Cardiology free book TABLE OF CONTENTS ( Click on the title of each chapter to see the selected chapter)

cardiology book online

Cardiology free e-book online 

TABLE OF CONTENTS ( Click on the title of each chapter to see the selected chapter)

The Electrocardiogram -ECG (adult and pediatric)

Assessment of left and right ventricular systolic and diastolic function with echocardiography

Arterial hypertension-hypertensive crisis-hypertension in pregnancy

Coronary artery disease stable and unstable-Cases and Notes

Congestive heart failure diagnosis and treatment and a case of heart failure (video)

The Cardiomyopathies

Pericarditis -pericardial effusion

Constrictive pericarditis: Pathophysiology, diagnosis, echocardiography and treatment

Aortic stenosis -A case of stenosis of the aortic valve

Aortic regurgitation (AR)

Mitral regurgitation. Diagnosis, echocardiography and management. / A clinical case (VIDEO)

Mitral stenosis

Tricuspid regurgitation

Stenosis of the right cardiac valves: Pulmonic stenosis, Tricuspid Stenosis

Prosthetic heart valves

Infective Endocarditis ( Diagnosis, treatment and a case)

Tachyarrhythmias-supraventricular and ventricular tachycardia

Bradycardia-Bradyarrhythias. Diagnosis,treatment and clinical cases

Pulmonary Hypertension and pulmonary arterial hypertension

Congenital heart disease. A concise introduction (overview)

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)

Cardiac tumors (cardiac neoplasms)


My free emergency medicine book online: Emergency Medicine and First Aid. A free ebook online.

A useful link for a free Cardiology journal  (Continuing Cardiology Education, a journal with review articles):

A Useful and interesting website about Cardiovascular Research
Cardiovascular Research Institute

A useful link for drug information : emc

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, 
 10 -year cardiovascular risk scores,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


Online Medical Calculators-Medicine World org

Medscape-Medical Calculators for medical professionals

LINKS TO OTHER FREE SOURCES OF MEDICAL INFORMATION  (About Cardiology, emergency medicine, internal medicine, and other clinical fields)

Cardiology cases-videos by Dr Chatziathanasiou  
(This is my own channel ! It contains cardiology cases. It is under development -more videos are being continuously added).

Clinical Advisor - Decision Support in Medicine

The Merck Manual - MSD Manual Professional Edition-Cardiovascular Disease

Radcliffe Cardiology - Information for Cardiology Professionals

NICE Evidence search: Cardiology

Continuing Cardiology Education, a journal with review articles):


E medicine-Medscape-Cardiology

The Echo-Journal-Echocardiography videos and Tutorials

123 sonography you tube channel (by Professor of Cardiology and echocardiography Thomas Binder) Link

ECG Library-Life in the fast lane medical blog

Dr. Smith's ECG blog

Cardioserv blog-Echocardiography

CCC Live Cases (Interventional cardiology cases and videos)

Cardiology News  (site for physicians about cardiology news and new developments in cardiovascular medicine)

European cardiology review (ECR)  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)

Prof N Kumar Cardiology lectures (videos about interventional cardiology -electrophysiology-ECG etc)

DeBakey Institute For Cardiovascular Education and Training-videos-cardiology lectures

UofL Internal Medicine Lecture Series-cardiology lectures (videos)

Dr. John M ( a medical-cardiology blog)


NEJM blog-cardiology posts


FREE BOOKS DOWNLOAD (freebookcentre net)


Cardiology free ebook online

Cardiac tumors (cardiac neoplasms)

Cardiac tumors (cardiac neoplasms)

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.

Primary tumors of the heart

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).
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
 can occur in any chamber of the heart but they are more frequently located in the right or left atrium. 
Malignant cardiac tumors have a poor prognosis.

