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Aortic regurgitation (AR)
The regurgitation of blood from the aorta to the left ventricle through the aortic valve in diastole.
Causes of aortic regurgitation (AR)
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).
Causes of AR due to aortic root disease are:
Degenerative dilatation of the aorta age-or hypertension-related.
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.
Aortic dissection involving the ascending aorta can cause acute AR.
Arteritis of the aorta caused by giant cell arteritis, seronegative arthropathies (ancylosing spondylitis, psoriatic arhritis, Reiter syndrome, reactive arthritis), Adamantiadis-Behcet syndrome.
Pathophysiology and haemodynamic consequences of AR
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 (regurgitant volume) in diastole. The LV works with an increased in total stroke volume, which is the sum of effective stroke volume plus regurgitant volume.
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 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.
LV end-diastolic pressure and 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 eccentric myocardial hypertrophy. An increase in LV end-diastolic volume is also the main compensatory mechanism to maintain an adequate effective stroke volume.
Left ventricular ejection fraction (EF) is initially normal, however, LV end diastolic pressure rises. Due to the chronic overload of the left ventricle in severe AR, as the disease progresses, EF decreases over time and this together with a further increase in LV volume, may precede the onset of symptoms.
Acute aortic regurgitation (causes : infective endocarditis, dissection of the ascending aorta, and 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 can be life-threatening. A regurgitant volume that would be well tolerated in chronic AR can lead to marked increases in LV end-diastolic pressure and a decrease in effective stroke volume. So acute AR can often lead to pulmonary edema, hypotension, and even cardiogenic shock. Indeed, in acute severe aortic regurgitation there is usually dyspnea or pulmonary edema with a normal left ventricular size and high ejection fraction.
Clinical presentation of chronic severe aortic regurgitation:
Patients with chronic aortic regurgitation can be asymptomatic for
many years, with symptoms developing in the late stages. The most common symptom is dyspnea (shortness of breath), initially during exercise, later also at rest. Other symptoms include palpitations due to ventricular or supraventricular arrhythmias, or a sensation of a prominent heart beat (due to the increased total stroke volume). Some patients also have angina, even in absence of coronary
artery disease, because of increased myocardial oxygen demand.
Physical examination in aortic regurgitation
A characteristic diastolic murmur, high-pitched, decrescendo (intensity shows a progressive decrease during diastole) can be heard 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 (A2) is decreased. The intensity of the AR diastolic murmur increases when the patient is sitting and leaning forward (this is also the best patient position for the murmur to be auscultated) or when the patient is squatting. The murmur intensity decreases with the strain phase of the Valsalva maneuver.
The severity of aortic regurgitation correlates with duration, not intensity, of the murmur. In moderate to severe AR, a short mid-systolic 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 also be present). In severe AR third heart sound (S3) is often heard, as a manifestation of the volume overload and it does not necessarily indicate congestive heart failure. Some patients with aortic regurgitation also have an Austin -Flint murmur (diastolic rumble at the apex).
Pulse pressure is widened, with low diastolic and increased systolic blood pressure. In severe AR the pulse pressure is usually 100 mmHg or higher and the diastolic pressure 60 mmHg, or less. A useful clinical sign that can exclude hemodynamically significant AR is a normal or elevated diastolic blood pressure. 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.
The left ventricular apical impulse is hyperdynamic (prominent),
broadened and is displaced laterally and inferiorly.
Peripheral signs, related to wide pulse pressure can be present:
Traube sign: pistol-shot murmur heard over the femoral artery
Duroziez sign: a murmur over the femoral artery when it is partially
compressed.
Quincke pulse: visible capillary pulsation in the nail bed after holding the tip of the nail.
Musset sign: head bobbing with each cardiac cycle
Müller sign: pulsation of the uvula.
The ECG 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.
Treatment of aortic regurgitation (AR)
In cases of rheumatic etiology, antibiotic prophylaxis for rheumatic fever is indicated.
Vasodilator treatment in AR, with ACE inhibitors and dihydropyridine calcium channel blockers (e. g. nifedipine) being the preferred drugs, is indicated if :
There is systemic hypertension
There are symptoms, or left ventricular (LV) dysfunction (in these cases surgery is the definitive treatment).
