size: large;">also show enlargement of the right heart chambers. The enlargement of the right atrium is seen as a protruding lower right heart border and the enlargement of the right ventricle as an elevated heart apex.</span><br />
<span style="font-size: large;">In other causes of PH, findings depend on the causative disease.</span><br />
<span style="font-size: large;">In PH caused by </span><span style="font-size: large;">parenchymal lung disease, the chest X-ray may show hyperinflation and </span><span style="font-size: large;">bullous disease (suggestive of COPD), </span><span style="font-size: large;">or increased interstitial lung markings (suggestive of interstitial lung disease).</span><br />
<span style="font-size: large;">In PH caused by left heart disease, the chest X-ray may show dilated left heart chambers and signs of pulmonary venous congestion.</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><b>A 30 years old woman with progressive dyspnea on exertion. Can you describe the findings in this chest X-ray ?</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi0KAXXXxfwHQ9xV_FvWWn1cNr_LY3uTraL2qdgzJIzyWCn80yOV_QqpDAUEcob05EegEot7x7K0pLtOKa44VQE9RZH0AGeu_8vSUz2KqYFfXiuuy0hIqi7kPl2fyRpd7DhSUS9c4mxBoQ/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+PAH+%25CE%25B3%25CF%2585%25CE%25BD%25CE%25B1%25CE%25AF%25CE%25BA%25CE%25B1+30+%25CE%25B5%25CF%2584%25CF%258E%25CE%25BD+radiopedia.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1024" data-original-width="1024" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi0KAXXXxfwHQ9xV_FvWWn1cNr_LY3uTraL2qdgzJIzyWCn80yOV_QqpDAUEcob05EegEot7x7K0pLtOKa44VQE9RZH0AGeu_8vSUz2KqYFfXiuuy0hIqi7kPl2fyRpd7DhSUS9c4mxBoQ/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+PAH+%25CE%25B3%25CF%2585%25CE%25BD%25CE%25B1%25CE%25AF%25CE%25BA%25CE%25B1+30+%25CE%25B5%25CF%2584%25CF%258E%25CE%25BD+radiopedia.jpg" width="640" /></a></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><b>An enlarged main pulmonary artery is seen, as a protruding arch of the main pulmonary artery at the mid-left heart border, between the aortic knob and the left atrial appendage. The proximal pulmonary arteries are also enlarged. The right atrium is dilated (note the increased prominence of the lower right heart border) These radiographic features raised the suspicion of pulmonary arterial hypertension. This diagnosis was proven after further diagnostic workup.</b></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;"><b>Image from <a href="https://radiopaedia.org/" target="_blank">Radiopaedia.org</a> case by </b></span><b><span style="font-family: Arial, Helvetica, sans-serif;"> A.Prof Frank Gaillard</span></b><br />
<b><span style="font-family: Arial, Helvetica, sans-serif;">Link <a href="https://radiopaedia.org/cases/pulmonary-arterial-hypertension-primary?lang=us" target="_blank">https://radiopaedia.org/cases/pulmonary-arterial-hypertension-primary?lang=us</a></span></b><br />
<b>Licence </b><a href="https://radiopaedia.org/licence" style="background: rgb(255, 255, 255); box-sizing: border-box; color: #698fc0; font-family: "Open Sans", sans-serif; font-size: 12.96px; outline-offset: -2px; outline: -webkit-focus-ring-color auto 5px;">modified creative commons license</a><br />
<h4>
<span style="font-size: large;">Echocardiography in the evaluation of pulmonary hypertension</span></h4>
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<span style="font-size: large; font-weight: normal;">It can demonstrate enlargement of the right heart chambers (right ventricle and right atrium), signs of right ventricular pressure overload, including paradoxical bulging of the septum into the left ventricle during systole and hypertrophy of the right ventricular free wall. (Normally the right ventricular</span><span style="font-size: large;"><span style="font-weight: normal;"> wall is thinner and more compliant </span></span><span style="font-size: large; font-weight: normal;">than the left ventricular wall. Right ventricular wall thickness in diastole can be measured in the subxiphoid echocardiographic view. Normally it is < 5 mm). </span><br />
<span style="font-size: large;"><span style="font-weight: normal;">A practical assessment of the right ventricular size is obtained by its comparison </span></span><span style="font-size: large; font-weight: normal;">with the size of the left ventricle in the apical four-chamber view. Normally the right ventricle( RV) </span><span style="font-size: large; font-weight: normal;">should be less than two-thirds of the </span><span style="font-size: large; font-weight: normal;">size of the left ventricle (LV). However, this may be misleading </span><span style="font-size: large; font-weight: normal;">when LV dilation coexists.</span><br />
<span style="font-size: large;"><span style="font-weight: 400;">Moreover, it can be roughly estimated that the right ventricle is enlarged when on the apical 4 chamber view, the size of the right ventricle is equal to or greater than the left ventricle and when the distal part of the right ventricle contributes together with the left ventricle in the formation of the heart apex. Normally the heart apex is formed solely by the left ventricle. Also, in the case of right ventricular dilatation, the interventricular septum is shifted towards the left ventricle, thus reducing the dimensions of the left ventricle. This has an adverse effect on left ventricular diastolic filling.</span></span><br />
<span style="font-size: large; font-weight: normal;">The most useful echocardiographic view for the assessment of right ventricular dimensions is the apical 4 chamber view. It is useful to have the transducer approximately at the position of the cardiac apex. If it is medially from the apex, then the view may represent a larger part of the right ventricle and a smaller part of the left one. This can sometimes give a false impression of a dilated right ventricle. In the 4 chamber view, the short axis (width) of the right ventricular cavity is normally at the base < 4.1 and at the mid-ventricular level ≤ 3.5 cm (normal values 2-3.5 cm).</span><br />
<span style="font-size: large;"><span style="font-weight: 400;">In the apical </span></span><span style="font-size: large; font-weight: 400;">4 chamber </span><span style="font-size: large;"><span style="font-weight: 400;">view, the right ventricle can be planimetered, that is, it's area can be measured. The right ventricular area at end-diastole with respect to the body surface area (BSA) normally is 5-12.6 c</span></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="font-weight: normal;"><span lang="EN-US" style="line-height: 115%;">m</span><sup><span style="line-height: 115%;">2</span></sup></span><span style="line-height: 115%;"> </span><span style="font-weight: 400;">/ </span><span style="font-weight: normal;"><span lang="EN-US" style="line-height: 115%;">m</span><sup><span style="line-height: 115%;">2</span></sup></span></span><span style="font-size: large;"><span style="font-weight: 400;">. </span></span><br />
<span style="font-size: large;"><span style="font-weight: 400;">The area of the right ventricle normally is less than 2/3 of the left ventricular area. When the ratio of the right ventricular area to the left ventricular area is between 1 and 1.5 then there is a moderate dilatation of the right ventricle while when it is > 1.5 then the dilatation of the right ventricle is severe. (In mild enlargement of the right ventricle, the ratio is between 0.6 and 1).</span></span><br />
<span style="font-size: large; font-weight: 400;"> I</span><span style="font-size: large; font-weight: 400;">n the apical 4-chamber view, t</span><span style="font-size: large; font-weight: 400;">he end systolic area of the right ventricle divided by the BSA normally is in men ≤ 7.4 c</span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: 400;">/ </span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="font-size: large; font-weight: 400;"> and in women ≤ 6.4 c</span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: 400;">/ </span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: normal;"><span lang="EN-US" style="line-height: 27.6px;">m</span><sup><span style="line-height: 23px;">2</span></sup></span><br />
<span style="font-size: large; font-weight: normal;">In the parasternal long axis view, an index of the size of the right ventricle is the end-diastolic width of the right ventricular outflow tract, which normally should be <3 cm.</span>
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<div style="font-size: medium; font-weight: normal;">
<span style="font-size: large;"><span style="font-size: large;">(Watch this <span style="background-color: #e06666;">video</span> from 123sonography, which demonstrates these echocardiographic findings Link:</span><span class="video-thumb yt-thumb yt-thumb-48 g-hovercard" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" style="background: rgb(241 , 241 , 241); border: 0px; color: #167ac6; cursor: pointer; display: inline-block; font-family: "roboto" , "arial" , sans-serif; font-size: 0px; margin: 0px; overflow: hidden; padding: 0px; position: relative; text-decoration: none; vertical-align: middle; width: 48px;"><span class="yt-thumb-square" style="background: transparent; border: 0px; display: inline !important; height: auto; margin: 0px; padding: 0px 0px 48px;"><span class="yt-thumb-clip" style="background: transparent; border: 0px; bottom: -100px; display: inline !important; left: -100px; margin: 0px; padding: 0px; position: absolute; right: -100px; text-align: center; top: -100px; white-space: nowrap; word-break: normal;"><a class="yt-user-photo g-hovercard yt-uix-sessionlink spf-link " data-sessionlink="itct=CDAQ4TkiEwiY8p3issDSAhXOWxYKHUbjDiYo-B0" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" href="https://www.youtube.com/user/123sonography" style="background: rgb(255, 255, 255); border: 0px; color: #167ac6; cursor: pointer; display: inline !important; font-family: Roboto, arial, sans-serif; font-size: 13px; margin: 0px; padding: 0px; text-decoration: none;"> </a><a class="yt-user-photo g-hovercard yt-uix-sessionlink spf-link " data-sessionlink="itct=CDAQ4TkiEwiY8p3issDSAhXOWxYKHUbjDiYo-B0" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" href="https://www.youtube.com/user/123sonography" style="background: rgb(255, 255, 255); border: 0px; color: #167ac6; cursor: pointer; display: inline !important; font-size: 13px; margin: 0px; padding: 0px; text-decoration: none;"><span class="video-thumb yt-thumb yt-thumb-48 g-hovercard" data-ytid="UCCII7b4o20jJI9DWm3FE-ww" style="background: rgb(241, 241, 241); border: 0px; display: inline-block; font-size: 0px; margin: 0px; overflow: hidden; padding: 0px; position: relative; vertical-align: middle; width: 48px;"><span class="yt-thumb-square" style="background: transparent; border: 0px; display: inline !important; height: auto; margin: 0px; padding: 0px 0px 48px;"><span class="yt-thumb-clip" style="background: transparent; border: 0px; bottom: -100px; display: inline !important; left: -100px; margin: 0px; padding: 0px; position: absolute; right: -100px; top: -100px; word-break: normal;"><span class="vertical-align" style="background: transparent; border: 0px; display: inline-block; height: 248px; margin: 0px; padding: 0px; vertical-align: middle;"><span style="background-color: transparent;">123sonography</span></span></span></span></span></a></span></span></span></span></div>
<span style="font-size: large;"> </span><span style="font-size: large;"></span><br />
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<div style="font-size: medium; font-weight: normal;">
<span style="font-size: large;"><span style="font-size: large;"><a href="https://www.youtube.com/watch?v=jpEXFf2tRL4" target="_blank">https://www.youtube.com/watch?v=jpEXFf2tRL4</a>)</span></span></div>
<div style="font-size: medium; font-weight: normal;">
<span style="font-size: large;"><span style="font-size: large; font-weight: normal;"><span style="font-weight: normal;"><br /></span></span></span></div>
<span style="font-size: large; font-weight: 400;">For the assessment of right ventricular contractile function, it is useful to examine the M-mode of the movement of the lateral annulus of the tricuspid valve in the apical 4-chamber view. The maximum displacement of the lateral tricuspid annulus in the direction of the cardiac apex during systole (TAPSE) is measured. After the M mode function is selected, the cursor is positioned along the right side wall of the right ventricle in the apical 4-chamber view. The displacement of the lateral tricuspid annulus from end-diastole to end-systole is measured. This index provides a reliable estimate of right ventricular systolic function and has a good association with the right ventricular ejection fraction. (Exception: in case of a severe tricuspid regurgitation, the association of TAPSE with the right ventricular ejection fraction is weaker.) TAPSE in normal subjects is on average 2.2-2.3 cm, while the lower normal limit is 1.8 cm. In the international guidelines for the echocardiographic assessment of the cardiac chambers, a TAPSE <17 mm is considered as a strong indication of right ventricular systolic dysfunction. TAPSE <1.5 cm indicates severe systolic dysfunction of the right ventricle. Prognostic significance: A low TAPSE indicates a worse prognosis in pulmonary hypertension, heart failure, or chronic obstructive pulmonary disease.</span><br />
<span style="font-size: large; font-weight: 400;">Right ventricular fractional area change (FAC) is calculated from the end-diastolic and the end-systolic surface of the right ventricle (RV), in an apical 4-chamber view. FAC provides an estimate of global right ventricular systolic function. When tracing the right ventricular cavity with the cursor, the entire RV must be contained in the imaging sector, including the apex and the free wall, during both diastole and systole. Also, care must be taken to include myocardial trabeculae, as part of the RV cavity. The fractional area change (FAC) is calculated as follows:</span><br />
<span style="font-size: large; font-weight: 400;">FAC = (EDA-ESA) / EDA (%).</span><br />
<span style="font-size: large; font-weight: 400;">Where EDA is the end-diastolic and ESA the end-systolic area of the right ventricle. Right ventricular systolic dysfunction is indicated by FAC <35%.</span><br />
<span style="font-size: large; font-weight: 400;">Another index of global right ventricular (RV) contractility is the peak systolic velocity S' of the lateral tricuspid annulus. This is obtained with pulse wave tissue Doppler imaging (TDI), by aligning the Doppler cursor with the lateral annulus and the basal segment of the right ventricular free wall, in the apical 4-chamber view. Suggestive of RV systolic dysfunction is S'< 9.5 cm/s. </span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">Estimation of pulmonary arterial systolic pressure</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large; font-weight: normal;"><span style="font-size: large; font-weight: normal;"><span style="font-weight: normal;">Estimation of pulmonary arterial systolic pressure based on the peak velocity of tricuspid regurgitation (TR) by using the continuous wave Doppler signal of TR, can suggest the presence of pulmonary hypertension. This is a good method to suspect, or suggest PH, but not to accurately measure PA pressure (Accurate measurement requires right heart catheterization). The peak systolic pressure gradient (pressure difference) between the right ventricle and the right atrium, according to the modified Bernoulli equation</span><span style="font-family: inherit; font-weight: normal;"> is 4V</span></span></span><span style="font-family: inherit; font-size: large; font-weight: normal;"><sup>2</sup> , where V= the peak velocity of the TR jet. Thus the peak right ventricular systolic pressure (RVSP) is </span><span style="font-size: large; font-weight: normal;"><span style="font-size: large; font-weight: normal;"><span style="font-family: inherit; font-weight: normal;"> 4V</span></span></span><span style="font-size: large; font-weight: normal;"><sup>2</sup></span><span style="font-size: large; font-weight: normal;">+ RAP (where RAP=right atrial pressure). When there is no pulmonary stenosis, RVSP=PASP (PASP: pulmonary artery systolic pressure). Thus,</span><span style="font-size: large; font-weight: normal;"> if </span><span style="font-size: large; font-weight: normal;">there is no pulmonary stenosis, </span><span style="font-size: large; font-weight: normal;"> </span><span style="font-size: large; font-weight: normal;">PASP=</span><span style="font-size: large; font-weight: normal;"><span style="font-size: large; font-weight: normal;"><span style="font-family: inherit; font-weight: normal;">4V</span></span></span><span style="font-size: large; font-weight: normal;"><sup>2</sup></span><span style="font-size: large; font-weight: normal;">+ RAP. </span></div>
<span style="font-weight: normal;"><span style="font-size: large;">Right atrial pressure (RAP) can be estimated by echocardiography based on the maximum diameter and respiratory variation in the diameter of the inferior vena cava (IVC): </span></span><br />
<span style="font-weight: normal;"><span style="font-size: large;">An IVC diameter < 2.1 cm that collapses > 50% with a sniff suggests a normal RAP of 3 mmHg (range 0–5 mmHg). </span></span><br />
<span style="font-weight: normal;"><span style="font-size: large;">An IVC diameter >2.1 cm that collapses < 50% with a sniff or < 20% on quiet inspiration suggests a high RA pressure of 15 mmHg (range 10–20 mmHg).</span></span><br />
<span style="font-weight: normal;"><span style="font-size: large;"> In cases in which the IVC diameter and collapse do not fit this description, an intermediate value of 8 mmHg (range 5–10 mmHg) may be used. Such an approach is more accurate than using for RAP a fixed value of 5 or 10 mmHg. </span></span><br />
<span style="font-weight: normal;"><span style="font-size: large;">However, given the inaccuracies of RAP estimation, it is better to use the continuous wave Doppler measurement of peak TR velocity (and not the estimated PASP) as the main variable for assigning the echocardiographic probability of PH. </span></span><span style="font-size: large; font-weight: normal;">The echocardiographic probability of pulmonary hypertension (PH) in symptomatic patients with a suspicion of PH can be estimated from the peak tricuspid regurgitation velocity TRV (expressed in m/s):</span><br />
<span style="font-size: large;"><span style="font-weight: normal;"> When the peak tricuspid regurgitation velocity, TRV </span></span><span style="font-size: large; font-weight: normal;">≤2.8, or is not measurable and other echocardiographic signs suggestive of PH are absent, then the probability of PH is low (for the other suggestive echocardiographic signs of PH see below). </span><br />
<span style="font-size: large;"><span style="font-weight: normal;">When TRV </span></span><span style="font-size: large; font-weight: normal;">≤2.8, or not measurable and other echocardiographic signs suggestive of PH are present, </span><span style="font-weight: normal;"><span style="font-size: large;">then the probability of PH is intermediate.</span></span><br />
<span style="font-weight: normal;"><span style="font-size: large;">When TRV 2.9–3.4, then </span></span><span style="font-size: large; font-weight: normal;">the probability of PH is intermediate if other echocardiographic signs suggestive of PH are absent, but the probability is high if other suggestive echocardiographic signs are present.</span><br />
<span style="font-size: large; font-weight: normal;">When TRV >3.4 there is a high probability of PH, regardless of the presence or absence of other echocardiographic signs</span>.<br />
<span style="font-weight: normal;"><span style="font-size: large;">For a good measurement to be obtained the entire Doppler envelope of tricuspid regurgitation (TR) should be visualized with the characteristic bullet-shaped form. Do not measure peak velocity if the jet is not fully formed. Every Doppler velocity measurement should be performed with the Doppler beam as parallel to blood flow as possible. (This rule applies to every Doppler velocity measurement and not only to the measurement of TRV).</span></span><br />
<span style="font-size: large; font-weight: normal;">Doppler-derived right ventricular systolic pressure estimation can be inaccurate in patients with severe tricuspid regurgitation (TR), where TRV may significantly underestimate the pulmonary artery systolic pressure. Thus in patients with severe TR, peak TR velocity should not be used to exclude PH.</span><br />
<h3>
<span style="font-size: large;">Other echocardiographic signs suggestive of pulmonary hypertension (PH) besides TRV</span></h3>
<span style="font-size: large; font-weight: normal;">There are several echocardiographic signs suggesting pulmonary hypertension. These signs are used to assess the probability of pulmonary hypertension in addition to tricuspid regurgitation velocity measurement and include: </span><br />
<span style="font-size: large; font-weight: normal;">An enlarged right ventricle (RV) with RV/ LV basal diameter ratio >1 (LV=left ventricle). </span><br />
<span style="font-size: large;"><span style="font-size: large; font-weight: normal;">An enlarged right atrium:</span><span style="font-size: large; font-weight: normal;"> </span></span><span style="font-weight: normal;"><span style="font-size: large;">Right atrial area (at end-systole) >18 c</span></span><span lang="EN-US" style="color: #222222; font-family: "times new roman" , serif; font-weight: normal; line-height: 107%;"><span style="font-size: large;">m<sup>2</sup></span></span><span style="font-weight: normal;"><span style="font-size: large;"> measured in the apical 4 chamber view.</span></span><br />
<span style="font-size: large; font-weight: normal;">A dilated pulmonary artery with a diameter >25 mm (measured in the parasternal basal short axis view).</span><br />
<span style="font-weight: normal;"><span style="font-size: large;">Flattening of the interventricular septum, which can be demonstrated in the parasternal short axis view (left ventricular eccentricity index >1.1 in systole and/or diastole). LV eccentricity index is </span></span><span style="font-size: large; font-weight: normal;">the ratio of the anterior-inferior and septal-posterolateral cavity dimensions at the mid-ventricular level in the parasternal short axis view.</span><br />
<span style="font-size: large;"><span style="font-size: large; font-weight: normal;">Right ventricular outflow tract(RVOT) acceleration time (AT) <105 msec and/or midsystolic notching of the Doppler signal. AT is the time from the onset to the peak velocity of flow. These two signs are assessed with the pulse wave Doppler immediately proximal to the pulmonary valve in the parasternal basal short axis view.</span></span><br />
<span style="font-size: large;"><span style="font-size: large; font-weight: normal;"><span class="fontstyle0">The RVOT or pulmonary arterial AT (measured with the pulse wave Doppler) can also be used to calculate </span></span></span><span style="font-size: large; font-weight: normal;">mean pulmonary arterial (PA) with</span><span style="font-size: large; font-weight: normal;"> the following formula</span><br />
<span style="font-size: large;"><span style="font-size: large; font-weight: normal;"><span class="fontstyle0">Mean PA pressure = 79 - 0.45(AT)</span> </span></span><br />
<span style="font-size: large;"><span style="font-size: large; font-weight: normal;"> </span></span><span style="font-size: large;"><span style="font-size: large; font-weight: normal;">From the same view with continuous wave Doppler interrogation of the flow through the pulmonic valve, an e</span></span><span style="font-family: inherit; font-size: large; font-weight: normal;">arly diastolic pulmonary regurgitation velocity >2.2 m/sec, is also suggestive of PH.</span><br />
<span style="font-size: large; font-weight: normal;">Inferior cava diameter >21 mm with decreased inspiratory collapse (<50 % with a sniff, or <20 % with quiet inspiration).</span><span style="font-size: large; font-weight: normal;">Echocardiography can also show evidence of some etiologies of PH such as left heart disease, or congenital heart disease with a left to right shunt.</span></div>
</h3>
<h4>
<span style="font-size: large;">General diagnostic workup of patients with suspected PH:</span></h4>
<span style="font-size: large; font-weight: normal;">Echocardiography is recommended as a first-line test in case of suspicion of PH.</span><br />
<span style="font-size: large; font-weight: normal;">Lung function test with DLCO </span><span style="font-size: large;">(diffusing capacity of the lung for carbon monoxide )</span><span style="font-size: large;"> is recommended in the initial evaluation of patients with PH and a high-resolution CT should be considered in all patients with PH, to search for pulmonary disease.</span><br />
<span style="font-size: large; font-weight: normal;">In patients with a working diagnosis of PAH right heart catheterization is needed to measure mean pulmonary arterial pressure, PVR, and PCWP.</span><br />
<span style="font-size: large; font-weight: normal;">When measurement of PCWP is unreliable, left heart catheterization should be considered to measure left ventricular end diastolic pressure (LVEDP). Diagnosis of PAH and specific treatment decisions always require prior diagnostic confirmation with right heart catheterization.</span><br />
<span style="font-size: large; font-weight: normal;">In all patients with PAH routine biochemistry, hematology, immunology, HIV testing and thyroid function tests are recommended to search for a specific associated condition.</span><br />
<span style="font-size: large; font-weight: normal;">Abdominal ultrasound is recommended to screen for portal hypertension.</span><br />
<span style="font-weight: normal;"><span style="font-size: large;">In patients with unexplained PH, a ventilation /perfusion lung scan is recommended to exclude chronic thromboembolic PH </span></span><span style="font-size: large; font-weight: normal;">(CTEPH). </span><br />
<span style="font-size: large; font-weight: normal;"> A contrast CT angiography of the pulmonary artery is recommended in the workup of patients with CTEPH.</span><br />
<span style="font-size: large; font-weight: normal;">Patients with CTEPH should undergo </span><span style="font-size: large; font-weight: normal;">screening for thrombophilia, including antiphospholipid antibodies, anticardiolipin antibodies, and lupus anticoagulant.</span><br />
<h3>
<span style="font-weight: normal;"><span style="font-size: large;">Note: lung biopsy (o<span style="font-family: inherit;">pen or thoracoscopic) is not recommended in patients with PAH, according to the recent ESC guidelines.</span></span></span></h3>
<h3>
<span style="font-size: large;">Clinical classification of pulmonary hypertension (PH) according to the etiology and pathophysiology: </span></h3>
<span style="font-size: large;">PH is classified into 5 groups: </span><br />
<h3>
<span style="font-size: large;">Group1. </span></h3>
<span style="font-size: large;">It contains 3 subgroups: </span><br />
<span style="font-size: large;">Pulmonary arterial hypertension (PAH), </span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Pulmonary veno-occlusive disease and/or pulmonary capillary haemangiomatosi</span><span style="font-size: large;">s,</span><span style="font-size: large;"> and</span><br />
<span style="font-size: large;"> Persistent pulmonary hypertension of the newborn.</span><br />
<span style="font-size: large;"></span><br />
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<h4>
<b style="font-size: x-large;">Pulmonary arterial hypertension (PAH, group 1</b><span style="font-size: large;">)</span></h4>
</div>
<div>
<span style="font-size: large;"> It is characterized by the presence of pre-capillary PH ( mean pulmonary arterial pressure </span><span style="font-size: large;"> </span><span style="color: #222222; font-family: "times new roman" , serif; font-size: large;">≥ </span><span style="font-size: large;">25 mmHg and </span><span style="font-size: large;"> </span><span style="font-size: large;">PCWP is normal ≤ 15 mmHg</span>) <span style="font-size: large;">and pulmonary vascular resistance >3 Wood units, in the absence of other causes of pre-capillary PH such as lung disease or chronic thromboembolic disease or other rare diseases such as pulmonary</span><span style="font-size: large;"> capillary haemangiomatosis</span><span style="font-size: large;">. Pulmonary arterial hypertension (PAH) includes several different etiologies of PH that share a similar clinical picture and virtually identical pathological changes of the lung microcirculation. </span> <span style="font-size: large;">These changes of the lung microcirculation include vasoconstriction, intimal proliferation and fibrosis, medial hypertrophy and in situ thrombosis. These changes cause a progressive increase in pulmonic vascular resistance (PVR) and thus in right ventricular afterload and right ventricular work.</span><br />
<div>
<span style="font-size: large;">Etiologically pulmonary arterial hypertension (PAH) is classified as </span></div>
<div>
<span style="font-size: large;">Idiopathic </span></div>
<div>
<span style="font-size: large;">Heritable (BMPR2 mutation /Other mutations )</span></div>
<div>
<span style="font-size: large;"> Induced by drugs and toxins </span></div>
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<span style="font-size: large;">PAH associated with: </span></div>
<div>
<span style="font-size: large;">Connective tissue disease</span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;">Human immunodeficiency virus </span><span style="font-size: large;">(HIV)</span><span style="font-size: large;"> infection</span></div>
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<span style="font-size: large;">Portal hypertension </span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;">Congenital heart disease</span></div>
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<span style="font-size: large;">Schistosomiasis</span></div>
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<span style="font-size: large;"></span><br />
<div>
<span style="font-size: large;">PAH is a relatively rare form of pulmonary hypertension. The characteristic symptoms of PAH are dyspnea, chest pain, and syncope and if left untreated, PAH carries a high mortality rate, with </span><span style="font-size: large;">the most common cause of death being decompensated right heart failure. There is often a considerable delay in the diagnosis of PAH because the symptoms are insidious and overlap with many common diseases including asthma, </span><span style="font-size: large;">chronic obstructive lung disease,</span><span style="font-size: large;"> and other lung disease and cardiac disease (such as congestive heart failure of many etiologies, or coronary artery disease).</span></div>
<div>
<span style="font-size: large;">Early diagnosis is important, so that specific treatment for PAH can be initiated because new drugs have been recently developed resulting in a change in the management of this disease, with significant improvement in the quality of life and mortality.</span><span style="font-size: large;">The current treatment for PAH can be divided into three main steps: The initial approach includes General measures such as counseling on physical activity and supervised rehabilitation, pregnancy, birth control, psychosocial support, etc. PAH patients should avoid pregnancy because it is associated with significant mortality. Immunization of PAH patients against influenza and pneumococcal infection is recommended. Supervised exercise training should be considered in physically deconditioned PAH patients under medical therapy. </span><span style="font-size: large;">PAH patients should be encouraged to be active within symptom limits,</span><span style="font-size: large;"> avoiding excessive physical activity that leads to distressing symptoms.</span><br />
<span style="font-size: large;">Supportive therapy such as oral anticoagulants, diuretics, oxygen, digoxin, is important.</span><br />
<span style="font-size: large;">Referral to expert centers for PAH treatment and right heart catheterization </span><span style="font-size: large;">is indicated in every patient with clinical suspicion of PAH. During right heart catheterization of patients with PAH </span><span style="font-size: large;">acute vasoreactivity testing is indicated. </span><br />
<span style="font-size: large;">The second step of PAH treatment includes initial therapy with high-dose with calcium channel blockers only in vasoreactive patients or </span><span style="font-size: large;">w</span><span style="font-size: large;">ith drugs approved for PAH in non-vasoreactive patients. These drugs include prostacyclin, an endothelin receptor antagonist, or a phosphodiesterase-5 inhibitor.</span><br />
<span style="font-size: large;">Prostacyclin (epoprostenol in continuous intravenous infusion) and prostacyclin analogues (</span><span style="font-size: large;"> treprostinil, iloprost</span><span style="font-size: large;">) are direct pulmonary vasodilators. </span><br />
<span style="font-size: large;">Endothelin receptor antagonists (e.g., bosentan,</span><br />
<span style="font-size: large;">ambrisentan) inhibit the vasoconstricting</span><br />
<span style="font-size: large;">effects of endothelin-1.</span><br />
<span style="font-size: large;">Phosphodiesterase-5 inhibitors (e.g., sildenafil,</span><br />
<span style="font-size: large;">tadalafil) enhance nitric oxide-mediated </span><span style="font-size: large;">vasodilation.</span><br />
<span style="font-size: large;">The third part of the treatment strategy is related to the response to the initial treatment. In case of an inadequate response, combinations of the above drugs for PAH, or lung transplantation are considered.</span></div>
<h4>
<span style="font-size: large;"> Pulmonary hypertension due to pulmonary veno-occlusive disease and/or pulmonary capillary haemangiomatosis,</span></h4>
<span style="font-size: large;"> etiologically is classified as: </span></div>
<div>
<span style="font-size: large;"> Idiopathic</span></div>
<div>
<span style="font-size: large;">Heritable (EIF2AK4 mutation/other mutations)</span></div>
<div>
<span style="font-size: large;">Induced by drugs, toxins and radiation, and </span></div>
<div>
<span style="font-size: large;"> Associated with: </span></div>
<div>
<span style="font-size: large;">Connective tissue disease</span></div>
<div>
<span style="font-size: large;">HIV infection</span><br />
<h4>
<span style="font-size: large;">Pulmonary veno-occlusive disease and pulmonary capillary haemangiomatosis,</span></h4>
<span style="font-size: large;"> These are uncommon causes of PH. These two conditions have similarities in pathologic features and clinical characteristics. Another feature, that they have in common is the risk of drug-induced pulmonary edema with PAH. Thus, there is evidence that these two conditions overlap. They also share some important clinical similarities with PAH. </span><br />
<span style="font-size: large;">Pulmonary veno‐occlusive disease is characterized by abnormalities of the pulmonary venules similar to the arteriolar abnormalities seen in idiopathic PAH. and may be idiopathic or associated with scleroderma. Similar to PAH, true pulmonary arterial wedging is difficult during catheterization, but, if successful, the truly wedged PCWP is approximately the same as the left atrial pressure and has normal value. Although the PCWP i.e. the LA pressure, is normal, the pulmonary capillary pressure is increased due to the obstructive disease of the pulmonary venules. Thus, pulmonary edema can develop.</span><br />
<h4>
<span style="font-size: large;">Group 2 of diseases causing pulmonary hypertension (PH) is PH due to left heart disease </span></h4>
<span style="font-size: large;">PH secondary to left heart disease is also called pulmonary venous hypertension or postcapillary PH, because the initial pathophysiologic and etiologic event is the elevated pulmonary venous pressure. This is the most common group of disorders causing PH.</span><br />
<span style="font-size: large;">Left heart ventricular or valvular diseases may produce an increase in left atrial pressure. This results in a passive backward transmission of pressure to the </span><span style="font-size: large;">pulmonary circulation. As a result, the first event is a rise in pulmonary </span><span style="font-size: large;">capillary</span><span style="font-size: large;"> wedge pressure(PCWP) and then also the pulmonary</span><span style="font-size: large;"> arterial pressure rises</span><span style="font-size: large;">. The hemodynamic features are: </span><br />
<span style="font-size: large;">PCWP is elevated (>15 mmHg).</span><br />
<span style="font-size: large;"> Diastolic PA pressure is passively increased </span><br />
<span style="font-size: large;"> Pulmonary vascular resistance (PVR) is <3 Wood units. </span><br />
<span style="font-size: large;">The transpulmonary gradient, which is the pressure difference that produces flow in the pulmonary circulation, i.e., mean PA pressure minus PCWP, is <12 mmHg</span><br />
<span style="font-size: large;">The transpulmonary gradient is the numerator in pulmonary vascular resistance (PVR) calculation: PVR = transpul</span><span style="font-size: large;">monary gradient/cardiac output.</span><br />
<span style="font-size: large;">Causes are classified as :</span><br />
<span style="font-size: large;"> Left ventricular systolic dysfunction </span><br />
<span style="font-size: large;">Left ventricular diastolic dysfunction </span><br />
<span style="font-size: large;">Valvular disease, obstruction, and congenital cardiomyopathies </span><br />
<span style="font-size: large;"> Congenital or acquired </span><span style="font-size: large;">stenosis of the </span><span style="font-size: large;">pulmonary veins </span><br />
<span style="font-size: large;">In PH of the group 2 treatment is of the underlying cause, e.g. treatment for congestive heart failure, or surgery for severe disease of the left heart valves.</span><br />
<h3>
<span style="font-size: large;">Group 3 of the causes of pulmonary hypertension (PH) : Pulmonary hypertension due to lung diseases and/or hypoxia </span></h3>
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<span style="font-size: large;">These causes of PH are classified as:</span></div>
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<span style="font-size: large;"> Chronic obstructive pulmonary disease (COPD)</span></div>
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<span style="font-size: large;"> Interstitial lung disease </span></div>
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<span style="font-size: large;">Other pulmonary diseases with mixed restrictive and obstructive pattern </span></div>
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<span style="font-size: large;">Sleep-disordered breathing (sleep apnea)</span></div>
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<span style="font-size: large;"> Alveolar hypoventilation disorders </span></div>
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<span style="font-size: large;">Chronic exposure to high altitude </span></div>
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<span style="font-size: large;">Developmental lung diseases </span></div>
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<span style="font-size: large;">In patients with COPD, mild pH is common, but moderate </span><span style="font-size: large;">PH is </span><span style="font-size: large;">only seen in about 5-10% of cases</span><br />
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<span style="font-size: large;">and severe PH is quite uncommon ( in 2% of cases). respectively. </span></div>
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<span style="font-size: large;">Sleep apnea also usually causes </span><span style="font-size: large;">mild PH. </span></div>
<span style="font-size: large;">Conversely, severe interstitial lung disease, especially advanced‐stage fibrotic lung disease that obliterates the pulmonary capillaries can cause severe PH. <br />Severe PH may also be seen with interstitial lung disease due to sarcoidosis and with obesity-hypoventilation syndrome.</span></div>
<span style="font-size: large;"></span><br />
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<span style="font-size: large;"><span style="font-size: large;">In group 3 PH, treatment is of the underlying lung disease or cause. Usually, in case of a lung disease bronchodilators and oxygen are used.</span></span></div>
<span style="font-size: large;"> </span>
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<h3>
<span style="font-size: large;">Group 4 of PH: Chronic thromboembolic pulmonary hypertension and other pulmonary artery obstructions </span></h3>
<span style="font-size: large;">This etiologic group includes</span><br />
<span style="font-size: large;">Chronic thromboembolic pulmonary hypertension 4 Other pulmonary artery obstructions </span><br />
<span style="font-size: large;"> Angiosarcoma </span><br />
<span style="font-size: large;">Other intravascular tumors </span><br />
<span style="font-size: large;">Arteritis </span><br />
<span style="font-size: large;">Congenital pulmonary arteries stenoses </span><br />
<span style="font-size: large;">Parasites (hydatidosis) </span><br />
<span style="font-size: large;"> I</span><span style="font-size: large;">n thromboembolic PH with proximal thromboembolic disease, the treatment is surgical: p</span><span style="font-size: large;">ulmonary thromboendarterectomy.</span><br />
<h3>
<span style="font-size: large;">Group 5 of pulmonary hypertension: PH with unclear and/or multifactorial mechanisms</span></h3>
<span style="font-size: large;"> Hematological disorders: chronic hemolytic anemia, myeloproliferative disorders, splenectomy</span><br />
<span style="font-size: large;"> Systemic disorders: sarcoidosis, pulmonary histiocytosis, lymphangioleiomyomatosis, neurofibromatosis </span><br />
<span style="font-size: large;">Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders </span><br />
<span style="font-size: large;"> Others: pulmonary tumoral thrombotic microangiopathy, chronic renal failure (with/without dialysis), segmental pulmonary hypertension</span><br />
<span style="font-size: large;">In these patients, there is no specific treatment for PH. Treatment is for the underlying disease. Drugs for PAH are not used in the treatment of group 5 disorders, since there are no randomized trials.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<span style="font-size: large;"><b style="background-color: lime;">Bibliography and links </b></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">LINK: <a href="https://academic.oup.com/eurheartj/article/37/1/67/2887599/2015-ESC-ERS-Guidelines-for-the-diagnosis-and" target="_blank">2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension</a> </span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /><br />Guazzi M1, Galiè N., et al. Pulmonary hypertension in left heart disease. Eur Respir Rev. 2012;21:338-46. doi:10.1183/09059180.00004612.</span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="http://err.ersjournals.com/content/21/126/338.long" target="_blank">http://err.ersjournals.com/content/21/126/338.long</a></span></b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Hoeper MM,et al. Treatment of pulmonary hypertension. The Lancet Respiratory Medicine 2016; 4, 323–336. </b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="doi: http://dx.doi.org/10.1016/S2213-2600(15)00542-1" target="_blank">DOI: http://dx.doi.org/10.1016/S2213-2600(15)00542-1 </a></b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Kiely DG, et al. Pulmonary hypertension: diagnosis and management. BMJ 2013;346:f2028</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="doi: https://doi.org/10.1136/bmj.f2028" target="_blank">doi: https://doi.org/10.1136/bmj.f2028 </a></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="doi: https://doi.org/10.1136/bmj.f2028" target="_blank"><br /></a></b></span> <b><span style="font-family: "arial" , "helvetica" , sans-serif;"></span></b><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Rudski LG,<span style="vertical-align: baseline;"> Wyman WW et </span><span style="vertical-align: baseline;">al.</span>Guidelines for the Echocardiographic Assessment of<span style="vertical-align: baseline;"> </span>the Right Heart in Adults: A Report from the American<span style="vertical-align: baseline;"> </span>Society of EchocardiographyJ Am Soc Echocardiogr 2010;23:685-713 </span></b></div>
<div style="direction: ltr; margin-bottom: 0pt; margin-left: 0in; margin-top: 0pt; unicode-bidi: embed; word-break: normal;">
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://www.onlinejase.com/article/S0894-7317(10)00434-7/pdf" target="_blank">http://www.onlinejase.com/article/S0894-7317(10)00434-7/pdf</a></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /><br />Lang, R. M., Badano, L. P., Mor-Avi, et al. Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015; 16 (3 ), 233-271. https://doi.org/10.1093/ehjci/jev014</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://academic.oup.com/ehjcimaging/article/16/3/233/2400086" target="_blank">https://academic.oup.com/ehjcimaging/article/16/3/233/2400086</a></b></span></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="doi: https://doi.org/10.1136/bmj.f2028" target="_blank"><br /></a></b></span> <span style="font-size: large;"><br /></span></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-15807372397492876462017-01-09T01:38:00.000+02:002018-09-13T22:00:54.556+03:00Infective Endocarditis<script async="" src="//pagead2.googlesyndication.com/pagead/js/adsbygoogle.js"></script> <script>
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<h2>
<span style="font-size: large;"><b>Infective Endocarditis</b></span></h2>
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>A cardiology case (video): Infective endocarditis of a prosthetic mitral valve -Transesophageal echocardiography </b></span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 115%;">This is a case of a 32 years old female with a history of mitral valve replacement (with a bileaflet mechanical valve) 3 years before, presenting with fever and a cerebrovascular stroke.</span></b></span><br />
<span style="font-size: large;">( Echo images are courtesy of Dr Abdallah Almaghraby )</span><br />
<span style="font-size: large;">To watch the video in full-screen click on the symbol [] at the lower right corner</span><br />
<span style="font-size: large;"><b><br /></b></span>
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<div class="separator" style="clear: both; text-align: center;">
<iframe allowfullscreen="" class="YOUTUBE-iframe-video" data-thumbnail-src="https://i.ytimg.com/vi/852e0Pc9DG4/0.jpg" frameborder="0" height="266" src="https://www.youtube.com/embed/852e0Pc9DG4?feature=player_embedded" width="320"></iframe></div>
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Infective endocarditis (IE) </b>is a microbial infection of the endocardium or implanted intracardiac materials (eg prosthetic valves, conduits), or pacing electrodes, and indwelling catheters. The most typical pathologic feature of IE is a mobile vegetation associated with valve leaflets.</span><span style="font-size: large;"> Vegetations are composed of fibrin, platelets, debris, and bacteria.</span><span style="font-size: large;"><span style="font-size: medium;"> </span>Left-sided lesions are more common than right-sided lesions (the latter are common in intravenous drug use and congenital abnormalities).</span><br />
<span style="font-size: large;">Infective endocarditis (IE) is a serious disease, carrying potential for high morbidity and mortality, in part due to the difficulty in establishing an accurate diagnosis early in the course of the disease.</span><br />
<span style="font-size: large;">The incidence of IE in the general population is approximately 3-4 cases in 100.000 people per year. </span><br />
<span style="font-size: large;">The most common microorganism involved is Staphylococcus aureus , the next most common are streptococci of the oropharyngeal cavity (mostly Streptococcus viridians), followed in order of frequency by Enterococcus, coagulase-negative staphylococci, other streptococcal species, microorganisms of the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella) group, non HACEK Gram-negative bacteria, and fungi. </span><br />
<h3>
<span style="font-size: large;"><b> Pathogenesis of infective endocarditis (IE)</b> </span></h3>
<span style="font-size: large;">In most cases, an injury to the endothelium is involved, caused by turbulent blood flow at the site of a preexisting cardiac lesion. This results in the deposition of platelets and fibrin on the site and these early deposits are called nonbacterial thrombotic endocarditis. In case of a microorganism present in the blood, for example due to a dental procedure, or an infection, the microorganism can enter </span><span style="font-size: large;">these thrombotic deposits </span><span style="font-size: large;">and grow, resulting in the development of vegetations, composed of fibrin, platelets, debris, and bacteria and also often in invasion and destruction of cardiac structures, such as valve tissue, or occasionally invasion of the adjacent myocardium (formation of an abscess). </span><br />
<h3>
<span lang="EN-US" style="font-family: "calibri" , "sans-serif"; font-size: 11.0pt; line-height: 115%;"> </span><span style="font-size: large;"><b>Heart conditions predisposing to endocarditis </b></span></h3>
<span style="font-size: large;">Conditions that predispose to the development of IE by order of frequency include degenerative valve disease, presence of a prosthetic heart valve, intravenous narcotic drug use, rheumatic heart disease and congenital heart disease. </span><br />
<span style="font-size: large;">C</span><span style="font-size: large;">onditions predisposing to endocarditis<b> </b></span><span style="font-size: large;">(if significant bacteremia also occurs) are classified according to their relative risk for endocarditis and are the following:</span><br />
<span style="font-size: large;"><u>Cardiac conditions with a relatively high or intermediate risk for IE</u></span><br />
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<span style="font-size: large;">Prosthetic valves, including surgically and </span><span style="font-size: large;">transcatheter-implanted prostheses, </span><span style="font-size: large;">or presence of </span><span style="font-size: large;">prosthetic material used for cardiac valve repair </span><span style="font-size: large;">(high risk -there is an indication of antibiotic prophylaxis for procedures that can cause bacteremia)</span></div>
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<span style="font-size: large;">Previous infective endocarditis (obviously </span><span style="font-size: large;">high risk)</span><span style="font-size: large;"><br />Indwelling right heart catheters for hyperalimentation are associated with </span><span style="font-size: large;">high risk for IE, </span><span style="font-size: large;">but indwelling right heart catheters for other purposes pose an intermediate</span><span style="font-size: large;"> risk</span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;">Unrepaired congenital heart disease:</span></div>
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<span style="font-size: large;"> Coarctation of the aorta, patent ductus arteriosus and </span><span style="font-size: large;">arteriovenous fistula</span><span style="font-size: large;"> are conditions with a high risk for IE. </span><span style="font-size: large;">Tetralogy of Fallot has an intermediate risk</span></div>
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<span style="font-size: large;">Marfan syndrome (relatively high risk)</span></div>
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<span style="font-size: large;">Valvular heart disease:</span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;">Aortic regurgitation is considered to be associated with a relatively high risk, but calcific aortic stenosis with an intermediate risk. </span><span style="font-size: large;">Mitral regurgitation, in general, is considered to have a relatively high risk, but specifically m</span><span style="font-size: large;">itral valve prolapse with regurgitation, as well as mitral</span><span style="font-size: large;"> stenosis are of intermediate risk for IE.</span><span style="font-size: large;"> Tricuspid valve disease is also an intermediate risk condition for IE. </span><br />
<span style="font-size: large;">Hypertrophic obstructive cardiomyopathy (intermediate risk)</span></div>
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<span style="font-size: large;">Nonvalvular intracardiac prosthesis </span><span style="font-size: large;">(intermediate risk)</span></div>
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<span style="font-size: large;"><u>Cardiac conditions with a low risk for IE</u> are:</span></div>
<span style="font-size: large;">Mitral valve prolapse without regurgitation <br />Congenital heart disease with low risk for IE: an uncorrected atrial septal defect and surgically corrected congenital lesions without a prosthesis >6 months after surgery<br />Cardiac pacemakers<br />Aortocoronary bypass surgery (negligible risk)</span><br />
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<br /></div>
<span style="font-size: large;">The most important <b>non-cardiac predisposing factors to bacterial endocarditis</b> (by causing bacteremia) are: </span><span style="font-size: large;">IV drug use, d</span><span style="font-size: large;">ental procedures that cause bleeding, oral and upper respiratory tract surgery, genitourinary surgery. </span></div>
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<h3>
<span style="font-size: large;"><b>Antibiotic prophylaxis for Infective Endocarditis</b></span></h3>
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<span style="font-size: large;">Current guidelines have restricted the indications for antibiotic prophylaxis compared to older common practice, because of changes in pathophysiological conceptions and risk-benefit analyses. Cardiac conditions which require prophylactic antibiotic therapy for the avoidance of IE, in case of a procedure predisposing to endocarditis (</span><span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;">dental procedures inducing gingival or mucosal bleeding, including professional cleaning, tonsillectomy, adenoidectomy, surgical operations that involve intestinal or respiratory mucosa</span><span style="font-size: large;">) are the following :</span></div>
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<span style="font-size: large;"> Prosthetic heart valves, including bioprosthetic and homograft valves, </span><span style="font-size: large;">or a prosthetic material (eg a prosthetic ring) placed for valve repair,</span></div>
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<span style="font-size: large;">Previous bacterial endocarditis, even in the absence of heart disease Most congenital cardiac malformations, </span><span style="font-size: large;">if not repaired,</span><span style="font-size: large;"> especially cyanotic lesions (except isolated atrial septum defect which is a low risk condition for IE) </span><span style="font-size: large;">or repaired congenital heart disease (CHD) with shunts or conduits, repaired CHD when a residual defect is present , and recent repair of CHD (<6 months) involving prosthetic device or material. </span><br />
<span style="font-size: large;">A cardiac transplant with valve regurgitation due to a structurally abnormal valve</span><br />
<span style="font-size: large;">Antibiotic prophylaxis is also recommended before implantation of pacemakers, or implantable defibrillators (ICDs), to avoid infection of the device.</span></div>
<span style="font-size: large;"><u>Procedures predisposing to endocarditis</u> are divided into: Procedures </span><span style="font-size: large;">with a clear indication for antibiotic prophylaxis (if one of the above cardiac conditions is present) such as </span><span style="font-size: large;">dental procedures which induce gingival or mucosal bleeding, (professional cleaning is included), tonsillectomy and adenoidectomy and</span><br />
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<span style="font-size: large;">Procedures with a less clear indication for </span><span style="font-size: large;">antibiotic prophylaxis, such as </span><span style="font-size: large;">operations that involve intestinal or respiratory mucosa.</span><span style="font-size: large;"> </span><br />
<b style="font-size: x-large;"><br /></b> <br />
<h3>
<b style="font-size: x-large;">Clinical manifestations of infective endocarditis</b></h3>
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<span style="font-size: large;">The most typical presentation of IE is the presence of fever and a new murmur (in about 85%) of cases. However, fever may be absent in the elderly, uremic, or immunosuppressed. A murmur may be absent with right-sided or mural infection or with </span><span style="font-size: large;">infection of an</span><span style="font-size: large;"> intracardiac device. Nonspecific symptoms such as malaise, fatigue and night sweats are common. Dyspnea is also common.</span><br />
<span style="font-size: large;">Congestive heart failure occurs in up to 55% of cases</span><span style="font-size: large;">. </span><br />
<span style="font-size: large;">Neurologic symptoms and findings, are usually indications of an embolic complication and may include clinically apparent cerebral emboli (20%), rupture of a </span><span style="font-size: large;">mycotic aneurysm (< 5%), meningitis, or brain abscess (< 5%).</span><br />
<span style="font-size: large;">Additional possible manifestations of IE, are due to <u>embolic or immune complex phenomena</u> and include mucosal petechiae (in about 20% -30% of cases), Osler’s nodes (painful, tender red nodules on the pads of fingers or toes: 10% -20%), splinter hemorrhages (dark red linear streaks under the nails in about 10% -20%), an arterial embolism (the clinical picture depends on the site of embolism, see below), Janeway lesions (these are more rare, they are red, macular, nontender lesions on the fingers, palms, or soles, observed in < 5% of IE cases), splenomegaly (in about 30% of cases), and Roth’s spots (retinal hemorrhages: < 5%). These classic physical findings are not sensitive and (also not specific) for the diagnosis of IE.</span><br />
<span style="font-size: large;">Systemic embolization occurs in about 20% - 40% of cases of IE and may result in manifestations of an </span><span style="font-size: large;">acute stroke (cerebral emboli), or it can mimic </span><span style="font-size: large;">peritonitis (embolization to the spleen, kidney, or bowel), a pulmonary embolism (from IE involving the right side of the heart), an </span><span style="font-size: large;">acute coronary syndrome (coronary artery emboli), or it may result in a cold extremity with reduced or absent pulse (embolization of a peripheral artery).</span><br />
<span style="font-size: large;">In summary, the clinical picture of IE is highly variable, ranging from subtle and slowly progressive symptoms to acute severe congestive heart failure due to severe valvular regurgitation. IE can be divided into acute and subacute.</span></div>
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<span style="font-size: large;">Acute infective endocarditis, the most common cause of which is staphylococcus aureus, is associated with rapid symptom onset, often with high fever and it is a more invasive infection which tends to produce large vegetations (2 mm to 2 cm), rapid valve destruction and, commonly, embolic complications. Invasion of myocardium with the formation of an abscess cavity, is also common.</span></div>
<span style="font-size: large;">With subacute infective endocarditis, streptococcus viridans (a microorganism of the oral cavity) is the most common causative agent.</span><span style="font-size: large;"> Clinical course is characterized by slow onset with vague or nospecific symptoms, such as low-grade fever, malaise, fatigue, weight loss, flulike symptoms, chills, night sweats, and musculoskeletal aches</span><span style="font-size: large;">.</span><span style="font-size: large;"> It leads to valve lesions and valve dysfunction but with a more gradual course, in comparison to acute IE. It tends to produce smaller vegetations than those observed in acute IE. </span></div>
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<h3>
<span style="font-size: large;"><b>Diagnosis of infective endocarditis</b></span></h3>
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<span style="font-size: large;"> The <u>modified Duke criteria</u> are widely used for the diagnosis of IE. </span><span style="font-size: large;">A combination of 2 major criteria, or the combination of 1 major and 3 minor criteria, </span><span style="font-size: large;">or five minor criteria </span><span style="font-size: large;">will constitute a definite clinical diagnosis. </span><br />
<span style="font-size: large;">The <u>major diagnostic criteria</u> can be summarized as </span></div>
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<span style="font-size: large;"> Positive blood cultures and </span></div>
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<span style="font-size: large;">An abnormal echocardiogram with typical findings for IE. </span><br />
<span style="font-size: large;">A more detailed description of the<u> major clinical diagnostic criteria </u>is the following:</span><br />
<span style="font-size: large;">• A positive blood culture for infective endocarditis, as defined by the recovery of a typical </span><span style="font-size: large;">microorganism from two separate blood cultures in the absence of a primary focus.</span><br />
<span style="font-size: large;">(Typical microorganisms include viridans streptococci, community-acquired staphylococcus aureus or enterococcus species, streptococcus bovis, HACEK group, abiotrophia species and granulicatella species), </span><span style="font-size: large;">or</span><br />
<span style="font-size: large;">• A persistently positive blood culture, for a microorganism consistent with IE from either blood samples obtained more than 12 hours apart, or all three, or a majority of four or more separate blood samples, with the first and last obtained at least 1 hour apart, or<br />• A positive serological test for Q fever, with an immunofluorescence assay showing phase 1 IgG antibodies at a titre >1 : 800, or</span></div>
<span style="font-size: large;">• Echocardiographic evidence of endocardial involvement:<br />-An oscillating intracardiac mass on a cardiac valve or its supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation, or<br />-An abscess, or<br />-New partial dehiscence of a prosthetic valve, or<br />-New valvular regurgitation.</span><br />
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<span style="font-size: large;"><br /></span> <span style="font-size: large;">The <u>minor criteria</u> are: </span><br />
<span style="font-size: large;"> Fever <br />Predisposing cardiac lesion <br />IV drug use <br />Vascular phenomena (arterial embolic, septic pulmonary infarcts, Janeway lesions),<br />Immunologic phenomena (such as Osler nodes, Roth spots, glomerulonephritis, or a positive rheumatoid factor) <br />Microbiologic evidence (positive blood cultures not meeting major criteria or evidence of active infection with an organism consistent with infective endocarditis)</span><br />
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<b><span style="font-family: "verdana" , sans-serif;">Infective endocarditis: A video. Clinical manifestations, diagnosis and echocardiography (The echo case is courtesy of Dr.</span></b></div>
<b><span style="font-family: "verdana" , sans-serif;">Vugar Guliyev </span></b></h5>
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<span style="font-size: medium;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b></span> <span style="font-size: medium;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;">After starting the video, you can click on the symbol [] on its lower right corner if you want to watch it in full screen</span></b></span> <span style="font-size: large;"><br /></span></div>
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<span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;"><b>I also recommend the following <span style="color: purple;">video</span><span style="color: purple;">,</span> because apart from a summary of the topic, they also provide images of some physical signs of IE, such as </b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>mucosal petechiae, Osler’s nodes, splinter hemorrhages</b></span><b style="font-family: "helvetica neue", arial, helvetica, sans-serif;">, Janeway's lesions, Roth spots. LINK :</b></div>
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<span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;"><a href="https://www.youtube.com/watch?v=yaxUur_7_ok"><b>https://www.youtube.com/watch?v=yaxUur_7_ok</b></a></span></div>
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<span style="font-size: large;"><br /></span><span style="font-size: large;"><b>Diagnostic tests for Infective Endocarditis (Echocardiography and blood cultures)</b></span></h3>
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<span style="font-size: large;">In IE, bacteremia is almost constant, therefore p</span><span style="font-size: large;">ositive blood cultures remain the cornerstone of diagnosis and permit identification of the causative micro-organism and susceptibility testing.</span><span style="font-size: large;"> Samples for blood culture should be taken </span><span style="font-size: large;">before antibiotic administration (</span><span style="font-size: large;">At least three sets of blood cultures </span><span style="font-size: large;">at 30-minute intervals, each containing 10 ml of blood, incubated in both aerobic and anaerobic culture media). The sample should be obtained from a peripheral vein rather than from a central venous catheter with a meticulous sterile technique. This almost always is sufficient to identify the <u>usual</u> causative microorganisms. </span></div>
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<span style="font-size: large;"><u>Blood culture-negative IE</u> refers to IE in which no causative microorganism can be grown and identified by the usual blood culture methods and it can occur in approximately 10- 20% of all cases of IE. It often poses important diagnostic and therapeutic dilemmas. </span><span style="font-size: large;">Blood culture-negative IE</span><span style="font-size: large;"> commonly arises as a consequence of previous antibiotic administration, or it is IE caused by fungi or fastidious bacteria (especially obligatory intracellular bacteria).</span><span style="background-color: #fffffe; color: #030303; font-family: "helvetica" , "arial" , sans-serif; font-size: 14px; line-height: 21px;"> </span><span style="font-size: large;">Such microorganisms need culture on specialized media, in order to be isolated. Moreover, their growth is relatively slow.</span></div>
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<span style="font-size: large;">Four <span style="background-color: white;"><u>echocardiographic findings</u> </span>are major criteria for the diagnosis of IE: a vegetation, an abscess or pseudoaneurysm , a new dehiscence of a prosthetic valve and a new valvular regugitation. With current technology the sensitivity for the diagnosis of vegetations </span><span style="font-size: large;">for transthoracic echocardiography (TTE) </span><span style="font-size: large;">in native and prosthetic valves is 70% and 50%, respectively, and </span><span style="font-size: large;">for transesophageal echocardiography (TEE)</span><span style="font-size: large;"> </span><span style="font-size: large;"> 95% and 92%, respectively (roughly let us say more than 90 %). Specificity is approximately 90% for both TTE and TEE.</span><br />
<span style="font-size: large;">Some echocardiographic findings, that can be observed in infective enocarditis (IE):</span></div>
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<span style="font-size: large;">A vegetation, on echocardiography, appears as an irregularly shaped, discrete echogenic mass which is adherent to, but distinct from, the endocardial surface or an intracardiac device. Oscillation of the mass is supportive for the diagnosis, but not mandatory.</span><br />
<span style="font-size: large;">An abscess, on echocardiography, is a thickened, nonhomogeneous area near a valve with echodense or echolucent appearance. Evidence of flow into the region is supportive for the diagnosis, but not mandatory.<br />Perforation of a valve leaflet is defined as interruption of tissue continuity of valve leaflet with demonstration of flow with color flow doppler, through the defect.<br />Dehiscence of a prosthetic valve is shown by demonstration of paravalvular regurgitation by transthoracic or transesophageal echocardiography, with or without a rocking motion of the prosthesis. <br />Pseudoaneurysm is a perivalvular cavity communicating with the cardiovascular lumen and in echocardiography it appears as a pulsatile perivalvular echo-free space (an echolucent cavity) with color-Doppler detected entering this space. <br />A valve aneurysm is a saccular outpouching or bulging of valvular tissue (meaning that a portion of the valvular tissue protrudes outward).</span><br />
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<span style="background-color: #ea9999; font-family: "youtube noto" , "roboto" , "arial" , sans-serif; font-size: x-large; font-weight: 500; line-height: 1em;">A video </span><span style="font-family: "youtube noto" , "roboto" , "arial" , sans-serif;"><span style="background-color: #ea9999; font-size: 18px; line-height: 32px;">A simple transesophageal echo quiz and introduction to TEE (TOE)</span></span></h1>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;"><i>(The case is courtesy of Dr. Lampros Lakkas ).</i></span><br />
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<span style="font-size: large;"><b>Treatment of infective endocarditis</b> </span></h3>
<span style="font-size: large;">According to the latest guidelines, the best management of </span><span style="font-size: large;">IE can be achieved </span><span style="font-size: large;"> via an "endocarditis team", a multidisciplinary collaboration among cardiologists, cardiac surgeons, and infectious </span><span style="font-size: large;"><br />disease specialists (Although, this is not always quite possible).<br />In IE, prompt initiation of parenteral antibiotic therapy is important, because the rate of complications, such as embolization, decreases rapidly within several days, after initiation of proper antibiotic treatment. </span><span style="font-size: large;">In severely ill patients with IE </span><span style="font-size: large;">initial empirical antibiotic treatment </span><span style="font-size: large;">(before pathogen identification) should start immediately after obtaining three separate blood cultures at 30 minute time intervals. When the pathogen is identified the antibiotic regimen can change according to the specific microorganism and its antibiotic subsceptibility. Generally in IE t</span><span style="font-size: large;">he duration of antibiotic treatment is usually about 4-6 weeks. </span><span style="font-size: large;">Repeat sets of blood cultures</span><br />
<span style="font-size: large;">after the initiation of antibiotic treatment are obtained every 48 hours, </span><span style="font-size: large;">until the resolution of bacteremia is confirmed.</span><br />
<span style="font-size: large;"><u>Indications for surgery in IE include: </u></span><br />
<span style="font-size: large;">H</span><span style="font-size: large;">eart failure with pulmonary edema or cardiogenic shock, or signs and symptoms of heart failure, or valve dysfunction with echocardiographic signs of poor hemodynamic tolerance.</span><br />
<span style="font-size: large;">Findings suggesting that the infection cannot be controlled or is already uncontrolled, such as persisting positive blood cultures despite appropriate antibiotic therapy and adequate control of septic metastatic foci, or</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">local findings of uncontrolled infection such as abscess, false aneurysm, fistula, or an enlarging vegetation,</span></div>
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<span style="font-size: large;">or IE by fungi or multiresistant organisms, or</span></div>
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<span style="font-size: large;"> prosthetic valve endocarditis caused by staphylococci or non-HACEK gram-negative bacteria (this is a class IIa indication, meaning that surgery probably should be considered but not as an absolute indication).</span></div>
<span style="font-size: large;">Surgery is also indicated in infective endocarditis for prevention of embolic complications:<br />After an embolic episode in a patient with IE involving a native or prosthetic aortic or mitral valve with persistent vegetations >10 mm despite appropriate antibiotic therapy.<br />IE involving an aortic or mitral valve (native or prosthetic) with very large vegetations >30 mm (this is a relative-class IIa-indication for surgery).</span><br />
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<span style="font-size: large;">The objective of surgery is the total removal of infected tissues and repair of cardiac damage, including repair of the affected valve, or replacement of the affected valve with a prosthetic one.</span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;"><u>Proposed antibiotic regimens for empirical treatment </u></span><span style="font-size: large;">(before pathogen identification)</span><span style="font-size: large;"> are the following: </span></div>
<span style="font-size: large;">For <u>community-acquired</u> endocarditis of native valves, or late endocarditis of prosthetic valves (≥12 months post surgery) : Ampicillin 12 g/day i.v. in 4–6 doses+ (Flu)cloxacillin or oxacillin + Gentamycin (for drug dosages see below) or</span></div>
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<span style="font-size: large;"> for patients allergic to penicillin, a very good regimen is Vancomycin + Gentamycin (for dosages see below)</span></div>
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<span style="font-size: large;"><u>For early prosthetic valve endocarditis (<12 months post surgery) or for healthcare associated endocarditis</u> </span></div>
<span style="font-size: large;">Vancomycin +Gentamycin +Rifampin (rifampin is recommended only for prosthetic valve IE and should be started 3–5 days later than the other two drugs). F</span><span style="font-size: large;">or drug dosages see below.</span><br />
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<b><span style="font-size: large;"><br /></span></b><b><span style="font-size: large;">Therapy of IE caused by some common specific microorganisms</span></b></h4>
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<span style="font-size: large;"><u>Treatment for Streptococus viridans</u>: (and also in general for oral and digestive streptococci) : Penicillin G 12–18 million U/day i.v. either in 4–6 doses or continuously </span><span style="font-size: large;">or </span></div>
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<span style="font-size: large;">Amoxicilline </span><span style="font-size: large;">100–200 mg/kg/day i.v. in 4–6 doses</span></div>
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<span style="font-size: large;">or Ceftriaxone </span><span style="font-size: large;">2 g/day i.v. or i.m. in one dose.</span></div>
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<span style="font-size: large;">Treatment duration is 4 weeks.</span></div>
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<span style="font-size: large;">Alternative treatment for 2 weeks : one of the above anibiotics + </span></div>
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<span style="font-size: large;">an aminoglycoside ( Gentamycin 3 mg/kg/day i.v. or i.m. in one dose, or Netilmycin 4–5 mg/kg/day i.v. in one dose).</span><br />
<span style="font-size: large;">For patients allergic to beta-lactam antibiotics (penicillines, cephalosporines) : Use for 4 weeks Vancomycin 30 mg/kg/day i.v. in 2 doses.</span></div>
<span style="font-size: large;">For strains relatively resistant to penicillin (MIC 0.250–2mg/l) : Penicillin G 24 million U/day i.v. either in 4–6 doses or continuously or Amoxicilline 200 mg/kg/day i.v. in 4–6 doses, or Ceftriaxone for 4 weeks + </span><br />
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<span style="font-size: large;">Gentamycin for 2 weeks (the last two antibiotics with dosages as above).</span><br />
<span style="font-size: large;">or in allergic patients </span>Vancomycin (4 weeks) + Gentamycin (2 weeks), dosages as above<br />
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<span style="font-size: large;"><u>Methicillin-sensitive staphylococcus (native valve</u> infection) treatment duration is for 4-6 weeks </span><span style="font-size: large;">: (Flu)cloxacillin or oxacillin 12 g/day i.v. in 4–6 doses</span></div>
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<span style="font-size: large;"> If the patient is</span><span style="font-size: large;"> </span><span style="font-size: large;">allergic to p</span><span style="font-size: large;">enicillin,</span> <span style="font-size: large;">or for methicillin-resistant staphylococci (native valves) treatment is for 4-6 weeks with: Vancomycin 30–60 mg/kg/day i.v. in 2–3 doses/ or Daptomycin 10 mg/kg/day i.v. once daily.</span></div>
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<span style="background-color: white;"><u><span style="font-size: large;">For staphylococcus (</span><span style="font-size: large;">Methicillin-susceptible) </span></u></span><span style="font-size: large;"><span style="background-color: white;"><u>endocarditis of prosthetic valves </u></span>(Flu)cloxacillin or Oxacillin </span><span style="font-size: large;">(for ≥ 6 weeks) +</span><span style="font-size: large;"> Rifampine </span><span style="font-size: large;">(for ≥ 6 weeks)</span> <b>900–1200 mg i.v. or orally in 2 - 3 divided doses </b> <span style="font-size: large;">+ </span><span style="font-size: large;">Gentamycin (for 2 weeks).</span><br />
<u><span style="font-size: large;">For staphylococcus (</span><span style="font-size: large;">Methicillin-resistant) </span><span style="font-size: large;">endocarditis of prosthetic </span></u><span style="font-size: large;"><u>valves, or allergy to penicillin,</u> instead of Flucloxacillin, or Oxacillin use </span><span style="font-size: large;">Vancomycin</span><span style="font-size: large;">, with the same other 2 drugs. Treatment duration is the same.</span><br />
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<span style="font-size: large;"><u>Enterococcus: </u> 4-6 weeks treatment with </span><span style="font-size: large;">Amoxicillin </span><b>200 mg/kg/day i.v. in 4–6 doses </b><span style="font-size: large;">+ Gentamycin for 2-6 weeks</span><br />
<span style="font-size: large;">Alternative treatment (in p</span><span style="font-size: large;">enicillin-allergic patient or resistant strain of enterococcus):</span><span style="font-size: large;">Vancomycin + Gentamycin, both for 6 weeks</span><span style="font-size: large;"> (Dosages as usual, see above).</span><span style="font-size: large;"> </span></div>
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<span style="font-size: large;"><br /></span> <span style="font-size: large;">(</span><span style="font-family: "verdana" , sans-serif;">Pediatric doses of antibiotics in IE: Penicillin G 200,000 U/kg/day i.v. in 4–6 divided doses, Amoxicillin 300 mg/kg/day i.v. in 4–6 divided doses ,</span><br />
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<span style="font-family: "verdana" , sans-serif;">Ceftriaxone 100 mg/kg/day i.v. or i.m. in one dose,</span></div>
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<span style="font-family: "verdana" , sans-serif;">Gentamycin 3 mg/kg/day i.v. or i.m. in 1 dose or 3 equally divided doses,</span></div>
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<span style="font-family: "verdana" , sans-serif;"> </span><span style="font-family: "verdana" , sans-serif;">Vancomycin 40 mg/kg/day i.v. in 2 or 3 equally divided doses,</span><br />
<span style="font-family: "verdana" , sans-serif;">Rifampin 20 mg/kg/day i.v. or orally in 3 equally divided doses</span><span style="font-size: large;">) </span><span style="font-size: large;"> </span><br />
<span style="font-size: large;"><br />Treatment for <u>HACEK group</u> microorganisms. These are slow growing fastidious gram negative bacilli. They are susceptible to ceftriaxone, other third-generation cephalosporins and quinolones. Standard treatment is ceftriaxone 2 g/day ( treatment duration in native valve enodcardis is 4 weeks and in prosthetic valve endocarditis is 6 weeks. <br /><br /><u> For Gram-negative bacteria that do not belong to the HACEK group</u> the recommended treatment is early surgery plus long-term (at least 6 weeks) therapy with bactericidal combinations of beta-lactams and aminoglycosides. A quinolone or cotrimoxazole may be added to the above treatment.</span></div>
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<span style="font-size: large;"><b>Cardiac device related endocarditis (CDRIE)</b> </span></h3>
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<span style="font-size: large;"><b>Cardiac device related endocarditis (CDRIE)</b> is a special and difficult problem (microbial infection of the leads of a pacemaker, or implanted defibrillator). Cardiac device (pacemaker, or implanted defibrillator) infection is generally classified in two categories: pocket infection and endocarditis. Patients may present with regional or systemic manifestations, which can include : </span><br />
<span style="font-size: large;">In cases of <u>pocket infection</u> : erythema (redness), pain, local warmth, purulent discharge, or erosion of the skin.</span><br />
<span style="font-size: large;">In cases of <u>endocarditis</u>: fever is the most common symptom, fatigue, malaise, loss of appetite are common, and local signs of pocket infection may be present. A septic pulmonary embolus may occur.</span><br />
<div class="t m0 xd h8 y43 ff6 fs5 fc4 sc0 ls42 ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 927.904px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.602845px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">with</span><span class="_ _18 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 40.2284px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">PM</span><span class="_ _7 current-selection" style="box-sizing: content-box; color: transparent; display: inline; margin-left: -2.22224px; position: relative;"></span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">/ICD</span><span class="_ _22 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 41.4023px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">infections</span><span class="_ _1b current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 35.9209px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">may</span><span class="_ _18 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 40.2284px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">present</span><span class="_ _18 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 40.2284px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">with</span><span class="_ _18 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 40.2284px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">regional</span><span class="_ _26 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 37.005px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">or</span></div>
<div class="t m0 xd h8 y44 ff6 fs5 fc4 sc0 ls40 ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 881.821px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.523901px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">systemic</span><span class="_ _27 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 43.2541px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">symptom</span><span class="_ _5 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 1.29097px;"></span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">s.</span><span class="_ _18 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 40.2284px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">Eryt</span><span class="_ _5 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 1.29097px;"></span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">hema,</span><span class="_ _22 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 41.4023px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">pain,</span><span class="_ _27 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 43.2541px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">erosion,</span><span class="_ _27 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 43.2541px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">redness,</span></div>
<div class="t m0 xd h8 y45 ff6 fs5 fc4 sc0 ls30 ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 836.7px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.509547px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">increased</span><span class="_ _11 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 15.4321px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">warmt</span><span class="_ _5 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 1.29097px;"></span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">h, purulent</span><span class="_ _11 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 15.4321px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">drainage,</span><span class="_ _11 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 15.4321px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">and</span><span class="_ _10 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 19.8928px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">cellulitis are fre-</span></div>
<div class="t m0 xd h8 y46 ff6 fs5 fc4 sc0 ls2f ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 790.619px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.559784px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">quent</span><span class="_ _a current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 9.07112px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">regional</span><span class="_ _13 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 10.4232px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">findings</span><span class="_ _a current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 9.07112px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">in</span><span class="_ _e current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 14.3041px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">pocket</span><span class="_ _a current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 9.07112px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">infections.</span><span class="_ _20 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 7.66804px;"></span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">In</span><span class="_ _e current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 14.3041px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">endocarditi</span><span class="_ _7 current-selection" style="box-sizing: content-box; color: transparent; display: inline; margin-left: -2.22224px; position: relative;"></span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">s,</span></div>
<div class="t m0 xd h8 y47 ff6 fs5 fc4 sc0 ls2f ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 744.538px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.559784px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">fever and</span><span class="_ _17 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 20.9716px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">rash</span><span class="_ _10 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 19.8928px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">are</span><span class="_ _17 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 20.9716px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">present in</span><span class="_ _10 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 19.8928px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">addition to</span><span class="_ _10 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 19.8928px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">regional findings.</span></div>
<div class="t m0 xd h8 y48 ff6 fs5 fc4 sc0 ls2f ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 699.419px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.559784px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">Positive</span><span class="_ _8 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 12.7497px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">surface</span><span class="_ _e current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 14.3041px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">and</span><span class="_ _11 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 15.4321px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">blood</span><span class="_ _11 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 15.4321px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">cultures</span><span class="_ _13 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 10.4232px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">suggest</span><span class="_ _e current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 14.3041px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">the</span><span class="_ _11 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 15.4321px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">presence</span><span class="_ _e current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 14.3041px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">of</span></div>
<div class="t m0 xd h8 y49 ff6 fs5 fc4 sc0 ls34 ws0" style="-webkit-text-stroke-width: 0.012em !important; background-color: white; bottom: 653.336px; box-sizing: content-box !important; color: #231f20; font-family: ff6; font-size: 71.7672px; height: 55.0454px; left: 1203.83px; letter-spacing: 0.581314px; line-height: 0.954; padding-right: 32px; padding-top: 32px; position: absolute; text-shadow: none !important; transform-origin: 0% 100% 0px; transform: matrix(0.5, 0, 0, 0.5, 0, 0); unicode-bidi: bidi-override; visibility: visible; white-space: pre;">
<span class="current-selection" style="box-sizing: content-box !important; position: relative;">a</span><span class="_ _17 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 20.9716px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">device</span><span class="_ _9 current-selection" style="box-sizing: content-box; color: transparent; display: inline-block; position: relative; width: 16.5796px;"> </span><span class="current-selection" style="box-sizing: content-box !important; position: relative;">infection. </span></div>
<span style="font-size: large;">Three or more sets of blood cultures are recommended before prompt initiation of antimicrobial therapy and a transesophageal echocardiogram (TEE) must be performed in patients with suspected CDRIE with positive or negative blood cultures, to assess for the presence of lead-related endocarditis and heart valve infection. TEE may show electrode or valvular vegetations.</span><br />
<span style="font-size: large;">In the majority of patients, </span><span style="font-size: large;">CDRIE</span><span style="font-size: large;"> must be treated by complete hardware (device and leads) removal and prolonged antibiotic therapy (i.e. before and after hardware removal). The same treatment is also recommended in presumably isolated pacemaker or defibrillator pocket infection (i.e infection at the site, where the battery of the device has been implanted).</span><span style="font-size: large;">Before reimplantation of the device a re-evaluation of the indication for implantation is necessary, because in some cases, reimplantation is not necessary. The new device should be implanted on the contralateral side. Immediate reimplantation should be avoided, because there is a significant risk of new infection. Blood cultures should be negative for at least 72 hours before placement of a new device. The decision on the timing of reimplantation needs a consideration of several factors such as persistent bacteremia, persistent vegetation and how dependent is the patient from the pacemaker or the implantable cardioverter defibrillator. When there is evidence of remnant valvular infection, implantation should be delayed for at least 14 days. Temporary pacing should be avoided if possible, because it is a risk factor for subsequent cardiac device infection. In a pacing-dependent patient, temporary use of active fixation leads connected to an external device can be a "bridging strategy", until the placement of a new permanent device is considered safe.</span></div>
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<span style="color: #38761d; font-size: large;"><b style="background-color: #f1c232;">Bibliography and Links :</b></span><br />
<span style="color: #38761d; font-family: "trebuchet ms" , sans-serif; font-size: large;"><b style="background-color: #f1c232;"><br /></b></span> <b><span style="background-color: white; color: #cc0000; font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;">I recommend this video (by 123sonography) showing echocardiography in native valve endocarditis Link:</span></b><br />
<span style="color: #38761d; font-size: medium;"><span style="background-color: #f1c232;"><a href="https://www.youtube.com/watch?v=H8z-2EvsxuY" style="background-color: white;" target="_blank"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Echo in Endocarditis-Prof. Thomas Binder</b></span></a></span></span></div>
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<span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/early/2015/08/28/eurheartj.ehv319" target="_blank">2015 ESC Guidelines for the management of infective endocarditis</a></span></h2>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b> Hoen B, Duval X. Infective endocarditis. N Engl J Med 2013; 368:1425–1433</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Baddour LM, Wilson WR, et al: Infective endocarditis: diagnosis, antimicrobial therapy and management of complications. Circulation</b></span><b style="font-family: Arial, Helvetica, sans-serif;"> 2005</b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>;111: e394–e434</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Li JS, Sexton DJ, et al: Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis, Clin Infect Dis 2000;30:633–638</b></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-843439026378412162016-12-18T22:43:00.004+02:002021-12-12T18:48:54.818+02:00The Cardiomyopathies<div dir="ltr" style="text-align: left;" trbidi="on">
<h2>
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</script> <span style="font-size: large;">The Cardiomyopathies</span></h2>
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<span style="font-size: large;"><b>Definition: Cardiomyopathy</b> is a disease of the heart muscle (myocardium) causing structural and functional abnormalities, which does not result from coronary artery disease, hypertension, valvular disease, or congenital heart disease.</span><br />
<span style="font-size: large;">The term "ischemic cardiomyopathy" continues to be in use for left ventricular systolic dysfunction caused by myocardial scar and left ventricular remodeling after myocardial infarction, although according to this definition it is not exactly a cardiomyopathy, but a secondary myocardial disease.</span><br />
<span style="font-size: large;">Most (but not all) cardiomyopathies are familial. Thus family screening is often mandatory to identify people with undiagnosed or subclinical disease. In familial cardiomyopathies, the inheritance is most often autosomal dominant and less often X- linked recessive, or autosomal recessive.</span><br />
<span style="font-size: large;">Cardiomyopathies are a heterogeneous group of diseases. Recently the MOGES classification system has been adopted, which describes the morphological and functional (morphofunctional) phenotype (M), organ involvement (O), genetic inheritance pattern (G), etiology (E), functional status (S).</span><br />
<span style="font-size: large;">Another classification of cardiomyopathies includes <b>primary cardiomyopathies</b> characterized by disease involving predominantly the myocardium and <b>secondary cardiomyopathies</b>, i.e. myocardial disease associated with a known specific etiology.</span><br />
<span style="font-size: large;"><b>Primary cardiomyopathies include: </b></span><br />
<span style="font-size: large;"><b>Cardiomyopathies of genetic etiology</b></span><br />
<span style="font-size: large;">Hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, myocardial noncompaction, glycogen storage disease (such as Danon's disease), mitochondrial myopathies and genetic ion channel disorders (channelopathies such as Brugada syndrome, congenital long QT syndrome, congenital short QT syndrome, catecholaminergic polymorphic ventricular tachycardia).</span><br />
<span style="font-size: large;"><b>Cardiomyopathies of mixed (genetic or acquired) etiology:</b></span><br />
<span style="font-size: large;"> This category includes dilated cardiomyopathy and restrictive cardiomyopathy</span><br />
<span style="font-size: large;"><b>Acquired cardiomyopathies</b> such as:</span><br />
<span style="font-size: large;"> inflammatory cardiomyopathy (caused by myocarditis), alcoholic cardiomyopathy, peripartum cardiomyopathy, tachycardiomyopathy (cardiomyopathy due to a persistent tachyarrhythmia), stress-induced cardiomyopathy also known as Tako-tsubo cardiomyopathy, cardiac sarcoidosis.</span><span style="font-size: large;"><br /><b><br /></b></span><br />
<span style="font-size: large;"><b>Hypertrophic cardiomyopathy (HCM) </b><br />It is the most common inherited cardiac disorder with a prevalence in the general population of approximately 1 per 500. </span><br />
<span style="font-size: large;">There is hypertrophy of left (usually), right, or both ventricles<br />with </span><span style="font-size: large;">preserved</span><span style="font-size: large;"> </span><span style="font-size: large;">or </span><span style="font-size: large;">reduced contractile function. </span><span style="font-size: large;">Hypertrophy (increased cardiac muscle thickness) is inappropriate (is not expected as a result of an etiologic condition, such as hypertension, aortic stenosis, etc) may be generalized or regional and it </span><span style="font-size: large;">almost always presents by the age of 30 years. </span><span style="font-size: large;">Histologically HCM is characterized by left ventricular </span><span style="font-size: large;">hypertrophy with malalignment of the myocardial fibers (myofibril disarray) and myocardial fibrosis. The hypertrophy may be </span><span style="font-size: large;">generalized or confined largely to the interventricular </span><span style="font-size: large;">septum (asymmetric septal hypertrophy) or other regions (e.g. apical hypertrophic cardiomyopathy).</span><br />
<span style="font-size: large;"><b>Causes of HCM</b></span><br />
<span style="font-size: large;">HCM is a </span><span style="font-size: large;">genetic disorder,</span><span style="font-size: large;"> caused by mutations of genes encoding proteins involved in the contractile apparatus of the myocardial cells. The most common mutation involves</span><span style="font-size: large;"> beta-myosin heavy chains. There are also other mutations involving </span><span style="font-size: large;">troponin T, tropomyosin, and other proteins. The mode of genetic </span><span style="font-size: large;">transmission is</span><span style="font-size: large;"> </span><span style="font-size: large;">usually autosomal dominant, with a high </span><span style="font-size: large;">degree of penetrance and variable expression.</span><br />
<span style="font-size: large;"><b>Clinical presentation</b>: most patients with HCM are asymptomatic, but some present with </span><span style="font-size: large;">dyspnea, effort angina palpitations (due to arrhythmias), syncope, or sudden </span><span style="font-size: large;">death. In summary, h</span><span style="font-size: large;">ypertrophic cardiomyopathy (HCM) can be asymptomatic or it c</span><span style="font-size: large;">an result in heart failure with preserved ejection fraction (EF), in sudden cardiac death, or rarely </span><span style="font-size: large;">in heart failure with reduced </span><span style="font-size: large;">EF.</span><br />
<span style="font-size: large;"> H</span><span style="font-size: large;">eart failure with preserved ejection fraction (EF), usually manifested by effort dyspnea (breathlessness during physical activity) can occur in HCM because myocardial hypertrophy can produce a stiff ventricle with reduced compliance. This results in an elevation of the diastolic filling pressure. </span><br />
<span style="font-size: large;">Angina, when present, in HCM usually results from increased myocardial oxygen demand due to the hypertrophy.</span><br />
<span style="font-size: large;">In hypertrophic obstructive cardiomyopathy (HOCM), a form of HCM characterized by the presence of </span><span style="font-size: large;">dynamic left ventricular </span><span style="font-size: large;">outflow tract (LVOT) obstruction, the systolic pressure gradient in the LVOT contributes to the development of symptoms. In HOCM the</span><span style="font-size: large;"> dynamic LVOT </span><span style="font-size: large;">obstruction is caused by the hypertrophy of the interventricular septum and the</span><span style="font-size: large;"> </span><span style="font-size: large;">abnormal systolic anterior motion (SAM) of the mitral </span><span style="font-size: large;">valve. SAM can also cause </span><span style="font-size: large;">mitral regurgitation.</span><br />
<span style="font-size: large;"><b>Physical examination in HCM</b> can be normal or reveal only a fourth (presystolic) heart sound S4 when there is no LVOT obstruction. The S4 is caused by LV diastolic dysfunction resulting in a forceful left atrial contraction against a stiff ventricle. The apical impulse is often forceful and diffuse. A double impulse can be present because of a presystolic impulse due to the forceful atrial contraction as a consequence of the reduced LV compliance.</span><br />
<span style="font-size: large;"><u>In hypertrophic obstructive cardiomyopathy (HOCM) </u>:</span><br />
<span style="font-size: large;"> >The carotid pulse typically rises sharply and then falls sharply in mid systole (because of the LVOT obstruction in mid systole) followed by a second rise</span><br />
<span style="font-size: large;">> There is a midsystolic crescendo-decrescendo murmur best heard at the left sternal border and at the area between the apex and the left sternal border. This murmur of dynamic LVOT obstruction is accentuated by maneuvers that decrease preload (abruptly standing up, which reduces venous return to the heart) or decrease afterload (vasodilation by administering sublingual nitrate) and does not radiate to the neck. These features help distinguish the murmur of HOCM from the murmur of valvular aortic stenosis (also see the chapter on aortic stenosis).</span><br />
<span style="font-size: large;">> A pansystolic murmur is often heard at the apex due to mitral regurgitation.</span><br />
<span style="font-size: large;">The <b>ECG</b> is abnormal in the majority of patients with hypertrophic cardiomyopathy (HCM). The commonest abnormalities are ST and T wave abnormalities followed by signs of left ventricular hypertrophy ( Tall R waves especially in mid-precordial leads and also in left precordial leads). Prominent Q waves may be present in the inferior and/or precordial leads, caused by septal hypertrophy. Giant negative T waves in the precordial leads occur in apical HCM. </span><br />