In childhood, primary cardiac tumors are extremely rare and mainly include rhabdomyoma and fibroma. Rhabdomyomas are the most common cardiac tumors in childhood. Cardiac rhabdomyomas are benign tumors that originate from cardiac myocytes. Some cases are sporadic and isolated, but in 50% of cases, they are associated with tuberous sclerosis. The most common malignant cardiac tumor in childhood is rhabdomyosarcoma. Cardiac tumors in children are often associated with genetic syndromes.
 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.
The perioperative mortality is about 8% overall but for myxoma, which is the most common cardiac tumor resected, the perioperative mortality is much lower, approximately 1% .

Metastatic cardiac tumors

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.
Metastases to the heart can occur by the following three mechanisms:
  • Direct extension of a neoplasm via adjacent tissues
  • Dissemination of cancer cells in the blood or the lymphatic system
  • Propagation through the superior or the inferior vena cava to the right atrium.
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 large and 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 of thickening of the visceral pericardium. Generally, pericardial metastases are common and they result in persistent pericardial effusions, also posing the risk of tamponade. The differential diagnosis in a patient with known malignant neoplasm and a pericardial effusion includes malignant pericardial effusion (metastasis to the pericardium), radiation-induced pericarditis, 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.
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  myocardial metastasis include nonspecific ST-T wave changes, cardiac arrhythmias, heart block, or myocardial dysfunction.  
Echocardiography is the most commonly used imaging method in suspected cardiac metastatic disease, but magnetic resonance imaging and computed tomography  are also valuable. Metastatic tumors affecting the myocardium, usually appear as distinct, brightly echogenic masses. Rarely, metastatic tumors may seed the endocardium and echocardiographically appear as intracavitary masses.
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.
The general prognosis of patients with cardiac metastases is poor. For patients with intramyocardial metastasis, survival generally is limited to a few months at most. Survival is longer for intracavitary tumors. Occasional patients have survived several years.

Symptoms and clinical findings of cardiac neoplasmatic disease

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.
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.
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 :
  • congestive (backward) heart failure, such as dyspnea, peripheral edema, or 
  •  low cardiac output (forward) heart failure, such as fatigue, or hypotension. 

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. Primary malignant cardiac tumors can also cause congestive heart failure when there is extensive myocardial involvement.

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.
The constitutional symptoms, signs and laboratory findings may resemble the findings of vasculitis or autoimmune connective tissue disease.
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.  The embolus consists either of tumor cells or of thrombi formed on the tumor surface.
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 (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.
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.

Diagnosis of cardiac tumors

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: 
  • the clinical context and presentation 
  • the location 
  • the imaging characteristics 
  • the findings of additional imaging tests (when necessary), such as CT or MRI
  • in case of a tumor the definitive diagnosis is by biopsy (histological examination), although imaging is in many cases suggestive of the correct diagnosis.
Generally, echocardiography (transthoracic followed in some cases by transesophageal) is the first diagnostic procedure.  Cardiac tumors may be intracavitary or intramural. Echocardiography depicts intracavitary tumors as sessile or mobile echo densities attached to the endocardium, whereas intramural tumors as a localized thickening of the left ventricular wall. Cardiac tumors may also involve the pericardium, with or without a concomitant pericardial effusion.
Differential diagnosis of an intracavitary cardiac tumor includes an intracavitary thrombus. Contrast injection can be helpful in the differential diagnosis because it will intensify the signals from tumors, but not from thrombi.   
If echocardiographic findings cannot suggest the diagnosis, further imaging procedures such as computed tomography (CT) or magnetic resonance imaging are employed. Magnetic resonance imaging (MRI) provides the best spatial resolution and allows exact localization of the tumor. It may also differentiate fat from a thrombus or tumor. It provides particularly valuable information for intramyocardial and malignant tumors.
 In differentiating between benign and malignant neoplasms, a useful test is18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT). If there is a decision to proceed with cardiac tumor surgery (surgical excision of the tumor under cardiopulmonary by-pass), in 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.

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 ?

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.

The patient was managed with a successful surgical resection of the tumor. Biopsy has proven that it was a myxoma.