There are no recommendations for vasodilator treatment in asymptomatic patients with severe AR without hypertension and LV dysfunction.
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).
In acute severe aortic regurgitation 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.
Important: Which invasive treatment often used to stabilize patients with low cardiac output is contraindicated in AR ?
Answer:
Intraortic balloon counterpulsation is contraindicated in AR ( it could increase regurgitation, since the balloon of the intraortic balloon pump dilates in diastole).
Indications for surgery in chronic severe aortic regurgitation (AR)
In patients with symptoms, due to the AR (regardless of LV function)
In patients with impaired left ventricular (LV) function (ejection fraction EF < 50%)
In patients with severe dilatation of the LV (LV end systolic dimension > 50 mm, or LV diastolic dimension > 75 mm)
(Mnemonic: "the rule of 50s" regarding the indications of surgery in severe asymptomatic chronic AR: EF <50, LVend systolic dimension > 50)
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)
A useful video :
Aortic regurgitation (AR)
The regurgitation of blood from the aorta to the left ventricle through the aortic valve in diastole.
Causes of aortic regurgitation (AR)
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).
Causes of AR due to aortic root disease are:
Degenerative dilatation of the aorta age-or hypertension-related.
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.
Aortic dissection involving the ascending aorta can cause acute AR.
Arteritis of the aorta caused by giant cell arteritis, seronegative arthropathies (ancylosing spondylitis, psoriatic arhritis, Reiter syndrome, reactive arthritis), Adamantiadis-Behcet syndrome.
Pathophysiology and haemodynamic consequences of AR
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 (regurgitant volume) in diastole. The LV works with an increased in total stroke volume, which is the sum of effective stroke volume plus regurgitant volume.
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 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.
LV end-diastolic pressure and 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 eccentric myocardial hypertrophy. An increase in LV end-diastolic volume is also the main compensatory mechanism to maintain an adequate effective stroke volume.
Left ventricular ejection fraction (EF) is initially normal, however, LV end diastolic pressure rises. Due to the chronic overload of the left ventricle in severe AR, as the disease progresses, EF decreases over time and this together with a further increase in LV volume, may precede the onset of symptoms.
Acute aortic regurgitation (causes : infective endocarditis, dissection of the ascending aorta, and 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 can be life-threatening. A regurgitant volume that would be well tolerated in chronic AR can lead to marked increases in LV end-diastolic pressure and a decrease in effective stroke volume. So acute AR can often lead to pulmonary edema, hypotension, and even cardiogenic shock. Indeed, in acute severe aortic regurgitation there is usually dyspnea or pulmonary edema with a normal left ventricular size and high ejection fraction.
Clinical presentation of chronic severe aortic regurgitation:
Patients with chronic aortic regurgitation can be asymptomatic for
many years, with symptoms developing in the late stages. The most common symptom is dyspnea (shortness of breath), initially during exercise, later also at rest. Other symptoms include palpitations due to ventricular or supraventricular arrhythmias, or a sensation of a prominent heart beat (due to the increased total stroke volume). Some patients also have angina, even in absence of coronary
artery disease, because of increased myocardial oxygen demand.
Physical examination in aortic regurgitation
A characteristic diastolic murmur, high-pitched, decrescendo (intensity shows a progressive decrease during diastole) can be heard 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 (A2) is decreased. The intensity of the AR diastolic murmur increases when the patient is sitting and leaning forward (this is also the best patient position for the murmur to be auscultated) or when the patient is squatting. The murmur intensity decreases with the strain phase of the Valsalva maneuver.
The severity of aortic regurgitation correlates with duration, not intensity, of the murmur. In moderate to severe AR, a short mid-systolic 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 also be present). In severe AR third heart sound (S3) is often heard, as a manifestation of the volume overload and it does not necessarily indicate congestive heart failure. Some patients with aortic regurgitation also have an Austin -Flint murmur (diastolic rumble at the apex).
Pulse pressure is widened, with low diastolic and increased systolic blood pressure. In severe AR the pulse pressure is usually 100 mmHg or higher and the diastolic pressure 60 mmHg, or less. A useful clinical sign that can exclude hemodynamically significant AR is a normal or elevated diastolic blood pressure. 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.