<span style="font-size: large;">The <b>chest X-ray</b> may demonstrate a normal heart size or cardiac enlargement due to LV hypertrophy and left atrial dilatation. </span><br />
<span style="font-size: large;">Echocardiography in HCM </span><br />
<span style="font-size: large;">There are <u>some characteristic features</u> that strongly indicate HCM:</span><br />
<span style="font-size: large;">1) Hypertrophy of any segment of the LV with wall thickness > 1,5 cm.</span><br />
<span style="font-size: large;">2) Asymmetric septal hypertrophy (the interventricular septum is much thicker than other segments of LV wall) with a ratio of wall thickness septum/posterior wall > 1.3 in normotensive and > 1.5 in hypertensive individuals. This is the commonest form of HCM.</span><br />
<span style="font-size: large;">3) In HOCM (a common type of HCM): Asymmetric hypertrophy of the interventricular septum with SAM of the anterior mitral leaflet, increased velocity of flow in the left ventricular outflow tract (LVOT) and a systolic pressure gradient in the LVOT. The latter two findings are evidence of LV dynamic obstruction. Obstruction is dynamic, meaning that it changes at different times at the same patient and especially with changes in preload, afterload or contractility. Some patients have an obstruction at rest, whereas others only during exercise. Obstruction is present when the peak intraventricular systolic gradient is </span><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 14pt;">≥ </span><span style="font-size: large;">30 mmHg. Severe obstruction is present when the peak gradient is > 50 mmHg. Mitral regurgitation is often present. </span><br />
<span style="font-size: large;">4) Concentric hypertrophy of the LV without any identifiable cause, especially with a wall thickness </span><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 14pt;">≥ </span><span style="font-size: large;">1.5 cm.</span><br />
<span style="font-size: large;">5) Apical hypertrophy of the LV (this is a rare form of HCM, about 1 % of cases)</span><br />
<span style="font-size: large;">6) Mid-ventricular hypertrophy of the LV with signs of systolic obstruction at the level of the papillary muscles (such signs are a turbulent high-velocity systolic flow at the midventricular level, demonstrated with color flow doppler and a systolic intraventricular gradient at this level, demonstrated with pulse wave spectral doppler.) The LV apex is usually aneurysmatic. This is a rare form of HCM.</span><br />
<span style="font-size: large;">7) In some cases of HCM hypertrophy of the right ventricle (RV) can also be present (RV wall thickness > 5 mm).</span><br />
<b style="font-size: x-large;">Differential diagnosis</b><span style="font-size: large;"> of HCM includes other causes of increased ventricular wall thickness: e.g. hypertensive heart disease, aortic stenosis, infiltrative and storage diseases (amyloidosis, Fabry disease).</span><br />
<span style="font-size: large;"><b>Treatment of HCM</b><br />In patients without an LVOT gradient pharmacologic therapy is administered if there are symptoms (dyspnea or chest pain): Beta-blockers (starting at a dose equivalent to propranolol 80-120 mg/day and titrated to achieve a heart rate of 50-70 beats per minute at rest ) or alternatively nondihydropyridine calcium antagonists (verapamil starting at a dose of 120 mg/day, or diltiazem starting at a dose of 180 mg/day).</span><br />
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<span style="font-size: large;">In patients with HOCM who have symptoms, treatment to reduce the LVOT gradient is indicated. Such treatment includes</span></div>
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<span style="font-size: large;">beta-blockers, usually in high doses. If this fails, combined treatment with a beta-blocker (in a small to moderate dose) plus disopyramide (an antiarrhythmic drug with potent negative inotropic properties) is an option. Disopyramide is usually given at a dose of 400-600 mg/day and can often cause side effects due to its anticholinergic action (dry mouth and eyes, urinary retention).</span></div>
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<span style="font-size: large;">Surgical myectomy, alcohol septal ablation or DDD pacing are treatment options (that act by reducing the LVOT gradient) selected in cases of HOCM with symptoms refractory to medical therapy, or who cannot tolerate medical therapy and a significant LVOT pressure gradient (i.e. a pressure gradient > 50 mmHg in the LVOT, in LV systole). DDD pacing generally is less effective than the other two treatments (surgery, or septal ablation). Both s</span><span style="font-size: large;">urgical myectomy and alcohol septal ablation</span><span style="font-size: large;"> are effective </span><span style="font-size: large;">procedures, </span><span style="font-size: large;">associated with low rates of complications </span><span style="font-size: large;">and high success rates when performed in centers with experience. There is a debate </span><span style="font-size: large;">regarding which procedure is best. Two basic concerns </span><span style="font-size: large;">with percutaneous septal </span><span style="font-size: large;">ablation </span><span style="font-size: large;">are the following:</span><span style="font-size: large;"> There is a potential for the creation of an </span><span style="font-size: large;">arrhythmogenic focus (since the procedure causes a myocardial infarct at the proximal interventricular septum) and there is also</span><span style="font-size: large;"> an increased risk of complete </span><span style="font-size: large;">heart block, as a procedural complication.</span><br />
<span style="font-size: large;">In summary, in HCM either with or without intraventricular obstruction, treatment is needed in patients who have symptoms and not in asymptomatic people. Evaluation of risk factors for sudden cardiac death is needed in all patients. </span><br />
<b style="font-size: x-large;"><br /></b> <b style="font-size: x-large;">Important: Risk factors for sudden death in HCM</b><span style="font-size: large;"> are as follows:</span><br />
<span style="font-size: large;">The most powerful, but also very obvious, risk factor is a personal history of resuscitated cardiac arrest, or sustained ventricular tachycardia. This is an indication for an implantable defibrillator (ICD). </span><br />
<span style="font-size: large;">Massive left ventricular hypertrophy (>30 mm on echocardiography)</span><br />
<span style="font-size: large;">Family history of sudden cardiac death (that has occured before the age of 50 in one or more first-degree relatives with or without a diagnosis of HCM, or sudden death in one or more first-degree relatives </span><span style="font-size: large;">irrespective of age, </span><span style="font-size: large;">with an established diagnosis of HCM).</span><br />
<span style="font-size: large;">Non-sustained ventricular tachycardia on 24-hour Holter monitoring</span><br />
<span style="font-size: large;">Prior unexplained syncope</span><br />
<span style="font-size: large;">Abnormal blood pressure (BP) response on exercise (failure of BP to rise, or a fall in BP with exercise).</span><span style="font-size: large;"></span><br />
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<span style="font-size: large;"> ICD insertion should be seriously considered in patients with 2 or more of these risk factors. When </span><span style="font-size: large;">the risk is less, amiodarone is an appropriate alternative.</span><br />
<span style="background-color: #fff2cc; color: #38761d; font-size: large;"><br /></span> <span face=""arial" , "helvetica" , sans-serif" style="color: #38761d; font-size: medium;"><b style="background-color: #fff2cc;">A VIDEO : Hypertrophic Cardiomyopathy: The ECG, echocardiography and treatment</b></span><br />
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</script> <span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"> <b>Dilated cardiomyopathy (DCM)</b>:</span><br />
<span style="font-size: large;">There is impaired systolic function and dilatation of one or both ventricles. It more often affects the left ventricle and then it is characterized by left ventricular dilatation associated with decreased contractile function (left ventricular EF <45%) in the absence of coronary artery disease sufficient to cause global systolic dysfunction and in the absence of abnormal ventricular loading conditions (hypertension, valvular heart disease, congenital heart disease). DCM can result in heart failure with reduced ejection fraction (EF). Right ventricular dilation and dysfunction may also </span><span style="font-size: large;">be present but are not necessary for the diagnosis.</span><br />
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<b style="font-size: x-large;">Causes of DCM </b></div>
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<span style="font-size: large;"> The most common causes are idiopathic and inherited (familial DCM, due to genetic defects).</span></div>
<span style="font-size: large;">Idiopathic DCM includes cases with no clearly identified cause </span><span style="font-size: large;">and is considered to result from an interplay of unclear familial, immune-mediated, toxic, or infectious mechanisms that ultimately result in myocardial systolic dysfunction. Some cases are due to a previous episode of subclinical viral myocarditis. Viral components present in the myocardial tissue may serve as antigens that can direct the immune system to attack the myocardium.</span><br />
<span style="font-size: large;">An abnormality of immune regulation may play a role in DCM, as suggested by the association of DCM with some HLA antigens (HLA DR4).</span><br />
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<span style="font-size: large;">Familial DCM accounts for about 30-50 % of cases and is due to mutations of genes that result in myocardial dysfunction and reduced contractile force. Most cases of familial DCM demonstrate an autosomal dominant mode of inheritance, although autosomal recessive and X-linked forms also exist. They are the result of mutations of genes encoding cytoskeletal, contractile or nuclear membrane proteins (dystrophin, desmin, actin, troponin, a-tropomyosin, beta-myosin heavy chain, lamin, vinculin). </span><br />
<span style="font-size: large;">Some n</span><span style="font-size: large;">euromuscular diseases of genetic origin also cause DCM (Duchenne muscular dystrophy).</span><span style="font-size: large;"><br /></span><br />
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<span style="font-size: large;">Other causes of DCM are due to myocardial inflammation and cell damage via infective, immunologic or toxic mechanisms.</span></div>
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<span style="font-size: large;">Such causes are:</span></div>
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<span style="font-size: large;"> Infections (viral myocarditis, Chagas disease)<br />Drugs and toxins (</span><span style="font-size: large;">Alcohol, </span><span style="font-size: large;">cocaine, </span><span style="font-size: large;">doxorubicin, cyclophosphamide,)</span></div>
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<span style="font-size: large;">Peripartum cardiomyopathy</span></div>
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<span style="font-size: large;">Systemic vasculitis (systemic lupus erythematosus)</span></div>
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<span style="font-size: large;">Other causes of DCM include various systemic diseases such as u</span><span style="font-size: large;">remia, t</span><span style="font-size: large;">hyroid disease, p</span><span style="font-size: large;">heochromocytoma, g</span><span style="font-size: large;">lycogen storage disease.</span></div>
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<span style="font-size: large;">Whereas coronary artery disease (CAD) is the most common cause of left ventricular (LV) systolic dysfunction and dilatation, this condition (often called ischemic cardiomyopathy) is not classified as dilated cardiomyopathy.</span></div>
<span style="font-size: large;"><b>Clinical presentation of DCM</b> </span></div>
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<span style="font-size: large;">DCM usually presents with signs and symptoms of congestive heart failure. Thus the major presenting symptoms are effort dyspnea or paroxysmal nocturnal dyspnea, fatigue and effort intolerance and edema. Other presentations include systemic emboli (from LV wall thrombus), syncope, </span><span style="font-size: large;">angina, cardiac arrhythmias, conduction defects </span><span style="font-size: large;">or sudden death (from ventricular arrhythmias). </span><span style="font-size: large;">Chest pain, including typical angina, may be </span><span style="font-size: large;">present in some patients with DCM (even though it is not considered one of the main symptoms) and should not be used as a proof of coronary artery disease as the etiology of myocardial systolic dysfunction.</span><span style="font-size: large;"> It may indicate a more limited coronary vascular reserve in these patients, despite normal epicardial coronary arteries.</span></div>
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<span style="font-size: large;"><b>Physical examination in DCM</b> can show:</span><br />
<span style="font-size: large;">An apical impulse which is laterally displaced, because of left ventricular (LV) enlargement.</span><br />
<span style="font-size: large;"> A narrow pulse pressure (this is a sign of a diminished stroke volume)</span><br />
<span style="font-size: large;">Pulsus alternans (in cases of severe LV dysfunction).</span><br />
<span style="font-size: large;">In auscultation a fourth (presystolic) heart sound (S4) is common and in case of decompensated heart failure, there is often a third (early diastolic) heart sound -S3. Systolic murmurs of mitral or tricuspid regurgitation are also common because dilated cardiomyopathy (DCM) is often associated with functional atrioventricular valve regurgitation.</span><br />
<span style="font-size: large;"><b>The ECG</b> in DCM often shows poor R wave progression (or even Q waves) in the precordial leads, because of myocardial fibrosis and P wave morphology indicative of left atrial dilatation. </span><span style="font-size: large;">ST and T wave abnormalities frequently occur.</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 11pt; line-height: 107%;"> </span></b> Another common finding is an intraventricular conduction defect (for example a LBBB) causing an increased QRS duration. Atrial or ventricular arrhythmias are also common. </span><br />
<span style="font-size: large;">The <b>chest X-ray</b> usually demonstrates a generalized enlargement of the cardiac silhouette due to the dilatation of the cardiac chambers (cardiomegaly= enlargement of the heart).</span><br />
<span style="font-size: large;"><b>Echocardiography</b> is valuable for the diagnosis since it can assess ventricular size and function. Usually, in DCM there is a diffuse reduction of LV contractility (hypokinesis) with LV dilation (often the best contracting LV segment is the basal posterior and /or the basal lateral). In ischemic cardiomyopathy, diffuse hypokinesis and LV dilatation can also be present, but there is akinesis and reduced thickness of the infarcted segments. This is a useful distinguishing feature between these two entities. </span><br />
<span style="font-size: large;">In some cases of mild DCM, or at an early stage of the disease echocardiography can show a mild diffuse hypokinesis of the left ventricle (LV) without LV dilatation and with an ejection fraction (EF) being at the lower normal limits or mildly abnormal.</span><br />
<span style="font-size: large;">Ventricular size and function can also be assessed </span><span style="font-size: large;">very accurately </span><span style="font-size: large;">with magnetic resonance imaging (MRI).</span><br />
<span style="font-size: large;"><b>Cardiac catheterization</b> and coronary angiography is often necessary to exclude coronary artery disease as the cause of LV dysfunction. Usual hemodynamic findings in cardiac catheterization include an elevated left ventricular end-diastolic pressure and pulmonary capillary wedge pressure and often modest pulmonary hypertension. Left ventriculography demonstrates diffuse contractile dysfunction of a dilated LV.</span><br />
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<span style="font-size: large;"><b>Treatment of DCM</b></span><br />
<span style="font-size: large;">Standard treatment for heart failure with reduced EF (systolic heart failure) which usually includes an ACE inhibitor, a beta-blocker, a diuretic (usually furosemide) and an aldosterone antagonist (MRA=mineralocorticoid receptor antagonist). Digoxin can be added if there is atrial fibrillation with a relatively rapid ventricular response, or in patients with sinus rhythm but persistent symptoms of heart failure despite the above standard treatment.</span><br />
<span style="font-size: large;">Regular exercise (as tolerated) is beneficial. </span><br />
<span style="font-size: large;">Cardiac resynchronization or an ICD (implantable cardioverter-defibrillator) may be needed in patients with an indication (see the chapter on heart failure for the indications).</span><br />
<span style="font-size: large;">For patients with end-stage heart failure, treatment options include ventricular assist devices and heart transplantation.</span><br />
<span style="font-size: large;"><b>Video</b></span><br />
<span style="font-size: large;"><b>A case of DCM (left parasternal long-axis view)</b></span><br />
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<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Restrictive cardiomyopathy (RCM)</b></span><br />
<span style="font-size: large;">Restrictive cardiomyopathy (RCM)</span><span style="font-size: large;"> is a rare type of cardiac muscle disease, in which symptoms and signs of congestive heart failure occur in a patient with normal or decreased volume of both ventricles and </span><span style="font-size: large;">bi-atrial enlargement (dilatation of both atria). The ventricles have a normal or near-normal systolic function as assessed visually with 2-dimensional imaging or with the ejection fraction, despite the manifestations of heart failure. (More sensitive echocardiographic techniques such as tissue doppler or myocardial strain and strain rate show an impairment of the systolic function, that is not apparent on visual estimation with 2-dimensional imaging or M-mode measurements). V</span><span style="font-size: large;">entricular wall thickness can be </span><span style="font-size: large;">normal or increased (depending on the etiology) and cardiac valves have no significant dysfunction.</span><br />
<span style="font-size: large;"> It should be emphasized that the predominant abnormality in these patients is a severely impaired ventricular </span><span style="font-size: large;">filling with restrictive physiology, which </span><span style="font-size: large;">produces symptoms and signs of heart failure.</span><br />
<span style="font-size: large;">The restrictive physiology is caused by severely reduced compliance (elasticity) of the ventricular walls and can be demonstrated by Doppler echocardiography, or cardiac catheterization.</span><br />
<span style="font-size: large;"><b>Causes of RCM</b></span><br />
<span style="font-size: large;">The most common cause is amyloidosis.</span><br />
<span style="font-size: large;">Other causes: Sarcoidosis, hemochromatosis, Loeffler's endocarditis, </span><span style="font-size: large;">endomyocardial fibrosis, </span><span style="font-size: large;">radiation,</span><span style="font-size: large;"> metastatic cancer, diabetic cardiomyopathy, systemic scleroderma, </span><span style="font-size: large;">idiopathic restrictive cardiomyopathy (it can </span><span style="font-size: large;">be familial). </span><br />
<span style="font-size: large;">In Loeffler's endocarditis and endomyocardial fibrosis, there is myocardial and endocardial fibrosis apparent in imaging tests (echocardiography or magnetic resonance imaging) and blood tests (complete blood count-CBC) show eosinophilia.</span><span style="font-size: large;"></span><br />
<span style="font-size: large;"><b>Investigations in RCM</b></span><br />
<span style="font-size: large;"> A <b>chest X-ray</b> may show pulmonary venous congestion. The cardiac silhouette can be normal </span><span style="font-size: large;">or mildly enlarged (because of atrial enlargement).</span><br />
<span style="font-family: inherit;"><span style="font-size: large;">The <b>ECG </b>may show low QRS voltage</span><span style="font-size: large;"> and nonspecific ST-segment and T-wave abnormalities.</span><span style="font-size: large;"></span></span><br />
<span style="font-family: inherit;"><span style="font-size: large;"><b> Echocardiogram</b> </span></span><span style="font-family: inherit; font-size: large;">demonstrates a normal or near-normal ejection fraction (EF), dilatation of both atria and impaired ventricular filling.<br /><u>The severely impaired ventricular filling (restrictive physiology) is characterized by the following findings</u> :<br />Significant dilatation of the atria<br />Mitral inflow pattern (obtained with the pulse wave doppler at the tips of the mitral valve) with <br />E wave peak velocity/ A wave peak velocity >1.5 <br />(E wave is the early diastolic velocity of the blood moving through the mitral valve and A wave is an end-diastolic velocity at the time of atrial contraction-absent in atrial fibrillation). The deceleration time (DT) of the E wave (the time from peak velocity of blood flow to zero velocity) is reduced: DT ≤ 150 msec.<br />( Isovolumic relaxation time is also reduced: IVRT < 60 msec).<br />Pulse wave Doppler examination of blood flow in a pulmonary vein (performed in the apical 4 chamber view) will show a marked predominance of the D wave (of early diastolic flow through the pulmonary veins) over the S wave (of systolic flow) with<br />peak S velocity/peak D velocity <0.5 The S and D waves are both positive waves (over the baseline) because they represent flow with direction into the left atrium and towards the transducer (which is at the apex of the heart). The peak velocity of the AR wave (a negative wave of reverse flow from the atrium into the pulmonary vein at end-diastole during atrial systole, in sinus rhythm) is elevated </span><span style="font-family: inherit; font-size: large;">(> 35 cm/s). </span><br />
<span style="font-family: inherit; font-size: large;">Tissue Doppler measurements of the velocity at the mitral annulus demonstrate reduced early diastolic peak velocity (E'): E'< 8 cm/s and E/E' > 15 (this indicates an elevated LV end-diastolic pressure). In this ratio E=the peak velocity of early diastolic blood flow through the mitral valve and E'=the peak early diastolic velocity of the mitral annulus. The first is measured with pulse wave flow doppler through the tips of the mitral valve (in the apical 4 chamber view) and the latter with the pulse wave tissue doppler at the mitral annulus.</span><br />
<span style="font-size: large;">In contrast, in constrictive pericarditis peak velocity E' of the septal mitral annulus > 8 cm/s. The differential diagnosis between restrictive cardiomyopathy and constrictive pericarditis is a classic problem because both conditions produce a clinical picture of heart failure caused by severe diastolic dysfunction. Another difference between these two entities is the following. In constrictive pericarditis, there is a marked respiratory variation (by more than 30%) of the peak E (early diastolic) blood flow velocity both in mitral and tricuspid flow, with mitral E velocity decreasing in inspiration and tricuspid E velocity increasing in inspiration. This is due to the phenomenon of the ventricular interdependence (for an explanation of this term see the chapter on constrictive pericarditis). This phenomenon of ventricular interdependence does not exist in restrictive cardiomyopathy (RCM), therefore in RCM the respiratory variation in the transmitral and transtricuspid flow is not augmented. In fact, in </span><span style="font-size: large;">RCM </span><span style="font-size: large;">respiratory variation in flow velocities through the atrioventricular valves is diminished or absent. </span><span style="font-size: large;"><br /><b>Cardiac catheterization in RCM</b> shows an elevation of filling pressures (diastolic pressures) in both ventricles, and a dip-and-plateau ventricular diastolic pressure tracing (a pattern like the symbol of a square root) is often seen. These are also features of constrictive pericarditis (CP). A difference is that in CP there is an equalization of diastolic pressures of both ventricles (the difference of end-diastolic pressure between the two ventricles is <5 mmHg in CP). On the contrary, in RCM this difference is usually > 5mmHg. Therefore, careful evaluation of simultaneously recorded LV and RV pressures helps in distinguishing between the two.</span><br />
<span style="font-size: large;"> A very useful parameter is the change in these simultaneously recorded ventricular pressures during respiration.<br />This pressure recording in CP demonstrates discordant changes in systolic pressures with respiration </span><span style="font-size: large;">(inspiratory increase in RV systolic pressure with a simultaneous </span><span style="font-size: large;">decrease in LV systolic pressure/ the opposite in expiration).</span><span style="font-size: large;"> In contrast, in RCM the change in the systolic pressure of the RV and the LV with respiration is concordant ( they increase or diminish concomitantly and their respiratory changes are small). </span><br />
<span style="font-family: inherit; font-size: large;"><b>Treatment of RCM</b><br />Diuretics are administered for heart failure symptoms, but cautiously (elevations in dosage must be cautious and gradual in order to relieve congestive symptoms, without reducing left ventricular filling pressures to the point of causing hypotension). Beta-blockers are commonly administered, especially if the heart rate is rapid but any reduction in heart rate should be moderate. These patients do not need a slow heart rate because diastolic filling occurs only at the beginning of diastole, so there is no point in increasing the duration of diastole. A slow heart rate in patients with RCM will usually decrease cardiac output and this results in worsening of symptoms. In patients with secondary restrictive cardiomyopathies, specific treatment of the underlying systemic disease is often indicated. In many cases, referral for transplant assessment should be considered early because severe pulmonary hypertension may develop.</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;">Video : A case of RCM due to cardiac amyloidosis </span><br />
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<span style="font-size: large;"><div style="font-family: inherit;"><span style="font-family: inherit; font-size: large;"><br /></span></div><div style="font-family: inherit;"><span style="font-family: inherit; font-size: large;"><br /></span></div><h4 style="text-align: left;"><span style="font-family: times; font-size: large;">Cardiac sarcoidosis </span></h4></span><span style="font-size: large;"><div><span style="font-size: large;"><br /></span></div>Sarcoidosis is a rare systemic (multisystem) inflammatory disease (age-adjusted incidence of 11 cases per 100,000 population in whites but 34 cases per 100,000 in African Americans. Sarcoidosis most commonly involves the lungs and intrathoracic lymph nodes but it may also involve other organs such as the skin, the liver, the eyes, and the heart (the heart is affected in about 5% of the cases). Its pathologic hallmark is the formation of noncaseating granulomas ( clusters of inflammatory cells without central necrosis).<br />Cardiac manifestations may include bundle branch block, atrioventricular block (which may manifest with syncope), ventricular arrhythmias/ and or sudden death, atrial arrhythmias, manifestations of heart failure due to diastolic or systolic dysfunction. Echocardiography may show akinesis and thinning, or aneurysm of the basal interventricular septum and/or the basal lateral, inferolateral (posterior) or inferior wall. Other common echocardiographic findings of cardiac sarcoidosis include left ventricular diastolic dysfunction (grade II or III), increased thickness of the right ventricular free wall ( > 5mm at end-diastole in the subcostal view), or increased thickness of the left ventricular wall, systolic dysfunction of either the left ventricle or the right ventricle with non-coronary distribution wall motion abnormalities and aneurysms, mitral regurgitation, or tricuspid regurgitation. Cardiac magnetic resonance imaging with late gadolinium enhancement provides important clues for the diagnosis.<br />The blood tests in sarcoidosis may show elevated levels of angiotensin converting enzyme, elevated calcium levels, and/ or elevated alkaline phosphatase ( ALP). The chest -X-ray often shows bilateral hilar adenopathy (enlarged hilar lymph nodes) and it may also show indications of interstitial pulmonary disease with a reticulonodular pattern.<br />The mainstay of medical therapy for cardiac sarcoidosis, as with other organ involvement, is immunosuppression, mostly in the form of corticosteroids. A number of different immunosuppressive agents may be used to avoid the side effects of chronic corticosteroid use.</span></div><div>
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<h4 style="text-align: left;"><span style="font-size: large;"><b>Arrhythmogenic right ventricular cardiomyopathy (AVRC)</b>. </span></h4></div>
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<span style="font-size: large;">It is also known as a</span><span style="font-size: large;">rrhythmogenic right ventricular dysplasia. </span><span style="font-size: large;">In this condition, </span><span style="font-size: large;">inherited as an autosomal dominant </span><span style="font-size: large;">trait, </span><span style="font-size: large;">patches of the right ventricular myo</span><span style="font-size: large;">cardium are replaced with fibrous and fatty tissue. Fibrofatty replacement can also occur in the left ventricle. It </span><span style="font-size: large;">has a prevalence of approximately 1 per </span><span style="font-size: large;">10000 to 1 per 5000 in the general adult population. The dominant clinical problems are ventricular </span><span style="font-size: large;">arrhythmias (ventricular tachycardia-VT, monomorphic with an LBBB pattern, or polymorphic VT), syncope, sudden death, and right-sided heart </span><span style="font-size: large;">failure. C</span><span style="font-size: large;">ommon presenting </span><span style="font-size: large;">symptoms are p</span><span style="font-size: large;">alpitations and syncope. Sudden cardiac death due to f</span><span style="font-size: large;">atal </span><span style="font-size: large;">ventricular arrhythmias is also a common first manifestation (in over 20% </span><span style="font-size: large;">of ARVC patients).</span><span style="font-size: large;"> Right ventricular or biventricular failure occurs in advanced stages of the disease, whereas sudden cardiac death can also occur at an early stage.</span><br />
<span style="font-size: large;">The <b>ECG </b>typically shows a slightly broadened </span><span style="font-size: large;">QRS complex often with incomplete or complete RBBB and inverted T waves in the right precor</span><span style="font-size: large;">dial leads (V1-V3, which are the leads related to the right ventricle).</span><span style="font-size: large;"> A</span><span style="font-size: large;">n </span><span style="font-size: large;">epsilon wave </span><span style="font-size: large;">can be present</span><span style="font-size: large;"> i.e. a</span><span style="font-size: large;"> terminal notch of the QRS (a small wave at the end of the QRS), </span><span style="font-size: large;">as a result of slowed intraventricular </span><span style="font-size: large;">conduction in an area of the right ventricle</span><span style="font-size: large;">. Often in arrhythmogenic cardiomyopathy, there is low QRS voltage and also right QRS axis deviation is present in many cases, although these findings are less common than T wave inversion. In some cases, the ECG can be normal. </span><span style="font-size: large;">Holter </span><span style="font-size: large;">monitoring may demonstrate frequent extrasystoles of right ventricular origin or runs of non-</span><span style="font-size: large;">sustained ventricular tachycardia.</span><br />
<span style="font-size: large;"> Echocardiography is frequently normal at an early stage, but in more advanced cases it often demonstrates right </span><span style="font-size: large;">ventricular dilatation and/or aneurysm of a segment of the RV wall. There may be left ventricular dilatation and dysfunction.</span><br />
<span style="font-size: large;"><b>Treatment of ARVC </b></span><br />
<span style="font-size: large;">Beta-blockers are first-line treatment for patients with non-life-threatening arrhythmias. </span><span style="font-size: large;">Amiodarone or sotalol can be used for symptomatic arrhythmias. In cases of life-</span><span style="font-size: large;">threatening arrhythmias, or indications of high risk for sudden cardiac death an implanted cardioverter defibrillator (ICD) is required. </span><span style="font-size: large;">Obviously, there is an indication for an ICD in patients who had a previous episode of cardiac arrest (aborted SCD) or of h</span><span style="font-size: large;">emodynamically unstable </span><span style="font-size: large;">sustained ventricular tachycardia (VT), but ICD implantation should also be seriously considered in patients with an episode of hemodynamically stable VT.</span><br />
<span style="font-size: large;"> Cardiac transplantation is indicated in some severe cases for end-stage heart failure or </span><span style="font-size: large;">for intractable arrhythmia. </span></div>
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<b><span style="font-size: large;"> Clinical risk factors that predict an increased risk of sudden cardiac death (SCD) in patients with arrhythmogenic right ventricular cardiomyopathy</span></b><span style="font-size: large;"> are the following:</span><br />
<span style="font-size: large;">Hemodynamically stable </span><span style="font-size: large;">sustained VT</span><br />
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<span style="font-size: large;">Non-sustained VT</span><br />
<span style="font-size: large;">History of unexplained syncope</span><br />
<span style="font-size: large;">Severe dilatation and/or </span><span style="font-size: large;">dysfunction of the right or the left ventricle, or </span><span style="font-size: large;">both</span><br />
<span style="font-size: large;">Early-onset </span><span style="font-size: large;"> </span><span style="font-size: large;">(age < 35 </span><span style="font-size: large;">years) of </span><span style="font-size: large;">severe</span><span style="font-size: large;"> </span><span style="font-size: large;">structural </span><span style="font-size: large;">disease (with prominent ventricular dilatation or dysfunction)</span><br />
<span style="font-size: large;">Left heart failure</span><span style="font-size: large;"> </span></div>
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<span style="font-size: large;">Family of history of SCD</span><br />
<span style="font-size: large;">An <b>ICD</b> is recommended for patients with ARVC for primary<br />prevention of SCD if such risk factors are present, as well as for secondary prevention of SCD (i.e. in patients who have been resuscitated and have survived an episode of cardiac arrest or sustained VT) regardless of risk factors.</span><br />
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<span face=""arial" , "helvetica" , sans-serif"><b><span style="background-color: #f6b26b;">VIDEO</span> Arrhythmogenic right ventricular cardiomyopathy (or dysplasia)-ARVC or ARVD. A cardiology case is presented in this Video. The findings with ECG and echocardiography and the diagnostic criteria of ARVC (Taskforce-2010) are shown and analyzed. Also, a concise review of the evaluation of the right ventricle (RV function) with echocardiography is presented. ( To watch the video full screen, start the video and click on the symbol [] at the lower right corner).</b></span></div>
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<span face=""arial" , "helvetica" , sans-serif" style="font-size: small;"><b>Another patient ( a male- age 41) with a different myocardial disorder... Describe each view (what kind of view it is what are the interesting findings and which diagnosis could be considered) </b></span><br />
<b style="font-family: arial, helvetica, sans-serif;"><span face=""arial" , "helvetica" , sans-serif">The following images are courtesy of <span style="background-color: yellow;">Dr. Vladyslav Kavalerchyk</span> (used with permission).</span></b><span face=""arial" , "helvetica" , sans-serif" style="font-size: small;"></span><br />
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<tr><td class="tr-caption" style="text-align: center;"><span face=""arial" , "helvetica" , sans-serif" style="font-size: small;"><b>Image 1</b></span></td></tr>
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<tr><td class="tr-caption" style="text-align: center;"><b><span face=""arial" , "helvetica" , sans-serif" style="font-size: small;">Image 2</span></b></td></tr>
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<tr><td class="tr-caption" style="text-align: center;"><span face=""arial" , "helvetica" , sans-serif" style="font-size: small;"><b>Image 3</b></span></td></tr>
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<tr><td class="tr-caption" style="text-align: center;"><span face=""arial" , "helvetica" , sans-serif" style="font-size: small;"><b>Image 4</b></span></td></tr>
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<span face=""arial" , "helvetica" , sans-serif"><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold;">Image 1 is an echocardiographic 2-dimensional apical 4-chamber view. Images 2 and 3 are 3 -dimensional (3D) echocardiographic views (apical 4-chamber) and Image 4 is a frame derived from the cardiac magnetic resonance imaging (MRI) examination of the same patient. All these views show large trabeculations and deep recesses in the apical and lateral segments of the left ventricle, a pattern that strongly suggests left ventricular non-compaction cardiomyopathy with a sponge-like appearance of an area of the left ventricle. Note: There is also a small proportion of the general population with an echocardiographic pattern of prominent left ventricular trabeculations and recesses but without any other abnormalities in left ventricular systolic and diastolic function and in the ECG. Therefore, the presence of recesses and trabeculations is not the only criterion that should be taken into account to make the diagnosis of this cardiomyopathy. Apart from the two characteristic myocardial layers in cardiac imaging, a thick </span></span><b><span face=""arial" , "helvetica" , sans-serif">noncompacted internal layer and a thinner compacted external layer,</span></b><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold;"> the patient should also have one or more of the following findings in order to be diagnosed with the cardiomyopathy: Symptoms (e.g. palpitations, syncope, exertional dyspnea), a positive family history for cardiomyopathy or sudden death, abnormalities of the ECG (eg. inverted T waves or LBBB), documented arrhythmias (in Holter monitoring or in an exercise ECG test), a reduced left ventricular ejection fraction (EF <50%), or left ventricular wall motion abnormalities, or left ventricular dilation or left ventricular diastolic dysfunction. </span><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold;"> For a description of this cardiomyopathy, a</span><span face=""arial" , "helvetica" , sans-serif"><b style="font-family: arial, helvetica, sans-serif;">lso see the paragraph below. (The case is courtesy of </b><span face=""arial" , "helvetica" , sans-serif" style="background-color: yellow; font-weight: bold;">Dr. Vladyslav Kavalerchyk</span><b style="font-family: arial, helvetica, sans-serif;"> (used with permission).</b><span style="font-family: "times" , "times new roman" , serif; font-size: large;"> Also, see the <span style="background-color: yellow;">Video : link</span> <a href="https://www.youtube.com/watch?v=8w5XjQ2E8po&app=desktop" target="_blank">Left Ventricular Non-Compaction Cardiomyopathy (LVNC)</a> from Dr. Kavalerchyk's YouTube channel <a href="https://www.youtube.com/channel/UC94Dpl_O6Kywp5wCJB8-NOA?app=desktop" target="_blank">Echocardiography step by step</a>)</span></span><br />
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<b style="font-size: x-large;">Left ventricular non-compaction</b></div>
<span style="font-size: large;">Left ventricular non-compaction is a sponge-like appearance of an area of the left ventricle (LV). It </span><span style="font-size: large;">results from an arrest of</span><br />
<span style="font-size: large;">myocardial maturation during embryogenesis. Familial and spontaneous cases have been described. I</span><span style="font-size: large;">n patients with LV noncompaction</span><span style="font-size: large;"> </span><span style="font-size: large;">mutations in several </span><span style="font-size: large;">genes </span><span style="font-size: large;">encoding proteins of the</span><br />
<span style="font-size: large;">cytoskeleton, sarcomere, and mitochondria have been implicated. </span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">The condition predominantly affects the apical segments of the LV and also the mid-inferior and mid-lateral wall. LV non-compaction can be isolated, or it may be associated with congenital heart abnormalities (such as an atrial or ventricular septum defect, or coarctation of the aorta). </span><br />
<span style="font-size: large;">The condition is diagnosed by echocardiography, cardiac MRI (magnetic resonance imaging) or left ventriculography (injection of contrast medium into the LV during cardiac catheterization). On these imaging studies, affected areas have a thick myocardium consisting of a thin compacted outer layer and a thicker noncompacted inner layer. The noncompacted myocardial layer has prominent trabeculations and deep endomyocardial recesses,</span><span style="font-size: large;"> that communicate </span><span style="font-size: large;">with the left ventricular cavity.</span><br />
<span style="font-size: large;"> Useful diagnostic criteria are the following:</span><br />
<span style="font-size: large;"> The thickness of the noncompacted endocardial layer is > 2 times the thickness of the compacted epicardial layer at end-systole.</span><br />
<span style="font-size: large;">The presence of blood flow should be demonstrated (with color flow doppler or contrast echocardiography) in the recesses between the myocardial trabeculations.</span><br />
<span style="font-size: large;">The presence of > 3 trabeculations visible in a single image, protruding from the left ventricular wall, apically to the papillary muscles, with intertrabecular spaces connected with the ventricular cavity.</span><br />
<span style="font-size: large;">Evidence of systolic and/or diastolic LV dysfunction should be present.</span><br />
<span style="font-size: large;">Cardiovascular magnetic r</span><span style="font-size: large;">esonance imaging (CMR) </span><span style="font-size: large;"> permits even </span><span style="font-size: large;">better visualization of trabeculations and recesses of the LV myocardium, therefore it is a useful diagnostic test for LV noncompaction.</span><br />
<span style="font-size: large;"><u>Important note</u>: There is also a small proportion of the general population with an echocardiographic pattern of prominent left ventricular trabeculations and recesses but without any other abnormalities in left ventricular systolic and diastolic function and in the ECG. Therefore, the presence of recesses and trabeculations and the ratio of the thickness of the noncompacted and the compacted myocardial layer is not the only criterion that should be taken into account to make the diagnosis of this cardiomyopathy. Apart from the two characteristic myocardial layers identified in cardiac imaging, a thick noncompacted endocardial layer and a thinner compacted epicardial layer, the patient should also have one or more of the following findings in order to be diagnosed with the cardiomyopathy: Symptoms (e.g. palpitations, syncope, exertional dyspnea), a positive family history for cardiomyopathy or sudden death, abnormalities of the ECG (eg. inverted T waves, or a left bundle branch block-LBBB, which is a usual finding in these patients), documented arrhythmias (in Holter monitoring or in an exercise ECG test), a reduced left ventricular ejection fraction (EF <50%), or left ventricular wall motion abnormalities of the noncompacted segments, or left ventricular dilation, or left ventricular diastolic dysfunction. <br />The cardiomyopathy, when present, often leads to the development of heart failure due to systolic and/or diastolic dysfunction. LV non-compaction, especially if it involves an extensive area of the myocardium, can result in congestive cardiac failure, thromboembolism, cardiac arrhythmias, and sudden death. Manifestations can appear in adult age, or in childhood.</span></div>
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<span style="font-size: large;"><b>Treatment</b>, when necessary, is for associated heart failure (the standard treatment for HF with reduced EF, see chapter on heart failure), </span><span style="font-size: large;">arrhythmias (beta-blockers, amiodarone, or an ICD may be needed depending on the clinical scenario and according to their standard indications), and the risk of emboli (anticoagulation may be needed). Regarding anticoagulation, one must take into account that p</span><span style="font-size: large;">atients with LV noncompaction with or without atrial fibrillation </span><span style="font-size: large;">are at high risk for thromboembolism if they have</span><span style="font-size: large;"> impaired left ventricular systolic function.</span><br />
<span style="font-size: large;">Therefore, </span><span style="font-size: large;">anticoagulation with a vitamin K antagonist (warfarin, or acenocoumarol) is recommended in </span><span style="font-size: large;">patients with LV noncompaction, </span><span style="font-size: large;">with </span><span style="font-size: large;">left ventricular EF <40 %,</span><span style="font-size: large;"> even if they do not have a history of atrial fibrillation.</span><br />
<span style="font-size: large;">I also recommend this <span style="background-color: yellow;">Video</span>, link: <a href="https://www.youtube.com/watch?v=WGOz_2FCwyw" target="_blank">LV hyper-trabeculation or non-compaction in athletes? S.Caselli</a></span><span style="font-size: large;"> from the IOC Course on Cardiovascular(CV) Evaluation of Olympic athletes (</span><span style="font-size: large;">Youtube channel of Dr. Antonio Pelliccia).</span></div>
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<span style="font-family: inherit; font-size: large;"><b>Takotsubo cardiomyopathy</b><br />Takotsubo cardiomyopathy is a syndrome of transient apical left ventricular dysfunction (which is apparent with echocardiography or left ventriculography) with a clinical picture that mimics a myocardial infarction (chest pain, or dyspnea, ST-segment elevation, and raised cardiac biomarkers). <br />Important features of the syndrome are its association with a period of emotional stress, normal epicardial coronary arteries (demonstrated with coronary angiography), and characteristic akinesia of the apical and occasionally also the midsegments of the LV on echocardiography or ventriculography with a good contractile function of the basal segments.<br />Possible mechanisms include a hyperadrenergic syndrome (i.e. the effects of increased levels of catecholamines), or coronary artery spasm.<br />Complete recovery of myocardial systolic function usually occurs within 4–6 weeks, but recurrences can occur.<br /><b><br /></b></span></div>
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<span style="font-family: inherit; font-size: large;"><b>Peripartum cardiomyopathy</b><br />This is a rare condition that occurs in the last trimester of pregnancy or within 5 months from delivery (more common between the 36th week of pregnancy and the first month after delivery) and presents clinically and echocardiographically as a dilated cardiomyopathy with left ventricular (LV) systolic dysfunction (with reduced LV ejection fraction) in a patient without a recognizable previous heart disease. This diagnosis is made, when no other cause of LV dysfunction is found. It is more common in multiparous, obese women over 30 years old. Peripartum cardiomyopathy occurs in about 1 every 2000 live births (this is an approximate number).<br />Recovery to normal ventricular systolic function within 6 months occurs in nearly half of the cases, but in some patients, peripartum cardiomyopathy can demonstrate a severe course with progressive heart failure, or it can cause sudden death. Thus, it can be a life-threatening condition.</span><br />
<span style="font-size: large;">Treatment of peripartum cardiomyopathy before delivery usually includes</span><span style="font-size: large;"> loop </span><span style="font-size: large;">diuretics, </span><span style="font-size: large;">beta-blockers, and digoxin. Hydralazine and nitrates can also be added to the above medications. These five drugs are safe in pregnancy and they are considered as the mainstay of heart failure treatment during pregnancy.</span><span style="font-size: large;"> Pregnant women should not receive angiotensin-converting enzyme inhibitors (ACE-inhibitors), angiotensin receptor blockers, or mineralocorticoid receptor antagonists (MRAs) because of potential teratogenic effects. Postpartum, the treatment is identical to the treatment of any dilated cardiomyopathy (ie. the treatment of heart failure with reduced ejection fraction). Therefore, an ACE-inhibitor (or an angiotensin receptor blocker) usually plus an MRA are also included in the treatment which should comply with the general heart failure guidelines.</span></div>
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<span style="font-size: large;"> I</span><span style="font-size: large;">n patients who present with acute peripartum cardiomyopathy, s</span><span style="font-size: large;">tudies have reported a beneficial effect of bromocriptine (a drug that inhibits the secretion of prolactin). Bromocriptine is currently being evaluated in larger studies to assess its cardiovascular effects.</span></div>
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<span style="font-size: large;">In peripartum cardiomyopathy, heart failure therapy should be continued for a minimum of 12 months after the time of diagnosis or even permanently in cases with severe persistent LV dysfunction.</span><br />
<span style="font-size: large;">In some patients who develop severe heart failure not responding to optimal medical treatment the implantation of a left ventricular assist device or heart trasplantation will be required.</span><br />
<span style="font-size: large;">There is a risk of relapse of the cardiomyopathy in a susequent pregnancy, therefore the physician should inform the patient regarding this issue. Relapse in a subsequent pregnancy is possible even in women who have fully recovered left ventricular function.</span><br />
<span style="font-size: large;">Recommendations of experts about a subsequent pregnancy are the following: In cases with a full recovery of LV function subsequent pregnancy is not contraindicated, but the patient should be informed that although the risk is relatively low, it is not absent. In cases with a partial recovery of LV function, a dobutamine stress echocardiography should be performed before counselling the patient on this issue. If the left ventricular inotropic response to dobutamine is normal, then patients can be counseled as above. If the left ventricular inotropic response to dobutamine is abnormal (ie. there is a reduced LV contractile reserve) then there is a higher risk and pregnancy is not recommended.<br />In patients with no recovery of LV function, the risk in case of a subsequent pregnancy is high, therefore it must be avoided.</span></div>
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<b>Ramaraj R, Sorrell VL. Peripartum cardiomyopathy: Causes, diagnosis, and treatment. Cleveland Clinic Journal of Medicine 2009 ;76(5):289–96. LINK <a href="https://www.mdedge.com/ccjm/article/95079/womens-health/peripartum-cardiomyopathy-causes-diagnosis-and-treatment">Peripartum cardiomyopathy: Causes, diagnosis, and treatment. </a><br /><br />Hilfiker-Kleiner D, Haghikia A, et al. Peripartum cardiomyopathy: current management and future perspectives. European Heart Journal 2015, doi:10.1093/eurheartj/ehv009<br />LINK <a href="http://eurheartj.oxfordjournals.org/content/early/2015/01/29/eurheartj.ehv009.full">http://eurheartj.oxfordjournals.org/content/early/2015/01/29/eurheartj.ehv009.ful</a></b><br />
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<span style="font-family: inherit; font-size: large;"><br /><b>Tachycardia induced cardiomyopathy</b><br />This is a rare form of dilated cardiomyopathy caused by prolonged periods of supraventricular or ventricular tachycardia, which is persistent or very frequent, in order to cause LV systolic dysfunction. Apart from tachyarrhythmias, also very frequent ventricular premature beats (PVCs) with a burden > 10-15% of total QRS complexes in Holter monitoring can occasionally cause this type of cardiomyopathy.</span><br />
<span style="font-family: inherit; font-size: large;">Apart from tachycardia duration, another significant factor that contributes to the development of ventricular dysfunction is the ventricular rate. </span><span style="font-size: large;">Patients with higher ventricular rates develop cardiomyopathy earlier.</span><br />
<span style="font-size: large;">A clinical problem is determining if the tachycardia is the cause of the cardiomyopathy or if the arrhythmia is a consequence of a cardiomyopathy of different etiology. Tachycardia induced cardiomyopathy should be suspected in every patient with LV dysfunction in the setting of a persistent tachyarrhythmia when another cause for the LV dysfunction cannot be found.</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px; line-height: 21.9988px;"><br /></span><span style="font-size: large;">Tachycardia induced cardiomyopathy is generally reversible once the underlying arrhythmia is controlled, therefore it is important to treat </span><span style="font-size: large;">promptly</span><span style="font-size: large;"> the tachycardia responsible for the condition.</span></div>
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<span style="font-family: inherit; font-size: large;">Successful treatment of the causative prolonged arrhythmia usually results in the recovery of cardiac function. Usually, </span><span style="font-size: large;">the greatest recovery of the LV ejection fraction (EF) is observed approximately 1 month after arrhythmia cessation and more gradual recovery, which may lead to a complete normalization in many cases, can be observed up to one year thereafter.</span><br />
<span style="font-family: inherit; font-size: large;"> </span><span style="font-size: large;">Heart rate normalization, either with rate or rhythm control, is the cornerstone of management. Most of the data available come from patients with atrial fibrillation. In these patients, normalization of heart rate using any of the two methods (rate or rhythm control) improves systolic function, in case of tachycardia-induced cardiomyopathy. However, in other clinical settings, treatment of tachycardia-induced cardiomyopathy should aim at the termination of the responsible arrhythmia, which may require </span><span style="font-size: large;">antiarrhythmic drug therapy, direct current (DC) cardioversion, or </span><span style="font-size: large;">catheter ablation. F</span><span style="font-size: large;">or patients with supraventricular tachyarrhythmias, if control of the arrhythmia cannot be achieved by other means, a</span><span style="font-size: large;">trioventricular junction conduction ablation combined with pacemaker implantation can be an option.</span><span style="font-size: large;"> </span><span style="font-size: large;"> Drug treatment of heart failure (HF) is also provided, as needed, according to the general indications and guidelines (e.g. an ACE-inhibitor, beta blocker-also useful for the control of heart rate, a loop diuretic, digoxin, aldosterone antagonist, may be needed as part of the HF treatment). </span><br />
<span style="font-size: large;"><br /></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<span style="font-size: large;"></span><br />
<br />
<b><span style="background-color: #990000; color: #f1c232; font-size: large;">Links and Bibliography</span></b><br />
<span style="font-family: arial;"><b><span style="color: #990000;"> </span></b></span></div><div><span style="font-family: arial;"><b><span style="color: #990000;"><span>A VIDEO : I highly recommend this video with clinical questions and most importantly echocardiographic images of various cardiomyopathies ( YouTube -Mayo Clinic -Dr. Steve R. Ommen)</span></span><br />
<span>LINK <a href="https://www.youtube.com/watch?v=aIlGrMUURQI" target="_blank">https://www.youtube.com/watch?v=aIlGrMUURQI</a></span><br />
<br />
<br />
<span><a href="http://eurheartj.oxfordjournals.org/content/29/2/270" target="_blank">Classification of the cardiomyopathies: a position statement from the European society of cardiology </a></span><br />
<br />
<span face=""arial" , "helvetica" , sans-serif">Maron BJ, Towbin JA, et al Contemporary Definitions and Classification of the Cardiomyopathies. Circulation. 2006;113:1807-1816 (AHA SCIENTIFIC STATEMENT)<br />LINK <a href="http://circ.ahajournals.org/content/113/14/1807">http://circ.ahajournals.org/content/113/14/1807</a><br /><br /><br />Nishimura RA, Holmes DR. Hypertrophic obstructive cardiomyopathy. N Engl J Med. 2004;350:1320-1327.<br /><br />Watkins H, Ashrafian H, Redwood C. Inherited cardiomyopathies. N Engl J Med 2011;<br />364:1643–1656.<br /><br />Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. Circulation. 2010;121:1533-1541<br /><br />Kushwaha SS, Fallon JT, Fuster V. Restrictive cardiomyopathy. N Engl J Med. 1997;336:267-276.<br /><br />Behere SP, Weindling SN. Inherited arrhythmias: The cardiac channelopathies.Annals of Pediatric Cardiology. 2015;8: 210-220. LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4608198/">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4608198/</a></span><br />
<br /> <span face=""arial" , "helvetica" , sans-serif">Hilfiker-Kleiner D, Haghikia A, et al. Peripartum cardiomyopathy: current management and future perspectives. European Heart Journal 2015, </span><span face=""arial" , "helvetica" , sans-serif">doi:10.1093/eurheartj/ehv009</span></b></span></div>
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<span style="font-family: arial;"><b>LINK <a href="http://eurheartj.oxfordjournals.org/content/early/2015/01/29/eurheartj.ehv009.full" target="_blank">http://eurheartj.oxfordjournals.org/content/early/2015/01/29/eurheartj.ehv009.ful</a><br />
<br />
<span face=""arial" , "helvetica" , sans-serif">Ramaraj R, Sorrell VL. Peripartum cardiomyopathy: Causes, diagnosis, and treatment. Cleveland Clinic Journal of Medicine 2009 ;76(5):289–96. LINK <a href="https://www.mdedge.com/ccjm/article/95079/womens-health/peripartum-cardiomyopathy-causes-diagnosis-and-treatment">Peripartum cardiomyopathy: Causes, diagnosis, and treatment.</a></span></b></span></div><div><span style="font-family: arial;"><span face=""arial" , "helvetica" , sans-serif"><b><a href="https://www.mdedge.com/ccjm/article/95079/womens-health/peripartum-cardiomyopathy-causes-diagnosis-and-treatment"></a></b></span><span face=""segoe_uiregular" , "helvetica neue" , "helvetica" , "arial" , sans-serif" style="line-height: 21.4286px;"><b><br /></b></span><span face=""arial" , "helvetica" , sans-serif"><b>Perez-Silva A, Merino JS, Tachycardia-induced cardiomyopathy E-Journal-of-Cardiology-Practice 2019;7 </b></span></span></div>
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<span style="font-family: arial;"><span face=""arial" , "helvetica" , sans-serif"><b>LINK <a href="http://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-7/Tachycardia-induced-cardiomyopathy">http://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-7/Tachycardia-induced-cardiomyopathy</a></b></span><b><a href="http://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-7/Tachycardia-induced-cardiomyopathy" target="_blank"> </a></b></span></div><div><span style="font-family: arial;"><b><br /></b></span></div><div><div style="background-color: white; color: #222222; widows: 1;"><span style="font-family: arial;"><b><div class="ref" style="animation-duration: 6s; animation-fill-mode: both; animation-name: latestRef; animation-timing-function: ease-out; box-sizing: border-box; color: black; transition: all 0.15s ease 0s; widows: 2;"><div class="csl-right-inline" style="box-sizing: border-box; display: inline;">Gilotra N, Okada D, Sharma A, Chrispin J. Management of Cardiac Sarcoidosis in 2020. </div></div><div class="ref" style="animation-duration: 6s; animation-fill-mode: both; animation-name: latestRef; animation-timing-function: ease-out; box-sizing: border-box; color: black; transition: all 0.15s ease 0s; widows: 2;"><div class="csl-right-inline" style="box-sizing: border-box; display: inline;">Arrhythm Electrophysiol Rev [Internet] 2020 ;9(4):182–8. Available from: <a href="https://doi.org/10.15420/aer.2020.09" style="box-sizing: border-box;" target="_blank">10.15420/aer.2020.09</a></div></div><div class="reference_buttons_container" style="background-attachment: initial; background-clip: initial; background-image: linear-gradient(90deg, rgba(255, 255, 255, 0) 0%, white 12%); background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; bottom: 0px; box-sizing: border-box; color: black; height: 76.8229px; position: absolute; right: 0px; top: 0px; widows: 2; width: 230px;"><div class="reference_buttons" style="box-sizing: border-box; height: 56px; margin-top: -28px; position: absolute; right: 0px; top: 38.4028px;"><button aria-label="Copy in-text reference" class="button intext_button hint--top hint--no-animate" style="-webkit-tap-highlight-color: transparent; appearance: button; background-color: white; background-position: left center; border-color: rgb(191, 191, 191); border-radius: 13px; border-style: solid; border-width: 1px; cursor: pointer; line-height: 1; margin: 2px 0px 2px 5px; padding: 4px 10px; vertical-align: baseline;">In-Text</button><button aria-label="Copy Reference" class="button copy_button hint--top hint--no-animate" style="-webkit-tap-highlight-color: transparent; appearance: button; background-color: white; background-position: left center; border-color: rgb(191, 191, 191); border-radius: 13px; border-style: solid; border-width: 1px; cursor: pointer; line-height: 1; margin: 2px 0px 2px 5px; padding: 4px 10px; vertical-align: baseline;">Copy</button><button aria-label="Add or Edit Note" class="button note_button hint--top hint--no-animate" style="-webkit-tap-highlight-color: transparent; appearance: button; background-color: white; background-position: left center; border-color: rgb(191, 191, 191); border-radius: 13px; border-style: solid; border-width: 1px; cursor: pointer; line-height: 1; margin: 2px 0px 2px 5px; padding: 4px 10px; vertical-align: baseline;">Note</button><br style="box-sizing: border-box;" /><button aria-label="Edit Reference" class="button edit_button hint--top hint--no-animate" style="-webkit-tap-highlight-color: transparent; appearance: button; background-color: white; background-position: left center; border-color: rgb(191, 191, 191); border-radius: 13px; border-style: solid; border-width: 1px; cursor: pointer; line-height: 1; margin: 2px 0px 2px 5px; padding: 4px 10px; vertical-align: baseline;">Edi</button></div></div></b></span></div><div style="background-color: white; widows: 1;"><span style="color: #222222; font-family: arial;"><b>LINK </b></span><span style="background-color: transparent;"><span style="color: #222222; font-family: arial;"><b><a href="https://www.aerjournal.com/articles/management-cardiac-sarcoidosis-2020">https://www.aerjournal.com/articles/management-cardiac-sarcoidosis-2020</a></b></span></span></div></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-6177488573781824902016-09-19T12:52:00.000+03:002019-12-26T00:13:17.580+02:00Tricuspid regurgitation<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: large;"><b>Tricuspid regurgitation (TR)</b></span></div>
<span style="font-size: large;"><b>Trivial</b> (small) TR is frequently detected by echocardiography in normal subjects, and should never be interpreted as an abnormal finding. </span><br />
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<span style="font-size: large;"><b>Pathological TR</b> is more often secondary (not due to a disorder of the valve structure) and less often it is attributed to a primary (structural) valve lesion. </span></div>
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<span style="font-size: large;"><b>Secondary TR </b>is due to </span><span style="font-size: large;">annular dilatation and increased tricuspid leaflet tethering</span><span style="font-size: large;"> and is caused by:</span></div>
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<span style="font-size: large;">1) Right ventricular (RV)</span><span style="font-size: large;"> pressure overload (usually caused by pulmonary hypertension as a consequence of left sided heart disease, chronic pulmonary disease, connective tissue disease, congenital heart disease, or idiopathic pulmonary hypertension) </span></div>
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<span style="font-size: large;">or</span></div>
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<span style="font-size: large;">2) RV volume overload (dilatation of the right ventricle due to an atrial septal defect, or due to intrinsic right ventricular disease with systolic dysfunction, as in right ventricular cardiomyopathy).</span></div>
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<b style="font-size: x-large;"><br /></b> <b style="font-size: x-large;">Primary TR</b><span style="font-size: large;"> (caused by structural alterations of the valve) can be caused by</span></div>
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<span style="font-size: large;"> Infective endocarditis (especially in intravenous drug addicts),<br />Myxomatous disease (leading to prolapse of the valve leaflets)<br />Rheumatic heart disease, <br />Iatrogenic causes (</span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>occasionally TR occurs after pacemaker implantation or after endomyocardial biopsy</b></span><span style="font-size: large;">)<br />Carcinoid syndrome</span><i><b><span style="font-family: "arial" , "helvetica" , sans-serif;">( carcinoid syndrome, is a type of neuroendocrine tumor, usually in the small bowel or appendix, with </span></b></i><i><b><span style="font-family: "arial" , "helvetica" , sans-serif;">metastases to the liver, which releases serotonin metabolites into the bloodstream. These metabolites are responsible for the formation of endocardial plaques in the right heart chambers. Involvement of the tricuspid valve causes thickening and immobilization of the leaflets, resulting in significant tricuspid regurgitation and, less often tricuspid stenosis.)</span></b></i><i><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b></i><span style="font-size: large;">Ebstein’s anomaly</span><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><i> is a congenital malformation characterized by apical displacement of the annular insertion of the septal and posterior leaflets of the tricuspid valve and atrialization of a portion of the ventricular myocardium.</i></span></b><br />
<span style="font-size: large;">Endomyocardial fibrosis,</span><br />
<span style="font-size: large;">Ergot-like drugs,</span><br />
<span style="font-size: large;">Thoracic trauma </span><br />
<b style="font-size: x-large;">Symptoms</b></div>
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<span style="font-size: large;">Often, even severe TR can be tolerated for a long period of time without significant symptoms. Symptoms of the causative disorder may be present. Eventually, severe TR will produce symptoms of right heart failure, such as fatigue, exercise intolerance, edema, vague abdominal discomfort due to hepatomegaly.</span><br />
<b style="font-size: x-large;">Physical examination in TR</b><span style="font-size: large;"></span><br />
<span style="font-size: large;"> The most common physical signs of severe TR are prominent v waves in the jugular veins and a pulsatile liver. Both these signs are due to regurgitation of right ventricular blood into the systemic veins. </span><br />
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<span style="font-size: large;">The systolic murmur of TR is heard at the lower left sternal border and at the xiphoid area. The holosystolic murmur of tricuspid regurgitation (TR) is often soft (and may be absent in many cases of severe TR, if flow is not turbulent enough) and it becomes louder on inspiration.</span></div>
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<span style="font-size: large;">In severe cases peripheral (ankle or leg) edema, or even ascites may be present.</span></div>
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<span style="font-size: large;"><b>ECG</b></span></div>
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<span style="font-size: large;">Frequent findings are an incomplete right bundle branch block and atrial fibrillation.</span></div>
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<span style="font-size: large;"><b>Echocardiography in tricuspid regurgitation (TR)</b></span></div>
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<span style="font-size: large;">TR is identified using color flow mapping of the systolic<br />regurgitant jet in the right atrium.</span></div>
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<span style="font-size: large;">Evaluation of the </span><span style="font-size: large;">pulmonary systolic pressure from the measurement of the peak velocity of the TR jet should be carried out in all cases. </span><span style="font-size: large;">This may be inaccurate </span><span style="font-size: large;">in the presence of severe TR (with a large regurgitant volume) because this leads to a lower pressure difference (pressure gradient) between the right ventricle and the right atrium </span><span style="font-size: large;">.</span></div>
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<span style="font-size: large;">The presence of associated lesions, particularly left ventricular systolic or diastolic dysfunction and lesions of the left-sided cardiac valves, should be assessed.</span></div>
<span style="font-size: large;">In primary TR, valve morphology can help determine the etiology: vegetations in endocarditis, leaflet retraction and thickened leaflet tips in rheumatic valve disease, prolapsing thickened leaflets in myxomatous disease, a flail leaflet in myxomatous or post-traumatic valve involvement.</span><br />
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<span style="font-size: large;">In secondary TR annular dilatation or leaflet tethering is observed:</span></div>
<span style="font-size: large;">Significant tricuspid annular dilatation is defined in the apical 4 chamber echocardiographic view by a diastolic diameter ≥40 mm </span><span style="font-size: large;">, or >21 mm/</span><span style="font-family: inherit; font-size: large;"> </span><span lang="EN-US" style="font-size: large;">m</span><sup>2 </sup><span style="font-size: large;">of body surface area. </span><br />
<span style="font-size: large;">S</span><span style="font-size: large;">ignificant tethering of the valve, i</span><span style="font-size: large;">n secondary TR, is characterized by a coaptation distance > 8 mm. This is the distance between the tricuspid annular plane and the point of coaptation of the valve leaflets in mid-systole from the apical 4-chamber view.</span><br />
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<span style="font-size: large;">Evaluation of the right ventricular (RV) dimensions and function should be performed. Indications of RV systolic dysfunction are: Tricuspid annular plane systolic excursion (TAPSE) <15 mm,</span></div>
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<span style="font-size: large;"> pulse wave TDI-derived peak </span><span style="font-size: large;">systolic velocity of the lateral</span><span style="font-size: large;"> </span><span style="font-size: large;">tricuspid annulus <11 cm/s, and</span></div>
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<span style="font-size: large;"> RV end-systolic area >20 c</span><span lang="EN-US" style="font-size: large;">m</span><sup>2</sup><span style="font-size: large;">. </span></div>
<span style="font-size: large;">Tricuspid regurgitation (TR) severity is estimated from the extent of the jet, or better by vena </span><span style="font-size: large;">contracta width (vena contracta is the narrowest portion of the jet, near its origin from the valve leaflets). </span><span style="font-size: large;">In many cases, just a visual estimate can allow judgment on the severity of regurgitation.</span><span style="font-size: large;"> </span><span style="font-size: large;"> In case of TR with an eccentric jet, a </span><span style="font-size: large;">large eccentric jet reaching the posterior wall </span><span style="font-size: large;">of the right atrium indicates significant TR. </span><span style="font-size: large;"> Conversely, small </span><span style="font-size: large;">jets and a normal size of the right atrium and right ventricle usually indicate mild TR.</span><br />
<span style="font-size: large;"> Regurgitant jet area correlates roughly with the severity of regurgitation:</span><span style="font-size: large;">mild <5 </span><span style="font-size: large;">c</span><span lang="EN-US" style="font-size: large;">m</span><sup>2</sup><span style="font-size: large;"> </span><br />
<span style="font-size: large;">moderate 6-10 </span><span style="font-size: large;">c</span><span lang="EN-US" style="font-size: large;">m</span><sup>2</sup><br />
<span style="font-size: large;">severe >10 </span><span style="font-size: large;">c</span><span lang="EN-US" style="font-size: large;">m</span><sup>2</sup><span style="font-size: large;">.</span><span style="font-size: large;"> </span><br />
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<span style="font-size: large;">Other more accurate indications of severe TR are:<br />Vena contracta ≥ 7 mm</span><br />
<span style="font-size: large;"> In continuous wave Doppler examination of TR, a dense/triangular TR Doppler signal with early peaking.</span><br />
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<span style="font-size: large;"> PISA radius >9 mm, at color Doppler examination with baseline shift, with a Nyquist limit (aliasing velocity) of 28 cm/s towards the direction of the regurgitation.</span></div>
<span style="font-size: large;">Effective regurgitant orifice area (EROA) ≥40 mm².</span><br />
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<span style="font-size: large;">Regurgitant Volume ≥45 ml/beat.</span><br />
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<span style="font-size: large;">In severe TR, enlargement of the right atrium, right ventricle, and inferior vena cava is almost always present.</span><span style="font-size: large;"><br /></span>
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<b style="font-size: x-large;"><br /></b> <b style="font-size: x-large;">Treatment</b><span style="font-size: large;"> </span></div>
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<span style="font-size: large;">Diuretics improve signs of congestion. Specific therapy of the underlying disease is necessary, when feasible.</span><span style="font-size: large;"></span><br />
<span style="font-size: large;"> </span></div>
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<span style="font-size: large;"><b>Surgery</b> (usually tricuspid annuloplasty with a prosthetic ring) is indicated in :</span></div>
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<span style="font-size: large;">Symptomatic patients with severe primary TR without severe right ventricular dysfunction. </span></div>
<span style="font-size: large;">In asymptomatic or mildly symptomatic patients with severe isolated primary TR and progressive right ventricular (RV) dilatation or progressive deterioration of RV function (class IIa indication).</span><br />
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<span style="font-size: large;">In patients with severe (indication class I) or moderate (indication class IIa) primary TR, or moderate secondaryTR with dilated annulus (for limits of annular diameter see above) undergoing left-sided valve surgery. <br />The surgical operation performed is usually annuloplasty with a prosthetic ring, but in advanced forms of tethering and RV dilatation, or in a severe valve deformity that cannot be corrected, valve replacement should be considered. Valve replacement is performed with large bioprostheses (these are preferred than mechanical valves in the tricuspid position).</span><span style="font-size: large;"><br /></span> <span style="font-size: large;">Tricuspid regurgitation (color doppler echocardiography). A video-link (by dr <a href="https://www.youtube.com/channel/UCfpGYcP8Li9mfNEcDbtcBrw">Luke Howard</a>)</span><span style="font-size: large;"> :</span><br />
<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=UHNKYKyorJo" target="_blank">https://www.youtube.com/watch?v=UHNKYKyorJo</a></span>
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<span style="font-size: large;"><b style="background-color: #e06666;">Useful links and bibliography</b><br /><br /><a href="http://content.onlinejacc.org/article.aspx?articleid=1838843">2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease</a><br /><br /><a href="http://www.sfcardio.fr/sites/default/files/pdf/Valvular_Heart_Dis_FT.pdf">ESC Guidelines on the management of valvular heart disease (version 2012)</a></span><span style="font-size: large;"><br /></span></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-13226422746457878742016-09-18T22:35:00.000+03:002018-08-16T23:40:35.799+03:00Mitral stenosis<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: large;"><br /></span><span style="font-size: large;"><b>Mitral stenosis (MS)</b></span><span style="font-size: large;"><br /><b>Causes</b> </span><br />
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<span style="font-size: large;">The most common underlying cause of MS is prior rheumatic fever<br />occurring, on average, 20 years before presentation of mitral stenosis. </span></div>
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<span style="font-size: large;"></span><br />
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<span style="font-size: large;">Rheumatic valve disease is characterized by fibrous thickening and calcification of the valve leaflets, fusion of the commissures (the borders where the leaflets meet), shortening and thickening of the chordae tendineae.</span></div>
<span style="font-size: large;"> </span></div>
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<span style="font-size: large;"> Other more rare etiologies of MS include calcification of the mitral annulus that extends onto the leafets, infective endocarditis with large vegetations obstructing the valve orifice, and rare congenital mitral stenosis (parachute mitral valve, s</span><span style="font-size: large;">upravalvular mitral ring</span><span style="font-size: large;">). In parachute mitral valve, there is a single papillary muscle to which chordae to both leaflets attach. It results in mitral stenosis or mitral regurgitation.</span></div>
<div>
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<span style="font-size: large;">Some systemic diseases can cause valvular fibrosis and stenosis (carcinoid, s</span><span style="font-size: large;">ystemic lupus erythematosus, rheumatoid arthritis, h</span><span style="font-size: large;">ealed endocarditis, m</span><span style="font-size: large;">ucopolysaccharidosis. </span></div>
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<span style="font-size: large;">Mitral valvular fibrosis and stenosis can also be caused by p</span><span style="font-size: large;">rior anorectic drug use.</span></div>
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<b><br /></b></div>
<div style="font-size: x-large;">
<b>Pathophysiology of mitral stenosis (MS)</b></div>
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<span style="font-size: large;">In the normal heart, the mitral valve opens in</span><span style="font-size: large;"> early diastole </span><span style="font-size: large;"> and blood flows freely rom the left atrium (LA) into the left ventricle (LV). Normally the pressure difference between these two chambers </span><span style="font-size: large;">in diastole </span><span style="font-size: large;">is negligible (the LA and the LV have almost the same diastolic pressure). The normal cross sectional area of the mitral valve orifice is 4-6</span><span style="font-family: inherit; font-size: large;"> </span><span style="font-size: large;"><span lang="EN-US" style="font-family: "times new roman" , serif; line-height: 115%;">cm</span><sup><span style="font-family: "times new roman" , serif; line-height: 115%;">2</span></sup></span><br />
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<span style="font-size: large;"> In MS, there is obstruction to blood flow across the mitral valve. This produces an abnormal pressure gradient (pressure difference)<br />between the LA and LV, resulting in an icreased left atrial (LA) pressure. Hemodynamic changes (a rise in transvalvular pressure gradient) begin when the cross-sectional area of the valve, is reduced to less than 2 </span><span style="font-family: inherit; font-size: large;"><span lang="EN-US" style="line-height: 27.6px;">cm</span><sup><span style="line-height: 23px;">2.</span></sup></span></div>
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<span style="font-family: inherit; font-size: large;">In MS the high LA pressure is transmitted retrograde to the pulmonary circulation, resulting in increased pulmonary venous and capillary pressures. The elevated pressure in the pulmonary vasculature may cause transudation of plasma into the lung interstitium and alveoli. This causes symptoms of heart failure, such as exertional dyspnea and paroxysmal nocturnal dyspnea, or orthopnea. </span></div>
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<span style="font-size: large;">In MS,</span><span style="font-size: large;"> c</span><span style="font-size: large;">hronic pressure overload of the LA (i.e. the chronically elevated LA pressure) leads to left atrial dilatation. This stretches the atrial conduction fibers and may adversely affect intra-atrial conduction of electric impulses, resulting in atrial fibrillation.</span></div>
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<span style="font-size: large;">Atrial fibrillation due to the increased heart rate leads to a shortened diastolic period. The contribution of atrial systole to diastolic filling is also lost. These factors worsen the patient's clinical condition, because they result in a further elevation in atrial and pulmonary venous pressures and in a diminished cardiac output. </span><br />
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Auscultatory findings in MS </b></span><br />
<span style="font-size: large;">The opening snap is an early diastolic sound of short duration, and it is considered as the most characteristic auscultatory finding of mitral stenosis (MS). </span><span style="font-size: large;">You can hear the opening snap near the cardiac apex, but it is more easily heard along the lower left sternal border.</span><span style="font-size: large;"> However, as the disease progresses and the valve becomes more calcified and immobile, the opening snap may be lost. Also the first heart sound (S1), which is usually accentuated (loud) in MS, for the same reason can become softer at a later stage of the disease. The murmur of MS is a low-pitched rumbling mid-diastolic murmur. It is best heard with the bell of the stethoscope with the patient in the left lateral decubitus position. Presystolic accentuation of the murmur can be present if the patient is in sinus rhythm. Auscultation after a brief period of exercise usually accentuates the murmur of MS, because exercise increases the transvalvular gradient, </span><span style="font-size: large;">due to the increased cardiac output and heart rate.</span><br />
<span style="font-size: large;"> The length of the murmur correlates better with the severity of MS than the loudness. MS is more severe when the murmur is longer and when the time interval from the second heart sound (S2) to the opening snap is short.</span><br />
<span style="font-size: large;"><b>ECG</b></span><br />
<span style="font-size: large;">The electrocardiogram (ECG) in MS, if the rhythm is sinus, shows left atrial enlargement. </span><span style="font-size: large;">Atrial fibrillation may be present (it is common in MS). </span><span style="font-size: large;">If pulmonary </span><span style="font-size: large;">hypertension has developed, then there is also ECG evidence of right ventricular hypertrophy.</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;"><b>Echocardiography in MS </b></span><br />
<span style="font-size: large;">It shows structural abnormalities of the valve (in rheumatic MS </span><span style="font-size: large;">mitral leaflets are </span><span style="font-size: large;">thickened </span><span style="font-size: large;">with abnormal fusion of their commissures). Echocardiography also shows restricted separation</span></div>
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<span style="font-size: large;">of the valve leaflets and </span><span style="font-size: large;">doming of leaflets </span><span style="font-size: large;">during diastole.</span><br />
<span style="font-size: large;"> Left atrial enlargement is also present.</span><br />
<span style="font-size: large;">The mitral valve area (MVA) can be measured directly from the parasternal short axis view at the level of the tips of the mitral valve. Optimal positioning of the echocardiographic view, in order to obtain this measurement, is done by first obtaining a parasternal long-axis view and placing the mitral valve orifice in the center of the scan plane. The transducer is then rotated 90° to obtain the short-axis view. Measurements are obtained at the tips of the mitral leaflets. </span><span style="font-size: large;">Three-dimensional echocardiography can provide a more accurate determination of the mitral valve area (MVA).</span><br />
<span style="font-size: large;">MVA can also be calculated from Doppler velocity measurements (</span><span style="font-size: large;">the diastolic pressure half time). In general, the pressure half time </span><span style="font-size: large;">(PHT) represents the time in </span><span style="font-size: large;">which the peak pressure gradient between two adjacent chambers </span><span style="font-size: large;">decreases to the half of its value. Thus, the </span><span style="font-size: large;">PHT is the time it takes for the pressure gradient across the valve to fall to one-half the starting value. (This is equal to the time for the velocity of the mitral E wave to decrease to 70% of peak velocity). The mitral inflow E wave is used in this calculation.</span><br />
<span style="font-size: large;"> MVA (in </span><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 14.0pt; line-height: 115%;">cm</span><sup><span style="font-family: "times new roman" , "serif"; font-size: 14.0pt; line-height: 115%;">2</span></sup><span style="font-size: large;">) = 220/PHT. </span><span style="font-size: large;"><br />PHT is measured by tracing the deceleration slope of the E wave on a continuous wave Doppler recording of diastolic mitral flow. In some cases, the deceleration slope can be bimodal with a more rapid decline of mitral flow velocity in early diastole. Then it is recommended to trace the deceleration slope in mid-diastole rather than the early one.</span><br />
<span style="font-size: large;">Another method to determine the mitral valve area (MVA) is the PISA (proximal isovelocity surface area) method, a method also used (more commonly) for the calculation of the effective regurgitant oriffice in cases of mitral regurgitation. In mitral stenosis (MS) the PISA method can be used to calculate the MVA and it </span><span style="font-size: large;">offers the advantage of being still accurate in case of concomitant mitral or </span><span style="font-size: large;">aortic regurgitation. </span><br />
<span style="font-size: large;">On the atrial side of the stenotic mitral valve, diastolic flow converges towards the stenotic valvular orifice, </span><span style="font-size: large;">producing multiple hemispheres of isovelocity (the velocity of blood is the same in every point of the surface of each of these converging hemispheres)</span><span style="font-size: large;">. As blood accelerates towards the stenotic orifice, the velocity at the outer hemispheres is lower than the velocity on the smaller inner hemispheres. </span><span style="font-size: large;">If</span><span style="font-size: large;"> π=3.14, r </span><span style="font-size: large;">(in cm) </span><span style="font-size: large;">is the PISA radius (the radius of flow convergence) which is the radius of the hemisphere where blood velocity is the aliasing velocity and a is </span><span style="font-size: large;">the opening angle of mitral leaflets, i.e. </span><span style="font-size: large;">the </span><span style="font-size: large;">angle between the two mitral leaflets at the atrial surface</span><span style="font-size: large;"> (in degrees), aliasing velocity is the velocity at which aliasing of color doppler occurs in the direction of flow through the mitral valve (this is set by the echocardiographer to 20-45 cm/s), then we can use the equation: </span><br />
<span style="font-size: large;">MVA= 2π <span style="font-family: inherit;"><span style="line-height: 19.9733px;">r</span><sup style="line-height: 107%;">2 </sup></span></span><span style="font-size: large;">x (aliasing velocity/p</span><span style="font-size: large;">eak MS velocity) x (a/180).</span><br />
<span style="font-size: large;">Thus,</span><br />
<span style="font-size: large;"> MVA=6,28 </span><span style="font-size: large;"><span style="font-family: inherit;"><span style="line-height: 19.9733px;">r</span><sup style="line-height: 21.4px;">2 </sup></span></span><span style="font-size: large;">x (aliasing velocity/p</span><span style="font-size: large;">eak MS velocity) x (a/180)</span><br />
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<span style="font-size: large;"> Measurement of the opening angle</span><span style="font-size: large;"> is demanding, however it has</span><br />
<span style="font-size: large;">been demonstrated that there is only a slight difference in the angle</span><br />
<span style="font-size: large;">between patients and the use of a fixed angle of 100 degrees can provide an </span><span style="font-size: large;">accurate estimation of MVA.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Current guidelines define clinically important, severe, MS as a valve area ≤1.5</span><span lang="EN-US" style="font-family: "times new roman" , serif; line-height: 115%;"><span style="font-size: large;">cm</span></span><sup><span style="line-height: 115%;"><span style="font-family: inherit; font-size: large;">2</span></span><span style="font-family: "times new roman" , "serif"; font-size: 14.0pt; line-height: 115%;"> </span></sup><span style="font-size: large;"> , because this valve area is typically accompanied by left atrial enlargement and elevated pulmonary artery systolic </span><span style="font-size: large;">pressure. A valve area ≤1.0 </span><span lang="EN-US" style="font-family: "times new roman" , serif; line-height: 18.4px;"><span style="font-size: large;">cm</span></span><sup><span style="font-family: "times new roman" , serif; line-height: 15.3333px;"><span style="font-size: large;">2</span></span><span style="font-family: "times new roman" , serif; font-size: 14pt; line-height: 21.4667px;"> </span></sup><span style="font-size: large;">is termed "very severe" MS.</span></div>
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<span style="font-size: large;">The transvalvular mean gradient (assessed by means of tracing mitral inflow continuous wave doppler signal) provides an estimate of s</span><span style="font-size: large;">tenosis</span><span style="font-size: large;"> severity. I</span><span style="font-size: large;">n mild stenosis : </span><span style="font-size: large;">mean gradient < 5 mm Hg Moderate stenosis : mean gradient between 5 and 10 mm Hg.</span><br />
<span style="font-size: large;"> Severe MS : mean gradient > 10 mm Hg. </span><br />
<span style="font-size: large;"><span class="fontstyle0">Tricuspid regurgitation (TR) often accompanies severe MS. It may be secondary to right ventricular dysfunction and tricuspid annular dilation or may be the result of the rheumatic involvement of the tricuspid valve </span> </span><br />
<span style="font-size: large;"><br /></span>
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<span style="font-size: large;"><b>Treatment of MS</b></span><br />
<span style="font-size: large;"> S</span><span style="font-size: large;">ymptoms due to vascular congestion can be improved by </span><span style="font-size: large;">restriction</span><span style="font-size: large;"> of s</span><span style="font-size: large;">alt intake and diuretic therapy.</span><br />
<span style="font-size: large;">Heart rate slowing agents, such as beta-blockers or nondihydropyridine calcium channel blockers (diltiazem or verapamil), increase diastolic left ventricular filling time and so they there decrease symptoms with exercise. These drugs, or digoxin, are also used to slow the ventricular rate in patients with rapid atrial brillation. </span><span style="font-size: large;">Anticoagulant therapy to prevent thromboembolism is indicated in MS patients with </span><span style="font-size: large;">atrial fibrillation, or an identied LA thrombus, or a prior embolic event.</span><br />
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<span style="font-size: large;">Percutaneous or surgical valve interventions are the only treatments that alter the natural </span><span style="font-size: large;">history of severe MS. They are indicated in patients with severe (see above for the echocardiographic criteria of MS severity), symptomatic MS. Percutaneous </span><span style="font-size: large;">mitral </span><span style="font-size: large;">balloon </span><br />
<span style="font-size: large;"> valvuloplasty is the treatment of choice in appropriately selected patients (those without </span><span style="font-size: large;">advanced anatomic deformity of the valve, and without moderate or severe mitral regurgitation, or left atrial thrombus).</span><span style="font-size: large;"> Transesophageal echocardiography (TEE) is indicated to exclude LA thrombus prior to valvuloplasty.</span><br />
<span style="font-size: large;">Percutaneous mitral valvuloplasty (PMV) is also indicated for asymptomatic patients with severe MS (valve area </span><span style="font-size: large;"> ≤1.5</span><span lang="EN-US" style="font-family: "times new roman" , serif; line-height: 18.4px;"><span style="font-size: large;">cm</span></span><sup><span style="font-family: "times new roman" , serif; line-height: 15.3333px;"><span style="font-size: large;">2</span></span></sup><span style="font-size: large;">) , who have pulmonary hypertension (pulmonary artery systolic pressure > 50 mm Hg at rest or > 60 mm Hg with exercise) if valve morphology is favorable for PMV, in the absence of left atrial thrombus or moderate to severe mitral regurgitation.</span><br />
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<span style="font-size: large;">In patients with severe MS causing symptoms, not suitable for percutaneous valvuloplasty, surgical treatment is indicated. This is true for patients with s</span><span style="font-size: large;">evere subvalvular disease or severe valvular calcification, or concomitant mitral regurgitation (moderate or severe).</span><span style="font-size: large;"> Surgical treatment choices include: </span></div>
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<span style="font-size: large;">Open mitral valvotomy: It involves direct visualization of the mitral valve (with cardiopulmonary bypass), debridement of calcium, and splitting of fused commissures and chordae.</span></div>
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<span style="font-size: large;"> Mitral valve replacement.</span><span style="font-size: large;">with a prosthetic valve</span><span style="font-size: large;"> is often required, when there is extensive fibrosis and calcification or concomitant moderate to severe mitral regurgitation.</span><br />
<span style="font-size: large;"><br /></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<span style="color: #cc0000; font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-size: x-large;"><br /></span> <span style="font-size: large;"></span> <span style="background-color: #e06666; color: #f6b26b; font-size: large;">LINKS : </span><br />
<span style="font-size: large;">Mitral stenosis and echocardiography. A good video by 123sonography</span><br />
<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=MQ5UyGoYhZ8" target="_blank">https://www.youtube.com/watch?v=MQ5UyGoYhZ8</a></span></div>
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<span style="font-size: large;">An echocardiogram of a patient with mitral stenosis (by dr Maged Al Ali)</span><br />
<a href="https://www.youtube.com/watch?v=9yPfTxBAq3s" target="_blank"><span style="font-size: large;">https://www.youtube.com/watch?v=9yPfTxBAq3s</span></a><br />
<span style="background-color: white; color: #2a2a2a; font-family: "source sans pro" , sans-serif;"><br /></span> <span style="background-color: white; color: #2a2a2a; font-family: "source sans pro" , sans-serif;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><span style="background-color: white; color: #2a2a2a;">Baumgarther H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease: The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), </span><em style="background-color: white; border: 0px; box-sizing: border-box; color: #2a2a2a; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">European Heart Journal</em><span style="background-color: white; color: #2a2a2a;">, , ehx391, </span><a href="https://doi.org/10.1093/eurheartj/ehx391" style="background-color: white; border: 0px; box-sizing: border-box; color: #006fb7; font-stretch: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">https://doi.org/10.1093/eurheartj/ehx391</a></b></span></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: medium;">LINK</span><a href="https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data" target="_blank"> https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data</a></b></span></div>
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</script></div>Stella Giotopoulouhttp://www.blogger.com/profile/08157744010315731907noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-26123038566363291702016-09-07T12:22:00.002+03:002018-07-21T18:32:23.926+03:00Bradyarrhythmias-Bradycardia : Diagnosis and treatment and a case-quiz<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: medium;"><b><span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;"><i>Cardiology free e-book online</i></span></b></span> <span style="font-size: large;"><b>ECG QUIZ 1. An electrocardiography CASE-QUIZ: A patient with weakness and lightheadedness. </b></span><span style="font-size: large;"><b>What is the diagnosis and which should be the management ?</b></span><br />
<span style="font-size: large;">Watch the video and answer the question. Click on the symbol [] at the lower right corner of the video to see it enlarged: full screen)</span> <span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b><br /></b></span>
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<span style="font-size: large;"><b>THE ANSWER </b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Heart rate (ventricular rate) 30- 35/min. P waves are more frequent than the QRS complexes and they do not have any temporal relation with QRS complexes (some P waves even fall in the ST segment). This is a case of complete atrioventricular block. QRS has a right bundle branch block morphology. In general, complete atrioventricular (AV) block would be an indication for permanent pacing, but in this case the complete (third degree) AV block could be possibly caused by verapamil, which the patient has been taking for hypertension. So there is a potentially reversible cause for the AV block. When we suspect a reversible cause we do not implant a permanent pacemaker. Instead there is an indication for temporary pacing and discontinuation of the causal drug. The patient was admitted to the hospital, verapamil was discontinued and replaced by another antihypertensive agent, with no effect on conduction. The patient remained under observation with temporary transvenous pacing for 2 days. Two days after the discontinuation of verapamil the normal heart rhythm (normal atrioventricular conduction) recovered. So a permanent pacemaker was not implanted. </b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>In cases, where the complete AV block persists and is not reversible, or if there is no revesible cause for the block, implantation of a permanent pacemaker is absolutely indicated.</b></span><br />
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Bradycardia</b> is a ventricular rate (at rest) < 50 beats per minute (bpm) (cycle length 1200 </span><span style="font-size: large;">ms). Some cardiologists use 60 bpm (cycle length 1000 ms) as the lower limit </span><span style="font-size: large;">of the normal resting heart rate. Bradycardia is not always an abnormal finding. It can be normal, especially in the absence of </span><span style="font-size: large;">symptoms. Trained athletes, especially endurance athletes, usually have </span><span style="font-size: large;">bradycardia at rest and this is normal.</span><br />
<span style="font-size: large;">Bradycardia due to an abnormality of the conducting system of the heart is called "<b>bradyarrhythmia</b>". Many of these rhythm disorders are asymptomatic and benign, requiring no treatment, whereas some cause symptoms and need treatment with pacemaker implantation and others can be life threatening requiring rapid intervention.</span><br />
<span style="font-size: large;"><b>Symptoms of bradycardia or bradyarrhythmias</b> are nonspecific (i.e. the </span><span style="font-size: large;">symptom is not always directly correlated to the bradycardia and other causes should also be sought). Symptoms </span><span style="font-size: large;">include: fatigue, generalized weakness, </span><span style="font-size: large;">lightheadedness, presyncope, syncope, </span><span style="font-size: large;">dyspnea </span><span style="font-size: large;">on exertion. </span><br />