Cardiac myxoma

Myxomas are the most common benign cardiac tumors in adults. A myxoma is an intracavitary mass, usually 4 -8 cm in diameter. In most cases, it is located in the left atrium (75%), attached to the interatrial septum, over the foramen ovale. More rarely, it is found in the right atrium and even less commonly in the ventricles. Most myxomas are sporadic (>90%) and seldom reoccur after complete resection. Multiple myxomas (synchronous, successive, or recurrent) are a feature of the myxoma syndromes (which account for 7% of cardiac myxoma cases). These cases are familial, as part of the rare Carney syndrome, which is a combination of cardiac and cutaneous myxomas, endocrine disorders (pituitary adenomas, adrenocortical disease, or testicular tumors), and cutaneous lentiginosis. (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)
When a familial myxoma syndrome is identified or suspected, screening first-degree relatives with echocardiography is mandatory.
Large myxomas are often mobile. They may move back and forth into the mitral valve annulus during a cardiac cycle.
Histologically, myxomas are neoplasms of multipotent mesenchymal cells in the subendocardial tissue. These are polygonal, occasionally multinucleate cells surrounded by a myxoid stroma. 
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.
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,
The treatment of a cardiac myxoma is surgical resection of the tumor.

Other benign cardiac tumors: Lipoma / Papillary fibroelastoma  (endocardial papilloma)

Lipomas result from a benign neoplastic proliferation of mature adipocytes and they are usually enclosed in a capsule in contrast to lipomatous hypertrophy (which is a condition that affects the interatrial septum). The majority of cardiac lipomas arise in the subepicardium, but occasionally they can be located in the pericardium and on the cardiac valves. Their size usually ranges from a few to several centimeters. On echocardiography, they appear homogenous, 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. Excision may be required because of the progressive growth of lipomas, as well as the above potential manifestations, 
Lipomatous hypertrophy of the interatrial septum is a prominent thickening of the septum due to the accumulation of adipose tissue. The proximal and distal portions of the atrial septum appear thickened, generally with sparing of the fossa ovalis. 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.

Papillary fibroelastoma of the aortic valve

Papillary fibroelastoma 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 a sea anemone, floating in the blood.  On echocardiography, these benign tumors have a small size, with independent motion and attachment to an endocardial surface (of a valve) via a central pedicle. The tumor typically has frond-like arms (small finger-like projections) and its 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. ,Papillary fibroelastomas may cause valvular incompetence and thromboembolic complications. Thromboembolic complications may manifest as a transient ischaemic attack, a stroke, myocardial infarction, sudden death, syncope, blindness, or pulmonary embolism. If the tumor is located on the arterial side of the aortic valve, it may cause coronary obstruction.Surgical excision of the tumor is curative and it is a reasonable decision in symptomatic patients or when the tumor has been diagnosed incidentally in a preoperative evaluation before cardiac surgery for another reason.

A Video Papillary fibroelastoma in 2D (modified short- and long-axis views) and 3D-transesophageal echocardiography. by the You Tube channel CDT

Cardiac sarcoma

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 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. Differential 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.

LINK: Cardiology book- Table of contents

Bibliography and links 

Paraskevaidis IA, Michalakeas CA, Papadopoulos CH, Anastasiou-Nana M. Cardiac Tumors. ISRN Oncology 2011:1-5.

Hoffmeier, A, Sindermann, JR, Scheld H, Martens, S. Cardiac Tumors-Diagnosis and Surgical Treatment. Deutsches Ärzteblatt International 2014; 111: 205-211.

Takahashi A, Otsuka H, Harada M. Multimodal Cardiovascular Imaging of Cardiac Tumors.  2015;2(1):61-67.

Mankad R, Herrmann J. Cardiac tumors: echo assessment. Echo Res Pract 2015;3(4):R65-R77.

LINK Cardiac tumors: echo assessment

Yuan S-M, Shinfeld A, Lavee J, et al. Imaging morphology of cardiac tumours. Cardiol J 2009; 16:26-35.