The left ventricular apical impulse is hyperdynamic (prominent),
broadened and is displaced laterally and inferiorly.
Peripheral signs, related to wide pulse pressure can be present:
Traube sign: pistol-shot murmur heard over the femoral artery
Duroziez sign: a murmur over the femoral artery when it is partially
compressed.
Quincke pulse: visible capillary pulsation in the nail bed after holding the tip of the nail.
Musset sign: head bobbing with each cardiac cycle
Müller sign: pulsation of the uvula.
The ECG 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.
Criteria for severe aortic regurgitation :
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 ≥ 65% of the left ventricular outflow tract (LVOT).
Pressure half time (PHT) of the aortic regurgitant jet, derived with continuous wave Doppler examination < 200 ms (milliseconds). Regurgitant orifice area (EROA) ≥ 0.3 cm2 / Regurgitant volume ≥ 60 ml.
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 ≥ 65% of the left ventricular outflow tract (LVOT).
Pressure half time (PHT) of the aortic regurgitant jet, derived with continuous wave Doppler examination < 200 ms (milliseconds). Regurgitant orifice area (EROA) ≥ 0.3 cm2 / Regurgitant volume ≥ 60 ml.
Left ventricular size: increased (always in chronic severe AR, but often is normal in acute AR)
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 assessing the severity of AR.
VIDEO An echocardiography quiz: What is the severity of aortic regurgitation?
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 assessing the severity of AR.
VIDEO An echocardiography quiz: What is the severity of aortic regurgitation?
Answers and a brief discussion are provided in the video.
(Video) (The images of this video are courtesy of Dr Ahmed Said).
(Video) (The images of this video are courtesy of Dr Ahmed Said).
To see the video on full-screen, after starting the video click on the symbol [] on the right lower corner.
Treatment of aortic regurgitation (AR)
In cases of rheumatic etiology, antibiotic prophylaxis for rheumatic fever is indicated.
Vasodilator treatment in AR, with ACE inhibitors and dihydropyridine calcium channel blockers (e. g. nifedipine) being the preferred drugs, is indicated if :
There is systemic hypertension
There are symptoms, or left ventricular (LV) dysfunction (in these cases surgery is the definitive treatment).
There are no recommendations for vasodilator treatment in asymptomatic patients with severe AR without hypertension and LV dysfunction.
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).
In acute severe aortic regurgitation 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.
Important: Which invasive treatment often used to stabilize patients with low cardiac output is contraindicated in AR ?
Answer:
Intraortic balloon counterpulsation is contraindicated in AR ( it could increase regurgitation, since the balloon of the intraortic balloon pump dilates in diastole).
Indications for surgery in chronic severe aortic regurgitation (AR)
In patients with symptoms, due to the AR (regardless of LV function)
In patients with impaired left ventricular (LV) function (ejection fraction EF < 50%)
In patients with severe dilatation of the LV (LV end systolic dimension > 50 mm, or LV diastolic dimension > 75 mm)
(Mnemonic: "the rule of 50s" regarding the indications of surgery in severe asymptomatic chronic AR: EF <50, LVend systolic dimension > 50)
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)
A useful video :
Echocardiographic assessment of aortic regurgitation (A lecture by dr Shantanu Shengupta) Link:
ASE GUIDELINES AND STANDARDS Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation A Report from the American Society of Echocardiography
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), European Heart Journal,ehx391, https://doi.org/10.1093/eurheartj/ehx391 LINK https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease
https://www.youtube.com/watch?v=mJLr4g9oUaY
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CARDIOLOGY BOOK ONLINE-HOME PAGE AND TABLE OF CONTENTS
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Useful links
ASE GUIDELINES AND STANDARDS Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation A Report from the American Society of Echocardiography
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), European Heart Journal,ehx391, https://doi.org/10.1093/eurheartj/ehx391 LINK https://academic.oup.com/eurheartj/article/4095039/2017-ESC-EACTS-Guidelines-for-the-management-of#supplementary-data
2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease
2015 ESC Guidelines for the management of infective endocarditis
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