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<span style="font-size: large;">Bradyarrhythmias arise from abnormalities in one or more of three locations in the heart's conducting system: sinoatrial node, atrioventricular node, or infranodal (the His -Purkinje system).</span><span style="font-size: large;"></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br style="font-size: x-large;" /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>A female patient 78 years old with a history of hypertension and one-vessel coronary artery disease treated with a percutaneous coronary intervention (PCI) of the right coronary artery 3 years before (because of effort angina). She also has a history of asthma. One year before she had a myocardial perfusion scintigraphy (a technetium 99m SPECT scan) which did not reveal any ischemia of significant extent or any myocardial scar. She complains of episodes of fainting, or near-fainting (one episode of syncope and two presyncopal episodes during the last month). She is currently on medication with irbesartan -hydrochlorothiazide 300/25 mg per day, aspirin 100 mg per day ,atorvastatin 20 mg per day and an inhaled bronchodilator. Physical examination is normal and it also did not reveal orthostatic hypotension. Her blood tests revealed no significant abnormalities. Her 12 lead ECG shows sinus rhythm, a prolonged PR interval (first degree AV block) and a LBBB . Here is a part of her 24-hours Holter ECG recording. The patient did not have any symptoms during the recording. What are the findings ? Which could be the most probable cause ? What treatment do you propose ?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /><br />THE ANSWER<br /><br />The presence of PR prolongation and/or a bundle branch block in a patient with presyncopal or syncopal episodes, should raise a suspicion of a bradyarrhytmic cause (e.g. pauses due to sinus node dysfunction, or a transient second or third degree atrioventicular block). In this case the holter ECG recording shows sinus pauses with a duration of about 3-3,5 seconds. The most probable cause of sinus node dysfunction in this age group is idiopathic degenerative fibrosis of the conductive system. The patient does not take any medications whith an influence on sinus node function. A permanent pacemaker (type DDDR) was implanted and the patient is asymptomatic since then. (There was a class II indication for permanent pacing, since there is ECG evidence of sinus node dysfunction and symptoms compatible with the disorder are present, in the absense of another identifiable cause. If the patient had symptoms at the time of the recorded pauses, then the indication for pacing would be absolute- class I).</b></span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span>
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<b><span style="font-size: large;"><br /></span></b> <b><span style="font-size: large;">Sinus nodal or sinoatrial nodal (SA nodal) dysfunction </span><span style="font-size: large;">(sick sinus syndrome)</span></b><span style="font-size: large;"> </span></div>
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<span style="font-size: large;"><b>Causes of sinus node dysfunction</b> </span><span style="font-size: large;">have been classified as intrinsic or extrinsic. This classification is practical because </span><span style="font-size: large;">extrinsic causes are often reversible. In this case they</span><span style="font-size: large;"> should be corrected (if it is possible) and this way unnecessary pacemaker therapy can be avoided. </span><span style="font-size: large;">The most common causes of extrinsic sinus </span><span style="font-size: large;">node dysfunction are drugs and </span><span style="font-size: large;">influences of the </span><span style="font-size: large;">autonomic nervous system (stimulation of the parasympathetic nervous system via the vagus nerve or inhibition of the activity of the sympathetic nervous system can </span><span style="font-size: large;">suppress automaticity and/or slow conduction).</span></div>
<span style="font-size: large;"><u>Drugs</u> that can cause sinus node dysfunction are beta-blockers, non-dihydropyridine calcium channel blockers (verapamil, diltiazem), digoxin, ivabradine, a</span><span style="font-size: large;">ntiarrhythmic drugs, such as t</span><span style="font-size: large;">ype IA (quinidine, procainamide, disopyramide) ,Type IC (flecainide and propafenone) Type III (sotalol and amiodarone), s</span><span style="font-size: large;">ympatholytic antihypertensives (clonidine, methyldopa, reserpine) and other miscellaneous drugs (lithium, cimetidine, amitriptyline, phenytoin).</span><br />
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<span style="font-size: large;">Causes of sinus node dysfunction related to effects of the <u>autonomic</u> </span><span style="font-size: large;">nervous system include vasovagal syncope and generally situations of excessive vagal tone, the carotid sinus syndrome and endotracheal suctioning (via activation of the vagus nerve).</span><br />
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<span style="font-size: large;"><u>Other </u></span><span style="font-size: large;"><u>extrinsic</u> causes include hypothyroidism, sleep apnea, hyperkalemia, increased intracranial pressure, sepsis, hypothermia and hypoxia.</span></div>
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<span style="font-size: large;"><u>Intrinsic sinus node dysfunction</u> is often degenerative due to </span><span style="font-size: large;">fibrous replacement of the sinus node or its </span><span style="font-size: large;">connections to the atrium. This is more common in elderly individuals.</span></div>
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<span style="font-size: large;">Other causes of i</span><span style="font-size: large;">ntrinsic sinus node dysfunction are :</span></div>
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<span style="font-size: large;">Acute and chronic coronary artery disease (</span><span style="font-size: large;">in the </span><span style="font-size: large;">setting of acute myocardial infarction, typically inferior, the </span><span style="font-size: large;">abnormality can be transient).</span></div>
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<span style="font-size: large;"> Inflammatory processes such as </span><span style="font-size: large;">myocarditis (e.g viral myocarditis), rheumatic heart disease, </span><span style="font-size: large;">systemic lupus erythematosus (SLE), rheumatoid </span><span style="font-size: large;">arthritis and mixed connective tissue disease. </span></div>
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<span style="font-size: large;">Congenital heart disease (transposition of the great arteries/Mustard and Fontan repairs)</span><span style="font-size: large;"></span><br />
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<span style="font-size: large;">Familial causes of sinus node disease (miscellaneous genetic causes and also in rare familial syndromes such as Kearns-Sayre syndrome and myotonic dystophy.</span><br />
<span style="font-size: large;">Iatrogenic damage of the sinus node from direct injury in cardiothoracic surgical procedures, or radiotherapy.</span></div>
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<span style="font-size: large;"><b>Sinus node dysfunction (sick sinus syndrome) can be manifested with</b>:</span><span style="font-size: large;"> sinus bradycardia (with heart rate ≤ 50/min)</span><br />
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<span style="font-size: large;">Sinus <u>pauses</u>, of duration > 2 seconds ( </span><span style="font-size: large;">Generally pauses < 3 seconds are not a serious concern. However, </span><span style="font-size: large;">pauses > 3 seconds while the patient is awake are generally concidered abnormal). For a description of sinus pauses and sinoatrial exit block see below.</span><br />
<span style="font-size: large;"><u>Chronotropic incompetence</u>: inability to attain 80% of the maximum predicted heart rate in response to exercise. It can be associated with symptoms (such as fatigue, reduced exercise toleralce, dizziness with exercise). </span></div>
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<span style="font-size: large;">The <u>"tachy-brady" (tachycardia-bradycardia) syndrome</u>: when there are alternating periods of a supraventricular tachycardia (most commonly atrial fibrillation, but atrial flutter, or atrial tachycardia can also occur) with periods of sinus bradycardia or sinus pauses > 2 seconds. </span><span style="font-size: large;">In patients with tachycardia-bradycardia syndrome after conversion of tachyarrhythmias, long pauses may occur (post-conversion pause). Sinus bradycardia in some patients can facilitate the occurence of reentrant tachycardias, by magnifying discrepancies in the duration of the refractory period between different areas of the cardiac tissue. This is a phenomenon that occurs with longer cycle lengths.</span><br />
<span style="font-size: large;"><u> Sinus pauses</u></span><br />
<span style="font-size: large;">The sinus node may fail to deliver an electrical impulse to the atria for a time interval and this is manifested on the ECG by the absence of P waves and also absence of cardiac electical activity, until a sinus impulse appears, or until an escape pacemaker (an other focus of conductive tissue) depolarizes and generates an impulse. This can happen because of a sinus arrest or sinus pause, which occurs when the sinus node does not depolarize on time, or because of sinoatrial (SA) exit block. In SA exit block the sinus node generates electrical impulses, some of which are blocked on their exit from the sinus node to the atrial tissue. SA exit block produces on the ECG an abnormality very similar to sinus arrest. SA exit block may be distinguished from sinus arrest by the fact that the pause is a multiple of the sinus PP interval (the interval between two consecutive sinus P waves before the pause)</span><br />
<span style="font-size: large;"></span><span style="font-size: large;">Brief, asymptomatic sinus pauses are a common finding and do not require treatment. Generally pauses < 3 seconds are not a serious concern and can be seen in Holter ECG monitoring in up to approximately 10% of normal persons. They are also more common in athletes. Pauses lasting > 3 seconds, especially if they occur while the patient is awake are considered abnormal.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <span style="font-size: large;"><u>Treatment</u>:<br />For sinus node dysfunction (sick sinus syndrome) implantation of a permanent pacemaker is generally indicated only when symptoms that correlate to this disorder </span><span style="font-size: large;">are present -this is a class I indication</span><span style="font-size: large;"> (or it may be indicated if symptoms compatible with the disorder are present, in the absense of another identifiable cause-a class II indication). These pacing indications are valid for cases where sinus node dysfunction is not the result of a reversible cause. 3) Sinus node disease. </span><br />
<span style="font-size: large;">Pacing is not indicated in patients with sinus node dysfunction, or sinus bradycardia which is asymptomatic or due to reversible causes. </span><br />
<span style="font-size: large;"><b>Atrioventricular (AV) node or His-Purkinje system disorders (disorders of atrioventricular conduction)</b></span><br />
<span style="font-size: large;">Their etiologies can classified as functional (which are often reversible) or structural. The most common</span><span style="font-size: large;"> cause of atrioventricular (AV) block is idiopathic fibrosis of the heart's conductive system (Lenegre’s disease and Lev’s disease). </span><span style="font-size: large;">This, of course, is a structural cause and it is not reversible also.</span></div>
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<span style="font-size: large;">Other structural causes include: Acute myocardial infarction (MI) : AV block in </span><span style="font-size: large;">patients with acute inferior MI</span><span style="font-size: large;"> is more common (occuring approximately in 14%-15 % of patients) and less common in </span><span style="font-size: large;">those with anterior infarction, (</span><span style="font-size: large;">2%). AV block occurs usually within the first 24 hours of an acute MI,</span><span style="font-size: large;"> most commonly, it is first-or second-degree AV </span><span style="font-size: large;">block, but complete heart block can also occur.</span><span style="font-size: large;"> I</span><span style="font-size: large;">n acute inferior MI the </span><span style="font-size: large;">level of block</span><span style="font-size: large;"> is usually </span><span style="font-size: large;">in the AV node, resulting in more stable, </span><span style="font-size: large;">escape rhythms with </span><span style="font-size: large;">narrow QRS complex . In </span><span style="font-size: large;">contrast in acute anterior MI </span><span style="font-size: large;"> the </span><span style="font-size: large;">level of block is usually </span><span style="font-size: large;"> in the </span><span style="font-size: large;">His bundle, or bundle branches resulting in </span><span style="font-size: large;">unstable escape rhythm with a</span><span style="font-size: large;"> wide QRS </span><span style="font-size: large;">complex and a worse prognosis (high </span><span style="font-size: large;">mortality rates).</span></div>
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<span style="font-size: large;">Chronic coronary artery disease can also cause AV block.</span></div>
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<span style="font-size: large;">Calcific valvular disease</span></div>
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<span style="font-size: large;">Cardiomyopathies and infiltrative diseases of the heart can also cause disorders of AV conduction (AV block). Infiltrative diseases are conditions caused by the accumulation in tissues of substances or cells not normally found in those tissues, such as amyloidosis, hemochromatosis and sarcoidosis</span><span style="font-size: large;"> </span></div>
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<span style="font-size: large;">Infectious and inflammatory disorders such as endocarditis myocarditis (Chagas disease, Lyme disease, rheumatic fever, etc)</span></div>
<span style="font-size: large;">Collagen vascular diseases (scleroderma, rheumatoid arthritis, systemic lupus erythematosus, Reiter’s syndrome, ankylosing spondylitis, and polymyositis)</span></div>
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<span style="font-size: large;">Iatrogenic AV block is not uncommon. It may occur as a consequence of mitral or aortic valve surgery, or catheter ablation.</span><span style="font-size: large;"></span><br />
<span style="font-size: large;"> Congenital heart disease, such as congenital complete heart block ostium primum atrial septal defect and transposition of the great vessels can also cause AV block</span></div>
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<span style="font-size: large;">Functional causes of AV block are common and include drugs ( beta-blockers, </span><span style="font-size: large;">nondihydropyridine </span><span style="font-size: large;">calcium channel blockers d</span><span style="font-size: large;">igoxin, </span><span style="font-size: large;">antiarrhythmic drugs)</span></div>
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<span style="font-size: large;">Effects exerted via the autonomic nervous system ( vasovagal syncope, carotid sinus syndrome) hyperkalemia, hypermagnesemia.</span></div>
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<b>Atrioventricular (AV) node or His-Purkinje system disorders can be manifested as:</b></div>
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<span style="font-size: large;">A <u>first-degree AV block</u>: </span><span style="font-size: large;">PR interval prolongation (PR duration >200 ms).</span><br />
<span style="font-size: large;">A <u>second-degree AV block</u>, which is further classified in two types:</span><br />
<span style="font-size: large;"><u>Mobitz I (Wenckebach)</u>: The ECG shows progressive PR interval</span><br />
<span style="font-size: large;">prolongation followed by a single blocked P wave. In some cases the progressive lengthening of the PR interval </span><span style="font-size: large;">may be subtle. The best way to assess it is to measure the PR interval of the beat which is </span><span style="font-size: large;">immediately prior to a blocked P wave and the PR of the beat immediately after </span><span style="font-size: large;">a blocked P wave. The latter should be shorter.</span><br />
<span style="font-size: large;">In this type of atrioventricular (AV) block, the most common site of block is in the AV node.</span><br />
<span style="font-size: large;"><u>Mobitz II:</u> There is no progressive PR interval prolongation</span><br />
<span style="font-size: large;">before a blocked P wave. The PR interval is constant but there is intermittent conduction of the atrial electrical impulses to the ventricles, so that some P waves are not followed by a QRS complex. In </span><span style="font-size: large;">Mobitz II AV block, the </span><span style="font-size: large;">most common site of block</span><br />
<span style="font-size: large;">is infranodal (in the His-Purkinje system).</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">A special case is a <u>2:1 AV block</u>, where every second P wave is conducted to the ventricles (followed by a QRS).</span><br />
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<span style="font-size: large;"><u>Third-degree (complete) AV block, or complete heart block</u></span><br />
<span style="font-size: large;">There is no temporal association between P waves and QRS</span><br />
<span style="font-size: large;">complexes, because there is no conduction of atrial impulses (P waves) to the ventricles. Thus, the ventricular rhythm is an escape rhythm originating from a secondary pacing site and not from transmission of sinus impulses.</span><br />
<span style="font-size: large;">This ventricular escape rhythm, if it is characterized by narrow QRS complexes, is called a junctional escape rhythm. Usually in these cases the site of block is</span><span style="font-size: large;"> in the AV node.</span><br />
<span style="font-family: inherit; font-size: large;">If QRS complexes are wide (≥ 120 msec) the </span><span style="font-size: large;">block is infranodal, i.e. below the AV node, in the His- Purkinje system.</span></div>
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<span style="font-size: large;">The autonomic nervous system exerts an important effect on the function of the AV node but it only minimally influences the His bundle and the distal conducting system. Thus, the influence of the autonomic system on the production and conduction of electrical impulses in the heart is mainly on the sinus node and the AV node.</span><br />
<span style="font-size: large;">The AV node is highly innervated with postganglionic sympathetic and </span><span style="font-size: large;">parasympathetic nerves.</span><br />
<span style="font-size: large;"><b>Treatment of bradycardia and heart block </b>is needed </span><span style="font-size: large;">if there are symptoms such as syncope, lightheadedness, dyspnea (shortness of breath), ischemic chest pain and/or evidence of hemodynamic compromise or low cardiac output. If bradycardia is attributed to the effect of a drug, then this drug should be discontinued, if possible.However, if cessation of drug therapy considered as the cause of the bradycardia for a reasonable duration of time does not result in improvement, or drug therapy is </span><span style="font-size: large;">needed for an indication (e.g. a paroxysmal tachyarrhythmia) then </span><span style="font-size: large;">the implantation of a permanent pacemaker should be considered.</span><br />
<span style="font-size: large;">If rapid treatment of bradycardia is needed, because of the presense of serious symptoms, or hypotension the next step is intravenous administration of atropine. Infusion of isoproterenol, may be required in acutely decompensated patients if atropine fails, until pacing can be initiated. Temporary pacing is more effective than atropine or isoproterenol for decompensated patients with serious bradycardia. Temporary pacing includes:<br />External transcutaneous pacing, which can be rapidly and easily instituded, but it is used only for a short period of time, due to the unpredictable transcutaneous capture and also because it is poorly tolerated by the patient.<br />Transvenous temporary pacing, via the insertion of a pacing electrode through the subclavian or the internal jugular vein into the right ventricle. This is the most effective and reliable method of temporary pacing.</span></div>
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<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Implantation of a permanent pacemaker</b> is indicated in all patients with <u>symptomatic</u> bradycardia (caused by sinus node dysfunction, or any type of second or third degree AV block-even Mobitz I if it results in <u>symptoms</u>), when bradycardia is not due to </span><span style="font-size: large;">a reversible cause. When symptomatic sinus bradycardia, sinus pauses, or AV block is attributed to the effects of drug treatment (for examle treatment with beta blockers, diltiazem, verapamil, or antiarrhythmic agents) the following general rules should be followed : </span></div>
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<span style="font-size: large;">If this treatment is not absolutely necessary, these drugs should be disontinued. Then, if the bradyarrhythmia terminates, no pacemaker is indicated. </span></div>
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<span style="font-size: large;">If symptomatic bradycardia is attributed to an absolutely necessary drug treatment, then a permanent pacemaker is implanted and drug treatment is continued.</span></div>
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<span style="font-size: large;"> A permanent pacemaker is also indicated <u> in asymptomatic patients with aqcuired Mobitz type 2 block, </u></span><span style="font-size: large;"><u> </u></span><span style="font-size: large;"><u>or complete (third degree) AV block,</u> because these types of block are assossiated with a high risk for the development of profound </span><span style="font-size: large;">bradycardia and syncope (This is a class I indication according to ESC guidelines on cardiac pacing-2013).</span><br />
<span style="font-size: large;"> Permanent pacing is also indicated in </span><span style="font-size: large;">2:1 infranodal block, and it </span><span style="font-size: large;"> should be considered in patients with second-degree type 1 AV block if it causes symptoms or if it is found to be located at intra- or infra-His levels at an electrophysiologic study.(This is a class IIa indication, according to the ESC guidelines on cardiac pacing-2013). Pacing is not indicated in patients with AV block which is due to reversible causes (i.e. a class III indication).</span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;"><br /></span></b></span>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<span style="color: #cc0000; font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-size: x-large;"><br /></span> <span style="font-size: large;"></span> <span style="color: #38761d; font-size: large;"><b>Bibliography and useful links :</b></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><a href="http://circ.ahajournals.org/content/112/24_suppl/IV-67" target="_blank">AHA Guideline: Management of Symptomatic Bradycardia and of Symptomatic Tachycardia in the acute setting.</a></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Harrigan R A, Brady W JThe Clinical Challenge of Bradycardia: Diagnosis, Evaluation, and Intervention in the Emergency Department. Emergency Medicine Reports, 2000, ahcmedia.com. </b></span><br />
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<span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b><br /></b></span> <span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b><br /></b></span> <span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b><br /></b></span> <span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b><br /></b></span> <span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b><br /></b></span> <span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b><br /></b></span><br />
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<span style="background-color: white; color: #444444; font-family: "roboto" , sans-serif; font-size: 16px; line-height: 26.4px;"><b>LINK: </b> </span><a href="https://www.ahcmedia.com/articles/58758-the-clinical-challenge-of-bradycardia-diagnosis-evaluation-and-intervention" style="font-family: Roboto, sans-serif; font-size: 16px; line-height: 26.4px;" target="_blank">https://www.ahcmedia.com/articles/58758-the-clinical-challenge-of-bradycardia-diagnosis-evaluation-and-intervention</a></div>
<span style="font-family: inherit; font-size: large;"></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/34/29/2281.full.pdf" target="_blank">ESC (2013) Guidelines on cardiac pacing and cardiac resynchronization therapy</a></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-family: inherit; font-size: medium;">Deal N.Evaluation And Management Of Bradydysrhythmias In The Emergency Department. </span><span style="font-size: medium;">Emergency Medicine Practice, 2013;15:1-16.</span></span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK</span> <a href="http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=377" target="_blank">http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=377</a></b><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <span style="font-size: large;"><a href="http://circ.ahajournals.org/content/127/3/e283" target="_blank">Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities</a></span><br />
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<a href="http://circ.ahajournals.org/content/circulationaha/117/21/e350.full.pdf" target="_blank"><span style="font-size: large;">ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities</span></a><br />
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<a href="http://eurheartj.oxfordjournals.org/content/ehj/30/21/2631.full.pdf" target="_blank"><span style="font-size: large;">Guidelines for the diagnosis and management of syncope (version 2009)</span></a></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-18547850706139855222016-08-20T22:59:00.003+03:002020-02-10T03:27:24.547+02:00Tachyarrhythmias-supraventricular and ventricular tachycardias <div dir="ltr" style="text-align: left;" trbidi="on">
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<h3>
<span style="font-size: large;">Tachycardia, sinus tachycardia and tachyarrhythmias</span></h3>
<span style="font-family: inherit; font-size: large;"><b>Tachycardia</b> is a heart rate >100 beats per minute. </span><br />
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<span style="font-family: inherit; font-size: large;"><b>Sinus tachycardia </b>is a normal response to physiologic demand, i.e. a need for an increased cardiac output under certain conditions such as exercise, emotional or physical stress, fever, anemia, hypermetabolic states (hyperthyroidism) and volume depletion. Tachycardias of other etiologies are <b>tachyarrhythmias.</b></span><br />
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<span style="font-size: large;"><b>Pathophysiologic mechanisms of tachyarrhythmias</b></span></h3>
<b><span style="font-family: inherit; font-size: large;"><span lang="EN-US">T</span></span><span style="font-size: large;">achyarrhythmias.</span></b><span style="font-family: inherit; font-size: large;"><span lang="EN-US"> </span><span lang="EN-US">like all arrhythmias, are caused by</span><span lang="EN-US"> disorders of impulse formation or </span><span lang="EN-US">disorders of impulse propagation. </span></span><br />
<span style="font-family: inherit; font-size: large;"><span lang="EN-US">Tachycardias caused by disorders of impulse formation are called focal tachycardias. In focal tachycardias, an ectopic (not the sinus node) site generates impulses, that propagate in the myocardium and overdrive the sinus node. This means that the sinus node undergoes <b>overdrive suppression</b>, which is the inhibition of pacing activity of an area of the myocardium, due to the higher frequency of the electrical impulses originating from another site.</span></span><span style="font-size: large;"> The increased frequency of depolarizations of a site in the myocardium </span><span style="font-size: large;">by electrical impulses conducted by adjacent cells has the following consequences. If that </span><span style="font-size: large;">frequency of depolarization of a myocardial area exceeds its intrinsic pacing rate, that leads to an increase in intracellular sodium ions in this area. </span><span style="font-family: inherit; font-size: large;">This increased sodium stimulates the Na</span><sup style="font-family: inherit;">+</sup><span style="font-family: inherit; font-size: large;">-K</span><sup style="font-family: inherit;">+</sup><span style="font-family: inherit; font-size: large;">-ATPase and because this pump is electrogenic it increases the amount of hyperpolarizing currents, driving the membrane potential more negative.</span><span style="font-size: large;">This prevents the depolarizing pacemaker currents (If) of the cells from depolarizing the cell membrane to its threshold potential, and thereby prevents the spontaneous generation of action potentials.</span><br />
<span style="font-size: large;"> On the contrary, in normal sinus rhythm, the sinus node, as the pacemaker with the highest intrinsic rate, exerts overdrive suppression to all other cardiac foci that have a capability of pacemaker function, by the above mechanism.</span><br />
<span style="font-size: large;"><b>Disorders of impulse formation</b> causing tachyarrhythmias consist of abnormal automaticity and triggered activity.</span><br />
<span style="font-size: large;"><b>Abnormal automaticity:</b> </span></div>
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<span style="font-size: large;">Automaticity is the capacity of pacemaker function and is due to a gradual depolarization of the resting (phase 4) membrane potential of a myocardial cell membrane to the point of the action potential threshold. Automaticity is abnormal when an ectopic site’s rate of discharge is accelerated to overdrive the natural sinus heart rate. <br /><b>Triggered activity</b></span></div>
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<span style="font-size: large;">It is the occurrence of afterdepolarizations, cell membrane depolarizations that occur after the initial phases of the action potential.Triggered activity can cause polymorphic ventricular tachycardia, (torsades de pointes), or ventricular fibrillationVF. There are two types of afterdepolarizations:<br />Early afterdepolarizations (EADs): Occur during the plateau (phase 2), or repolarization (phase 3) of the action potential and are probably associated with calcium overload. They are associated with prolonged QT and torsades de pointes<br />Delayed afterdepolarizations (AEDs): Occur after repolarization (phase 3) is complete.They are associated clinically with digoxin toxicity.</span></div>
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<span style="font-size: large;"><b>Disorders of impulse propagation:</b> </span></div>
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<span style="font-size: large;">They include reentry and fibrillation.</span></div>
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<span style="font-size: large;"><b>Reentry</b> occurs when there is a functional circuit, where the electrical impulse can circulate repeatedly. A functional circuit can be defined by an anatomic obstacle, such as the scar of a previous myocardial infarction, or the tricuspid valve, or the circuit can be not anatomical but physiological, such as created by an area of abnormal electrophysiologic properties (refractoriness). Reentry also requires the presence of unidirectional conduction block in one limb of the circuit (typically refractoriness to a premature impulse). The impulse is then conducted through the other limb of the circuit which has a shorter refractory period and slower conduction. If the refractory limb recovers excitability as the impulse returns in the retrograde direction, the impulse will circulate through the circuit. So reentry is a circular conduction of an electrical impulse through a circuit in the myocardium. <br /><b>Fibrillation</b> is the chaotic, disorganized electrical activation of the muscle. It may involve both abnormal impulse formation and abnormal impulse propagation. <br />Tachyarrhythmias are classified in: <br /><b>Supraventricular</b> where the origin of the abnormal rhythm is confined to the atrium (atrial arrhythmias) or the mechanism that generates the arrhythmia is not confined to the atria but includes various supraventricular structures (paroxysmal supraventricular arrhythmias-PSVTs).</span><span style="font-size: large;"> A better definition is that supraventricular tachyarrhythmias originate from or are dependent on conduction through the atrium, or atrioventricular (AV) node to the ventricle. In supraventricular arrhythmias, the arrhythmia circuit always involves supraventricular tissue and depending on the type of the arrhythmia it may also involve ventricular tissue or not.</span><br />
<span style="font-size: large;"><b>Ventricular</b>: The abnormal rhythm originates in ventricular structures (usually ventricular myocardium, but may also originate in the His-Purkinje system). The arrhythmia circuit involves only ventricular tissue.</span><br />
<h3>
<br style="font-size: x-large;" /><b style="font-size: x-large;">Supraventricular tachyarrhythmias</b></h3>
<span style="font-size: large;"><b>Symptoms of supraventricular arrhythmia</b> depend on the rate, duration, associated heart disease, and comorbidities and include palpitations (which is the most common presenting symptom), fatigue or diminished exertional capacity, dyspnea, chest pain and rarely syncope. Rarely, a supraventricular arrhythmia can precipitate cardiac arrest in patients with the Wolff-Parkinson-White syndrome, or in patients with severe heart disease, such as hypertrophic cardiomyopathy, or severe aortic valve stenosis.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">Most supraventricular tachyarrhythmias produce tachycardia with a narrow <b>QRS complex </b>(QRS duration <120 ms). The presence of a narrow QRS is characteristic of ventricular activation over the physiologic route, the His- Purkinje system. </span></div>
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<span style="font-size: large;">A supraventricular tachycardia may have </span><span style="font-size: large;">a wide QRS complex when there is</span><span style="font-size: large;"> c</span><span style="font-size: large;">onduction block in the left or right bundle branch, or if there is activation of the ventricle from an accessory pathway. Such a tachyarrhythmia must be distinguished from ventricular tachycardia. The prognosis of a supraventricular tachyarrhythmia varies depending on the mechanism and more importantly on the underlying cardiac disease (if any). </span><br />
<span style="font-size: large;">A nonsustained supraventricular tachycardia is one of brief duration with spontaneous termination. </span></div>
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<span style="font-size: large;">A sustained supraventricular tachycardia has a longer duration and an intervention, such as cardioversion or drug administration, is required for termination.</span><br />
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<span style="font-size: large;"><b>Paroxysmal supraventricular tachycardia (PSVT)</b>: </span></h4>
<span style="font-size: large;">is characterized by episodes of tachycardia that occur with sudden onset and termination. It includes atrioventicular node reentry tachycardia (AVNRT), atrioventricular reentry tachycardia using an accessory pathway (AVRT) and some cases of atrial tachycardia (AT). </span><br />
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<h4>
<span style="font-size: large;"><b>Differential Diagnosis for Narrow QRS-Complex Tachycardia </b></span></h4>
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<span style="font-size: large;">If ventricular activation (QRS) is narrow (less than 120 msec), then the tachycardia is almost always supraventricular. To diagnose its mechanism (the specific type of the tachycardia) one must know the following: If no P waves or evidence of atrial activity is apparent and the RR interval is regular, then the tachycardia is more commonly an atrioventricular nodal reentry tachycardia AVNRT. Sometimes P-wave activity in AVNRT may be only partially hidden within the QRS complex and may deform the QRS to give a pseudo-R wave in lead V1 and/or a pseudo-S wave in inferior leads (II, III,avF).</span><br />
<span style="font-size: large;"> If a P wave is present in the ST segment and separated from the QRS by 70 ms or more, then the tachycardia </span><span style="font-size: large;">is most likely an atrioventricular reentry tachycardia </span><span style="font-size: large;">AVRT . Typical AVNRT and AVRT are <u>tachycardias with a short RP</u> (i.e. a short time interval from the QRS to the next P wave: the P wave is nearer to the preceding than the next QRS). </span><br />
<span style="font-size: large;"><u>Tachycardias with RP longer than PR </u>(the P waves are near the next QRS complex), are the following : sinus tachycardia, atypical AVNRT, permanent form of junctional reciprocating tachycardia (PJRT, which is a type of AVRT via a slowly conducting accessory pathway, or atrial tachycardia (AT).</span><br />
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<h4>
<span style="font-size: large;"><b>Differential Diagnosis for Wide QRS-Complex Tachycardia:</b></span></h4>
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<span style="font-size: large;"> If the QRS is >120 ms, then it is important to differentiate between </span><span style="font-size: large;">ventricular tachycardia (VT) which is the most probable cause and supraventricular tachycardia.</span><span style="font-size: large;"> In case of a wide QRS tachycardia intravenous verapamil or diltiazem, should be avoided. They may be deleterious because they can precipitate hemodynamic collapse for a patient with ventricular tachycardia.</span></div>
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<span style="font-size: large;">Stable vital signs during tachycardias cannot be used to reliably distinguish supraventricular tachycardia (SVT) from VT. If the diagnosis of SVT cannot be proven or cannot be made easily, then the patient should be treated as a patient with VT.</span></div>
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<span style="font-size: large;"> Wide-QRS tachycardia can be divided into three groups: VT, SVT with bundle-branch block (BBB) or aberration and SVT with AV conduction over an accessory pathway.</span></div>
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<h4>
<span style="font-size: large;"><b>Atrioventricular nodal reentry tachycardia (AVNRT)</b></span></h4>
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<span style="font-size: large;">In AVNRT there are two functionally different </span><span style="font-size: large;">pathways predominantly within the atrioventricular node (AV node). This is termed "dual AV nodal physiology". In order to understand the physiology of reentry one must remember the concept of the refractory period. </span><span style="font-size: large;">Once a myocardial cell has an action potential (electrical activation) its</span><span style="font-size: large;"> sensitivity to further stimulation </span><span style="font-size: large;">decreases for a time interval, called the <b>refractory </b></span><span style="font-size: large;"><b>period</b>. The first part of the refractory period, during which complete </span><span style="font-size: large;">insensitivity to any stimulus </span><span style="font-size: large;">exists, is called the absolute refractory period. </span><span style="font-size: large;">The second part of the refractory period, called the relative </span><span style="font-size: large;">refractory period, follows the absolute refractory period. During the relative refractory period the cell can be stimulated but a stronger than usual electrical signal is needed to achieve stimulation of the cell and initiation of a new action potential. </span><span style="font-size: large;">In AVNRT the <b>two functionally different </b></span><span style="font-size: large;"><b>pathways</b> that exist predominantly within the AV node are the following: </span><span style="font-size: large;">There is a pathway with a short refractory period and slow conduction and another pathway with a longer refractory period and fast conduction. In sinus rhythm, the atrial impulse is usually conducted to the ventricles through </span><span style="font-size: large;">the </span><span style="font-size: large;">fast </span><span style="font-size: large;">pathway. If an atrial impulse (an atrial premature </span><span style="font-size: large;">beat) </span><span style="font-size: large;">occurs early when the fast pathway is still refractory, </span><span style="font-size: large;">the impulse is conducted to the ventricles through the slow pathway (since it has a shorter refractory period)</span><br />
<span style="font-size: large;">Meanwhile, the fast pathway has the time to recover its excitability and so the electrical impulse travels back through the fast pathway. Then it is conducted again through the slow pathway and this circular movement of the impulse continues.</span><span style="font-size: large;"> initiating the </span><span style="font-size: large;">most </span><span style="font-size: large;">common "slow-fast", or <b>typical, AVNRT.</b></span><br />
<span style="font-size: large;">In atrioventricular </span><span style="font-size: large;">nodal reentry tachycardia (AVNRT) <b>the ECG </b>shows regular QRS </span><span style="font-size: large;">complexes, usually at a rate of 140–240/minute. The QRS complexes are usually narrow but s</span><span style="font-size: large;">ometimes they have a typical bundle </span><span style="font-size: large;">branch block morphology.</span><br />
<span style="font-size: large;">In AVNRT <u>P waves</u> are either:</span><br />
<span style="font-size: large;"> Not visible ("buried" in the QRS complex- this is common) or </span><br />
<span style="font-size: large;">seen </span><span style="font-size: large;">immediately before the </span><span style="font-size: large;">QRS complex</span><span style="font-size: large;"> (this is rare and is manifested by pseudo-q waves in the inferior leads) or</span><br />
<span style="font-size: large;"> seen immediately after the QRS complex (this is common and is manifested as pseudo -r wave in V1, and small pseudo-s waves in leads II, III, and avF).</span><br />
<span style="font-size: large;"> This close proximity of the P wave to the QRS, occurs because the reentrant circuit is in the AV node- in proximity to both the atria and the ventricles- and retrograde atrial activatio</span><span style="font-size: large;">n is usually through the fast pathway. </span><span style="font-size: large;">Thus, <u>in AVNRT there is almost simultaneous atrial and ventricular activation</u></span><span style="font-size: large;"><u>.</u></span><br />
<span style="font-size: large;">An exception to the above, is <u>fast-slow or atypical AVNRT</u> (</span><span style="font-size: large;">5% of cases), where the electrical stimulus is conducted antegradely, from atria to ventricles, through the fast pathway and retrogradely from the ventricles to the atria through the slow pathway. This causes</span><span style="font-size: large;"> the P wave to be near the next QRS complex (since conduction from the atria to the ventricles is rapid, through the fast pathway) and away from the previous QRS complex (since conduction from the ventricles to the atria is through the slow pathway). This situation is the opposite of what is happening in the usual (typical) form of AVNRT (which is a tachycardia with a short RP interval). Thus, the atypical fast-slow AVNRT is a supraventricular tachycardia with a short PR and long RP interval, thus </span><span style="font-size: large;">mimicking an atrial tachycardia or a permanent junctional reciprocating tachycardia (PJRT). </span><br />
<span style="font-size: large;"><u>P </u></span><span style="font-size: large;"><u>wave morphology in AVNRT :</u> In all kinds of AVNRT (typical slow-fast, or atypical fast-slow) the P wave (when it is identifiable) is negative in leads II, III </span><span style="font-size: large;">and aVF, and biphasic with a terminal positive com</span><span style="font-size: large;">ponent in V1. (These characteristics are opposite of those of the sinus P wave). </span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi40G29gmFVA54VTiwQVmlG2STqPA-YXC2_bdwwxF1MM2OlXDg3t6peXK87rvL_gmUgPRPfd4raJfT4bwa55Wn5KvTgzB1koiT2Ec_reF50ymfut-TBuZcxqYb8GlcjVIIHSC3YlmTwfms/s1600/%25CE%25B7%25CE%25BA%25CE%25B3+AVNRT+%25CE%25BD%25CE%25AC%25CF%2583%25CF%2584%25CE%25B1%25CF%2582+%25CF%2583%25CF%2580%25CF%2585%25CF%2581%25CE%25AF%25CE%25B4%25CF%2589%25CE%25BD+%25CF%2580%25CE%25B1%25CF%2581%25CE%25BF%25CE%25BE%25CF%2585%25CF%2583%25CE%25BC+%25CF%2585%25CF%2580%25CE%25B5%25CF%2581%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB+%25CF%2584%25CE%25B1%25CF%2587%25CF%2585%25CE%25BA%25CE%25B1%25CF%2581%25CE%25B4%25CE%25AF%25CE%25B1+001.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="" border="0" data-original-height="292" data-original-width="1600" height="116" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi40G29gmFVA54VTiwQVmlG2STqPA-YXC2_bdwwxF1MM2OlXDg3t6peXK87rvL_gmUgPRPfd4raJfT4bwa55Wn5KvTgzB1koiT2Ec_reF50ymfut-TBuZcxqYb8GlcjVIIHSC3YlmTwfms/s640/%25CE%25B7%25CE%25BA%25CE%25B3+AVNRT+%25CE%25BD%25CE%25AC%25CF%2583%25CF%2584%25CE%25B1%25CF%2582+%25CF%2583%25CF%2580%25CF%2585%25CF%2581%25CE%25AF%25CE%25B4%25CF%2589%25CE%25BD+%25CF%2580%25CE%25B1%25CF%2581%25CE%25BF%25CE%25BE%25CF%2585%25CF%2583%25CE%25BC+%25CF%2585%25CF%2580%25CE%25B5%25CF%2581%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB+%25CF%2584%25CE%25B1%25CF%2587%25CF%2585%25CE%25BA%25CE%25B1%25CF%2581%25CE%25B4%25CE%25AF%25CE%25B1+001.jpg" title="ECG AVNRT supraventricular tachycardia- cardiology book" width="640" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>ECG: atrioventricular nodal reentry tachycardia AVNRT (Click on the photo to see it larger )</b></span></td></tr>
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<h4>
<b style="font-size: x-large;">Atrioventricular reentry (or atrioventricular reciprocating) tachycardia -AVRT </b></h4>
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<span style="font-size: large;">It is the most common arrhythmia that can occur in Wolff Parkinson White (WPW) syndrome. (The second most common arrhythmia in WPW is atrial fibrillation.) The mechanism of AVRT involves a reentrant circuit that includes the atrioventricular (AV) node and an accessory pathway.<br />AVRT is classified into orthodromic or antidromic depending on the direction of conduction over the atrioventricular (AV) node.<br />Orthodromic AV reciprocating tachycardia (Orthothromic AVRT): The antegrade conduction of the electrical impulse (from the atria towards the ventricles) occurs down the AV node and retrograde conduction (from the ventricles to the atria) occurs through the accessory pathway.This is the most common form of AVRT (95%)<br />Orthodromic AVRT may occur with a manifest or concealed accessory pathway. A manifest accessory pathway is one that has the capability of antegrade conduction (from the atria to the ventricles) and usually these pathways have the capability of retrograde conduction (from the ventricles to the atria) as well. It is called a manifest accessory pathway because in sinus rhythm its presence can be recognized from the ECG findings (short PR interval < 120 msec, a slurring of the initial part of the QRS called delta wave, prolonged QRS and secondary ST-T wave changes. This the ECG pattern of the Wolff-Parkinson -White syndrome).</span></div>
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<span style="font-size: large;">On the contrary, a concealed accessory pathway can conduct only in </span><span style="font-size: large;">the retrograde direction and so its presence cannot be detected in the baseline ECG: In this case the baseline ECG in sinus rhythm has a normal appearance.</span></div>
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<span style="font-size: large;"> In summary, both these types of accessory pathways can participate in the mechanism of AVRT (atrioventricular reciprocating or atrioventricular reentry tachycardia).</span></div>
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<span style="font-size: large;">In orthodromic AVRT the ECG shows a narrow-complex regular tachycardia (the QRS is not prolonged since conduction to the ventricles occurs through the normal route: AV node and His-Purkinje system, except if there is a bundle branch block) and usually a retrograde P wave can be seen after the QRS complex, on the ST segment. In orthodromic AVRT the RP interval is smaller than the PR interval, but there is also another useful feature: In orthodromic AVRT the RP is usually > 70 msec (in contrast to the AVNRT where RP < 70 msec and the P waves are often "hidden" in the QRS). In some cases of orthodromic AVRT, P waves cannot be seen on the ECG (this is not infrequent). Then the ECG cannot be distinguished from the ECG of AVNRT. Orthodromic AVRT represents about 30% of all regular supraventricular tachycardias (supraventricular tachycardias with an almost constant heart rate during the tachycardia).</span></div>
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<span style="font-size: large;">In contrast to AV nodal reentry tachycardia (AVNRT), in </span><span style="font-size: large;"> </span><span style="font-size: large;">AVRT atrial and ventricular activation is not </span><span style="font-size: large;">simultaneous and for this reason, t</span><span style="font-size: large;">he symptom of neck pounding, often </span><span style="font-size: large;">experienced by patients with AVNRT, usually is not present in AVRT. For the same reason, </span><span style="font-size: large;">cannon A waves usually do not occur in AVRT.</span></div>
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<span style="font-size: large;">Antidromic AV reciprocating tachycardia (ART):<br />Tachycardia conducts antegrade down the accessory pathway and retrograde up the AV node, or a second accessory pathway. Antidromic AVRT, since ventricular activation occurs via the accessory pathway and not via the normal conduction system, shows on the ECG broad QRS complexes >120 msec. Thus antidromic AVRT is a wide- complex tachycardia which can be mistaken for a ventricular tachycardia. It is rare (about 5 % of AVRT).</span></div>
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<span style="font-size: large;">The acute management of both AV reciprocating tachycardia via an accessory pathway (AVRT) and AV node reentry tachycardia (AVNRT) is the same : vagal maneuvers (that activate the parasympathetic nervous system) or intravenous administration of drugs blocking conduction in the AV node (such as adenosine, beta blockers, verapamil)-see the section below.</span></div>
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<span style="font-size: medium;"><br /></span> <span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>What kind of rhythm is that?</b></span></span><br />
<span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>The initial ECG and the ECG after administration of intravenous adenosine is shown</b></span></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEicP_ewWwCw5Z-SOvKD3yRBpdIgVQYIyBANLsGnzIhM8VfaWek8SPPF5phuQeCPSHRZrnc4QqCfzXbbNUWY_9duEF33t5LDXe5lGIYZ1LsaCbB_X9Zy2X7uQdgbuVK6uEjDeEdxVJd-EoU/s1600/Orthodromic-AVRT+life+in+the+fast++lane.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1057" data-original-width="1600" height="422" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEicP_ewWwCw5Z-SOvKD3yRBpdIgVQYIyBANLsGnzIhM8VfaWek8SPPF5phuQeCPSHRZrnc4QqCfzXbbNUWY_9duEF33t5LDXe5lGIYZ1LsaCbB_X9Zy2X7uQdgbuVK6uEjDeEdxVJd-EoU/s640/Orthodromic-AVRT+life+in+the+fast++lane.jpg" width="640" /></a></div>
<span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span></span> <span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span></span>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj0xtvXxrNp0hUywsj1K_9FlC5q9RVl3iZLM0RwTgfC-L_M7eJ1njwccXmtH9MjZ_JdEWPxLH4nZyHyfjDuNz8NzdKUkzMBK2aVMU1T7_1YRunh-WbtkD7_xPxCl4oE6z_k-SGObSRzg2Q/s1600/Orthodromic-AVRT-post-adenosine-+WPW+life+in+the+fast+lane.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1081" data-original-width="1597" height="432" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj0xtvXxrNp0hUywsj1K_9FlC5q9RVl3iZLM0RwTgfC-L_M7eJ1njwccXmtH9MjZ_JdEWPxLH4nZyHyfjDuNz8NzdKUkzMBK2aVMU1T7_1YRunh-WbtkD7_xPxCl4oE6z_k-SGObSRzg2Q/s640/Orthodromic-AVRT-post-adenosine-+WPW+life+in+the+fast+lane.jpg" width="640" /></a></div>
<span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span></span> <span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span></span> <span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>The first ECG shows a regular narrow complex supraventricular tachycardia. P waves cannot be seen . It can be AVNRT or orthodromic AVRT After the administration of adenosine the tachycardia stopped and the second ECG shows sinus rhythm with short PR interval and a delta wave (a slurring at the onset of the QRS) can be seen clearly in some leads. So this is a case of a patient with Wolff Parkinson White syndrome and the tachycardia in a patient with a by-pass tract (accessory pathway) probably was AVRT </b></span></span><br />
<span style="font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>THIS CASE IS FROM THE SITE: LIFE IN THE FAST LANE , LINK <a href="https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/" target="_blank">https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/</a></b></span></span></div>
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<h4>
<span style="font-size: large;"><b>Acute management of narrow QRS paroxysmal supraventricular tachycardia (AVNRT or AVRT)</b> </span></h4>
<span style="font-size: large;">Acute treatment is guided by the clinical presentation. If the patient is hemodynamically stable (without significant hypotension or symptoms of acute heart failure) termination of the tachycardia is accomplished with </span><span style="font-size: large;">vagotonic maneuvers or drugs. </span><span style="font-size: large;">In the presence of hypotension with unconsciousness or respiratory </span><span style="font-size: large;">distress, QRS-synchronous direct current cardioversion is indicated. Generally this is rarely needed, because intravenous adenosine can terminate the tachycardia promptly in most situations. </span></div>
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<span style="font-size: large;">For stable individuals, initial management</span><span style="font-size: large;"> is based on the fact that most paroxysmal supraventricular tachycardias (PSVTs), such as A</span><span style="font-size: large;">V nodal reentry tachycardia or AV reentry tachycardia,</span><span style="font-size: large;"> are dependent on atrioventricular (AV) nodal conduction. So, treatment that slows conduction through the AV node is usually effective. This treatment consists of sympatholytic and vagotonic maneuvers (maneuvers that block the activity of the sympathetic and increase the activity of the parasympathetic nervous system) or the administration of drugs slowing atrioventricular (AV) conduction.</span></div>
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<span style="font-size: large;">As treatment is administered, the ECG should be continuously recorded, to observe for tachycardia termination, an occurrence of another arrhythmia (rare), or a response that can establish the diagnosis. Cases in which the response to AV blocking maneuvers or drugs can indicate the diagnosis are the following: AV block with transient slowing of tachycardia may expose ongoing P waves, indicating atrial tachycardia, or atrial flutter F waves, which have a frequency of about 250-300/minute and in contrast to the P waves of atrial tachycardia, they have a "saw tooth" appearance and there is no isoelectric line between them. </span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;">A Valsalva maneuver should be attempted in patients with a PSVT who are able to cooperate for its performance. The patient can be taught to perform this maneuver when needed.</span></div>
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<span style="font-size: large;">For the termination of a PSVT also carotid sinus massage is a reasonable maneuver, provided there is no</span><span style="font-size: large;"> carotid bruit and no prior history of stroke, or known carotid arterial stenosis. </span><span style="font-size: large;">If vagal maneuvers fail or cannot be performed, the next step for PSVT termination is intravenous adenosine (initial dose 6 mg by i.v. push, followed by 12 mg if needed). Adenosine blocks transiently conduction in the AV node and can terminate the vast majority of paroxysmal supraventricular tachycardias (PSVTs) . Adenosine may occasionally cause transient dyspnea, chest pain and anxiety, but side effects are of very short duration, because of the drug's short duration of action. Adenosine can also aggravate bronchospasm and occasionally it may precipitate atrial fibrillation, which is usually brief.</span></div>
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<span style="font-size: large;">Intravenous beta blockers, or calcium channel blockers (the nondihydropyridine calcium channel blockers verapamil or diltiazem) are also effective treatment options for PSVT termination. They can cause hypotension and have a longer duration of action. Intravenous digoxin can also be effective in some cases.<br />Beta blockers, verapamil, or diltiazem can also be given orally (PO) and they can be taken by the patient on an as-needed basis to terminate the tachycardia, or to facilitate tachycardia termination by theValsalva maneuver. PO drugs have a slower onset of action than IV treatment, but it can be an option in stable cases, where the arrhythmia is well tolerated by the patient.</span><span style="font-size: large;"><br /></span><br />
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<h3>
<span style="font-size: large;"><b>Atrial fibrillation (AF)</b></span></h3>
<span style="font-size: large;">AF is a supraventricular arrhythmia with uncoordinated atrial activation and as a consequence, there is no effective atrial </span><span style="font-size: large;">c</span><span style="font-size: large;">ontraction. ECG) characteristics of AF include: </span><br />
<span style="font-size: large;">1) Absolutely irregular R-R intervals (This is the general rule, with an exception </span><span style="font-size: large;">in the rare occasion of a patient with AF and a complete atrioventricular block: then the RR intervals will be regular and the heart rate low), </span><br />
<span style="font-size: large;">2) Absence of distinct repeating P waves, and </span><br />
<span style="font-size: large;">3)</span><span style="font-size: large;"> Irregular atrial activity (irregular waves of low amplitude are seen between QRS complexes).</span><br />
<span style="font-size: large;">The duration of an arrhythmia with the above characteristics on the ECG must be at least 30 seconds in order for the diagnosis of AF to be made (according to the ESC guidelines 2016).</span></div>
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<span style="font-size: large;">In AF, QRS complexes are usually of normal duration (< 120msec). However, they can be wide if there is a bundle branch block, or if conduction to the ventricles is through a by-pass tract (this can occur in Wolff-Parkinson-White syndrome), or in complete heart block with a ventricular escape rhythm. </span><span style="font-size: large;">The incidence of atrial fibrillation (AF) increases with age. <br />AF is associated with increased risk of stroke, heart failure exacerbation, and all-cause mortality. The mortality rate in patients with AF is about twice that of patients with sinus rhythm. However, in patients with AF the treatment strategy of maintaining sinus rhythm does not decrease mortality in comparison to the treatment strategy of controlling heart rate.<br />Etiology: AF is most commonly associated with advanced age, hypertension, valvular heart disease, congestive heart failure (CHF), and coronary artery disease (CAD), cardiomyopathy, chronic lung disease, hyperthyroidism, obesity and sleep apnea and cardiac surgery (cardiac surgery is associated with a high risk of postoperative atrial fibrillation). There are also idiopathic cases of AF without any clear underlying etiology. The term lone AF is used to describe cases of AF without evidence of an underlying cardiopulmonary disease.<br />Pathophysiologically, factors that contribute to the development of Atrial Fibrillation (AF) are the following : Atrial fibrosis, </span><span style="font-size: large;">reduced atrial contractility, atrial dilation,</span><span style="font-size: large;"> pulmonary vein dilation, local conduction heterogeneities within the atrial myocardium and increased sympathetic stimulation. This substrate permits the development of multiple small reentrant circuits in the atria that induce and stabilize the arrhythmia.</span><span style="font-size: large;"> Recent data support that the mechanism of AF involves both increased automaticity and multiple reentrant wavelets, occurring predominantly in the left atrium around the pulmonary veins.</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: bold;">ECG of a woman, 70 years old with a history of hypertension, treated with an ACE inhibitor and diuretic and hypercholesterolemia treated with simvastatin 20 mg daily. She complains of palpitations and fatigue since two hours. She does not have breathlessness or chest pain. Blood pressure is 155-80 mmHg. What are the ECG findings and what is the appropriate initial treatment and further diagnostic testing?</span><br />
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<span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-weight: bold;"><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgkRDNXdI5om55FyUXUcWJo_1V2gRcr_tFK3jhRLGyPpuio1Mo5U9ydKX4Z8HxBCQCIBUPcHNgH7fMPoZOMAZ27dJ_JNTpt-UrIqF-WQq_jmPJLUesn5cvBAom45bqGusas2RIRSsIxYFSS/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%2597%25CE%259A%25CE%2593+%25CE%25B2%25CE%25AC%25CF%2581%25CE%25BB%25CE%25B1+%25CF%2584%25CE%25B1%25CF%2587%25CE%25B5%25CE%25AF%25CE%25B1+%25CE%25BA%25CE%25BF%25CE%25BB%25CF%2580+%25CE%25BC%25CE%25B1%25CF%2581%25CE%25BC%25CE%25B1%25CF%2581.jpg" /></span><br />
<span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-weight: bold;"><br /></span> <span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-weight: bold;">Answer:</span><br />
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<span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-weight: bold;">The RR intervals are completely irregular, there are no distinguishable P waves, only small uneven fluctuations of the baseline. Therefore, it is atrial fibrillation. Also a mild non-specific repolarization disorder is noted (slightly negative T waves and a minimal ST depression) are observed in leads II, aVF, V4-V6) These non specific ST-T changes are not diagnostic for a certain disease and in the setting of a tachyarrhythmia, they cannot even be evaluated. The heart rate is markedly accelerated (there is a rapid ventricular response). Since the arrhythmia is of recent onset (less than 48 hours) , cardioversion can be attempted either with an antiarrhythmic drug, or electrical synchronized DC cardioversion. The patient is hemodynamically stable (no hypotension) and there are no symptoms of acute heart failure or cardiac ischemia, so an immediate emergency electrical DC cardioversion is NOT required. An initial attempt to control the heart rate ( with intravenous administration of a beta-blocker or digoxin ), while administering also an antiarrhythmic drug for cardioversion (usual options include flecainide or propafenone PO, if the patient does not have significant structural heart disease, or IV amiodarone in cases of concomitant structural heart disease). In addition, anticoagulation is initiated ( a vitamin K antagonist such as acenocoumarol, or warfarin, or one of the newer anticoagulants-dabigatran, apixaban, or rivaroxaban). If pharmaceutical cardioversion fails. then electrical cardioversion (synchronized DC cardioversion). can be attempted. </span><br />
<span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif; font-weight: bold;">Alternatively, one could choose not to attempt cardioversion, but only to control (slow) the heart rate, for example with a beta-blocker, verapamil or digoxin and start PO anticoagulation with one of the anticoagulants mentioned above. However, in recent onset atrial fibrillation, the success rate of cardioversion is high and it is usually attempted. We should also schedule to check for possible underlying causes of atrial fibrillation (hyperthyroidism, valvular heart disease, hypertensive heart disease, ischemic heart disease). This testing includes blood levels of TSH (thyroid stimulating hormone), echocardiography and possibly, depending on indications and the degree of clinical suspicion, a scheduled functional test for ischemia detection (eg exercise test or myocardial perfusion scintigraphy).</span><br />
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<h4>
<b style="font-size: x-large;">Management of atrial fibrillation</b></h4>
<span style="font-size: large;">Treatment of atrial fibrillation consists of:</span><br />
<span style="font-size: large;">a) Anticoagulation to prevent embolic complications (mainly stroke) on the short term for new-onset atrial fibrillation converted to sinus rhythm, or on the long term for people who have risk factors that increase the thromboembolic risk.</span><br />
<span style="font-size: large;">b) Rate control (control of the ventricular rate)</span><br />
<span style="font-size: large;">c) Rhythm control when appropriate and feasible (restoration and maintanance of sinus rhythm).</span><br />
<span style="font-size: large;">Atrial fibrillation (AF) is a factor that increases a person's risk for embolic stroke (embolic cerebrovascular accident -CVA). For a discussion of anticoagulation in atrial fibrillation see below in this chapter, but some general facts are the following. As a general rule therapy with an oral anticoagulant (OAC) can prevent the majority of ischemic strokes in AF patients and can prolong life (according to the ESC guidelines 2016). OAC treatment is superior to no treatment or aspirin in patients with AFwith risk factors for stroke.</span><br />
<span style="font-size: large;">Apart from the issue of anticoagulation, two strategies are available for AF treatment:</span><br />
<span style="font-size: large;">1) Rate control without conversion to sinus rhythm (AV nodal slowing agents to control the resting heart rate at about 70-100 beats per minute (bpm) and heart rate during exercise <140 bpm, plus oral </span><span style="font-size: large;">anticoagulation if the<span style="font-family: inherit;"> </span><span style="font-family: inherit;">CHA<sub>2</sub>DS<sub>2</sub>-VASc stroke risk score is<span style="font-family: inherit;"> </span></span></span><span style="font-family: inherit; font-size: large;">≥ 1, to prevent thromboembolic complications of AF, such as an embolic stroke). For the </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score see below...</span><br />
<span style="font-size: large;">2) Rhythm control : Antiarrhythmic drugs and if needed direct current (DC) </span><span style="font-size: large;">cardioversion, to convert to sinus rhythm and continuation of antiarrhythmic drugs for maintenance of sinus rhythm, plus oral anticoagulant for at least 4 weeks in sinus rhythm after cardioversion. The decision if the anticoagulant will be discontinued after 4 weeks of sinus rhythm or if it will be continued permanently depends on the presence or absence of risk factors for thromboembolism. If there are no risk factors, the anticoagulant will be stopped after 4 weeks : Generally, if AF does not recur and </span><span style="font-size: large;">the<span style="font-family: inherit;"> </span><span style="font-family: inherit;">CHA<sub>2</sub>DS<sub>2</sub>-VASc stroke risk score is<span style="font-family: inherit;"> 0 or 1, anticoagulation can be discontinued.</span></span></span><span style="font-size: large;"> Anticoagulation will be permanent </span><span style="font-size: large;">if the<span style="font-family: inherit;"> </span><span style="font-family: inherit;">CHA<sub>2</sub>DS<sub>2</sub>-VASc risk score is<span style="font-family: inherit;"> </span></span></span><span style="font-size: large;">≥ 2, even if the arrhythmia does not reccur, or if the patient has </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score=1 and a </span><span style="font-size: large;">high likelihood of AF recurrence (e.g. history of AF recurrences, significant enlargement of the left atrium) in order to prevent embolic complications</span><span style="font-size: large;">.</span><br />
<span style="font-size: large;"><span style="font-size: large;">Major randomized studies in patients with atrial fibrillation (AF) predominantly over </span><span style="font-size: large;">the age of 65 years (AFFIRM), or in patients with heart failure (</span><span style="font-size: large;">AF-CHF) have shown that there is no net mortality or </span><span style="font-size: large;">symptom benefit to be gained from one strategy (rhythm control or rate control) compared </span><span style="font-size: large;">with the other. Which strategy to adopt needs to be assessed and decided </span><span style="font-size: large;">for each individual patient. Factors considered in order to make this decision, include: The </span><span style="font-size: large;">likelihood of maintaining sinus rhythm (low likelihood favors rate control and the opposite is true for high likelihood),</span></span><br />
<span style="font-size: large;"><span style="font-size: large;"> The safety and </span><span style="font-size: large;">tolerability of antiarrhythmic </span><span style="font-size: large;">drugs in a particular patient (if there is problematic safety or tolerability of antiarrhythmics this favors rate control), </span></span><br />
<span style="font-size: large;"><span style="font-size: large;">If there is a history of failed cardioversions or many AF recurrences (this favors rate control), </span></span><br />
<span style="font-size: large;"><span style="font-size: large;">The age of the patient (younger age usually favors rhythm control whereas older age rate control)</span></span><br />
<span style="font-size: large;"><span style="font-size: large;">If AF is accompanied by symptoms and their intensity (significant symptoms with AF favor rhythm control)</span></span><br />
<span style="font-size: large;"><span style="font-size: large;"> Generally, a rhythm control strategy is prefered in younger and more symptomatic patients and if AF is of new onset.</span></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><b>Risk Score for embolic risk in non-valvular atrial fibrillation (AF): The </b></span><span style="font-size: large;"><b>CHA2DS2-VASc score</b> is calculated by summing the points corresponding to the risk factors present in given patient: Risk factors for thromboembolism included in this score (the name of the score stems from the initial letters of these factors) are :</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">Congestive heart failure or left ventricular dysfunction= 1 point,</span><br />
<span style="font-size: large;"> Hypertension= 1 point, </span><br />
<span style="font-size: large;">Age >75 =2 points,</span><br />
<span style="font-size: large;"> Diabetes mellitus= 1 point, </span><br />
<span style="font-size: large;">Stroke (history of previous stroke or transient ischemic attack-TIA, or other arterial </span><span style="font-size: large;">thrombo-embolism</span><span style="font-size: large;">) = 2 points </span><br />
<span style="font-size: large;">Vascular disease </span><span style="font-size: large;">(a prior myocardial infarction, peripheral arterial disease, aortic plaque)</span><span style="font-size: large;"> = 1 point </span><br />
<span style="font-size: large;">Age 65–74 = 1 point</span><br />
<span style="font-size: large;">Sex category (female sex) = 1 point. </span><br />
<span style="font-size: large;">(Maximum score= 9 / minimum score=0) </span><br />
<span style="font-size: large;"><span style="font-size: large;">Hence, there are 2 major risk factors (history of previous </span><span style="font-size: large;">thromboembolic event or stroke and age >75) each having a value of</span><span style="font-size: large;"> 2 points in the score. The rest of the risk factors are minor risk factors (1 point each)</span></span><br />
<span style="font-size: large;">Patients with paroxysmal AF should be regarded as having a stroke risk similar to those with persistent or permanent AF, in the presence of risk factors. (Let's remember this fact, it is important).</span><br />
<span style="font-size: large;"> Patients aged </span><span style="font-family: "times new roman" , serif; font-size: 14pt; line-height: 115%;">≤ </span><span style="font-size: large;">60 years, with lone AF, i.e. no clinical history or echocardiographic evidence of cardiovascular disease, have a very low stroke risk, about 1.3% over 15 years. However, the probability of stroke will increase with advancing age or development of hypertension, therefore re-assessment of risk factors for stroke over time is important. </span><u><span style="font-size: large;">In general, patients without clinical stroke risk factors do not need antithrombotic therapy, while patients with stroke risk factors (i.e. </span><span style="line-height: 115%;"><span style="font-family: inherit; font-size: large;">CHA<sub>2</sub>DS<sub>2</sub>-VASc</span></span><span style="font-size: large;"><span style="font-family: inherit;"> </span>score of 1 or more for men, and 2 or more for women) are likely to benefit from oral anticoagulants.</span></u><br />
<u><span style="font-size: large;">Another important note is that the </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score does not cover all cases. In patients with AF that have significant structural heart disease (for example valvular, or congenital heart disease, or hypertrophic cardiomyopathy,</span></u><u><span style="font-size: large;"> etc</span></u><u><span style="font-size: large;"> / or in patients with uncontrolled hyperthyroidism (thyrotoxicosis) anticoagulation is definitely needed regardless of the </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score.</span></u><br />
<u><span style="font-size: large;">Another consideration in such cases is the type of anticoagulation. </span></u><br />
<u><span style="font-size: large;">The term "valvular AF" in the guidelines does not include all patients with AF that have significant valvular heart disease. It is used to indicate which AF patients are </span></u><u><span style="font-size: large;">treated only with vitamin K antagonists and should not be treated with the new oral anticoagulants (NOACS):</span></u><br />
<span style="font-size: large;">The distinction between <b>"valvular" and "non-valvular" AF</b> remains a matter of debate. <u>Currently, "valvular AF" refers to patients with moderate or severe mitral stenosis (MS) or mechanical heart valves (and valve repair in North American guidelines only). These patients with AF should be treated with a vitamin K antagonist -not with a new oral anticoagulant (NOAC)</u>. Other valvular heart diseases, such as mitral regurgitation, aortic stenosis, and aortic regurgitation, do not result in conditions of low flow in the left atrium and do not apparently increase as much the risk of thromboembolism brought by AF. These patients should receive anticoagulation in case of AF, but both vitamin K antagonists and NOACs are acceptable alternatives ( in contrast to patients with MS, or prosthetic valves, or a history of valve repair, for whom only vitamin K antagonists are recommended).</span><b style="font-size: x-large;"><br /></b> <b style="font-size: x-large;">In case of a new patient presenting with atrial fibrillation the management is </b><span style="font-size: large;">as follows: If the patient is hemodynamically unstable (systolic blood pressure < 90, acute pulmonary edema, ischemic chest pain) give heparin and proceed quickly to synchronized DC cardioversion.</span><br />
<span style="font-size: large;">If the patient is not unstable and the heart rate is fast, an AV node slowing medication is given ( a beta-blocker, or verapamil, or diltiazem, or digoxin either intravenously or orally, to slow the ventricular response) and also a decision must be made about the treatment strategy (rate control, or rhythm control). </span><br />
<span style="font-size: large;">If rate control is chosen then a rate slowing medication is prescribed and </span><span style="font-size: large;">if </span><span style="font-size: large;">CHA<sub>2</sub>DS<sub>2</sub>-VASc score is </span><span style="font-size: large;">≥ 1 </span><span style="font-size: large;">an anticoagulant medication should also be included in the treatment ( a vitamin K antagonist with target INR 2-3, or dabigatran, or apixaban, or rivaroxaban).</span><br />
<span style="font-size: large;">If a rhythm control strategy is chosen, we should carefully define from patient's history the time of onset of AF:</span><br />
<span style="font-size: large;"> If it is a new onset AF (<48 hours) then we can proceed to cardioversion (restoration of sinus rhythm) either electrically (synchronized DC cardioversion) or with an antiarrhythmic medication. (If the patient has risk factors for thromboembolism, before cardioversion therapeutic dose of unfractionated heparin, or low molecular weight heparin or of one of the new oral anticoagulants should be given, but if the patient does not have significant risk factors this is not necessary). After cardioversion, anticoagulation is given for at least 4 weeks, but if the patient has moderate to high risk for thromboembolism (</span><span style="font-size: large;">CHA<sub>2</sub>DS<sub>2</sub>-VASc score </span><span style="font-size: large;">≥ 2) </span><span style="font-size: large;"> </span><span style="font-size: large;">anticoagulation is continued permanently.</span><br />
<span style="font-size: large;">If AF duration is > 48 hours, or if it is unknown, or we have reasonable doubt, then there is a risk that a thrombus may </span><span style="font-size: large;">already </span><span style="font-size: large;">be present in the left atrium or in the left atrial appendage. In such case, cardioversion to sinus rhythm leading to the resumption of atrial contraction, may "push" thrombus into the circulation and lead to an arterial thromboembolic complication. Hence, to avoid that, in AF of > 48 hours duration or of unknown duration we have the following two choices: </span><br />
<span style="font-size: large;">1) Give therapeutic anticoagulation for 3-4 weeks, then cardiovert (electrically or pharmacologically) and then continue anticoagulation for at least 4 weeks (permanently if there are risk factors for thromboembolism). </span><br />
<span style="font-size: large;">or</span><br />
<span style="font-size: large;">2) Give heparin (unfractionated or low molecular weight) and conduct a transesophageal echocardiogram (TEE) to assess the left atrium (LA) and the left atrial appendage: If there is no thrombus proceed to cardioversion and then give anticoagulation for at least 4 weeks (or permanently if there are is moderate or severe risk for thromboembolism with </span><span style="font-size: large;">CHA<sub>2</sub>DS<sub>2</sub>-VASc </span><span style="font-size: large;">≥ 2). If there is thrombus in the LA or its appendage, give anticoagulation for 4 weeks and then carry out a new TEE. If there is no thrombus then proceed to cardioversion and continue anticoagulation for at least 4 weeks. </span><br />
<span style="font-size: large;">The choices of oral (PO) anticoagulation are either a vitamin K antagonist (target INR 2-3), or one of the newer oral anticoagulants (dabigatran, apixaban, or rivaroxaban-for dosages see below) </span><br />
<span style="font-size: large;">The newer oral anticoagulants (NOACS) are at least as efficacious as warfarin in preventing stroke and are associated with a lower risk of intracranial bleeding. However, they are excreted primarily by the kidney, therefore renal function should be assessed before treatment initiation (and after treatment initiation at regular time intervals e.g. 2 times/year) and they are not readily monitored with standard laboratory tests.</span><br />
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<h4>
<span style="font-size: large;"><b>Recommendations for chronic antithrombotic prophylaxis (anticoagulation) for atrial fibrillation (AF)</b> : </span></h4>
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<span style="font-size: large;">According to</span><span style="font-size: large; text-align: justify;"> ESC guidelines of 2016, a general rule is that patients with non-valvular AF without clinical risk factors for thromboembolism (i.e. men with </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score =0, or women with </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score=1), </span><span style="font-size: large;">do not need anticoagulation.</span><span style="font-size: large;"> Then treatment options are aspirin, or no antithrombotic treatment (with the latter being preferable). whereas: </span><br />
<span style="font-size: large;">There is benefit from anticoagulation for AF patients </span><span style="font-size: large;">with risk factors (</span><span style="font-size: large;">i.e. men with </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc score </span><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 14pt; line-height: 21.4667px;">≥</span><span style="font-size: large;">1 </span><span style="font-size: large;"> or women with </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc sc</span><span style="font-size: large;">ore <span lang="EN-US" style="font-family: "times new roman" , "serif"; line-height: 21.4667px;">≥2</span>). </span><br />
<span style="font-size: large;">There is an absolute (class I) indication for anticoagulation in AF patients having at least 1 major or 2 minor risk factors for thromboembolism (except female sex), i.e. men with </span><span style="font-size: large;">CHA</span><sub>2</sub><span style="font-size: large;">DS</span><sub>2</sub><span style="font-size: large;">-VASc</span><span style="font-size: large;"> score</span><span style="font-size: large;"> </span><span style="font-family: "times new roman" , serif; font-size: large; line-height: 21.4667px;">≥ 2 and women with score </span><span style="font-family: "times new roman" , serif; font-size: large; line-height: 21.4667px;">≥ 3. </span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">In patients having only 1 minor clinical risk factor (except from female sex) , i.e in men with score =1, or women with score =2, there is generally a logical, but not absolute, indication for anticoagulation (class IIa indication).</span><br />
<span style="font-size: large;">The above guidelines are applied if there is <u>no contraindication </u>for anticoagulation (e.g. active pathological bleeding, severe hepatic disease, etc)</span><br />
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<span style="font-size: large;"> Anticoagulation is achieved with the administration of a vitamin K antagonist (warfarin, or acenocoumarol), with target INR 2-3, or one of the newer oral anticoagulants (NOACS): dabigatran, apixaban, or rivaroxaban. According to the guidelines, NOACS are generally preferable to vitamin K antagonists, but both are correct treatment options and the choice is made by the physician after taking into consideration the characteristics of each patient case.</span></div>
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<h4>
<br /><span style="font-size: large;"><b>Dosages of the new oral anticoagulants (NOACS) for patients with non-valvular atrial fibrillation with risk factors for thromboembolism :</b></span></h4>
<span style="font-size: large;"><u>Dabigatran</u> 150 mg x 2 times/day (150 mg bid), or 110 mg x 2 /day if there is a high estimated bleeding risk, or i</span><span style="font-size: large;">f age > 75 years. </span><span style="font-size: large;">Dabigatran is a direct thrombin inhibitor.</span><br />
<span style="font-size: large;"> Caution is needed for patients with moderate renal impairment (CrCl or GFR 30-50 mL/min).</span><br />
<span style="font-size: large;"> European Medicines Agency (EMA) based primarily on pharmacokinetic evidence, recommends a reduction of the daily dabigatran dose to 150 mg (75 mg x 2) if patients are aged >75 years and have a CrCl between 30 and 50 mL/min, or need treatment with verapamil or amiodarone (these two drugs have an interaction with dabigatran).</span> <span style="font-size: large;">Reduce the dose of dabigatran (to75 mg twice daily) in patients with severe renal impairment (CrCl 15-30 mL/min).</span> <span style="font-size: large;">The drug should not be administered to patients with CrCl < 15 mL/min or on dialysis.</span><br />
<span style="font-size: large;">Discontinuation for surgery and other interventions, that can cause bleeding: In patients with </span><span style="font-size: large;">CrCl ≥ 50 mL/min) </span><span style="font-size: large;">discontinue dabigatran 1 to 2 days </span><span style="font-size: large;">before invasive or surgical procedures because of the increased risk of bleeding. For patients with less adequate renal function</span><span style="font-size: large;"> </span><span style="font-size: large;">(CrCl < 50 mL/min) </span><span style="font-size: large;">discontinue dabigatran for </span><span style="font-size: large;">3 to 5 days. I</span><span style="font-size: large;">n case of emergency surgery use the </span><span style="font-size: large;">specific reversal agent (antidote) idarucizumab for reversal of the anticoagulant effect of dabigatran. </span></div>
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<span style="font-size: large;">Restart </span><span style="font-size: large;">dabigatran</span><span style="font-size: large;"> as soon as medically appropriate.</span></div>
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<span style="font-size: large;"><br /></span></div>
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<span style="font-size: large;"><u>Rivaroxaban</u> (a factor Xa inhibitor), dosage: 20 mg x 1 time/day (20 mg qd). Rivaroxaban is taken with a meal (this provides better absorption)</span><br />
<span style="font-size: large;"> I</span><span style="font-size: large;">f </span><span style="font-size: large;">creatinine clearance (</span><span style="font-size: large;">CrCl)</span><span style="font-size: large;"> or glomerular filtration rate (GFR) is 15-50 mL/min, then r</span><span style="font-size: large;">ivaroxaban</span><span style="font-size: large;"> dosage is 15</span><span style="font-size: large;"> mg 1 time per day.</span><br />
<span style="font-size: large;"> It is contraindicated in very severe renal failure with CrCl < 15 mL/min). Rivaroxaban was tested in patients with non valvular AF in the</span><span style="font-size: large;"> ROCKET AF trial.</span><br />
<span style="font-size: large;">Discontinuation for surgery and other interventions, that can cause bleeding: D</span><span style="font-size: large;">abigatran should be stopped at least 24 hours before the intervention and restarted as soon as possible after the procedure, provided the clinical situation allows and adequate haemostasis has been established.</span><br />
<span style="font-size: large;"></span><br />
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<br /></div>
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><u>Apixaban </u>(a factor Xa inhibitor), dosage: 5 mg x 2 times per day, </span><span style="font-size: large;">swallowed with water, with or without food. </span><span style="font-size: large;">Reduced dosage of 2.5 mg x 2 times/day is prescribed if </span><br />
<span style="font-size: large;">a) 2 or more of the following factors are present : </span><span style="font-size: large;">age > 80, body weight ≤ 60 kg, </span><span style="font-size: large;">creatinine ≥ 1.5 mg/dL).</span><br />
<span style="font-size: large;">b) </span><span style="font-size: large;">there is severe renal impairment (creatinine clearance 15-30 mL/min) </span><br />
<span style="font-size: large;">Apixaban must not be used in patients with serum creatinine >2.5 mg/dL, or CrCl <15 mL/min (these were exclusion criteria </span><br />
<span style="font-size: large;">T</span><span style="font-size: large;">he drug was tested for patients with non valnular AF i</span><span style="font-size: large;">n ARISTOTLE study.</span><br />
<span style="font-size: large;">Discontinuation for surgery and other interventions, that can cause bleeding: </span><span style="font-size: large;">Apixaban should be discontinued at least 48 hours prior to elective surgery or invasive procedures with a moderate or high risk of bleeding (interventions for which clinically significant bleeding cannot be excluded or for which the risk of bleeding would be unacceptable).<br />In case of surgery or invasive procedures with a low risk of bleeding (</span><span style="font-size: large;">interventions for which any bleeding that occurs is expected to be minimal, non-critical in its location): </span><span style="font-size: large;">apixaban </span><span style="font-size: large;">should be discontinued at least 24 hours before the procedure</span><span style="font-size: large;"> </span><span style="font-size: large;">.</span></div>
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<span style="font-size: large;"><br /></span> <span style="font-size: large;">Note: Great caution is needed in patients on treatment with anticoagulants who need e</span><span style="font-size: large;">pidural or spinal anesthesia because if an e</span><span style="font-size: large;">pidural or spinal hematoma occurs, it can cause long term paralysis. The discontinuation of any anticoagulat drug in such cases should be such as to avoid any periprocedural anticoagulant effect</span></div>
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<h3>
<b style="font-size: x-large;"><br /></b></h3>
<h3>
<b style="font-size: x-large;">Atrial flutter </b></h3>
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<span style="font-size: large;">Atrial flutter is a supraventricular arrhythmia that in many aspects has a similar treatment with atrial fibrillation, but it is less common than atrial fibrillation. These two arrhythmias can also commonly coexist, appearing in the same patient at a different time.</span></div>
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<span style="font-size: large;">Usual symptoms are palpitations, or </span><span style="font-size: large;">fatigue (these are also usual symptoms of atrial fibrillation). </span></div>
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<span style="font-size: large;"><b>Etiology</b></span></div>
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<span style="font-size: large;">Atrial flutter is o</span><span style="font-size: large;">ften seen in conjunction with structural heart </span><span style="font-size: large;">disease or chronic obstructive pulmonary disease </span><span style="font-size: large;">(COPD) and only rarely in patients without an underlying cardiac or pulmonary disease. Atrial flutter</span><span style="font-size: large;"> may occur </span><span style="font-size: large;">in patients with</span><span style="font-size: large;"> coro</span><span style="font-size: large;">nary heart disease, heart failure (of any cause), valvular heart disease, </span><span style="font-size: large;">rheumatic heart disease, atrial septal defect</span><span style="font-size: large;">, or surgically repaired </span><span style="font-size: large;">congenital heart disease.</span></div>
<span style="font-size: large;">Heart rhythm is usually regular but can be irregular when there is a variation in the conduction of atrial impulses through the atrioventricular (AV) node to the ventricles. There is usually tachycardia (100-150 beats/min). The ECG shows a "sawtooth" pattern of atrial activity in the inferior leads II, III, and AVF. The sawtooth atrial flutter waves have a rate of 250-350/min. The transmission of atrial impulses through the AV node to the ventricles usually occurs every second, third, or fourth impulse.<span style="font-family: inherit;"> </span></span></div>
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<span style="font-size: large;"><span style="font-family: inherit;">When there is 2:1 conduction of the flutter waves to the ventricles there is usually a rhythmic supraventricular tachycardia, with a ventricular rate typically about 150/minute and it is relatively difficut to recognize the flutter waves. In case of a supraventricular tachycardia with a regular ventricular rhythm at a rate of about 150/min always consider atrial flutter in the differential diagnosis! </span></span><span style="font-size: large;">Another diagnostic pitfall is that flutter waves can deform the ST segment in a manner that may mimic an ischemic pattern on the ECG.</span><span style="font-family: "times new roman" , serif; font-size: 14pt; line-height: 115%;"> </span><span style="font-size: large;"><span style="font-family: inherit;">If atrial flutter is suspected but flutter waves are not clearly visible, vagal maneuvers or the administration of a drug that reduces conduction through the AV node, such as adenosine, can help unmask the flutter waves by enhancing the degree of AV block.</span> Then the flutter waves (F waves) can be clearly seen between the QRS complexes.</span><span class="fontstyle0"><span style="font-family: inherit; font-size: large;"> </span></span></div>
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<span class="fontstyle0"><span style="font-family: inherit; font-size: large;">There are three categories of atrial flutter: </span></span></div>
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<span class="fontstyle0"><span style="font-family: inherit; font-size: large;">The </span></span><span style="font-size: large;">isthmus-dependent counterclockwise (typical) atrial flutter is the </span><span style="font-family: inherit; font-size: large;">most common form. It is recognized by the </span><span style="font-family: inherit; font-size: large;">negative flutter waves (F </span><span style="font-family: inherit; font-size: large;">waves) in leads II, III, and aVF and positive F waves in lead V1.</span><span style="font-family: inherit; font-size: large;"> In V6 they are negative.</span> <span style="font-family: inherit; font-size: large;">This form is called counterclockwise because the</span><span style="font-size: large;"> reentrant electrical current (the reentrant wavefront) is traveling on a counterclockwise course: It travels up the interatrial septum, across the roof of the right atrium, down the lateral wallof the right atrium and across its inferior wall.</span><span style="font-size: large;"> </span></div>
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<span style="font-family: inherit; font-size: large;"> The isthmus-dependent clockwise atrial flutter is the next most common form. </span><span style="font-size: large;">The reentrant circuit moves in the reverse direction from that of the counterclockwise flutter. </span><span style="font-family: inherit; font-size: large;">On ECG the </span><span style="font-size: large;">F waves are</span><span style="font-size: large;"> positive in leads II, III, and aVF and negative in lead V1.</span></div>
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<span style="font-family: inherit; font-size: large;"> </span><span class="fontstyle0"><span style="font-family: inherit; font-size: large;">In both of the isthmus-dependent types of atrial flutter (counterclockwise and clockwise) the atrial rate, i.e. the rate of the F waves, ranges between 250 and 340 beats per minute.</span></span></div>
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<span style="font-family: inherit; font-size: large;">The atypical, non-isthmus dependent atrial flutter is the least common variety. </span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b> What is the type of rhythm shown on this ECG ?</b></span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhUsHU7Kyqy_9w1hD4YQsGAWu7OwEZ5toeFx8M8gbgLDnjzbWLIgJcOeyxoIV0adig5EmAnDHM5T7OsVv0yyMCmSw-SuevrLBblpWy7kZ0qIDk_oNFj_EM9h-bg81AosbvNaj0hRRSHqRs/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25B7%25CE%25BA%25CE%25B3+%25CE%25BC%25CF%2580%25CE%25AC%25CE%25BB%25CE%25BB%25CE%25BF%25CF%2585+%25CE%25B3%25CE%25B5%25CF%2589%25CF%2581%25CE%25B3%25CE%25AF%25CE%25B1+%25CE%25BA%25CE%25BF%25CE%25BB%25CF%2580%25CE%25B9%25CE%25BA%25CF%258C%25CF%2582+%25CF%2580%25CF%2584%25CE%25B5%25CF%2581%25CF%2585%25CE%25B3+001.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" data-original-height="862" data-original-width="1600" height="344" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhUsHU7Kyqy_9w1hD4YQsGAWu7OwEZ5toeFx8M8gbgLDnjzbWLIgJcOeyxoIV0adig5EmAnDHM5T7OsVv0yyMCmSw-SuevrLBblpWy7kZ0qIDk_oNFj_EM9h-bg81AosbvNaj0hRRSHqRs/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25B7%25CE%25BA%25CE%25B3+%25CE%25BC%25CF%2580%25CE%25AC%25CE%25BB%25CE%25BB%25CE%25BF%25CF%2585+%25CE%25B3%25CE%25B5%25CF%2589%25CF%2581%25CE%25B3%25CE%25AF%25CE%25B1+%25CE%25BA%25CE%25BF%25CE%25BB%25CF%2580%25CE%25B9%25CE%25BA%25CF%258C%25CF%2582+%25CF%2580%25CF%2584%25CE%25B5%25CF%2581%25CF%2585%25CE%25B3+001.jpg" width="640" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Answer</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Atrial flutter : In this case there is a slow ventricular rate (a rapid ventricular rate is more common in patients with atrial flutter, in contrast to this example). Here, flutter waves can be clearly seen between the QRS complexes. Flutter (F) waves have a "sawtooth" morphology in leads II, III and avF. They are also prominent in lead V1.</span><span style="font-family: "arial" , "helvetica" , sans-serif;"> Here there are</span></b></span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b> negative F waves in leads II, III, and aVF and positive F waves in lead V1. So it is a case of </b></span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>isthmus-dependent counterclockwise (typical) atrial flutter which is the most common form</b></span></td></tr>
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<b style="font-size: x-large;">Treatment of atrial flutter</b><br />
<span style="font-size: large;">For ventricular rate control the same drugs are used as in atrial fibrillation, but it is more difficult to achieve with atrial flutter than with atrial fibrillation.<br />Cardioversion and anticoagulation:</span><span style="font-size: large;">The risk of thromboembolism in atrial flutter is generally considered equivalent to the risk in atrial fibrillation and anticoagulation treatment for atrial flutter follows the same rules as for atrial fibrillation. As with atrial fibrillation, precardioversion anticoagulation is not necessary in atrial flutter when the arrhythmia is of <48 hours duration, except in the setting of mitral valve disease</span><span style="font-size: large;">.</span></div>
<span style="font-size: large;">In atrial flutter of > 48 hours duration or of unknown duration </span><span style="font-size: large;">therapeutic anticoagulation must be administered for 3-4 weeks and then cardioversion (electrical or pharmacological) can be attempted.</span><br />
<span style="font-size: large;"> In atrial flutter anticoagulation must be continued at least 4 weeks after electrical or chemical cardioversion. Long term anticoagulation is indicated in patients with risk factors for thromboembolism (</span><span style="font-size: large;">CHA<sub>2</sub>DS<sub>2</sub>-VASc score </span><span style="font-size: large;">≥ 1). Note that these rules are the same, as for atrial fibrillation. </span><br />
<span style="font-size: large;">For the pharmacological cardiovesion of atrial flutter the most effective drug is ibutilide, an intravenous (IV) class</span><span style="font-size: large;"> III antiarrhythmic agent. W</span><span style="font-size: large;">ithin </span><span style="font-size: large;">60-90 minutes following IV </span><span style="font-size: large;">ibutilide </span><span style="font-size: large;">1-2 mg, conversion to sinus rhythm occurs in about</span><span style="font-size: large;"> </span><span style="font-size: large;">50–70% of patients. </span><br />
<span style="font-size: large;">For the conversion of atrial flutter to sinus rhythm amiodarone (a class III antiarrhythmic agent), or class I antiarrhythmic drugs can also be used. Conversion of atrial flutter with </span><span style="font-size: large;">class I antiarrhythmic drugs is difficult to achieve (relatively low success rates). When these drugs </span><span style="font-size: large;">are used,</span><span style="font-size: large;"> (e.g. drugs of the category Ic such as flecainide or propafenone) concomitant administration of rate lowering drugs that lower AV conduction (such as beta-blockers, verapamil, diltiazem, or digoxin) is indicated. This is advised in order to avoid the following rare but dangerous complication: Administration of class I drugs can slow the atrial flutter rate and this in some cases can reach a point where 1:1 atrioventricular (AV) conduction of the atrial flutter waves to the ventricles can occur, with a resulting ventricular rate of 200 beats/minute or higher, leading to hemodynamic collapse.</span><br />
<span style="font-size: large;">Another risk associated with the use of antiarrhythmic drugs and especially sotalol and drugs of class Ic (flecainide, propafenone) is the risk of proarrhythmia (the relatively rare but dangerous possibility of the occurence of ventricular arrhythmias as a result of these drugs). This risk is probably greatest in the first 24-48 hours after the initiation of antiarrhythmics, therefore careful assessment of the patient with repeated ECGs is needed during of the first days of treatment or after dose increments.</span><br />
<span style="font-size: large;">The most effective treatment (with the highest success rate) to achieve cardioversion of atrial flutter is eletrical cardioversion. With a synchronized electric shock of low energy, </span><span style="font-size: large;">25-50 Joules (J), </span><span style="font-size: large;"> conversion to sinus rhythm is accomplished in about</span><span style="font-size: large;"> 90% of patients. </span><br />
<span style="font-size: large;"><b>Catheter ablation</b> is a highly successful treatment for atrial flutter to prevent recurrences. It is the prefferred treatment option for patients with reccurent typical atrial flutter. </span><span style="font-size: large;"><br />Radiofrequency ablation (RFA) is often used as first-line therapy to permanently restore sinus rhythm. For patients with recurrent symptomatic isthmus-dependent atrial flutter the current success rate is ≥ 95%.</span><br />
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<span style="font-size: large;">Ventricular arrhythmias </span></h3>
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<span style="font-size: large;">Sustained ventricular tachycardia </span><span style="font-size: large;">with hemodynamic instability (e.g. syncope, hypotension) </span><span style="font-size: large;">and ventricular fibrillation </span><span style="font-size: large;">are life-threatening ventricular tachyarrhythmias. Therefore, there is no doupt about their importance and the need for very prompt treatment in the acute episode and also for long term treatment to prevent sudden cardiac death in patients who have previously manifested such arrhythmias, or in patients with a cardiac disorder </span><span style="font-size: large;">accompanied by a high risk to develop such arrhythmias.</span><br />