Assessment of left and right ventricular systolic and diastolic function with echocardiography

Echocardiography: Useful indices of left ventricular systolic function

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 tissue Doppler imaging (TDI), speckle tracking imaging, three-dimensional (3D) echocardiography, computed tomography (CT), and cardiac magnetic resonance imaging (CMR).
 M-mode echocardiography, 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 in the parasternal long-axis view by positioning the cursor through the LV minor axis at the level of the tips of the mitral leaflets. Then fractional shortening (FS) can be calculated 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).

Fractional shortening (FS) is calculated from linear measurements

of LV dimensions from M-mode or 2D images:

FS = 100% × (LVDd – LVDs)/LVDd 

where LVDd and LVDs are the LV end-diastolic dimension and

end-systolic dimension, respectively. FS normal values: 25-45 %
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.

Two-dimensional (2D) echocardiography for the evaluation of LV systolic function

This is the primary mode for evaluation of LV systolic function. Endocardial border 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 discs of equal height. Individual disc volume is calculated as height x disc area. LV volume is then calculated as the sum of disc volumes.
The ejection fraction (EF)= stroke volume/end diastolic volume.
Stroke volume= the volume of blood ejected by a ventricle in systole= EDV-ESV. 

(EDV= end diastolic volume, ESV= end systolic volume). 
Thus,  EF=  (EDV-ESV)/ EDV. 
The left ventricular EF generally has a normal value   55%.
 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 ≥ 60%.)  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%.
 Left ventricular EF is a strong predictor of clinical outcome and is widely used to make clinical decisions.
EF should be calculated from volumetric measurements
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.

Echocardiography quiz. Any abnormality in the systolic function of the left ventricle?

(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.

Parasternal long axis echocardiogram of a patient with dilated cardiomyopathy

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.

Doppler Echocardiography derived systolic indices (stroke volume)

Doppler echocardiography also provides some indices of LV systolic function, such as the stroke volume (SV), i.e. the 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).  
SV= VTI (LVOT) x area (LVOT)
VTI is the velocity time integral (also named time velocity integral-TVI) of blood flow through the LVOT during systole. 
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).  Assuming a circular LVOT with radius r and diameter D (=2r) : 
LVOT area = πr2=3,14r2=3,14(D/2)2 =
 (3,14 D2)/4= 0,785D2 
In the absence of aortic 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.
It is better to express the normal values of stroke volume per mof body surface area: 
Normal values of SV(ml/m2):  26-54

Tissue Doppler Imaging (TDI)

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.
The systolic annular velocity of the mitral valve (Sm) 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 ≥ 8 cm/sec, 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).
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).
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.

Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and Limitations.Heart, Lung and Circulation 2015;24:224-233
  LINK Tissue Doppler Imaging in Echocardiography

Myocardial strain and strain rate imaging

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. Strain 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). Strain = L-Lo /Lo, where L is the current length and Lo is the original length of a myocardial segment. 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. During systole the left ventricle undergoes longitudinal and circumferential shortening,(denoted by a negative value of longitudinal and circumferential strain) and radial
thickening (positive value of radial strain in systole).

Strain rate (SR) is the rate of change of the strain value= the proportional change in length per unit of time. SR units are s-1SR 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.
 Global longitudinal strain (GLS) is derived from averaging multiple 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%. 
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).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). The normal value for the peak systolic strain rate of the left ventricular myocardium is between  - 1.2  and  - 2  s-1 (sec-1=1/s). 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.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.
A diminished peak systolic strain or strain rate is a sensitive marker of an impairment in systolic function.Need more information about these modern echocardiographic techniques? In that case, here is a link for you to click on (free review article with the option to download PDF) ...

Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability

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. 