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<span style="font-size: large;"><b>Ventricular tachycardia (VT)</b></span></h3>
<span style="font-size: large;">A tachycardia with a heart rate of 120 / minute or greater comprising of at least three or more consecutive systoles of ventricular origin.<br />Ventricular tachycardias originate from sites located distally to the bifurcation of the bundle of His. The circuit from which the tachycardia originates may include specialized conductive myocardial tissue, common contractile myocardium, or both types of myocardial tissue.<br />A VT is called <b>sustained (persistent)</b> when it lasts> 30 seconds, or if electrical DC cardioversion is required to manage the hemodynamic consequences, whereas when none of these two conditions is fulfilled, the tachycardia is called <b>non sustained</b>(<b>non-persistent).</b> <br />Ventricular tachycardia (VT) is also divided into<b> monomorphi</b>c in which the morphology of QRS waves is stable and <b>polymorphic</b>, with a varying QRS.morphology.</span><br />
<span style="font-size: large;"><b>Clinical Presentation</b></span><br />
<span style="font-size: large;">Nonsustained VT: May be asymptomatic or cause </span><span style="font-size: large;">palpitations</span><br />
<span style="font-size: large;">Sustained VT: It is more likely to cause palpitations, and it may also present with </span><span style="font-size: large;">lightheadedness, near-syncope, syncope, or cardiac arrest.</span><br />
<span style="font-size: large;">A tachycardia with a frequency of 120 / minute or more (some electrophysiologists set the heart rate threshold at 100 beats/ minute) and wide QRS (120 msec or greater) should be considered as ventricular tachycardia, unless proven otherwise.<br />Less commonly, a tachycardia with wide QRS may be of supraventricular origin, if one of the following occurs: <br />a) There is aberrant conduction, i.e. it is a supraventricular tachycardia with bundle branch block , a preexisting block, or one that appears only at an increased heart rate, or<br />b) There is a supraventricular tachycardia with pre-excitation, i.e. conduction of the electrical impulse to the ventricles through an accessory pathway <br />c) An antidromic AV reentry tachycardia (antidromic AVRT) which is the least common type of AV re-entrant tachycardia, in which the impulse is conducted downward (anterogradely) from the atria to the ventricles through an accessory pathway and then retrogradely from the ventricles to the atria through the normal conduction system (ie the bundle of His and the atrioventricular node).<br />d) A supraventricular tachycardia with wide QRS due to the effect of an antiarrhythmic drug that causes QRS prolongation. ( Class Ic antiarrhythmics, such as flecainide and propafenone).<br />If there is doubt whether it is a ventricular or supraventricular tachycardia, an intravenous calcium receptor blocker (verapamil or diltiazem).should never be administered for diagnostic purposes. The calcium channel blocker </span><span style="font-size: large;">if the tachycardia is supraventricular,</span><span style="font-size: large;">will usually terminate it, but if it is ventricular it may cause severe hypotension, or frank circulatory collapse (shock).</span><br />
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<b><span style="font-size: large;">The ECG in ventricular tachycardia and ECG criteria for the differential diagnosis of a wide QRS tachycardia</span></b></h4>
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<span style="font-size: large;">There is tachycardia with wide QRS complexes ≥ 120 msec and heart rate > 100-120 beats / min (bpm). As mentioned above, ventricular tachycardia (VT) can be non sustained ( duration from only 3 consecutive ventricular beats to 30 seconds, with spontaneous termination) or sustained (duration >30 seconds, or when treatment was needed for tachycardia termination).<br />ECG findings suggestive of a ventricular origin of the tachycardia are the following:<br />1) P waves that have no temporal relationship to the QRS. This is called atrioventricular dissociation and strongly favours the diagnosis of VT.<br />2) The presence of fusion beats: The presense of one or more beats within the tachycardia with a QRS morphology originating from the concomitant occurence of a ventricular and supraventricular beat. Fusion beats have a QRS morphology with features intermediate between these two beats. This is due to the simultaneous stimulation of the myocardium by an impulse of supraventricular origin and one of ventricular origin and strongly suggests VT.<br />3) The presence of capture beats is also strongly suggestive of VT: This is the occurence between the wide QRS complexes of the tachycardia, of one or more supraventricular beats with a narrow QRS complex.<br />4) Concordance (r</span><span style="font-size: large;">elative uniformity) in the appearance of the QRS in the precordial leads (i,e. when QRS is positive or negative in all the precordial leads)</span></div>
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<span style="font-size: large;">5) QRS axis: A left axis in the frontal plane, more negative than -30, or a rightward axis more positive than +90˚, is suggestive of a VT.<br />6) Occasionally in ventricular tachycardia there may be a temporal relationship between the QRS and P waves, when the atria are stimulated retorgradely from the ventricles, resulting in P waves following the QRS complexes. Then, if there is evidence that the atrial depolarizations (P waves) have a temporal dependence on the ventricular ones (QRS complexes), i.e. when there is a degree of a ventriculoatrial conduction block, this is suggestive of VT. (E.g., a 2: 1 ventriculoatrial block, where there is 1 P wave for every 2 QRS complexes).<br />In contrast, if the ventricular depolarizations show a temporal dependence on atrial depolarizations, e.g. a 2: 1 block of AV conduction, where every second P-wave is followed by a QRS complex, the diagnosis of supraventricular tachycardia is supported.<br />7) A QRS duration > 140 msec when the tachycardia has a right bundle branch block morphology, or > 160 msec when there is a left bundle branch block QRS morphology suggests a ventricular tachycardia.<br />8) In the case of a tachycardia with wide QRS complexes and a right bundle branch block (RBBB) morphology, i.e. a positive QRS in lead V1, the presence in this lead of a monophasic or biphasic QRS (consisting of only one positive wave or two waves, a positive and a negative one) is an indication of VT, as is the presense in lead V6 of a deep S wave with an R / S ratio <1. </span></div>
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<span style="font-size: large;">This criterion is based on the fact that typically a RBBB does not have such an appearence (it is characterized by a three-wave QRS complex - rSR '- in V1 and in V6, although there is a broad S wave, its depth is smaller than the the height of the of R wave).<br />Therefore, if a three-wave ( rSR') morphology is present in V1 with the first R being smaller than the second (R'), this is suggestive of a supraventricular tachycardia, as is a R / S ratio > 1 in V6 in the presence of an RBBB morphology of the QRS.<br />9) In the case of a tachycardia with a wide QRS, showing a left bundle branch block (LBBB)-like QRS morphology , i.e. a positive QRS in left-oriented leads (I, aVL, V5, V6), one can use the following rules: When there is an initial r wave in leads V1, V2 , the following criteria can be applied: If r in V1 or V2 has</span></div>
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<span style="font-size: large;"> a duration > 40 msec (1 mm with the standard ECG paper speed ) or the time from the onset of QRS to the deepest point (the nadir) of the S wave is> 70 msec, or the descending limb of the S wave is notched, a diagnosis of ventricular tachycardia is supported.<br />10) In case of a tachycardia with a LBBB morphology, the presence of an initial q wave in lead V6 is an indication of VT (This criterion is based on the fact that in a true left bundle branch block, there is no q wave in this lead).</span><br />
<span style="font-size: large;">A history of structural heart disease, if present, also increases the likelihood that a broad QRS tachycardia is of ventricular origin (VT).</span><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: large;"><br /></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A male 73 years old with a history of diabetes-type 2 , permanent atrial fibrillation with an adequately controlled heart rate (ventricular response) and known mild global left ventricular systolic dysfunction (ejection fraction EF= 45%). He did not have a history of smoking , or increased alcohol consumption. He was on treatment with ramipril, metoprolol (sustained relase tablets) and acenocoumarol (a vitamin K antagonist- same drug category with warfarin). A recent coonary angiography showed no significant stenoses of the coronary arteries, and he had no history of chronic unregulated hypertension or a history of cardiac valvulopathy.</b></span><br /><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>He presented for examination because he was feeling fast pulpitations, fatigue and a mild nonspecific and poorly described precordial discomfort of approximately one hour. He did not have breathlessness or chest pain. Blood pressure was 120/90 mmHg and a brief targeted physical examination was without significant findings except from tachycardia. What is the type of the observed tachycardia (a reasoned answer is requested), in the context of which heart disease did the arrhythmia propably occur and what is the proposed treatment?</b></span><br /><br /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhftYY68wKDNXq0N2_Hl8eCR2h4-6moIQQYcI58xnd9ZiQLMP6LyaLJLHPTm_ZvXHvvIqo83BrzGjYba0wEOUgqDKrxUtIIuh7Hca4fyA-hb2K1Pu5ceI2WaM2pCF2xA-ZKCjZCyV6JaRwI/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B7%25CE%25BA%25CE%25B3+%25CF%2580%25CE%25B1%25CF%2583%25CF%2583%25CE%25AC%25CF%2582+%25CE%25BA%25CF%2589%25CE%25BD%25CF%2583%25CF%2584+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB+%25CF%2584%25CE%25B1%25CF%2587%25CF%2585%25CE%25BA%25CE%25B1%25CF%2581%25CE%25B4%25CE%25AF%25CE%25B1_Fotor.jpg" style="font-family: arial, helvetica, sans-serif; font-weight: bold;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhftYY68wKDNXq0N2_Hl8eCR2h4-6moIQQYcI58xnd9ZiQLMP6LyaLJLHPTm_ZvXHvvIqo83BrzGjYba0wEOUgqDKrxUtIIuh7Hca4fyA-hb2K1Pu5ceI2WaM2pCF2xA-ZKCjZCyV6JaRwI/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B7%25CE%25BA%25CE%25B3+%25CF%2580%25CE%25B1%25CF%2583%25CF%2583%25CE%25AC%25CF%2582+%25CE%25BA%25CF%2589%25CE%25BD%25CF%2583%25CF%2584+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB+%25CF%2584%25CE%25B1%25CF%2587%25CF%2585%25CE%25BA%25CE%25B1%25CF%2581%25CE%25B4%25CE%25AF%25CE%25B1_Fotor.jpg" /></a><br /><br /><br /><br /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg8eh-O9utx564Xw-pyd1DIl1rdOmJCCN0DtR99oCXK-2LPgEWvjTFtAUEq_wkZ2tY-ORjf52hKSS6c1wloykzi59txHyqowW2ioa8p23324BQjCI7pnG8CZmpu5PirQzDdX-ctixVC02Bw/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B7%25CE%25BA%25CE%25B3+%25CF%2580%25CE%25B1%25CF%2583%25CF%2583%25CE%25AC%25CF%2582+%25CE%25BA%25CF%2589%25CE%25BD%25CF%2583%25CF%2584+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB+%25CF%2584%25CE%25B1%25CF%2587%25CF%2585%25CE%25BA%25CE%25B1%25CF%2581%25CE%25B4%25CE%25AF%25CE%25B1_Fotor-2.jpg" style="font-family: arial, helvetica, sans-serif; font-weight: bold;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg8eh-O9utx564Xw-pyd1DIl1rdOmJCCN0DtR99oCXK-2LPgEWvjTFtAUEq_wkZ2tY-ORjf52hKSS6c1wloykzi59txHyqowW2ioa8p23324BQjCI7pnG8CZmpu5PirQzDdX-ctixVC02Bw/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B7%25CE%25BA%25CE%25B3+%25CF%2580%25CE%25B1%25CF%2583%25CF%2583%25CE%25AC%25CF%2582+%25CE%25BA%25CF%2589%25CE%25BD%25CF%2583%25CF%2584+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB+%25CF%2584%25CE%25B1%25CF%2587%25CF%2585%25CE%25BA%25CE%25B1%25CF%2581%25CE%25B4%25CE%25AF%25CE%25B1_Fotor-2.jpg" /></a><br /><br /><br /><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>ANSWER:</b></span><br /><br /><br /><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A tachycardia with a regular rhythm, heart rate around 140 beats per minute (bpm) and wide QRS complexes in a patient with a history of structural heart disease (mild global reduction of systolic left ventricular function). A regular tachycardia with wide QRS, (especially in a patient with structural heart disease) is very likely to be a ventricular tachycardia (VT). In this case, some of the morphological criteria of VT are also present (see above): The tachycardia has a left bundle branch block morphology and a QRS duration marginally exceeding 160 msec [QRS width here, is more clearly discerned on leads V2-V4 , while in leads V1, V2 there is an r wave clearly more than 40 msec wide and the interval from the beginning of the QRS to the deepest point (the nadir) of the S wave is greater than 70 msec]. The above findings are suggestive of a ventricular tachycardia (VT). Since the patient is hemodynamically stable, initial treatment can be by intravenous infusion of amiodarone or lidocaine. If this fails to terminate the VT, then electrical cardioversion is employed by administering an electric shock (initially 100-200 Joules) synchronized to the R wave of the QRS complex (synchronized cardioversion-press the defibrillator's sync button).</b></span><br /><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Regarding the underlying heart disease, diabetic cardiomyopathy would be most likely and as a second possibility idiopathic dilated cardiomyopathy (often resulting from unrecognized prior viral myocarditis, but a genetic predisposition is also commonly involved). One can arrive to these two possibilities, relying upon the patient's history, since from the history other common causes of systolic left ventricular dysfunction (such as coronary heart disease, chronic uncontrolled hypertension, chronic severe valvular disease, alcoholic cardiomyopathy, cardiomyopathy due to chronic tachyarrhythmia) propably can be ruled out. </b></span></span></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Regarding long-term management, sustained ventricular tachycardia in a patient with organic heart disease, poses an indication for implantation of an implanted cardioverter-defibrillator (ICD).</span></b><br />
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<span style="font-family: inherit; font-size: large;"><br /></span><span style="font-size: large;">Prognosis and treatment of ventricular tachycardia (VT): </span></h4>
<span style="font-size: large;">These depend </span><span style="font-size: large;">on the presence of underlying structural heart disease. </span><span style="font-size: large;">The most common causes of VT are ischemic heart disease and cardiomyopathies (dilated or hypertrophic) but there are also other more rare causes. </span><br />
<span style="font-size: large;">In ischemic heart disease the underlying substrate for VT is usually a scar in ventricular myocardium, i.e an area of fibrosis due to a previous myocardial infarction (MI), arround which the reentrant impulse propagates.</span><span style="font-size: large;"> Another cause is acute myocardial ischemia or an acute MI, which can produce non-homogeneous electrophysiologic properties (slow conduction, differences in refractory period) in areas of the ventricular myocardium), which can lead to the occurence of V</span><span style="font-size: large;">T. </span><br />
<span style="font-size: large;">In dilated cardiomyopathy the most common underlying substrate, responsible for ventricular tachycardia (VT) is myocardial fibrosis. However, there is also another important mechanism causing VT in some of the patients with dilated cardiomyopathy, called "bundle branch reentry". In these cases VT is caused by a reentrant circuit, which uses the bundle of His and its branches. Since the electrical impulse uses the bundle branches to enter the ventricles, the ECG, unlike the usual pattern of VT, shows a typical bundle branch block morphology, usually LBBB and rarely RBBB. Appart from dilated cardiomyopathy, VT from bundle branch reentry can also occur in patients with aortic or mitral valve disease. This is attributed to the anatomical proximity between the annuli of these valves and the bundle of His and the proximal parts of its branches. </span><br />
<span style="font-size: large;">Less common causes of VT include congenital heart disease, arrhytmogenic right ventricular dysplasia-ARVD (better term: </span><span style="font-size: large;">arrhytmogenic right ventricular cardiomyopathy), mitral valve prolapse (very rarely it can cause VT) and various genetic disorders of ion channels of the myocardial cell membrane (Brugada syndrome, congenital long QT syndrome, etc).</span></div>
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<span style="font-size: large;">As mentioned above, most cases of VT are assossiated with underlying heart disease, but there are also cases with no underlying heart disease (idiopathic VT).<br /><b>Idiopathic ventricular tachycardia</b> is a VT occuring in otherwise healthy people, with structurally normal hearts and it is usually benign (good prognosis). The most common type of idiopathic VT is right ventricular outflow tract (RVOT) ventricular tachycardia. </span><br />
<h4>
<span style="font-size: large;"><br /></span><span style="font-size: large;">Diagnostic assessment of a patient with ventricular arrhythmias</span></h4>
<span style="font-size: large;">In patients with a diagnosed ventricular arrhythmia, the next step is a careful evaluation to exclude or confirm the presence any structural heart disease. Evaluation for structural heart disease is necessary and besides a careful history (including family history) physical examination and ECG it should always include echocardiography. Note that the family history can provide clues for an inherited cardiomyopathy, or an inherited disorder of the ion channels. Depending on the specific characteristics of each case and the suspected probable etiology, additional studies can include stress testing with ECG or imaging, cardiac computed tomography-angiography or conventional coronary angiography. Cardiac magnetic resonance imaging (CMR) is indicated only in selected cases, when there is a suspicion of arrhythmogenic right ventricular cardiomyopathy (</span><span style="font-size: large;">ARVC) or </span><span style="font-size: large;">sarcoidosis.</span></div>
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<span style="font-size: large;">Monitoring: Depending on symptom frequency, appropriate options can include </span><span style="font-size: large;">24- to 48-hour Holter monitor, 30-day event </span><span style="font-size: large;">monitor, or long-term implantable loop recorder (ILR).</span><br />
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<h4>
<span style="font-family: inherit; font-size: large;"> <span style="font-family: inherit; font-size: large;"><b>Idiopathic ventricular tachycardia </b></span></span></h4>
<span style="font-family: inherit; font-size: large;"> Despite a comprehensive evaluation, about 10 to 15% of patients with VT will not have an identifiable cause. Most of the idiopathic monomorphic VTs are in one of two categories, defined by the absence of indications of an underlying heart disorder and by ECG morphology. These most prevalent categories of idiopathic VT are VTs that arise in the right or left ventricular outflow tract. The ECG in those VTs typically shows an inferiorly directed frontal axis (the QRS is markedly positive in inferior leads)</span><br />
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<span style="font-size: large;"><b>Inherited Arrhythmia Syndromes</b><br />These are inherited syndromes that can be manifested with ventricular tachycardia (VT), ventricular fibrillation (VF) and sudden death. They incude the congenital long QT syndromes (LQTS), the </span><span style="font-size: large;">short QT syndrome,</span><span style="font-family: inherit; font-size: large;"> the Brugada syndrome and catecholaminergic polymorphic VT</span><br />
<span style="font-size: large;"> The <b>congenital long QT syndromes</b></span><span style="font-size: large;"> form </span><span style="font-size: large;">a family of disorders characterized by prolongation of </span><span style="font-size: large;">cardiac repolarization with a prolonged QT interval. These patients have a tendency to develop</span><br />
<span style="font-size: large;">polymorphic VT (torsades de pointes) which is often transient (self-terminating) causing syncope but in some cases it can degenerate to ventricular fibrillation causing sudden death. </span><span style="font-size: large;">These patients, although they have structuraly normal hearts and they are usually otherwise healthy individuals, have an increased risk for syncope and sudden cardiac death.</span><br />
<span style="font-size: large;">The estimated prevalence of the LQTS </span><span style="font-size: large;">in the general population is about </span><span style="font-size: large;">1 in 3000 - 5000 people. The LQTS </span><span style="font-size: large;">are caused by mutations in genes that encode ion channel proteins, with the resultant ion channel dysfunction leading to</span><span style="font-size: large;"> a prolonged repolarization phase of the ventricular action potential.</span><span style="font-size: large;"><span class="fontstyle0">A prolonged QT is defined </span></span><span style="font-size: large;">in women </span><span style="font-size: large;">as a QTc >460 ms and </span><span style="font-size: large;">in men a QTc </span><span style="font-size: large;">>450 ms. A congenital long </span><span style="font-size: large;">QT syndrome is suspected in a person with a prolonged QTc</span><span style="font-size: large;"> (particularly if QTc>480ms) if there is not any </span><span style="font-size: large;">reversible cause of QT prolongation (metabolic, drug, ischemia, or cardiomyopathy)</span><span class="fontstyle0" style="font-size: large;">.</span><span style="font-size: large;"> Some other findings that are supportive of this diagnosis are </span><span style="font-size: large;">the following: The presence of T wave alternans (beat to beat variation in the morphology of the T wave), syncope, family history of long QT or family history of sudden death, ECG screening of family members (marked<br />prolongation of QTc in a family member).</span><br />
<span style="font-size: large;"> In people with congenital long QT syndrome (LQTS), f</span><span style="font-size: large;">actors associated with higher risk for polymorphic VT and sudden death are:</span><span style="font-size: large;"> QTc > 500 ms, syncope despite treatment with a beta-blocker, age-gender</span><span style="font-size: large;"> interactions (increased event rate in males during childhood and females after </span><span style="font-size: large;">onset of adolescence), LQTS genotype (LQT3, which responds less to beta blocker treatment). There are also some factors that can further prolong repolarization in people with LQTS and thereby they can trigger an episode of VT or sudden death. Such factors are</span><span style="font-size: large;"> e</span><span style="font-size: large;">lectrolyte disorders, bradycardia or pauses, sudden sympathetic stimulation, and drug effects</span><span style="font-size: large;">. </span><br />
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<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>ECG: Congenital Long QT syndrome (LQTS). Leads V1 and II are shown here. Note the very prominent QT prolongation in this example</b></span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiLOeU1p1vzy5eRxldEomHcNFWJhL9sZUy5eEzPFetlVVigdsg-PgkivlhfzRMc2Jad7eM6Po3wLDo1w32VMhalLJB9WvAT6c9-qbvr36fk_U338pGAHts6b_Lj6VsZ6MK6kFvl6cUFgLM/s1600/%25CE%2595%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2583%25CF%258D%25CE%25BD%25CE%25B4%25CF%2581%25CE%25BF%25CE%25BC%25CE%25BF+%25CE%25BC%25CE%25B1%25CE%25BA%25CF%2581%25CE%25BF%25CF%258D+Q%25CE%25A4-2.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="" border="0" data-original-height="205" data-original-width="360" height="363" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiLOeU1p1vzy5eRxldEomHcNFWJhL9sZUy5eEzPFetlVVigdsg-PgkivlhfzRMc2Jad7eM6Po3wLDo1w32VMhalLJB9WvAT6c9-qbvr36fk_U338pGAHts6b_Lj6VsZ6MK6kFvl6cUFgLM/s640/%25CE%2595%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2583%25CF%258D%25CE%25BD%25CE%25B4%25CF%2581%25CE%25BF%25CE%25BC%25CE%25BF+%25CE%25BC%25CE%25B1%25CE%25BA%25CF%2581%25CE%25BF%25CF%258D+Q%25CE%25A4-2.jpg" title="ECG: a case of congenital long QT syndrome (LQTS)-cardiology book" width="640" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><b style="font-family: arial, helvetica, sans-serif; font-size: medium;">ECG: another case of a congenital long QT syndrome (LQTS). The limb leads are shown here.</b></td></tr>
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<br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <span style="font-size: large;">A <b>congenital short QT syndrome</b> </span><span style="font-size: large;">has also been described. The cause is a mutation enhancing a repolarizing potassium current. To date, mutations in six genes have been implicated in the pathogenesis. The syndrome has most often an autosomal dominant inheritance, but some de novo sporadic cases have also been described. </span><span style="font-size: large;">This uncommon syndrome, </span><span style="font-size: large;">first described in 2000, </span><span style="font-size: large;">is characterized </span><span style="font-size: large;">by a short QT interval (usually QT ≤ 320 msec or QTc ≤ 340msec</span><span style="font-size: large;"> </span><span class="fontstyle0" style="font-size: large;">),</span><span style="font-size: large;"> a high incidence of syncope and </span><span style="font-size: large;">atrial fibrillation </span><span style="font-size: large;">and an increased risk for </span><span style="font-size: large;">sudden death. </span><span style="font-size: large;">Symptoms, including syncope or cardiac </span><span style="font-size: large;">arrest, occur most often during periods of rest or sleep. A</span><span class="fontstyle0" style="font-size: large;">trial fibrillation occurs in approximately a third (1/3 ) of the patients. </span><span style="font-size: large;"><br />ECG features consists of a short QT interval (QTc ≤340 msec), an ST segment which is absent or short and T waves in the precordial leads are usually tall and peaked. In some cases T waves can be inverted.</span><br />
<span style="font-size: large;"> <br style="line-height: normal; text-align: -webkit-auto; text-size-adjust: auto;" />The<b> Brugada syndrome</b> is another familial condition</span><span style="font-size: large;"> </span><span style="font-size: large;">associated with sudden death.</span><span style="font-size: large;"> </span><span style="font-size: large;">It is caused by a mutation in an ion- channel gene (causing reduced function of a sodium channnel) </span><span style="font-size: large;">.</span><span style="font-family: inherit; font-size: large;">The inheritance is autosomal dominant but the mutations are heterogenous. It usually affects males (90% of the affected people are males).</span><br />
<span style="font-size: large;"> The ECG shows an </span><span style="font-size: large;"> incomplete or complete right bundle branch block with a coved ST-segment</span><span style="font-family: inherit; font-size: large;"> elevation in leads V1 and V2. </span><br />
<span style="font-size: large;">There are three types of Brugada ECG pattern, but only type 1 is associated with a risk of clinical events such as VT, syncope or sudden death.</span><span style="font-size: large;"> These patients can manifest episodes of polymorphic VT and </span><span style="font-size: large;">ventricular fibrillation (but not monomorphic VT) often during sleep, or at rest, or during a febrile illness (fever can trigger polymorphic VT in these patients).</span><br />
<span style="font-size: large;"> Type 1: coved ST elevation ≥ 2mm at the J point in at least two of the leads V1-V3, with T‐wave inversion<br />Type 2: saddleback ST elevation >1mm with upright or biphasic T wave<br />Type 3: coved ST< 2mm or saddleback ST<1mm<br />Brugada ECG patterns can be transient and they can be unveiled by Na channel blockers, such as flecainide, or by fever, propofol, cocaine, or tricyclic antidepressant use.</span><br />
<span style="font-size: large;">The spontaneous type 1 Brugada pattern is the one most specifically associated with sudden death and this is called Brugada syndrome. The other two patterns are suspicious but may often be seen in absolutely healthy individuals and they require provocative testing with flecainide to make the diagnosis of Brugada syndrome. Provocation of type 1 pattern with flecainide establishes the diagnosis, but provoked type1 Brugada has a much lower event risk than the spontaneous type 1. The </span><span style="font-size: large;">spontaneous type 1 Brugada pattern is associated with a </span><span style="font-size: large;">syncope/sudden death rate of approximately </span><span style="font-size: large;">0.5% per year.Types 2 and 3 are not clearly associated with an increased event rate.</span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg6yTqsHgX-xfoyUCye_g3hDYzDtG9tFgVLGHFiwOw880w-hSXpoKSGLZrqoTjiVB6LE15UJT1syHJC6yqfMuXmijIwPrBPLahNKxsnPrEUig6JEyb28G2FEzUFogh4dsU5SUWuZYqiB_g/s1600/Brugada-type-1-leads+V1%252CV2_F.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="" border="0" data-original-height="248" data-original-width="127" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg6yTqsHgX-xfoyUCye_g3hDYzDtG9tFgVLGHFiwOw880w-hSXpoKSGLZrqoTjiVB6LE15UJT1syHJC6yqfMuXmijIwPrBPLahNKxsnPrEUig6JEyb28G2FEzUFogh4dsU5SUWuZYqiB_g/s400/Brugada-type-1-leads+V1%252CV2_F.jpg" title="ECG Brugada syndrome type -1 cardiology book" width="204" /></a> </td></tr>
<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>ECG leads V1 and V2 showing a right bundle branch block (rSR΄) morphology and a coved-slowly descending ST elevation > 2mm in these right precordial leads with a negative T wave This is the ECG pattern of Brugada syndrome type 1, which is the type that has clinical significance</b></span></td></tr>
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<span class="fontstyle0" style="font-size: large;"><span class="fontstyle0">In asymptomatic type 1 Brugada pattern, an electrophysiologic study may be performed, during which an inducible VF implies a higher risk of sudden death, although this is still controversial.<br />Asymptomatic type 2 or 3 patterns do not require any specific workup and are normal variants rather than specific predictors of life‐threatening<br />ventricular arrhythmias.</span> </span><br />
<span class="fontstyle0" style="font-size: large;">In persons with the Brugada syndrome </span><span style="font-size: large;">the risk of VT can be reduced by treatment with </span><span class="fontstyle0" style="font-size: large;">quinidine.</span><br />
<span class="fontstyle0" style="font-size: large;"> Indications for</span><span style="font-size: large;"> ICD implantation include patients who have been resuscitated from an episode of cardiac arrest, or patients with Brugada type 1 (</span><span style="font-size: large;">spontaneous or inducible) and</span><span style="font-size: large;"> a history of syncope.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><b>Catecholaminergic polymorphic VT</b></span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Catecholaminergic polymorphic ventricular tachycardia (CPVT), </span><span style="font-size: large;">a rare genetic condition resulting from abnormal calcium homeostasis in the myocardial cells,</span><span style="font-size: large;"> is an inheritable cardiac channelopathy, i.e. a genetic disorder of the ion channels of the cardiac myocytes. CPVT is considered as a highly malignant channelopathy because it predisposes to sudden cardiac death. It is thought to affect 1 in 10,000 people and is estimated to cause 15% of all unexplained sudden cardiac deaths in young people.</span><br />
<span style="font-size: large;">CPVT </span><span style="font-size: large;">results from mutations in the genes encoding the cardiac ryanodine receptor type II or encoding calsequestrin and also some other mutations (mutations </span><span style="font-size: large;">in the genes encoding the calcium signaling protein calmodulin, another gene located in the chromosome 7, etc).</span><span style="background-color: white; font-family: "times new roman" , "stixgeneral" , serif; font-size: 15.9991px; line-height: 21.9988px;"> </span><span style="font-size: large;"> These mutations cause an increased intracellular calcium and this predisposes to an increased risk of ventricular arrhythmias.</span><br />
<span style="font-size: large;">Symptom onset most often occurs in the first two decades of life, with a median age at diagnosis of 15 ± 10 years but there is also a type with delayed symptom onset in patients aged 30-50 years. The older age group has a larger proportion of females. </span></div>
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<div class="MsoNormal" style="margin-bottom: 0.0001pt;">
<span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 18pt;">When symptoms appear, they occur with exercise or
emotional stress and they include palpitations, syncope, or sudden death. When
a young person with a structurally normal heart has syncope or cardiac arrest
during exercise or emotional upset, the diagnosis of CPVT should be considered.</span><span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 13.5pt;"><o:p></o:p></span></div>
<div class="MsoNormal" style="margin-bottom: 0.0001pt;">
<span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 18pt;">The resting ECG is usually normal. In some patients
sinus bradycardia, indications of sick sinus syndrome, or intermittent atrial
tachycardia may be present. Exercise ECG is helpful for the diagnosis
because it often demonstrates ventricular arrhythmias that become more
pronounced as the sinus rate increases with exercise at about 110-130 beats per
minute. The arrhythmias often start to appear as multiform premature
ventricular complexes, progressing to ventricular couplets and triplets (often
with non-uniform QRS morphologies), and then to ventricular tachycardia
(VT). The tachycardia is typically a bidirectional VT which is
characterized by beat-to-beat alternation of the axis and the morphology of the
QRS, although just a polymorphic ventricular tachycardia may also appear.
Usually the arrhythmias gradually resolve after the end of the exercise. Holter
ECG monitoring can also be helful in the diagnosis.</span><span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 13.5pt;"><o:p></o:p></span></div>
<span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 18pt; line-height: 115%;"> Symptomatic patients
are treated with beta-blockers. An ICD is indicated for patients with
catecholaminergic polymorphic VT who survive from sudden death or manifest
syncope or sustained VT despite treatment with beta-blockers.</span></div>
<div>
<span style="font-family: inherit; font-size: large;"> </span><br />
<span style="font-family: inherit; font-size: large;"><b>Arrhythmiogenic right ventricular cardiomyopathy</b> :</span><br />
<span style="font-size: large;">See the chapter on cardiomyopathies, where this entity is described. (link: <a href="http://cardiologybookandcases.blogspot.com/2016/12/cardiomyopathies-cardiomyopathy-diagnosis-treatment-cardiologyfreebook.html" target="_blank">The cardiomyopathies</a>)</span><br />
<h3>
<span style="font-size: large;"><br /></span></h3>
<h3>
<span style="font-size: large;">Impantable cardioverter defibrillator (ICD) for the secondary prevention of sudden cardiac death (SCD) and ventricular tachycardia (VT): </span></h3>
<br />
<span style="font-size: large;">ICDs are implantable electronic devices highly effective for termination of VT and ventricular fibrillation (VF), which also provide pacing in case of bradycardia. The main benefit of</span><span style="font-size: large;"> ICDs is that they decrease mortality in patients with </span><span style="font-size: large;">structural heart diseases, with increased</span><span style="font-size: large;"> risk </span><span style="font-size: large;">for sudden death.</span><br />
<span style="font-size: large;">The components of an ICD are the following: The ICD generator which is implanted in the subcutaneous tissue of the upper chest at the subclavicular area, an atrial pacing lead which is placed in the right atrium, and a ventricular pacing and defibrillating lead in the right ventricle. If it is a unit also capable of biventricular pacing (used in patients with symptomatic heart failure with EF<35% and prolonged QRS duration, see chapter on heart failure) then it also includes a lead for pacing the left ventricle, usually placed in the left ventricular branch of the coronary sinus (LV lead).</span><span style="font-size: large;"> </span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">ICDs can terminate ventricular arrhythmias in two ways: </span><br />
<span style="font-size: large;">a) They can terminate a monomorphic VT by antitachycardia pacing, which is a burst of rapid </span><span style="font-size: large;">pacing, at a rate faster than the VT.</span><br />
<span style="font-size: large;">b) An electric</span><span style="font-size: large;"> shock is delivered i</span><span style="font-size: large;">f </span><span style="font-size: large;">antitachycardia pacing</span><span style="font-size: large;"> fails, or in case of rapid</span><span style="font-size: large;"> VT or VF. </span><span style="font-size: large;">Shocks are often lifesaving, but they are also painful. </span><br />
<span style="font-size: large;">ICD complications: <br />The most common complication is the delivery of inappropriate (unnecessary) shocks in response to a rapid supraventricular tachycardia or to electrical noise (resulting from an ICD lead fracture).<br />Another complication is infection of the device ( in about 1% of patients).</span><span style="font-size: large;">As a general rule ICDs are implanted only if there is also a reasonable expectation for survival of at least 1 year (with the planned treatment), with acceptable functional capacity.</span><br />
<span style="font-size: large;">ICD implantation is recommended in patients with documented VF or haemodynamically not tolerated VT in the absence of reversible causes and not within 48 h after myocardial infarction, who are receiving chronic optimal medical therapy. </span><br />
<span style="font-size: large;">This is class I recommendation and is based on a meta-analysis of three trials, Antiarrhythmic drugs Versus Implantable Defibrillator</span><span style="font-size: large;">(AVID), </span><span style="font-size: large;">Cardiac Arrest Study Hamburg (CASH) and </span><span style="font-size: large;"> Canadian Implantable Defibrillator Study (CIDS), conducted in patients who had suffered a cardiac arrest or hemodynamically unstable VT, or VT with syncope. </span><span style="font-size: large;">These studies, compared treatment with an ICD with anti-arrhythmic drug therapy, predominantly amiodarone.</span><br />
<span style="font-size: large;">ICD implantation should be considered in patients with recurrent sustained VT (not within 48 h after myocardial infarction) who are receiving chronic optimal medical therapy, even if they have a normal left ventricular EF (class IIa).</span><br />
<span style="font-size: large;">In patients with VF or VT and an indication for ICD, amiodarone may be considered as an alternative treatment (instead of the ICD), when an ICD is not available, contraindicated for concurrent medical reasons or refused by the patient.</span><br />
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<b style="color: #274e13; font-size: x-large;">Links and bibliography</b><span style="font-family: inherit; font-size: large;"></span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: large;"> </span><span style="font-size: small;">Brugada J. Katritsis DG, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. </span><span style="font-size: small;"><i>European Heart Journal</i>, 2020;41,(5):655–720. LINK<a href="https://academic.oup.com/eurheartj/article/41/5/655/5556821#" target="_blank">2019 ESC Guidelines for the management of patients with supraventricular tachycardia</a></span></span></b><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><br />Tang PT, Do DH, et al. Team Management of the Ventricular Tachycardia Patient. Arrhythmia & Electrophysiology Review 2018;7(4):238–46. LINK <a href="https://www.aerjournal.com/articles/Management-Ventricular-Tachycardia" target="_blank">Team Management of the Ventricular Tachycardia Patient </a></span></b></span> <br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: small;">Brugada J, Diez DP. How to recognise and manage idiopathic ventricular tachycardia. T</span></span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: small;">he e-journal of the ESC Council for Cardiology Practice 2010;8 (26) </span></span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: small;">LINK <a href="https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-8/How-to-recognise-and-manage-idiopathic-ventricular-tachycardia" target="_blank">How to recognise and manage idiopathic ventricular tachycardia</a></span></span></b><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;">Medi C, Kalman JM, Freedman SM. Supraventricular Tachycardia. Med J Aust 2009;190 (5): 255-260 LINK <a href="https://www.mja.com.au/journal/2009/190/5/supraventricular-tachycardia#panel-article" target="_blank">Supraventricular Tachycardia</a></span></b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: large;"> </span></span></b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"> </span></b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><a href="https://www.escardio.org/static_file/Escardio/Guidelines/publications/SVAguidelines-SVA-FT.pdf">Guidelines on supraventricular tachycardias </a></span></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"> <br /><br /><a href="http://eurheartj.oxfordjournals.org/content/early/2016/08/26/eurheartj.ehw210" target="_blank">2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS</a><br /><br /> <a href="http://eurheartj.oxfordjournals.org/content/36/41/2793">Guidelines on ventricular arrhythmias and the prevention of sudden cardiac death- ESC 2015</a><br /><br /><a href="http://content.onlinejacc.org/article.aspx?articleid=1659563">ACCF/HRS/AHA 2013 Appropriate Use Criteria for Implantable Cardioverter-Defibrillators and Cardiac Resynchronization Therapy</a><br /><br /><a href="http://content.onlinejacc.org/article.aspx?articleid=1871606">HRS/ACC/AHA Expert Consensus Statement on the Use of Implantable Cardioverter-Defibrillator Therapy in Patients Who Are Not Well Represented in Clinical Trials</a><br /><br /><br /><a href="http://eurheartj.oxfordjournals.org/content/ehj/31/19/2369.full.pdf">Atrial Fibrillation Guideline ESC 2010</a><br /><br /><br /><a href="http://eurheartj.oxfordjournals.org/content/ehj/33/21/2719.full.pdf">Focused update of the guidelines for atrial fibrillation .2012- ESC</a><br /><br /><a href="http://circ.ahajournals.org/content/early/2014/04/10/CIR.0000000000000041">Atrial Fibrillation Guideline2014 AHA/ACC/HRS -Click on the link and download PDF !</a><br /><br /><br /><a href="https://www.nice.org.uk/guidance/cg180/resources/atrial-fibrillation-management-35109805981381">Guideline on atrial fibrillation -NICE</a><br /><br /><br /> <a href="http://circ.ahajournals.org/content/132/18_suppl_2.toc">2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care</a></span></b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><br /></span></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278051/pdf/112292.pdf" style="font-size: x-large;" target="_blank">Oral Anticoagulant Therapy Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Clinical Practice Guidelines</a></span></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><br /></span></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278055/" target="_blank">Evidence-Based Management of Anticoagulant Therapy</a></span><span style="font-size: small;"> <span style="font-size: medium;"><br /></span></span></b></span>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-size: small;"><a href="http://www.jgh.ca/uploads/Hematology/JGH%20ACO%20Guidelines%20Final%2006-29-2012.pdf" target="_blank">PRACTICE GUIDELINES FOR ANTICOAGULATION MANAGEMENT</a></span></b></span><br />
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-81091214812570901212016-08-19T01:40:00.000+03:002020-02-02T23:30:20.904+02:00Mitral regurgitation. Diagnosis, echocardiography and management. <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: large;"><br /></span> <span style="font-size: large;">IMPORTANT NOTE : THE SITE IS UNDER DEVELOPMENT AND CONTENTS ARE CONTINUOUSLY ADDED.</span><br />
<span style="font-size: medium;"><span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;"><b><i>Cardiology free e-book online</i></b></span></span><br />
<span style="font-size: large;">A VIDEO : </span><br />
<span style="font-size: large;"><b>A case</b> of a 65- years- old man with effort dyspnea and nocturnal dyspnea, atrial fibrillation and an apical systolic murmur. Echo showed severe mitral regurgitation A discussion of the ECG, chest X-ray, echocardiogram and indications for surgical treatment. Analysis of how to assess the severity of mitral regurgitation with echocardiography and of the indications for surgery and the therapeutic desicion on the type of surgery.</span><br />
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<h2>
<span style="font-family: inherit; font-size: large;"><b>Mitral Regurgitation (MR) -Important Notes</b></span></h2>
<span style="font-family: inherit; font-size: large;"><b><br /></b></span> <span style="font-size: large;"> The role of the <b>mitral valve (MV)</b> is to permit unidirectional flow from the left atrium (LA) to the left </span><span style="font-size: large;">ventricle (LV).</span><br />
<span style="font-size: large;">The mitral apparatus is composed of an annulus, two leaflets, </span><span style="font-size: large;">chordae tendinae and two </span><span style="font-size: large;">papillary muscles</span><span style="font-size: large;"> (</span><span style="font-size: large;">anterolateral and </span><span style="font-size: large;">posteromedial). </span><span style="font-size: large;">The </span><span style="font-size: large;">mitral subvalvular apparatus is a term, that includes the </span><span style="font-size: large;">chordae tendinae and the two </span><span style="font-size: large;">papillary muscles.</span><br />
<span style="font-size: large;">For adequate function of the mitral valve, </span><span style="font-size: large;">proper function and interaction between these parts, t</span><span style="font-size: large;">ogether with the LV and the LA, is </span><span style="font-size: large;">necessary. Abnormal function of any one of these </span><span style="font-size: large;">components can lead to mitral regurgitation (MR).</span><br />
<span style="font-size: large;">MR is the presence of </span><span style="font-size: large;">backward flow of blood from the left ventricle (LV) into the left atrium (LA) during systole, </span><span style="font-size: large;">caused by inadequate coaptation of the valve leaflets.</span><br />
<h3>
<span style="font-size: large;"><b>Mechanisms and causes of mitral regurgitation</b></span></h3>
<span style="font-size: large;">There are three <b>basic mechanisms of mitral regurgitation</b> (MR): 1) Alterat</span><span style="font-size: large;">ion of mitral leaflets, commissures, or annulus </span><br />
<span style="font-size: large;">2) Defective subvalvular (tensor) </span><span style="font-size: large;">apparatus and</span><br />
<span style="font-size: large;"> 3) Alterations of left ventricular and left atrial </span><span style="font-size: large;">size and function (i.e dilatation of the LV or the LA can cause MR).</span><br />
<span style="font-size: large;"><b>Organic (primary) MR</b> is caused primarily by abnormalities of the valve leaflets </span><span style="font-size: large;">and/or chordae tendinae. </span><br />
<span style="font-size: large;"><u>Causes of primary MR </u></span><br />
<span style="font-size: large;">Myxomatous degeneration (mitral valve prolapse is caused by myxomatous degeneration and it is also the most common cause of isolated severe mitral </span><span style="font-size: large;">regurgitation),</span><br />
<span style="font-size: large;"> Infective endocarditis (it </span><span style="font-size: large;">may cause </span><span style="font-size: large;">valve leaflet perforation or a vege</span><span style="font-size: large;">tation interfering with leaflet coaptation),</span><br />
<span style="font-size: large;"> Rheumatic valve disease,(it is caused by rheumatic fever and gradually deforms the valve over many years, with thickening of the leaflet tips, chordal shortening, and calcification of the valve. Usually, in rheumatic valve disease, the regurgitation is in combination with stenosis, but pure MR can also occasionally occur. </span><br />
<span style="font-size: large;">A congenital cleft of the anterior mitral leaflet (associated with a </span><span style="font-size: large;">primum atrial septal defect or an </span><span style="font-size: large;">atrioven</span><span style="font-size: large;">tricular canal defect, but it can also occur in isolation</span><span style="font-size: large;">). </span><br />
<span style="font-size: large;">Ruptured chordae tendinae are </span><span style="font-size: large;">responsible for a considerable percentage of cases of mitral regur</span><span style="font-size: large;">gitation.</span><span style="font-size: large;">Rupture of chordae can be </span><span style="font-size: large;">a result of myxomatous degeneration in the setting of mitral valve </span><span style="font-size: large;">prolapse</span><span style="font-size: large;">, a complication of endocarditis,</span><span style="font-size: large;"> </span><span style="font-size: large;">a complication of a blunt or penetrating thoracic trauma, </span><span style="font-size: large;">or idiopathic (not attributed to a specific cause).</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Degenerative MR is caused by myxomatous degeneration of the valve (m</span><span style="font-size: large;">yxomatous proliferation can occur in the leaflets, </span><span style="font-size: large;">chordae tendineae, and/or annulus). This is the cause of the</span><span style="font-size: large;"> mitral valve prolapse syndrome. It u</span><span style="font-size: large;">sually occurs as a primary condition-the most common form (Barlow's disease or fibroelastic </span><span style="font-size: large;">deficiency) which can be familial or non familial. However, it has also been associated with genetic syndromes affecting the </span><span style="font-size: large;">connective tissue, including Marfan syndrome, Ehlers–Danlos syndrome, </span><span style="font-size: large;">osteogenesis imperfecta, etc.</span><br />
<span style="font-size: large;">A p</span><span style="font-size: large;">aravalvular prosthetic leak (PVL)</span><span style="font-family: inherit; font-size: large;"> is another cause of MR, in cases of prosthetic valves, where blood flows through a gap between the structure of the implanted valve and the mitral annulus. It can be related to disruption of sewing ring sutures caused by infectious endocarditis, accompanied by an abscess formation. Another cause is calcification and fibrosis of the annulus or even technical factors of the surgical procedure (incomplete apposition of the valvular structure against the annulus). In most cases, paravalvular leaks are mild and cause no symptoms but sometimes they are large.</span><span style="font-size: large;"> A significant PVL can cause heart failure, or hemolytic anemia. </span><br />
<span style="font-size: large;"><span class="fontstyle0"><b>Carpentier’s classification</b> is used to classify MR according to its mechanism, specifically relying on </span><span class="fontstyle0">the pattern of leaflet motion. It categorizes MR into:</span></span><br />
<span style="font-size: large;"><span class="fontstyle0"> Type I: MR with normal leaflet motion (i.e. annular dilatation, or leaflet perforation), </span></span><br />
<span style="font-size: large;"><span class="fontstyle0">Type II: MR due to excessive leaflet motion (mitral valve prolapse or a flail mitral leaflet</span><span class="fontstyle0">), </span></span><br />
<span style="font-size: large;"><span class="fontstyle0">type III: MR due to a restricted motion of its leaflets, with the following subtypes:</span></span><br />
<span style="font-size: large;"><span class="fontstyle0"> IIIa systolic and diastolic restrictive leaflet motion (such as in rheumatic MR) and</span></span><br />
<span style="font-size: large;"><span class="fontstyle0"> IIIb leaflet motion is </span></span><span style="font-size: large;">restrictive</span><span class="fontstyle0" style="font-size: large;"> only in systole (such as in secondary MR).</span><br />
<h4>
<span style="font-size: large;"><b>Causes of Secondary (functional) mitral regurgitation</b></span></h4>
<span style="font-size: large;"> Functional MR is caused primarily by ventricular dysfunction usually accompanied by </span><span style="font-size: large;">annular dilatation (e.g., in dilated cardiomyopathy and ischemic MR). </span><span style="font-size: large;">Ischemia can cause either dysfunction or rupture of a papillary </span><span style="font-size: large;">muscle. Rupture can occur in acute myocardial infarction (either transmural, or subendocardial). The posteromedial papillary muscle is </span><span style="font-size: large;">most often </span><span style="font-size: large;">affected by ischemic dysfunction or rupture </span><span style="font-size: large;">because it has a single-arterial blood supply. </span><br />
<span style="font-size: large;">Global or regional left ventricular dysfunction and enlargement can alter the position of the papillary muscles and can also cause dilatation of the mitral ring. These are changes that often result in mitral regurgitation (MR).</span><br />
<span style="font-size: large;">In hypertrophic obstructive cardiomyop</span><span style="font-size: large;">athy, MR results from distortion of the mitral valve apparatus due to the </span><span style="font-size: large;">systolic anterior motion of the mitral valve.</span><br />
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<span style="font-size: large;"><b>Physical examination findings in mitral regurgitation</b></span></h3>
<span style="font-size: large;">In clinical examination, </span><span style="font-size: large;"> </span><span style="font-size: large;">the hallmark of chronic mitral regurgitation (MR) is a </span><span style="font-size: large;"> holosystolic murmur heard with maximum intensity at the position of the heart apex (fifth intercostal space at the midclavicular line). T</span><span style="font-size: large;">he murmur fre</span><span style="font-size: large;">quently radiates to the axilla. Occasionally </span><span style="font-size: large;">(if the regurgitant jet is directed anteriorly, in</span><span style="font-size: large;"> a primary posterior leaflet abnor</span><span style="font-size: large;">mality)</span><span style="font-size: large;"> the radiation can be toward </span><span style="font-size: large;">the anterior chest wall or toward the aortic area.</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;"> </span><span style="font-size: large;">The intensity of the murmur does not correlate reliably with </span><span style="font-size: large;">the severity of MR. In significant MR a third heart sound (</span><span style="font-size: large;">S3) that does not necessarily indicate left ventricular dysfunction and/or an early diastolic flow rumble may be present. These are due to an increased </span><span style="font-size: large;">antegrade flow through the mitral valve in early diastole. This happens because not only blood returning from the pulmonary circulation to the left atrium (LA) passes</span><span style="font-size: large;"> </span><span style="font-size: large;">through the mitral orifice in diastole,</span><span style="font-size: large;"> but also blood, that has regurgitated into the LA during the previous systole. </span><br />
<span style="font-size: large;">In </span><span style="font-size: large;">severe </span><span style="font-size: large;">chronic mitral regurgitation</span><span style="font-size: large;"> the </span><span style="font-size: large;">apical impulse</span><span style="font-size: large;"> is usually brief (of small duration), laterally displaced </span><span style="font-size: large;">and enlarged. (If </span><span style="font-size: large;">ventricular systolic function gradually deteriorates, then the </span><span style="font-size: large;">duration of the apical impulse increases).</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;"> The presence of an apical thrill indicates severe MR.</span><br />
<span style="font-size: large;">In mitral valve prolapse, the murmur is endsystolic and a midsystolic click is heard before the murmur. </span><br />
<span style="font-size: large;"> It is important to know that in acute severe mitral regurgitation the systolic apical murmur may be short (not holosystolic), or soft, or even completely absent, </span><span style="font-size: large;">because of the low left ventricular-to-atrial pressure gradient. This lower pressure gradient is due to the markedly elevated left atrial (LA) pressure, since the LA in acute MR, does not have the time to dilate, in order to accommodate the regurgitant volume without a marked pressure elevation.</span><span style="font-size: large;"> Because of the markedly raised LA pressure, if acute MR is severe, it </span><span style="font-size: large;">promptly</span><span style="font-size: large;"> results in severe pulmo</span><span style="font-size: large;">nary congestion. A third or fourth heart sound (S3, S4) may also be present due to the elevated atrial and ventricular diastolic pressures.</span><span style="font-size: large;"> </span><span style="font-size: large;">Acute MR usually results from infective endo</span><span style="font-size: large;">carditis, myocardial infarction, </span><span style="font-size: large;">chordal </span><span style="font-size: large;">rupture (rupture of chordae tendinae),</span><span style="font-size: large;"> or trauma.</span><br />
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<h3>
<span style="font-family: inherit; font-size: large;"><b>Echocardiographic assessment of the etiology of mitral regurgitation</b></span></h3>
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<span style="font-size: large;">In degenerative mitral valve disease, the leaflets are thick and redundant (with excessive, unnecessary tissue) and the chordae are elongated. In some cases, there is a rupture of one or more chordae tendinae. Ruptured chordae appear echocardiographically as flail segments. To diagnose mitral valve prolapse, the following echocardiographic criteria should be fulfilled: Movement of any part of either leaflet more than 2 mm behind the annular plane (towards the left atrium) in systole, in the parasternal long axis view and the point of leaflet coaptation being located behind the annular plane in apical 4 chamber view.</span><span style="font-size: large;"></span></div>
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<span style="font-size: large;">In rheumatic mitral regurgitation, echocardiographic findings include thickening </span><span style="font-size: large;">of the tips of the mitral leaflets and </span><span style="font-size: large;">some degree of commissural fusion. The movement of the valve leaflets is restricted. </span></div>
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<span style="font-size: large;"> Secondary or functional MR results from local or global left ventricular remodeling (a pathologic change in the shape of the left ventricle). This leads to the </span><span style="font-size: large;">displacement of the </span><span style="font-size: large;">papillary muscles resulting in tethering of mitral leaflets. Tethering means that the leaflets are pulled and their closing motion is restricted.</span><span style="font-size: large;"> This causes a failure of coaptation of the mitral valve leaflets. An echocardiographic parameter which reflects tethering is the coaptation distance or coaptation height</span><span style="font-size: large;">. This is the</span><span style="font-size: large;"> </span><span style="font-size: large;">end-systolic distance between the center of the mitral annular plane and the coaptation point of the leaflets. It can be evaluated in </span><span style="font-size: large;">transthoracic</span><span style="font-size: large;"> </span><span style="font-size: large;">parasternal long axis view or </span><span style="font-size: large;">transoesophageal</span><span style="font-size: large;"> a long axis view at 135°. Normal coaptation height or distance is ≤ 10 mm. When it exceeds this value, it is an indication of tethering of the mitral valve leaflets. Another parameter which reflects tethering is the tenting area. This is t</span><span style="font-size: large;">he triangular zone comprised between the mitral annulus, both leaflets and the coaptation point.</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="background-color: orange;"> Video</span> Transesophageal echocardiographic views ( 2D midesophageal 4 chamber view at 0 degrees and 2D midesophageal long axis view at 120-130 degrees ) and also a 3D transoesophageal view (3D-zoom) of the mitral valve from the left atrial aspect. A patient with severe mitral regurgitation (MR) due to tethering of the valve leaflets as a result of systolic left ventricular dysfunction. The patient had ischemic cardiomyopathy due to a previous posterolateral infarction. He was treated surgically with CABG and mitral valve replacement.</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>To watch the video in a large screen, after starting it, click on the symbol [] on the lower right corner.</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b style="background-color: orange;"><span style="font-family: "arial" , "helvetica" , sans-serif;">Video</span><span style="font-family: "arial" , "helvetica" , sans-serif;"> </span></b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />A case of mitral regurgitation due to a flail P2 scallop of the posterior mitral leaflet (TEE 2D and 3D echocardiography </b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>The case is courtesy of Dr. Özge Özden Tok. </b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>To watch the video in a large screen, after starting it, click on the symbol [] on the lower right corner.</b></span>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Link to the video <a href="https://www.youtube.com/watch?v=Y4WPWluZFfQ" target="_blank">https://www.youtube.com/watch?v=Y4WPWluZFfQ</a></b></span>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b style="font-size: x-large;">Echocardiographic criteria of severe MR </b></span><br />
<span style="font-size: large;">Vena contracta, which is the narrowest portion ("the neck") of the regurgitant </span><span style="font-size: large;">jet-at the level of the valve: with width </span><span style="line-height: 18.4px;"><span style="font-family: inherit; font-size: large;">≥ </span></span><span style="font-size: large;">7 mm.</span><br />
<span style="line-height: 21.4667px;"><span style="font-size: large;">Color jet area >8.0 cm</span></span><span style="font-size: large;"><span style="font-family: inherit; line-height: 21.4667px; vertical-align: super;"><span style="line-height: 21.4667px;"><sup>2</sup></span></span><span style="font-size: medium;"> (t</span>he color jet area is not a very accurate index and it can underestimate MR when the jet is eccentric. The color doppler gain must be properly</span><span style="font-size: large;"> set and color doppler aliasing velocity should be at about 55-60 cm/s).</span><br />
<span style="font-size: large;">An effective regurgitant orifice area <span lang="EN-US" style="line-height: 27.6px;">ERO</span><span style="line-height: 27.6px;"> >0.</span><span lang="EN-US" style="line-height: 27.6px;">4</span><span lang="EN-US" style="line-height: 27.6px;"> </span><span lang="EN-US" style="line-height: 27.6px;">cm<sup>2 </sup></span><span style="line-height: 27.6px;">in primary (organic) MR. or > 0.2</span><span lang="EN-US" style="line-height: 27.6px;"> </span><span lang="EN-US" style="line-height: 27.6px;">cm<sup>2 </sup></span>in functional MR. ERO area is usually calculated with the PISA method (see the video on the top of the page for details about the assessment of mitral regurgitation severity with echocardiography and for a simple and complete description of the PISA-proximal isovelocity area- method).</span><br />
<span style="font-size: large;">CW Doppler signal intensity: A dense CW Doppler signal of MR is suggestive of severe MR.</span><br />
<span style="font-size: large;">Transmitral PW peak early diastolic flow velocity E >1.5 m/s (for a native mitral valve) / E > 2 m/s (for a prosthetic valve), are suggestive of severe MR, if there is no indication of concomitant valve stenosis (PHT of the E wave of the early diastolic transmitral flow is normal).</span><br />
<span style="font-size: large;">Regurgitant volume in primary MR >60 ml / in secondary (functional) MR > 30 ml.</span><br />
<span style="font-size: large;"><u>Magnetic resonance imaging (MRI) </u>is the most accurate method for the assessment of the regurgitant volume and can also provide an accurate assessment of the left ventricular end diastolic and end systolic volume.</span><br />
<h4>
<span style="font-size: large;">Cardiac catheterization findings in mitral regurgitation</span></h4>
<span style="font-size: large;">The pulmonary capillary wedge pressure (PCWP) tracing or the left atrial pressure tracing show an increased amplitude of the v wave and y descent is particularly rapid. Severe mitral regurgitation is suggested by an amplitude of the v wave > 2-3 times the mean PCWP. However, occasionally in slow developing MR, the amplitude of the v wave is not markedly elevated. </span><br />
<span style="font-size: large;">With left ventriculography (infusion of contrast into the left ventricle with a pig-tail angiographic catheter) the severity of MR can be visually assessed, using Seller's criteria: There are four grades of MR (1+/4+, 2+/4+, 3+/4+, 4+/4+). In moderately severe MR (3+) contrast opacifies (makes visible) the entire left atrium (LA) with the same intensity of opacification as the left ventricle (LV), in 2-3 beats after its infusion in the LV. </span><br />
<span style="font-size: large;">In severe MR (4+) contrast completely opacifies the LA in one beat and there is also contrast reflux into the pulmonary veins.</span><span style="font-family: "helvetica neue" , "arial" , "helvetica" , sans-serif;"> <b><i>(In mild to moderate MR of 2+ , the entire LA is fairly opacified but the intensity of opacification of the LA is less than of the LV, and in mild MR of 1+ contrast does not opacify the entire LA and clears from the LA in one heartbeat.)</i></b></span><br />
<span style="font-size: large;"></span><br />
<span style="font-size: large;">Generally in severe valve disease with an indication for surgery coronary angiography is performed before surgery in patients >40 years old, or with multiple risk factors or suspicion for coronary artery disease.</span><br />
<h3>
<b style="font-size: x-large;">Treatment of chronic mitral regurgitation</b></h3>
<span style="font-size: large;">Drugs such as ACE inhibitors, diuretics, beta blockers and/or digoxin are given in cases of symptomatic patients due to left ventricular dysfunction. However definitive treatment is surgery.</span><br />
<span style="font-size: large;">Valve repair, when feasible, is preferable to valve replacement (with a prosthetic valve) because it is associated with less morbidity and mortality.</span><br />
<h4>
<span style="font-size: large;"><b>Indications for surgery in chronic severe MR</b></span></h4>
<span style="font-size: large;">Patients with symptoms NYHA II-IV</span><br />
<span style="font-size: large;">Asymptomatic patients with evidence of left ventricular (LV) dysfunction : LV ejection fraction (EF) 30-60 % and/or LV end systolic dimension </span><span style="font-size: large;"> </span><span style="line-height: 18.4px;"><span style="font-family: inherit; font-size: large;">≥ 45</span></span><span style="font-size: large;"> mm ( in cases, where valve repair is feasible with low surgical risk, the decision for surgery can be made with LV end systolic dimension > </span><span style="line-height: 18.4px;"><span style="font-family: inherit; font-size: large;">40</span></span><span style="font-size: large;"> mm).</span><br />
<span style="font-size: large;">Asymptomatic patients with new onset atrial fibrillation.</span><br />
<span style="font-size: large;">Asymptomatic patients with pulmonary hypertension (pulmonary artery systolic pressure at rest >50 mmHg, or with exercise >60 mmHg.)</span><br />
<h3>
<span style="font-size: large;"><b>Acute mitral regurgitation</b></span></h3>
<span style="font-size: large;">It is characterized by a left atrium (LA) of normal or almost normal size, but with acute rise of LA pressure, because in acute MR the LA does not have the time to dilate, in order to accommodate an increased volume load. For this reason acute MR often leads to pulmonary edema and pulmonary hypertension. </span><br />
<span style="font-size: large;">In contrast to chronic MR, in acute MR the systolic murmur is decrescendo, softer in intensity and not holosystolic (it does not last in all the period of systole and ends well before the aortic component of the second heart sound-A2). This happens because the increased LA pressure results in a lower pressure gradient between the left ventricle (LV) and LA in systole. A fourth heart sound (S4) is frequently audible in acute MR. Echocardiography in acute MR shows no (or only little) dilation of the LA and the LV and a hyperkinetic (with increased systolic motion) LV.</span><br />
<span style="font-size: large;"><u>Treatment of acute MR</u></span><br />
<span style="font-size: large;">Afterload reduction with intravenous nitroprusside and if there is hypotension an inotrope (eg dobutamine) is administered. Afterload reduction is beneficial because it helps to increase forward flow of blood into the aorta in systole and thus it decreases regurgitant flow through the mitral valve. Intraortic balloon counterpulsation can help stabilize the patient. Surgery (this the definitive and absolutely necessary treatment) is generally performed promptly, after initial patient stabilization.</span><br />
<b style="background-color: white; font-family: times, "times new roman", serif; font-size: x-large;"><span style="color: #990000;"><br /></span></b> <b style="background-color: white; font-family: times, "times new roman", serif; font-size: x-large;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><span style="background-color: #ffe599;">More details in ... <br /><b>Useful links </b></span><br /><span style="background-color: white; color: #2a2a2a; font-family: "source sans pro" , sans-serif;"><br /></span></span><br />
<span style="font-size: large;"><span style="background-color: white; color: #2a2a2a; font-family: "source sans pro" , sans-serif;">Baumgarther H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease: The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), </span><em style="background-color: white; border: 0px; box-sizing: border-box; color: #2a2a2a; font-family: "Source Sans Pro", sans-serif; font-stretch: inherit; font-variant-numeric: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">European Heart Journal</em><span style="background-color: white; color: #2a2a2a; font-family: "source sans pro" , sans-serif;"> ehx391, </span><a href="https://doi.org/10.1093/eurheartj/ehx391" style="background-color: white; border: 0px; box-sizing: border-box; color: #006fb7; font-family: "Source Sans Pro", sans-serif; font-stretch: inherit; font-variant-numeric: inherit; line-height: inherit; margin: 0px; padding: 0px; text-decoration-line: none; vertical-align: baseline;">https://doi.org/10.1093/eurheartj/ehx391</a> </span><br />
<span style="font-size: large;">LINK<a href="https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data" target="_blank"> https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data</a><br /><br /><a href="http://content.onlinejacc.org/article.aspx?articleid=1838843">2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease</a><br /><br /><br /><a href="http://www.sfcardio.fr/sites/default/files/pdf/Valvular_Heart_Dis_FT.pdf">ESC Guidelines on the management of valvular heart disease (version 2012)</a></span><span style="font-size: large;"><br /></span><br />
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<span style="color: #0000ee; font-size: large; text-decoration: underline;">2015 ESC Guidelines for the management of infective endocarditis</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <a href="http://www.wikiecho.org/wiki/Mitral_regurgitation" target="_blank"><span style="font-family: inherit; font-size: large;"> Wikiecho/Mitral_regurgitation</span></a><br />
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-45506710112669235912016-07-30T23:01:00.001+03:002018-07-21T18:34:53.610+03:00Aortic regurgitation<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: medium;"><b style="font-size: x-large;">Aortic regurgitation (AR)</b><br /><br /><span style="font-size: large;">The regurgitation of blood from the aorta to the left ventricle through the aortic valve in diastole.</span><br /><b style="font-size: x-large;">Causes of aortic regurgitation (AR)</b><br /><span style="font-size: large;">AR can be caused by primary disease of the aortic valve leaflets and/or abnormalities of the aortic root geometry. The two most common causes of AR is an abnormality (dilation) of the aortic root and degenerative calcification of the aortic valve. Another common cause is bicuspid aortic valve, which is a congenital abnormality, in which the valve has two cusps (instead of the normal three cusps, named right coronary cusp, left coronary cusp and noncoronary cusp). Bicuspid aortic valve causes more often valvular stenosis than regurgitation, but regurgitation is not infrequent in this condition. Other causes of AR are infective endocarditis (it is a cause of acute AR), rheumatic fever, in case of a prosthetic valve: degeneration, paravalvular leak or malfunction. Some more causes (that are due to damage of the leaflets) : trauma, myxomatous degeneration of the aortic valve leaflets, congenital conditions such as a subaortic membranous stenosis or a subaortic ventricular septal defect, drugs (ergot derivatives, fenfluramine).</span><br /><span style="font-size: large;">Causes of AR due to aortic root disease are:</span><br /><span style="font-size: large;">Degenerative dilatation of the aorta age-or hypertension-related.</span><br /><span style="font-size: large;">Dilatation of the aorta due to cystic medial necrosis. This condition, when it is an isolated finding is called annuloaortic ectasia. When it is not an isolated finding, then it is associated with a syndrome, such as Marfan's, or Ehlers Danlos, or osteogenesis imperfecta.</span><br /><span style="font-size: large;">Aortic dissection involving the ascending aorta can cause acute AR.</span><br /><span style="font-size: large;">Arteritis of the aorta caused by giant cell arteritis, seronegative arthropathies (ancylosing spondylitis, psoriatic arhritis, Reiter syndrome, reactive arthritis), Adamantiadis-Behcet syndrome.</span></span><br />
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Pathophysiology and haemodynamic consequences of AR</b> </span><br />
<span style="font-size: large;">In AR there is left ventricular (LV) volume overload because a larger volume of blood enters the left ventricle (LV) in diastole: Besides blood retuning from the pulmonary veins, there is also a volume of blood that regurgitates from the aorta into the LV (</span><span style="font-size: large;">regurgitant volume) in diastole</span><span style="font-size: large;">. The LV works with an i</span><span style="font-size: large;">ncreased in total stroke volume, which is the sum of effective </span><span style="font-size: large;">stroke volume </span><span style="font-size: large;">plus regurgitant volume.</span><br />
<span style="font-size: large;">Aortic regurgitation also causes an increased pulse pressure, with low arterial diastolic pressure (because of the regurgitation of blood from the aorta in diastole) and </span><span style="font-size: large;">increased systolic blood pressure (because of the larger stroke volume ejected by the LV in systole). The pulse pressure is the difference: systolic minus diastolic pressure.</span><br />
<span style="font-size: large;"> LV end-diastolic pressure and </span><span style="font-size: large;">LV end-diastolic volume are increased in aortic regurgitation (AR) because, as mentioned above, a larger volume of blood enters the left ventricle in diastole. This situation leads to e</span><span style="font-size: large;">ccentric myocardial hypertrophy. </span><span style="font-size: large;">An increase in LV end-diastolic volume is also the main com</span><span style="font-size: large;">pensatory mechanism to maintain an adequate effective </span><span style="font-size: large;">stroke volume.</span><br />
<span style="font-size: large;">Left ventricular ejection fraction (EF) is initially normal, </span><span style="font-size: large;">however, LV end </span><span style="font-size: large;">diastolic pressure rises. D</span><span style="font-size: large;">ue to the chronic overload of the left ventricle in severe AR, as the disease progresses, EF decreases over </span><span style="font-size: large;">time and this together with a further increase in LV</span><span style="font-size: large;"> volume, may precede the </span><span style="font-size: large;">onset </span><span style="font-size: large;">of symptoms. </span><br />
<span style="font-size: large;"><b>Acute aortic regurgitation</b> (causes : </span><span style="font-size: large;">infective endocarditis, dissection of the ascending aorta, and </span><span style="font-size: large;">trauma), also causes volume overload of the left ventricle (LV), but in this case the hemodynamic burden imposed on the LV is sudden, and so the LV does not have the time to compensate by dilatation and hypertrophy. For this reason acute severe AR </span><span style="font-size: large;">can be </span><span style="font-size: large;">life-threatening.</span><span style="font-size: large;"> A regur</span><span style="font-size: large;">gitant volume that would be well tolerated in chronic AR </span><span style="font-size: large;">can lead to marked increases in LV end-diastolic pressure </span><span style="font-size: large;">and a decrease </span><span style="font-size: large;">in effective stroke volume. So acute AR can often lead to pul</span><span style="font-size: large;">monary edema, hypotension, and even cardiogenic shock. Indeed, in a</span><span style="font-size: large;">cute severe aortic regurgitation there is usually </span><span style="font-size: large;">dyspnea or pulmonary </span><span style="font-size: large;">edema with a normal </span><span style="font-size: large;">left </span><span style="font-size: large;">ventricular size and high ejection fraction.</span><br />
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Clinical presentation</b> of chronic severe aortic regurgitation:</span><br />
<span style="font-size: large;">Patients with chronic aortic regurgitation can be asymptomatic for</span><br />
<span style="font-size: large;">ma</span><span style="font-size: large;">ny years, with symptoms developing in the late </span><span style="font-size: large;">stages. The most common symptom is dyspnea (</span><span style="font-size: large;">shortness of breath), </span><span style="font-size: large;">i</span><span style="font-size: large;">nitially during exercise, later also at rest. Other </span><span style="font-size: large;">symptoms include </span><span style="font-size: large;">palpitations due to ventricu</span><span style="font-size: large;">lar or supraventricular arrhythmias, or a sensation of a prominent heart beat (due to the increased total stroke volume). Some patients also have </span><span style="font-size: large;">angina, even </span><span style="font-size: large;">in absence of coronary</span><br />
<span style="font-size: large;">artery disease, because of increased myocardial oxygen demand. </span><br />
<span style="font-size: large;"><b>Physical examination in aortic regurgitation</b> </span><br />
<span style="font-size: large;">A characteristic</span><span style="font-size: large;"> </span><span style="font-size: large;">diasto</span><span style="font-size: large;">lic murmur,</span><span style="font-size: large;"> high-pitched, decrescendo (intensity shows a progressive decrease during diastole)</span><span style="font-size: large;"> can be heard </span><span style="font-size: large;">at left sternal border, 3rd-4th intercostal space. If AR is due primarily to aortic root dilatation, then the diastolic murmur usually is best heard at the second right intercostal space.The intensity of the aortic component of the second heart sound (</span><span style="font-size: large;">A2)</span><span style="font-size: large;"> is decreased. </span><span style="font-size: large;"> The intensity of the AR diastolic murmur increases when the <span class="LK">patient</span> is sitting and leaning forward (this is also the best patient position f</span><span style="font-size: large;">o</span><span style="font-size: large;">r the murmur to be auscultated) or when the patient is squatting. The murmur intensity decreases with the strain phase of the Valsalva maneuver. </span><br />
<span style="font-size: large;">The </span><span style="font-size: large;">severity of aortic regurgitation correlates with duration, not </span><span style="font-size: large;">intensity, of the murmur.</span><span style="font-size: large;"> In moderate to severe AR, a short mid-s</span><span style="font-size: large;">ystolic flow murmur can be present at the second right intercostal space (due mostly to volume overload, causing increased flow through the aortic valve in systole, but concomitant aortic stenosis can </span><span style="font-size: large;">also be present). In severe AR third heart sound (</span><span style="font-size: large;">S3) is often heard, as a manifestation of the volume overload and it does not </span><span style="font-size: large;">necessarily indicate congestive heart failure.</span><span style="font-size: large;"> Some patients with aortic regurgitation also have an Austin -Flint murmur (diastolic rumble at the apex).</span><br />
<span style="font-size: large;">Pulse pressure is widened, with low diastolic and </span><span style="font-size: large;">increased systolic blood pressure.</span><span style="font-size: large;"> </span><span style="font-size: large;"> In severe AR the pulse pressure is usually 100 mmHg or higher and the diastolic pressure 60 mmHg, or less.</span><span style="font-size: large;"> </span><span style="font-size: large;">A useful clinical sign that can exclude hemodynamically significant AR is a normal or elevated diastolic blood pressure. </span><span style="font-size: large;">Corrigan's pulse is observed in aortic regurgitation due to the wide pulse pressure. It is characterized by a rapid carotid upstroke followed by sudden collapse.</span><br />
<span style="font-size: large;">The left ventricular apical impulse </span><span style="font-size: large;">is hyperdynamic (prominent),</span><br />
<span style="font-size: large;">broadened and is di</span><span style="font-size: large;">splaced laterally and inferiorly.</span><br />
<span style="font-size: large;">Peripheral signs, related to wide pulse pressure can be present:</span><br />
<span style="font-size: large;">Traube sign: pistol-shot murmur heard over the femoral artery</span><br />
<span style="font-size: large;">Duroziez sign: a murmur over the femoral artery when it is partially</span><br />
<span style="font-size: large;">compressed.</span><br />
<span style="font-size: large;">Quincke pulse: visible capillary pulsation in the nail bed after holding the tip </span><span style="font-size: large;">of the nail.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Musset sign: head bobbing with each cardiac cycle</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Müller sign: pulsation of the uvula.</span><br />
<span style="font-size: large;">The <b>ECG </b>in chronic severe aortic regurgitation usually shows evidence of left ventricular enlargement (eccentric hypertrophy) which electrocardiographically has almost the same pattern with left ventricular concentric hypertrophy, with increased amplitude of the R waves in leads V5, V6, and of the QS, or S wave in lead V1, due to the increased left ventricular electrical forces. The T waves often are upward and tall (this is a difference from the usual strain pattern seen in concentric LV hypertrophy-e.g. in aortic stenosis). However, later in the course, T waves may become inverted. The appearance of a new conduction abnormality (e.g a left bundle branch block) in a patient with severe AR, often signifies the development of LV dysfunction.</span><br />
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<span style="font-size: large;"><b>Criteria for severe aortic regurgitation :</b></span><br />
<span style="font-size: large;">Doppler jet with vena contracta (the narrowest portion of the regurgitant jet-at the level of the valve) > 6 mm, or the width of the jet<span style="font-family: inherit;"> </span></span><span style="line-height: 115%;"><span style="font-family: inherit; font-size: large;">≥ 65% of the left ventricular outflow tract (LVOT).</span></span><br />
<span style="font-family: inherit; font-size: large;">Pressure half time (PHT) of the aortic regurgitant jet, derived with continuous wave Doppler examination < 200 ms (milliseconds). Regurgitant orifice area (EROA) </span><span style="font-size: large; line-height: 18.4px;">≥</span><span style="font-family: inherit; font-size: large;"> 0.3 </span><span style="font-size: large;"><span style="font-family: "times new roman" , serif;">cm</span></span><sup><span style="font-family: "times new roman" , "serif"; font-size: 14.0pt; line-height: 115%;">2</span></sup><span style="font-family: inherit; font-size: large;"> / Regurgitant volume </span><span style="font-size: large; line-height: 18.4px;">≥</span><span style="font-family: inherit; font-size: large;"> 60 ml.</span></div>
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<span style="font-size: large;">Left ventricular size: increased (always in chronic severe AR, but often is normal in acute AR)</span>
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<span style="font-size: large;">In cases where echocardiographic assessment of the severity of aortic regurgitation is inadequate, magnetic resonance imaging (MRI), or left cardiac catheterization with aortography, is useful for </span><span style="font-size: large;">assessing the severity of AR.</span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="background-color: #ea9999;">VIDEO</span> An echocardiography quiz: What is the severity of aortic regurgitation?</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Answers and a brief discussion are provided in the video.<br />(Video) (The images of this video are courtesy of Dr Ahmed Said).</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>To see the video on full-screen, after starting the video click on the symbol [] on the right lower corner.</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span><b style="font-size: x-large;">Treatment of aortic regurgitation (AR)</b><br />
<span style="font-size: large;">In cases of rheumatic etiology, antibiotic prophylaxis for rheumatic fever is indicated.</span><br />
<span style="font-size: large;">Vasodilator treatment in AR, with ACE inhibitors and dihydropyridine calcium channel blockers (e. g. nifedipine) being the preferred drugs, is indicated if :</span><br />
<span style="font-size: large;">There is systemic hypertension</span><br />
<span style="font-size: large;">There are symptoms, or left ventricular (LV) dysfunction (in these cases surgery is the definitive treatment).</span><br />
<span style="font-size: large;">There are no recommendations for vasodilator treatment in asymptomatic patients with severe AR without hypertension and LV dysfunction. </span><br />
<span style="font-size: large;">Beta-blockers should be better avoided in severe AR, because by slowing the heart rate they increase the duration of diastole (and this may increase regurgitation, since AR occurs in diastole) and also because of their negative inotropic action (reduction of the force of contraction).</span><br />
<span style="font-size: large;"><b>In acute severe aortic regurgitation</b> vasodilators (intravenous nitroprusside) and also inotropes (dobutamine or dopamine) may be needed to stabilize the patient, while preparing for surgery. Surgery must be performed promptly.</span><br />
<span style="font-size: large;"> Important: Which invasive treatment often used to stabilize patients with low cardiac output is contraindicated in AR ?</span><br />
<span style="font-size: large;">Answer:</span><br />
<span style="font-size: large;">Intraortic balloon counterpulsation is contraindicated in AR ( it could increase regurgitation, since the balloon of the intraortic balloon pump dilates in diastole).</span><br />
<span style="font-size: large;"><b>Indications for surgery in chronic severe aortic regurgitation (AR)</b></span><br />
<span style="font-size: large;">In patients with symptoms, due to the AR (regardless of LV function)</span><br />
<span style="font-size: large;">In patients with impaired left ventricular (LV) function (ejection fraction EF < 50%)</span><br />
<span style="font-size: large;">In patients with severe dilatation of the LV (LV end systolic dimension <span style="line-height: 18.4px;">></span> 50 mm, or LV diastolic dimension ></span><span style="font-size: large; line-height: 18.4px;"> 75 mm)</span><span style="font-family: inherit; font-size: large;"> </span><br />
<span style="font-size: large;">(Mnemonic: "the rule of 50s" regarding the indications of surgery in severe asymptomatic chronic AR: EF <50, LVend systolic dimension <span style="line-height: 18.4px;">></span></span><span style="font-family: inherit; font-size: large;"> 50)</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">In patients with severe or moderately severe AR undergoing heart surgery for another reason, such as coronary artery by-pass grafting (CABG), an aneurysm of the ascending aorta, or surgery of another valve, the aortic valve should also be replaced (This way, a possible second heart surgery in the future, for the AR is avoided. A second heart surgery carries increased surgical risk compared to the first)</span><br />
<span style="color: #38761d; font-size: large;"><br /></span> <b><span style="color: #38761d;"> <span style="font-size: large;"></span> <span style="font-size: large;">A useful video : </span></span></b></div>
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<span style="font-size: large;">Echocardiographic assessment of aortic regurgitation (A lecture by dr Shantanu Shengupta) Link:</span><br />
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<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=mJLr4g9oUaY" target="_blank">https://www.youtube.com/watch?v=mJLr4g9oUaY</a></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span></div>
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<span style="color: #274e13; font-family: inherit; font-size: x-large;"><b>Useful links</b> </span></div>
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<span style="font-family: inherit; font-size: large;"><a href="http://asecho.org/wordpress/wp-content/uploads/2017/04/2017VavularRegurgitationGuideline.pdf" target="_blank">ASE GUIDELINES AND STANDARDS Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation A Report from the American Society of Echocardiography</a></span><br />
<span style="font-family: inherit; font-size: large;"><span style="color: #2a2a2a; font-family: "source sans pro" , sans-serif;"><br /></span></span> <span style="font-family: inherit; font-size: large;"><span style="color: #2a2a2a; font-family: "source sans pro" , sans-serif;">Baumgarther H, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease: The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), </span><em style="border: 0px; box-sizing: border-box; color: #2a2a2a; font-family: "Source Sans Pro", sans-serif; font-stretch: inherit; font-variant-numeric: inherit; line-height: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">European Heart Journal</em><span style="color: #2a2a2a; font-family: "source sans pro" , sans-serif;">,ehx391, </span><a href="https://doi.org/10.1093/eurheartj/ehx391" style="border: 0px; box-sizing: border-box; color: #006fb7; font-family: "Source Sans Pro", sans-serif; font-stretch: inherit; font-variant-numeric: inherit; line-height: inherit; margin: 0px; padding: 0px; text-decoration-line: none; vertical-align: baseline;">https://doi.org/10.1093/eurheartj/ehx391</a> </span><span style="font-size: large;">LINK</span><a href="https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data" style="font-size: x-large;" target="_blank"> https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data</a><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><b style="color: #551a8b; cursor: text;"><a href="http://content.onlinejacc.org/article.aspx?articleid=1838843" style="color: #551a8b; cursor: text;" target="_blank">2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease</a></b></span></div>
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<span style="font-family: inherit; font-size: large;"><b style="color: #551a8b; cursor: text;"><a href="http://www.sfcardio.fr/sites/default/files/pdf/Valvular_Heart_Dis_FT.pdf" style="color: #551a8b; cursor: text;" target="_blank">ESC Guidelines on the management of valvular heart disease (version 2012)</a></b></span></div>
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<a href="http://eurheartj.oxfordjournals.org/content/early/2014/08/28/eurheartj.ehu281" target="_blank"><span style="color: #351c75; font-size: large;">2014 ESC Guidelines on the diagnosis and treatment of aortic disease</span></a></div>
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<span style="font-size: large;"><span style="color: #0000ee; text-decoration: underline;">2015 ESC Guidelines for the management of infective endocarditis</span></span></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-91217483156624462512016-07-14T11:01:00.000+03:002018-07-21T18:35:36.384+03:00Arterial hypertension-hypertensive crisis-hypertension in pregnancy<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-family: inherit; font-size: large;">IMPORTANT NOTE: THE SITE IS UNDER DEVELOPMENT AND CONTENTS ARE CONTINUOUSLY ADDED.</span><br />
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<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>VIDEO : A case of a hypertensive patient. Discussion of her ECG, echocardiogram (echo) 2-dimensional and tissue doppler (TDI) , diastolic dysfunction and management issues</b></span><br />
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<span style="font-size: large;">What is pressure, what is force and what is afterload? (Some physics)</span></h3>
<span style="font-size: large;"><i>Pressure (P) is the force applied perpendicular to the surface of an object per unit area, therefore it is force (F) divided by surface area (A)<br />P = F / A<br />Force is the physical quantity, that acting on a body can cause acceleration (change in its velocity) or distortion (a change in its shape).<br />Elevated blood pressure causes an increase in left ventricular afterload. The afterload is the force that the heart must overcome in order to eject blood.The afterload is usually expressed as ventricular wall stress and, denoted as σ<br />σ = P r / h = Pd / 2h<br />(P is the pressure inside the ventricle, r the radius, h the wall thickness and d of the diameter of the ventricle).<br />This equation shows, that for a given pressure, the wall tension and hence the afterload increase with increasing radius (ventricular dilatation). Also, an increase in pressure causes an increase in the afterload. Instead, increasing the thickness of the walls of a cardiac ventricle (hypertrophy) is an adaptive mechanism that reduces the afterload. (However, hypertrophy is harmful because it is associated with increased myocardial oxygen needs and with increased risk for future adverse cardiovascular events.) Hypertrophy allows more sarcomere units to share wall tension.<br />To summarize, the left ventricular afterload increases with:<br />An elevation of blood pressure and systemic vascular resistance,<br />Stenosis (narrowing) of the aortic valve <br />Left ventricular distension (increased left ventricular dimensions)<br />A significant increase of the afterload can lead to a reduction of the systolic performance of a cardiac ventricle. Then it can cause a reduction in stroke volume and an increase in the end-systolic volume.</i></span><br />
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<b style="font-family: inherit; font-size: x-large;">Definition of arterial hypertension</b></h3>
<span style="font-family: inherit; font-size: large;"><b>Arterial Hypertension</b> is defined as systolic blood pressure (BP) ≥140 and /or diastolic ≥ 90 mmHg at least twice on two separate visits, unless stage 2 hypertension (systolic BP ≥ 160 mm Hg, or diastolic BP ≥ 100 mm Hg) is diagnosed on the first visit, or the need for medication to keep the blood pressure < 140/90. Blood pressure (BP) should be taken in a seated position, with the arm supported, the patient at rest for 5 minutes, and without recent smoking or caffeine intake.</span><br />
<span style="font-size: large;">Generally, patients should be informed that a single elevated BP measurement, does not suffice for the diagnosis of hypertension and should lead to observation and repeated measurements on different occasions.</span></div>
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<span style="font-family: inherit; font-size: large;">Hypertension is a modifiable <b>risk factor</b> for heart disease, stroke, and chronic kidney disease.</span><span style="font-size: large;"> In people of middle or old age, an increment of the systolic BP by 20 mmHg or of the diastolic BP by 10 is associated with a 2-fold increase in mortality risk from ischemic heart disease or stroke (cerebrovascular accident).</span><br />
<span style="font-size: large;">Hypertension is a risk factor, predisposing for </span><span style="font-size: large;">cerebrovascular accident (CVA),</span><span style="font-size: large;"> </span><span style="font-size: large;">systolic heart failure, diastolic heart failure,</span><span style="font-size: large;"> coronary artery disease (CAD)-myocardial infarction, sudden death, atrial fibrillation and peripheral vascular disease (PVD). It is associated with increased total mortality among men and women of all ages and ethnic groups, regardless of CAD. </span><br />
<span style="font-size: large;">The positive correlation between blood pressure (BP) and cardiovascular mortality (i.e.the correlation between increased BP and increased probability of death from a cardiovascular cause) is stronger for systolic BP than for diastolic. Raised diastolic BP also increases cardiovascular morbidity and mortality but less than raised systolic BP).</span><br />
<span style="font-size: large;"> Older age is related to an increase in systolic BP, whereas diastolic BP after age 60 tends to plateau or fall. So, older age is related to an increase in pulse pressure=the difference between systolic and diastolic BP. This is caused by a reduction in the compliance (elasticity) of the large arteries. Isolated systolic hypertension (systolic BP >140 and diastolic < 90), is the predominant form of hypertension in the elderly.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">Hypertension is very common, estimated to be present in 25-30 % of the adult population in western countries. The prevalence (frequency) of hypertension increases with age (> the age of 55 years more than 50% of the people have hypertension). </span><br />
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<br /><b style="font-size: x-large;">Classification of hypertension</b></h3>
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<span style="font-family: inherit; font-size: large;">The World Health Organization, International Society of Hypertension, European Society of Hypertension, and the European </span><span style="font-family: inherit; font-size: large;">Society of Cardiology have published a<b> classification of hypertension</b>.</span></div>
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<span style="font-family: inherit; font-size: large;">They define: </span><br />
<span style="font-family: inherit; font-size: large;">Optimal BP as a systolic BP <120 mm Hg and diastolic BP <80 mmHg. </span></div>
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<span style="font-family: inherit; font-size: large;">Normal blood pressure (BP) is systolic 120 to 129 mm Hg and diastolic 80 to 84 mm Hg. </span></div>
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<span style="font-family: inherit; font-size: large;">High-normal is systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg.</span></div>
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<span style="font-family: inherit; font-size: large;">Stage 1 hypertension is systolic BP 140 to 159 mm Hg or diastolic BP 90 to 99 mm Hg </span></div>
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<span style="font-family: inherit; font-size: large;">Stage 2 hypertension is systolic BP 160 to 179 mmHg or diastolic BP 100 to 109 mmHg. </span></div>
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<span style="font-family: inherit; font-size: large;">Stage 3 hypertension is systolic BP ≥ 180 mm Hg or diastolic BP ≥ 110 mm Hg.</span></div>
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<span style="font-family: inherit; font-size: large;">An interesting fact is, that individuals that do not have hypertension, but have systolic BP in the range of 120-139 and/or diastolic BP 80-89 have a higher incidence of cardiovascular events than people with o</span><span style="font-size: large;">ptimal BP (systolic <120 mm Hg and diastolic <80 mmHg). </span><br />
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<span style="font-family: inherit; font-size: large;">According to JNC 7, normal BP is defined as systolic BP <120 mm Hg and diastolic BP < 80 mm Hg.<br />Prehypertension is systolic BP 120 to 139 mm Hg or diastolic BP 80 to 89 mm Hg.<br />Stage 1 hypertension is systolic BP 140 to 159 mm Hg or diastolic BP 90 to 99 mm Hg.<br />Stage 2 hypertension is systolic BP ≥ 160 mm Hg, or diastolic BP ≥ 100 mm Hg<b>. </b></span><br />
<span style="font-size: large;">The majority of hypertensive patients (95 % or more) have essential (primary or idiopathic) hypertension, in which an underlying cause of the hypertension is not found. Secondary hypertension (with an identifiable underlying cause) accounts for about 5 % or less of cases.</span><br />
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<span style="font-family: inherit; font-size: large;"><b>For children and adolescents the blood pressure (BP) limits are different (lower):</b><br />It is recommended to measure BP as a routine practice on examination of children ≥ 3 years of age. Hypertension in children and adolescents is defined as systolic or diastolic BP ≥ 95th percentile in repeated measurements (ie, a pressure equal to or above the value, below which the BP of 95% of children of the same age and sex is found.). Systolic and diastolic BP percentiles based on age and gender can be found in specific tables. Pre-hypertension in children and adolescents is defined as systolic or diastolic BP between the 90th and 95th percentile. In this link, you can see blood pressure percentiles for boys and girls by age and height. <b>LINK</b></span><span style="font-size: 24px;"> </span><a href="https://www.nhlbi.nih.gov/files/docs/guidelines/child_tbl.pdf" style="font-size: 24px;" target="_blank">https://www.nhlbi.nih.gov/files/docs/guidelines/child_tbl.pdf</a></div>
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<span style="font-size: large;"><b>Pathophysiology of hypertension</b> </span></h4>
<span style="font-size: large;">The etiology and pathophysiology of essential (primary) hypertension is multifactorial. Hypertension results </span><span style="font-size: large;">from a gain in function of n</span><span style="font-size: large;">eural, hormonal, or renal mechanisms </span><span style="font-size: large;">that induce vasoconstriction and renal </span><span style="font-size: large;">sodium retention or a reduction in function of mechanisms that promote vasodilation </span><span style="font-size: large;">and renal sodium excretion. Factors enhancing mechanisms that promote hypertension include: </span><br />
<span style="font-size: large;">G</span><span style="font-family: inherit; font-size: large;">enetic predisposition (S</span><span style="font-family: inherit; font-size: large;">tudies using twin data and data from Framingham Heart Study families reveal that the etiology of essential hypertension includes a substantial heritable component, ranging from about 30-55%. Further studies have shown that many different genes predispose to hypertension).</span><br />
<span style="font-size: large;">Behavioral factors: Excess dietary salt intake, increased consumption of calories resulting in obesity (a predisposing factor for hypertension-especially abdominal obesity), increased alcohol consumption.</span><span style="font-family: inherit; font-size: large;">Increased adrenergic tone. </span><br />
<span style="font-size: large;">N</span><span style="font-size: large;">eurohormonal activa</span><span style="font-size: large;">tion contributes to the early pathogenesis by adversely affecting vascular function </span><span style="font-size: large;">(e.g., reduction of endothelium-dependent vasodilation). </span><br />
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<span style="font-size: large;"><b>Causes of secondary hypertension </b>:</span></h4>
<span style="font-size: large;">Renovascular disease (renal artery stenosis,</span><span style="font-size: large;"> caused by atherosclerosis or fibromuscular dysplasia)</span><span style="font-size: large;"><br />Renal parenchymal disease: <br />Diabetic nephropathy, glomerulonephritis, vasculitides, polycystic kidneys, chronic pyelonephritis <br />Endocrine disease <br />Conn’s syndrome, Cushing’s syndrome, <br />hypertension caused by chronic glucocorticoid treatment, pheochromocytoma, hyperparathyroidism,</span><span style="font-size: large;"> </span><span style="font-size: large;">acromegaly.</span><br />
<span style="font-size: large;">Other causes : </span><br />
<span style="font-size: large;"> O</span><span style="font-size: large;">besity, a</span><span style="font-size: large;">ortic coarctation, pre</span><span style="font-size: large;">eclampsia, </span><br />
<span style="font-size: large;">drugs </span><span style="font-size: large;">(non-steroidal anti-inflammatory drugs -NSAIDs, sympathomimetics, </span><span style="font-size: large;">illicit stimulants, e.g. amphetamine,</span><span style="font-size: large;"> </span><span style="font-size: large;">cocaine,</span><span style="font-size: large;"> </span><span style="font-size: large;"> MDMA (‘ecstasy’). </span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">The heart responds to long-term pressure overload in an attempt to stabilize cardiac output by means of :</span><br />
<span style="font-size: large;">1. Left ventricular hypertrophy due to an increase in myocyte thickness and increased deposition of extracellular matrix,</span></div>
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<span style="font-size: large;">(Left ventricular hypertrophy is secondary to pressure </span><span style="font-size: large;">overload and neurohormonal effects).</span><span style="font-size: large;"><br />2. Adrenergic stimulation of the heart,<br />and <br />3. At later stages dilation (increased dimensions and volume) of the left ventricle.</span><br />
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<b><span style="font-family: inherit; font-size: large;">E</span></b><span style="font-size: large;"><b>valuation of hypertension</b></span></h4>
<span style="font-family: inherit; font-size: large;">E</span><span style="font-size: large;">valuation of hypertension<b> </b>is conducted through the medical history, physical examination, laboratory tests, and other diagnostic procedures. Evaluation has the following goals: </span><br />
<span style="font-size: large;">To identify known causes of high blood pressure</span><br />
<span style="font-size: large;">To assess the presence or absence of end-organ damage and cardiovascular disease and the severity of the disease.</span><br />
<span style="font-size: large;">To identify other cardiovascular risk factors or concomitant disorders that may influence prognosis and guide treatment.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">Hypertension is asymptomatic in most cases, although a patient will occasionally </span><span style="font-size: large;">complain of headache. If left untreated, later in the course symptoms of a cardiovascular complication may appear (for example symptoms of a stroke, or heart failure, or coronary artery disease). A history of cardiac or neurologic symptoms</span><br />
<span style="font-size: large;">should </span><span style="font-size: large;">be sought and the cardiovascular system should be examined</span><br />
<span style="font-size: large;">in </span><span style="font-size: large;">detail.</span><br />
<span style="font-size: large;">Clinical signs of an underlying cause should be sought (radio-femoral delay or weak femoral </span><span style="font-size: large;">pulses in aortic coarctation, renal enlargement in polycystic kidneys, an abdominal bruit in renovascular hypertension, caused by renal artery stenosis or cushingoid features. </span><br />
<span style="font-size: large;">Also, clinical signs of target-organ damage should be sought (signs of heart failure, a palpable abdominal aortic aneurysm, a carotid or femoral bruit, retinopathy).</span><span style="font-size: large;"><br /></span>
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<span style="font-size: large;">Findings suggesting the presence of hypertensive heart disease (a form of target organ damage) are the auscultation of a fourth heart sound (S4 gallop), or features of left ventricular hypertrophy (LVH) in the ECG or echocardiogram (which is more sensitive than the ECG for LVH). ECG evidence of LVH is associated with an about 3-fold increase in cardiovascular events. LVH is more powerful than the other 'traditional" cardiovascular risk factors for predicting an adverse outcome in hypertensive patients (such as the development of heart failure, stroke, myocardial infarction or death). In terms of estimated left ventricular mass (with echocardiography) the threshold for LVH in men is > 115 g/</span><span style="font-size: large;">m</span><sup>2 </sup><span style="font-size: large;">and in wo</span><span style="font-size: large;">men > 105 g/</span><span style="font-size: large;">m</span><sup>2</sup><span style="font-size: large;">.</span><br />
<span style="font-size: large;">LVH is associated with increased risk of developing myocardial ischemia (due to increased myocardial oxygen demand and increased resistance of the coronary arterial system), increased frequency of ventricular arrhythmias and diastolic dysfunction. Diastolic dysfunction, if severe, can lead to dyspnea on exertion and even pulmonary edema, in patients with normal left ventricular ejection fraction.</span><br />
<span style="font-size: large;">Findings of target organ damage (for example LVH) in a patient with stage-1 hypertension indicate the need for earlier and more aggressive antihypertensive treatment.</span><br />
<span style="font-size: large;">Grading of hypertensive retinopathy</span><br />
<span style="font-size: large;">Grades I-IV </span><br />
<span style="font-size: large;"> I. Tortuous arteries, with thickened bright walls ("silver wiring") </span><br />
<span style="font-size: large;"> II. Narrowing in a vein where crossed by an </span><span style="font-size: large;">artery </span><br />
<span style="font-size: large;"> III. S</span><span style="font-size: large;">mall retinal bleeds ("f</span><span style="font-size: large;">lame haemorrhages") </span><span style="font-size: large;">and exudates (described as</span><span style="font-size: large;"> "cotton wool spots").</span><br />
<span style="font-size: large;">IV.</span><span style="font-size: large;"> Papilloedema ( Optic disc swelling that is caused by increased intracranial pressure, or malignant hypertension.The optic disc represents the beginning of the optic nerve because it is the point where the axons of retinal ganglion cells come together. The optic disc is also the entry point for the retinal blood vessels</span><span style="font-size: large;">).</span><br />
<span style="font-size: large;">Ultrasound examination of the carotid arteries with measurement of the intima-media thickness (IMT) and detection of atheromatous plaques has also prognostic significance. An increased IMT </span><span style="font-family: "times new roman" , serif; line-height: 115%;"><span style="font-size: large;">≥ 9 mm</span></span><span style="font-size: large;">, or the presence of plaques are findings that indicate target organ damage (of the arterial system) and increase the risk of a stroke or a myocardial infarction. </span><br />
<span style="font-family: "calibri" , sans-serif; font-size: 11pt; line-height: 115%;"> </span><span style="font-size: large;"> </span><br />
<b style="font-size: x-large;">Treatment of hypertension</b></div>
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<span style="font-size: large;">The objective of antihypertensive therapy is to reduce the incidence of adverse cardiovascular events (i.e. to reduce the long-term risk of cardiovascular morbidity and mortality). The benefit of therapy of hypertension is a reduction in the risk of stroke by about 30% and in the risk of coronary artery disease (CAD) by 20%.</span><span style="font-size: large;">Placebo-controlled trials have proven that any blood pressure lowering drug treatment reduces strokes, the incidence of heart failure, coronary events, and deaths in hypertensive patients and this is true even for elderly patients > 80 years.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">According to current guidelines, the goal of treatment for all hypertensive patients, even in high-risk patients with diabetes or chronic kidney disease, or indications of target organ damage is systolic pressure < 140 and diastolic < 90 mmHg. An exception are very elderly patients, 80 years or older, where the goal is to slowly achieve systolic BP < 150.</span><br />
<span style="font-size: large;"><b>Lifestyle modification</b> should be the first line of treatment for patients with hypertension. Start with lifestyle modification even if drug therapy is also needed</span><span style="font-family: inherit; font-size: large;">. L</span><span style="font-size: large;">ifestyle measures include the following:</span><span style="font-size: large;"> Restricting salt (a </span><span style="font-size: large;">low sodium intake of 100 mmol/day, i.e. </span><span style="font-size: large;">6 g NaCl, or less), </span><br />
<span style="font-size: large;">starting </span><span style="font-size: large;"> a diet high in fruits, vegetables, </span><span style="font-size: large;">and low-fat dairy products (Dietary Approaches </span><span style="font-size: large;">to Stop Hypertension -DASH) diet plan),</span><br />
<span style="font-size: large;"> c</span><span style="font-size: large;">orrecting obesity (</span><span style="font-size: large;">weight loss with a goal of achieving a </span><span style="font-size: large;">body mass index <<span style="font-family: inherit;">25 kg/</span></span><span style="font-family: inherit; font-size: large;"> m</span><span style="font-size: large;"><span style="font-family: inherit;"><span lang="EN-US" style="line-height: 115%;"><sup>2</sup></span> </span>of body surface area can improve hypertension control),</span><br />
<span style="font-size: large;">reducing alcohol intake, smoking cessation </span><span style="font-size: large;">and taking regular physical exercise. M</span><span style="font-size: large;">oderately </span><span style="font-size: large;">intense physical activity (e.g., brisk walking, or cycling) for</span><span style="font-size: large;"> 30 minutes or more,</span><span style="font-size: large;"> four </span><span style="font-size: large;">or more times a week, is beneficial for BP lowering.</span><br />
<span style="font-size: large;">There are no strong recommendations for altering caffeine </span><span style="font-size: large;">intake. Chronic caffeine intake has not been shown to </span><span style="font-size: large;">correlate with elevated blood pressure (BP), but probably excessive caffeine intake should be discouraged because caffeine can lead to transient elevations in BP.</span><br />
<span style="font-size: large;">Relaxation therapy and stress management can be useful in some cases, but generally, they are of </span><span style="font-size: large;">uncertain benefit.</span><br />
<br />
<span style="font-family: inherit; font-size: large;">When <b>medications</b> are needed, adequate control of hypertension is more important than the category of medication used, with the exception of compelling indications. Compelling indications are indications, in case of patients who have other coexisting health problems, to use the drug category, which is more suitable for the specific coexisting diseases (comorbidities). </span><br />
<br /></div>
<span style="font-family: inherit; font-size: large;"> </span>
<br />
<div>
<span style="font-family: inherit; font-size: large;"> According to the latest guidelines (JNC 8), four classes of antihypertensive drugs are recommended as choices for <b>first-line treatment (initial drug choices)</b>. The physician should choose one of the following for treatment initiation: These are an angiotensin-converting enzyme inhibitor (ACEI), or an angiotensin receptor blocker (ARB), a calcium-channel blocker (CCB), or a diuretic (D), usually a thiazide-type diuretic (but in patients with moderate to severe renal dysfunction thiazide diuretics have reduced effect and a loop diuretic can be used instead). This selection of first-line drugs is based on evidence from randomized control trials (RCTs). </span><span style="font-size: large;">In the general population, including those with diabetes mellitus</span><span style="font-size: large;">, treatment should start with these drugs either with one drug (monotherapy, usually selected in cases of stage 1 hypertension), or with a combination of 2 drugs from these categories (usually selected for stage 2 hypertension, i.e systolic BP </span><span style="font-size: large;">≥ </span><span style="font-size: large;"> 160 and/or diastolic BP </span><span style="font-size: large;">≥ 100).</span><span style="font-size: large;"> </span><span style="font-size: large;">In most cases, choose agents with a 24-hour duration </span><span style="font-size: large;">of action and once-daily dosing, for better patient compliance.</span><br />
<span style="font-size: large;">When a drug combination is needed, any of these drug categories can be combined with each other, in combinations of 2 (or if necessary 3) drugs, with one exception: A combination of </span><span style="font-size: large;">ACEIs and ARBs is not preferable and should generally not be used. (This combination is used for some patients with systolic heart failure and persistent symptoms, who are intolerant to mineralocorticoid antagonists, but in this case, the goal of treatment is to treat heart failure, not hypertension- see chapter on <a href="https://cardiologybookandcases.blogspot.gr/2016/05/a-case-of-ischemic-cardiomyopathy-ecg.html" target="_blank">Heart Failure</a>)</span><br />
<span style="font-size: large;">In patients with chronic kidney disease (CKD), antihypertensive treatment should start with either an ACEI </span><span style="font-size: large;">or an ARB, because these drugs have been shown to demonstrate renoprotective effects.</span><br />
<span style="font-size: large;">In the general black population, including </span><span style="font-size: large;">patients with diabetes mellitus, treatment for hypertension should start either with a thiazide-type </span><span style="font-family: inherit; font-size: large;">diuretic or with a calcium channel blocker (CCB), because </span><span style="font-size: large;">ACEIs and ARBs, generally have been found not to achieve an adequate control of hypertension in black people.</span><br />
<span style="font-size: large;"> Monotherapy is successful in approximately 40% </span><span style="font-size: large;">of patients, but in the rest (about 60%), </span><span style="font-size: large;">to attain goal BP, </span><span style="font-size: large;">a combination of </span><span style="font-size: large;">two or more drugs will be needed. The latter is </span><span style="font-size: large;">often </span><span style="font-size: large;">the rule in </span><span style="font-size: large;">patients with a BP > 160/100 mm Hg.</span><br />
<span style="font-size: large;">If there is a partial but inadequate response to the first antihypertensive drug, or to the initial drug combination used, either increase the dose of the first drug, or a drug included in the initial combination or add an agent from a different class. Every dosage adjustment should be within the recommended dose limits of each drug (mentioned in textbooks, guidelines, or in the summary of product characteristics published for each drug). Dose increments generally should be gradual and moderate, not sudden and "aggressive", especially in elderly patients and a renal or hepatic dysfunction, or any other comorbidity, should be taken into account, if present. </span><span style="font-size: large;"> </span><span style="font-family: inherit; font-size: large;"> The previous guideline, JNC 7, recommended five drug classes as initial therapy, which include the above 4 classes and beta-blockers, emphasizing the use of thiazide diuretics for most patients, who do not have a compelling indication for a specific class.</span><br />
<span style="font-size: large;"> In patients whose goal blood pressure (BP) cannot be reached with 3 agents from the first line drug classes, agents from other drug classes should be added. </span></div>
<span style="font-family: inherit; font-size: large;"> </span>
<br />
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<span style="font-family: inherit; font-size: large;">Beta-blockers (BB) are not recommended as initial therapy for patients with hypertension in the recent guideline of JNC (JNC 8). They should be used as initial therapy, only if a compelling indication is present </span><span style="font-size: large;">(for example angina, previous myocardial infarction, heart failure with reduced ejection fraction, tachyarrhythmias)</span><span style="font-family: inherit; font-size: large;">. The exclusion of beta-blockers from first-line drugs in JNC 8 was related to less satisfactory results in blood pressure (BP) lowering and a smaller reduction of the overall </span><span style="font-family: inherit; font-size: large;">cardiovascular mortality in the general hypertensive population with beta blockers in comparison to the 4 other first-line drug categories. </span><br />
<h4>
<span style="font-size: large;"><b>Preferred antihypertensive treatment in specific situations:</b></span></h4>
<span style="font-size: large;">(For abbreviations see above)<br />Hypertension in elderly patients: CCB, D, ACEI or ARB, <br />Hypertension in patients with diabetes: CCB, ACEI or ARB, D<br />Hypertension in patients with diabetic nephropathy: ACEI or ARB, D<br />Hypertension in nondiabetic chronic kidney disease: </span></div>
<div>
<span style="font-size: large;">ACE-I or ARB, BB, D<br />Hypertension with left ventricular hypertrophy ARB, D, CCB<br />Hypertension in patients with a history of stroke (for secondary prevention of stroke): ACEI + D, CCB<br />Hypertension and coronary artery disease (BP reduction for secondary prevention of coronary events) : ACEI, BB, CCB, D<br />Hypertension and heart failure: D, ACE-I or ARB, BB, aldosterone antagonist<br />Hypertension and a thoracic aortic aneurysm: BB, ACE-I or ARB, D<br />Hypertension in patients with atrial fibrillation and increased heart rate (need for ventricular rate control): BB, nondihydropyridine CCB (diltiazem or verapamil)</span></div>
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<span style="font-size: large;">Gestational hypertension (stage 2):</span></div>
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<span style="font-size: large;"> Labetalol, methyldopa, nifedipine.</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span>
<br />
<span style="font-family: "arial" , "helvetica" , sans-serif;">James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline forthe management of high blood pressure in adults: report from the</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;">panel members appointed to the Eighth Joint National Committee</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;">(JNC 8). JAMA. 2014;311:507-520.</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;">Kaplan NM. Clinical Hypertension. 11th ed. Baltimore: Lippincott</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;">Williams & Wilkins; 2014.</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"></span>
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<h3>
<span style="font-family: inherit; font-size: large;"><b>Resistant hypertension (RH)</b></span></h3>
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<span style="font-family: inherit; font-size: large;">RH is systolic BP >140 and/or diastolic BP> 90 mmHg despite adequate doses of three or more antihypertensive medications, including a diuretic for at least 1 month, or hypertension requiring 4 or more antihypertensive drugs, in order to be adequately controlled. </span><br />
<span style="font-size: large;">Resistant hypertension can be real or spurious (not real resistance to treatment). Causes of spurious resistant hypertension: </span></div>
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<span style="font-size: large;">Non-adherence to treatment (common phenomenon: many patients do not take their medications according to the prescription, "forget" doses, etc).</span></div>
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<span style="font-size: large;">White coat hypertension: Persistence of an alerting reaction to the BP-measuring procedure: BP is elevated at the doctor's office, but home BP measurements are normal.</span></div>
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<span style="font-size: large;">Technical errors in measurement: Use of small cuffs on large arms, leading to inadequate compression of the artery.</span></div>
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<span style="font-size: large;">Pseudo-hypertension: Marked arterial stiffening in elderly persons with heavily calcified arteries. This prevents occlusion of the brachial artery by cuff pressure and leads to measuring higher BP than its real value.</span></div>
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<span style="font-size: large;">True resistant hypertension is associated with a high risk of cardiovascular disease, acute cardiovascular events and renal dysfunction.</span><span style="font-family: inherit; font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></span> <span style="font-family: inherit; font-size: medium;"><span style="font-family: "arial" , "helvetica" , sans-serif;">Fagard RH. Resistant hypertension. Heart 2012;98:254–261.</span><b style="font-family: inherit; font-size: x-large;"><br /></b></span>
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<h3>
<span style="font-family: inherit; font-size: large;"><b>Hypertensive crisis, hypertensive urgencies and hypertensive emergencies.</b></span></h3>
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<span style="font-family: inherit; font-size: large;"><b>Hypertensive crisis </b>is defined as a systolic blood pressure (SBP) of 190-200 mm Hg or greater and/or a diastolic blood pressure (DBP) of 120 mm Hg or greater. It is a broad term encompassing hypertensive urgency and emergency. Patients without acute or rapidly developing end-organ damage are classified as having a hypertensive urgency. </span><br />
<span style="font-family: inherit; font-size: large;">When individuals meet the criteria for hypertensive crisis and also have evidence of </span><span style="font-size: large;">rapidly progres</span><span style="font-family: inherit; font-size: large;">sive target organ dysfunction (</span><span style="font-family: inherit; font-size: large;">end-organ damage), it is a hypertensive emergency. </span><span style="font-size: large;">The rate of change in BP is important. A rapid rise is </span><span style="font-size: large;">poorly tolerated and leads to end-organ damage, whereas a gradual blood pressure rise in </span><span style="font-size: large;">a patient with preexistent poor BP control is tolerated better. </span><br />
<span style="font-size: large;">A hypertensive urgency or emergency can occur in patients with primary or secondary hypertension (for example renovascular hypertension, acute glomerulonephritis, scleroderma, pheochromocytoma, thyrotoxicosis, eclampsia, and pre-eclampsia, etc). </span><br />
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<span style="font-family: inherit; font-size: large;">Risk factors for developing hypertensive crisis include female sex, obesity, hypertensive heart disease, coronary heart disease, presence of a somatoform disorder ( a mental disorder causing bodily symptoms and anxiety), medication nonadherence and a high number of antihypertensive drugs.</span></div>
<span style="font-family: inherit; font-size: large;">Hypertensive emergencies typically present as sudden, high elevations in blood pressure associated with acute target organ dysfunction. Presentations include hypertensive encephalopathy, malignant hypertension, acute coronary syndromes, acute pulmonary edema, acute cerebrovascular events, aortic dissection, eclampsia and acute renal dysfunction. The initial examination should include a focused history, cardiovascular, mental and funduscopic examinations, as well as pertinent laboratory values.<br />Once the diagnosis of a hypertensive emergency has been made, drug therapy should be initiated promptly, even before laboratory results are available.</span><span style="font-family: inherit; font-size: large;"><br /></span><br />
<span style="font-size: large;">Malignant hypertension </span><span style="font-size: large;">is a medical emergen</span><span style="font-size: large;">cy, </span><span style="font-size: large;">diagnosed when there is severe hypertension (systolic </span><span style="font-size: large;">blood pressure > 200 mmHg ± diastolic blood pressure > 130, (</span><span style="font-size: large;">typically there is BP above 220/130 mmHg) ,</span><span style="font-size: large;"> together with </span><span style="font-size: large;">retinopathy, </span><span style="font-size: large;">of </span><span style="font-size: large;">grade III-IV. H</span><span style="font-size: large;">eadache is often present and occasionally visual disturbance (</span><span style="font-size: large;">blurred vision),</span><span style="font-size: large;"> </span><span style="font-size: large;"> nausea </span><span style="font-size: large;">and vomiting. Besides headache and blurred vision, more severe manifestations of central nervous system dysfunction can also be present, such as </span><span style="font-size: large;">confusion and </span><span style="font-size: large;">seizures (hypertensive encephalopathy) with or without manifestations of acute heart or renal dysfunction, such as pulmonary edema and oliguria. Hypertensive encephalopathy requires differential diagnosis from an intracranial hemorrhage or an acute ischemic stroke. </span><span style="font-size: large;">A new focal neurologic deficit </span><span style="font-size: large;">suggests an ischemic stroke in evolution. Brain CT or MRI may be needed to aid the diagnosis. An ischemic stroke demands a much more conservative</span><br />
<span style="font-size: large;">approach to hypertension (gradual and not rapid pressure lowering) in comparison to hypertensive encephalopathy, which demands a more rapid pressure lowering to a BP, initially about 160-170/100-110. Laboratory findings in malignant hypertension: </span><span style="font-size: large;">Proteinuria and hematuria are often present. In cases of malignant hypertension, i</span><span style="font-size: large;">mmediate treatment is required to prevent complications, such as </span><span style="font-size: large;">rapid progression to renal failure, heart failure, or stroke. If malignant hypertension is un</span><span style="font-size: large;">treated, the 1-year mortality is approximately 90 %. </span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;">In a hypertensive crisis, rapid lowering of BP may </span><span style="font-size: large;">compromise tissue perfusion, leading to cerebral damage or to coronary </span><span style="font-size: large;">or renal insufficiency. Thus, r</span><span style="font-size: large;">apid reduction of BP must be avoided, because it</span><span style="font-size: large;"> can result in cerebral and cardiac hypoperfusion </span><span style="font-size: large;">(abrupt change of >25% in BP will exceed cerebral BP autoregulation).</span><br />
<span style="font-size: large;">A good rule</span><span style="font-size: large;"> is to lower initially the elevated BP by 10% in the first </span><span style="font-size: large;">hour and by an additional 15% during the next 3 to 12 hours to a blood pres</span><span style="font-size: large;">sure of no less than 160/100-110 mmHg.</span><br />
<span style="font-size: large;">This rule has some exceptions, where BP must be lowered more rapidly. Such situations are aortic dissection, postoperative hemorrhage, and acute myocardial infarction. </span><br />
<span style="font-size: large;">Most patients, </span><span style="font-size: large;">with a hypertensive crisis,</span><span style="font-size: large;"> i</span><span style="font-size: large;">n the absence of manifestations of </span><span style="font-size: large;">acute target organ damage, even if blood pressure (BP) is 220/130 mmHg </span><span style="font-size: large;">or higher, should be treated with short-acting oral medications</span><span style="font-size: large;">. </span><span style="font-size: large;"> </span><span style="font-size: large;">First-line treatment should be with a </span><span style="font-size: large;">diuretic, a</span><span style="font-size: large;"> beta-blocker (unless contraindicated) ,</span><span style="font-size: large;"> a low-dose calcium antagonist, or an ACE inhibitor. A combination of two or more of these drug-classes may be needed. (Sublingual nifedipine should be avoided because it can result in rapid changes in blood pressure). </span><br />
<span style="font-size: large;">In real hypertensive emergencies with manifestations of acute target organ damage, the patient is admitted to an intensive care unit (ICU) and antihypertensive treatment starts with intravenous agents.</span><br />
<span style="font-size: large;">Where </span><span style="font-size: large;">necessary, intravenous administration of labetalol, nitroglycerine (GTN-glycerine trinitrate) and sodium nitroprusside are effective treatment options. Intravenous treatment requires careful patient supervision. </span><br />
<span style="font-size: large;">Labetalol is the drug of choice in pheochromocytoma or aortic dissection. It must be avoided if there is left ventricular failure.</span><br />
<span style="font-size: large;">Intravenously (IV) it is given as a </span><span style="font-size: large;">bolus</span><span style="font-size: large;"> of </span><span style="font-size: large;">20–80 mg and administration is continued with </span><span style="font-size: large;"> </span><span style="font-size: large;">IV infusion, (</span><span style="font-size: large;">20–200 mg/min, start with a low dose and increase every </span><span style="font-size: large;">15 minutes, if needed for blood pressure control. IV treatment has an onset of action after 2-5 minutes. Labetalol can be continued orally (PO) </span><span style="font-size: large;">100–400 mg /12 hours. If the patient does not need parenteral treatment (in less severe emergencies) treatment can start PO. Then the onset of action is in 30-60 minutes (min). It is also safe for pregnant patients. </span><br />
<span style="font-size: large;">Nitroprusside is the drug of choice for hypertensive emergencies with acute left ventricular failure and/or hypertensive encephalopathy. It is administered by </span><span style="font-size: large;">IV infusion </span><span style="font-size: large;">0.25–10 µg/kg of body weight/min and the onset of action is in seconds.</span><br />
<span style="font-size: large;">Nitroglycerine is useful in hypertensive emergencies with left ventricular failure or acute coronary ischemia. It is given in </span><span style="font-size: large;">IV infusion </span><span style="font-size: large;">1–10 mg/hour and the onset of action is in 2-5 minutes. </span><br />
<span style="font-size: large;">Hydralazine is given IV 5–10 mg over 20 minutes and then by IV infusion 50–300 µg/min</span><span style="font-size: large;"> (µg = </span><span style="font-size: large;">microgram= </span><span style="font-family: inherit; font-size: large;"><span style="line-height: 115%;">10</span><sup style="line-height: 115%;">-6 </sup></span><span style="font-family: inherit; font-size: large;">gram).</span><br />
<span style="font-size: large;">Esmolol HCl is a s</span><span style="font-size: large;">hort-acting beta-blocker (it is also used for supraventricular tachycardias) It is given in an </span><span style="font-size: large;">IV </span><span style="font-size: large;"> </span><span style="font-size: large;">loading dose</span><br />
<span style="font-size: large;">500 µg/kg/min and continuous IV </span><span style="font-size: large;">infusion </span><span style="font-size: large;">50–200 µg/kg/min. </span><br />
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<div>
<span style="font-family: inherit; font-size: large;">BIBLIOGRAPHY- LINKS : </span></div>
<div class="MsoNoSpacing" style="text-align: justify; text-justify: inter-ideograph;">
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Doroszko A, Janus A, Szahidewicz-Krupska E,, et al. Resistant Hypertension.Adv Clin Exp Med. 2016 ;25:173-18</span></b></div>
<div class="MsoNoSpacing" style="text-align: justify; text-justify: inter-ideograph;">
<b style="font-family: Arial, Helvetica, sans-serif;">Link : <a href="http://www.advances.umed.wroc.pl/pdf/2016/25/1/173.pdf" target="_blank">Resistant hypertension</a></b></div>
<br />
<a href="http://eurheartj.oxfordjournals.org/content/ehj/34/28/2159.full.pdf" style="font-size: x-large;" target="_blank">ESC GUIDELINES ON HYPERTENSION</a><br />
<br />
<a href="https://www.nice.org.uk/guidance/cg127/resources/hypertension-in-adults-diagnosis-and-management-35109454941637"><span style="font-size: large;">Hypertension in adults: diagnosis and management (NICE guideline)</span></a><br />
<h3>
<span style="font-family: inherit; font-size: large;"><br /></span><b style="font-size: x-large;">Hypertensive disorders in pregnancy- Arterial hypertension in pregnancy-Preeclampsia</b></h3>
<span style="font-size: large;">Hypertensive disorders of pregnancy are the most common medical</span><br />
<span style="font-size: large;">disorder in pregnancy. Hypertension is estimated to occur in</span><br />
<span style="font-size: large;">5% - 10% of all pregnancies and it is a major cause of maternal</span><br />
<span style="font-size: large;">and fetal morbidity and mortality.</span><br />
<span style="font-size: large;">Hypertension in pregnancy is defined as </span><br />
<span style="font-size: large;">blood pressure (BP) </span><span style="font-family: inherit; font-size: large;">≥ 140/90 in two measurements, at least 4 hours apart.</span><br />
<span style="font-family: inherit; font-size: large;">Hypertension in pregnancy includes the following categories :</span><br />
<span style="font-family: inherit; font-size: large;"><u>Chronic hypertension.</u> </span><br />
<span style="font-family: inherit; font-size: large;"> It refers to hypertension that has appeared prior to pregnancy or before 20 weeks of gestation</span><br />
<span style="font-family: inherit; font-size: large;"><u>Gestational hypertension:</u></span><br />
<span style="font-family: inherit; font-size: large;">The development of hypertension without proteinuria after 20 weeks of gestation. It can evolve into preeclampsia.</span><br />
<span style="font-family: inherit; font-size: large;"><u>Preeclampsia/Eclampsia</u></span><br />
<span style="font-family: inherit; font-size: large;"> Hypertension in a pregnant woman accompanied by proteinuria (pathologic excretion of protein in the urine) >300mg/24 hours, developing after 20 weeks of gestation. Preeclampsia (or even eclampsia) less commonly may occur postpartum, usually in the first 4 days but it may develop up to 6 weeks postpartum. Preeclampsia is more common in women with multiple gestations, a history of hypertension for 4 years or more, renal disease, history of hypertension in a previous pregnancy, family history of preeclampsia. Preeclampsia can progress to eclampsia (in this case seizures appear).</span><span style="font-size: large;"> Eclampsia is defined as seizures that cannot be attributed to another cause in a woman with preeclampsia.</span><br />
<span style="font-family: inherit; font-size: large;"><u>Chronic hypertension with superimposed preeclampsia</u>:</span><br />
<span style="font-family: inherit; font-size: large;">When in a woman with hypertension, there is a new onset of proteinuria after 20 weeks of gestation. In a woman with hypertension and proteinuria prior to 20 weeks of gestation, superimposed preeclampsia is recognised by a sudden 2-3 fold increase in proteinuria, or the development of thrombocytopenia (pathologic reduction of the platelet count in the blood), or the development of an elevation of alanine aminotransferase (ALT), or aspartate aminotransferase (AST).</span><br />
<span style="font-family: inherit; font-size: large;"><u>Transient hypertension</u></span><br />
<span style="font-size: large;">This is a retrospective diagnosis. It denotes hypertension in pregnancy with subsequent normalization of blood pressure in 12 weeks postpartum. It may predict re-occurence of hypertension in a next pregnancy, or the later development of primary hypertension. </span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;">The pathophysiology of hypertension in pregnancy includes an increased cardiac output and vasoconstriction due to an increased central and peripheral sympathetic activity.</span><span style="font-family: inherit; font-size: large;">Preeclampsia is associated with an immunologic mechanism.</span><br />
<h4>
<span style="font-family: inherit; font-size: large;"><b>Treatment of hypertension in pregnancy</b></span></h4>
<span style="font-family: inherit; font-size: large;">Women with mild hypertension (</span><span style="font-size: large;">systolic BP 140 to 159 mm Hg or diastolic BP 90 to 99 mm Hg) </span><span style="font-family: inherit; font-size: large;"> are low risk for cardiovascular complications in pregnancy and they are treated with lifestyle modification only (salt restriction) and a restriction of physical activity. Women with target organ damage should receive antihypertensive medication, even with mild hypertension. Women with a prior requirement for multiple antihypertensive agents to control their BP, should also receive medication.</span><br />
<span style="font-family: inherit; font-size: large;">If blood pressure (BP) reaches 160 systolic or 100 diastolic, treatment with antihypertensive medications should be instituted in every case. Effective treatment of severe hypertension especially in the first trimester of pregnancy is mandatory. </span><br />
<span style="font-family: inherit; font-size: large;">Treatment for preeclampsia includes hospitalization, bed rest, control of BP, seizure prophylaxis in cases of severe preeclampsia (treatment with intravenous magnesium sulfate) and timely delivery. Magnesium sulfate has shown excellent results in the prevention and treatment of convulsions. Delivery should be strongly considered regardless of gestational age if there are signs of fetal distress, or signs of maternal problems including severe hypertension, headache, visual disturbance, epigastric pain, deteriorating renal function, elevated liver enzymes, hemolysis, low platelet count. </span><br />
<h4>
<span style="font-family: inherit; font-size: large;">Antihypertensive drug treatment in pregnancy.</span></h4>
<span style="font-size: large;">Methyldopa is generally preferred (first line drug in pregnancy ) because it does not affect uteroplacental blood flow and does not have short or long-term adverse effects on the development of children. Labetalol can also be used as a first -line drug instead of methyldopa. Beta-adrenergic blockers and the calcium channel blocker nifedipine, are generally safe and can be administered for the treatment of hypertension in pregnancy, but there are some reports of fetal growth retardation with the beta-blocker, atenolol. Diuretics are considered relatively safe but they should not be used as first-line agents. Pregnancy is a contraindication for ACE-inhibitors and angiotensin receptor blockers (ARBs) and this a fact that every physician should remember.</span><br />
<span style="font-size: large;"><b>In breastfeeding</b>, antihypertensive medications that are safe include ACE inhibitors, beta-blockers, and nifedipine. Methyldopa should be avoided in the postpartum period because of the risk of depression.</span><span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b></b></span> <span style="font-size: large;"><b>A USEFUL LINK </b></span><br />
<span style="font-size: large;"><b><a href="http://www.escardio.org/static_file/Escardio/Guidelines/publications/PREGN%20Guidelines-Pregnancy-FT.pdf" target="_blank">ESC Guidelines on the management of cardiovascular diseases during pregnancy</a></b></span><br />
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<h3>
<span style="font-size: large;"><b>Echocardiography in hypertension and echocardiography in diastolic dysfunction.</b></span></h3>
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<span style="font-size: large;">Hypertensive heart disease can be defined as the response of the heart to the increased afterload, imposed on the left ventricle by the increased arterial pressure and total peripheral resistance, as a consequence of hypertensive vascular disease. Usual sequelae of hypertension are the following: left ventricular hypertrophy, diastolic dysfunction, cardiac arrhythmias, congestive heart failure and ischemic heart disease. Depending on the severity of hypertensive heart disease a patient can have one or more of the above disorders.<br /><br />The primary echocardiographic finding in many patients with long- standing hypertension is left ventricular hypertrophy. The threshold for defining left ventricular hypertrophy in the average adult is left ventricular wall thickness</span><span style="font-size: large;"> </span><span style="font-size: large;">> 11 mm</span><span style="font-size: large;"> (measured by M- mode or 2 -dimensional echocardiography). A usual additional echocardiographic finding of </span><span style="font-size: large;">hypertensive heart disease is left atrial enlargement (dilation) in response to increased left ventricular diastolic filling pressures. The upper normal limit of the anteroposterior left atrial end-systolic dimension in adults is about 4cm (40 mm).</span><br />
<span style="font-size: large;">Measurement of maximum </span><span style="font-size: large;">left atrial volume (at end-systole) can be performed </span><span style="font-size: large;">in the apical four-chamber view </span><span style="font-size: large;">by the multiple discs </span><span style="font-size: large;">method. (The machine divides the cavity in parallel discs and calculates the sum of their volumes).</span></div>
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<span style="font-size: large;"><b><br /></b></span>
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<h4>
<span style="font-size: large;"><b>Assesment of left ventricular diastolic function (a summary)</b></span></h4>
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<span style="font-size: large;">Another usual finding in hypertension is<b> diastolic dysfunction </b>which usually is mild or moderate, but sometimes it can be severe. </span></div>
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<span style="font-size: large;"> Diastolic dysfunction can occur in many kinds of heart disease such as hypertensive heart disease, diabetes, hypertrophic cardiomyopathy, aortic stenosis with left ventricular hypertrophy, ischemic heart disease, restrictive cardiomyopathy, constrictive pericarditis, etc.</span><br />
<span style="font-size: large;">Assessment of left ventricular (LV) diastolic function with echocardiography is a part of the routine evaluation of patients presenting with symptoms of dyspnea or heart failure. </span><br />
<span style="font-size: large;">There are four key variables for a quick assessment of LV diastolic function. LV diastolic dysfunction is present if more than half of these parameters meet the abnormal cutoff values. These key parameters are:</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b>The peak early diastolic velocity of the mitral annulus </span><span style="font-size: large;">e΄</span><span style="font-size: large;">, obtained from the pulse wave tissue Doppler velocity tracing of the septal and lateral mitral annulus, in the apical 4 chamber view. The velocity </span><span style="font-size: large;">e΄is a marker of myocardial relaxation and it is reduced in all stages of diastolic dysfunction. A normal </span><span style="font-size: large;">e΄ is a strong indication that the diastolic function is normal, except in patients with constrictive pericarditis or significant mitral regurgitation.</span><br />
<span style="font-size: large;">The normal septal </span><span style="font-size: large;">e΄ </span><span style="font-family: "times new roman" , serif; font-size: 18pt;">≥ 8 cm/ s (centimeters per second). The lateral </span><span style="font-size: large;">e΄ is normally higher than the septal (> 10 cm/s). Abnormal values suggestive of diastolic dysfunction: a septal </span><span style="font-size: large;">e΄< 7 and a lateral </span><span style="font-size: large;">e΄< 10 cm/s.</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The average E/</span><span style="font-size: large;">e΄ ratio. This is the ratio of the peak early diastolic mitral inflow velocity E to the average of the </span><span style="font-size: large;">e΄ velocities of the septal and lateral mitral annulus. Abnormal is a ratio E/</span><span style="font-size: large;">e΄>14. The ratio E/</span><span style="font-size: large;">e΄ is less age-dependent than other indices of LV diastolic function. A ratio > 14, regardless of the patient's age, is almost always abnormal, suggesting elevated LV diastolic pressures (and thus, an elevated mean left atrial pressure and pulmonary capillary wedge pressure)</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The LA volume index is the maximum volume of the left atrium (LA), measured at the end of ventricular systole, divided by the patient's body surface area (BSA). </span><span style="font-size: large;">LA volume index > 34 ml/</span><span style="font-family: inherit; font-size: large;">m<sup>2 </sup></span><span style="font-size: large;">is considered abnormal, indicating left atrial dilation. LA dilation in the absence of a chronic atrial arrhythmia (e.g. atrial fibrillation), or mitral valve disease, is an indication of increased LV filling pressures, resulting in chronically elevated left atrial pressures.</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The peak tricuspid regurgitation (TR) velocity measured with the continuous wave Doppler. A peak TR velocity > 2.8 m/s is suggestive of an elevated pulmonary arterial systolic pressure (with the exception of pulmonary stenosis). This can often result from elevated pulmonary venous pressures due to the elevated left atrial pressure caused by LV diastolic dysfunction (provided that there are no indications suggestive of another cause of pulmonary hypertension e.g. pulmonary arterial hypertension, lung disease, valvular heart disease, LV systolic dysfunction).</span><br />
<span style="font-size: large;">A more detailed discussion follows:</span><br />
<span style="font-size: large;">Evaluation of left ventricular (LV) diastolic function begins with M-mode and 2D echocardiography : </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> Assessment of </span><span style="font-size: large;"> LV size, and wall thickness and </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b>Assessment of left atrial (LA) </span><span style="font-size: large;">volume and anteroposterior dimension. </span><br />
<span style="font-size: large;">In patients with LV diastolic dysfunction, concentric or</span><br />
<span style="font-size: large;">eccentric LV hypertrophy can be found. Pathologic LV hypertrophy is usually associated with an increased left ventricular stiffness which results in diastolic dysfunction. </span><br />
<span style="font-size: large;">Increased LA volume reflects the effects of the </span><span style="font-size: large;">increased LV filling pressures over time. </span><span style="font-size: large;"> Elevated left ventricular filling pressures can occur in patients with diastolic or systolic dysfunction. LA dilation can also occur in patients with mitral stenosis or regurgitation and in patients with chronic permanent atrial fibrillation. LA volume is measured at end-systole in the apical 4 chamber view with the same method (Simpson's method of summation of disks) used for the measurement of left ventricular volume.</span><span style="font-size: large;"></span></div>
<span style="font-size: large;">Doppler assessment: To assess the mitral inflow a</span><span style="font-size: large;">lign the Doppler beam with the inflow direction and p</span><span style="font-size: large;">lace a 1-3 mm pulse wave (PW) Doppler sample volume between the </span><span style="font-size: large;">tips of the </span><span style="font-size: large;">mitral leaflets. If the </span><span style="font-size: large;"> PW sample volume position is not at the valve tips, but </span><span style="font-size: large;">towards the mitral annulus or towards the </span><span style="font-size: large;">apex, this can alter significantly the mitral flow </span><span style="font-size: large;">velocities.</span><br />
<span style="font-size: large;">E is the peak early diastolic velocity of transmitral flow and A is the peak late diastolic velocity at the time of atrial contraction. In adults with normal diastolic function E/A has a value between 0.8 and 2, but less than 2 (In younger people E>A and in middle-aged or older people E wave normally becomes lower and A increases and can be higher than A).<br /> In adults with <b>normal diastolic function (normal pattern)</b> the E > A but is less than 2A (except in very young persons), or E may be a little smaller than A, but more than 0.8 A (the E wave can be lower than the A wave by less than 20 %). The deceleration time (DT) of the E wave (time from the peak of the E wave to its end at the baseline) is </span><span style="font-size: large;">150-200 ms (milliseconds). Isovolumic relaxation time (the time from the end of aortic flow to the beginning of mitral flow) is IVRT = 50-100 ms. </span><span style="font-size: large;">Measure isovolumic relaxation time (IVRT) by placing </span><span style="font-size: large;">the PW Doppler sample volume in- between LV inflow and </span><span style="font-size: large;">outflow to simultaneously display the end of aortic flow </span><span style="font-size: large;">and the onset of mitral E-wave velocity. </span><br />
<span style="font-size: large;">In very young people with normal diastolic function E/A can be >2, but this is not due to an increased LA pressure as in the restrictive pattern. This pattern in young people is normal and is due to a more active relaxation of the left ventricle (LV) in early diastole so that early diastolic flow velocity is increased. It is easy to distinguish this from the restrictive pattern because these are very young individuals with no heart disease, no symptoms of effort dyspnea, normal left atrial size and normal tissue Doppler velocities of the mitral annulus.</span></div>
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<span style="font-size: large;">Pulse wave Doppler of pulmonary venous flow (obtained in the apical 4 chamber view) in adults with normal diastolic function and also in those with mildly impaired diastolic function (delayed relaxation) shows S ≥ D. S is the peak velocity of the systolic wave and D the peak velocity of the early diastolic wave of pulmonary venous flow. </span><br />
<div>
<span style="font-size: large;">In people with normal diastolic function and also in those with mild diastolic dysfunction (impaired relaxation) </span><span style="font-size: large;">the ratio E/e΄ is <10. E is the peak velocity of the early transmitral flow and e'</span><span style="font-size: large;"> (or </span><span style="font-size: large;">Ea) is the peak early diastolic velocity of the mitral annulus measured by pulse wave tissue Doppler.</span></div>
<div>
<span style="font-size: large;">In more advanced forms of diastolic dysfunction (moderate or grade- 2 diastolic dysfunction with a pseudonormal pattern of transmitral flow-see below, or severe diastolic dysfunction with the restrictive pattern), the pulmonary venous flow shows S<D and tissue Doppler of the mitral annulus shows an elevated ratio E/</span><span style="font-size: large;">e΄</span><span style="font-size: large;"> and a reduced velocity </span><span style="font-size: large;">e΄</span><span style="font-size: large;">. According to the recent ASE (American Society of Echocardiography) and EACVI (European Association for Cardiovascular Imaging) recommendations, abnormal values indicating left ventricular (LV) diastolic dysfunction are the following: Peak early diastolic velocity (</span><span style="font-size: large;">e΄) of the septal mitral annulus< 7 cm/s, </span><span style="font-size: large;">e΄ of the lateral mitral annulus < 10 cm/s and an average ratio E/</span><span style="font-size: large;">e΄> 14. </span><br />
<span style="font-size: large;"><b>Mild (grade 1) diastolic dysfunction</b> is characterized by the impaired relaxation (or delayed relaxation) mitral inflow pattern with E/A<0.8, </span><span style="font-size: large; text-align: justify;">E </span><span style="font-family: "times new roman" , serif; font-size: 18pt; text-align: justify;">≤ </span><span style="font-size: large; text-align: justify;">50 cm/s </span><span style="font-size: large;">and a prolonged deceleration time DT of the mitral flow E wave ( DT> 200 ms). DT is the time from the peak to the end </span><span style="font-size: large;">of the E wave</span><span style="font-size: large;">. There is also prolongation of isovolumic relaxation time, </span><span style="font-size: medium;"><span style="font-size: large;">IVRT ≥ 100 ms. </span><span style="font-family: "arial" , "helvetica" , sans-serif;">The IVRT is the time from the closure of the aortic valve (end of left ventricular ejection) to the opening of the mitral valve (onset of ventricular filling). In this time interval, left ventricular dimensions are constant and the mitral annulus does not move. So, the IVRT can be measured on the pulse wave tissue Doppler tracing of the mitral annulus as the time from the end of the systolic S wave to the onset of the </span></span><span style="font-family: "arial" , "helvetica" , sans-serif;">e΄ (Ea) wave.</span><br />
<span style="font-size: large;">In grade 1 diastolic dysfunction the pulse wave Doppler of pulmonary venous flow shows S>D, where S is the peak velocity of the systolic flow in the pulmonary vein and D the peak velocity of the early diastolic flow.</span><br />
<span style="font-size: large;">In grade 1 diastolic dysfunction mean left atrial pressure and left ventricular filling pressure is not elevated.</span><br />
<span style="font-size: large;">An important point is that <b>age </b>should be taken into account when evaluating LV diastolic function since the LV filling pattern in healthy elderly individuals resembles that of younger people (e.g. 40-60 years old) with mild (grade 1) diastolic dysfunction. Indeed, healthy sedentary elderly people usually have a mild degree of diastolic dysfunction (grade 1) as a result of an increased left ventricular stiffness and a slower myocardial relaxation in comparison to younger individuals.</span><br />
<span style="font-size: large;"><b>Moderate (grade 2) diastolic dysfunction </b>shows the same transmitral flow pattern (</span><span style="font-size: large;">0.8 < E/A <2), as that observed in people with normal diastolic function. It is called <b>pseudonormal pattern</b>.</span><br />
<span style="font-size: large;">In the pseudonormal pattern (as well as in the normal pattern),</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">150 <DT <200 ms and </span><span style="font-size: large;">IVRT is <100 msec (range 60-100 msec).</span><br />
<span style="font-size: large;">This pattern can be distinguished from the normal pattern of diastolic inflow because at the peak of the Valsalva maneuver (which causes a reduction of preload = a reduction of ventricular filling) in people with grade-2 diastolic dysfunction, the pattern of mitral inflow takes the morphology of impaired relaxation (E< A). Other features of the pseudonormal pattern which allow its differentiation from the normal pattern are the following:</span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> A reduced mitral annular e΄ velocity (this is a simple way to distinguish it from normal diastolic function, which is characterized by a normal </span><span style="font-size: large;">e΄).</span><span style="font-size: large;"> </span><span style="font-size: large;">The normal and pseudonormal filling pattern have the same pattern of transmitral flow (generally E>A), but </span><span style="font-size: large;">in case</span><span style="font-family: inherit; font-size: large;"> of a pseudonormal pattern,</span> <span style="font-size: large;">the </span><span style="font-size: large;">e΄</span><span style="font-size: large;"> velocity is reduced. </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The increased E/e΄ </span><br />
<span style="font-size: large;"><b><span lang="EN-US" style="font-family: "arial" , sans-serif; font-size: 14pt;">►</span></b> The pulse wave Doppler signal of the pulmonary venous flow showing S<D (S/D <1). </span><span style="font-size: large;">The peak velocity of the end systolic pulmonary vein reverse flow wave at atrial systole </span><span style="font-size: large;">(AR)</span><span style="font-size: large;"> is elevated ( > 35 cm/s) and the duration of AR wave is increased: </span><br />
<span style="font-size: large;">AR wave duration-mitral<span style="font-family: inherit;"> A wave duration </span></span><span style="font-family: inherit;"><span style="font-size: large;"><span style="background-color: white; color: #222222; text-align: justify;">≥</span> </span><span style="font-size: large;">30 msec.</span></span><br />
<span style="font-size: large;">The pseudonormal mitral inflow pattern can change to a delayed relaxation pattern by reducing preload with diuretic treatment.</span><br />
<span style="font-size: large;"></span><br />
<b><span style="font-size: large;">Severe diastolic dysfunction is characterized by the </span><span style="font-size: large;">restrictive left ventricular </span></b><span style="font-size: large;"><b>filling pattern</b>, where the markedly elevated left atrial pressure causes an increased early transmitral pressure gradient (pressure difference between the left atrium and the left ventricle) in early diastole. This causes the following findings: </span><br />
<span style="font-size: large;"> E/A ratio >2, a short deceleration time (DT </span><span style="font-size: large;"><150 ms) and also a short IVRT < 60 ms. Due to the severe impairment of diastolic function, </span><span style="font-size: large;">mitral annular e΄ velocity is usually severely reduced, the ratio E/e΄ is increased and </span><span style="font-size: large;">pulmonary venous flow shows S<<D (the peak velocity of the S wave is much lower than the peak velocity of the D wave). </span><span style="font-size: large;">The peak velocity of the end systolic pulmonary vein reverse flow wave at atrial systole </span><span style="font-size: large;">(AR)</span><span style="font-size: large;"> is elevated ( > 35 cm/s) and </span><span style="font-size: large;">AR wave duration-mitral<span style="font-family: inherit;"> A wave duration </span></span><span style="font-family: inherit;"><span style="font-size: large;"><span style="background-color: white; color: #222222; text-align: justify;">≥</span> </span><span style="font-size: large;">30 msec.</span></span><br />
<span style="font-size: large;">The restrictive pattern </span><span style="font-size: large;">is called <b>stage 3 diastolic dysfunction</b></span><span style="font-size: large;"> if it can change, by reducing preload with diuretic treatment, </span><span style="font-size: large;">to a pattern of stage 1 or 2 diastolic dysfunction. If treatment cannot change the restrictive pattern of left ventricular filling, then there is <b>stage-4 diastolic dysfunction </b>which carries a severe prognosis.</span><br />
<span style="font-size: large;">Regarding the tissue Doppler examination of the velocities of the mitral annulus, the early diastolic peak velocity of the mitral annulus (</span><span style="font-size: large;">e΄ or </span><span style="font-size: large;">Ea) is generally a good index of diastolic function. It is </span><span style="font-size: large;">higher at the lateral mitral annulus than at the septal </span><span style="font-size: large;">annulus. An indication of diastolic dysfunction is </span><span style="font-size: large;">an e΄ < 7 cm/s at the septal annulus,</span><span style="font-size: large;"> </span><span style="font-size: large;">or <10 cm/sec at the lateral annulus. Moreover, </span><span style="font-size: large;">e΄</span><span style="font-size: large;"> has a </span><span style="font-size: large;">reasonable accuracy in</span><span style="font-size: large;"> identifying patients with diastolic dysfunction </span><span style="font-size: large;">and pseudonormal LV filling. </span><br />
<span style="font-size: large;">In people with cardiac disease, an increased E/e΄ ratio can provide an indication of the presence of an elevated left ventricular filling pressure and pulmonary capillary wedge pressure, </span></div>
<div>
<span style="font-size: large;">if the ratio is > 15 for the septal mitral annulus or > 13 for the lateral mitral annulus. For the septal mitral annulus, an E/e΄ between 10 and 15 is borderline, and cannot predict if the left ventricular diastolic pressures are elevated or normal.</span><span style="font-size: large;">When an average (septal, and lateral) e΄ velocity is available, a cutoff value of 14 should be considered for the E/e΄ ratio.</span><span style="font-size: large;"><br /></span>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<span style="font-size: large;"> A USEFUL LINK</span><br />
<a href="http://asecho.org/wordpress/wp-content/uploads/2016/03/2016_LVDiastolicFunction.pdf" target="_blank"><span style="color: red; font-size: large;">Guideline ASE -2016 : Echocardiographic evaluation of diastolic function</span></a><br />
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-25746869332048940182016-06-02T11:25:00.001+03:002020-01-06T20:50:43.048+02:00The Electrocardiogram -ECG (adult and pediatric) <script async="" src="//pagead2.googlesyndication.com/pagead/js/adsbygoogle.js"></script> <script>
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<span style="font-size: large;"><b><u><br /></u></b></span> <span style="font-size: large;"><b><u><br /></u></b></span> <span style="font-size: large;"><b><u>The ECG</u></b><br />(Note: at the bottom of the page, there are 2 useful video links with ECG examples).<br /><br />In a resting cardiac muscle cell, there are mostly positively charged ions on the outer surface and negatively charged ions on the inner surface of the cell membrane. Then the cell is in the polarized, resting state. When the cell is stimulated by an excitatory electrical wave, the negative ions pass to the outer surface of the cell and the positively charged ions pass into the cell. This reversal of polarity is called depolarization.<br />If an electrode is placed so that the depolarization wave has a direction toward the electrode, it will record an upward or positive deflection. This happens because the cells near the electrode have not yet depolarized and so they have a positive membrane potential, and some myocardial cells away from the electrode have depolarized and so they have a negative potential, as the depolarization wave spreads toward the electrode. When all the myocardial cells have depolarized, then there is no potential difference and so the potential difference recorded by the electrode is zero. The opposite phenomena happen during repolarization.<br />The electrocardiogram (ECG) is the graphic representation of the heart’s electrical activity recorded through electrodes positioned on the body. The electrocardiograph makes the recording of the electrical currents, their magnitude and their direction. It is a sensitive galvanometer. It's deflections are recorded on moving, specially prepared paper. <br />The ECG paper is covered with a grid of squares. Five small squares on the paper form a larger square. The width of a single small square on the horizontal axis (1mm) represents 0.04 seconds =40 msec (40 milliseconds), with the usual ECG paper speed (25mm/sec) and its height (1mm) on the vertical axis represents 0,1 mV (millivolts) On the horizontal axis a second will be 25 small squares (25 mm) across, or 5 large squares.<br />The ECG was introduced by Willem Einthoven in 1903,The electrocardiogram is a graphical representation of changes in electrical potential recorded from the body surface. When skeletal muscle is at rest, changes in surface potential reflect cardiac electric activity (propagation of the cardiac depolarization and<br />then repolarization).<br />The basic waves of the electrocardiogram (ECG) correspond to the electrical events, which take place during the cardiac cycle.<br />The P wave represents atrial muscle depolarization. The QRS complex represents ventricular muscle depolarization. Because ventricular muscle mass is much larger than atrial muscle mass, typically the QRS complex is much larger in voltage amplitude than the P wave.<br />Recorded from multiple points, the QRS complex harbors information about the structure and function of ventricular tissue.<br />The PR interval, which is the segment from the onset of the P wave to the onset of the QRS complex, represents the delay<br />between atrial and ventricular depolarization. <br />The ST segment and T wave (and occasionally the U wave) correspond to the period of ventricular repolarization, a process of electrical recovery that must take place before the ventricle can be depolarized again. The J (junction) point denotes the end of the QRS complex and beginning of the ST segment.</span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>ECG Waves and the ECG paper. From the website ECG Learning Center <a href="https://ecg.utah.edu/lesson/12" target="_blank">https://ecg.utah.edu/lesson/12</a></b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Licence: Creative commons <a href="https://creativecommons.org/licenses/by-nd-nc/1.0/" target="_blank">https://creativecommons.org/licenses/by-nd-nc/1.0/</a></b></span></div>
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<span style="font-size: large;"><br />The twelve ECG leads can be described as 12 different positions from which, the electric activity of the heart is recorded and combining the information from multiple leads, with each lead giving a different perspective of the same phenomenon, the spatial orientation of the cardiac electric phenomena is made possible.<br />Each limb (frontal) lead has its own orientation (or axis) corresponding to the position of its positive and negative poles.A wave of depolarization proceeding along the axis of a lead, toward its positive pole,will result in a maximal positive deflection in that lead, and a less positive deflection in neighboring leads. A wave of depolarization propagating in a direction opposite to the positive pole of a lead (toward its negative pole) will produce a negative wave (a negative deflection).<br />Lead aVL is –30°.<br />Lead I is 0°.<br />Lead II is 60°.<br />Lead aVF is 90°.<br />Lead III is 120°.<br />Lead aVR is –150° <br />Each of the 6 precordial leads presents its own “perspective,” recording electrical potentials from a different chest surface location.</span><br />
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<span style="font-size: large;"><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjc4GdzupBg_WA_qLcM-AB_6TjkTXRl1Z9uKnOF9VQ5WMsDB-tlxxdyXnb1Zp0gRSJLW4nT4SR-lHh70Oknrr0E38FviX21bLy8tOapaNCZsP9MZzGyoaIX7F8p6usRpTtdaMNpeRSamTc/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+ecg-lead-planes.png" imageanchor="1" style="font-size: medium; margin-left: 1em; margin-right: 1em; text-align: center;"><img border="0" height="370" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjc4GdzupBg_WA_qLcM-AB_6TjkTXRl1Z9uKnOF9VQ5WMsDB-tlxxdyXnb1Zp0gRSJLW4nT4SR-lHh70Oknrr0E38FviX21bLy8tOapaNCZsP9MZzGyoaIX7F8p6usRpTtdaMNpeRSamTc/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+ecg-lead-planes.png" width="400" /></a><br />Limb leads (axis direction) <br />From http://www.emtresource.com/ <br /><br /><br /><br /><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_er66bI-KQInntvEVflQ_uFyBmym2EtVyadBBjnoTjcXGEwGGNkiq1pwY5EudURkglNSctaBdi9QEAM1mIv4ERhMOq94P0-n8xgvUlfxhklR6SElsTPsAkhRvL_8YfTlzeNxqDHvgl0g/s1600/%25CE%2595%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%2592%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2580%25CF%2581%25CE%25BF%25CE%25BA+%25CE%2591%25CF%2580%25CE%25B1%25CE%25B3.jpg" imageanchor="1" style="font-size: medium; margin-left: 1em; margin-right: 1em; text-align: center;"><img border="0" height="305" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_er66bI-KQInntvEVflQ_uFyBmym2EtVyadBBjnoTjcXGEwGGNkiq1pwY5EudURkglNSctaBdi9QEAM1mIv4ERhMOq94P0-n8xgvUlfxhklR6SElsTPsAkhRvL_8YfTlzeNxqDHvgl0g/s400/%25CE%2595%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%2592%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CF%2580%25CF%2581%25CE%25BF%25CE%25BA+%25CE%2591%25CF%2580%25CE%25B1%25CE%25B3.jpg" width="400" /></a><br /><br />Position of precordial leads on the chest <br />From http://www.nottingham.ac.uk/ <br /><br /><br />The first step in examining an ECG is making sure that the correct name of the patient and date are written on the ECG recording ! The second step is to determine heart rate and rhythm. <br />In order to understand the ECG, one must know at first the<b> sequence of the electrical activation of the heart</b>. Normally the electrical impulses are generated in the sinoatrial node (SA node) which is the heart's natural pacemaker and consists of a cluster of cells, situated in the upper part of the wall of right atrium, near the origin of the superior vena cava. An electrical signal generated by the SA node is conducted from cell to cell, through the heart. At first the electrical impulse (signal) travels through the atria. Right atrial activation begins before activation of the left atrium, then the impulse is conducted to the left atrium. Both atria undergo activation during much of the middle of the overall atrial activation period and left atrial activation continues after the end of right atrial activation. After atrial activation the impulse reaches the atrioventricular (AV) node, a cluster of cells situated in the center of the heart, between the atria and ventricles. The AV node is characterized by slow conduction of the electrical signal. It serves as a gate, slowing the electrical signal before it is permitted to pass down to the ventricles. This delay ensures that the atria have a chance to fully contract before the ventricles are stimulated. After passing the AV node, the impulse rapidly traverses the bundle of His to enter the bundle branches, and it then travels through the specialized intraventricular conduction paths (Purkinje fibers) to activate ventricular myocardium.<br /><b>Heart rate</b> determination (pulses per minute, or beats per minute- bpm). <br />At the usual ECG paper speed (25 mm/s), a distance of 25 mm represents 1 second. Since 1 minute=60 seconds, a distance of 60 x 25 mm=1500 mm represents 1 minute. If the rhythm is regular, a cardiac beat appears at a constant dinstance (D) from the previous one, and so every time the ECG paper runs this distance D, a new cardiac beat appears. Thus, if we measure this distance (D) between two consecutine QRS comlexes in mm, in a situation of a regular heart rate (HR): HR= 1500/D. From this simple rule, and by taking into account that every large square of the ECG paper represents a distance of 5 mm, if the distance D between 2 consecutive R waves is 1 large square, then HR=1500/5=300 bpm. If the distance is 2 large squares HR=150, 3 large squares : HR=100, <br />4 large squares HR=75, 5 large squares, HR=60, 6 large squares: HR=50, 7 large squares HR=43, <br />8 large squares : HR=37.5 , 9 large squares HR=33, 10 large squares HR=30, 11 large squares HR=27. It is easy to remember these numbers.<br />If heart rhythm is irregular (for example in patients with atrial fibrillation) then you can measure how many QRS complexes occur in 6 seconds (in a paper distance of 6 x 25=150 mm= 15 cm=30 large squares) and then multiply this number of QRS comlexes by 10, in order to see how many QRS complexes occur in a minute. Some measure the number of QRS complexes in 3 seconds (15 large squares) and multiply x20. It is essentially the same.<br />In adults normal heart rate at rest is usually considered to range from 60 to 100 beats per minute (bpm) , but these values are not absolute, because sleeping heart rate may normally fall to about 50 bpm and the normal daytime resting heart rate rarely exceeds 90 bpm. So, from a practical point of view, many doctors consider as normal range of resting heart rate 50-90 bpm. In infants and children heart rate is normally higher.<br />Normal sinus rhythm is considered to be present when the P wave is positive in I, II, negative in aVR, positive in V2–V6, and positive or biphasic (+/–) in V1, III and posive or biphasic (-/+) in aVL. (this is the morphology of the normal sinus P wave, when the origin of atrial depolarization is from the spread of a sinus electrical impulse). <br /><br /><b>An abnormal morphology of the P</b> wave can indicate atrial activation from an ectopic focus, or left or right atrial abnormality. With the term atrial abnormality we mean a P wave morphology suggesting dilation of an atrium (hypertrophy of its myocarium may also coexist), or interatrial and intra-atrial conduction delay.<br />Atrial activation from an ectopic focus is indicated by a P wave with abnormal polarity. For example, a negative P wave in lead<br />I suggests activation beginning in the left atrium. Inverted P waves in the inferior leads generally indicate a posterior atrial activation<br />site.<br /><b>Features indicative of a left atrial abnormality</b> : <br />Prolonged P wave duration (>120 msec), prominent notching of P wave, with the interval between notches of >40 msec (“P mitrale”), increased duration and depth of the terminal negative portion of P wave in lead V1, so that the area subtended by it >0.04 mm.sec ( > 1 mm</span><sup><span style="font-size: 14pt; line-height: 107%;"><span style="font-family: inherit;">2</span></span></sup><span style="font-size: large;">), leftward shift of mean P wave axis to between −30 and −45 degrees. The terminal negative portion of the P wave in lead V1 has a duration > 40 msec or depth > 1mm.</span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>This is lead II. Can you describe any abnormalities ?</b></span><br />
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<span style="font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>Answer </b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b> Increased duration of the P wave (> 3mm, i.e > 120 msec) and nospecific ST-T wave changes. The increased duration of the P wave indicates left atrial enlargement.</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>[This ECG lead is from a 70 years old man who presented with dyspnea with mild exertion and an enlarged cardiac shadow on chest x ray . After testing with echocardiography (which showed left ventricular systolic dysfunction and left ventricular and left atrial enlargement) and coronary arteriography (which showed no significant stenoses of the coronary arteries) he was diagnosed with dilated cardiomyopathy ] </b></span><br />
<span style="font-size: large;"><br /></span> <b style="font-size: x-large;">Features indicative of a right atrial abnormality</b><br />
<span style="font-size: large;">Peaked P waves with increased amplitude: in lead II >0.25 mV(> 2.5 mm). This is called P pulmonale, because it is often present in cor pulmonale (right heart failure due to severe chronic pulmonary disease), but it can also be noticed in other conditions leading to a dilation of the right atrium.<br />Prominent initial positive portion of the P wave in lead V1 or V2 >0.15 mV (>1.5 mm).<br />Increased area under initial positive portion of the P wave in lead V1 >0.06 mm-sec (>1.5 mm</span><sup><span style="font-size: 14pt; line-height: 107%;"><span style="font-family: inherit;">2</span></span></sup><span style="font-size: large;">)<br />Rightward shift of mean P wave axis to more than +75 degrees.<br /><br />The <b>PR interval</b> is the distance from the beginning of the P wave to the beginning of the QRS complex.<br />The normal PR interval in adults ranges from 120-200 msec (3-5 mm).<br />A longer PR interval is seen in cases of atrioventricular (AV) block (delayed or abnormal conduction properties of the AV node, or the bundle of His, or its branches) and shorter PR interval in pre-excitation syndromes and various arrhythmias.</span><br />
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<span style="font-family: inherit; font-size: large;">The <b>PR segment</b> is the last part of the PR interval. It is the distance from the end of the P wave to the onset of the QRS and is usually isoelectric (isoelectric in the ECG means a straight line of zero electric potential).</span></div>
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<span style="font-family: inherit; font-size: large;"><b>The QRS complex</b> represents ventricular depolarization, which occurs in three consecutive phases that give rise to the generation of three electrical vectors (meaning that each of these 3 phases has a different magnitude and spatial direction of the measured electrical potential). Among the waves constituting the QRS complex, the positive ones are termed R, the negatives are called Q waves when they appear as the initial phase of the QRS, and when they are not the initial waves, the are called S waves. If there are two positive waves (deflections) the first is called R and the second R'. The R, Q, and S, when they are of small amplitude are indicated by a lowercase letter (r,q,s), while when they are larger in size they are denoted by a capital letter. If the QRS consists of a monophasic negative wave, this is called a QS wave.</span></div>
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<span style="font-family: inherit; font-size: large;">A normal initial negative wave of ventricular depolarization is called <b>a q </b><b>wave.</b> <u>Normally </u>it must be narrow (< 40msec) and should not usually exceed 25% of the amplitude of the following R wave, but exceptions exist in leads III, aVL and aVF. If the initial negative deflection is wider or deeper, it is known as a Q wave.</span><br />
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<tr><td class="tr-caption" style="text-align: center;"><b><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;">A normal ECG</span></b></td></tr>
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<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <b style="font-family: inherit; font-size: x-large;"><br /></b> <b style="font-family: inherit; font-size: x-large;"><br /></b> <b style="font-family: inherit; font-size: x-large;">With infarction,</b><span style="font-family: inherit; font-size: large;"> depolarization (QRS) changes often accompany repolarization (ST-T) abnormalities, if some time has passed and there is necrosis of sufficient myocardial tissue. This can lead to decreased R wave amplitude or abnormal Q waves in the anterior, lateral, or inferior leads as a result of loss of electrical forces in the infarcted area.</span></div>
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<span style="font-family: inherit; font-size: large;"><b>Normal ventricular depolarization</b> has 3 phases. The first phase is the depolarization of the left side of the middle third of the interventricular septum, with a direction from left toward the right side of the septum, with a small resultant electric vector directed rightward and anteriorly. This produces the small initial deflection of the QRS complex. Because depolarization is directed from left to right it produces a small positive (r) wave in leads with a right position, such as avR, V1 and V2 and a small negative wave (septal q wave) in leads with a left orientation, such as I, avL, V5,V6. Then the impulse spreads throughout the apical and free walls of both ventricles in an endocardial to epicardial direction. Because the myocardial mass of the left ventricle is greater than that of the right ventricle, the resultant vector of this main phase of ventricular depolarization is directed leftward and inferiorly. This produces the largest wave of the QRS complex: in leads avR, V1,V2 it is a large negative deflection (S) and in leads I, avL, V5,V6, it is a large positive deflection (R). Finally depolarization arrives at the posterolateral left ventricular wall and the posterobasal septum. This gives rise to a small resultant vector, directed posteriorly and superiorly. </span><br />
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<span style="font-family: inherit; font-size: large;"><b>The QRS axis in the frontal plane</b> (the mean direction and amplitude of ventricular electrical activation in this plane) can be assessed from the bipolar and augmented unipolar limb leads (leads I, II, III and avR, avL, avF). By convention, the axis of lead I, toward the left, is called 0 degrees.</span></div>
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<span style="font-family: inherit; font-size: large;">The exact method to calculate the axis, would be to calculate the algebric sum of the area of the positive and negative waves of the QRS complex, for each of two leads. If this value is plotted as a vector on the axis of each of the two leads used, the mean frontal plane QRS axis will be the resultant of these 2 vectors. Note that for axis determination the area of a deflection (ECG wave) is more important than its amplitude.This method of axis determination can only be used by a machine (computerized analysis). There are simpler ways to determine (in approximation) the mean frontal plane QRS axis, by applying the following rules: </span></div>
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<span style="font-family: inherit; font-size: large;">The axis can be estimated by identifying the limb lead in which the QRS complex is most nearly isoelectric ( the algebric sum of the positive and negative waves is about zero- almost equal positive and negative deflections). The frontal plane axis is perpendicular to that lead. The direction of ventricular depolarization on that frontal plane QRS axis is easily determined, because it must be towards the direction of the leads having a positive net QRS deflection. Another rule is that the QRS axis is approximately the axis of the lead having the most positive algebric sum of the QRS waves (the lead with the most positive net QRS deflection).</span></div>
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<span style="font-family: inherit; font-size: large;">A tip for quick analysis of the axis: </span></div>
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<span style="font-family: inherit; font-size: large;">If the QRS is net positive in Lead I and in Lead II the axis is normal.</span></div>
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<span style="font-family: inherit; font-size: large;">If the net QRS is positive in Lead I but negative in Lead II, there is usually left axis deviation.</span></div>
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<span style="font-family: inherit; font-size: large;">If the net QRS is negative in Lead I but positive in Lead II, there is usually right axis deviation.</span></div>
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<span style="font-family: inherit; font-size: large;">A frontal plane axis between −30 and +90 degrees is normal, whereas other axes are abnormal in adults. </span></div>
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<span style="font-family: inherit; font-size: large;">Right axis deviation: axis between +90 and 180 degrees. Left axis deviation : axis between -30 and -90. </span></div>
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<span style="font-family: inherit; font-size: large;">Indeterminate axis : between -90 and 180 (this axis can be extreme left, or extreme right axis deviation). The axis is considered as indeterminate also when positive and negative deflections in all limb leads are equal.</span></div>
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<span style="font-family: inherit; font-size: large;">Right axis deviation beyond +90 degrees is often a normal variant in children and adolescents. </span></div>
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<span style="font-family: inherit; font-size: large;">Common <u>causes of left axis deviation</u>: left anterior fascicular block (a non- conducting anterior fascicle of the left bundle branch, also called left anterior hemiblock-LAH), inferior wall myocardial infarction, chronic obstructive pulmonary disease (COPD), and Wolff -Parkinson-White syndrome with a posteroseptal accessory pathway.</span></div>
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<span style="font-family: inherit; font-size: large;"><u>Causes of right axis deviation</u> include right ventricular hypertrophy or dilation, left posterior fascicular block (also called left posterior hemiblock-LPH), lateral wall myocardial infarction, , Wolff -Parkinson-White syndrome with a left free wall accessory pathway, or a normal variant (in some young people with mild right axis deviation).</span></div>
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<span style="font-family: inherit; font-size: large;"><b>In the precordial leads,</b> QRS is normally characterized by<b> progression</b> from an rS pattern= small r and large S (or sometimes QS in V1) in the right precordial leads to a qR (small q, large R) pattern in the left precordial leads. From the right toward the left precordial leads the R wave progressively enlarges and the S wave decreases.</span></div>
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<span style="font-family: inherit; font-size: large;"> The <b>transitional zone</b> is the lead in which the change of this QRS pattern occurs, where the R and S waves are almost equal in size. Normally the transitional zone is lead V3 or V4.</span></div>
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<span style="font-family: inherit; font-size: large;">A <b>shift of the transitional zone</b> to the right (in leads V2 or V1) is called an early transition,or early R wave progression, or counterclockwise rotation of the heart and to the left (in leads V5 or V6) is called delayed transition, or clockwise rotation.</span></div>
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<span style="font-family: inherit; font-size: large;">A shift of the transitional zone to the right with an<u> R>S in lead V2 and possibly in lead V1 </u>can occur as a normal variant, or in right ventricular hypertrophy, or in posterior myocardial infarction (MI).</span></div>
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<span style="font-family: inherit; font-size: large;">So, the differential diagnosis of a tall R wave (> 7mm or R>S) in the right precordial leads V1,V2 is the following:</span></div>
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<span style="font-family: inherit; font-size: large;">RBBB, right ventricular hypertrophy (usually the T wave is negative), posterior MI (usually the T wave is positive in the right precordial leads), Wolff- Parkinson -White (WPW) syndrome with a left sided accessory pathway (because in that case ventricular depolarization begins from the left ventricle through the accesory pathway with a direction from left to right, causing the appearance of a big R wave in right sided leads), rarely a normal variant (in some normal people), Duchenne's muscular dystrophy.</span></div>
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<span style="font-family: inherit; font-size: large;">A shift of the transitional zone to the left denoting a delayed or poor R wave progression (clockwise rotation) can occur in lead malpositioning, mild right ventricular hypertrophy as in chronic obstructive pulmonary disease, left bundle branch block (LBBB), left anterior hemiblock (LAH) ,anteroseptal MI, pectus excavatum (the most common congenital chest deformity, with a sunken-concave appearance of the sternum), corrected transposition of the great arteries and congenital absence of the left pericardium.</span></div>
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<span style="font-family: inherit; font-size: large;"><b>QRS duration </b>The normal QRS is narrow (normal duration < 100 msec, which means < 2.5 mm), because the His-Purkinje system spreads activation rapidly throughout the ventricles. A prolonged QRS implies slow conduction through the ventricles due to dysfunction ,or circumvention of the His-Purkinje system. This is explained by the fact that conduction through ventricular myocardium is relatively slow. </span></div>
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<span style="font-family: inherit; font-size: large;"><b>Aberrancy </b></span></div>
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<span style="font-family: inherit; font-size: large;">Aberrancy refers to patterns of slowed conduction through the ventricles, due to failure of part of the His-Purkinje system.</span></div>
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<span style="font-family: inherit; font-size: large;">There are some patterns of aberrancy:</span></div>
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<span style="font-family: inherit; font-size: large;"><b>Bundle branch blocks.</b> The bundle of His divides distally in the left and right bundle branches. The left bundle branch further splits into anterior and posterior fascicles. In bundle branch blocks the QRS duration is ≥120 ms (≥ 3 mm wide). This is a feature of both left and right bundle branch block.</span></div>
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<span style="font-family: inherit; font-size: large;">A <u>left bundle branch block (LBBB) </u>is characterized by the following : In lead V1 there is a small narrow r wave (if any) and a deep wide S, or a wide QS wave. and in lead V6: a wide monophasic R wave or RsR' pattern (R, small s and a second R). It is also characterized by the absence of septal q waves in leads I, V5, and V6 (the left-oriented leads). In most cases, the ST segment and T wave are discordant with the QRS complex, meaning that the ST segment is depressed and the T wave is inverted in leads with positive QRS waves ( I, aVL, V5, V6), and the ST segment is elevated with an upright T wave in leads with a predominantly negative QRS complex (V1 ,V2).</span></div>
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<span style="font-family: inherit; font-size: large;">LBBB occurs in less than 1% of the general population. More commonly it it occurs in people with heart disorders (for example coronary artery disease, dilative cardiomyopathy, hypertensive heart disease, valvular heart disease etc). </span></div>
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<span style="font-family: inherit; font-size: large;">However, approximately 10% of the persons with LBBB have no clinically demonstrable heart disease. </span></div>
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<span style="font-family: inherit; font-size: large;">LBBB is an ECG pattern with prognostic implications. In persons with or without overt heart disease, LBBB is associated with a higher risk of mortality and morbidity from infarction, heart failure and arrhythmias (including high-grade atrioventricular block) in comparison to the the risk observed in the general population.</span></div>
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<span style="font-family: inherit; font-size: large;">A <u>right bundle branch block (RBBB)</u>: is characterized by a primarily positive deflection in lead V1, classically with a rSR' pattern, but sometimes with a rsR' or rsr' pattern (“rabbit ears” in V1) and the presence of terminal S waves in leads I and V6 ≥40 msec (1mm) wide. The ST-T waves are (as in LBBB) discordant with the QRS complex : T waves are negative in the right precordial leads (V1,V2) and upright in the left precordial leads (V5,V6) and also in leads I and aVL.</span></div>
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<span style="font-family: inherit; font-size: large;">RBBB is a common finding in the general population. Many persons with RBBB have no evidence of structural heart disease.</span></div>
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<span style="font-family: inherit; font-size: large;"> In people with no manifest cardiac disease, RBBB is not associated with an increased risk of cardiac morbidity or mortality.</span></div>
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<span style="font-family: inherit; font-size: large;"> In persons with cardiac disease, the presence of RBBB generally suggests more advanced disease (for example this is true for patients with coronary artery disease).</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>Which are the abnormal findings in this ECG ?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Rhythm : sinus. PR interval prolonged (first degree atrioventricular block).</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Some supraventricular premature beats. Left bundle branch block (LBBB). Frontal QRS axis with left deviation. </b></span></div>
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: medium;"><br /></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>What are the findings in this ECG ?</b></span></div>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiT_THHexuQhdEp_cCNnQgWG07GJRPwRggm2uS844RCN6RmBtrXkr01th4td5H7b5lFMTx0thQ-3oVC1fP781rrkwtjhqJSdeyk5VVAe4Jj6MAOaCmd9vPde1PYxckCyRrSReAwSBbeVu_s/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25BA%25CE%25AF%25CF%2584%25CF%2583%25CE%25B7%25CF%2582+%25CE%25B5%25CF%2585%25CF%2583%25CF%2584%25CE%25AC%25CE%25B8%25CE%25B9%25CE%25BF%25CF%2582+%25CE%25B1%25CF%2580%25CE%25BF%25CE%25BA%25CE%25BB+%25CE%25B4%25CE%25B5%25CE%25BE+%25CF%2583%25CE%25BA%25CE%25AD%25CE%25BB%25CE%25BF%25CF%2585%25CF%2582+%25CE%25BA%25CE%25B1%25CE%25B9+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB%25CE%25B9%25CE%25B1%25CE%25BA%25CE%25AD%25CF%2582+%25CE%25B5%25CE%25BA%25CF%2584%25CE%25B1%25CE%25BA%25CF%2584%25CE%25BF%25CF%2583%25CF%2585%25CF%2583%25CF%2584%25CE%25BF%25CE%25BB%25CE%25AD%25CF%2582.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="" border="0" height="342" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiT_THHexuQhdEp_cCNnQgWG07GJRPwRggm2uS844RCN6RmBtrXkr01th4td5H7b5lFMTx0thQ-3oVC1fP781rrkwtjhqJSdeyk5VVAe4Jj6MAOaCmd9vPde1PYxckCyRrSReAwSBbeVu_s/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25BA%25CE%25AF%25CF%2584%25CF%2583%25CE%25B7%25CF%2582+%25CE%25B5%25CF%2585%25CF%2583%25CF%2584%25CE%25AC%25CE%25B8%25CE%25B9%25CE%25BF%25CF%2582+%25CE%25B1%25CF%2580%25CE%25BF%25CE%25BA%25CE%25BB+%25CE%25B4%25CE%25B5%25CE%25BE+%25CF%2583%25CE%25BA%25CE%25AD%25CE%25BB%25CE%25BF%25CF%2585%25CF%2582+%25CE%25BA%25CE%25B1%25CE%25B9+%25CE%25BA%25CE%25BF%25CE%25B9%25CE%25BB%25CE%25B9%25CE%25B1%25CE%25BA%25CE%25AD%25CF%2582+%25CE%25B5%25CE%25BA%25CF%2584%25CE%25B1%25CE%25BA%25CF%2584%25CE%25BF%25CF%2583%25CF%2585%25CF%2583%25CF%2584%25CE%25BF%25CE%25BB%25CE%25AD%25CF%2582.jpg" title="ECG (Electrocardiogram) RBBB" width="640" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Electrocardiogram (ECG) case-1</b></span></td></tr>
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<span style="font-family: inherit; font-size: large;"> </span><b style="font-family: arial, helvetica, sans-serif; text-align: justify;">Rhythm : sinus. PR interval : normal , V</b><b style="font-family: arial, helvetica, sans-serif; text-align: justify;">entricular premature beats (3)</b><span style="text-align: justify;"><span style="font-size: large;">.</span></span><b style="font-family: arial, helvetica, sans-serif; text-align: justify;"> There is a Right bundle branch block (RBBB). </b><br />
<b style="font-family: arial, helvetica, sans-serif; text-align: justify;">Frontal QRS axis is at about -30 degrees, since the net QRS is almost isoelectric in lead II. This fact alone indicates that the axis can be either -30 degrees, or +150 degrees, but the QRS is positive in lead avL, so the axis cannot be + 150 degrees. It is at -30 degrees. Also note that lead avL has the larger positive algebric sum of the QRS waves. </b><br />
<span style="font-family: inherit; font-size: large;"><br /></span><span style="font-size: large;">The <u>Brugada syndrome</u> </span><span style="font-family: inherit; font-size: large;">is a condition, in which an RBBB-like pattern in the ECG </span><span style="font-size: large;">(incomplete or complete)</span><span style="font-family: inherit; font-size: large;"> with persistent ST segment elevation in the right precordial leads, is associated with susceptibility to ventricular tachyarrhythmias and sudden cardiac death. A number of diagnostic criteria for this entity have been described. The</span><span style="font-size: large;"> syndrome has been associated with a predisposition for ventricular tachyarrhythmia (polymorphic ventricular tachycardia or ventricular fibrillation) and sudden death. There are three ECG forms of the Brugada syndrome, but only type 1 has been clearly associated with ventricular arrhythmias and a risk of sudden death. Type 1 is characterized by an ST segment elevation ≥ 2mm at the J point (at the junction point of QRS and ST) with the ST segment having the convex upward and forming a downward slope in at least two of the leads V1-V3, with a negative T wave.</span><br />
<span style="font-size: large;">Type 2 and type 3 are also characterized by a right bundle branch block morphology (incomplete or complete) with ST segment elevation in the right precordial leads. In type 2, the ST elevation has a concave upward - saddle morphology - and is > 1 mm with a positive or biphasic T wave. Type 3 has an ST pattern similar to type 1 but with an elevation of <2 mm or an ST morphology similar to type 2 but with an elevation <1mm.</span><br />
<span style="font-size: large;"> Types 2 and 3 are usually normal variants in healthy individuals. However, if there are symptoms (e.g., palpitations- episodes of syncope), then type 2 or 3 poses a diagnostic problem, because it can rarely transiently change into type 1. Then a diagnostic test with flecainide admonistration can be performed, which may in some of these individuals induce the appearance of a type 1 ECG morphology. If administration of flecainide causes this unmasking of type 1, then Brugada syndrome is also diagnosed in these patients, but they have a much lower risk of events than in the spontaneous type 1. The spontaneous type 1 Brugada syndrome has been associated with risk of syncope or sudden death of approximately 0.5% per year.</span><br />
<span style="font-size: large;">Asymptomatic individuals with Brugada type 2 or 3 do not require any diagnostic testing.</span><br />
<span style="font-size: large;">Brugada syndrome is about 8-9 times more common in men than in women. It results from a mutation of the SCN5A gene coding for a sodium ion channel (INa). Brugada syndrome type 1 may be manifested by either syncope or cardiac arrest (sudden cardiac death) in the third or fourth decade of life (often during sleep) in individuals without stuctural heart disease.</span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGiCkczAKDBcrVpBBHwRucPYxWP9g51fQfAUxZQDRu7bsyPTHbI0dlKQeRbVyHwjqUJiCoIlwj_KopqGoXrGK7jkWgO1YyX441eHIlj_MdXWMjDAtByZKT9xfRqJtzxaR5godt8qF7CqM/s1600/Brugada-type-1-leads+V1%252CV2_F.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="248" data-original-width="127" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGiCkczAKDBcrVpBBHwRucPYxWP9g51fQfAUxZQDRu7bsyPTHbI0dlKQeRbVyHwjqUJiCoIlwj_KopqGoXrGK7jkWgO1YyX441eHIlj_MdXWMjDAtByZKT9xfRqJtzxaR5godt8qF7CqM/s400/Brugada-type-1-leads+V1%252CV2_F.jpg" title="Electrocardiogram-ECG Brugada syndrome type 1-cardiology book" width="204" /></a></div>
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><u>Arrhythmogenic right ventricular cardiomyopathy (AVRC) or arrhythmogenic right ventricular dysplasia </u>is another condition where the ECG often shows an RBBB pattern (complete or incomplete) and inverted T waves in the leads V1-V3 (</span><span style="font-size: large;">the leads related to the right ventricle).</span><span style="font-size: large;"> A</span><span style="font-size: large;">n </span><span style="font-size: large;">epsilon wave </span><span style="font-size: large;">can be present</span><span style="font-size: large;"> i.e. a</span><span style="font-size: large;"> terminal notch of the QRS (a small wave at the end of the QRS), </span><span style="font-size: large;">as a result of slowed intraventricular </span><span style="font-size: large;">conduction in an area of the right ventricle. AVRC is a cardiomyopathy caused by a defective gene, characterized by right ventricular systolic dysfunction (global or segmental) due to infiltration of a part of the right ventricle by fbrofatty tissue (in some cases also left ventricular dysfunction) and episodes of monomorphic ventricular tachycardia with an LBBB morphology, which pose a risk of sudden cardiac death.</span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjS0SBAFfouTtcy4CYnG__NnqYOkXzM3Xq1ODQ8Ia5NL0iWjSkdZnzmu8ryNC1ZbExeo861WXLuwpLNbkhwK2pi4tZoYRb2hL9CqoE0t113VyZKT4jKUilY-_JC0cccUi7BMUs9WTYEOTE/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+ARVC.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="" border="0" data-original-height="162" data-original-width="239" height="271" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjS0SBAFfouTtcy4CYnG__NnqYOkXzM3Xq1ODQ8Ia5NL0iWjSkdZnzmu8ryNC1ZbExeo861WXLuwpLNbkhwK2pi4tZoYRb2hL9CqoE0t113VyZKT4jKUilY-_JC0cccUi7BMUs9WTYEOTE/s400/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+ARVC.jpg" title="ECG: epsilon wave -arrhythmogenic right ventricular cardiomyopathy-cardiology book" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Lead V1 with epsilon wave at the end of the QRS. From the ECG of a patient with arrhytmogenic right ventricular cardiomyopathy</b></span></td></tr>