Assesment of left ventricular diastolic function (a summary)

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.
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. 
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:
The peak early diastolic velocity of the mitral annulus , obtained from the pulse wave tissue Doppler velocity tracing of the septal and lateral mitral annulus, in the apical 4 chamber view. The velocity e΄is a marker of myocardial relaxation and it is reduced in all stages of diastolic dysfunction. A normal e΄ is a strong indication that the diastolic function is normal, except in patients with constrictive pericarditis or significant mitral regurgitation.
The normal septal e΄ ≥ 8 cm/ s (centimeters per second). The lateral e΄ is normally higher than the septal (> 10 cm/s). Abnormal values suggestive of diastolic dysfunction: a septal e΄< 7 and a lateral e΄< 10 cm/s.
 The average E/e΄ ratio. This is the ratio of the peak early diastolic mitral inflow velocity E to the average of the e΄ velocities of the septal and lateral mitral annulus. Abnormal is a ratio E/e΄>14. The ratio E/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)
 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). LA volume index > 34 ml/mis 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.
 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).
A more detailed discussion follows:
Evaluation of left ventricular (LV) diastolic function begins with M-mode and 2D echocardiography : 
 Assessment of  LV size,  and wall thickness and 
Assessment of left atrial (LA) volume and anteroposterior dimension. 
In patients with LV diastolic dysfunction, concentric or
eccentric LV hypertrophy can be found. Pathologic LV hypertrophy is usually associated with an increased left ventricular stiffness which results in diastolic dysfunction. 
Increased LA volume reflects the effects of the increased LV filling pressures over time.  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.
Doppler assessment:  To assess the mitral inflow align the Doppler beam with the inflow direction and place a 1-3 mm pulse wave (PW) Doppler sample volume between the tips of the mitral leaflets. If the  PW sample volume position is not at the valve tips, but towards the mitral annulus or towards the apex, this can alter significantly the mitral flow velocities.
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).
 In adults with normal diastolic function (normal pattern) 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 
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. Measure isovolumic relaxation time (IVRT) by placing the PW Doppler sample volume in- between LV inflow and outflow to simultaneously display the end of aortic flow and the onset of mitral E-wave velocity. 
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.
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. 
In people with normal diastolic function and also in those with mild diastolic dysfunction (impaired relaxation) the ratio E/e΄ is <10. E is the peak velocity of the early transmitral flow and e' (or Ea) is the peak early diastolic velocity of the mitral annulus measured by pulse wave tissue Doppler.
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/  and a reduced velocity . 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 (e΄) of the septal mitral annulus< 7 cm/s, e΄ of the lateral mitral annulus < 10 cm/s  and an average ratio E/e΄> 14. 
Mild (grade 1) diastolic dysfunction is characterized by the impaired relaxation (or delayed relaxation) mitral inflow pattern with E/A<0.8, E  ≤ 50 cm/s 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 of the E wave. There is also prolongation of isovolumic relaxation time,  IVRT ≥ 100 ms. 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 e΄ (Ea) wave.
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.
In grade 1 diastolic dysfunction mean left atrial pressure and left ventricular filling pressure is not elevated.
An important point is that age 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.
Moderate (grade 2) diastolic dysfunction shows the same transmitral flow pattern (0.8 < E/A <2), as that observed in people with normal diastolic function. It is called pseudonormal pattern.
In the pseudonormal pattern (as well as in the normal pattern),
 150 <DT  <200 ms and IVRT is  <100 msec (range 60-100 msec).
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:
 A reduced mitral annular e΄ velocity (this is a simple way to distinguish it from normal diastolic function, which is characterized by a normal e΄). The normal and pseudonormal filling pattern have the same pattern of transmitral flow (generally E>A), but in case of a pseudonormal pattern, the  velocity is reduced. 
 The increased E/e΄ 
 The pulse wave Doppler signal of the pulmonary venous flow showing S<D (S/D <1). The peak velocity of the end systolic pulmonary vein reverse flow wave at atrial systole (AR) is elevated ( > 35 cm/s) and the duration of AR wave is increased: 
AR wave duration-mitral A wave duration    30 msec.
The pseudonormal mitral inflow pattern can change to a delayed relaxation pattern by reducing preload with diuretic treatment.