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<span style="font-size: large;"><b style="font-family: arial, helvetica, sans-serif; font-size: medium;"><br /></b></span> <span style="font-size: large;"><b style="font-family: arial, helvetica, sans-serif; font-size: medium;"><br /></b></span> <span style="font-size: large;"><b style="font-family: arial, helvetica, sans-serif; font-size: medium;">Lead V5 of the same patient with the epsilon wave at the end of the QRS (less prominent than in lead V1).</b></span> <span style="font-size: large;"><br /></span> <span style="font-size: large;">Another entity characterized by a prolonged QRS interval is <b>pre-excitation</b>. This ECG pattern is caused by the presence of a congenital abnormal pathway of conductive cardiac tissue, between the atria and the ventricles. Such a pathway is called a by-pass tract, or an accessory pathway, through which conduction of electrical impulses can occur, occasionaly resulting in a capacity to form a reentrant circuit, which can function as an arrhythmogenic substrate. The presence of an accessory pathway is an abnormality</span><span style="font-size: large;">, since normally the atria and the ventricles are electrically isolated, and electrical contact between them exists only at the atrioventricular node-His bundle conductive tissue. </span><span style="font-size: large;">The majority of accessory pathways are capable of conduction in both directions, with retrograde </span><span style="font-size: large;">only </span><span style="font-size: large;">conduction </span><span style="font-size: large;">(from ventricles to atria) occurring in 15% of cases, and antegrade only conduction (only from atria to ventricles) rarely seen.</span><span style="color: #222222; font-family: "roboto" , sans-serif;"><span style="line-height: 26px;">. </span></span><span style="font-size: large;">Accessory pathways that are capable of only retrograde conduction are referred to as "concealed", whereas those capable of antegrade </span><span style="font-size: large;">conduction</span><span style="font-size: large;"> (from the atria down to the ventricles) are referred to as "manifest", because a standard ECG reveals their presence by demontrating pre-excitation. Manifest accessory pathways usually conduct in both anterograde and retrograde directions. </span><span style="font-size: large;">In pre-excitation, the ventricles are depolarized by an electrical signal concomitantly conducted through both the accessory pathway and the atrioventricular (AV) node. The part of the ventricle where the accessory pathway connects is the first to depolarize, resulting in a short PR interval and a delta wave on the ECG (a slurring and slow rise of the initial upstroke of the QRS complex). The remaining portion of the ventricular myocardium is depolarized via the normal conductive system (AV node-His bundle-Purkinje fibers) </span><span style="font-size: large;">Thus, the typical ECG features of preexcitation include: </span><span style="font-size: large;"> A short PR interval <120 ms, a slurring and slow rise of the initial upstroke of the QRS complex (called a delta wave), a wide QRS complex > 120 ms and ST segment-T wave changes directed opposite the delta wave and QRS complex, (reflecting altered depolarization). </span><br />
<span style="font-size: large;">Accessory pathways usually can conduct rapidly (i.e. an electrical impulse moves through the pathway at a fast velocity), but they frequently have a longer refractory period than the AV node (Refractory period is the time after tissue is activated by an electrical impulse, during which it cannot conduct another impulse).</span><br />
<span style="font-size: large;">Although a by-pass (accessory pathway) tract can result in arrhythmias, not all patients with a by-pass tract or with preexcitation manifest tachyarrhythmias. The diagnosis of Wolff-Parkinson-White (WPW) syndrome is reserved for patients who have both preexcitation on the ECG and also manifest tachyarrhythmias. (also see chapter on arrhythmias). The most common arrhythmia encountered in people with pre-excitation is atrioventricular reentry tachycardia (AVRT),a reentrant supraventricular arrhythmia. In AVRT, the </span><span style="font-size: large;">AV node is one portion </span><span style="font-size: large;"> </span><span style="font-size: large;">of the reentrant circuit </span><span style="font-size: large;">and the other portion is the accessory pathway (most usually the accessory pathway forms the retrograde limb of the circuit, by conducting from the ventricles to the atria, but rarely it forms the antegrade limb).</span><br />
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<b><b>Bibliography</b></b></div>
<b> Sethi KK, Dhall A ,et al. </b><b>WPW and Preexcitation Syndromes. JAPI supplement 2007;55: 10-15</b></div>
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<b>LINK <a href="http://www.japi.org/april2007/suppliment/Suppliment_10-15.pdf" target="_blank">http://www.japi.org/april2007/suppliment/Suppliment_10-15.pdf</a></b></div>
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<span style="font-family: inherit; font-size: large;"><b>Fascicular blocks</b> typically prolong the QRS slightly, QRS duration is < 120 ms and cause an abnormal frontal QRS axis (see the section on the frontal plane axis of the QRS)</span></div>
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<span style="font-family: inherit; font-size: large;">In <u>Left anterior fascicular block or left anterior hemiblock (LAFB or LAH)</u> there is left axis deviation. There is a qR pattern in lead aVL and the time to peak R wave in aVL ≥45 msec. Left anterior fascicular block also can produce some changes in the precordial leads: Leads V4 - V6 commonly show deep S waves. Damage to the left anterior fascicle is very common because of its delicate nature. Left anterior fascicular block is common in persons without cardiac disease, but it is also common in various cardiac pathologic conditions.</span></div>
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<span style="font-family: inherit; font-size: large;">In<u> Left posterior fascicular block or left posterior hemiblock</u> (LPFB or LPH) there is a right axis deviation</span></div>
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<span style="font-family: inherit; font-size: large;">A left posterior fascicular block is relatively rare, since the posterior fascicle is wider and highly branched, and loss of all the branches is uncommon. Besides right axis deviation, there is an rS pattern in leads I and aVL and qR complexes in the inferior leads.</span></div>
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<span style="font-family: inherit; font-size: large;">A left posterior fascicular block can occur in patients with any cardiac disease, but is unusual in people without cardiac disease.</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>A man 60 years old with a history of paroxysmal atrial fibrillation and hypertension. Can you list 4 abnormalities in his ECG ?</b></span><br />
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<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Sinus rhythm. Abnormalities : 1 supraventricular premature beat, 1 ventricular premature beat, prolonged sinus P wave (see lead II) consistent with possible left atrial enlargement and l</b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>eft anterior fascicular block or left anterior hemiblock (LAFB or LAH)</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A 62 years old male with mechanical prosthetic valves in the aortic and mitral position (because of rheumatic valve disease) on anticoagulation treatment with acenocoumarol, states that in the last month he experienced episodes of a transient discomfort (felt like pressure and vague pain). The discomfort was rather diffuse, on the central area of the chest, lasting a few minutes, appearing with physical activity (brisk walking) and resolvin</b></span><b style="font-family: Arial, Helvetica, sans-serif;">g with discontinuation of activity. Physical examination revealed no significant findings. His ECG is shown. What is the most probable cause of the patient's symptoms? What does the ECG show ? Is the ECG helpful for the diagnosis in this case?</b><br />
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<b style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: normal; text-align: justify;"><b><br /></b></span></b> <b style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: normal; text-align: justify;"><b>ANSWER</b></span><span style="font-family: "times new roman"; font-weight: normal; text-align: justify;"></span><span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: normal; text-align: justify;"><b><br /></b></span></b><br />
<b style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: normal; text-align: justify;"><b>The history alone is sufficient to lead to the most probable diagnosis in this case. The description of the symptoms is typical for effort angina, and the most probable underlying condition in males of this age group is coronary artery disease (CAD).</b></span></b><br />
<b style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: normal; text-align: justify;"><b>The ECG shows features of preexcitation, as in </b></span></b><b style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-weight: normal; text-align: justify;"><b>Wolff-Parkinson-White (WPW) syndrome : A</b></span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;"> short PR interval <120 ms, a</span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;"> slurring and slow rise of the initial upstroke of the QRS complex (called a delta wave), a </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">wide QRS complex > 120 ms</span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">and ST segment-T wave changes directed opposite the delta wave and QRS complex, (reflecting altered depolarization). These ECG findings are of course urelated to the patient's symptoms and can in many cases obscure ischemic ECG changes (posing difficulties in the diagnosis of CAD, especially with an ECG exercise test, which would be an innappropriate diagnostic test for CAD in a patient with a preexcited ECG). </span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">The patient had a coronary angiography and he was diagnosed with CAD ( he had a severe stenosis of the left main coronary artery).</span></b></div>
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<span style="font-family: inherit; font-size: large;"><u>A nonspecific intraventricular conduction delay </u>is a condition characterized by widening (prolongation) of the QRS that does not conform to a specific pattern.</span></div>
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<span style="font-family: inherit; font-size: large;"><b>Low QRS voltage</b>: Low ampitude of the whole QRS in limb leads is defined as the sum of the absolute amplitude of the R and S wave in every limb lead 5mm (0.5mV) or less and in the precordial leads a sum of 10mm or less in every precordial lead. </span></div>
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<span style="font-family: inherit; font-size: large;">Causes of low QRS voltage include obesity, chronic obstructive pulmonary disease, a large pleural effusion, pericardial effusion , pneumothorax, dilative or ischemic cardiomyopathy. </span></div>
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<span style="font-family: inherit; font-size: large;">In <u>dilative cardiomyopathy</u> sometimes we have the following characteristic findings: A relatively low whole QRS amplitude in limb leads (<8mm), with a large QRS amplitude in the precordial leads (the sum of S wave in V1 or V2 and the R wave in V5 or V6 is > 35mm) and slow R wave progression in the precordial leads (R<S in leads V1-V4). </span></div>
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<span style="font-family: inherit; font-size: large;">The T wave, together with the preceding ST segment, is formed during ventricular repolarization.</span></div>
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<span style="font-family: inherit; font-size: large;">The</span><b style="font-family: inherit; font-size: x-large;"> ST segment</b><span style="font-family: inherit; font-size: large;"> normally is isoelectric, or shows only a slight depression (< 0.5 mm).</span><span style="font-family: inherit; font-size: large;"></span><br />
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<span style="font-family: inherit; font-size: large;">The point at the end of the QRS complex and the beginning of the ST segment is called the <b>junctional point (J point)</b> and is normally at or near the isoelectric line.</span><br />
<span style="font-family: inherit; font-size: large;">The<b> T wave</b> normally has an ascending slope with slower inscription than the descending slope. </span><span style="font-family: inherit; font-size: large;">The </span><b style="font-family: inherit; font-size: x-large;">polarity of the T wave</b><span style="font-family: inherit; font-size: large;"> normally is essentially the same as the net polarity of the preceding QRS complex because normally the mean vector of the T wave has roughly the same orientation as the mean QRS vector. The T wave normally is generally positive in all leads except aVR, but there are some normal exceptions :</span></div>
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<span style="font-family: inherit; font-size: large;"> 1) In lead</span><span style="font-size: large;"> V1 t</span><span style="font-family: inherit; font-size: large;">he T wave often is negative, flattened or only slightly positive </span><br />
<span style="font-family: inherit; font-size: large;">2) Also in some normal people the T wave can be flattened or slightly negative in leads V2, III and aVF.</span></div>
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<span style="font-family: inherit; font-size: large;">3) In children, a negative T wave is normal when seen in the right precordial leads V1-V3 and occasionally V4 (pediatric repolarization pattern). This pattern usually changes with puberty of after puberty to the normal adult pattern with positive T waves in all the precordial leads (except V1 which may have a negative T wave. Some normal adults may have a negative T wave also in V2).</span><br />
<span style="font-family: inherit; font-size: large;">4) S</span><span style="font-size: large;">ome normal adults have a persistent juvenile T wave inversion pattern, with negative T waves in the right and middle precordial leads (typically in V1-V3, occasionally also V4 ).</span><br />
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<span style="font-family: inherit; font-size: large;">A <b>U wave </b>is a small wave, which is occasionally present, after the T wave (a small rounded wave </span><span style="font-size: large;">≤1 mm that follows the T wave).</span><span style="font-family: inherit; font-size: large;"> Normally it is smaller than the preceding T wave and has the same polarity. </span><span style="font-size: large;">An abnormal increase in U wave amplitude is most commonly due to some antiarrhythmic drugs (such as ibutilide, dofetilide, sotalol, quinidine, procainamide, or disopyramide) or hyperkalemia (elevated </span><span style="font-size: large;">serum </span><span style="font-size: large;">potasium concentration).</span><br />
<span style="font-family: inherit; font-size: large;"><u>U wave inversion</u> is a sign of ischemia and it can be sometimes the earliest ECG sign of an acute coronary syndrome, although it is not often found. Transient inversion of the precordial U waves induced by exercise, is a sign of ischemia and has been correlated with a significant stenosis of the left anterior descending (LAD) coronary artery.</span><br />
<span style="font-size: large;"><b>Abnormalities of the ST segment and the T wave</b> are often characterized as nonspesific especially if these abnormalities are minor. There are also some prominent ST-T wave abnormalities which are considered diagnostic for important clinical disorders, e.g. a typical ECG pattern suggestive of transmural ischemia with ST elevation (which may or may not be preceded by tall "hyperacute" T waves ) or subendocardial ischemia with ST segment depression or T wave inversion in the appropriate clinical situation, see below. </span><br />
<span style="font-size: large;">In the case of minor ST-T wave abnormalities, the physician should decide if they have diagnostic significance or not, depending on the clinical situation (the patient's history and physical findings e.g. symptoms, risk factors etc.). Minor ST and T wave abnormalities are usually not considered important (except if the patient has many risk factors for coronary artery disease or symptoms). In some cases they appear in people with a normal heart (without any cardiac disease), whereas in some other cases they are associated with left ventricular diastolic dysfunction (eg. in hypertensive individuals) or with left ventricular hypertrophy or with subclinical coronary artery disease (coronary artery disease that has not yet resulted in symptoms). T wave inversion has a higher probability to be due to myocardial ischemic disease or another pathologic condition when it is</span><span style="font-size: large;"> ≥ 2 mm and ST depression when it is > 0.5 mm.</span><br />
<span style="font-size: large;">Usually most physicians ignore minor ST-T wave abnormalities in people without significant cardiovascular risk factors and without symptoms on physical exertion. If significant cardiovascular risk factors or symptoms with physical exertion are present, then further testing is usually indicated (e.g. echocardiography, exercise ECG testing or stress testing with imaging such as myocardial scintigraphy or stress echocardiography).<br /><b>Etiology:</b> Minor T wave changes are non-specific, because they have many different etiologies. Prominent T wave abnormalities also have multiple etiologies but in some cases they provide a more specific pattern. They can occur with: </span><br />
<span style="font-size: large;">Anxiety -heightened adrenergic state (influences of the sympathetic nervous system)</span><br />
<span style="font-size: large;">Hyperventilation (it can cause ST segment depression)</span><br />
<span style="font-size: large;">Changes in position</span><br />
<span style="font-size: large;">Drinking hot or cold beverages</span><br />
<span style="font-size: large;">After a meal</span><br />
<span style="font-size: large;">As a normal variant </span><br />
<span style="font-size: large;">(The ST or T wave abnormalities in the above cases, when present, are usually minor- not very prominent)</span><br />
<span style="font-size: large;">The <u>athletic </u>heart (a constellation of findings present in people that undergo intensive training which is not due to any heart disorder). Some normal athletes have prominent T wave inversions</span><br />
<span style="font-size: large;"><u>CNS</u> events (stroke, intracranial hemorrhage) can cause ST-T wave changes, sometimes prominent.</span><br />
<span style="font-size: large;"><u>Hyperkalemia </u>can cause tall, narrow peaked T waves.</span><br />
<span style="font-size: large;"><u>Hypokalemia </u>can cause low amplitude or inverted T waves</span><br />
<span style="font-size: large;"><u>Ischemia</u> can cause mild ST-T wave changes such as low amplitude T waves or small inverted T waves. It can also cause prominent abnormalities such as deep inverted or biphasic T waves, prominent ST elevation or ST depression (usually horizontal or downsloping)</span><br />
<span style="font-size: large;"><u>Myocardial hypertrophy</u> either secondary to hypertension or aortic stenosis, or associated with hypertrophic cardiomyopathy can cause ST-T wave abnormalities (minor or prominent) with or without the voltage criteria of left ventricular hypertrophy. Typically, apical hypertrophic cardiomyopathy is associated with prominent (deep) T wave inversions in the precordial leads. Left ventricular hypertrophy typically is associated with the ECG pattern of <u>left ventricular strain </u>in leads facing the left ventricle (I, avL, V5, V6). This pattern is characterized by ST segment depression (usually downsloping) and T wave inversion (negative T wave). Left ventricular strain is a term meaning that the ECG abnormality results from the increased workload of the left ventricle usually due to pressure overload (e.g in hypertension or significant stenosis of the aortic valve).</span><br />
<span style="font-size: large;">Other <u>cardiomyopathies</u> such as Tako-tsubo cardiomyopathy (stress cardiomyopathy) and arrhytmogenic right ventricular cardiomyopathy can be associated with T wave inversions (see chapter on cardiomyopathies- link <a href="http://cardiologybookandcases.blogspot.com/2016/12/cardiomyopathies-cardiomyopathy-diagnosis-treatment-cardiologyfreebook.html" target="_blank">The Cardiomyopathies</a>)</span><br />
<span style="font-size: large;"><u>Myocarditis</u> can be associated with ST segment elevation, diffuse T wave inversion or arrhythmias. It is an inflammatory disease of the myocardium that more commonly results from a viral infection but it can also result from mycoplasma infection, drugs and toxins or diseases which can lead to an immune-mediated myocardial inflammation such as systemic lupus erythematosus, scleroderma, Kawasaki's disease. It can cause systolic heart failure.</span><br />
<span style="font-size: large;">In <u>pericarditis </u>after the normalization of the ST segment, which is initially elevated, a phase of diffuse T wave inversion follows.</span><br />
<span style="font-size: large;">Pericarditis is an inflammation of the pericardium, caused by a viral (usually), or a bacterial (rare) infection, immunologic reactions (e.g. autoimmune disease, postpericardiectomy syndrome after heart surgery), uremia, malignancies etc.</span><br />
<span style="font-size: large;"><u>Global idiopathic T wave inversion</u>: The rare occurence of negative T waves in all chest leads (V1-V6) in an adult without evidence of heart disease. </span><br />
<span style="font-size: large;"><u>Right ventricular strain</u> Pulmonary embolism, pulmonary hypertension or right ventricular hypertrophy can cause inverted T waves with or without ST depression in leads that have an orientation roughly toward the right ventricle </span><span style="font-size: large;">due to right ventricular strain (meaning right ventricular pressure overload which adversely affects its function).</span><span style="font-size: large;"> These are the right precordial leads (V1-V3 and occasionally V4) and the inferior leads II, III, aVF (among these inferior leads, the ST-T wave abnormality is often more pronounced in lead III because this the most rightward facing lead).</span><br />
<span style="font-size: large;"><u>Secondary ST-T wave abnormalities</u> T</span><span style="font-size: large;">hese are ST-T wave changes solely due an alteration in the sequence of ventricular activation. T</span><span style="font-size: large;">he ST segment and the T wave have a direction </span><span style="font-size: large;">opposite</span><span style="font-size: large;"> </span><span style="font-size: large;"> to the QRS, e.g. there is ST depression and a negative T wave in leads with a positive net QRS). This is observed in</span><span style="font-size: large;"> bundle branch blocks, Wolff-Parkinson-White (WPW) syndrome, paced ventricular beats and ventricular arrhythmias (premature ventricular beats and ventricular tachycardia).</span><br />
<span style="font-size: large;"><u>"Memory T waves"</u> are inverted T waves that may appear after periods of i</span><span style="font-size: large;">ntermittent rate dependent left bundle branch block, preexcita</span><span style="font-size: large;">tion (WPW pattern), or ventricular pacing.</span><br />
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<span style="font-size: large;"><b>A general approach to the patient with nospecific ST-T wave abnormalities.</b></span><br />
<span style="font-size: large;">The patient with ST- T wave abnormalities should be questioned regarding past or present symptoms of myocardial ischemia including chest pain. In some patients a history of athletic training, or symptoms and signs of stroke could explain the electrocardiographic abnormality. Physical examination may reveal hypertension, signs of valve disease or signs of cardiomyopathy in some patients with T wave abnormalities. Echocardiography is generally a very helpful test to diagnose left ventricular hypertrophy, a cardiomyopathy or valve disease.</span><span style="font-size: large;">Blood tests should also be obtained including electrolytes (potassium , sodium, calcium magnesium), glucose, BUN (blood urea nitrogen), creatinine and also a complete blood count to look for anemia.</span><br />
<span style="font-size: large;"><b>Prominent ST-T wave abnormalities</b> raise more concerns and they also have many etiologies. Some of these etiologic conditions are emergencies, such as the acute coronary syndrome (STEMI or non-STEMI), other conditions are chronic but important, such as hypertrophic cardiomyopathy, but there is also a condition termed idiopathic T wave inversion, where despite the presence of prominent T wave inversion, diagnostic tests do not reveal an underlying heart disease.<br />Some important abnormalities of the ST segment and the T wave are listed below.</span></div>
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<span style="font-family: inherit; font-size: large;"><u><b>Transmural ischemia </b></u>: An ST segment elevation occurring in leads representing an identifiable coronary distribution (e.g., inferior, anterior, lateral), suggests acute and ongoing myocardial transmural ischemic injury, as seen in acute coronary occlusion (myocardial infarction). It can also occur in a case of coronary artery spasm (a condition called variant angina or Prinzmetal's angina), see the first case in the chapter on coronary artery disease (link :<a href="http://cardiologybookandcases.blogspot.gr/2016/05/coronary-artery-disease-stable-unstable.html" target="_blank">Coronary artery disease</a>)</span><br />
<span style="font-size: large;">In an appropriate clinical setting (acute symptoms raising suspicion of an acute coronary syndrome) coronary occlusion causing <b>transmural myocardial ischemia (an ST elevation myocardial infarction STEMI</b>) is diagnosed by the following ECG findings:</span><br />
<span style="font-size: large;">1) In leads V2 -V3, ST segment elevation of 2 mm (0.2 mV) or more at the J point in men, or 1.5 mm (0.15 mV) or more in women in the absence of left ventricular hypertrophy, or</span><br />
<span style="font-size: large;">2) </span><span style="font-size: large;">in two or more other contiguous chest or limb leads</span><span style="font-size: large;"> the presence of an ST elevation of 1 mm (0.1 mV) or more. In such patients, emergency reperfusion (primary angioplasty or fibrinolysis) should be performed, unless there is a contraindication. </span><br />
<span style="font-size: large;">3) Another diagnostic </span><span style="font-size: large;">ECG</span><span style="font-size: large;"> </span><span style="font-size: large;"> criterion for a STEMI, if compatible symptoms are also present (i.e., in the appropriate clinical setting) is a </span><span style="font-size: large;">new or pre</span><span style="font-size: large;">sumably new LBBB (which may obscure ST elevation analysis). In this case emergency reperfusion is also indicated.</span><br />
<span style="font-size: large;">4) Another type of STEMI (in which prompt emergency reperfusion is performed, as for any STEMI) is a true posterior myocardial infarction (MI). True posterior MI in the acute phase presents ST depression in leads V1, V2 (and sometimes also in V3, V4). This is a mirror-image of ST elevation in the posterior leads V7-V9 and is usually caused by an acute infarction in the territoty of a non dominant left circumflex (LCX) coronary artery. In case of suspicion, e</span><span style="font-size: large;">xtending the ECG to left posterior leads V7 -V9 increases sensitiv</span><span style="font-size: large;">ity (also </span><span style="font-size: large;">with excellent specificity)</span><span style="font-size: large;"> for detection of acute LCX injury patterns, with the detection of ST </span><span style="font-size: large;">segment elevation in these leads. Later i</span><span style="font-size: large;">n the acute phase, as</span><span style="font-size: large;"> myocardial necrosis is evolving and also in the chronic </span><span style="font-size: large;">phase, there is an increased </span><span style="font-size: large;">amplitude and widening of the </span><span style="font-size: large;">R wave in V1, V2 ( as a mirror image of the Q waves of myocardial necrosis in the posterior leads overlying the area of necrosis).</span><span style="font-size: large;"> In true posterior MI, injury is </span><span style="font-size: large;">actually located in portions of the lateral wall of the left ventricle.</span><br />
<span style="font-size: large;">Recognition of a true posterior acute MI pattern is important</span><br />
<span style="font-size: large;">because it leads to an immediate reperfusion strategy (as in every STEMI). </span><span style="font-size: large;">New appear</span><span style="font-size: large;">ance of these ECG changes, compatible clinical manifestations, or the association with an acute inferior MI are clues to </span><span style="font-size: large;">this diagnosis.</span></div>
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<span style="font-family: inherit; font-size: large;">With</span><u style="font-family: inherit; font-size: x-large;"> infarction</u><span style="font-family: inherit; font-size: large;">, depolarization (QRS) changes often accompany repolarization (ST-T) abnormalities, if some time has passed and there is necrosis of sufficient myocardial tissue. This can lead to decreased R wave amplitude or abnormal Q waves in the anterior, lateral, or inferior leads as a result of loss of electrical forces in the infarcted area.</span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>The ECG of a male patient, 65 years old, who complained of retrosternal pain since about half an hour, with perspiration. What is: 1) the diagnosis and 2) the proposed treatment?</b></span><br />
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<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Answer </b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>1.Acute anterolateral ST elevation myocardial infarction (STEMI). Note the ST segment elevation in the anterior leads V1-V4 and the lateral leads V5,V6 and I and a mirror ST depression in leads III and aVF.</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>2. N</b></span><b style="font-family: Arial, Helvetica, sans-serif;">itrates (if there is no hypotension)</b><b style="font-family: Arial, Helvetica, sans-serif;">, aspirin, clopidogrel loading dose (or ticagrelor loading dose),morphine, oxygen administration (particularly if the hemoglobin saturation is below normal) and as soon as possible primary angioplasty (if it can be done within 120 minutes) or thrombolysis if primary angioplasty cannot be performed promptly (at most within 120 minutes). Also heparin (standard or low molecular weight heparin), a beta-blocker (if there is no bradycardia or hypotension), an ACE inhibitor (if there is no hypotension) and a statin.</b><br />
<b style="font-family: Arial, Helvetica, sans-serif;"><br /></b> <b style="font-family: Arial, Helvetica, sans-serif;"><br /></b> <span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i>A man 52 years old, with crushing substernal chest pain. What is the diagnosis and which artery is probably responsible?</i></span><span style="font-family: "times" , "times new roman" , serif; font-size: large; font-weight: bold;"><i> (the ECG is courtesy of Dr </i></span><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><i><a ajaxify="/groups/member_bio/bio_dialog/?group_id=425106461001292&member_id=100000482760981&ref=floc2" aria-describedby="u_4k_1" aria-owns="js_1p7" data-hovercard-prefer-more-content-show="1" data-hovercard-referer="ARTdEGs4r5snJIcQ9ncwgXK6i6LRD-gdVi8XRvspIDieQG-UIG1kEhZwHYWFa2-ioKg" data-hovercard="/ajax/hovercard/user.php?id=100000482760981&extragetparams=%7B%22__tn__%22%3A%22%2CdC-R-R%22%2C%22eid%22%3A%22ARCfrEvvAqViYH9lwY1LW24NpGCfs3t5NTegHh1tWyHrnr2oe4xzvPACa-khH5xGONmzwV2Vvb-zLdJn%22%2C%22hc_ref%22%3A%22ARTdEGs4r5snJIcQ9ncwgXK6i6LRD-gdVi8XRvspIDieQG-UIG1kEhZwHYWFa2-ioKg%22%2C%22fref%22%3A%22gs%22%2C%22directed_target_id%22%3A425106461001292%2C%22dti%22%3A425106461001292%2C%22hc_location%22%3A%22group%22%7D" href="https://www.facebook.com/nusajid1969?fref=gs&__tn__=%2CdC-R-R&eid=ARCfrEvvAqViYH9lwY1LW24NpGCfs3t5NTegHh1tWyHrnr2oe4xzvPACa-khH5xGONmzwV2Vvb-zLdJn&hc_ref=ARTdEGs4r5snJIcQ9ncwgXK6i6LRD-gdVi8XRvspIDieQG-UIG1kEhZwHYWFa2-ioKg&dti=425106461001292&hc_location=group" id="js_1pa" rel="dialog" role="button" style="background-color: white; color: #365899; cursor: pointer; font-weight: 600;">Najeebullah Sajid</a> (facebook group <a href="https://www.facebook.com/groups/425106461001292/" target="_blank">CARDIOCARE</a>)</i></span><br />
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<b style="font-family: Arial, Helvetica, sans-serif;"><br /></b> <b style="font-family: Arial, Helvetica, sans-serif;"><br /></b> <b style="font-family: Arial, Helvetica, sans-serif;">The rhythm is sinus. There is ST elevation in the lateral leads (I, avL, V5, V6) , thus this is a lateral acute myocardial infarction (STEMI). There is also ST depression in V1 and V2 which can be attributed to an acute posterior myocardial infarction. (If we had placed an ECG lead at the patient's back, facing the posterior wall, this lead would show an ST-segment elevation). ST depression in leads III and avF is due to a mirror image of the ST elevation in the lateral leads. Often in an acute STEMI there is a mirror image of ST depression in leads having a different or opposite direction than the leads which are close to the site of the infarction. Conclusion: An acute ST-elevation myocardial infarction (STEMI) of the lateral and posterior wall (territory of the left circumflex coronary artery-LCX, which is the occluded artery in this case). Emergency reperfusion with a PCI or thrombolysis is required for this patient. </b><br />
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<span style="font-family: inherit; font-size: large;">In the chronic phase of a myocardial infarction ST segments may remain elevated suggesting the presence of a </span><u style="font-family: inherit; font-size: x-large;">dyskinetic or aneurysmatic segment</u><span style="font-family: inherit; font-size: large;"> of the left ventricular wall.</span><br />
<span style="font-family: inherit; font-size: large;"><b>Subendocardial ischemia</b></span></div>
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<span style="font-family: inherit; font-size: large;"><u>When ischemia is confined primarily to the subendocardium,</u> the ST vector typically shifts toward the inner ventricular layer and </span><span style="font-family: inherit; font-size: large;">the ventricular cavity. Since the current of injury is located only in the inner aspect of the myocardium if we imagine a theoretical lead located into the left ventricle near the ischemic area of the endocardium, this imaginary lead would show ST segment elevation. The leads of the ECG that we obtain in clinical practice are directed toward the epicardial (outer) layer of the heart. Therefore, they will show a mirror image of this current of injury and this is the characteristic <b>ischemic ST-segment depression.</b> The </span><u style="font-family: inherit; font-size: x-large;">ischemic ST depression</u><span style="font-family: inherit; font-size: large;"> is usually horizontal or downsloping and less often slowly upsloping. An ST-segment elevation may be present in lead aVR, which is oriented toward the ventricular cavity.</span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>A male patient, age 53, smoker with a history of low HDL cholesterol ( 33 mg/dl) and a sedentary lifestyle. He did not have a known history of heart disease. He complained of anterior chest pain felt around the sternum. What abnormalities can you see in his ECG and what is the probable diagnosis ?</b></span><br />
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The rhythm is sinus and the QRS axis is normal. There is a horizontal ST segment depression in leads I, aVL (which also displays T wave inversion), V5 and V6. There is also a subtle ST segment elevation in lead aVR ( because it faces in an opposite direction than the other leads which show ST depression). Although the ST depressions are not very deep in this case (about 1 mm=0.1 mV) they have a characteristic ischemic morphology. The diagnosis is a non ST elevation acute coronary syndrome (NSTEMI or </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">unstable angina </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">depending whether there will be a rise in cardiac troponin or not). The patient should be admitted to the hospital, started on double antiplatelet and anticoagulant treatment (e.g. low molecular weight heparin) plus anti-ischemic treatment (beta-blockers and nitrates if there is no hypotension or other containdications ) and a statin. A coronary angiography is also required preferrably within the first 12-24 hours.</span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>In this case there was a rise and fall in cardiac troponin I, therefore a NSTEMI was confirmed. The coronary angiography showed significant lesions of the circumflex (LCX) and the right coronary artery (RCA) which were both succesfully treated with PCI with placement of drug eluting stents (DES).</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Female 70 years old diabetic with dizziness, fatigue, sweating, and vomiting since one hour. On physical examination she has jugular vein distension and hypotension (systolic blood pressure 85 mmHg) What is the cause of hypotension? What should be the treatment and what medication is contraindicated?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>The ECG shows sinus rhythm (there are normal P waves) and ST elevation in the inferior leads (II, III, avF) and the right precordial leads V3R, V4R . There is also "mirror" ST depression in leads I, avL. Therefore, the diagnosis is an acute inferior myocardial infarcion (MI) with acute right ventricular infarction . This type of infarction is due to an occlusion in the right coronary artery (RCA). In this case, the patient did not have the pain of the infarction, </b></span><b style="font-family: Arial, Helvetica, sans-serif;">probably due to diabetic neuropathy</b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b> </b></span><b style="font-family: Arial, Helvetica, sans-serif;">(typically she should feel pain or pressure on the central area of the chest, sometimes also at the epigastrium). Perspiration (sweating), fatique and nausea are common nonspecific symptoms accompanying an acute MI. Hypotension and jugular vein distention are common clinical findings in a right ventricular (RV) infarction, due to the impairment of the RV contractile function. Right ventricular dysfunction causes both the reduction in cardiac output (leading to hypotension) and the increase in RV diastolic pressure with a consequent increase in right atrial and central venous pressure (leading to jugular venous distention).</b><br />
<b style="font-family: Arial, Helvetica, sans-serif;"> In such cases, of an acute inferior MI accompanied by an RV infarction and hypotension, intravenous saline (0.9 % NaCl solution) is administered to raise blood pressure, antiplatelet and anticoagulant treatment (as in every acute MI) and promptly (without delay) urgent reperfusion with angioplasty and stenting. If primary angioplasty within less than 90 minutes is not possible, then thrombolysis is administered. Nitrates are containdicated in an acute RV infarction, even if hypotension is not present.</b><br />
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<span style="font-family: inherit; font-size: large;">The<b> negative T wave of ischemic origin </b> is symmetric, usually with an isoelectric or a mildly upsloping ST segment or a horizontally depressed ST segment and appears in leads normally expected to have an upright T wave. It is a common finding, caused either by subendocardial ischemia or by subendocardial necrosis of the myocardium. It may occur as a manifestation of acute </span><span style="font-family: inherit; font-size: large;">coronary syndromes (Non ST elevation myocardial infarction or unstable angina) or in the long term after a Q-wave myocardial infarction. The inverted Q waves often appear after the ischemic episode but they may also appear during the episode with concomitant ST segment depression.</span></div>
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<span style="font-family: inherit; font-size: large;">In <b>N<u>on ST elevation acute coronary syndromes </u></b>(unstable angina or non ST elevation MI-NSTEMI) the ECG often shows negative T waves > 1 mm in leads expected to show an upright T wave, or ST segment depression (usually horizontal or downsloping, less frequently slowly upsloping).</span><br />
<span style="font-family: inherit; font-size: large;"><br /></span> <b><span style="font-family: "arial" , "helvetica" , sans-serif;">A male patient, 57 years old, smoker with hypercholesterolemia and without any history of cardiac disease, is describing episodes of " squeezing and heaviness" on the central area of the chest, when walking at a usual speed on level ground. Chest discomfort lasts about five minutes and stops when he interrupts walking and rests for a couple of minutes. These symptoms started 15 days ago. Diagnosis? Is there any significant risk on the short-term ? Management?</span></b><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Answer:</span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b><span style="font-family: "arial" , "helvetica" , sans-serif;">Typical history </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">of recent onset </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">angina at a small effort, . Therefore the history suggests unstable angina, since unstable angina is either angina of recent onset < month at a low workload , or angina with recent increase in symptom severity or frequency (crescendo angina), or angina at rest. The ECG findings are suggestive of a high-risk patient (deep negative, or biphasic T waves in multiple precordial leads). So there is a significant short-term risk of an adverse cardiovascular event (myocardial infarction or death). The ECG pattern cannot be distinguished from the ECG of a patient with a non ST elevation myocardial infarction (NSTEMI). However, the duration of the chest discomfort is consistent with angina (in myocardial infarction chest discomfor lasts usually more than 20 minutes). The distinction between unstable angina and NSTEMI is based on troponin blood levels (the best biomarker for myocardial necrosis), or CKMB, which begin to increase 6-8 hours after the onset of a myocardial infarction. These biomarkers (of myocardial necrosis) do not rise in unstable angina. </span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Management : Admit to the hospital as a case of probable unstable angina (ECG features of relatively high risk), immediate initiation of antiplatelet (usually aspirin plus loading dose of clopidogrel, or aspirin plus loading dose of one of the newer antiplatelet agents), and anticoagulation treatment (low molecular weight heparin or unfractionated heparin), nitrates, a beta -blocker, initiation of a statin drug and coronary angiography, preferably within the first or second day of hospital stay. </span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b><span style="font-family: "arial" , "helvetica" , sans-serif;">Question 2: On the basis of the ECG picture is it possible to suspect which should be the culprit vessel?</span></b><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"> This pattern of diffuse prominent T wave inversion in the precordial leads is usually suggestive of a severe stenosis of the proximal left anterior descending (LAD) branch of the left coronary artery. </span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Indeed, the patient's coronary angiography showed this type of lesion. He was treated with angioplasty and placement of a coronary stent (percutaneous coronary intervention -PCI). </span></b><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A man, 55 years old, with a history of hypercholesterolemia and no other cardiac history. In the last four days, he had several episodes of constrictive retrosternal pain, of a few minutes duration, occurring with physical activity of low intensity. Physical examination was without remarkable findings. His resting ECG (he had no discomfort during the ECG) is given below. What are the ECG findings? In this case, what is of greater diagnostic importance, the patient's history or the ECG findings? What is the proposed further diagnostic and therapeutic strategy?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Sinus rhythm, normal QRS frontal plane axis, small negative T wave in aVL, V4, V5 and flattened T wave in lead I. These ECG findings can raise a suspicion of underlying coronary artery disease but they are not specific. In this case, the history is more important for the diagnosis, and it is suggestive of angina on small effort of a very recent onset. Therefore, the history suggests unstable angina. In this context, ECG findings of inverted T waves enhance these diagnostic thoughts. The patient was admitted to the hospital, treatment for unstable angina was initiated, with dual antiplatelet drug treatment, low molecular weight heparin, a nitroglycerin patch, a beta-blocker, a statin and a decision to proceed with coronary angiography (within 24-48 hours). There was no rise in troponin, so it was not a NSTEMI, but unstable angina. Coronary angiography showed a severe stenosis (90% in the mid-right coronary artery), which was treated by angioplasty with stenting. Dual antiplatelet therapy was given for 12 months (together with pantoprazole for gastric protection), and then antiplatelet therapy was continued with aspirin only, while the administration of a statin and a low dose of a beta-blocker was also continued.</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Note: The ECG findings (small inverted T waves) resolved promptly after percutaneous coronary intervention (PCI). An important observation is that the leads with T wave inversion do not accurately identify the coronary artery involved (as opposed to the finding of ST-segment elevation). An exception is Wellens syndrome in which deep symmetric negative or biphasic T waves are present in the precordial leads (usually from V2 to V4 but quite often also in V5 and V6), without Q waves or ST-segment elevation ≥1 mm in these leads. This syndrome is associated with a severe proximal stenosis of the left anterior descending coronary artery (LAD).</b></span><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b style="font-size: x-large;">Acute pericarditis </b><span style="font-size: large;">(due to an acute inflammation of the pericardium) typically is characterized by diffuse ST segment elevation, usually in most of the chest leads and also in leads I, aVL, II, and aVF. Reciprocal ST segment depression is often present in lead aVR. The diffuse nature of the ST segment elevation in acute pericarditis is an important difference from the pattern seen in acute ST elevation myocardial infarction (STEMI). (In STEMI the ST segment elevation is not diffuse. It is observed in leads corresponding to a coronary artery territory and there are often reciprocal ST depressions in leads located away from the area of the infarction). Another important characteristic in acute pericarditis is the frequent presence of PR segment elevation in aVR, with reciprocal PR segment depression in many other leads, caused by the coexistence of an atrial current of injury. In acute pericarditis abnormal Q waves do not appear and the ST segment elevation may be followed by T wave inversion after a variable period of time.</span><br />
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<span style="font-family: inherit; font-size: large;"><br /></span><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>A woman 60 years old presenting with pain on the substernal area and the precordium since 12 hours. The pain increases when lying flat and with deep inspiration. What are the ECG findings and what is the proposed diagnostic testing and probable treatment ?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Answer <br /><br />The ECG shows sinus rhythm and normal QRS frontal axis. There is PR segment depression (note that the PR segment is at a lower level than the TP segment) in many leads (II, aVF, V2-V6) and PR segment elevation in avR. There is also a mild ST segment elevation (concave upward) in some leads (V2-V5, II). These ECG findings and the characteristics of the pain raise a suspicion of acute pericarditis, although the ECG is not completely typical (usually in acute pericarditis the concave upward ST segment elevation is more diffuse-present in more leads- and more prominent, than in this ECG). However the ECG , as mentioned above, shows some features suggestive of acute pericarditis. Testing should include the usual general blood tests plus c-reactive protein (CRP) and echocardiography. In this case, blood tests showed an elevated leukocyte count (13000/ μL) and moderately elevated CRP. Cardiac troponin test was negative. Echocardiography in this case showed a small pericardial effusion. Treatment of acute pericarditis should be with non steroidal anti-inflammatory drugs (NSAIDs: usually aspirin, ibuprofen, indomethacin, or naproxen) at least for about 2 weeks usually in combination with a drug protective for the stomach (e.g. omeprazol, lansoprazol, pantoprazol, or ranitidine). A full-dose NSAID should be maintained until normalization of the C-reactive protein (CRP) followed by gradual tapering of the drug for another 1-2 weeks to prevent early reoccurrence. In more severe cases of acute pericarditis (e.g. with severe pain showing a delayed response to treatment with a NSAID, or with a moderate to large pericardial effusion), or in reccurent pericarditis concomitant administration of colchicine (combined with the administration of NSAIDS) can improve treatment effectiveness and reduce the posibility of further recurrences. (See chapter "Acute pericarditis -pericardial effusion").</b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span></div>
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<b style="font-family: inherit; font-size: x-large;">The QT interval,</b><span style="font-family: inherit; font-size: large;"> is measured from the onset of the QRS complex to the end of the T wave. The QT interval is generally measured in leads II, V5 and V6 and reported as the longest interval among the three. If the QT interval cannot be accurately measured in these leads, other leads can be used. The QT interval increases in slow heart rates and decreases in fast heart rates, so it must be corrected for the heart rate, in order to assess if it is normal, prolonged or decreased.</span></div>
<span style="font-family: inherit; font-size: large;"> Bazett’s formula defines a corrected QT interval (QTc):<br />QTc=QT/√RR<br />Bazett’s formula works well at heart rates within the normal range but overcorrects at high rates (so at high rates it gives a QTc relatively greater than real) and undercorrects at low rates (estimating again a QTc relatively greater than real). The upper limit of a normal QTc is in men 0.45 second (450 msec) and in women 0.46 second (460 msec) . Patients with a congenital or acquired prolonged QTc, especially if it is markedly prolonged (480 msec or more) may be at risk for torsades de pointes ventricular tachycardia.A short QTc interval (<390 msec) is rare, but it also carries an increased risk of malignant ventricular arrhythmias.</span></div>
<span style="font-family: inherit; font-size: large;"><u>Hypercalcemia and hypocalcemia</u> predominantly alter the action potential duration and so they influence the QT interval. Hypercalcemia (increased calcium concentration in the blood) results in a shortened QT interval. Severe hypercalcemia also can be associated with decreased T wave amplitude, T wave notching, or inversion and sometimes with a high takeoff of the ST segment in leads V1 and V2. Hypocalcemia ( reduced calcium concentration in the blood) causes prolongation of the QT interval, due to prolongation of the ST segment. </span></div>
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<span style="font-family: inherit; font-size: large;"><u>Hypokalemia</u> (reduced potasium concentration in the blood) causes prolongation of the QTc ( for the ECG features of hypokalemia see below).</span></div>
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<span style="font-family: inherit; font-size: large;"><b>Left ventricular hypertrophy (LVH)</b><br />The most characteristic finding is increased amplitude of the R waves in leads facing the left ventricle ( I, aVL, V5, and V6), which are taller than normal, and S waves in leads V1 and V2, overlying the opposite side of the heart, are deeper than normal. <br />In leads with tall R waves usually the ST segment is depressed (typically, it slopes downward from a depressed J point) and the T wave is inverted and asymmetric. In some patients in leads with a tall R wave the ST segment may be normal or somewhat elevated. These repolarization changes (ST depression and T wave inversion) in patients with left ventricular hypertrophy (LVH) usually occur in <br />patients with QRS changes, but they may also appear alone. There are numerous criteria for diagnosing LVH and they are more reliable in people over 40 years of age (because in some normal young persons there is an increased amplitude of the QRS ). Some useful criteria are: The Sokolow-Lyon voltage criteria : <br />The sum of the S wave in V1 or V2 and the R-wave in V5 or V6 > 35 mm (3.5 mV). The R wave in aVL ≥ 12 mm (1.2 mV).<br />The Romhilt-Estes point score system (probable LVH=4 points/ definite LVH=5 points) <br />Any limb lead R wave or S wave > 20 mm , or SV1 or SV2 ≥ 30 mm , or RV5 to RV6 ≥ 30 mm (3 points) <br />ST-T wave abnormality in a patient with no digitalis therapy (3 points) <br />ST-T wave abnormality in a patient receiving digitalis therapy (1 point) <br />Left atrial abnormality (3 points) <br />Left axis deviation ≥−30 degrees (2 points) <br />QRS duration ≥90 msec (1 point) <br />Intrinsicoid deflection (the time interval from the onset of the QRS to the peak of the R wave) in V5 or V6 ≥50 msec (1 point). <br />ECG criteria for LVH, have a high specificity (when they are present, there is a high probability that LVH is actually present, (this corresponds to a low proportion of false positive findings), but a low sensitivity (there is a relatively high proportion of false negative findings : people that have LVH as shown with echocardiography, but do not have the ECG criteria.) <br />LVH usually occurs with left ventricular pressure overload (work of the left ventricle under conditions of increased systolic ventricular pressure, for example in arterial hypertension, or in aortic valve stenosis). Hypertrophic cardiomyopathy is another cause of left ventricular hypertrophy, often asymmetric.</span><br />
<span style="font-family: inherit; font-size: large;">The ECG has a low sensitivity (about 15 %) , but a high specificity (about 80%) for the diagnosis of LVH. So it cannot exclude LVH (many people with LVH can have a normal ECG, due to the low specificity), but if it shows features of LVH, there is a high probability that more accurate tests (usually echocardiogaphy) will confirm that the patient indeed has LVH. The latter is a feature of high specificity (low number of false positive results).<br /><b><br />Right Ventricular Hypertrophy (RVH )</b> occurs with right ventricular pressure overload (due to pulmonary valve stenosis, which is usually a congenital condition, or pulmonary hypertension)<br />Typically there is a right axis deviation and an increased R-wave amplitude in the right precordial leads (R wave > S wave in lead V1).<br />Common diagnostic criteria for RVH are the following: <br />The QRS in lead V1: an R ≥ 7 mm (0.7 mV), an R/S >1 with an R > 5 mm, or a QR or qR pattern. <br />The increased R in V1 is due to this lead's position in proximity of the right ventricle, recording its increased electrical forces in RVH. <br />Criteria regarding the QRS in V5 or V6 are based on the fact that these leads are oriented towards the left ventricle and away from the right ventricle. So, the increased right ventricular electrical activity causes a partial cancellation of left ventricular electrical forces in these leads ( low R wave) and also the appearance of a more prominent S wave. So in leads V5 or V6 common criteria for RVH include R/S <1 (S>R), or an S wave> 7 mm. <br />Other criteria of RVH : <br />Right axis deviation (>90 degrees) <br />S1Q3 pattern (this means the presence of a large S wave in lead I, either a RS or rS pattern, and an abnormal Q wave in lead III). <br />S1S2S3 pattern (large S waves in leads I, II and III) <br />P pulmonale (ECG pattern of a right atrial abnormality-see section on P wave). </span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Woman, age 27 with effort dyspnea and fatigue. These symptoms worsened progressively in the last 6 months. Physical examination showed blood pressure 110/80 mmHg, jugular venous distention with increased height of visible jugular venous pulsations , with prominent a and v waves. Auscultation revealed an increased intensity of the second heart sound parasternally at the second and third left intercostal space and no audible murmurs. Auscultation of the lungs was normal. The ECG is given below. What are the ECG findings and what is the differential diagnosis?</b></span><span style="font-family: inherit; font-size: large;"><b style="font-family: arial, helvetica, sans-serif; font-size: medium; text-align: justify;"><br /></b></span>
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<span style="font-size: large;">Answer</span></div>
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /><br />Physical examination showed signs compatible with right ventricular (RV) dysfunction: Dilated external jugular veins and increased height of visible pulsations of the internal jugular veins, which indicate an elevated central venous pressure/ prominent a-wave of the jugular venous pulse indicative of an elevated RV end diastolic pressure/ prominent v wave indicative of tricuspid regurgitation (which in many cases can be severe, without an audible holosystolic murmur). The increased intensity of the second heart sound (S2) parasternally at the second left intercostal space, since this is the area of the pulmonic valve, is due to an augmented pulmonic component of the second heart sound (P2) and is suggestive of pulmonary hypertension. <br />The ECG shows sinus rhythm, P waves have an increased amplitude (indicative of right atrial enlargement) and QRS frontal plain axis shows right deviation, In the right precordial leads R waves have an increased amplitude and in lead V1 there is a qR pattern. There are also inverted Τ waves in the precordial leads and in the left precordial leads V5 and V6 an increased amplitude of the S wave is noted. This ECG pattern indicates right ventricular hypertrophy. The ECG picture, combined with the symptoms and physical signs is suggestive of pulmonary hypertension. Another cause of RV hypertrophy is pulmonic stenosis (PS), but in this case the physical findings do not support this diagnosis ( in PS there is a systolic ejection murmur heard over the pulmonic area and a diminished intensity of P2). Thus the differential diagnosis in this case includes causes of pulmonary hypertension. Echocardiography is absolutely necessary and other diagnostic tests will follow depending on the findings, in order to reach an etiologic diagnosis. (Note :Tricuspid regurgitation is often secondary, due to RV enlargement, which causes displacement of the papillary muscles and dilatation of the tricuspid annulus). In this case the final diagnosis was idiopathic pulmonary hypertension (a rare cause of pulmonary arterial hypertension).</b></span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Male patient 69 years old with a history of hypertension and hypercholesterolemia. The patient denies any anginal symptoms or any other symptoms on ordinary physical activity. Physical examination revealed arrhythmia, normal heart sounds without a cardiac murmur and blood pressure 170/80 mmHg. What abnormalities can you see in his ECG, what are your diagnostic thoughts and what is the proposed further diagnostic evaluation and treatment?</span></b><span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>The rhythm is atrial fibrillation (absent P waves, fine fibrillatory waves and variable RR intervals) with a slow ventricular rate. QRS frontal plane axis is normal. There is a deep S wave in lead V2, tall R wave in leads V5 ( almost 30 mm), a positive Sokolow index ( RV5+SV1 > 35 mm) and abnormal negative T waves in leads I, avL, V4-V6 (the T wave is biphasic in lead V3). The voltage criteria and the T wave abnormalities are consistent with a diagnosis of left ventricular hypertrophy due to hypertensive heart disease. Atrial fibrillation is also common in hypertensive heart disease. Although the diagnosis of secondary T wave changes due to left ventricular hypertrophy is the most probable explanation for the inverted T waves in this ECG, they could also be due to coronary artery disease. Further diagnostic testing was with echocardiography, which revealed concentric left ventricular (LV) hypertrophy (diastolic wall thickness of the interventricular septum and the posterior wall of 13 mm-upper limit of normal 11mm) with normal LV dimensions and normal systolic function. The left atrium was enlarged and there was a moderate mitral regurgitation (functional due to a dilated mitral annulus). Myocardial perfusion scintigraphy (cardiac SPECT scan) was also undertaken to assess for myocardial ischemic disease. The SPECT was almost normal, without perfusion defects of a significant extent or severity. Hypertension was controlled (with an ACE inhibitor in combination with thiazide diuretic plus a calcium channel blocker) and oral anticoagulation was started, because of atrial fibrillation with a </b></span><b><span style="font-family: "arial" , "helvetica" , sans-serif;">CHA<sub>2</sub>DS<sub>2</sub>-VASc score of 2. When this score in patients with atrial fibrillation (permanent, persistent or paroxysmal) is 1 or more in men and 2 or more in women, chronic thromboembolic prophylaxis with an oral anticoagulant is indicated. (see the chapter on tachyarrhythmias <a href="http://cardiologybookandcases.blogspot.com/2016/08/tachyarrhythmias-cardiac-arrhythmias-supraventricular-and-ventricular-tachycardia-atrial-fibrillation.html" target="_blank">Tachyarrhythmias-supraventricular and ventricular tachycardias</a>) Choices for anticoagulation include one of the newer anticoagulants (non vitamin K antagonist oral anticoagulants-NOACS, e.g dabigatran, apixaban, rivaroxaban or endoxaban) or a vitamin K antagonist (such as warfarin or acenocoumarol) with a target INR 2-3.</span></b><br />
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<b style="font-family: inherit; font-size: x-large;">Hyperkalemia </b><br />
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<span style="font-family: inherit; font-size: large;">The earliest effect is peaking (tenting) and narrowing of the T wave, which becomes tall. With progressive hyperkalemia P wave amplitude decreases and QRS begins to widen. PR interval prolongation can occur (and sometimes second or third degree atioventricular block). Complete loss of P waves may occur, associated with a junctional escape rhythm or so-called sinoventricular rhythm. Moderate to severe hyperkalemia occasionally induces elevation of the ST segment in the right precordial leads (V1 and V2).</span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhQCdYwCxgnZgymeqy1toKBUxG2YbN14rkHeTRmTWpt8bS0_RKmdupto7jxVbf2BdhX4JCjjn4p1kFQV0jFZYFUIiolnI96kDVeBQWuPG2eWJr0Q42mOCTo9FgYj4OsGqcqnEPvKTazeII/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25B7%25CE%25BA%25CE%25B3+%25CF%2585%25CF%2580%25CE%25B5%25CF%2581%25CE%25BA%25CE%25B1%25CE%25BB%25CE%25B9%25CE%25B1%25CE%25B9%25CE%25BC%25CE%25AF%25CE%25B1+peaked-t-waves1+life+in+the+fast+lane.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="" border="0" data-original-height="544" data-original-width="409" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhQCdYwCxgnZgymeqy1toKBUxG2YbN14rkHeTRmTWpt8bS0_RKmdupto7jxVbf2BdhX4JCjjn4p1kFQV0jFZYFUIiolnI96kDVeBQWuPG2eWJr0Q42mOCTo9FgYj4OsGqcqnEPvKTazeII/s320/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+%25CE%25B7%25CE%25BA%25CE%25B3+%25CF%2585%25CF%2580%25CE%25B5%25CF%2581%25CE%25BA%25CE%25B1%25CE%25BB%25CE%25B9%25CE%25B1%25CE%25B9%25CE%25BC%25CE%25AF%25CE%25B1+peaked-t-waves1+life+in+the+fast+lane.jpg" title="Electrocardiogram (ECG)-hyperkalemia-cardiology book" width="240" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Lead V5 of a patient with hyperkalemia. Note the T wave which becomes tall and narrow.</b></span></td></tr>
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<span style="font-family: inherit; font-size: large;"><br /></span> <span style="font-family: inherit; font-size: large;"><br /><u>Chronic renal failure </u>The ECG triad of peaked T waves (from hyperkalemia), QT prolongation (from hypocalcemia), and left ventricular hypertrophy (from hypertension) is suggestive of chronic renal failure.<br /><b>Hypokalemia,</b> causes hyperpolarization of myocardial cell membranes and increased action potential duration. The ECG <br />manifestations include ST depression with flattened T waves and increased U wave prominence (U waves become enlarged). The U waves can exceed in amplitude the T waves. The T waves can be flattened or negative. The QT interval is prolonged.</span><span style="font-size: large;"> Because the T waves and U waves often merge, in some cases the QT interval cannot be accurately measured.</span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>Describe the findings in this ECG</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgaumweja1Zt4WI-yj02y5ukOAKZAsdCvhDUpynbNXCC0x2VrX9ytgn4h7s5ohkCkesz64NHw1lCG7LvTJ2eqLzMnWsKC41u9IUDigPpVun6fUeJHb4ji2eZSJrqJ9pSSy50Qh7jQ0mu1Y/s1600/%25CE%259D%25CE%25AD%25CE%25B1+%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="" border="0" data-original-height="142" data-original-width="480" height="187" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgaumweja1Zt4WI-yj02y5ukOAKZAsdCvhDUpynbNXCC0x2VrX9ytgn4h7s5ohkCkesz64NHw1lCG7LvTJ2eqLzMnWsKC41u9IUDigPpVun6fUeJHb4ji2eZSJrqJ9pSSy50Qh7jQ0mu1Y/s640/%25CE%259D%25CE%25AD%25CE%25B1+%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1.png" title="ECG quiz Cardiology book online" width="640" /></a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b>Rhythm sinus, QRS axis normal, widespread ST depression and T wave inversion and prominent (large) U waves (here especially in the leads II, aVF, V2-V5). These are findings suggestive of hypokalemia. Serum potasium was 2 mEq/L in this patient (Normal K levels 3.5-5.5 </b></span><b><span style="font-family: "arial" , "helvetica" , sans-serif;">mEq/L). </span></b><br />
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<b><span style="font-family: inherit; font-size: large;"><br /></span></b> <b><span style="font-family: inherit; font-size: large;">The pediatric ECG</span></b><br />
<span style="font-family: inherit; font-size: large;"><br />The normal resting heart rate varies with age. The average resting heart rate increases from birth to 1 month of age and subsequently decreases.The increase in heart rate in the first month of life is related to the activity of the autonomic nervous system, but the subsequent decrease of heart rate is primarily related to age-dependent changes in the intrinsic sinus node activity. <br /><br />Here are some normal limits (simplified ) in beats per minute (bpm) :<br />first week of life 90-160 (mean 124) bpm</span></div>
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<span style="font-family: inherit; font-size: large;">7 days –6 months 105–180 (mean 145) bpm<br />6-12 months 105–170 (mean 130) bpm<br />Years 1–3 90–150 (mean 120) bpm<br />Years 3–5 70–135 (mean 105) bpm<br />Years 5–12 60–130 (mean 95) bpm<br />Years 12-16 60–120 (mean 80) bpm<br /><br />The morphology of a normal ECG varies with age. In young children the electrical forces of the right ventricle are more evident than in adults. A right deviation of the QRS frontal axis is normal through the first year of life.<br />Three patterns can be distinguished, through the morphology of the QRS complex (ventricular depolarization) and the T wave (ventricular repolarization):<br />The neonatal pattern ECG is typical in the first month of life. <br />In a normal child, this ECG pattern changes after the first month and takes on the characteristics of the infant pattern, which can last up to the age of three. <br />After the age of 3 years the ECG changes again, gradually taking the characteristics of the adult pattern.<br />Normally, the ECG pattern is in concordance with the age of the patient. <br />An ECG pattern different from what would be expected according to the patient’s age, (for example a neonatal pattern after the first month of life), should lead to the suspision of a pathological reason.<br />Important note : The term “infant”, referring to a child in the first year of life, is not equivalent to the term “infant ECG pattern”, which can last until the age of about 3 years.<br />The neonate ECG pattern, normally shows a prevalent electrical activity of the right ventricle.<br />This is a result of the hemodynamic condition of a fetus. After the 31st week of gestation until term, the right ventricle of the fetus gains myocardial mass because it pumps against the high resistance of the small muscular pulmonary arteries. The left ventricle pumps against the low resistance of the placenta’s blood vessels. At birth the mass of the right and left ventricles have a ratio of 1 :1.3 . This ratio is quite different from the adult person, where left ventricular mass is much larger than right ventricular mass. <br />Lead V1 is the precordial lead facing the right ventricle. Thus, in lead V1 the depolarizing electrical activity of the right ventricle is represented by the R wave (the positive deflection) and the depolarizing electrical activity of the left ventricle is represented by the S wave. <br />Lead V6 faces the left ventricle. Thus in this lead, the R wave (positive deflection) corresponds to the depolarizing electrical activity of the left ventricle and the S wave (negative deflection) represents the depolarization of the right ventricle.<br />Since the electrical activity of the right ventricle prevails in the first mont of age, the neonate ECG pattern has the following features: In lead V1 the R wave is dominant (R/S > 1) and in lead V6 the dominant wave is S (R/S < 1). <br />In V1 the R wave can be exclusive (without an S), but in that case, its voltage should be less than 13 mm (1.3 mV) in the first week of life and less than 10 mm (1 mV) afterwards. If an S wave is also present in V1, then the R/S ratio: is from 1 to 7, R wave < 25 mm and S wave < 20 mm.<br />In lead V6 R< S and also S wave < 10 mm.<br />With regards to the morphology of the T wave, in the first week of life, in lead V1 T wave can be positive or negative and T wave in lead V6 usually is positive (but a flat or negative T wave in V6 in the first week of life is considered at the limits of normal, i.e. a normal variant ).<br />After the first week of life the neonatal pattern is characterized by the following : T wave in leads V1 and V2 must be negative and in V6 it must be positive.<br />A positive T wave in V1 after the first week of life should be regarded with suspicion and investigated because it can indicate right ventricular hypertrophy, elevated systolic pressure in the right ventricle and /or elevated pulmonary vascular resistance (PVR). These findings can be caused by congenital heart disease.<br />Within the first few hours after birth hemodynamic changes begin, which continue over the next months and years and form the basis of the changes in the ECG. After birth and as the child grows, there is a gradual fall in pulmonary vascular resistance (PVR) which causes a gradual reduction in right ventricular systolic pressure. Consequently, right ventricular mass (in comparison to left ventricular mass) and right ventricular electrical forces gradually decrease, as the circulation of the growing child matures.<br />The left ventricle, after birth and as the child grows, follows the opposite course. After birth it ceases to pump against the low resistance of the blood vessels in the placenta and begins pumping against the high resistance of the peripheral blood vessels. This causes a rise in left ventricular systolic pressure and a gradual rise in left ventricular mass, and left ventricular electrical force. These changes continue throughout the first years of life, with the right ventricle (having to pump against a smaller resistance) growing more slowly than the left ventricle and this reflects on the evolution of the ventricular electrical forces in the ECG.<br /><br />The “infant ECG pattern” is characterized by balanced ventricular electrical forces. This is the normal ECG pattern found after the first month of life up to 2-3 years. After the first month of life the electrical forces of the ventricles are balanced, therefore, the infant ECG pattern shows equal electrical weight of the two ventricles. <br />In lead V1 the R wave will still be dominant ( R/S > 1) but the normal R wave voltage is < 20 mm (2 mV). Sometimes in V1 the R wave may be exclusive. In that case, to be normal, its voltage should be < 10 mm (1 mV). An exclusive R in V1 should never be present after the first year of life.<br />In V6 the R wave will be dominant over the S wave (R/S > 1). The normal R in V6 should be < 25 mm (2.5 mV) and the S wave <10 mm (1 mV). As a general rule, R waves are usually prominent in the right precordial leads in neonates and infants but gradually decrease in amplitude with age.<br />A unique characteristic of the infant pattern, is that potentially a narrow Q wave ≤ 10 mm can be present in the inferior leads (II, III, aVF) and/or lead V6. <br />In infants, Q waves are usually absent in leads I and aVL, and if they are present, they are often suggestive of cardiac pathology. A deep (.3 mm) and broad (.30 ms) Q wave in leads I and aVL, especially when Q waves are absent in the inferior leads, may suggest the diagnosis of anomalous origin of the left coronary artery from the pulmonary artery. The presence of Q waves in the right precordial leads in infants and children is always pathologic. They are commonly associated with right ventricular hypertrophy.<br />Deep Q waves in the left lateral precordial leads (V5,V6) are often present in left ventricular hypertrophy of many etiologies. Q waves ≥ .3mm in depth or ≥ . .40 ms in duration, in .two or more leads other than V1,V2, or III, raise a suspicion of familial hypertrophic cardiomyopathy (this finding has low sensitivity, but high specificity).<br />Regarding repolarization, in the infant ECG pattern the T wave in leads V1-V3 is normally negative and this finding can be present as late, as the age of 8-10 years (or sometimes even persist in an adult as a normal variant). <br />Upright T waves in the right precordial leads prior to age 7 years can raise a suspicion of right ventricular hypertrophy.<br />The infant ECG pattern, as well as the ECG pattern later in life, is characterized by a T wave in lead V6, which is normally positive.</span></div>
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<span style="font-family: inherit; font-size: medium;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Is this ECG of a 1 year old child, normal ?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Normal. For details see text. </b></span><br />
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<span style="font-family: inherit; font-size: large;"><u>The adult ECG pattern (in childhood)</u><br />The adult ECG pattern usually appears in children older than 2 years and is characterized by prevalent electrical activity in the left ventricle, which is dominant over the electrical activity of the right ventricle. This ECG pattern is the norm after 2–3 years of life.<br />In V1 the S wave will dominate (R/S <1) . Although the R wave in V1 tends to be taller in a child than in an adult, after the age of 3 years, it will usually be smaller than the S wave. The normal S in V1 must be < 25 mm.<br />In V6 the R wave is dominant ( R/S > 1) Normally in V6, R wave < 25 mm and S wave < 5 mm.</span><br />
<span style="font-family: inherit; font-size: large;"><span style="text-align: justify;">[In case of an increased amplitude (exceeding normal limits) of the R or S wave in lead V1, or in leads V5, or V6 – or in case of an abnormal R/S relation in these leads- in comparison with the expected findings according to age, or in case of an ECG pattern different from that expected with respect to age : Then there will be a suspicion of hypertrophy or dilatation of one of the two ventricles. In such cases echocardiography is the next step, to search for (or exclude) any abnormality.]</span></span><br />
<span style="font-family: inherit; font-size: large;">The T wave in lead V6 is positive and in leads V1-V3 is negative up until adolescence (in girls, even later). A positive T wave in leads V2 and V3 may be present in childhood, as a normal variant.</span><br />
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<span style="text-align: left;"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Νormal ECG : Sinus rhythm, normal QRS axis, QT interval within normal limits. The R wave in V1 is somewhat taller than what would be expected in the ECG of an adult person, but this a usual finding in children. It is smaller than the S wave, so it is normal. In leads V5 and V6 R/S is >1 which is normal. The negative T waves in the right precordial leads are normal for a child. Moreover, in order to characterize this ECG as normal the T wave must be positive in leads V5, V6 (it is in this case). For more details see text .</b></span></span></div>
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<span style="font-family: inherit; font-size: large;"><u><br />QRS axis </u></span><br />
<span style="font-family: inherit; font-size: large;">As would be expected from the right ventricular dominance of the term infant, the frontal plane QRS axis in term infants is usually directed rightward and inferiorly. Healthy preterm infants may have a more leftward QRS axis.<br />In term infants, the rightward QRS axis usually within the first year of life changes to a more adult (less rightward) pattern.</span><span style="font-size: large;">Thus, the initial </span><span style="font-size: large;">right deviation of </span><span style="font-size: large;">the QRS frontal axis progressively </span><span style="font-size: large;">reduces and turns toward normal.</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">In the 1st month of life the QRS axis is normally over +120° (right deviated). In the first week of life it can be </span><span style="font-size: large;">up to +180°/+210° . Except for individual variation, the </span><span style="font-size: large;">QRS frontal axis generally </span><span style="font-size: large;">after the age of 6 months </span><span style="font-size: large;"> should be under </span><span style="font-size: large;">+120° , and </span><span style="font-size: large;">after the age of 1 year, it should be </span><span style="font-size: large;">under +100° .</span><br />
<span style="font-size: large;">While </span><span style="font-size: large;">in adults </span><span style="font-size: large;">the left and superior frontal QRS </span><span style="font-size: large;">axis is defined as at least a -30 degrees</span><span style="font-size: large;">, during the first month of life, it is </span><span style="font-size: large;">defined as less than +30 degrees.</span><br />
<span style="font-size: large;">In children, a QRS frontal axis directed </span><span style="font-size: large;">to the left should be regarded with suspicion. It is often a </span><span style="font-size: large;">typical marker of some congenital </span><span style="font-size: large;">heart diseases, such as </span><span style="font-size: large;">ostium primum atrial septal defect,</span><span style="font-size: large;"> complete form of atrioventricular </span><span style="font-size: large;">septal defect or atrioventricular canal </span><span style="font-size: large;">defect, </span><span style="font-size: large;">inlet-type ventricular septal defect, atrioventricular </span><span style="font-size: large;">septal defect with tetralogy of Fallot, </span><span style="font-size: large;">Ebstein’s anomaly, </span><span style="font-size: large;">tricuspid atresia, </span><span style="font-size: large;">and univentricular heart with </span><span style="font-size: large;">double inlet.</span><br />
<span style="font-size: large;">The leftward and superior QRS frontal axis </span><span style="font-size: large;">can be present even in pediatric patients with </span><span style="font-size: large;">structurally normal hearts, due to a </span><span style="font-size: large;">delay in intraventricular conduction ( left anterior </span><span style="font-size: large;">fascicular block-LAFB or LAH). So a child with a left QRS axis can have a sructurally normal heart, but this s</span><span style="font-size: large;">hould always be </span><span style="font-size: large;">confirmed by a physical examination and </span><span style="font-size: large;">an echocardiogram.</span><br />
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<b><span style="font-size: large;"><br /></span> </b><span style="font-size: large;"><b>TWO USEFUL ECG VIDEOS SHOWING EXAMLES :</b><br /><br />A good video showing the basic interpretation of normal and abnormal ECG with ECG examples presented. <br />(From MED tube). Link :</span><br />
<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=Iv_MyCAIEo0" target="_blank">https://www.youtube.com/watch?v=Iv_MyCAIEo0</a></span></div>
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<span style="font-family: "trebuchet ms" , sans-serif; font-size: large; text-align: left;">Most Important ECG Findings in Major Diseases (from USMLEVideoLectures) Link:</span></div>
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<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=A_xHXvWBNLU" target="_blank">https://www.youtube.com/watch?v=A_xHXvWBNLU</a></span></div>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b><a href="https://cardiologybookandcases.blogspot.com/">CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</a></b></span><br />
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<b><span style="font-size: large;">Bibliography and links </span></b><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">A website about the intepretation of the electrocardiogram (ECG) LINK: <a href="https://ecgwaves.com/systematic-clinical-ecg-interpretation-review-guide/">Clinical ECG interpretation</a><br /><br /><br />Price D. How to read an Electrocardiogram (ECG). Part One: Basic principles of the ECG. The normal ECG. Southern Sudan Medical Journal 2010; 3(2) 26-28<br />LINK: <a href="http://www.southsudanmedicaljournal.com/archive/may-2010/how-to-read-an-electrocardiogram-ecg.-part-one-basic-principles-of-the-ecg.-the-normal-ecg.html">How to read an electrocardiogram (ECG). Part One</a> <br /><br /><br />How to read an electrocardiogram (ECG). Part 2: Abnormalities of Electrical Conduction Southern Sudan Medical Journal 2010; 3(4)<br />LINK: <a href="http://www.southsudanmedicaljournal.com/archive/november-2010/how-to-read-an-electrocardiogram-ecg.-part-2-abnormalities-of-electrical-conduction.html">http://www.southsudanmedicaljournal.com/archive/november-2010/how-to-read-an-electrocardiogram-ecg.-part-2-abnormalities-of-electrical-conduction.html</a><br /><br />Becker DE. Fundamentals of Electrocardiography Interpretation. Anesthesia Progress. 2006;53(2):53-64. doi:10.2344/0003-3006(2006)53[53:FOEI]2.0.CO;2.<br />LINK: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1614214/">Fundamentals of Electrocardiography Interpretation</a><br /><br />Gurm HS. The ECG in acute coronary syndromes: new tricks from an old dog. Heart 2005;91(7):851-3. Available from: http://dx.doi.org/10.1136/hrt.2004.047258<br />LINK: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1769008/">The ECG in acute coronary syndromes: new tricks from an old dog</a><br /><br />Wellens, H. J.j. "The Electrocardiogram 102 Years After Einthoven." Circulation 2004; 109(5 : 562-64. doi:10.1161/01.cir.0000117293.30403.8f.<br />LINK: <a href="https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000117293.30403.8F">The Electrocardiogram 102 Years After Einthoven</a><br /><br />Farhan H, Hassan K, Al-Belushi A, Sallam M, Al-Zakwani I. Diagnostic Value of Electrocardiographic T Wave Inversion in Lead aVL in Diagnosing Coronary Artery Disease in Patients with Chronic Stable Angina. <a href="https://www.ncbi.nlm.nih.gov/pmc/journals/1561/">Oman Med </a>2010 ; 25(2): 124–127.<br />LINK: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3215494/">Diagnostic Value of Electrocardiographic T Wave Inversion in Lead aVL in Diagnosing Coronary Artery Disease in Patients with Chronic Stable Angina</a></span></b><b><span style="font-size: large;"><br /></span></b> <b><span style="font-size: large;"><br /><a href="https://www.healio.com/cardiology/learn-the-heart/blogs/68-causes-of-t-wave-st-segment-abnormalities" target="_blank">68 causes of T wave, ST segment abnormalities. From Healio.com</a></span></b> <b><span style="font-size: large;"><br /></span></b></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-45568063896631822712016-06-02T11:02:00.003+03:002018-08-12T00:16:40.633+03:00 Acute pericarditis -pericardial effusion<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="font-size: large;">IMPORTANT NOTE : THE SITE IS UNDER DEVELOPMENT AND CONTENTS ARE CONTINUOUSLY ADDED.<br /><b><u><br /></u></b></span><br />
<span style="font-size: large;"><b><u>Acute pericarditis</u></b> <br />It is an inflammation of the pericardium characterized by chest pain, pericardial friction rub, and serial ECG changes. A pericardial effusion (increased pericardial fluid) is commonly-but not always-present.<br />Viral infection is the most common cause of acute pericarditis. The disease is usually self-limited with a relatively short duration (about 1-3 weeks). Viruses that can cause pericarditis include coxsackievirus B, echovirus, adenoviruses, influenza A and B viruses, enterovirus, Epstein-Barr, herpes simplex virus (HSV) type 1, varicella-zoster virus, measles virus, parainfluenza virus, respiratory syncytial virus (RSV), cytomegalovirus (CMV), hepatitis viruses A, B, and C and human immunodeficiency virus (HIV). <br />Idiopathic acute pericarditis, i.e. acute pericarditis with no clearly identified cause, is common. There are no differences in clinical features distinguishing idiopathic cases from viral pericarditis. Most cases of idiopathic pericarditis are propably undiagnosed viral infections. Seasonal peaks occur in spring and fall.</span><br />
<span style="font-size: large;"> Other causes of pericarditis include connective tissue disease (systemic lupus erythematosus, rheumatoid arthritis), myocardial infarction, postpericardiotomy syndrome, radiation, trauma, bacterial infection, tuberculosis, uremic pericarditis, malignancy, etc. Malignancy is a cause that we should have in mind in the process of differential diagnosis, especially in patients with moderate to large pericardial effusions. In patients presenting with acute pericarditis or pericardial effusion, 4-7% have an unsuspected malignancy. Most cases of neoplasm-related pericarditis result from metastatic disease, because primary neoplasms of the heart and pericardium are rare.<br /><b>Symptoms of acute pericarditis</b>: Chest pain, which may be intense, and usually is sharp, pleuritic (this means that the pain increases with deep respiration), and positional (worse when lying flat, relieved by leaning forward). The pain may also increase with body movements. Chest pain is usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. Fever is common.</span><span style="font-size: large;"> Other symptoms are due to pressure on adjacent structures from a pericardial effusion and may include dyspnea (common symptom in pericarditis or pericardial effusion), cough, dysphagia and hiccups. </span><br />
<span style="font-size: large;"><b>Physical Findings</b>: Tachycardia is a usual finding. There is often a pericardial friction rub, a coarse high pitched sound with a scratching quality, described as two pieces of leather being rubbed together. This sound</span><span style="font-size: large;"> is best heard at the left sternal border at end-expiration with the patient sitting and leaning forward. It can have up to three components which correspond to the movement of the heart (a systolic component, an early diastolic component corresponding to the movement of the heart due to rapid ventricular filling and a late diastolic component at atrial systole). It is present in about 85% of the patients with acute pericarditis. The rub may be intermittent.</span><br />
<span style="font-size: large;">If you click on this video you can listen to a pericardial friction rub.</span><br />
<span style="font-size: large;">Link: <a href="https://www.youtube.com/watch?v=J1R8Oxgqhfk" target="_blank">https://www.youtube.com/watch?v=J1R8Oxgqhfk</a> </span><br />
<b style="font-family: 'courier new', courier, monospace;">From: You Tube channel Rombero 123</b><br />
<span style="font-size: large;"><br /><b>Electrocardiogram</b> : In acute pericarditis there is diffuse ST segment elevation (concave upward) usually present in almost all leads, except aVR and V1. PR-segment depression may be present, but in aVR there is a PR-segment elevation ( this is useful to differentiate from early repolarization and myocardial infarction).<br />Days later, ST segments return to baseline before T-wave inversion develops.<br />A useful feature in the differentiation of the concave ST segment elevation of acute pericarditis from the similar ST elevation present in early repolarization, is the following: In early repolarization there is also an increased amplitude of the T wave, so that the ratio of the elevation of the ST segment to the height of the T wave (ST-T ratio) < 0.25 . This ratio in acute pericarditisis is usually > 0.25. <br />Moreover, in acute pericarditis depression of the PR segment is often present and ST elevation is more diffuse ( compared to the ST elevation of early repolarization, or acute myocardial infarction). <br />In ST elevation myocardial infarction (STEMI) the leads with ST elevation correspond to a specific left ventricular wall (depending on the blocked coronary artery) and the elevated ST segment usually has a convex morphology. Often reciprocal ST segment depression in leads with an opposite orientation is also present in STEMI. These features differ from the pattern seen in acute pericarditis. <br /><br /><b>Echocardiography:</b><br />It is the most sensitive test for detection of pericardial effusion, which commonly (but not always) accompanies acute pericarditis.<br />If there is a drop in ejection fraction, one must suspect that myocardial involvement is also present and the diagnosis of concomitant inflammatory disease of the myocardium (myocarditis) is made. In this case blood tests usually show a marked elevation of troponin and CKMB. This condition (concomitant pericarditis and myocarditis) is called myopericarditis.<br /><b><br />Treatment of acute pericarditis</b><br />The first line therapy for acute pericarditis is the administration of non steroidal anti-inflamatory drugs (NSAIDs):<br />High-dose aspirin 650 mg -1 g x 3-4 times per day, or ibuprofen 600 mg PO x 3 times per day, or indomethacin 75 mg PO x2 times per day).<br />Useful is the co-administration with an H2-antagonist (e.g. ranitidine) or proton pump inhibitor (e.g. pantoprazol, lansoprazol etc) to reduce the risk of gastrointestinal bleeding.<br />Concomitant administration of colchicine (combined with the administration of NSAIDS) can reduce the chances of recurrent<br />pericarditis. ( Dosage : 1–2 mg for the first day followed by 0.6–1 mg/day for 3 months).<br />For recurrent pericarditis, colchicine can be used with NSAIDs or instead of NSAIDs (1–2 mg/day followed by 0.6–1 mg/day).<br />Colchicine side effects: It can cause gastrointestinal symptoms (in that case the lower dose may be selected). Infrequently it can cause bone marrow suppression (chronic kidney disease is a risk factor for this side effect).</span><span style="font-size: large;"> In acute pericarditis strenuous physical activity should be limited for at least 2 months.</span><span style="font-size: large;"><br />Corticosteroids should be avoided as a treatment for pericarditis, since recurrence rate is increased with steroid treatment. <br />Steroids can be considered in cases of failure of NSAID and colchicine therapy. (Prednisone 0.2 - 0.5 mg/kg/day) for 4 weeks until symptoms and elevated C-reactive protein have resolved). The dose of corticosteroids is gradually reduced before discontinuation of this treatment. </span><span style="font-size: large;">Avoid anticoagulants in the acute phase of pericarditis (if they are not absolutely necessary for a serious reason) to decrease the risk of intrapericardial hemorrhage and tamponade.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><b> Pericardial effusion</b><br /><b>Causes</b> of a pericardial effusion (an abnormal accumulation of pericardial fluid) include all the causes of acute pericarditis listed above but occasionaly it also occurs with some non-inflamatory states that induce fluid retention or increased cardiac filling pressures and consequently an increased central venous pressure (heart failure, pulmonary hypertension, renal failure, or cirrhosis). Other causes: hypothyroidism, amyloidosis, hemopericardium.</span><br />
<span style="font-size: large;">Hemopericardium is bleading into the pericardial sac, due to trauma (blunt or penetrating), as a complication of dissection of the ascending aorta, left ventricular rupture due to myocardial infarction, or as a complication of cardiac interventions.</span><br />
<span style="font-size: large;">Accumulation of pericardial fluid leads to a rise in intrapericardial pressure, which in turn can cause a rise in right and left atrial pressure and in right and left ventricular diastolic pressures. </span><br />
<span style="font-size: large;">Cardiac tamponade is the condition in which pericardial fluid causes a rise in intrapericardiac pressure that significantly impairs diastolic filling of the heart, in other words when the fluid compresses the heart and reduces diastolic filling with </span><span style="font-size: large;">subsequent hemodynamic compromise.</span><span style="font-size: large;"> This is a medical emergency. In severe tamponade diastolic pressures in all 4 cardiac chambers typically equalize and become equal to the intrapericardial pressure (about 15-20 mmHg). As the pressure exerted on the heart by the pericardia</span><span style="font-size: large;">l fluid increases, cardiac volumes progressively decline and the decreased ventricular end diastolic volumes lead to a reduction in stroke volume (because of Frank-Starling law). This leads to a reduction in cardiac output. A compensatory mechanism to the decreased cardiac output is sympathetic stimulation producing tachycardia and increased contractility. </span><br />
<span style="font-size: large;">For clinical symptoms </span><span style="font-size: large;">(caused by increased intrapericardial pressure) </span><span style="font-size: large;">to develop, two main factors are significant:<br />1)The </span><span style="font-size: large;"> rate</span><span style="font-size: large;"> of fluid accumulation. This is the most important factor, since rapid accumulation of a moderate quantity of fluid, such as 80-200 ml, will result in markedly increased intrapericardial pressures and can often cause symptoms or even the full clinical picture of cardiac tamponade.</span><span style="font-size: large;"> On the other hand, gradual accumulations of up to 1 to 2 L are </span><span style="font-size: large;">often well tolerated, because the pericardium in such cases has enough time to dilate.</span><span style="font-size: large;"><br />2) The fluid volume. A large pericardial effusion is much more likely to cause symptoms than a small one, although the rate of fluid accumulation plays a major role.</span><br />
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<span style="font-size: large;"><b>Symptoms-clinical presentation</b></span></div>
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<span style="font-size: large;">A patient with a pericardial effusion can be asymptomatic, or present with typical symptoms of pericarditis, or with symptoms related to compression of adjacent structures by the effusion, or the clinical picture of cardiac tamponade, which is an emergency.</span></div>
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<span style="font-size: large;">Large effusions can present with a sensation of dull chest pain or pressure, or a nonspecific sense of chest discomfort, or with dyspnea (dyspnea is a common symptom).</span></div>
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<span style="font-size: large;">Other symptoms related to mechanical compression of adjacent structures may include dysphagia, cough, hoarseness (due to compression of the left recurrent laryngeal nerve), hiccups (</span><span style="font-size: large;">compression of the </span><span style="font-size: large;">phrenic nerve) and </span><span style="font-size: large;">nausea.</span></div>
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<span style="font-size: large;">On physical examination, in a large pericardial effusion, there is often reduced intensity of the heart sounds (muffled heart sounds) and the apex beat cannot be palpated.</span></div>
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<span style="font-size: large;"><b>In tamponade</b>, symptoms include fatigue and lightheadedness (due to a low cardiac output caused by the restricted cardiac diastolic filling ) and dyspnea. Patients with tamponade are more comfortable sitting and leaning forward.</span></div>
<span style="font-size: large;">Physical signs of cardiac tamponade include tachycardia, hypotension, muffled heart sounds, elevated jugular venous pressure, loss of the Y descent in the jugular venous pulse and pulsus paradoxus</span><span style="font-size: large;"> (decrease in systolic blood pressure with inspiration greater than 10 mm Hg). Tachypnea may also be present.</span><br />
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<span style="font-size: large;">Pulsus paradoxus is not entirely specific for cardiac tamponade. Other conditions that can cause pulsus paradoxus are constrictive pericarditis, pulmonary embolism, pulmonary emphysema and severe asthma.</span><br />
<span style="font-size: large;">In tamponade often there are also some signs commonly present in patients with reduced cardiac output, such as cool </span><span style="font-size: large;">extremities, peripheral cyanosis, diaphoresis (sweating, due to compensatory sympathetic stimulation). </span></div>
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<span style="font-size: large;">The classic presentation of tamponade is referred to as Beck triad: <br />1) elevated jugular venous pressure, <br />2) arterial hypotension, and <br />3) quiet ("muffled") heart sounds.</span><br />
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<span style="font-size: large;"><b>The ECG</b> in a large pericardial effusion or tamponade can show: reduced QRS voltage, </span><span style="font-size: large;">nonspecific T-wave flattening, and electrical</span><br />
<span style="font-size: large;">alternans (often with sinus tachycardia).<br />Electrical alternans is the phenomenon of alternation of QRS complex amplitude or axis between beats. This is due to the swinging motion of the heart in the pericardial cavity causing a change in QRS voltage and axis from beat to beat.</span><br />
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<span style="font-size: large;"><b>Echocardiography in pericardial effusion :</b> It<b> </b>takes advantage of the different acoustic </span><span style="font-size: large;">properties of pericardial fluid as compared with the myocardium </span><span style="font-size: large;">and parietal pericardium. Pericardial fluid is typically echolucent (black or almost black in the echo image), whereas</span><span style="font-size: large;"> myocardium and pericardial membrane are echodense (white or gray).</span><span style="font-size: large;"></span><span style="font-size: large;">Pericardial effusion is seen on 2D echocardiography as an echolucenr space surrounding </span><span style="font-size: large;">the heart.</span><span style="font-size: large;"> Occasionaly </span><span style="font-size: large;">fibrinous strands, and/or thrombus</span><span style="font-size: large;"> can be present in the effusion.</span><br />
<span style="font-size: large;">Pericardial effusions are not always completely echolucent and may have varying degrees of echogenicity when they contain fibrin or clot, protein, chyle, tumor cells, or bacteria.</span><br />
<span style="font-size: large;">The size of the pericardial effusion can be assessed in the parasternal long axis, apical four chamber and subcostal views. Measurements of the width (thickness) of a pericardial effusion are taken during end-diastole and according to these measurements the effusion is generally classified as:<br />Small if <1 cm<br />Moderate if between 1 to 2 cm<br /> Large if >2 cm.</span></div>
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<span style="font-size: large;">Small pericardial effusions often can be seen only posteriorly (but sometimes they can also be seen as circumferential). Moderate-sized and large-sized effusions are circumferential.</span><span style="font-size: large;">Epicardial fat occasionally can be confused with a pericardial effusion. It appears as a relatively echolucent space usually anteriorly from the heart (less often posteriorly). However, epicardial fat usually has more echogenicity than fluid, usually with a “stippled appearance” ( with multiple dots). Increased epicardial fat is more commonly seen in the elderly, particularly in obese women.</span><br />
<span style="font-size: large;">In case of an echolucent space posterior to the heart, we should distinguish if this is a pericardial or a left pleural effusion. The parasternal long-axis view shows pericardial fluid as an echolucent space located anterior to the descending aorta, whereas pleural fluid lies posterior to the descending thoracic aorta.</span><br />
<span style="color: #990000; font-size: large;"><br /></span> <span style="color: #990000; font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><span style="background-color: #f6f6f6;"><b>VIDEO A cardiology case of a postoperative (loculated) pericardial effusion. The chest x ray, echocardiography and treatment are being shown.</b></span></span><br />
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<span style="font-size: large;"><u>Echocardiographic findings suggestive of tamponade </u></span><br />
<span style="font-size: large;">Pericardial tamponade is mainly a clinical diagnosis, but the following echocardiographic findings are suggestive of tamponade:</span><br />
<span style="font-size: large;">1 Right atrial collapse: An inward displacement of the right atrial (RA) free wall seen in the apical 4 chamber view or the subcostal (subxiphoid) view, in late diastole, or in systole. This is due to compression from the pericardial fluid, when intrapericardial pressure exceeds RA pressure. This sign appears earlier than right ventricular (RV) collapse, since RA pressure is smaller than RV pressure.</span><br />
<span style="font-size: large;">2 Right ventricular (RV) early diastolic collapse (an inward motion of the RV free wall because of compression from the pericardial fluid).</span><br />
<span style="font-size: large;">3 Marked respiratory variation in Doppler inflow velocities across mitral and tricuspid valves. (This finding is also seen in constrictive pericarditis). This can be assessed more easily if you slow the sweep speed (at the doppler menu) to 25 cm/s, to allow for an increased number of cardiac cycles to be displayed. In tamponade, </span><span style="font-size: large;">in inspiration</span><span style="font-size: large;"> </span><span style="font-size: large;">there is</span><span style="font-size: large;"> an increase in tricuspid valve inflow velocity of 40% or </span><span style="font-size: large;">greater and a decrease in mitral inflow velocity of 25% or</span></div>
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<span style="font-size: large;">greater .</span></div>
<span style="font-size: large;">4 Dilatation of the inferior vena cava, because of increased central venous pressure (due to the pressure exerted by the pericardial effusion on the RA).</span><br />
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<span style="font-size: large;"><b>Hemodynamic features of cardiac tamponade</b> include an elevated right atrial pressure with marked reduction or absense of the Y descent in right atrial pressure curve (or central venous pressure curve) . The loss of the Y descent is explained as following: The Y descent is a drop in central venous pressure at the time of early diastolic filling of the right ventricle. In tamponade heart volume is fixed (restricted) as a result of compression of the heart by pericardial fluid. So blood can move from the central veins into the heart only when its volume reduces (only when blood is leaving from the heart), that is during systole and not in diastole. For this reason the Y descent in tamponade is lost, but the X descent is not lost. </span></div>
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<span style="font-size: large;">In tamponade RA pressure, </span><span style="font-size: large;">diastolic RV pressure, and pulmonary capillary wedge </span><span style="font-size: large;">pressures are almost equal, with a difference </span><span style="font-family: "georgia" , "times new roman" , serif; font-size: large;">≤</span><span style="font-family: inherit; font-size: large;"> 5 mmHg (This finding, called equalization of pressures, is also observed in constrictive pericarditis, but in constrictive pericarditis the Y descent is not reduced, on the contrary there is a prominent X and Y descent ).</span><br />
<span style="font-family: inherit; font-size: large;"><b>Treatment of tamponade</b></span><br />
<span style="font-size: large;">Cardiac tamponade is a medical emergency. Evacuation of the pericardial fluid is needed promptly via needle pericardiocentesis with the insertion of an intrapericardial catheter, or via surgical treatment. A useful <u>t</u></span><span style="font-size: large;"><u>emporary</u> measure, that helps to stabilize blood pressure before pericardial fluid </span><span style="font-size: large;">evacuation, is expansion of intravascular </span><span style="font-size: large;">volume with intravenous infusion of saline (normal saline 0,9%).</span></div>
<span style="font-size: large;"><br /></span> <span style="font-size: large;"> </span><span style="font-size: large;">A case of a large pericardial effusion due to pericarditis. A video by the EchoWeb. Link: </span><br />
<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=hzo9HE9LV9g" target="_blank">https://www.youtube.com/watch?v=hzo9HE9LV9g</a></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
<b style="font-size: x-large;"><br /></b>
<b style="background-color: #e69138; font-size: x-large;">Useful links and bibliography</b><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br />Lazaros G, Imazio M, Brucato A, Tousoulis D. </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Untying the Gordian knot of pericardial diseases: A pragmatic approach. </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Hellenic J Cardiol. 2016;57(5):315-322. doi: 10.1016/j.hjc.2016.11.024. </span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://www.sciencedirect.com/science/article/pii/S1109966616303050?via%3Dihub" target="_blank">http://www.sciencedirect.com/science/article/pii/S1109966616303050?via%3Dihub</a></b></span></div>
<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span></b> <b><span style="font-family: "arial" , "helvetica" , sans-serif;">Kyriakakis CG, Mayosi BM, de Vries E, Isaacs A, Doubell AF.An approach to the patient with suspected pericardial disease. S Afr Med J. 2016 Feb;106:151-155.</span></b><span style="font-size: large;"><br /></span><br />
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<span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/early/2015/08/28/eurheartj.ehv318">2015 ESC Guidelines for the diagnosis and management of pericardial diseases</a></span><br />
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br />Yusuf SW, Hassan SA, Mouhayar E, Negi SI, Banchs J, O'Gara PT. Pericardial disease: a clinical review. Expert Rev Cardiovasc Ther. 2016; 14:525-539.</span></b><br />
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-91807188252736120022016-05-11T21:29:00.002+03:002020-10-04T20:51:20.855+03:00Congestive heart failure diagnosis and treatment / and A case of Heart Failure from ischemic cardiomyopathy. ECG, echo, SPECT, coronary angiography and treatment. <div dir="ltr" style="text-align: left;" trbidi="on">
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Congestive heart failure diagnosis and treatment / and A case of Heart Failure</h2>
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<span style="font-size: large;">IMPORTANT NOTE: THE SITE IS UNDER DEVELOPMENT AND CONTENTS ARE CONTINUOUSLY ADDED.</span><br />
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<span style="font-size: large;"><br /><br />One of my medical videos. A case of ischemic cardiomyopathy The patient presented with effort dyspnea, in the context of coronary artery disease and a previous myocardial infarction. The ECG, the echocardiogram, the myocardial perfusion scan (SPECT) and the coronary angiography of the patient are presented and the appropriate treatment is discussed.</span><br />
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>NOTES </b></span><br />
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<span style="font-size: large;"><b>Definition of heart failure and general considerations </b></span></h3>
<span style="font-size: large;"><b>Definition: Heart failure (HF)</b> is a progressive pathologic condition. It is defined as a clinical syndrome that results from any structural or functional abnormality of the heart </span><span style="font-size: large;">resulting in a reduced cardiac output and/ or elevated intracardiac pressures at rest or during stress (physical activity) and is c</span><span style="font-size: large;">haracterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) and/or signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema).</span><span style="font-size: large;"> HF can also be defined as an abnormality of cardiac structure or function </span><span style="font-size: large;">that impairs the ability of the left ventricle, or the right ventricle, or both ventricles, to eject blood, or to fill with blood,</span><span style="font-size: large;"> leading to failure of the heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolizing tissues, despite normal filling pressures, or the situation in which the heart is able to deliver to the tissues, blood and oxygen at a sufficient rate only at the expense of increased filling pressures. </span><span style="font-size: large;">HF may involve the left heart, the right heart, or be biventricular.</span><br />
<span style="font-size: large;">HF is characterized by dyspnea and/or fatigue on exertion (and occasionally at rest) and evidence of fluid retention, which can manifest as peripheral edema or pulmonary congestion. Clinically HF can be defined, as a syndrome in which patients have typical symptoms (e.g. breathlessness, ankle swelling, and fatigue) and signs (e.g. elevated jugular venous pressure, pulmonary crackles, and displaced apex beat), resulting from an abnormality of cardiac structure or function.<br />The prevalence of HF is increasing. The <b>prognosis </b>is severe for symptomatic HF (50 % or more of patients hospitalized for heart failure die within the next 5 years.) HF is a significant cause of morbidity and mortality. Death in HF can occur as sudden cardiac death (due to the sudden occurrence of a ventricular tachyarrhythmia: ventricular tachycardia or ventricular fibrillation), or as a result of end stage HF with worsening heart failure symptoms and fluid overload.<br />Many of the signs of HF result from sodium and water retention and resolve quickly with diuretic therapy.<br />Very important for the diagnosis of HF is <b>demonstration of an underlying cardiac cause</b> This is usually myocardial disease causing systolic ventricular dysfunction (for example ischemic cardiomyopathy in the context of a previous myocardial infarction, dilated cardiomyopathy). However, abnormalities of ventricular diastolic function or of the valves (for example severe aortic or mitral valve disease, severe stenosis of the pulmonary valve,etc), pericardium (for example constrictive pericarditis), endocardium, heart rhythm (heart failure due to a tachyarrhythmia), and conduction (heart failure caused by serious bradycardia,advanced atrioventricular block) can also cause HF. Occasionally, more than one abnormality can be present.</span><br />
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<span style="font-size: large;"><br /></span><span style="font-size: large;"><b>Systolic HF, or heart failure with reduced ejection fraction</b></span></h3>
<span style="font-size: large;"><b>Systolic HF, or HF with reduced ejection fraction</b>, is due to an impaired left ventricular systolic function: It is a failure of the left ventricle to eject blood in order to maintain a cardiac output adequate to meet the total metabolic needs of the body, under normal ventricular filling pressures. The cardiac output can be reduced (manifestations of inadequate cardiac output are fatigue on exertion, or even hypotension and shock) or more commonly cardiac output may be normal, but under the expense of abnormally elevated ventricular filling pressures, causing the manifestations of congestion (effort dyspnea, nocturnal dyspnea and orthopnea, acute pulmonary edema, pleural effusion, peripheral edema, hepatomegaly, jugular venous distention, etc.). Systolic HF is caused by damage to the cardiac muscle (myocardium) from infarction, inflamation (myocarditis), toxicity (alcohol, chemotherapeutic drugs used for the treatment of malignancies), chronic pressure overload (chronic hypertension, severe aortic valve stenosis), chronic volume overload ( severe aortic or mitral regurgitation, large cardiac shunts due to congenital heart disease), etc.</span><br />
<span style="font-size: large;">According to the recent guidelines (ESC 2016) HF with reduced EF is defined by the presence of symptoms and/or signs of HF in patients with left ventricular EF <40 % .<br /><b><br /></b></span><br />
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<span style="font-size: large;"><b>Diastolic HF, or heart failure with preserved ejection fraction (EF)</b></span></h3>
<span style="font-size: large;"><b>Diastolic HF, or HF with preserved ejection fraction (EF)</b>: However, there is also a large group of patients with signs and symptoms of heart failure, but apparently preserved left ventricular systolic function, with left ventricular ejection fraction ≥ 50%. These patients have diastolic HF or HF with preserved ejection fraction (EF). The latter term is better, because often patients with this type of HF, do not have a completely normal systolic function, when they are examined with more sensitive tests, such as tissue Doppler echocardiography or myocardial strain imaging. These sensitive tests show that these patients usually also have subtle abnormalities of systolic function. The important fact is, that in these patients the predominant disorder, causing the manifestations of HF, is a disorder of the ventricular diastolic function. In simple words, there is an abnormality in the ability of the left ventricle to fill in diastole, causing elevated filling pressures and manifestations of pulmonary congestion (effort dyspnea, nocturnal dyspnea, orthopnea, even acute pulmonary edema). The severe impairment of diastolic function may be transient (e.g. acute ischemia) or persistent ( e.g. left ventricular hypertrophy due to hypertension, or hypertrophic cardiomyopathy /restrictive or infiltrative cardiomyopathy/ diabetic cardiomyopathy).</span><br />
<span style="font-size: large;">Recent guidelines (ESC 2016) define HF with preserved EF by the following criteria: </span><br />
<span style="font-size: large;">(a) Patients with symptoms and /or signs of HF,</span><br />
<span style="font-size: large;">(b) left ventricular EF </span><span style="font-size: large;"> </span><span style="font-size: large;">≥ 50%, </span><br />
<span style="font-size: large;">(c) elevated natriuretic peptide (BNP> 35 pg/ml or NTProBNP> 125 pg/ml) and</span><br />
<span style="font-size: large;">(d) at least one of the following:</span><br />
<span style="font-size: large;">Evidence of a relevant structural heart disease (e.g. left ventricular hypertrophy, left atrial enlargement), or</span><br />
<span style="font-size: large;">Evidence of diastolic dysfunction (usually obtained with echocardiography).</span><br />
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<span style="font-size: large;"><b>Heart failure with mid-range EF </b></span></h4>
<span style="font-size: large;">Recent guidelines also define a form of HF between HF with reduced and HF with preserved EF. This is:</span><br />
<span style="font-size: large;"><b>HF with mid-range EF </b> and it is defined by the following criteria:</span></div>
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<span style="font-size: large;">Patients with symptoms and /or signs of HF,</span><br />
<span style="font-size: large;">left ventricular EF between 40 and 50 % (41-49%) plus the criteria (c) and (d) mentioned above for HF with preserved EF.</span><br />
<span style="font-size: large;">The symptoms of these patients most probably are caused primarily by mild systolic dysfunction, or by a combination of diastolic and systolic dysfunction.</span><br />
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<span style="font-size: large;"><b>Stages of heart failure </b></span></h3>
<span style="font-size: large;">This staging classification has been adopted by the guidelines with the purpose to emphasize the progressive nature and the evolution of heart disease leading to the development of HF.<br /><br />Stage A: People without significant structural heart disease, being at risk for future development of heart failure, based on the presence of risk factors such as hypertension, atherosclerotic disease, diabetes mellitus, prior exposure to cardiotoxic agents (such as doxorubicin), or a family history of a cardiomyopathy. These predisposing factors do not constitute the syndrome of heart failure, so the importance of this stage is to emphasize the need for early identification of individuals with risk factors for a better follow up and for treatment of any modifiable risk factors. </span></div>
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<span style="font-size: large;"><b>Stage B </b>includes patients with structural heart disease, but without signs or symptoms of heart failure (HF), such as patients with<br />previous myocardial infarction, low ejection fraction (EF), left ventricular hypertrophy, or asymptomatic valvular disease.</span><span style="font-size: large;">Patients with asymptomatic left ventricular systolic dysfunction (of ischemic or nonischemic etiology) </span><span style="font-size: large;">should receive an ACE inhibitor </span><span style="font-size: large;">to reduce of developing symptomatic heart failure and death. If there is an intolerance to an ACE- inh because of cough or angioedema, an </span><span style="font-size: large;">angiotensin receptor blocker- ARB( especially valsartan) is an effective treatment alternative. I</span><span style="font-size: large;">n patients with left ventricular dysfunction </span><span style="font-size: large;">in the context of a myocardial infarction, the combination </span><span style="font-size: large;">of an ACE inhibitor and ARB is </span><span style="font-size: large;">not better than either alone, so in this setting, combination therapy is not recommended. </span><br />
<span style="font-size: large;">Beta -blockers </span><span style="font-size: large;">in patients with a recent </span><span style="font-size: large;">myocardial infarction and reduced left ventricular EF (≤40%) </span><span style="font-size: large;">also improve sur</span><span style="font-size: large;">vival and reduce subsequent nonfatal myocardial infarctions,</span><span style="font-size: large;"> when added to an ACE inhibitor.</span><br />
<span style="font-size: large;"><b>Stage C: </b> Patients with structural heart disease </span><span style="font-size: large;">with prior or current </span><span style="font-size: large;">symptoms of HF (e.g. s</span><span style="font-size: large;">hortness of breath, </span><span style="font-size: large;">fatigue, reduced exercise </span><span style="font-size: large;">tolerance, edema)</span><br />
<span style="font-size: large;">Usual treatment includes diuretics for fluid retention (symptoms and signs of congestion) and for patients with stage C heart failure with reduced left ventricular EF drug cate proven by randomized trials to reduce </span><span style="font-size: large;">mortality (and also reduce hospitalizations): </span><span style="font-size: large;">ACE inhibitors (or ARBs) beta- b</span><span style="font-size: large;">lockers, m</span><span style="font-size: large;">ineralocorticoid antagonists. (See below, the chapter on treatment and the links to the guidelines).</span><br />
<span style="font-size: large;"><b>Stage D</b></span><br />
<span style="font-size: large;">Refractory HF requiring </span><span style="font-size: large;">specialized interventions. </span><span style="font-size: large;"><span style="font-family: "times" , "times new roman" , serif; font-size: large;">Patients with end stage (stage D) heart failure have the following characteristics: severe symptoms at rest or with minimal activity despite optimal medical treatment, </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">recurrent decompensation with hospitalizations, severe </span><span style="font-family: "times" , "times new roman" , serif; font-size: large;">cardiac dysfunction and often a need for treatment with inotropes.</span> Besides optimal medical treatment, with the drugs used for stage C, these patients often require treatment in specialized centers and for some of them, advanced forms of treatment are required (such as chronic-permanent mechanical circulatory assist devices, heart transplantation, treatment with intravenous inotropic medications).</span><br />
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<span style="font-size: large;"><b>The NYHA classification of heart failure (HF) </b></span></h3>
<span style="font-size: large;">The New York Heart Association (NYHA) classification is a scale used for classifying patients with HF according to the severity of symptoms and has prognostic and therapeutic implications:</span></div>
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<span style="font-size: large;"> NYHA I: asymptomatic </span></div>
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<span style="font-size: large;">NYHA II: symptomatic with moderate exertion </span></div>
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<span style="font-size: large;">NYHA III: symptomatic with mild exertion and may limit activities of daily living</span></div>
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<span style="font-size: large;">NYHA IV: symptomatic at rest.</span><b style="font-size: x-large;"><br /></b>
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<h4>
<b style="font-size: x-large;">A practical clinical classification of patients with heart failure</b></h4>
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<span style="font-size: large;">Is it possible to classify patients with heart failure (HF), especially those with acute HF, into hemodynamic categories according to their clinical manifestations, and can this influence the treatment strategy?</span><br />
<span style="font-size: large;">Yes...The manifestations (signs and symptoms) of HF can be classified into those caused by low perfusion (i.e., "cool" hemodynamics) and those caused by congestion (increased pulmonary and systemic venous pressure and salt and water retention = "wet hemodynamics"). </span><br />
<span style="font-size: large;">The manifestations of low perfusion (decreased cardiac output=is decreased volume of blood passing through the circulation per minute) are the following: </span><br />
<span style="font-size: large;">Decreased pulse pressure (pulse pressure = systolic pressure –diastolic pressure), cool </span><span style="font-size: large;">extremities, altered mental status and decreased urine output. Some or all of these manifestations can be present depending on the severity of the patient's condition.</span><br />
<span style="font-size: large;">The manifestaitons of congestion (i.e., wet hemodynamics) can be some or all of the following :</span><br />
<span style="font-size: large;"> Dyspnea on exertion, p</span><span style="font-size: large;">aroxysmal nocturnal dyspnea, o</span><span style="font-size: large;">rthopnea, edema, </span><span style="font-size: large;">elevated jugular venous pressure (external jugular veins become distended and the pulsations of the internal jugular vein are visible at an increased height, measured from the sternal angle),</span><span style="font-size: large;"> ascites (abdomimal distention due to the accumulation of fluid), an </span><span style="font-size: large;">audible third heart sound </span><span style="font-size: large;">at early diastole, crackles on lung auscultation, hepatojugular reflux.</span><br />
<span style="font-size: large;">A practical, simplified, approach is to classify the patient with HF into one of the following hemodynamic profiles: </span><br />
<span style="font-size: large;"> Warm and dry: the patient is well compensated, with no manifestations of low tissue perfusion or congestion. No change in medical management is needed on the basis of the clinical manifestations.</span><br />
<span style="font-size: large;"> Warm and wet: The patient is congested but has no manifestations of decreased perfusion. Diuretic treatment should be increased to reduce congestion.</span><br />
<span style="font-size: large;"> Cool and dry: The patient has manifestations of diminished perfusion, but no manifestations of congestion. A general rule is to add inotropic support to improve perfusion, especially if the manifestations are severe, but also the dosage of vasodilators such as ACE inhibitors can be increased (with caution to avoid hypotension), in order to reduce afterload and hence increase cardiac output. </span><br />
<span style="font-size: large;">Cool and wet: </span><span style="font-size: large;">The patient has manifestations of diminished perfusion as well as manifestations of congestion. A general rule is to increase </span><span style="font-size: large;">diuretic therapy, to treat congestion and add inotropic support (especially if the patient has severe signs of diminished perfusion or significant hypotension).</span><br />
<span style="font-size: large;">The above classification is simplified and schematic, but it is often helpful, especially in some cases of acute heart failure. We should emphasize that the cornerstone of the treatment of HF with reduced EF (systolic HF) is formed by those medications proved in major clinical trials to increase survival: angiotensin converting enzyme inhibitors (ACE-inhibitors) or angiotensin receptor blockers (ARBs), beta-blockers and aldosterone antagonists</span><span style="font-size: large;">.</span><br />
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<b style="font-size: x-large;">Imaging in heart failure ( Chest radiography / Echocardiography)</b></h3>
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<span style="font-size: large;"><b>The chest x -ray</b> is a simple and widely available imaging study that can provide some important clues, but the most useful study in a patient with suspected or known HF is echocardiography.</span><br />
<span face=""arial" , sans-serif"><br /></span> <span face=""arial" , sans-serif"><b>The chest X-ray of a male patient, 60 years old, ex-smoker (15 pack-years), with no history of increased alcohol consumption and with no previous history of cardiac or respiratory disease. He presented with effort dyspnea class NYHA-3 in the last 2 months and a general feeling of tiredness. The physical examination revealed no significant findings, other than </b></span><b style="font-family: arial, sans-serif;">reduced intensity</b><b style="font-family: arial, sans-serif;"> of heart sounds. Auscultation of the lungs was also normal. </b><b style="font-family: arial, sans-serif;">Is the shortness of breath most probably due to a cardiac or a respiratory disorder? What further testing is indicated ?</b><br />
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<span face=""arial" , "helvetica" , sans-serif"><b><span face=""arial" , "helvetica" , sans-serif"><b>THE ANSWER</b></span><br />Findings include enlargement of the hilar shadows, dilatation of the lung vessels and more prominent vascular markings in the upper lung fields. These are signs suggestive of elevated pulmonary venous pressure due to heart disease. In contrast there are no findings indicative of a pulmonary disease. Increased dimensions of the cardiac shadow are also observed with an increased prominence of the lower portion of its left margin. The latter finding suggests dilatation of the left ventricle (LV). These findings in conjunction with the presenting symptom of effort dyspnea favor the diagnosis of heart failure (HF), the cause and the severity of which can be investigated by means of further tests. An ECG and an echocardiogram are absolutely mandatory. According to the ESC guidelines (2016) the following laboratory tests are recommended for a patient with newly diagnosed HF in order to evaluate the patient’s suitability for particular therapies and to detect treatable causes and comorbidities: Hemoglobin and WBC - </b></span><b style="font-family: Arial, Helvetica, sans-serif;">urea, creatinine (with estimated GFR), </b><span face=""arial" , "helvetica" , sans-serif"><b>sodium, potassium, </b></span><b style="font-family: Arial, Helvetica, sans-serif;">- glucose, HbA1c -</b><span face=""arial" , "helvetica" , sans-serif"><b>-lipid profile- liver function tests (</b></span><b style="font-family: Arial, Helvetica, sans-serif;">AST, ALT, </b><span face=""arial" , "helvetica" , sans-serif"><b>bilirubin,GGT) TSH - ferritin. Natriuretic peptides can also be cosidered as a part of the evaluation. Depending on the findings and the pretest probability of coronary artery disease (risk factors), coronary angiography is often indicated in cases of HF, especially with LV systolic dysfunction, to confirm </b></span><b style="font-family: Arial, Helvetica, sans-serif;">or exclude </b><b style="font-family: Arial, Helvetica, sans-serif;">coronary artery disease, as a common underlying cause.</b><br />
<b style="font-family: Arial, Helvetica, sans-serif;">On echocardiography t</b><b style="font-family: Arial, Helvetica, sans-serif;">his patient had a dilated and diffusely hypokinetic LV with an EF 35 % and also a dilated left atrium. The right heart chambers and the valves were without significant abnormalities (appart from moderate functional mitral regurgitation). Coronary angiography did not reveal significant coronary arterial stenoses. He was diagnosed with HFrEF due to dilated cardiomyopathy and treated with an ACE inhibitor (quinapril), a beta blocker (carvedilol), an MRA (eplerenone) and a loop diuretic (furosemide). Symptoms resolved and on re-evaluation after three months of treatment his EF had improved (40 %) and the dilatation of the LV had decreased. Subsequently, the dosage of the diuretic was reduced and the dosage of the ACE inhibitor was increased.</b><br />
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<h4>
<span style="font-family: inherit; font-size: large;"><b><span style="font-family: inherit;">A reminder of relevant chest X ray anatomy</span></b><span style="font-family: inherit;"> : </span></span></h4>
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<span style="font-family: inherit; font-size: large;"><span style="font-family: inherit;">In the </span><u style="font-family: inherit;">posteroanterior</u><span style="font-family: inherit;"> chest radiograph the right border of the cardiomediastinal shadow is formed (from its lower to its upper parts), by the right atrium, the ascending aorta, and superior vena cava and further cranially it widens into a funnel shape, where its right border is formed by the brachiocephalic trunk. The upper margin of the left cardiomediastinal silhouette (from its upper to its lower portions) is formed by the aortic arch, the left pulmonary artery and the atrial appendage. The lower part of the left cardiomediastinal silhouette is formed by the left ventricle. The contour of the left hemidiaphragm is visible through the heart shadow almost as far as the shadow of the vertebral column.</span></span></div>
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<span style="font-size: large;"><u>Lateral chest x ray</u>: The anterior cardiac border is formed by the right ventricle. and its upper part by the shadow of the </span><span style="font-size: large;">aortic root continuing to the shadow of the aortic arch.</span><span style="font-size: large;"> The anterior surface of the right ventricle normally is in contact with the sternum along less than one-third of the length of the sternum </span></div>
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<span style="font-size: large;">The cranial border of the middle mediastinum is defined by the shadow of the aortic arch. The shadow of the arch is interrupted by the radiolucent (black) band of the trachea and main bronchi. </span><span style="font-size: large;">The lower part of the posterior heart border is formed by the left ventricle and its upper part by the left atrium.</span><br />
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<h4>
<span style="font-size: large;"><b>Chest radiography in heart failure:</b></span></h4>
<span style="font-family: inherit; font-size: large;">It is indicated for patients with suspected new-onset HF or with worsening HF. The goal is to assess heart size and to detect signs of pulmonary congestion, as well as to search for a possible pulmonary disease that may cause or contribute to the patient’s symptoms.</span><br />
<span style="font-family: inherit; font-size: large;">A usual finding in patients with HF with reduced EF is an e</span><span style="font-size: large;">nlarged cardiac silhouette (</span><span style="font-size: large;">cardiomegaly): In an inspiratory posteroanterior chest x ray the width if the cardiac silhouette is more than half of the width of the maximum internal diameter of the thorax. Cardiomegaly is almost always present in chronic systolic HF. In some forms of acute-new onset systolic HF, such as in the context of an acute myocardial infarction, cardiomegally often is not present (because the left ventricle did not have time to dilate), but there are signs of pulmonary congestion. </span><br />
<span style="font-size: large;">Clear signs of pulmonary congestion (elevated pulmonary venous pressure) are usually present in acute heart failure, but in much fewer patients with chronic heart failure. Such signs are</span><br />
<span style="font-size: large;"> U</span><span style="font-size: large;">pper lobe redistribution (enlarged upper lobe vessels in comparison to lower lobe vessels-in other words: p</span><span style="font-size: large;">rominence of upper lobe blood vessels. Normally, on the erect radiograph upper lobe vessels are less prominent and have a smaller diameter than lower lobe vessels.Important:</span><span style="font-size: large;"> The term redistribution applies to chest x-rays taken in full inspiration in the erect position</span><span style="font-size: large;">), </span><br />
<span style="font-size: large;">Enlarged hilar shadows of the lungs (due to dilated pulmonary veins) and increased diameter of the pulmonary vessels,</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">Septal or </span><span style="font-size: large;">Kerley B lines</span><span face=""arial" , "helvetica" , sans-serif"><br /><i><b>[These lines-named after Peter Kerley, a radiologist from Ireland- are short,</b></i></span><i><b><span face=""arial" , "helvetica" , sans-serif"> </span><span face=""arial" , "helvetica" , sans-serif">usually 1 -2 cm in length,</span><span face=""arial" , "helvetica" , sans-serif"> parallel horizontal thin lines at the lung periphery, They represent thickened interlobular septa (because of interstitial edema, i.e increased interstitial fluid).They are parallel to one another, at right angles to the pleura. kerley B lines</span><span face=""arial" , "helvetica" , sans-serif"> may be seen in any lung zone, but usually they are observed at the bases </span><span face=""arial" , "helvetica" , sans-serif">on the PA radiograph, and in the substernal region on lateral radiographs. The usual cause of</span><span face=""arial" , "helvetica" , sans-serif"> Kerley B lines is interstitial pulmonary edema from congestive heart failure,. There are also other causes that can produce Kerley B lines by thickening of the septa between pulmonary lobules, </span><span face=""arial" , "helvetica" , sans-serif">such as </span><span face=""arial" , "helvetica" , sans-serif">pulmonary fibrosis, pneumoconiosis</span><span face=""arial" , "helvetica" , sans-serif">, lymphangitis carcinomatosa, malignant lymphoma, viral and mycoplasmal pneumonia.]</span></b></i><br />
<span style="font-size: large;"> When fluid leaks into the peribronchovascular interstitium it is seen as thickening of the bronchial walls (peribronchial cuffing) and as loss of definition of hilar vessels (perihilar haze). Τhe above signs (Kerley B lines, peribronchial cuffing and perihilar haze) are signs of interstitial pulmonary edema (leakage of fluid into the interstitium of the lungs).</span><span style="font-size: large;"><span style="font-size: large;">and in more severe cases of congestion: </span></span><br />
<span style="font-size: large;">Alveolar pulmonary edema, due to leakage of fluid into the alveoli : Alveolar pulmonary edema is characterized by perihilar consolidations, i.e.large shadows or infiltrates (white areas like mist) surrounding the pulmonary hilae and air bronchograms within these consolidations. </span><span face=""arial" , "helvetica" , sans-serif"><i><b>Air bronchogram is the appearance of air-containing bronchi within an area of consolidation, as branching radiolucent (=black) lines.</b></i></span><span style="font-size: large;"> </span><br />
<span style="font-family: inherit; font-size: large;">Pleural effusions are not rare in HF, </span><span style="font-size: large;">often bilateral. In HF when there is a </span><span style="font-size: large;">unilateral pleural effusion, it is </span><span style="font-family: inherit; font-size: large;">usually on the right side.</span><br />
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<h4>
<b style="font-size: x-large;">Echocardiography: Useful indices of left ventricular systolic function</b></h4>
<span style="font-size: large;">The most frequently used methods for the assessment of left ventricular (LV) systolic function are LV ejection fraction (EF) and regional wall motion analysis. Two dimensional (and also M-mode) echocardiography is the most common technique used but other tests that can examine LV systolic function are </span><span style="font-size: large;">tissue Doppler imaging (TDI), speckle tracking imaging, three-dimensional (3D) echocardiography, </span><span style="font-size: large;">computed tomography (CT), and cardiac magnetic resonance imaging </span><span style="font-size: large;">(CMR).</span></div>
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<span style="font-size: large;"> </span><span style="font-size: large;"><u>M-mode echocardiography</u>, which records the motion of cardiac structures in one dimension, can be used to obtain some indices of left ventricular (LV) systolic function. Measurements of LV dimensions are made </span><span style="font-size: large;">in the parasternal long-axis view </span><span style="font-size: large;">by positioning the cursor through the LV minor axis at the level of the tips of the mitral leaflets. Then fractional shortening (FS) </span><span style="font-size: large;">can be calcu</span><span style="font-size: large;">lated </span><span style="font-size: large;">and even ejection fraction (EF) can be calculated with geometric assumptions (that are not accurate, if there are significant differences in regional contractile function, between various segments of the LV walls).</span><br />
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<span style="font-size: large;"><u>Fractional shortening (FS)</u> is calculated from linear measurements</span></div>
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<span style="font-size: large;">of LV dimensions from M-mode or 2D images:</span></div>
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<span style="font-size: large;">FS = 100% × (LVDd – LVDs)/LVDd </span></div>
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<span style="font-size: large;">where LVDd and LVDs are the LV end-diastolic dimension and</span></div>
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<span style="font-size: large;">end-systolic dimension, respectively. FS normal values: 25-45 %</span><br />
<span style="font-size: large;">FS as an index of global LV function can be problematic when there is a marked difference in regional function, in patients with a previous myocardial infarction.</span></div>
<h4>
<span style="font-size: large;">Two-dimensional (2D) echocardiography for the evaluation of LV systolic function</span></h4>
<div>
<span style="font-size: large;">This is the primary mode for evaluation of LV systolic function. Endocardial border </span><span style="font-size: large;">motion and wall thickening can be visualized and an experienced examiner can assess regional and global contractile function and roughly estimate the ejection fraction (EF) just by visualizing the LV in various echocardiographic views ("eyeball approach"). Quantitative measurements are obtained by tracing the endocardial border in end diastole and end systole in the apical 4- and 2-chamber views using the method of discs (modified Simpson rule). The machine software divides the LV along its long axis into a series of </span><span style="font-size: large;">discs of equal height. Individual disc volume is calculated as </span><span style="font-size: large;">height x disc area. LV volume is then calculated as the sum of disc volumes.</span></div>
<span style="font-size: large;"></span><span style="font-size: large;"><b>The ejection fraction (EF)</b>= stroke volume/end diastolic volume.<br />Stroke volume= the volume of blood ejected by a ventricle in systole= EDV-ESV. </span><br />
<div>
<span style="font-size: large;">(EDV= end diastolic volume, ESV= end systolic volume). </span><br />
<span style="font-size: large;">Thus, </span><span style="font-size: large;">EF= </span><span style="font-size: large;"> (</span><span style="font-size: large;">EDV-ESV)/ EDV. </span></div>
<div>
<span style="font-size: large;">The left ventricular EF generally has a normal value </span><span style="font-family: "times new roman" , serif; line-height: 18.4px;"><span style="font-size: large;">≥</span></span><span style="font-size: large;"> 55%.</span><br />
<span style="font-size: large;"> It is a measure of global LV systolic function, with established prognostic significance (the lower the EF, the worse the prognosis), but it is also influenced by preload, afterload, heart rate, and valvular function. (In patients with severe aortic or mitral regurgitation, conditions causing volume overload of the left ventricle, the normal value for the EF is </span><span style="font-family: "times new roman" , serif; font-size: 18pt; line-height: 107%;">≥ 60%.) </span><span style="font-size: large;"> Systolic function of the left ventricle (LV) is considered as mildly reduced when EF is between 45 and 55 %, moderately reduced with EF between 30 and 45 % and severely reduced with EF< 30%.</span><br />
<span style="font-size: large;"> Left ventricular </span><span style="font-size: large;">EF is a strong predictor of clinical outcome </span><span style="font-size: large;">and is widely used to make clinical decisions.</span><br />
<span style="font-size: large;">EF should be calculated from volumetric measurements</span><br />
<span style="font-size: large;">by 2D echocardiography. Even more accurate measurements of left ventricular volumes and EF are obtained with three dimensional (3D) echocardiography, or magnetic resonance imaging (MRI). The latter two techniques have similar accuracy.</span><br />
<h4>
<span style="font-size: large;">Doppler Echocardiography derived systolic indices (stroke volume)</span></h4>
<span style="font-size: large;">Doppler echocardiography also provides some indices of LV systolic function, such as the stroke volume </span><span style="font-size: large;">(SV), i.e. the </span><span style="font-size: large;">blood volume ejected per beat. For this measurement one obtains from the apical 5 chamber view the pulse wave doppler signal of the velocity in the left ventricular outflow tract (LVOT) and also measures the diameter of the LVOT (in the parasternal long axis view at the base of the aortic valve leaflets or immediately proximal to the aortic valve). </span><br />
<span style="font-size: large;">SV= VTI</span> (LVOT) <span style="font-size: large;">x area </span>(LVOT)<br />
<span style="font-size: large;">VTI is the </span><span style="font-size: large;">velocity time </span><span style="font-size: large;">integral (also named time velocity integral-TVI) of blood flow through the LVOT during systole. </span><br />
<span style="font-size: large;">This formula is explained as follows: VTI is calculated as the area under the curve of the Doppler velocity signal (which displays velocity on the vertical axis and time on the horizontal axis). This area of the Doppler signal is automatically calculated by the machine software, after the examiner manually traces the doppler velocity signal. It mathematically represents a velocity time integral, i.e. the sum of many products of velocity x time, each corresponding to every small time interval in systole. Since in every small time interval the column of blood moves by a distance given by the product of blood velocity x time interval, the VTI as a sum represents the total distance the column of blood has "traveled" in systole. This distance multiplied by the area of the orifice through which blood has passed, is the volume of blood which passed through the orifice in systole= the stroke volume (SV). </span><span style="font-size: large;"> A</span><span style="font-size: large;">ssuming a circular </span><span style="font-family: inherit; font-size: large;">LVOT with radius r and diameter D (=2r) :</span><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold;"> </span><br />
<span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold;">LVOT area = </span><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold; text-align: justify;">πr<sup>2</sup>=3,14r<sup>2</sup>=3,14(D/2)</span><sup style="font-family: Arial, Helvetica, sans-serif; font-weight: bold; text-align: justify;"><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 14pt;">2</span></sup><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold; text-align: justify;"> </span><span face=""arial" , "helvetica" , sans-serif" style="font-weight: bold; text-align: justify;">= (3,14 D</span><sup style="font-family: Arial, Helvetica, sans-serif; font-weight: bold; text-align: justify;"><span lang="EN-US" style="font-family: "times new roman" , "serif"; font-size: 14pt;">2</span></sup><span style="text-align: justify;"><b style="font-family: Arial, Helvetica, sans-serif;">)/4=</b><span style="font-size: large;"> <span style="font-family: inherit;">0,785D</span></span></span><span style="font-size: large;"><sup style="text-align: justify;"><span lang="EN-US" style="font-family: inherit; font-size: 14pt;">2</span></sup> </span><br />
<span style="font-size: large;">In the absence of aortic</span> <span style="font-size: large;">regurgitation, SV reflects the forward effective blood flow in a cardiac beat and multiplied by heart rate (beats per minute) it gives the cardiac output (= the volume of blood passing through the circulation per minute). Strictly speaking, the SV is the hemodynamic result of LV function and not a true index of systolic function. Normal values of SV: 55-80 mL.</span><br />
<span style="font-family: inherit; font-size: large;">It is better to express the normal values of stroke volume per </span><span style="font-size: large;">m</span><sup style="text-align: justify;"><span lang="EN-US" style="font-family: inherit; font-size: 14pt;">2 </span></sup><span style="font-size: large;">of body surface area: </span><br />
<span style="font-size: large;">Normal values of </span><span style="font-family: inherit; font-size: large;">SV(ml/m</span><sup style="font-family: inherit; text-align: justify;"><span lang="EN-US" style="font-family: inherit; font-size: 14pt;">2</span></sup><span style="font-size: large;">): </span><span style="font-size: large;">26-54</span><br />
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<h4>
<span style="font-size: large;">Tissue Doppler Imaging (TDI)</span></h4>
<span style="font-size: large;">Measurement of mitral ring velocities or myocardial velocities of the basal segments (velocity of the movement of these tissues along the longitudinal axis of the heart) is a simple and sensitive method for the assessment of the left ventricular systolic and diastolic function. Both peak systolic (Sm) and early diastolic (Em) mitral annular or left ventricular basal velocities are nearly always reduced in patients presenting with the clinical syndrome of systolic heart failure.</span><br />
<span style="font-size: large;">The systolic annular velocity of the mitral valve (<b>Sm</b>) is a measure of left ventricular longitudinal contraction (contraction of the long axis oft the ventricle). It generally correlates well with the left ventricular EF. Normally Sm of the septal mitral annulus is > 6.5 cm/sec, and Sm of the lateral mitral annulus </span><span style="font-size: large;">≥ 8 cm/sec</span><span style="font-size: large;">, when measured with pulse wave tissue doppler (PW-TDI). It is better to assess the mean Sm of the septal and lateral mitral annulus (normal value > 7.5 cm/sec). Note that myocardial velocities measured by the color TDI method are lower than velocities by pulsed Doppler (typically about 25% lower).</span><br />
<span style="font-size: large;">Early myocardial damage often involves the subendocardial fibres, with impairment in long-axis contraction occuring before changes in short-axis function. Thus, the Sm is a sensitive marker of mildly impaired left ventricular systolic function, even in people with apparently preserved systolic function and a normal EF, for example in those with diastolic heart failure, or in some diabetic patients without overt heart disease. Reduced annular TDI velocities are also present in subjects with hypertrophic cardiomyopathy, (even in people having the related gene mutations, who are at the stage of subclinical disease, with no cardiac hypertrophy).</span><br />
<span style="font-size: large;">Note that whereas the Sm velocity is an index of left ventricular systolic function, the Em or E΄velocity (the peak early diastolic mitral annular velocity, which is a negative wave) is an index of LV diastolic function and the Am or A΄velocity (an end-diastolic negative wave) is an index of the systolic function of the left atrium.</span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><span face=""arial" , "helvetica" , sans-serif" style="font-size: small; font-weight: 700;">Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and Limitations.Heart, Lung and Circulation 2015;24:224-233</span></span><br />
<span style="font-size: large;"><span face=""arial" , "helvetica" , sans-serif" style="font-size: small; font-weight: 700;"> LINK </span><a href="http://www.heartlungcirc.org/article/S1443-9506(14)00733-1/pdf" style="font-family: Arial, Helvetica, sans-serif; font-size: medium; font-weight: 700;" target="_blank">Tissue Doppler Imaging in Echocardiography</a></span><br />
<span style="font-size: large;"><br /></span>
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<h4>
<span style="font-size: large;"><b>Myocardial strain and strain rate</b> imaging</span></h4>
<span style="font-size: large;">In general, in myocardial segments with diminished systolic function, systolic velocities are typically reduced and there are also reductions in systolic strain and strain rate. <b>Strain</b> is the proportion (percentage) of change in length of the myocardium (units %) and it is negative in systole, since there is a negative change in length (shortening), and positive in diastole (because in diastole the length increases).</span><br />
<span style="font-size: large;"> Strain = L-Lo /Lo, where L is the current length and Lo is the original length of a myocardial segment. </span><br />
<span style="font-size: large;">Strain describes deformation (change in length) of the myocardium which occurs in three different directions, therefore there are three different types of strain, longitudinal (which is most often measured), circumferential and radial. Deformation in these three directions results from the different orientation of subepicardial and epicardial myofibers, that also generate a counterclockwise twist at the apex of the left ventricle and a clockwise twist at the base. </span><br />
<span style="font-size: large;"><b><br /></b></span> <span style="font-size: large;"><b>Strain rate (SR)</b> is the rate of change of the strain value= the proportional change in length per unit of time. SR units are </span><span style="font-family: inherit; font-size: large;">s<sup>-1</sup></span><br />
<div class="MsoNormal">
<span face=""arial" , "sans-serif"" lang="EN-US" style="font-size: 14pt;"><sup><o:p></o:p></sup></span></div>
<span style="font-family: inherit; font-size: large;">SR is negative in systole (because it represents the rate of proportional decrease in myocardial length) and positive in diastole (because it represents the rate of increase in length). LV longitudinal velocities measured from an apical window increase progressively from the apical toward the basal myocardial segments. Longitudinal strain and strain rate, however, are essentially similar between apical and basal segments.</span><span style="font-size: large;"></span><br />
<span style="font-size: large;">The normal value of the peak systolic strain (percentage of shortening) of the left ventricle during systole in the longitudinal axis is greater than 15%. To be more accurate, let us mention that normal peak systolic strain has a value more negative than -15%, usually between -15 and -25%. (The negative sign indicates a decrease in the length of the myocardium, i.e. shortening).</span><br />
<span style="font-size: large;">Peak systolic strain is influenced by preload (like the ejection fraction which is also influenced by the ventricular loading conditions) and can be used as an indicator of the total, and of the regional systolic function (when measured at a segment of the left ventricle). </span><br />
<span style="font-size: large;">The normal value for the peak systolic strain rate of the left ventricular myocardium is between - 1.2 and - 2 </span><span style="font-size: large;"> </span><span style="font-family: inherit; font-size: large;">s<sup>-1 </sup></span><span style="font-size: large;">(sec</span><sup><span style="font-family: inherit; font-size: large;">-1</span></sup><span style="font-size: large;">=1/s).</span><br />
<span style="font-size: large;"> In normal hearts the value of strain rate and strain is about the same in all myocardial segments from the base to the apex of the heart, (showing no significant difference). Conversely, myocardial velocity recorded by the tissue Doppler (in cm/s), and the displacement (change in position) of a given point of the myocardium (in mm) is greater in the basal portions and is getting smaller towards the apex.</span><br />
<span style="font-family: inherit; font-size: large;">An advantage of the percentage of myocardial deformation (strain) and of the rate of the proportional change in deformation (strain rate) is the following: Strain and strain rate is not affected by the translational motion of the heart ("bouncing" movements in the chest during systole). In contrast, the myocardial velocities recorded with tissue Doppler (TDI) are affected by the translational motion of the heart within the chest and not only by the motion of myocardial shortening in systole or lengthening in diastole.</span><br />
<span style="font-family: inherit; font-size: large;">A diminished peak systolic strain or strain rate is a sensitive marker of an impairment in systolic function.</span><br />
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</script> <span style="font-family: inherit; font-size: large;">Need more information about these modern echocardiographic techniques? In that case, here is a link </span><span style="font-size: large;">for you to click on</span><span style="font-family: inherit; font-size: large;"> (free review article with the option to download PDF) ...</span><br />
<br />
<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805816/" target="_blank"><span style="font-size: large;">Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability</span></a><br />
<span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span><span face=""arial" , "helvetica" , sans-serif"><b>Dandel Μ ,Lehmkuhl H, et al. Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability. Current Cardiology Reviews, 2009, 5, 133-148.</b></span><span style="font-family: inherit; font-size: large;"> </span></div>
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<b style="font-size: x-large;"><br /></b>
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<h3>
<b style="font-size: x-large;">Treatment of systolic heart failure (HF with reduced ejection fraction)</b></h3>
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<span style="font-size: large;"><b>The first step in the treatment of heart failure (HF) with reduced EF usually is starting three medications (an ACE-inhibitor, or an ARB, a beta blocker and a diuretic</b>-see below). The diuretic is indicated if there are signs or symptoms of congestion, because it reduces symptoms, improves exercise tolerance and reduces the risk of hospitalization for HF. The ACE-inhibitor and the beta blocker are very important because they reduce mortality and the risk of HF hospitalization. ARBs are recommended only as an alternative (instead of an ACE inhibitor), in patients intolerant of an ACE-inhibitor.</span><br />
<span style="font-size: large;">Important: In every patient with ejection fraction (EF) </span><span style="font-family: "times new roman" , serif; line-height: 115%;"><span style="font-size: large;">≤ 40 % there </span></span><span style="font-size: large;">is a class I indication (i.e. a "strong and clear" indication) for treatment with an</span><span style="font-size: large;"> ACE-inhibitor, (or an ARB, if the first is not well tolerated) and a beta blocker, because this treatment reduces mortality (rates of death) and the rate of hospitalizations for HF.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;"><span style="font-family: "times new roman" , serif; font-size: 14pt; line-height: 115%;"> </span></span><span style="font-size: large;">Diuretics are clearly indicated in parients with HF (systolic or diastolic) if they have symptoms or signs of congestion and provide improvement of symptoms. They have not been shown in trials to reduce mortality.</span><br />
<span style="font-size: large;">Angiotensin converting enzyme </span><span style="font-size: large;">(ACE)</span><span style="font-size: large;"> inhibitors are first line drugs in systolic heart failure (heart failure with reduced EF).</span><span style="font-size: large;"> ACE-inhibitors prevent conversion of angiotensin I to angiotensin II. This results in lower systemic vascular resistance (since angiotensin II induces vasoconstriction) and less secretion of aldosterone. Use of ACE inhibitors in patients with HFrEF increases survival, improves symptoms, decreases hospitalizations and improves left ventricular systolic function (the EF). </span><br />
<span style="font-size: large;">An Angiotensin receptor blocker (ARB) can be given instead, if the ACE inhibitor is not well tolerated by the patient. ARBs are </span><span style="font-size: large;">specific antagonists to the angiotensin II type 1 receptors and so they act by inhibiting the effects of angiotensin II.</span><br />
<span style="font-size: large;">Absolute contraindications for an an ACE inhibitor or an ARB include pregnancy and bilateral renal artery stenosis. An absolute contraindication for an ACE inhibitor (and relative contraindication for an ARB) is a history of angioedema.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">When using an ACE-inh or an ARB, caution is required in hyperkalemia (these drugs can cause elevation of potasium levels), in hepatic i</span><span style="font-size: large;">mpairment, in </span><span style="font-size: large;">renal dysfunction or unilateral stenosis of the renal artery (in this case there is a risk of causing deterioration of renal function), in aortic or mitral valve stenosis (risk of causing hypotension-if treament with these drugs is needed, one must be cautious to avoid rapid dose increments).</span><br />
<span style="font-size: large;"> </span><span style="font-size: large;">Relative contraindications for an ACE inhibitor or an ARB include</span><span style="font-size: large;"> </span><span style="font-size: large;">hypotension (systolic blood pressure < 90 mm Hg),</span><span style="font-size: large;"> hyperkalemia (potassium > 5.5 mEq/L), severe renal insufficiency (creatinine > 3.0 mg/dL). </span><br />
<span style="font-size: large;">Unique side effects of ACE inhibitors are cough and angioedema. Chronic nonproductive cough associated with ACE inhibitors is caused by elevated levels of bradykinin. All attempts should be made to identify an alternative cause of cough before discontinuing the ACE inhibitor and replacing it with an ARB. </span><br />
<span style="font-size: large;">Angioedema is a rare complication of ACE inhibitors (0.4%) manifested by soft tissue edema of the lips, face, tongue, and, occasionally, the oro- pharynx and epiglottis. This rare complication typically begins in the first 2 weeks of ACE inhibitor therapy, but in some patients it presents months to years after starting therapy.</span><br />
<span style="font-size: large;">ARBs are used and monitored in the same manner as ACE inhibitors. ARBs have a similar side-effect profile to ACE inhibitors (e.g.they can induce hypotension, or occasionally they can induce renal insufficiency and hyperkalemia in some patients), but unlike </span><span style="font-size: large;">ACE-inhibitors, ARBs do not induce cough and angioedema is a much more rare side effect with ARBs than with ACE inhibitors.</span><span style="font-size: large;"> Among ARBs, </span><span style="font-size: large;">the best studied in patients with heart failure are</span><span style="font-size: large;"> v</span><span style="font-size: large;">alsartan and candesartan and they should be preferred.</span><br />
<br />
<div>
<span style="font-size: large;">A beta blocker (carvedilol, bisoprolol, or metoprolol sustained release tablets, or nebivolol) is initiated with a low dose. </span></div>
<span style="font-size: large;">The dosage of ACE inhibitor or ARB and beta-blocker (starting from a low dosage) should be gradually titrated to the evidence-based dose, used in the major trials, or to the maximum tolerated dose below the evidence based dose. </span><br />
<span style="font-size: large;">Thus, in a symptomatic patient (NYHA II-IV) with HF with reduced left ventricular ejection fraction (EF<40%) according to the current guidelines (ESC-2016) initial treatment must include an ACE inh (or an ARB), a beta blocker and if there are </span><span style="font-size: large;"> </span><span style="font-size: large;">symptoms or signs of congestion </span><span style="font-size: large;">a diuretic (usually loop diuretic, e.g. furosemide). </span><br />
<span style="font-size: large;"> The dose of the ACE inh (or ARB) and of the beta blocker should be gradually increased (up-titrated) to reach the evidence based dosage, or the maximum tolerated dosage below the evience based dosage. If the patient becomes asymptomatic no further medications are added (and we can consider reducing the diuretic dose). </span><br />
<span style="font-size: large;">If a patient with HF with reduced LVEF remains symptomatic (has symptoms NYHA II-IV) despite the above therapy with an ACE-inh and a beta blocker, then there is a clear indication to add a <b>mineralocorticoid receptor antagonist (MRA).</b> Thus, in this case treatment includes ACE-inh+beta blocker+MRA (+diuretic for symptoms or signs of congestion). </span><br />
<span style="font-size: large;">To summarize the indication of an MRA as mentioned in the guidelines : For patients who remain symptomatic (NYHA class II-IV) under treatment with diuretic+ACE inh. (or ARB) + beta blocker and also </span><span style="font-size: large;">have an EF ≤ 35 %, a mineralocorticoid receptor antagonist (MRA) is added to this treatment scheme. </span><br />
<span style="font-size: large;">MRAs (spironolactone and eplerenone) are aldosterone antagonists, i.e. they prevent aldosterone from binding to its receptors. In such patients they reduce mortality and hospitalizations for HF.</span><br />
<span style="font-size: large;">Contraindications of aldosterone receptor antagonists (MRAs): potassium> 5 mmol / lt before the initiation of treatment, or severe renal failure: creatinine ≥2,5 mg / dL ,or calculated creatinine clearance ≤30 mL / min / 1,73 <span style="font-size: large; text-align: justify;">m</span><span style="font-size: large; text-align: justify;"><sup>2</sup></span> body surface area.</span><br />
<span style="font-size: large;"> For patients with EF ≤ 40% who remain symptomatic on treatment with a beta blocker, an ACE-inh. and a diuretic, if they cannot tolerate an MRA (or if this drug is contraindicated) an ARB can be added instead of the MRA and so treatment will include a beta blocker, an ACE-inh and an ARB (and a diuretic). </span><br />
<span style="font-size: large;">For patients with EF </span><span style="font-size: large;">≤ 40 % who cannot tolerate an ACE inh. because of cough, the treatment should include a beta blocker plus an ARB plus an MRA.</span><br />
<span style="font-size: large;">Note : A combination of three drugs blocking the renin-angiotensin-aldosterone axis, i.e. </span><span style="font-size: large;">an ACE-inh plus an ARB plus an MRA should never be used, due to adverse effects.</span><br />
<span style="font-family: inherit; font-size: large;">For patients with systolic HF who remain symptomatic despite the above treatment (including a beta blocker, an ACE-inh or ARB, an MRA and a diuretic = 4 drugs) , if LVEF is ≤ 35 % and the patient can tolerate an ACE-inh or an ARB, then there is an indication to replace the ACE inh or ARB used in the above drug regimen with a new drug : <b>ARNI</b> (angiotensin receptor neprilysin inhibitor). Thus treatment includes then : beta blocker+ diuretic+ARNI+ MRA. </span><span style="font-size: large;">ARNI is a new therapeutic class acting on the renin -angiotensin-aldosterone system (RAAS) and the neutral endopeptidase system. The first drug in this class is LCZ696, a molecule that combines the moieties of valsartan and sacubitril in a single substance. Sacubitril is a neprilysin inhibitor</span><span style="font-size: large;">. By inhibiting neprilysin, the degradation of netriuretic peptides, bradykinin and other peptides is slowed and this has beneficial effects in the course of systolic HF, because natriuretic peptides</span><span style="font-size: large;"> enhance diuresis, natriuresis and myocardial relaxation, reduce the progress of adverse LV remodelling and inhibit renin and aldosterone secretion. </span><br />
<div style="text-align: justify;">
<u><span style="font-size: large;">Contraindications and precautions regarding the use of ARNI (</span><span style="font-size: large; text-align: left;">LCZ696)</span></u></div>
<div style="text-align: justify;">
<span style="font-size: large;"> Concomitant treatment with an ACE-inh , or an ARB is contraindicated. C</span><span style="text-align: left;"><span style="font-size: large;">oadministration with direct renin inhibitor (aliskiren) is also not recommended.</span></span></div>
<div style="text-align: justify;">
<span style="font-size: large;">Contraindications include: </span></div>
<div style="text-align: justify;">
<span style="font-size: large;">H</span><span style="font-size: large;">ypersensitivity (allergy) to the active substance or ingredients</span><span style="font-size: large;"> </span></div>
<div style="text-align: justify;">
<span style="font-size: large;">Second and third trimesters of pregnancy</span><span style="font-size: large;"> </span></div>
<div style="text-align: justify;">
<span style="font-size: large;">History of angioedema related to a previous treatment with an ACE inhibitor or an ARB, or history of h</span><span style="font-size: large;">ereditary or idiopathic angioedema</span></div>
<div style="text-align: justify;">
<span style="font-size: large;"> Severe hepatic dysfunction or cholestasis</span></div>
<div style="text-align: justify;">
<span style="text-align: left;"><span style="font-size: large;"><u>Treatment onset</u> with ARNI should be at least 36 hours after discontinuation of treatment with ACE-inh (due to the potential risk of angioedema).</span></span></div>
<span style="font-size: large;"><br /></span> <span style="font-size: large;">The addition of <b>ivabradine</b> to</span><span style="font-family: inherit; font-size: large;"> the above treatment is indicated to reduce hospitalization rates in patients with EF≤ 35 %, in sinus rhythm with heart rate ≥ 70 beats /minute who remain symptomatic, despite the above drug combination (including an evidence based ,or maximum tolerated dose of a beta-blocker combined with 2 inhibitory drugs of the renin-angiotensin-aldosterone axis: an ACE-inh or an ARB or ARNI plus an MRA / or an ACE inh plus an ARB). Ivabradine has an indication of class IIa.</span><br />
<br />
<div>
<span style="font-size: large;"><b>Digoxin</b> may be considered (indication of class IIb) to reduce the risk of HF hospitalization in patients </span><span style="font-size: large;"> </span><span style="font-size: large;">with an EF ≤ 45%</span><span style="font-size: large;"> : </span><span style="font-size: large;">1) in sinus rhythm who are unable to tolerate a beta-blocker (ivabradine is an alternative in patients with symptomatic HF with reduced LVEF unable to tolerate a beta- blocker and sinus rate ≥70/min.), or 2) with persisting symptoms despite optimal treatment (with the above medications) or with atrial fibrilation and inadequately controlled ventricular response (ventricular rate).</span><br />
<span style="font-size: large;"><br /></span>
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<h4>
<span style="font-size: large;"><b>Cardiac resynchronization treatment (CRT)</b>, </span></h4>
<span style="font-size: large;">i.e. the implantation of a biventricular pacemaker is generally recommended for </span><span style="font-size: large;">patients with symptomatic systolic HF (despite optimal medical treatment), with </span><span style="font-size: large;"> a </span><span style="font-size: large;"> QRS duration is ≥ 130 ms (miliseconds) and left ventricular ejection fraction </span><span style="font-size: large;">LVEF</span><span style="font-size: large;">≤ 35%. </span><br />
<span style="font-size: large;"> It is not recommended for patients with a QRS duration < 130 ms.</span><br />
<span style="font-size: large;">The specific indications are as follows: CRT is recommended for symptomatic patients with HF in sinus rhythm with a QRS duration ≥ 130 ms and left bundle branch block (LBBB) and with LVEF ≤35% despite optimal medical treatment </span><span style="font-size: large;">(a class I </span><span style="font-size: large;">indication</span><span style="font-size: large;">). </span><br />
<span style="font-size: large;">In patients with systolic HF, (HFrEF) with LVEF</span><span style="font-size: large;">≤ 35% and symptoms despite optimal medical treatment : </span><span style="font-size: large;">CRT should/may be considered (class II indication) if :</span><br />
<span style="font-size: large;"> QRS ≥ 130 msec with non-LBBB in sinus rhythm, or </span><br />
<span style="font-size: large;">for patients in AF and </span><span style="font-size: large;"> </span><span style="font-size: large;">QRS ≥ 130 msec with NYHA Class III–IV provided there is a strategy to ensure bi-ventricular capture, or the patient is expected to return to sinus rhythm.</span><br />
<span style="font-size: large;"></span><br />
<span style="font-size: large;">CRT in patients with the above characteristics has been shown in trials to improve symptoms and reduce morbidity and mortality. Biventricular pacing (CRT) rather than right ventricular pacing is recommended for patients with systolic heart failure (HFrEF) regardless of NYHA class with an indication for ventricular pacing, because of high degree AV block in order to reduce morbidity. This also includes patients with AF.</span><br />
<h4>
<span style="font-size: large;"><br /></span><span style="font-size: large;"><b>Indications for an </b></span><span style="font-size: large;"><b>implantable cardioverter-defibrillator (ICD) in patients with heart failure</b> </span></h4>
<span style="font-size: large;">to reduce the risk of sudden death and imrove survival are the following:</span><br />
<span style="font-size: large;">Primary prevention : In symptomatic patients (NYHA class II-III) with systolic HF an implantable cardioverter-defibrillator (ICD) is indicated if </span><span style="font-size: large;"> LVEF</span><span style="font-size: large;">≤ 35%, despite</span><span style="font-size: large;"> </span><span style="font-size: large;">≥3 months</span><span style="font-size: large;"> of</span><span style="font-size: large;"> optimal medical treatment </span><span style="font-size: large;">provided they are expected to survive longer than one year with good functional status. This indication is for sympomatic patients with EF</span><span style="font-size: large;">≤ 35% who have: </span><br />
<span style="font-size: large;">a) ischemic heart disease</span><span style="font-size: large;"> but they did not have a myocardial infarction</span><span style="font-size: large;"> in the prior 40 days or </span><br />
<span style="font-size: large;">b) dilated cardiomyopathy DCM.</span><br />
<span style="font-size: large;">ICD implantation is not recommended in patients with HFrEF in NYHA class IV with severe symptoms refractory to pharmacological therapy because these patients will not have a survival benefit. Exceptions to this rule are patients with HFrEF class NYHA IV who are candidates for a treatment cabable of improving the course of their end stage HF, such as cardiac resynchronization treatment (CRT), a ventricular assist device, or cardiac transplantation. </span><br />
<span style="font-size: large;">For secondary prevention : </span><span style="font-size: large;">If the patient has recovered after an episode of </span><span style="font-size: large;">ventricular arrhythmia causing haemodynamic instability (</span><span style="font-size: large;">ventricular tachycardia, or ventricular fibrillation) not due to an identifiable reversible cause and expected to survive for >1 year with good functional status.</span><br />
<span style="font-size: large;">An ICD in asymptomatic patients with systolic HF (HFrEF) is recommended in patients receiving optimal medical treatment with severe systolic dysfunction : LVEF ≤30% either of ischemic origin, who are at least 40 days after acute myocardial infarction, or of non-ischemic origin (with asymptomatic non-ischemic dilated cardiomyopathy).ICD is recommended in patients: a) with asymptomatic. </span><br />
<span style="font-size: large;"> In patients with the above indications randomized controled trials have shown that an ICD prevents sudden death and prolonsg life.</span><br />
<span style="font-size: large;">As mentioned above, since the implantation of an ICD aims to increase survival, it is considered in the absence of other diseases likely to cause death within the following year.</span><br />
<span style="font-size: large;">Patients with systolic HF, with one of the above indications for ICD implantation, if they have οn the ECG a QRS duration ≥130 ms should be considered for a defibrillator with biventricular pacing, i.e. with cardiac resynchronization treatment (CRT-D= cardiac resynchronization treatment and defibrillator) rather than ICD.</span><br />
<h4>
<span style="font-size: large;"> Treatment of</span><b><span style="font-size: large;"> Heart Failure with preserved ejection fraction (</span><span style="font-size: large;">HFpEF) and of </span><span style="font-size: large;"> </span><span style="font-size: large;">Heart Failure with middle range ejection fraction (</span><span style="font-size: large;">HFmrEF)</span></b></h4>
<br />
<span style="font-size: large;">Diuretics are recommended in patients with HFpEF or HFmrEF, who have symptoms or signs of congestion. They are effective in alleviating symptoms. A study has also shown improvement in NYHA class with candesartan.</span><br />
<span style="font-size: large;">Patients with HFpEF or HFmrEF should be screened for both cardiovascular and noncardiovascular comorbidities, which, if present, should be treated in order to improve symptoms, well-being and/or prognosis. For example these patients often have hypertension, diabetes mellitus, or coronary artery disease. These conditions, which are also known to cause diastolic dysfunction, should be diagnosed, their severity should be assessed and effectively treated. Coronary reperfusion should be considered if there is symptomatic coronary heart disease (angina), or in cases where significant ischemia is demonstrated by non invasive diagnostic tests, if ischemia is considered to be involved in symptom worsening.</span><br />
<span style="font-size: large;">An important note is that <u>no treatment has yet been shown convincingly, to reduce mortality</u> in patients with HFpEF or HFmrEF. Trials of ACE-inhs, ARBs, beta-blockers and MRAs have failed to show mortality reduction in patients with HFpEF or HFmrEF. However, there is an exception to that general rule : N</span><span style="font-size: large;">ebivolol</span><span style="font-size: large;"> in older patients with HFrEF, HFpEF or HFmrEF, reduced the combined endpoint of death or cardiovascular hospitalization, with no significant association between treatment effect and left ventricular EF.</span><br />
<span style="font-size: large;">Patients with diastolic LV dysfunction often deteriorate in case of a tachycardia or tachyarrhythmia (because the duration of diastole is reduced). Then </span><span style="font-size: large;">control of heart rate (eg with beta-blockers or diltiazem) or restoration of normal sinus rhythm (when possible) is an important aspect of treatment.</span><br />
<h3>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Other treatment options for severe acute decompensated or chronic end stage heart failure with reduced EF.</span></h3>
<h4>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Ventricular assist devices (VADs) </span></h4>
</div>
<div>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">These devices are used for patients with acutely </span><span style="font-size: large;">decompensated heart failure (HF) not responding to medical treatment and also f</span><span style="font-size: large;">or end-stage </span><span style="font-size: large;">(ie, ACC/AHA stage D)</span><span style="font-size: large;"> chronic HF. Patients with end stage (stage D) heart failure have the following characteristics: severe symptoms at rest or with minimal activity despite optimal medical treatment, </span><span style="font-size: large;">recurrent decompensation with hospitalizations, severe </span><span style="font-size: large;">cardiac dysfunction and often a need for treatment with inotropes.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;"> The </span><span style="font-size: large;">left ventricle can be supported with a left ventricular assist device (LVAD), </span><span style="font-size: large;">the right ventricle with a right ventricular assist device (RVAD), or both ventricles with a biventricular assist device (BiVAD). Another term for a VAD is a ventricular assist system (VAS).</span></span></div>
<div>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-size: large;">A LVAD can be placed temporarily i</span><span style="font-family: inherit; font-size: large;">n acute refractory left ventricular failure (for example in </span><span style="font-size: large;">patients acute, severe myocarditis)</span><span style="font-size: large;"> </span><span style="font-size: large;">as a bridge to recovery. This can be achieved by unloading the dysfunctional heart to allow reverse remodeling, i.e. reduction of the left ventricular (LV) dilatation and improvement in systolic function.</span><span style="font-family: inherit; font-size: large;"> </span></span></div>
<div>
<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: inherit; font-size: large;">A VAD can also be used in patients with end-stage heart failure, either as a bridge to heart transplantation or for long term destination (permanent) treatment. A VAD as a destination therapy can be used in p</span><span style="font-family: inherit; font-size: large;">atients with end-stage heart failure, refractory to all other treatment options who are not transplant candidates and who otherwise would die without treatment.. </span></span></div>
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<span style="font-family: "times" , "times new roman" , serif;"><span style="font-family: inherit; font-size: large;">For patients with end stage HF, destination therapy with LVADs compared to medical therapy has shown better results (than medical therapy) in terms of quality of life and longer survival. This has been shown in the </span><span style="font-size: large;">REMATCH trial (</span><span style="font-family: inherit; font-size: large;">Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure) and also confirmed by newer data.</span></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><u>Potential complications of ventricular assist devices (VADs)</u></span></div>
<div>
<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Although VADs improve survival and quality of life in patients with end-stage HF, complications can occur and patients need expert follow up. Potential complications include mechanical dysfunction, infection, bleeding, and thromboembolic events. </span></div><div><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><br /></span></div><div><span style="font-family: "times" , "times new roman" , serif; font-size: large;"><span style="background-color: #ea9999;">A Video</span>: </span><span style="color: var(--yt-spec-text-primary); letter-spacing: var(--ytd-user-comment_-_letter-spacing); white-space: pre-wrap;"><b><span style="font-family: arial;">Echocardiography in advanced (end-stage ) heart failure with reduced EF. A concise introduction with a case presentation. The common echo findings. (To watch the video on a large screen, after you have started playing the video, click on the symbol [] at the lower right corner of the video.</span></b></span></div><div><span style="color: var(--yt-spec-text-primary); letter-spacing: var(--ytd-user-comment_-_letter-spacing); white-space: pre-wrap;"><b><span style="font-family: arial;"><br /></span></b></span></div><div><span style="color: var(--yt-spec-text-primary); letter-spacing: var(--ytd-user-comment_-_letter-spacing); white-space: pre-wrap;"><b><span style="font-family: arial;"><br /></span></b></span></div><div><span style="color: var(--yt-spec-text-primary); letter-spacing: var(--ytd-user-comment_-_letter-spacing); white-space: pre-wrap;"><b><div class="separator" style="clear: both; text-align: center;"><iframe allowfullscreen="" class="BLOG_video_class" height="331" src="https://www.youtube.com/embed/F-ooV5kOmzA" width="398" youtube-src-id="F-ooV5kOmzA"></iframe></div><br /><span style="font-family: arial;"><br /></span></b></span></div><div><br /></div><div><u style="font-family: times, "times new roman", serif; font-size: x-large;">For a detailed analysis of the management of HF, please use the links to heart failure-guidelines given at the bottom of this page. </u></div><div>
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Also see (LINK):</h3>
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<b style="font-family: inherit; font-size: x-large;"><a href="https://cardiologybookandcases.blogspot.com/p/heart-failure-and-heart-disorders-due.html">Heart failure and heart disorders caused by cancer teatment (cardio-oncology)</a></b></h3>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<b style="font-size: x-large;">BIBLIOGRAPHY AND USEFUL LINKS ABOUT HEART FAILURE MANAGEMENT</b><br />
<b><span face=""arial" , "helvetica" , sans-serif"><span face=""arial" , "helvetica" , sans-serif"><br /></span> <span face=""arial" , "helvetica" , sans-serif">Okwuosa IS, Princewill O, Nwabueze C, et al.The ABCs of managing systolic heart failure: Past, present, and future. Cleve Clin J Med. 2016 Oct;83:753-765.</span></span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif"><span face=""arial" , "helvetica" , sans-serif">Link : <a href="http://www.ccjm.org/view-pdf.html?file=uploads/media/Okwuosa_ManagingSystolicHeartFailure" target="_blank">The ABCs of managing systolic heart failure: Past, present, and future.</a></span> </span></b> <b><span style="font-size: large;"><br /></span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif"><br /></span></b> <span face=""arial" , "helvetica" , sans-serif"><b>Reed BN, Sueta CA .A practical guide for the treatment of symptomatic heart failure with reduced ejection fraction (HFrEF). Curr Cardiol Rev. 2015;11:23-32.</b></span></div>
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<span face=""arial" , "helvetica" , sans-serif"><b>LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4347206/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4347206/</a></b></span><b><span face=""arial" , "helvetica" , sans-serif"><br /></span></b> <span face=""arial" , "helvetica" , sans-serif" style="text-align: justify;"><b>Heart failure with preserved ejection fraction: </b></span><b style="font-family: arial, helvetica, sans-serif; text-align: justify;">pathophysiology, diagnosis, and treatment. European Heart Journal (2011) 32, 670–679.</b><br />
<b style="font-family: arial, helvetica, sans-serif; text-align: justify;">LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056204/pdf/ehq426.pdf" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056204/pdf/ehq426.pdf</a></b><br />
<b style="font-family: arial, helvetica, sans-serif; text-align: justify;"><br /></b> <span face=""arial" , "helvetica" , sans-serif"><b>Sanderson J E. Heart failure with a normal ejection fraction.Heart 2007;93:155-158. doi:10.1136/hrt.2005.074187 </b></span><br />
<span face=""arial" , "helvetica" , sans-serif"><b><br /></b></span> <span face=""arial" , "helvetica" , sans-serif"><b>Rose-Jones LJ, Rommel JJ, Chang PP. </b></span><b style="font-family: Arial, Helvetica, sans-serif;">Heart failure with preserved ejection fraction: an ongoing enigma. </b><b style="font-family: Arial, Helvetica, sans-serif;">Cardiol Clin. 2014; 32:151-61.</b></div>
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<b><br /></b> <b><span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/early/2016/05/19/eurheartj.ehw128.full.pdf" target="_blank">2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure</a></span></b><br />
<b><br /></b> <b><span face=""arial" , "helvetica" , sans-serif" style="font-size: large;"><br /></span></b><br />
<b><span face=""arial" , "helvetica" , sans-serif" style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/33/14/1787.full.pdf" target="_blank">Guidelines ESC Heart failure acute and chronic -2012</a></span></b><br />
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<span style="font-size: large;"><b><br /></b></span></div>
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<span style="font-size: large;"><b><a href="http://circ.ahajournals.org/content/128/16/e240.full.pdf+html" target="_blank">ACC/AHA Guidelines Heart failure -2013</a></b></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/29/2/270" target="_blank">Classification of the cardiomyopathies: a position statement from the european society of cardiology </a></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/early/2014/08/28/eurheartj.ehu284" target="_blank">2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy </a></span><br />
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<a href="http://content.onlinejacc.org/article.aspx?articleid=1893784" target="_blank"><span style="font-size: large;">2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery</span></a><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/35/35/2383.full.pdf" target="_blank">2014 ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management</a></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span> <span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/31/23/2915.full.pdf" target="_blank">ESC Guidelines for the management of grown-up congenital heart disease</a></span><br />
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<span style="font-size: large;"><a href="http://content.onlinejacc.org/article.aspx?articleid=1188032" target="_blank">ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease</a></span><br />
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<span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/37/1/67" target="_blank">2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension</a></span><br />
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<a href="http://eurheartj.oxfordjournals.org/content/35/43/3033" target="_blank"><span style="font-size: large;">2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism</span></a></div>
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-37444726856635976462016-05-09T19:31:00.001+03:002020-05-17T16:28:46.732+03:00Coronary artery disease: Stable-unstable angina and myocardial infarction - Cases of coronary artery disease. <div dir="ltr" style="text-align: left;" trbidi="on">
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Coronary artery disease: Stable-unstable angina and myocardial infarction - Cases of coronary artery disease. </h2>
<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="font-size: large;">IMPORTANT NOTE : THE SITE IS UNDER DEVELOPMENT AND CONTENTS ARE CONTINUOUSLY ADDED.</span><br />
<b><span style="font-size: large;"><br /></span></b> <b><span style="font-size: large;">VIDEO: A case of coronary artery disease: ECG, echocardiogram, coronary angiography and treatment.</span></b><br />
<span style="font-size: large;"><span style="font-size: 13.3333px;"><span style="font-size: large;"><b><br /></b></span></span></span> <iframe allowfullscreen="" class="YOUTUBE-iframe-video" data-thumbnail-src="https://i.ytimg.com/vi/I0c7D0Dvr5Q/0.jpg" frameborder="0" height="266" src="https://www.youtube.com/embed/I0c7D0Dvr5Q?feature=player_embedded" width="320"></iframe><span style="font-size: large;"><br /></span><br />
<span style="font-size: large;"><br /></span> <span style="font-size: large;"><br /></span><span style="font-size: large;"><b>NOTES</b></span><br />
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<b><span style="font-size: medium;"><br /></span></b></div>
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<h2>
<span style="font-size: large;">Coronary artery disease</span></h2>
<span style="font-size: large;">DEFINITION<br />Coronary artery disease (CAD) is a disease characterized by limitation of coronary blood flow to the myocardium as a result of atherosclerotic lesions. It usually manifests with exertional symptoms (such as stable angina) but also by non-exertional manifestations such as an acute coronary syndrome (unstable angina, Non-ST elevation myocardial infarction, ST- elevation myocardial infarction), arrhythmias and sudden cardiac death.</span><br />
<h3>
<span style="font-size: large;">Risk factors for coronary artery disease </span></h3>
<span style="font-size: large;">These are factors that are linked to an increased probability of a person to have coronary artery disease: Age, male sex, hypertension, hyperlipidemia, diabetes mellitus, tobacco use, family history, obesity, peripheral vascular disease. </span><span style="font-size: large;">Cigarette smoking is probably the most important of the modifiable cardiovascular risk factors. I</span><span style="font-size: large;">n smokers, t</span><span style="font-size: large;">he incidence of CAD is about 3 times higher than in nonsmokers.</span><br />
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<h3>
<span style="font-size: large;"><b>Causes and manifestations of myocardial ischemia and coronary artery disease (CAD)</b></span></h3>
<span style="font-size: large;">Myocardial ischemia is a condition caused by the impairment of coronary blood flow, or by a coronary blood flow which is not adequate to fulfill the needs of the myocardium, either because of a decreased coronary blood flow, or because of an increased myocardial oxygen demand. <br />The most common cause of myocardial ischemia is atherosclerotic coronary artery disease (CAD), which decreases coronary blood flow, but there are also other causes, for example coronary arterial spasm, coronary arterial embolism, congenital anomalies of the coronary arteries, and also conditions causing an increased myocardial oxygen demand, such as myocardial hypertrophy (due to hypertension, aortic stenosis, or cardiomyopathy), severe aortic regurgitation, etc. <br />Manifestations of myocardial ischemia are the following: </span><br />
<span style="font-size: large;">Stable angina, acute coronary syndromes (acute myocardial infarction or unstable angina), arrhythmias and sudden cardiac death.</span><br />
<span style="font-size: large;">The pain or discomfort, that commonly occurs in myocardial ischemia has the following characteristics:</span><br />
<span style="font-size: large;">Central (retrosternal) or left anterior chest discomfort, which is rather diffuse and not sharply localized, often described as squeezing, choking, heavy, and occasionally burning sensation. Discomfort is usually located in the retrosternal (central chest) area with possible radiation to the neck, shoulders, arms, jaw, epigastrium, or back. In some instances, it is located in these areas of radiation without affecting the retrosternal region. This description of the location of the ischemic discomfort holds true not only for stable angina, but also for unstable angina or acute myocardial infarction.</span><br />
<span style="font-size: large;">Angina typically lasts 3 to 5 minutes and usually does not last more than 20 minutes.The pain of acute myocardial infarction usually lasts more than 20-30 minutes and is often more severe than the pain of angina. </span><br />
<span style="font-size: large;">Women and diabetics often may </span><span style="font-size: large;">not </span><span style="font-size: large;">present with the classic symptoms, but they may have dyspnea as the main manifestation. </span><br />
<span style="font-size: large;">The pain of angina is elicited by physical exertion (this is the most usual and characteristic precipitating condition), emotional stress, cold exposure, smoking, sometimes even with light physical activity after consumption of a heavy meal.<br />Associated symptoms can include fatigue, dyspnea, weakness, nausea, diaphoresis (sweating), lightheadedness, altered mental status, and syncope.<br />The transition from stable coronary artery disease to <b>unstable</b> angina must be carefully monitored. Symptoms of concern include <br />more frequent episodes of chest pain, chest pain that occurs at a lower level of exercise than before, has a larger duration, or is less responsive to nitroglycerin than before, or a first episode of chest pain, with characteristics suggestive of myocardial ischemia, in a person with a high or intermediate pretest probability for CAD. <br />A person's <b>pretest probability</b> for CAD is estimated according to age, sex, risk factors and typical or atypical characteristics of symptoms.</span><br />
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<h3>
<span style="font-size: large;">Diagnostic tests for patients with suspected or known coronary artery disease</span></h3>
<span style="font-size: large;">These diagnostic studies are useful to establish the diagnosis, to determine the prognosis and to guide treatment decisions. </span><br />
<span style="font-size: large;">The </span><span style="font-size: large;"><b>Electrocardiogram (</b></span><span style="font-size: large;"><b>ECG)</b> is useful in the assessment of chest pain and helps to stratify patients who are at risk for an adverse event. The baseline ECG of a person with chronic CAD can often be normal (in about 50% of the cases)</span><span style="font-size: large;">. The resting, baseline ECG in some patients with chronic CAD, or stable angina shows focal </span><span style="font-size: large;">abnormal findings of ST segment depression or T wave inversions (negative T waves in leads with a positive net QRS, where a positive T wave, would be expected, see chapter <a href="https://cardiologybookandcases.blogspot.gr/2016/06/the-electrocardiogram-ecg-adult-and.html" target="_blank">The Electrocardiogram</a>). In such cases, ECG findings, although not entirely specific, can raise suspicion of CAD, especially in individuals with risk factors. However, many people with chronic ischemic </span><span style="font-size: large;">heart disease, </span><span style="font-size: large;">have a normal tracing at rest (</span><span style="font-size: large;">even patients with extensive coronary artery disease).</span><span style="font-size: large;"> Moreover, in addition to myocardial ischemia, other </span><span style="font-size: large;">conditions can also produce ST-T wave </span><span style="font-size: large;">abnormalities, such as left ventricular hypertrophy or dilation due to long-standing hypertension, or due to valvular heart disease, cardiomyopathies (especially hypertrophic cardiomyopathy), neurogenic effects, electrolyte abnormali</span><span style="font-size: large;">ties and antiarrhythmic drugs. An important diagnostic finding is a relatively recent change in the ECG in comparison to a previous one, with new ST-T </span><span style="font-size: large;">wave abnormalities on the resting ECG. This finding leads to serious suspicion of CAD</span><span style="font-size: large;"> and often also correlates with the severity of the disease.</span><br />
<span style="font-size: large;"> The presence of pathologic Q waves indicating a previous myocardial infarction, or the presence of persistent ST depression is associated with worse prognosis (higher probability for an unfavorable outcome). </span><br />
<span style="font-size: large;">In patients with chronic CAD, the</span><span style="font-size: large;"> ECG often may reveal various</span><br />
<span style="font-size: large;">conduction disturbances, most frequently left bundle branch block (LBBB) or left </span><span style="font-size: large;">anterior fascicular block. Such findings can raise a suspicion of underlying CAD, especially in people with risk factors, but they are not specific for CAD. They can also occur in patients with another underlying cardiac disorder and in some cases they are idiopathic (occurring in people without any detectable underlying cardiac disorder). </span><span style="font-size: large;">Arrhythmias, especially ventricular premature</span><br />
<span style="font-size: large;">beats, are relatively frequent findings in the ECG of CAD patients, but they are not diagnostic for CAD since they have a low sensitivity </span><span style="font-size: large;">and specificity for coronary artery disease.</span><br />
<span style="font-size: large;">An Electrocardiogram (ECG) is also important for the diagnosis of an acute coronary syndrome (ACS). If the ECG is recorded during cardiac ischemic pain, it usually shows abnormalities such as horizontal or downsloping ST segment depression, or negative T waves 1 mm (0.1mV) or deeper, in leads having a QRS complex with dominant R wave. The ischemic changes often resolve completely after the ischemic pain has subsided, or some abnormalities may persist. In general, t</span><span style="font-size: large;">ransient changes in the T-wave, ST-segment, or conduction patterns point toward a cardiac source of the chest pain. </span><span style="font-size: large;">Less frequently there is ST segment elevation during the ischemic symptoms, which signifies severe transmural myocardial ischemia due to an evolving ST-segment elevation myocardial infarction (STEMI), or rarely due to coronary arterial spasm (variant angina, or Prinzmetal's angina-see the video above). In some cases, the ischemic ST elevation may be preceded by the appearance of tall peaked symmetric T waves. </span><br />
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<span style="font-family: Arial, Helvetica, sans-serif;"><b>A 65-year-old male, smoker, with a history of mild hypercholesterolemia, without any previous history of cardiovascular disease. He had a normal exercise ECG test 8 years ago. He has episodes of substernal pain lasting 15-20 minutes at rest with concomitant numbness in the upper extremities. What does the ECG show and what is the diagnosis?</b></span><br />
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<span style="font-family: Arial, Helvetica, sans-serif;"><b>The ECG shows sinus rhythm and a normal QRS axis but there is ST segment depression with an ischemic pattern in the leads I, V4, V5, V6 . The differential diagnosis is between unstable angina and non ST elevation myocardial infarction (NSTEMI) and the distinction between the two is based on cardiac troponin (which increases in NSTEMI but not in unstable angina). In this case, an increase in troponin was found and the diagnosis of NSTEMI was made. Coronary angiography showed two successive stenoses of 70-80% in the middle portion of the left circumflex coronary artery (LCX) which were treated with angioplasty and stent placement.</b></span><br />
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<span style="font-size: large;">The exercise ECG test </span></h4>
<span style="font-size: large;"> Exercise ECG treadmill test (ETT), or a bicycle exercise ECG test is a useful test especially for people with intermediate risk of CAD for making the diagnosis of CAD, and for people with high risk of CAD , or known CAD, not for diagnostic but mainly for prognostic reasons (to determine the prognosis, which can guide subsequent therapeutic decisions). <br />The exercise ECG test can be selected as a diagnostic test for CAD under the conditions that the patient is able to exercise, has no contraindications for an exercise test and has a normal baseline ECG [so that ischemic ST segment changes with exercise can be assessed and not obscured in the context of an abnormal baseline ECG. Conditions that can obscure exercise ECG findings are a left bundle branch block, a paced rhythm, Wolff Parkinson White syndrome, an ECG pattern of left ventricular hypertrophy with strain, a baseline ST depression of > 1mm (0,1 mV), or treatment with digitalis (digoxin). Usually in these conditions, the usefulness of an ECG exercise test is very limited and it is not selected as a diagnostic test].<br />Stress tests combined with imaging (e.g. myocardial perfusion scintigraphy scan-SPECT, or stress echocardiography) are more expensive but have a higher sensitivity and specificity than the ECG exercise test. They present a good option in order to obtain diagnostic and prognostic information (which can guide treatment decisions). </span><br />
<span style="font-size: large;">These tests are preferred for people with a high pretest probability of CAD because they are more accurate and can provide information regarding the location and the extent of ischemia. They are also preferable for patients with known CAD (for prognostic assessment) and for people with intermediate pretest probability of CAD if they are unable to exercise, or if they have baseline ECG abnormalities that can limit the diagnostic accuracy of an exercise ECG test.</span><br />
<span style="font-size: large;"><b>The resting echocardiogram</b><br />The resting echocardiogram is used to assess left ventricular ejection fraction (LVEF), which is an important prognostic factor that influences therapeutic decisions. It can also demonstrate segmental wall motion abnormalities of the left ventricle, in patients with a previous (old) myocardial infarction, or in patients with active acute myocardial ischemia (during the symptoms of an acute coronary syndrome).</span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>An echocardiographic quiz <span style="background-color: orange;">(Video)</span><span style="background-color: white;">: </span>A diabetic patient. Two echocardiographic views are provided in the video. Which are these views and what is the diagnosis? The answer is provided in the video (at the end).</b></span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">Coronary CT angiography (CTA)</span></h4>
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;">This noninvasive diagnostic test requires intravenous administration of a contrast agent. It is discussed in a separate page, click on this link: <a href="https://cardiologybookandcases.blogspot.com/p/computed-tomography-ct-is-based-on-x.html"><b>CT coronary angiography-CTA (or multidetector computed tomography - MDCT )</b></a></span></div>
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<span style="font-size: large;">Coronary angiography: </span></h3>
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<span style="font-size: large;"> The following patient categories should undergo coronary angiography to assess coronary anatomy for revascularization:</span><span style="font-size: large;"> Patients with high-risk features on non -invasive testing, or </span><br />
<span style="font-size: large;">Patients with angina that limits their daily activities and does not respond adequately to medical treatment, or </span><br />