Severe diastolic dysfunction is characterized by the restrictive left ventricular filling pattern, 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: 
 E/A ratio >2,  a short deceleration time (DT <150 ms) and also a short IVRT < 60 ms. Due to the severe impairment of diastolic function, mitral annular e΄ velocity is usually severely reduced, the ratio E/e΄ is increased and pulmonary venous flow shows S<<D (the peak velocity of the S wave is much lower than the peak velocity of the D wave). The peak velocity of the end systolic pulmonary vein reverse flow wave at atrial systole (AR) is elevated ( > 35 cm/s) and AR wave duration-mitral A wave duration    30 msec.
The restrictive pattern is called stage 3 diastolic dysfunction if it can change, by reducing preload with diuretic treatment, to a pattern of stage 1 or 2 diastolic dysfunction. If treatment cannot change the restrictive pattern of left ventricular filling, then there is  stage-4 diastolic dysfunction which carries a severe prognosis.
Regarding the tissue Doppler examination of the velocities of the mitral annulus, the early diastolic peak velocity of the mitral annulus (e΄ or Ea) is generally a good index of diastolic function. It is higher at the lateral mitral annulus than at the septal annulus. An indication of diastolic dysfunction is an e΄ < 7 cm/s at the septal annulus, or <10 cm/sec at the lateral annulus. Moreover,  has a reasonable accuracy in identifying patients with diastolic dysfunction and pseudonormal LV filling. 
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, 
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.When an average (septal, and lateral) e΄ velocity is available, a cutoff value of 14 should be considered for the E/e΄ ratio.

Assessment of the dimensions and function of the right ventricle with echocardiography

Evaluation of right ventricular (RV) function is important because RV dysfunction has been associated with increased morbidity and mortality in patients with valvular heart disease, congenital heart disease, pulmonary hypertension, heart failure and coronary artery disease.
Assessment of the size and function of the right ventricle (RV) is complex because it has a  unique crescentic geometry, and also because changes in its shape and orientation occur under conditions of increased volume or resistance loading. Generally, the contractile pattern of the RV involves longitudinal 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.
.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.
A practical assessment of the right ventricular size is obtained by its comparison with the size of the left ventricle in the apical four-chamber view. Normally the right ventricle( RV)  should be less than two-thirds of the size of the left ventricle (LV). However, this may be misleading when LV dilation coexists.
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.
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).
In the apical 4 chamber 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 cm2 m2.   
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).
 In the apical 4-chamber view, the end systolic area of the right ventricle divided by the BSA normally is in men ≤ 7.4 cm2m2 and in women ≤ 6.4 cm2m2
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.
(Watch this video from 123sonography, which demonstrates these echocardiographic findings Link: 123sonography

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.
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:
FAC = (EDA-ESA) / EDA (%).
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%.
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. 
Another technique used for the assessment of  RV function is the myocardial performance index (MPI). It has the unique feature of incorporating both systolic and diastolic function. Isovolumic relaxation time (IVRT), isovolumic contraction time (IVCT), and RV ejection time (RVET) are measured. These time intervals are better measured with the tissue Doppler technique, by using the tissue Doppler velocity signal of the lateral tricuspid annulus. In this way, measurements are obtained from the same heartbeat. (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.)
Myocardial performance index MPI= (IVRT + IVCT) / RVET
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.
Abnormal tissue Doppler MPI ≥ 0.54
Abnormal pulsed Doppler MPI  ≥ 0.43

For a better understanding of these time intervals and of the method used to calculate the MPI see below:
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. 
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. 
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.
 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,
therefore IVCT + IVRT = TCOT-ET   and 
MPI = (IVCT + IVRT) / ET =  (TCOT-ET) / ET


LINK: Cardiology book- Table of contents

Bibliography and links 

Guideline ASE -2016 : Echocardiographic evaluation of diastolic function
Cardiology free e-book online

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.


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.