<span style="font-size: large;">Patients presenting with an acute coronary syndrome (especially an ST elevation myocardial infarction which needs prompt revascularization with a primary PCI, or a non-ST elevation acute coronary syndrome with high, or intermediate risk features). (PCI= percutaneous coronary intervention). <br />Coronary angiography is performed by the insertion of catheters (plastic tubes of specific design and function) through the femoral, radial, or brachial artery into the aortic root in order to engage the ostium of the left and right coronary artery and to achieve a selective infusion of a contrast medium into the coronary arteries. The contrast medium can make the arteries visible on a fluoroscopic screen. Contrast medium, a viscous iodinated solution used to opacify the coronary arteries is usually injected by hand through a multivalve manifold. This is performed with the handle of the syringe raised up (the tip pointing down), in order to avoid injecting any small air bubbles into the arterial circulation (this way any small bubbles float up in the syringe). The contrast medium injection flow rate is usually 2-4 ml/sec, with volumes of 7-10 ml administered in the left coronary artery (LCA) and 2-6 ml in the right coronary artery. </span><br />
<span style="font-size: large;">In coronary angiography, the source of the X-rays is under the patient and the image intensifier, which receives the x rays, is directly above the patient. The image intensifier can be described simply, for practical reasons, as the position of an observer looking at the heart. In right anterior oblique (RAO) views the image intensifier is on the right side of the patient, in left anterior oblique (LAO) views it is on the left side of the patient and in the anteroposterior (AP) view the image intensifier is directly over the patient with the X-ray beam traveling perpendicularly from back to front. In caudal views, the image intensifier is tilted towards the feet of the patient and in cranial views towards the head of the patient. The degrees of the angle that the image intensifier forms with the vertical line to the right or to the left, in RAO and LAO views respectively characterize the view. Moreover, the degrees of the angle between the image intensifier and the vertical axis at the cranial or caudal direction are also mentioned.<br />In the Right Anterior Oblique (RAO) projection the Image intensifier is angled above the right side of the patient’s chest and the heart is visualized from the right side. In the fluoroscopic image, the heart is on the right, its apex points to the right , the ribs go down to the right, the left anterior descending coronary artery (LAD) is on the right side and the circumflex coronary artery (LCX) and the spine are on the left.<br />In the Left Anterior Oblique (LAO) projection the Image intensifier is angled above the left side of the patient’s chest and the heart is visualized from the left side. A general description of the fluoroscopic image is the following: The spine is on the right side, the heart is on the left of the spine, the LAD is on the left and extends to the apex and the LCX is on the right. The ribs go down to the left.<br />In the Anterior- Posterior (AP) projection the Image intensifier is positioned directly above the patient’s mid-chest. The heart is visualized in the image from front to back. <br />In the Lateral projection, the Image intensifier is angled at a 90° angle to the left from the vertical axis, visualizing the heart from the far left side. In the fluoroscopic image, the LAD is on the far left and nearest to the sternum and the LCX and the spine are on the right side. <br />In Caudal views the Image intensifier is angled toward the patient’s feet, visualizing the heart from below. These projections tend to foreshorten LAD and elongate the LCx. So, they optimize visualization of LCx and OM (obtuse marginal branches of the LCX). </span></div>
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<span style="font-size: large;">The LAO caudal view of the left coronary artery, also called Spider view, permits a good visualization of the left main coronary artery (LM) and its bifurcation to the LAD and LCx. It is also an excellent view for the proximal and mid LCx, but a poor view for the LAD (considerably foreshortened). <br />In Cranial projections the Image intensifier is angled toward the patient’s head, visualizing the heart from above. They tend to elongate the LAD and foreshorten the LCx. So these views optimize visualization of LAD, and its septal and diagonal branches. <br />Visualization of the right coronary artery (RCA) <br />The Right coronary artery is engaged in the LAO position. Initial imaging of the RCA in this view (LAO 30 degrees) gives the best view of ostial and proximal RCA disease. In the LAO projection, the RCA looks like the letter “C”, the spine is on the right and the ribs are pointed down to the left. <br />In the RAO projection the RCA looks like the letter “L. The ribs point down to the right and the spine is on the left side. The 45 degrees RAO projection permits an excellent visualization of the second (vertical) segment of the RCA and its branches (right ventricular and right marginal artery) and a good view of the posterior descending (posterior interventricular) artery, but the posterolateral branch (retroventricular artery) is not clearly defined. <br />The RAO projection at 120 degrees with cranial angulation at 10 degrees permits a good visualization of the third (horizontal) segment of the right coronary artery and of the retroventricular artery (posterolateral branch) and its branches. </span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: large;"><b style="background-color: #f6b26b;"><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: large;"><b><span style="background-color: #f6b26b;">The procedure of coronary angiography demonstrated in a video</span> (you tube channel Media Space Plus LINK <a href="https://www.youtube.com/watch?v=u7V1KeJBHKM">https://www.youtube.com/watch?v=u7V1KeJBHKM</a></b></span><br />
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<span style="background-color: yellow;"><span class="watch-title" dir="ltr" id="eow-title" style="border: 0px; font-family: "youtube noto" , "roboto" , "arial" , sans-serif; font-size: 20px; font-weight: normal; margin: 0px; padding: 0px;" title="A Patient with NSTEMI Undergoing Complex PCI">A Patient with NSTEMI Undergoing Complex PCI with stenting (a video by </span><span style="font-weight: normal;"><span style="font-size: large;">IsraelHeartOrg</span></span></span></h1>
<span style="font-size: large;"><a href="https://www.youtube.com/watch?v=lHYw37M1A-Q">https://www.youtube.com/watch?v=lHYw37M1A-Q</a></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b style="background-color: orange;">A video of a percutaneous coronary intervention (PCI) of coronary artery bifurcation lesion</b></span><br />
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<span class="watch-title" dir="ltr" id="eow-title" style="background: transparent; border: 0px; margin: 0px; padding: 0px;" title="LAD Bifurcation Lesion By Dr. Samin Sharma From Mount Sinai - New York"><span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;">By Dr. Samin Sharma From Mount Sinai - New York</span></span></h1>
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<span class="watch-title" dir="ltr" style="background: transparent; border: 0px; margin: 0px; padding: 0px;" title="LAD Bifurcation Lesion By Dr. Samin Sharma From Mount Sinai - New York"><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.youtube.com/watch?v=z-3qlpfE1n8">https://www.youtube.com/watch?v=z-3qlpfE1n8</a></b></span></span></div>
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<span style="font-size: large;"><br /><b>Useful links to comprehensive powerpoint presentations on CAD, emphasizing on the basics </b><br />(the first by Dr. Haider Baqai and the second by Dr Ahmed Dabour, Hussain Salha and Osama Nofal )<br /><br /><a href="http://www.slideshare.net/ahsanshafiq90/ihd-30049709">A comprehensive powerpoint presentation of coronary artery disease</a><br /><br /><a href="http://www.slideshare.net/hus100/ischemic-heart-disease-15776504?next_slideshow=1">Coronary artery disease and myocardial infarction PPT</a><br /><br /><br /><b>VIDEO : A case of coronary artery disease. Exercise stress echo and coronary angiography</b></span><br />
<span style="font-size: large;">A case of treadmill exercise stress echocardiography. Τhis is a male patient 50 years old, smoker, with high cholesterol, who presented with mild dyspnea on exertion of 3 months duration. Physical examination and the ECG were without abnormal findings. Echocardiogram at rest was normal. He was tested with a treadmill exercise ECG test combined with echo. The echocardiogram was performed before and immediately after exercise. The stress echocardiography findings, the coronary angiography, and treatment are shown and discussed.</span><br />
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<span style="font-size: large;">Testing for coronary artery disease</span></h3>
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<span style="font-size: large;">Stress echocardiography</span></h4>
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<span style="font-size: large;">Stress echocardiography, introduced in 1979, is used for detec</span><span style="font-size: large;">tion of coronary artery disease and</span><span style="font-size: large;"> for determination of prognosis. S</span><span style="font-size: large;">tress (conditions that increase cardiac work, for example exercise or dobutamine administration) results in wall </span><span style="font-size: large;">motion abnormalities in regions supplied by a stenosed cor</span><span style="font-size: large;">onary artery. These wall motion abnormalities can be recognized </span><span style="font-size: large;">with echocardiography. </span></div>
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<span style="font-size: large;">Treadmill exercise echocardiography is the </span><span style="font-size: large;">most widely used form of exercise echocardiography. Images are </span><span style="font-size: large;">obtained before and immediately after symptom-limited tread</span><span style="font-size: large;">mill exercise, for evaluation of changes in regional </span><span style="font-size: large;">wall motion, ejection fraction and</span></div>
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<span style="font-size: large;">systolic volume. The standard views in stress echocardiography are parasternal long- and </span><span style="font-size: large;">short-axis and apical 4 chamber and 2 chamber views. The </span><span style="font-size: large;">side by side comparison of rest and stress images can make possible the recognition of even </span><span style="font-size: large;">subtle changes. Alternatively, the test may be performed during </span><span style="font-size: large;">either supine or upright bicycling, a technique having the </span><span style="font-size: large;">advantage, that images can be obtained during exercise. Interpretation of a stress echocardiogram depends on a v</span><span style="font-size: large;">isual assessment of left ventricular wall thickening and motion.</span></div>
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<span style="font-size: large;">The hallmark of stress- induced ischemia (inadequate blood supply with respect to the demand) is the development of a new wall motion abnormality </span><span style="font-size: large;">( an abnormal contractile function of one or more myocardial segments)</span><span style="font-size: large;"> during stress or worsening of a wall motion abnormality that was present at rest.</span></div>
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<span style="font-size: large;">Normally with exercise, ejection fraction markedly increases and all left ventricular walls become hyperdynamic (that is, they demonstrate increased contractility). </span></div>
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<span style="font-size: large;">For patients who are unable to perform physical exercise, </span><span style="font-size: large;">pharmacologic stress testing with dobutamine (a β-1 adrenergic receptor agonist that increases contractility and heart rate), or the vasodilators </span><span style="font-size: large;">dipyridamole or adenosine can be used. Dobutamine is the </span><span style="font-size: large;">pharmacologic stress agent</span><span style="font-size: large;"> most </span><span style="font-size: large;">commonly used in stress </span><span style="font-size: large;">echocardiography.</span></div>
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<span style="font-size: large;">Coronary angiography in stable CAD</span></h4>
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<span style="font-size: large;">Coronary angiography is indicated for the diagnosis </span><span style="font-size: large;">of coronary artery disease when the risks of the procedure are </span><span style="font-size: large;">outweighed by the likely benefits of accurate diagnosis and the </span><span style="font-size: large;">patient is willing to consider a therapeutic procedure, if a sig</span><span style="font-size: large;">nificant problem is found. </span></div>
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<span style="font-size: large;">In </span><span style="font-size: large;">stable coronary artery disease coronary angiography has a class I indication for purposes of revascularization, for patients whose angina is poorly controlled by medical treatment or who are intolerant of antianginal medications.</span></div>
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<span style="font-size: large;">In patients with an abnormal stress test (for example ECG exercise test, or stress echocardiography, or myocardial perfusion scintigr</span><span style="font-size: large;">aphy-SPECT scan) the main indications for coronary angiography are the following: A stress test that is positive at a low workload (6 metabolic equivalents of oxygen consumption or less) or that is classified as high risk, is a class I (absolute) indication for coronary angiography, even if the patient is asymptomatic. </span></div>
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<span style="font-size: large;">High-risk findings in noninvasive (stress) tests for coronary artery disease </span></h4>
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<span style="font-size: large;"> A high-risk ECG exercise test is characterized by an ST depression horizontal or downsloping of at least 2 mm in multiple leads or persisting into recovery for 5 minutes or more, or an ST elevation of 2 mm in leads without Q waves, a drop in blood pressure of > 10 mm Hg with exercise, or development of ventricular tachycardia with exercise.</span></div>
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<span style="font-size: large;"> A high-risk stress test on a concomitant imaging modality (scintigraphy, echocardiography) is one showing left ventricle dilatation with stress, or a drop in ejection fraction with exercise, or multiple areas of ischemia suggesting multivessel disease, or an extensive area of reversible ischemia. </span></div>
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<span style="font-size: large;">A positive stress test without high-risk criteria is a relative indication for coronary angiography (class II indication): The doctor may decide to proceed with coronary angiography based on his clinical judgment and the patient's preference if the stress test is positive, with intermediate risk findings. </span></div>
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<h3>
<b style="font-size: x-large;">Medical treatment of chronic coronary artery disease (CAD):</b></h3>
<span style="font-size: large;"><b>Modifiable risk factors</b> such as hypertension, hyperlipidemia (dyslipidemia), obesity and smoking should be suitably treated, to stop the progress of CAD and reduce the risk of acute events. </span><span style="font-size: large;"><br /></span><br />
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<span style="font-size: large;">Lowering of LDL-cholesterol and the role of statins</span></h4>
<span style="font-size: large;">Lowering of LDL-cholesterol has been shown to reduce cardiovascular disease event rates, not only in patients with CAD, but also in people with hypercholesterolemia (elevated blood cholesterol) but without diagnosed cardiovascular disease. <br />Trials have shown that in patients with evidence of CAD or vascular disease, with normal or elevated cholesterol levels, statins decrease mortality, the rate of myocardial infarction (MI) and stroke, and the need for coronary artery by-pass grafting surgery (CABG). These trials are the following: Scandinavian Simvastatin Survival Study (4S), Cholesterol and Recurrent Events (CARE), Long-term Intervention with Pravastatin in Ischemic Disease (LIPID), and Heart Protection Study (HPS).</span><span style="font-size: large;"> </span></div>
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<span style="font-size: large;"> In CAD patients guidelines recommend achieving LDL-cholesterol levels <70 mg/dL or reduction in LDL-cholesterol by more than 50% with high-intensity treatment with statins (3-hydroxy-3-methylglutaryl coenzyme reductase inhibitors </span><span style="font-size: large;">= HMG-CoA reductase inhibitors). </span><span style="font-size: large;">The side effects of statin therapy, including myositis and hepatitis, are rare. Liver tests (transaminases-AST, ALT) and blood levels of CPK evaluation are recommended prior to initiation of therapy (or increase in dose) and 2- 3 months there- after. Blood tests are not necessary for routine follow-up of patients who are stable on statins and should only be measured in case of clinical suspicion of a side effect.</span><br />
<span style="font-size: large;"> Secondary goals of dietary, lifestyle, and pharmacologic therapies are HDL cholesterol > 45 mg/dL and triglycerides < 150 mg/dL. </span><br />
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<span style="font-size: large;">Nitrates</span></h4>
<span style="font-size: large;">Nitrates are indicated in patients with angina. They provide a source of nitric oxide, which relaxes vascular smooth muscle and inhibits platelet aggregation. Nitrates are strong venodilators, and in higher doses they can also induce arterial dilatation. They reduce myocardial oxygen demand by reducing preload through venodilatation and in high doses they also induce coronary artery dilatation of stenotic vessels and intracoronary collaterals. Nitrates<br />prevent recurrent episodes of angina and increase exercise tolerance. Despite the improvement in symptoms, a survival benefit with the use of nitrates for chronic stable angina has not been shown by any randomized study. Dosing should allow for a nitrate-free interval of about 8 hours (usually at night) for preventing tolerance. (Tolerance is a gradual reduction in drug effectiveness during chronic treatment with nitrates). Use of long-acting tablets or transcutaneous delivery systems (nitrate patches) improves compliance but still necessitates a nitrate-free interval. <br />Side effects of nitrates: Oral nitrates should be taken with meals to prevent gastrointestinal disturbances, such as the burning sensation of gastrointestinal reflux (heartburn). Headache is common but is severity usually decreases with continued treatment and often can be controlled by decreasing the dose and/or paracetamol. Nitrates decrease blood pressure due to vasodilation, thus postural hypo- tension or dizziness can occur. Concurrent use of nitrates and PDE5 inhibitors like sildenafil (Viagra), tadalafil, etc can lead to severe hypotension and is absolutely contraindicated.</span><br />
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<h4>
<span style="font-size: large;">Beta-Blockers</span></h4>
<span style="font-size: large;">Beta-Blockers competitively inhibit catecholamines from binding<br />to beta-adrenergic receptors. Beta-Blockers reduce myocardial oxygen demand through a negative inotropic effect (reduction in the force of myocardial contraction), a negative chronotropic effect (reduction of heart rate), and a reduction in left ventricular wall stress. When beta-blockers are used in the treatment of angina, a goal resting heart rate should be between about 55 -60 beats/minute. Beta-Blockers decrease mortality after myocardial infarction (MI). Among patients with stable angina without prior MI mortality reduction is not proven, although symptomatic improvement is well documented. Beta blockers also reduce mortality in patients with heart failure with reduced ejection fraction.<br />Side effects of beta blockers: The most important side effects are caused by blockade of beta -2 receptors. However, significant side effects do not occur frequently and as mentioned above, for some patient subsets beta blockers are a potentially lifesaving therapy. Thus we should try to offer this therapy (with caution) even to some patients considered to be at greatest risk for adverse effects.<br />Potential side effects: bronchoconstriction, masking of symptoms caused by hypoglycemic reaction among patients receiving treatment for diabetes, exacerbation of symptoms of peripheral vascular disease, and side effects from the central nervous system (CNS) and occasionally decreased libido (decrease in sexual drive), impotence, and reversible alopecia can occur. The CNS side effects such as somnolence, depression and vivid dreaming are thought to be related to the lipid solubility of these drugs (they are more frequent with the more lipid soluble beta- blockers).<br />In patients with a pre-existing conduction system disorder beta- blockers can lead to symptomatic bradycardia.<br />In patients with left ventricular (LV) systolic dysfunction beta blockers especially if they are not initiated in small doses can cause precipitation or worsening of heart failure (due to their negative inotropic effect). It is a fact that beta blockers are indicated for patients with LV systolic dysfunction, but they should be initiated in small doses and increases in dosage should be gradual. In this way, they are usually well tolerated and have beneficial effects on these patients. The condition of a patient with NYHA class III or IV heart failure should be stabilized before beta-blocker therapy is instituted.<br />Beta blockers are contraindicated in patients with bradycardia and caution is needed in those with reactive airway disease (asthma, bronchospasm), because they may aggravate bronchospasm (especially the non-selective beta-blockers)<br />Beta blockers have a small adverse effect on the lipid profile by mildly increasing LDL cholesterol and triglycerides and decreasing HDL cholesterol.<br />Drug interactions: The combination if a beta blocker with a non-dihydropyridine calcium channel blocker (verapamil or diltiazem) should be avoided (in most cases) because there is a risk of severe bradycardia or hypotension.</span><br />
<span style="font-size: large;"> Atenolol is renally excreted and should be used with caution in patients with renal dysfunction and in the elderly. </span><span style="font-size: large;"></span><br />
<span style="font-size: large;">[Doses of beta blockers usually prescribed for angina:<br />Metoprolol (tartrate</span><span style="font-size: large;">)</span><span style="font-size: large;"> 25–200 mg x 2 times/day</span><br />
<span style="font-size: large;">Metoprolol succinate (sustained release form) 25-200 mg x 1 time/day</span><br />
<span style="font-size: large;">Atenolol 25–200 mg PO one time/day</span><br />
<span style="font-size: large;">Propranolol 80–320 mg/day, divided in 2 -3 doses </span><br />
<span style="font-size: large;">Propranolol (long-acting form) 80–160 mg x 1 time/day.</span><br />
<span style="font-size: large;">Carvedilol 6.25–25 mg x 2 times/day]</span><br />
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<h4>
<span style="font-size: large;">Calcium channel blockers (CCBs)</span></h4>
<span style="font-size: large;">Calcium channel blockers (CCBs) are classified as dihydropyridines, or non-dihydropyridines (the latter category includes only verapamil and diltiazem). Calcium channel blockers positively alter myocardial oxygen supply and demand, through direct arterial vasodilatation. The non-dihydropyridines also have useful negative chronotropic and inotropic effects, which result in further lowering myocardial oxygen demand. Thus, CCBs have antianginal effect. Dihydropyridines, when used, should be given in the form of sustained-release preparations. CCBs must be avoided </span><span style="font-size: large;">in patients with </span><span style="font-size: large;">left ventricular systolic dysfunction, with the exception of </span><span style="font-size: large;">amlodipine and felodipine, which are usually well tolerated in these patients.</span></div>
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<h4>
<span style="font-size: large;">Ranolazine</span></h4>
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<span style="font-size: large;">Ranolazine is a new antianginal agent, for the treatment of stable angina indicated for patients who remain symptomatic while on standard antianginal medical treatment. Its mechanism of </span><span style="font-size: large;">action is probably through effects on sodium shifts and intracellular </span><span style="font-size: large;">levels of </span><span style="font-size: large;">calcium.</span><span style="font-size: large;"> Side effects include dizziness, nausea, constipation, and mild prolongation of the QT interval. Dosage is 500-1000 mg x 2 times/day. Ranolazine should </span><span style="font-size: large;">be used with caution in patients who are taking other medications that can </span><span style="font-size: large;">prolong the QT interval and in </span><span style="font-size: large;">patients with hepatic dysfunction.</span><br />
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<span style="font-size: large;">Ivabradine</span></h4>
<span style="font-size: large;">It inhibits the I</span>f<span style="font-size: large;"> current in the pacemaker cells of the sinus node, producing a bradycardic effect, without other hemodynamic effects. As with beta- blockers, also with ivabradine target resting heart rate should be about 55-60 /minute (dosage is individualized to achieve this heart rate). In patients with stable angina, it increases exercise tolerance and time from the onset of exercise to the onset of ischemia. </span><br />
<span style="font-size: large;">Ivabradine is used as an adjunct to beta-blocker therapy for treatment of chronic stable angina pectoris in patients with inadequately controlled symptoms or as a substitute for beta-blocker therapy in patients with a contraindication or intolerance to beta-blockers. </span><span style="font-size: large;"> </span><span style="font-size: large;">It has shown improvement in anginal symptoms but did not show a reduction in adverse cardiovascular outcomes (new myocardial infarction or death). Ivabradine</span><span style="font-size: large;"> is not used in patients with atrial fibrillation and it is contraindicated in patients with bradycardic disorders (e.g. sick sinus syndrome), generally when resting heart rate is < 60/min prior to treatment, or severe hepatic dysfunction. </span><br />
<span style="font-size: large;">Concomitant use with non-dihydropyridine calcium-channel blockers (diltiazem, verapamil) should be avoided because it increases plasma ivabradine concentrations, and may also exacerbate bradycardia </span><br />
<span style="font-size: large;">No dosage adjustment is required for patients with renal dysfunction and creatinine clearance 15-60 mL/minute and in patients with mild to moderate hepatic dysfunction. </span><br />
<span style="font-size: large;">Dose range is 2.5-10 mg x 2 times/day.</span><br />
<span style="font-size: large;">Potential adverse effects: sinus bradycardia, a mild visual disturbance (due to an effect on retinal ion channels )</span></div>
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<h4>
<span style="font-size: large;">Antiplatelet Therapy</span></h4>
<span style="font-size: large;">An acute coronary syndrome is usually caused by a platelet-rich thrombus (an intravascular blood clot) occurring at the site of a coronary artery stenosis, after </span><span style="font-size: large;">rupture of an atheromatic</span><span style="font-size: large;"> plaque. Antiplatelet medications decrease morbidity and mortality in patients with coronary artery disease (CAD) or peripheral vascular disease, because they decrease the rate of myocardial infarction. For patients with stable CAD, low-dose aspirin (80–100 mg daily) is as effective as higher doses (300 mg). In patients with CAD, aspirin therapy achieves a 26% reduction in myocardial infarction. The number of patients needed to treat to prevent a myocardial infarction is 83. The Antiplatelet Trialists’ Collaboration Study demonstrated in high-risk cardiovascular patients treated with antiplatelet therapy a reduction in myocardial infarction, stroke, and death. </span><span style="font-size: large;">Thus, guidelines recommend in all patients with CAD indefinite (life-long) aspirin treatment for the secondary prevention of cardiovascular events. In patients with allergy or intolerance to aspirin, clopidogrel is given instead of aspirin. Among patients with allergy or intolerance to aspirin, clopidogrel has been shown to decrease the frequency of fatal and nonfatal vascular events in peripheral arterial, cerebral arterial disease, and CAD.</span><br />
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<span style="font-size: large;">D</span><span style="font-size: large;">ual antipla</span><span style="font-size: large;">telet therapy with aspirin and clopidogrel or aspirin plus one of the newer antiplatelet agents, </span><span style="font-size: large;">ticagrelor or</span><span style="font-size: large;"> </span><span style="font-size: large;">prasugrel,</span><span style="font-size: large;"> is administered to patients with an </span><span style="font-size: large;">ACS ( </span><span style="font-size: large;">unstable angina, or acute myocardial infarction). Aspirin plus clopidogrel is administered after a percutaneous coronary intervention -PCI (angioplasty usually with stenting) in cases of stable CAD for 1-2 months after intracoronary placement of a bare metal stent (BMS) or for 6-12 months after placement of a drug-eluting stent-DES (these stents are preferred due to a lower rate of in-stent restenosis of the artery). In patients treated with PCI for an acute coronary syndrome (ACS) aspirin plus clopidogrel, or aspirin plus ticagrelor, or aspirin plus prasugrel are given preferably for 12 months (in patients with a BMS or a DES). When the appropriate time of dual antiplatelet therapy elapses, antiplatelet therapy only with aspirin continues indefinitely.</span></div>
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<h4>
<span style="font-size: large;">Revascularization for coronary artery disease (CAD)</span></h4>
<span style="font-size: large;">Besides medical treatment, other treatment options for CAD are therapies, that achieve <b>revascularization</b>, i.e. the restoration of </span><span style="font-size: large;">blood flow to myocardial territories with reduced blood flow, due to significantly stenotic or occluded arteries. These treatment options include percutaneous coronary intervention i.e. percutaneous transluminal angioplasty with stent placement (PCI) or coronary artery by-pass grafting (CABG). CABG </span><span style="font-size: large;">compared with medical treatment </span><span style="font-size: large;">has been proven to decrease cardiovascular mortality in specific patient subsets with CAD. </span><br />
<span style="font-size: large;">Randomized trials of patients with mild to moderate stable angina have shown </span><span style="font-size: large;">an improved survival rate for patients treated with</span><br />
<span style="font-size: large;">initial CABG, compared with those treated with initial medical treatment, in the following circumstances:</span><br />
<span style="font-size: large;">A left main (LM) stenosis > 50% of the diameter,</span><br />
<span style="font-size: large;">Triple- </span><span style="font-size: large;">vessel disease (significant stenosis of three coronary arterial vessels)</span><br />
<span style="font-size: large;"> Double-vessel disease (significant stenosis in 2 arteries) with a proximal left anterior descending LAD lesion, </span><br />
<span style="font-size: large;">Double vessel disease with abnormal </span><span style="font-size: large;">left ventricular systolic function, or a strongly positive exercise test result,</span><br />
<span style="font-size: large;">A proximal LAD lesion causing documented myocardial isch</span><span style="font-size: large;">emia. </span><br />
<span style="font-size: large;">Therefore, the above patient subsets, are these that have a survival benefit from surgical revascularization (coronary artery by- pass grafting-CABG).</span><br />
<span style="font-size: large;"> In patients with stable CAD, </span><span style="font-size: large;">PCI has been shown to effectively improve anginal symptoms and quality of life in comparison with medical treatment. </span><span style="font-size: large;">For patients with stable CAD and significant coronary lesions </span><span style="font-size: large;">(i.e. lesions with stenosis </span><span style="font-size: large;">≥50% </span><span style="font-size: large;"> that causes reversible ischemia in non-invasive functional tests, or </span><span style="font-size: large;">with reduced fractional flow reserve: FFR < </span><span style="font-size: large;">0.8 measured invasively at the time of coronary arteriography, or with stenosis </span><span style="font-size: large;">≥ 90%)</span><span style="font-size: large;"> in one or more arteries, an initial PCI results in the following : A signifi</span><span style="font-size: large;">cant reduction in anginal symptoms and in the need for hospitalization for urgent revascularization. (For an explanation of FFR see below) Thus, PCI is a reasonable choice for these patients, especially if there are anginal symptoms despite medical treatment or evidence of substantial ischemia. However, PCI has </span><span style="font-size: large;">not been shown to reduce the composite endpoint of MI or death in these patients. A </span><span style="font-size: large;">decrease in mortality has not been proven with PCI in randomized controlled trials (RCTs) in comparison with optimal medical treatment. </span><br />
<span style="font-size: large;">Thus, </span><span style="font-size: large;">a trial </span><span style="font-size: large;">of optimal medical therapy to control symptoms and reduce mortality is justifiable and cost-</span><span style="font-size: large;">effective, for patients with stable coronary disease not associated with </span><span style="font-size: large;">anatomic features for which revascularization has been shown to prolong life, and not accompanied by anginal symptoms resistant to medical treatment.</span><br />
<span style="font-size: large;"> PCI in patients with chronic CAD should not be performed for coronary lesions causing stenosis of the arterial diameter <50 %, or a stenosis 50-90% with FFR > 0.8</span><span style="font-size: large;">, or without documented substantial ischemia on non-invasive testing. </span><br />
<span style="font-size: large;">The </span><span style="font-size: large;">fractional flow reserve (FFR), during maximum hyperemia (usually </span><span style="font-size: large;">induced by vasodilation of the peripheral coronary circulation-the arterioles- with intravenous adenosine) is the ratio of the pressure distal, divided by the pressure proximal to a coronary arterial stenosis. These pressures can be measured at coronary angiography with the appropriate equipment ( a pressure wire that is advanced through the arterial stenosis) after maximal peripheral vasodilation of the coronary arterial bed with the administration of adenosine. </span><br />
<span style="font-size: large;">An FFR (distal pressure/proximal pressure) <0.80 documents the hemodynamic severity of the coronary lesion and predicts</span><span style="font-size: large;"> a clinical benefit from PCI, whereas an FFR greater than 0.80 has been correlated with clinical harm from PCI, which should not be performed in this case. FFR measurement is not necessary if noninvasive tests have shown that a coronary stenosis causes substantial reversible ischemia, because this is an adequate proof, that the coronary lesion is hemodynamically significant. FFR measurement is also not necessary if there is a diameter stenosis of the arterial lumen </span><span style="font-size: large;"> </span><span style="font-size: large;">≥ 90%.</span><br />
<span style="font-size: large;"><b>Revascularization,</b> with either PCI or CABG (depending on the extent and anatomic-angiographic characteristics of coronary artery disease), is <b>appropriate</b>, for the following patient categories:</span><br />
<span style="font-size: large;">Patients who remain symptomatic despite intensive medical (drug) therapy.</span><br />
<span style="font-size: large;">Patients with evidence of ischemia of substantial severity, or involving an extensive myocardial region, regardless of the presence or absence of symptoms. Severe or extensive ischemia is documented by high-risk findings in functional tests, such exercise ECG testing, stress echocardiography, or myocardial perfusion scintigraphy (SPECT imaging).</span><br />
<span style="font-size: large;">Patients with stable (or unstable) CAD </span><span style="font-size: large;">who meet certain anatomic criteria: Signifi</span><span style="font-size: large;">cant LM coronary artery disease, significant three-vessel disease, or significant two-vessel </span><span style="font-size: large;">coronary artery disease with left ventricular systolic dysfunction ( EF< 50%), or significant stenosis at the proximal segment of the LAD.</span><br />
<span style="font-size: large;"></span><br />
<span style="font-size: large;">Patients with a STEMI (ECG findings of ST elevation, or new or presumably new left bundle branch block, or ECG findings of a true posterior myocardial infarction- click on the link to see chapter about the <a href="https://cardiologybookandcases.blogspot.gr/2016/06/the-electrocardiogram-ecg-adult-and.html" target="_blank">ECG</a> </span><span style="font-size: large;">for details- and symptoms compatible with an acute coronary syndrome ) in the first 12 hours of symptom onset. For these patients, a primary PCI is the preferred reperfusion strategy.</span><br />
<span style="font-size: large;">Patients with unstable angina or NSTEMI and high (or even intermediate) risk features. </span></div>
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<h4>
<br /><span style="font-size: large;">The choice between PCI and CABG for revascularization in coronary artery disease (CAD) and the SYNTAX score</span></h4>
<span style="font-size: large;">In patients with stable CAD and an indication for revascularization (eg anginal symptoms despite medical treatment, or findings of severe or extensive ischemia in noninvasive tests), the choice is between PCI and CABG. In such patients significant lesions in one or two coronary arteries (ie 1 or 2 vessel disease) with a normal, or near normal left ventricular contractile function generally favor the choice of PCI, if the anatomy of the lesions is suitable (eg lesions of small to moderate length, without severe calcification, without total vessel occlusion, or vessel tortuosity etc). The presence of left main or 3 vessel disease generally favors CABG, but if the SYNTAX score is low, then PCI can also be an appropriate option. The SYNTAX score is used to grade the anatomic complexity of the coronary lesions and thus the difficulty of PCI, in patients with left main or multivessel disease and generally, a high SYNTAX score suggests selecting CABG and not PCI as the revascularization strategy (see below).</span><br />
<span style="font-size: large;">In general, CABG improves survival among patients with complex multivessel or left main CAD. Patients especially likely to benefit from CABG are those with </span><span style="font-size: large;">more severe, more diffuse and complex CAD (a high SYNTAX score) and apart from the extent of CAD, also the presence of diabetes, left ventricular dysfunction, or mitral valve dysfunction (moderate to severe) are factors that tend to support the choice of CABG. </span><br />
<span style="font-size: large;"><span style="font-family: inherit;"><span style="background-color: white;">T</span></span>he SYNTAX score is an anatomic scoring system, based on the coronary angiogram, which quantifies CAD lesion complexity </span><span style="font-size: large;">in patients with multivascular and/or left main disease </span><span style="font-size: large;">and predicts clinical outcomes after percutaneous coronary intervention (PCI) or coronary artery by-pass grafting (CABG). The drawback to this score is that it does not include clinical features, such as the age of the patient, left ventricular function, the presence of diabetes, chronic renal failure or neurologic impairment, which also profoundly affect the treatment decision.</span><br />
<span style="font-size: large;">A newer development is the<u> SYNTAX score II,</u> which apart from the anatomy of the coronary lesions, also takes into account some clinical variables, such as age, sex, renal function (creatinine clearance), the presence of peripheral vascular disease or chronic obstructive lung disease and the left ventricular EF.</span></div>
<span style="font-size: large;">The SYNTAX score was initially established by the SYNTAX </span><span style="font-family: "arial" , "helvetica" , sans-serif;"><b>( Synergy between PCI with Taxus and Cardiac Surgery) </b></span><span style="font-size: large;">study, which randomly assigned 1800 patients with either three-vessel or left main stable coronary artery disease to CABG or PCI. For each patient, the SYNTAX score was determined, as a measure of the extent and complexity of CAD and the anticipated complexity and risk of PCI.</span></div>
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<span style="font-size: large;">The complexity of coronary artery disease (CAD) and the risk associated with PCI is classified with the SYNTAX score as:</span></div>
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<span style="font-size: large;"> low ( score ≤22), </span></div>
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<span style="font-size: large;">intermediate ( score 23 - 32), </span></div>
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<span style="font-size: large;">or high (score ≥33).</span><br />
<span style="font-size: large;">As a general rule, this randomized study demonstrated that patients who had SYNTAX scores >34 appeared to do much better with bypass surgery than those with lower SYNTAX scores, in whom PCI was just as good for major adverse cardiac events, with lower stroke rates.</span></div>
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<span style="font-size: large;"> In patients with the least complex three-vessel disease (SYNTAX score ≤22), the SYNTAX trial showed that PCI was non-inferior to CABG.<br />In patients with more complex three-vessel disease (SYNTAX score ≥23), CABG was superior to PCI.<br />In the SYNTAX study, </span><span style="font-size: large;">in patients with isolated left main coronary artery disease or left main coronary artery disease and single-vessel coronary artery disease (SYNTAX score <33) </span><span style="font-size: large;">the outcomes of the two procedures were the same. </span></div>
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<span style="font-size: large;">However, in patients with left main and two- or three-vessel coronary artery disease (SYNTAX score ≥33), the outcome was better with CABG (in this group CABG resulted in a significant reduction in the rate of the composite endpoint of death, myocardial infarction, stroke, or repeat revascularization compared with PCI). </span><br />
<span style="font-size: large;">To calculate the SYNTAX score for a patient the following site provides you with directions and a calculator:</span><br />
<span style="font-size: large;"><a href="http://www.syntaxscore.com/" target="_blank">http://www.syntaxscore.com/</a></span><br />
<h3>
<span style="font-size: large;">Choice between </span><span style="font-size: large;">PCI and </span><span style="font-size: large;">CABG in patients with acute coronary syndromes</span></h3>
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<span style="font-size: large;">The evidence for the comparison of these two methods of revascularization is almost entirely based on studies of patients with stable CAD. Nevertheless, the recommendations for CABG are commonly extended to include patients with unstable angina and stable NSTEMI, with a high SYNTAX score. </span></div>
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<span style="font-size: large;">For patients with acute STEMI</span><span style="font-size: large;">, the best initial treatment is prompt reperfusion therapy with either PCI or fibrinolytic therapy. In patients with acute STEMI, </span><span style="font-size: large;">PCI </span><span style="font-size: large;">restores coronary blood flow more rapidly, preserves more myocardium, and improves outcomes, </span><span style="font-size: large;">compared with CABG. CABG in patients with acute STEMI is reserved for those who have a coronary anatomy that is not amenable to PCI or who have mechanical complications, such as ventricular septal defect, myocardial rupture, or papillary muscle rupture with acute, severe mitral regurgitation.</span><br />
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<span style="font-size: large;"><span class="fontstyle0">The cardiac syndrome X </span></span></h3>
<span style="font-size: large;"><span class="fontstyle2">This term refers to those patients with a history of angina (usually a typical history), a positive ECG exercise test or an imaging test positive for ischemia and angiographically normal coronary arteries. Cardiac syndrome X is much more common in women<br />than in men. The prognosis of these patients is good, but they are<br />often highly symptomatic and can be difficult to treat. The most probable cause of this condition is an abnormal vasodilator response of the coronary microvasculature to stress</span> (e.g. during exercise). </span><br />
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<span style="font-size: large;">The acute coronary syndromes (unstable angina and acute myocardial infarction STEMI or NSTEMI) </span></h3>
<span style="font-size: large;"><span class="fontstyle0">The term acute coronary syndrome (ACS) encompasses a group of conditions in which acute myocardial ischemia occurs secondary to a sudden disruption in coronary blood supply to a territory of the heart. This disorder ranges from myocardial tissue ischemia (unstable angina) to the development of necrosis (non-ST or ST elevation myocardial infarction -NSTEMI and STEMI respectively).</span></span><span style="font-size: large;"><br />In an ST-elevation myocardial infarction</span><span style="font-size: large;"> </span><span style="font-size: large;">(STEMI)</span><span style="font-size: large;">, there is a complete occlusion of the coronary artery. This is characterized by ST elevation on ECG.</span><br />
<span style="font-size: large;">In non-ST elevation myocardial infarction (NSTEMI) or unstable angina, there is a partial occlusion of a coronary artery and this usually manifests on the ECG by ST segment depression or T wave inversion. The severity of ischemia depends on the degree of obstruction, the extent of collateral circulation and the presence of emboli. In unstable angina, there is no myocardial necrosis and troponin is not raised., whereas in non-ST elevation myocardial infarction (NSTEMI) there is a rise in troponin, indicating the presence of myocardial necrosis of variable extent.</span><br />
<span style="font-size: large;"><span class="fontstyle0">These conditions are classified according to the findings in the electrocardiogram (ECG) and biochemical markers of myocardial necrosis.</span> An ACS is</span><span style="font-size: large;"> almost always associated with rupture of an atherosclerotic plaque and thrombus formation with partial or complete occlusion of a coronary artery.</span><br />
<span style="font-size: large;"><span class="fontstyle0">The acute coronary syndromes (ACS) are a major cause of mortality since they account for an estimated 30% of all deaths worldwide. They are more common in males, but they may be underdiagnosed in women.</span> </span><br />
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<h4>
<span style="font-size: large;"><span class="fontstyle0">Clinical presentation of patients with an acute coronary syndrome (ACS)</span></span></h4>
<span style="font-size: large;"><span class="fontstyle2">Patients with an acute coronary syndrome (ACS) usually have a new onset of </span><span class="fontstyle3">chest pain</span><span class="fontstyle2">, chest pain at rest, or a deterioration (worsening) of pre-existing angina. In patients with an ACS, the chest discomfort is usually a </span></span><span style="font-size: large;">crushing </span><span style="font-size: large;">central retrosternal or </span><span style="font-size: large;">left-sided (on the left of the sternum) </span><span style="font-size: large;">pain. The pain is often severe and it</span><span style="font-size: large;"> may radiate to the jaw, neck or arm (usually the left and less commonly to both arms).</span><br />
<span style="font-size: large;">Often the patient does not have a previous history of stable angina (a history of long-standing angina is present in only 20% of the patients with an ACS)</span><span style="font-size: large;"><span class="fontstyle2">However, some patients manifest atypical presenting symptoms such as</span></span><span style="font-size: large;"> </span><span style="font-size: large;">dyspnea, a sense of</span><span style="font-size: large;"> "indigestion" or epigastric pain, syncope, hypotension, or an acute confusional state (especially in elderly patients), or rarely pleuritic chest pain.</span><br />
<span style="font-size: large;">Apart from chest pain, other coexisting features that are often present include a sense of impending doom (angor animi), sweating, pallor, dyspnea (breathlessness), nausea and vomiting. <br />Atypical presentations occur in about 20% of ACS patients, particularly in those with dysfunction </span><span style="font-size: large;">of the </span><span style="font-size: large;">autonomic nervous system (some patients with diabetes mellitus and elderly patients). A myocardial infarction without chest pain is an atypical presentation, referred to as "a silent myocardial infarction".</span></div>
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<h4>
<span style="font-size: large;">Physical examination in acute coronary syndromes </span></h4>
<span style="font-size: large;">Common findings that may be present include Levine’s sign: the patient describes the discomfort with a clenched fist on the chest (specificity about 80%), pallor, diaphoresis (sweating) and anxiety, occasionally a fourth heart sound and low-grade pyrexia can be present in some cases.</span></div>
<span style="font-size: large;">Physical examination can also detect clinical signs indicating an increased severity of the patient's condition such as hypotension, basal crackles, or a systolic apical murmur of mitral regurgitation.</span></div>
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<span style="font-size: large;">The ECG in unstable angina or acute myocardial infarction </span></h4>
<span style="font-size: large;"> ST depression and/or T wave inversion are highly suggestive for unstable angina or NSTEMI, particularly if they are new or associated with anginal chest pain. In some cases, </span><span style="font-size: large;">the 12-lead ECG may be normal in patients with an </span><span style="font-size: large;">ACS, but a normal initial ECG can change later. </span><span style="font-size: large;">The ECG should be repeated when the patient is in </span><span style="font-size: large;">pain, or if there is a clinical suspicion of an ACS. and continuous ST-segment monitoring is recommended. In</span><span style="font-size: large;"> STEMI, </span><span style="font-size: large;">complete occlusion of a coronary artery manifests on the ECG with </span><span style="font-size: large;">persistent ST-elevation or a new left bundle </span><span style="font-size: large;">branch block. (A transient ST elevation can be seen in </span><span style="font-size: large;">coronary vasospasm, a condition called Prinzmetal’s angina). </span><br />
<span style="font-size: large;">ECG features of STEMI are the following:</span></div>
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<span style="font-size: large;">in at least 2 adjacent limb leads: 1 mm ST elevation or<br />in at least 2 contiguous precordial leads 2 mm ST elevation or new<br />onset left bundle branch block (LBBB). </span><br />
<span style="font-size: large;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>A man 70 years old with crushing pain on the center of the chest, nausea, and vomiting. The symptoms started 1 hour ago. What are the ECG findings, which is the diagnosis and what is the preferred treatment?</b></span><br />
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<h4>
<span style="font-size: large;">Answer</span></h4>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Rhythm: sinus with first-degree atrioventricular block (prolonged PR interval). ST segment elevation in leads II, II, avF, diagnostic of an acute inferior wall myocardial infarction (acute inferior STEMI). Q waves are also developing in leads III and avF. The ST segment depression in leads avL and I represent "mirror changes". The ST depression in leads V1, V2 is indicative of a concomitant posterior wall infarction. </b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>Management consists of initial measures such as continuous rhythm monitoring, antiplatelet treatment, morphine, metoclopramide( for vomiting), oxygen if needed (if hemoglobin saturation is<95%), normal saline infusion if there is hypotension, anticoagulation, and emergent coronary reperfusion treatment : Primary PCI if it can be performed within 120 minutes by an experienced team, or otherwise fibrinolysis as soon as possible (within 30 minutes from the first medical contact/ provided there are no contraindications to fibrinolysis).</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif; font-size: medium;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif; font-size: small;"><b>A patient with crushing pain in the central area of the chest, sweating, and pallor. Which is the culprit artery?</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b>ANSWER An acute ST elevation myocardial infarction with ST elevation in leads I, avL, V1-V6</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><span style="font-family: "arial" , "helvetica" , sans-serif;">ST depressions in leads II, III, AVF are reciprocal ("mirror") changes. IT is an extensive anterior acute STEMI and this type of STEMI is usually the result of an occlusion of the LAD ( This case is courtesy of<span style="background-color: yellow;"> Dr. Kazi Ferdous-</span> </span> Dhaka Medical College and Hospital). The patient was treated successfully with primary PCI. You can see below this patient's left coronary angiography before (Image A) and after (Image B) the procedure of primary PCI ( LM left main coronary artery LAD left anterior descending artery LCX left circumflex artery)</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>A</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>B</b></span><br />
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<h4>
<span style="font-size: large;">Biomarkers in acute myocardial infarction</span></h4>
<span style="font-size: large;"><span class="fontstyle0">The best biochemical markers of myocardial infarction are the <b>cardiac troponins</b></span><span class="fontstyle2">: cardiac troponin I and T have a high sensitivity and specificity for acute myocardial infarction. Troponin is useful for the diagnosis, as well as for the assessment of the prognosis in patients with an acute coronary syndrome (ACS).</span></span><span style="font-size: large;"><br />A meta-analysis has shown that an elevated troponin level in patients with ACS without ST-segment elevation is associated with a nearly 4-fold increase in cardiac mortality rate. </span><br />
<span style="font-size: large;">Many trials (such as the TIMI IIIB, GUSTO IIa, GUSTO IV-ACS, and FRISC trial</span><span style="font-size: large;">)</span><span style="font-size: large;"> demonstrated a direct correlation between the level of cardiac troponin (TnI or TnT) and the rate of adverse cardiac events and mortality in patients with ACS.</span><br />
<span style="font-size: large;"><span class="fontstyle2"> Cardiac troponin should be requested on patient presentation and 12 hours after onset of symptoms. Troponin is a marker of myocardial necrosis which starts to be elevated in acute myocardial infarction at 2-4 hours after symptom onset, peaks at about 12-18 hours, and usually remains elevated for approximately 10-14 days.</span></span><br />
<span style="font-size: large;"><span class="fontstyle2"><u>Important Note: In a case of a suspected acute coronary syndrome (ACS) appropriate treatment must start as early as possible (including emergency myocardial reperfusion if there is a STEMI) and so do not wait for the result of troponin to start treatment.</u></span><span class="fontstyle2"><br /></span><span class="fontstyle2">Troponin can also be elevated in other conditions and should not be used in isolation for the diagnosis</span> of acute myocardial infarction. Other conditions in which troponin may be elevated are the following: </span><span style="font-size: large;">myocarditis, pericarditis, acute heart failure, pulmonary embolism, prolonged tachyarrhythmia, renal failure, and sepsis.</span><br />
<span style="font-size: large;"><b>Creatine phosphokinase-MB (CPK-MB)</b></span><span style="font-size: large;">, is the form of the enzyme creatine phosphokinase which is more specific to the heart muscle. It is a good biomarker indicating myocardial necrosis, although it is less sensitive and less specific </span><span style="font-size: large;">compared to cardiac troponin</span><span style="font-size: large;">. In the setting of myocardial infarction, plasma </span><span style="font-size: large;">CK-MB concentrations start to rise about 4-6 hours after the onset of chest pain, peak at 12-24 hours and return to normal (baseline) levels within 24-48 hours. A</span><span style="font-size: large;"> reliable estimate of the size of the infarct can be provided by t</span><span style="font-size: large;">he area under the concentration-time curve for </span><span style="font-size: large;">CK-MB created with serial measurements of its levels. </span><span style="font-size: large;">CK-MB values can </span><span style="font-size: large;">also </span><span style="font-size: large;">rise in conditions different</span><span style="font-size: large;"> than ACS, such as trauma, heavy exertion, and skeletal muscle disease (eg rhabdomyolysis).</span></div>
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<span style="font-size: large;">An overview of the initial treatment of an acute coronary syndrome (unstable angina or acute myocardial infarction)</span></h4>
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<span style="font-family: inherit; font-size: large;">Establish intravenous access (preferably two large bore peripheral venous catheters). </span><span style="font-family: inherit; font-size: large;">Start pulse oximetry and continuous ECG monitoring, and give supplemental oxygen if the oxygen saturation (</span><span lang="EN-US" style="font-size: large; line-height: 25.68px;">SaO<sub>2</sub></span><span style="font-family: inherit; font-size: large;">) is less than 95%, or if the patient manifests dyspnea (breathlessness), or signs and symptoms of acute heart failure. </span><br />
<span style="font-size: large;">ECG monitoring is very useful because most deaths caused by an acute myocardial infarction occur early and are due to ventricular fibrillation (VF). Prompt electric defibrillation is mandatory in cases of VF.</span><br />
<span style="font-family: inherit; font-size: large;">Give immediately</span><span style="font-family: inherit; font-size: large;"> aspirin 250-325 mg (usually we give 1/2 tablet 500 mg, which is chewed by the patient, for quick absorption).</span><span style="font-size: large;"> Apart from aspirin, a second antiplatelet agent is given to patients with an ACS: A loading dose of clopidogrel (300 to 600 mg PO once), or ticagrelor</span><span style="font-size: large;"> (180 mg PO once), or prasugrel (60 mg PO once), improves outcomes. Prasugrel and ticagrelor are more rapid in onset and may be preferred in cases of urgent percutaneous coronary intervention (PCI).</span></div>
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<span style="font-family: inherit; font-size: large;"> If there is active chest pain, n</span><span style="font-size: large;">itroglycerin is </span><span style="font-family: inherit; font-size: large;">given sublingually or by spray, provided there are no contraindications (contraindications include hypotension <100 mmHg, acute inferior STEMI with right ventricular infarction, severe stenosis of the aortic valve, recent use of a phosphodiesterase inhibitor-eg sildenafil within the last 24 hours).</span><br />
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<span style="font-family: inherit; font-size: large;">Relief of pain is important because it is associated with sympathetic activation. Sympathetic activation causes vasoconstriction and increases the workload of the heart. For the relief of pain intravenous (IV) morphine is administered</span><span style="color: #2a2a2a; font-family: "proxima_nova_rgregular" , "arial" , sans-serif; font-size: 18px; line-height: 22px;">:</span><span style="font-size: large;"> 2.5-5 mg over 4-5 minutes. It can be repeated, if necessary, every 5-15 minutes. Prior to each dose of morphine, the rate of respiration (number of breaths/minute), the heart rate and blood pressure is assessed, because morphine can cause suppression of the respiratory center and bradycardia or hypotension due to stimulation of the parasympathetic nervous system. The latter two conditions are treated with IV atropine 0.5 mg. In the case of respiratory depression, the action of morphine can be reversed by the intravenous (IV) administration of naloxone (an antidote for opioid drugs) 0.4-0.8 mg. Also, because morphine can cause nausea or vomiting, the antiemetic metoclopramide (Primperan) 5-10 mg is administered IV.</span><br />
<span style="font-size: large;">To patients with an ACS besides antiplatelet drugs, aspirin and clopidogrel (ticagrelor, or prasugrel can be used instead of clopidogrel), also anticoagulant treatment must be initiated with low molecular weight heparin or unfractionated heparin, or bivalirudin.</span><br />
<span style="font-size: large;">Bivalirudin is recommended as an anticoagulant for patients with a known or suspected history of heparin-induced thrombocytopenia.</span><br />
<span style="font-size: large;">Oral treatment with beta-blockers should be administered early to patients with ACS, (or an initial intravenous dose, followed by oral treatment) </span><span style="font-size: large;">and continued thereafter </span><span style="font-size: large;">unless there is a contraindication. Contraindications of beta-blockers include bradycardia, hypotension, acute congestive heart failure, severe bronchospasm. Non-stabilized patients with acute heart failure are <u>not </u>treated with beta-blockers, but beta blockers (especially carvedilol, bisoprolol, or metoprolol) are indicated in the treatment of patients with chronic heart failure with systolic left ventricular dysfunction after the acute non-compensated phase. </span><br />
<span style="font-size: large;">Prompt initiation of statin therapy (high dose of a statin e.g. atorvastatin 40-80mg/day) regardless of the baseline levels of LDL cholesterol is recommended </span><span style="font-size: large;">during hospitalization</span><span style="font-size: large;"> in all patients with an acute coronary syndrome (ACS) </span><span style="font-size: large;">to promote plaque stabilization and to restore endothelial function. </span></div>
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<span style="font-size: large;"><u>Timely treatment of the patient with an ACS (and especially STEMI) is very important, thus minimizing delays in the administration of appropriate treatment and in the transfer to the appropriate facility (hospital) is associated with improved outcomes</u>.</span>
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<span style="font-size: large;">To minimize patient delay, the public should be made aware of how to recognize common symptoms of acute myocardial infarction and instructed to call the emergency services immediately on such an occasion.</span><br />
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<span style="font-size: large;">Reperfusion treatment in patients with STEMI</span></h4>
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<span style="font-size: large;">In patients with ST segment elevation myocardial infarction (STEMI) reperfusion therapy (restoration of flow in the occluded coronary artery) is indicated in all patients with symptoms of <12 h duration and persistent ST-segment elevation or new (or presumed new) left bundle branch block (LBBB). </span></div>
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<span style="font-size: large;">Reperfusion therapy (preferably primary PCI) is also indicated</span><span style="font-size: large;"> </span><span style="font-size: large;">even if symptoms have started >12 h before,</span><span style="font-size: large;"> if there is evidence of ongoing myocardial ischemia. </span><span style="font-size: large;">Primary PCI is defined as an emergent percutaneous catheter intervention in the setting of STEMI, without previous fibrinolytic treatment. Fibrinolytic treatment is defined as the IV administration of a drug that can achieve thrombolysis, ie the lysis (breakdown) of thrombus in a blood vessel. (General indications of thrombolysis include</span><span style="font-size: large;"> ST elevation myocardial infarction, acute ischemic stroke, and a very large pulmonary embolism causing hypotension). Primary PCI </span><span style="font-size: large;">is the preferred reperfusion strategy in patients with STEMI, provided it can be performed within guideline-mandated times (within 120 minutes from first medical contact), by an experienced team. When primary PCI cannot be performed within the guideline-mandated time limits, then fibrinolytic treatment is indicated (provided that specific contraindications to thrombolysis are not present). An acceptable time interval from first medical contact to primary PCI is ≤120 min (≤90 min if the patient presents early after symptom onset with a large area at risk, ie a large estimated area of acute myocardial ischemia). If this time criterion cannot be met, consider fibrinolysis.</span><br />
<span style="font-size: large;">If fibrinolysis is chosen as reperfusion strategy (eg in a STEMI patient if primary PCI is not available within 2 hours from first medical contact), then current guidelines recommend coronary angiography to be performed 3-24 hours after successful fibrinolysis.</span><br />
<span style="font-size: large;">Another indication for primary PCI is for STEMI patients with severe acute heart failure or cardiogenic shock unless the expected PCI related delay is excessive and the patient presents early after symptom onset.</span></div>
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<span style="font-size: large;">In STEMI, the sooner reperfusion of the culprit coronary artery is achieved the better the outcome for the patient. Hospitals and emergency medical services (EMSs) managing patients with STEMI must monitor delay times and work to achieve the following quality targets: </span></div>
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<span style="font-size: large;">• first medical contact to first ECG ≤10 min</span></div>
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<span style="font-size: large;">• first medical contact to reperfusion therapy, if fibrinolysis is used ≤30 min. In case of primary percutaneous coronary intervention (primary PCI) ≤90 min (≤60 min if the patient presents within 2 hours of symptom onset or directly to a PCI- capable hospital). Note that 90 minutes is the preferred time interval for primary PCI, but a time interval up to 120 minutes is acceptable.</span><br />
<span style="font-size: large;">The time intervals mentioned above, are defined as the time from first medical contact to the beginning of thrombolytic drug administration, or the time from first medical contact to the passage of the angioplasty wire into the culprit artery, during primary PCI.</span><br />
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<span style="font-size: large;">Guidelines regarding procedural aspects of primary PCI </span></h4>
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<span style="font-size: large;">Primary PCI should be limited to the culprit vessel with the exception of cardiogenic shock in the presence of multiple truly critical stenoses,(≥90% diameter) or persistent ischemia after PCI of the supposed culprit lesion. When performing primary PCI, routine</span><span style="font-size: large;"> thrombus aspiration should be considered. </span><span style="font-size: large;">Stenting is recommended (over balloon angioplasty alone) for primary PCI. A drug eluting stent</span><span style="font-size: large;"> (</span><span style="font-size: large;">DES) should be preferred over a bare metal stent (BMS)</span> <span style="font-size: large;">if the patient is likely to be compliant and has no contraindications to prolonged dual antiplatelet therapy (DAPT), such as an indication for oral anticoagulation, or estimated high long-term bleeding risk.</span><span style="font-size: large;"> R</span><span style="font-size: large;">adial access should be preferred over femoral access i</span><span style="font-size: large;">f performed by an experienced radial operator, otherwise, femoral access is used. The radial approach has been shown to reduce the incidence of acute bleeding events on the arterial puncture site.</span><br />
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<span style="font-size: large;">Antithrombotic treatment in STEMI patients treated with primary PCI</span></h4>
<span style="font-size: large;">Aspirin is given and a platelet ADP-receptor blocking drug is recommended in addition to aspirin. Options are: </span><br />
<span style="font-size: large;">Ticagrelor or </span><br />
<span style="font-size: large;">Prasugrel (if there is no history of prior stroke or transient ischemic attack and age <75 years) or</span><br />
<span style="font-size: large;"> Clopidogrel.</span><br />
<span style="font-size: large;"> Glycoprotein (GP) IIb/IIIa inhibitors should be considered if there is angiographic evidence of massive thrombus, slow reflow or no-reflow or a thrombotic complication. Upstream use of a GP IIb/IIIa inhibitor (versus </span><span style="font-size: large;">use in the </span><span style="font-size: large;">catheterization lab ) may be considered in high-risk patients being transferred for primary PCI. </span><br />
<span style="font-size: large;">If a GP IIb/IIIa inhibitor is administered options include Abciximab, Eptifibatide, or Tirofiban</span><br />
<span style="font-size: large;">An injectable anticoagulant must be used in primary PCI and this anticoagulant can be bivalirudin, or enoxaparin, on unfractionat</span><span style="font-size: large;">ed</span> <span style="font-size: large;">heparin.</span><span style="font-size: large;"> Fondaparinux is not recommended for primary PCI. Moreover, the use of fibrinolysis before planned primary PCI is not recommended. <i>(The text of the chapter continues after the images)</i></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: medium;"><b>A female patient 55 years old, smoker, came to the emergency department with pain in the lower sternal area and epigastrium, vomiting, and perspiration. Suddenly, she lost consciousness and collapsed. From the images below, can you tell what happened to the patient, what was the cause and what kind of treatment she has received ? </b></span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="font-size: medium;"><b>The images of this case are courtesy of </b></span></span><span style="font-size: large;">Dr. Alma Sthela Arrioja.</span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh98Jg-imOvl9utmZR3p90-fALdtmK3dZ-JD8Fw5Y-wBrC25UqpGlApKYHi1SAY0jnTC0XHM42fW5_RTBvDLMN6nmwDPquiyKlht6QRZF6MzE5iYSPZCSqNHzfo5I8SjKCeV3ombOFYkbQ/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+ventricular+fibrillation.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="Cardiac arrest due to ventricular fibrillation (VF)" border="0" data-original-height="140" data-original-width="838" height="105" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh98Jg-imOvl9utmZR3p90-fALdtmK3dZ-JD8Fw5Y-wBrC25UqpGlApKYHi1SAY0jnTC0XHM42fW5_RTBvDLMN6nmwDPquiyKlht6QRZF6MzE5iYSPZCSqNHzfo5I8SjKCeV3ombOFYkbQ/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+ventricular+fibrillation.jpg" title="cardiology book and cases-chapter : acute myocardial infarction" width="640" /></a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b style="background-color: white;">2</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjMZZnua85RUG65RLuOdjMrnHLOUzQ7lpp1Igm2CS0dqu9EHGXg4SY4HsxFwMN0WTeOdSfpS21dxhKc9QxTv-aHf3OulVPHeli5x2IvYhWkzFnoA3K_m8aZmjwMZg9QOiwEPnPZf2o__Zo/s1600/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+acute+inferior+myocardial+infarction.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em; text-align: center;"><img alt="acute myocardial infarction (inferior wall STEMI)" border="0" data-original-height="496" data-original-width="960" height="330" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjMZZnua85RUG65RLuOdjMrnHLOUzQ7lpp1Igm2CS0dqu9EHGXg4SY4HsxFwMN0WTeOdSfpS21dxhKc9QxTv-aHf3OulVPHeli5x2IvYhWkzFnoA3K_m8aZmjwMZg9QOiwEPnPZf2o__Zo/s640/%25CE%25B5%25CE%25B9%25CE%25BA%25CF%258C%25CE%25BD%25CE%25B1+%25CE%25B2%25CE%25B9%25CE%25B2%25CE%25BB%25CE%25AF%25CE%25BF%25CF%2585+acute+inferior+myocardial+infarction.jpg" title="cardiology book and cases-chapter : acute myocardial infarction" width="640" /></a></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">3</span></b></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiPpTzcqSQ5Nhv4J8aWFAp9rfjEJhEl4dq5jmmfc4DdktfGnBdu6or8Xx-bz6CKlGtVvUv8Aduq9xa-opunYmNabg8RDHLvm_RW6zpqq0vljEGpNbJMxGKss0eh0Nq3J-IIHk85832O3QY/s1600/accluded+RCA+Dr+alma+sthela+arrijola.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em; text-align: center;"><img alt="coronary angiography" border="0" data-original-height="391" data-original-width="426" height="584" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiPpTzcqSQ5Nhv4J8aWFAp9rfjEJhEl4dq5jmmfc4DdktfGnBdu6or8Xx-bz6CKlGtVvUv8Aduq9xa-opunYmNabg8RDHLvm_RW6zpqq0vljEGpNbJMxGKss0eh0Nq3J-IIHk85832O3QY/s640/accluded+RCA+Dr+alma+sthela+arrijola.png" title="cardiology book and cases-chapter : acute myocardial infarction" width="640" /></a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>4</b></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKfhAQt_vAt9thxOidfKg0Ww_2mVY93V9_VzpRtKi8xevGi5W_gBkGIVm7M9TY7z-3GPSpIhGiKafJbWoimssq0Byb4JhUtzfVHWDkYfLVvT6FPKcHXuDngV9ICtz0iTib0dt4g_-u99U/s1600/accluded+RCA++after+primary+PCI+Dr+alma+sthela+arrijola.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img alt="coronary angiography (right coronary artery-RCA)" border="0" data-original-height="437" data-original-width="433" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKfhAQt_vAt9thxOidfKg0Ww_2mVY93V9_VzpRtKi8xevGi5W_gBkGIVm7M9TY7z-3GPSpIhGiKafJbWoimssq0Byb4JhUtzfVHWDkYfLVvT6FPKcHXuDngV9ICtz0iTib0dt4g_-u99U/s640/accluded+RCA++after+primary+PCI+Dr+alma+sthela+arrijola.png" title="cardiology book and cases-chapter: acute myocardial infarction" width="634" /></a></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Image 1, shows that the patient had an episode of cardiac arrest caused by ventricular fibrillation (VF) The ECG shows the characteristics of VF with rapid, c</b></span><b style="font-family: Arial, Helvetica, sans-serif; text-align: left;">haotic, irregular deflections of varying amplitude and no</b><b style="font-family: Arial, Helvetica, sans-serif; text-align: left;"> identifiable P waves, QRS complexes, or T waves. This irregular electrical activity inevitably causes the loss of any effective ventricular contraction, resulting in immediate loss of pulses and cardiac output. Treatment consists of immediate CPR (cardiopulmonary resuscitation with a ratio f 30 chest compressions</b><b><span style="font-family: "arial" , "helvetica" , sans-serif;"> (cardiopulmonary resuscitation with a repeated sequence of 30 chest compressions and 2 rescue breaths. External electrical defibrillation should be performed as soon as possible (immediately when the defibrillator is brought, connected to the patient and charged) starting with 200 Joules in the adult ( in children 2 Joules/kg body weight). <br />Image 2 shows that, obviously, successful CPR with defibrillation was performed on this patient, since this subsequent ECG, shows sinus rhythm (note the positive P waves in leads I and II and the negative ones in AVR) with tachycardia (about 110-120 pulse/min) and a clear ECG picture of an acute inferior wall STEMI (with ST-segment elevation in the inferior leads and reciprocal ST depression in leads I and avL). Thus, the cause of the VF was acute myocardial ischemia (here the acute phase of an inferior STEMI). In general, acute inferior STEMI is caused by an RCA lesion in 80% of cases, or an LCX lesions in 20% of cases.The best definitive treatment for an acute STEMI is primary PCI of the culprit coronary artery (if this is available within the appropriate time limits- otherwise the second best option is fibrinolysis).</span></b></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;">Images 3 and 4, show that the patient has undergone a successful primary PCI of a totally occluded right coronary artery (RCA). Image 3 shows the initial coronary angiography of the proximally occluded RCA and image 4 shows the same artery after PCI, with successful reperfusion. </span></b></div>
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<span style="font-size: large;"> </span><br />
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<span style="font-size: large;">Fibrinolysis in patients with acute STEMI </span></h4>
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<span style="font-size: large;">Fibrinolysis (thrombolysis) is chosen as a reperfusion strategy in patients with acute MI and ST elevation or LBBB (not known to be old) presenting < 12 hours from symptom onset if primary PCI is not available within 120 minutes from first medical contact.</span></div>
<span style="font-size: large;">Fibrinolysis should also be considered for STEMI patients presenting early (<2 h after symptom onset) with a large estimated myocardial area at risk (ECG or echocardiographic evidence of a large infarction) and low bleeding risk, if estimated time from first medical contact to primary PCI is >90 min.</span><br />
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<span style="font-size: large;">These two indications for fibrinolysis apply only when there is no contraindication to thrombolysis.</span><br />
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<span style="font-size: large;"><span class="fontstyle0">Contraindications to fibrinolysis (thrombolysis)</span></span></h4>
<span style="font-size: large;"><span class="fontstyle1"><u>Absolute contraindications</u></span><span class="fontstyle2">Active bleeding<br />Prior intracranial hemorrhage, other strokes or neurologic<br />events within</span><span class="fontstyle4">1 </span><span class="fontstyle2">year, intracranial neoplasm<br />Recent major surgery (</span><span class="fontstyle5"><</span><span class="fontstyle4">6 </span><span class="fontstyle2">weeks) or major trauma (</span><span class="fontstyle5"><</span><span class="fontstyle4">2 </span><span class="fontstyle2">weeks)<br />Recent vascular puncture in a noncompressible site (</span><span class="fontstyle5"><</span><span class="fontstyle4">2 </span><span class="fontstyle2">weeks)<br />Suspected aortic dissection</span><span class="fontstyle1"><u>Relative contraindications</u></span><span class="fontstyle2">Active peptic ulcer disease or recent gastrointestinal bleeding<br />(</span><span class="fontstyle5"><</span><span class="fontstyle4">4 </span><span class="fontstyle2">weeks)<br />Severe uncontrolled hypertension on presentation (BP</span><span class="fontstyle5">></span><span class="fontstyle4">180</span><span class="fontstyle2">/</span><span class="fontstyle4">110 </span><span class="fontstyle2">mm Hg) or chronic severe hypertension<br />Cardiopulmonary resuscitation</span><span class="fontstyle5">></span><span class="fontstyle4">10 </span><span class="fontstyle2">min<br />Prior nonhemorrhagic stroke<br />Pregnancy<br />Bleeding diathesis or INR</span><span class="fontstyle5">></span><span class="fontstyle4">2</span> </span><br />
<span style="font-size: large;">Coronary artery bypass grafting (CABG) for acute ST elevation myocardial infarction (STEMI) patients:<br />In contrast to primary PCI or fibrinolysis, CABG has a limited role in the acute management of STEMI. However, CABG is indicated alone or as part of the surgical treatment in cases of failed PCI, coronary anatomy of high risk for PCI, surgical repair of a mechanical complication of STEMI (eg, ventricular septal rupture, rupture of ventricular free wall, or severe mitral regurgitation from papillary muscle dysfunction or rupture).</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<span style="color: #38761d; font-size: large;"><b style="background-color: yellow;">Bibliography and links</b></span><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Archbold RA. </b></span><b style="font-family: Arial, Helvetica, sans-serif;">Comparison between National Institute for Health and Care Excellence (NICE) and European Society of Cardiology (ESC) guidelines for the diagnosis and management of stable angina: implications for clinical practice. </b><b style="font-family: Arial, Helvetica, sans-serif;">Open Heart. 2016;3(1):e000406. doi: 10.1136/openhrt-2016-000406. eCollection 2016.</b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908898/pdf/openhrt-2016-000406.pdf" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908898/pdf/openhrt-2016-000406.pdf</a><br /><br />Smith JN, Negrelli JM, et al. Diagnosis and management of acute coronary syndrome: an evidence-based update. J Am Board Fam Med. 2015;28:283-93.</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://www.jabfm.org/content/28/2/283.full.pdf+html" target="_blank">http://www.jabfm.org/content/28/2/283.full.pdf+html</a></b></span><b style="font-family: arial, helvetica, sans-serif;"><br /></b> <b style="font-family: arial, helvetica, sans-serif;"><br /></b> <b style="font-family: arial, helvetica, sans-serif;">Fathala A. Myocardial Perfusion Scintigraphy: Techniques, Interpretation, Indications and Reporting Ann Saudi Med. 2011; 31: 625–634.</b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221136/" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221136/</a></b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><br /></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br />Noninvasive Testing for Coronary Artery Disease. </b></span><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Agency for Healthcare Research and Quality (AHRQ)Publication No. 16-EHC011-EF March 2016 .</span></b><br />
<b><span style="font-family: "arial" , "helvetica" , sans-serif;">LINK <a href="https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0087137/pdf/PubMedHealth_PMH0087137.pdf" target="_blank">https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0087137/pdf/PubMedHealth_PMH0087137.pdf</a></span></b><br />
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><a href="http://blogs.nejm.org/now/index.php/coronary-artery-bypass-grafting/2016/05/20/">Coronary-Artery Bypass Grafting versus PCI</a> (blogs NEJM org.)</b></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><b><br /></b></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="background-color: white; color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"><b>Sianos G, Morel MA,, et al. The SYNTAX score: an angiographic tool grading the complexity of CAD. EuroInterv 2005; 1: 219-227</b></span></span><br />
<span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="background-color: white; color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"><b><br /></b></span></span> <span style="font-family: "arial" , "helvetica" , sans-serif;"><span style="background-color: white; color: #333333; font-family: "helvetica neue" , "helvetica" , "arial" , sans-serif; font-size: 14px;"><b>Valgimigli M, Serruys PW, et al. Cyphering the complexity of coronary artery disease using the syntax score to predict clinical outcome in patients with three-vessel lumen obstruction undergoing percutaneous coronary intervention. Am J Cardiol 2007;99:1072-1081.</b></span></span><br />
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<span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/34/38/2949.full.pdf">2013 ESC guidelines on the management of stable coronary artery disease</a><br /><br /><a href="http://circ.ahajournals.org/content/126/25/e354.full.pdf+html">ACC/AHA Guideline : Stable ischemic heart disease -2012</a><br /><br /><br /><a href="http://circ.ahajournals.org/content/127/4/e362.full.pdf+html">2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction</a><br /><br /><br /><a href="http://circ.ahajournals.org/content/130/25/e344.full.pdf+html">2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes</a><br /><br /><br /><br /><a href="http://eurheartj.oxfordjournals.org/content/ehj/early/2015/09/09/eurheartj.ehv320.full.pdf">2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation</a><br /><br /><br /><a href="http://eurheartj.oxfordjournals.org/content/ehj/33/20/2569.full.pdf">ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation (2012)</a><br /><br /><br /><a href="http://eurheartj.oxfordjournals.org/content/ehj/35/37/2541.full.pdf">2014 ESC/EACTS Guidelines on myocardial revascularization</a></span><br />
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<a href="http://eurheartj.oxfordjournals.org/content/ehj/33/20/2551.full.pdf" target="_blank"><span style="font-size: large;">Third universal definition of myocardial infarction</span></a><br />
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<span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/early/2016/08/26/eurheartj.ehw272.full.pdf" target="_blank">2016 ESC/EAS Guidelines for the Management of Dyslipidaemias</a></span><br />
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<span style="font-size: large;"><a href="http://eurheartj.oxfordjournals.org/content/ehj/37/29/2315.full.pdf" target="_blank">2016 European Guidelines on cardiovascular disease prevention in clinical practice</a></span><br />
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<a href="http://eurheartj.oxfordjournals.org/content/ehj/32/22/2851.full.pdf" target="_blank"><span style="font-size: large;">ESC Guidelines on the diagnosis and treatment of peripheral artery diseases</span></a><br />
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<a href="http://eurheartj.oxfordjournals.org/content/ehj/35/35/2383.full.pdf" target="_blank"><span style="font-size: large;">2014 ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management</span></a><br />
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Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0tag:blogger.com,1999:blog-8796590064874667605.post-6460495881486635982016-05-08T20:20:00.003+03:002018-08-12T00:18:50.604+03:00 Constrictive pericarditis: Pathophysiology, diagnosis, echocardiography and treatment . A cardiology case (video) and notes<div dir="ltr" trbidi="on">
<span style="font-size: large;">IMPORTANT NOTE : THE SITE IS UNDER DEVELOPMENT AND CONTENTS ARE CONTINUOUSLY ADDED.</span><br />
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<span style="font-size: large;">Constrictive pericarditis: Pathophysiology, diagnosis, echocardiography and treatment</span></h2>
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<span style="font-size: large;">A Cardiology Video: Constrictive pericarditis: A condition difficult to diagnose ! </span></h3>
<span style="font-size: large;">The pathophysiology, diagnosis, echocardiography and treatment of constrictive pericarditis are being explained. A presentation </span><span style="font-size: large;">of the important facts, </span><span style="font-size: large;">with images and videos for review purposes.</span><br />
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<span style="font-size: large;">NOTES<br /><b>The pericardium</b> is a two-layered sac that encircles the heart, consisting of an inner serosal layer (visceral pericardium) adhering to the surface of the heart,which is reflected at the origin of the great vessels and continuous to an outer fibrous layer (parietal pericardium). Normally the two layers are separated by a small amount of fluid (about 10 - 50 ml), which reduces friction. The pericardium prevents extreme dilatation of the heart during sudden rises of intracardiac volume and acts as a barrier to limit spread of infection from the adjacent lungs. Nevertheless, its physiological significance is limited. Patients with absense of the pericardium, either congenital, or after heart surgery generally do very well, without it.</span><span style="font-size: large;"><b><br />Constrictive pericarditis (CP)</b> is present when a thickened and fibrotic (and often calcified) pericardium restricts the filling of the heart.The consequence is elevation and equlibration of filling pressures in all cardiac chambers, as well as in the systemic and pulmonary veins. The diastolic filling pressures are almost the same in all cardiac chambers. In the early phase of diastole there is an abnormally rapid ventricular filling due to the elevated atrial pressures. Then, during early to mid diastole, ventricular filling is abruptly halted, when ventricular volume reaches the limit set by the rigid pericardium. CP is characterized by a uniform impairment of filling of all heart chambers. Impaired left ventricular filling causes a reduction of cardiac output, resulting in easy fatiguability. Moreover, the elevated systemic venous pressure and reduced cadiac output causes retention of sodium and water by the kidneys, contributing to edema and ascites. Myocardial contractile function is usually preserved (normal). CP is a rare disease (about 1 case in every 100,000 hospital admissions).</span><span style="font-size: large;"><br /></span><br />
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<span style="font-size: large;">Etiology of constrictive pericarditis</span></h3>
<span style="font-size: large;"><b>Causes</b> : CP can occur after acute pericarditis which is usually idiopathic or viral (9 % of the cases of acute pericarditis will develop CP), also after heart surgery, therapeutic mediastinal radiation, as a complication of an autoimmune connective tissue disease (for example systemic lupus erythematosus), after an infection (i.e. after purulent pericarditis or tuberculosis, which was a common cause in the past, but it is now rare). The above causes are mentioned according to their frequency (the commonest first). Miscellaneous, less common, causes include malignancy, trauma, uremic pericarditis, drug-induced, asbestosis, sarcoidosis.</span><span style="font-size: large;"><br /></span><br />
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<span style="font-size: large;"><b>Symptoms and signs (clinical manifestations) of constrictive pericarditis</b></span></h3>
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<span style="font-size: large;"><b>Symptoms and signs</b> : Patiens usually present with symptoms of heart failure (HF) : dyspnea (due to pumonary venous congestion) easy fatiguability, edema, ascites, hepatomegaly (hepatic enlargement), jugular venous distention. Edema, ascites, hepatomegaly and jugular venous distention are due to systemic venous congestion (elevated systemic venous pressure).Usually the manifestations of right heart failure (due to systemic venous congestion) precede the manifestations of left heart failure due to pulmonary venous congestion (exertional dyspnea, nocturnal dyspnea, orthopnea, cough) that appear later in the course of the disease. Less commonly patients present with chest pain, atrial arrhythmia (impaired ventricular filling causes result in raised atrial pressures and atrial dilatation, which predisposes to atrial arrhythmias such as atrial fibrillation) or abdominal symptoms (due to hepatomegaly, or ascites). Sometimes cardiac cirrhosis can ensue with prominent ascites and jaundice.</span><br />
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<span style="font-size: large;">The ECG and chest X-ray in CP</span></h3>
<span style="font-size: large;">The ECG in constrictive pericarditis (CP) often shows nonspecific findings such as T-wave flattening or inversions.<br />Chest radiography may show a calcified pericardium (rare).</span><br />
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<span style="font-size: large;">Echocardiography in constrictive pericarditis</span></h3>
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<span style="font-size: large;">Suspect and include in your differential diagnosis constrictive pericaditis (CP) and restrictive cardiomyopathy (RC) in patients with symptoms and signs of heart failure (especially with prominent symptoms and signs of right sided heart failure), normal size of both ventricles, normal or near-normal contractile function of the ventricles (this is the general rule but there are also exceptions), absence of a significant valvular disease that can explain heart failure and dilated atria. Note that there is a need to differentiate between these two conditions (CP and RC), because they have many similarities but treatment is different. The atria can be dilated in both conditions but in constrictive pericarditis (CP) they are usually mildly dilated, whereas in restrictive cardiomyopathy (RC) theey are markedly dilated. The echocardiogram in CP shows an abnormal diastolic </span><span style="font-size: large;">motion of the </span><span style="font-size: large;">ventricular septum called a septal bounce. This is due to the competitive filling of the right and left ventricle in diastole, which have to fill while they are confined within a rigid pericardial cavity. This abnormal abrupt septal motion in diastole does not occur in RC.</span><span style="font-size: large;"> </span><br />
<span style="font-size: large;">With respect to the pulse wave Doppler examination of the mitral valve inflow velocities, obtained at the tips of the mitral valve, both CP and RC usually demonstrate a restrictive filling pattern (or sometimes a pseudonormal pattern earlier in the disease course), which is an indication of increased diastolic filling pressures.</span><br />
<span style="font-size: large;"> In both conditions, the mitral early diastolic peak velocity E is > 1.5 A, where A </span><span style="font-size: large;">is the end-diastolic peak velocity during atrial contraction.</span><span style="font-size: large;"> </span><span style="font-size: large;">( In patients with atrial fibrillation the A wave is absent).</span><span style="font-size: large;">The deceleration time of the E wave (the time from its peak until it reaches the baseline of zero velocity) is usually reduced < 160 msec, in both CP and RC. </span><br />
<span style="font-size: large;">There is also in CP a marked respiratory variation in </span><span style="font-size: large;">ventricular size and in ventricular filling (>25% respiratory variation of the peak early diastolic velocity of the transmitral flow E). These findings described above are due to the ventricular interdependence and they are not present in RC. </span><br />
<span style="font-size: large;">In CP there is also a significant respiratory variation in the pulse wave doppler velocities of the hepatic vein and the pulmonary vein flow, whereas in RC, there is no significant variation in these flow patterns with respiration. (in normal persons there is also no significant respiratory variation). </span><span style="font-size: large;"> In CP, the hepatic vein S (systolic) and D (diastolic) flow velocity increase with inspiration </span><span style="font-size: large;"> but with expiration both these two waves of blood velocity decrease markedly and both waves are accompanied by a terminal velocity reversal (SR and DR waves). The end-diastolic AR wave (of flow reversal during atrial contraction) increases markedly with expiration in CP. Minimal respiratory variations are </span><span style="font-size: large;">seen in normal individuals and in RC. </span><br />
<span style="font-size: large;">I</span><span style="font-size: large;">nferior vena </span><span style="font-size: large;">cava is </span><span style="font-size: large;">dilated (it is seen in the subcostal view) in both CP and RC due to the elevated central venous pressure.</span><br />
<span style="font-size: large;">A useful distinguishing feature between CP and RC, is that in CP with pulse wave tissue Doppler imaging (PW-TDI) the early diastolic velocity of the medial mitral annulus (E') is not decreased: E' is usually > 8 cm/s. This is not the case in RC, where the E' tissue Doppler velocity is reduced (usually markedly reduced).</span></div>
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<span style="font-size: large;">A</span><span style="font-size: large;">t times, a thickened pericardium (>4 mm) can be seen with transthoracic echocardiography (TTE) from the subcostal view, but usually TTE does not allow an assessment of pericardial thickness. Transesophageal echocardiography (TEE) performs better that TTE in the assessment of pericardial thickness.</span></div>
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<span style="font-size: large;">Useful for </span><span style="font-size: large;">identifying a thickened </span><span style="font-size: large;">(>4 mm) and / or calcified pericardium is computerized tomography (</span><span style="font-size: large;">CT) or magnetic resonance imaging (MRI).</span><br />
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<span style="font-size: large;">Findings in right heart catheterization</span></h3>
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<span style="font-size: large;">Right-heart catheterization is important for diagnosing constrictive pericarditis, because there are some characteristic hemodynamic findings, such as : </span></div>
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<span style="font-size: large;">The pressure curves of the right and left ventricles in diastole show a characteristic dip and plateau pattern, (it looks like the symbol of square root : "rhe square root sign"). At early diastolic filling there is a rapid rise in diastolic pressure which abruptly reaches a plateau because the ventricles quickly reach the limit set by the rigid pericardium. Thus, they cannot dilate in order to allow further filling with blood.</span></div>
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<span style="font-size: large;">Diastolic pressures of the cardiac chambers: Elevation and equalization of right atrial diastolic pressure, right ventricular diastolic pressure, pulmonary capillary wedge pressure (which is used as a measure of left atrial pressure, since it is an approximation of the left atrial pressure), and left ventricular diastolic pressure is observed in constrictive pericarditis.</span></div>
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<span style="font-size: large;"> The right atrial pressure tracing shows prominent X and Y descents (resulting in a W configuration).</span></div>
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<span style="font-size: large;">Treatment of constrictive pericarditis</span></h3>
<span style="font-size: large;">Diuretics can be useful for congestive manifestations, but caution is advised to avoid hypotension.<br />Avoid calcium channel blockers and beta-blockers because in constrictive pericarditis sinus tachycardia is a compensatory mechanism for impaired cardiac filling. Thus these drugs, by reducing the heart rate, can also reduce cardiac output in this condition.<br />The definitive treatment for CP is total pericardiectomy (surgical<br />removal of the pericardium). Pericardiectomy has a high surgical mortality (about </span><span style="font-size: large;">5% -15%), but it is also a very effective treatment,</span><span style="font-size: large;"> leading to symptomatic improvement in </span><span style="font-size: large;">the majority of patients (</span><span style="font-size: large;">90% of the patiens).</span></div>
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<span style="font-size: large;">Occasionally, in some of the patients who develop constrictive pericarditis after radiation therapy, restrictive cardiomyopathy may also be present. In such cases surgical pericardiectomy is less effective.</span><br />
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<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><b style="background-color: white;"><span style="color: #990000;">GO BACK TO THE HOME PAGE AND TABLE OF CONTENTS </span>LINK<span style="color: #990000;"> </span>:</b></span><br />
<span style="font-family: "times" , "times new roman" , serif; font-size: large;"><a href="https://cardiologybookandcases.blogspot.com/"><b>CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS</b></a></span><br />
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<span style="font-size: large;"><b style="background-color: orange;">BIBLIOGRAPHY AND LINKS TO FREE RESOURCES</b></span></div>
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For the ESC guidelines on diagnosis and treatment of pericardial disease (including acute pericarditis, pericardial effusion,<br />
constrictive pericarditis, etc), please use this link:<br />
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<span style="font-size: large;"><br /><b><span style="color: blue;"><a href="http://eurheartj.oxfordjournals.org/content/36/42/2921">2015 ESC Guidelines for the diagnosis and management of pericardial diseases</a></span></b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>Garcia MJ1.Constrictive Pericarditis Versus Restrictive Cardiomyopathy? <a href="https://www.ncbi.nlm.nih.gov/pubmed/27126534#">J Am Coll Cardiol.</a> 2016;67:2061-76. doi: 10.1016/j.jacc.2016.01.076.</b></span></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://www.sciencedirect.com/science/article/pii/S0735109716008457?via%3Dihub" target="_blank">http://www.sciencedirect.com/science/article/pii/S0735109716008457?via%3Dihub</a></b></span></div>
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<b><span style="font-family: "arial" , "helvetica" , sans-serif;"><br /><br />Lazaros G, Imazio M, Brucato A, Tousoulis D. </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Untying the Gordian knot of pericardial diseases: A pragmatic approach. </span></b><b><span style="font-family: "arial" , "helvetica" , sans-serif;">Hellenic J Cardiol. 2016;57(5):315-322. doi: 10.1016/j.hjc.2016.11.024. </span></b></div>
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<span style="font-family: "arial" , "helvetica" , sans-serif;"><b>LINK <a href="http://www.sciencedirect.com/science/article/pii/S1109966616303050?via%3Dihub" target="_blank">http://www.sciencedirect.com/science/article/pii/S1109966616303050?via%3Dihub</a></b></span><br />
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</script>Georgios Chatziathanasiou Γεώργιος Χατζηαθανασίουhttp://www.blogger.com/profile/09105240057755687474noreply@blogger.com0