Acute aortic regurgitation is caused by either damage to the valve leaflets or dilation of the aortic root, or both in some cases. In the developed world, the most common causes are:
In the developing world, the most common cause is rheumatic fever.
Connective tissue diseases, syphilitic aortitis, and aging can lead to chronic dilation of the aortic root, resulting in aortic regurgitation.
Acute aortic regurgitation presents with the rapid onset of severe congestive left heart failure, cardiovascular collapse, and manifestations of cardiogenic shock (profound hypotension, pallor, and diaphoresis) with a thready pulse and normal to reduced pulse pressure.
In chronic aortic regurgitation, the left ventricle dilates to accommodate the volume of the backflow without increasing filling pressure or left atrial pressure. These individuals may be asymptomatic until eventually the heart can no longer compensate and symptoms of congestive left heart failure develop.
Since aortic regurgitation leads to congestive left heart failure, it is exacerbated by volume overload conditions (such as a high-salt diet) and strenuous exercise.
Aortic regurgitation causes a high-pitched diastolic murmur, often with a blowing quality, beginning immediately after A2. It may decrescendo or persist throughout diastole, and is enhanced by the patient leaning forward and holding his breath at end-expiration.
The spot at which the murmur is best appreciated depends on the cause of the regurgitation:
The Austin-Flint murmur is a low-pitched mid- to late-diastolic rumble best heard at the apex that is associated with aortic regurgitation. It is caused by the turbulence of the anterograde stream from the left atrium competing with retrograde flow across the insufficient aortic valve.
The Austin-Flint murmur is best heard with the patient in the left lateral decubitus position, as this brings the left ventricle closer to the chest wall.
The Austin-Flint murmur of chronic aortic regurgitation can be distinguished from the murmur of mitral stenosis by the absence of the loud S1 and opening snap which characterize mitral stenosis.
Clinical signs commonly associated with chronic aortic regurgitation include:
Patients with chronic aortic regurgitation have a widened pulse pressure (high systolic blood pressure with a low diastolic blood pressure).
Electrocardiogram will show left ventricular hypertrophy, left atrial dilation, and abnormal repolarization with ST segment depression at rest or during exercise.
Dilation of the left ventricle leads to an enlarged cardiac silhouette and in severe cases aortic dilation on chest x-ray.
Echocardiography shows a dilated left ventricle with regurgitation visible on color Doppler, and is the gold standard for diagnosis and staging.
Pulsus bisferiens (or biphasic pulse) refers to 2 strong systolic peaks of the aortic pulse from left ventricular ejection separated by a midsystolic dip. It can be palpated in patients with significant aortic regurgitation (with or without aortic stenosis), hypertrophic obstructive cardiomyopathy, and, occasionally, large patent ductus arteriosus.
Chronic aortic regurgitation is often associated with an S3 heart sound.
In acute onset aortic regurgitation, rapid decompensation causes flash pulmonary edema. In chronic aortic regurgitation, the left ventricular end-diastolic volume increases slowly enough that the ventricle is able to remodel, so pulmonary edema is seen only later.
Medical management of aortic regurgitation is aimed at reducing afterload, but plays a limited role because symptomatic patients require valve replacement.
In acute aortic regurgitation patients generally require emergent valve replacement. Temporary stabilization may be provided with IV nitroprusside to reduce afterload and dopamine or dobutamine for inotropic support. Note that intra-aortic balloon pumps are CONTRAINDICATED because they worsen the retrograde filling of the ventricle when the balloon inflates during diastole. Left-ventricular assist devices (LVADS) provide no therapeutic benefit.
Surgical replacement of the valve is indicated for symptomatic patients prior to the development of heart failure. If the aortic root is involved it is simultaneously replaced with a composite graft.
Medical management with a low-sodium diet, ACE inhibitors, and **calcium channel blockers **(nifedipine) is appropriate for patients with chronic, asymptomatic aortic regurgitation and an ejection fraction > 50%.
Note that beta-blockers are relatively contraindicated due to their tendency to lengthen diastole, thereby worsening the regurgitation.
Recall that patients with midsystolic murmurs (grade ≤2) without associated findings and symptoms do not require further workup for a murmur.
In contrast, patients with murmurs with any of the following characteristics require further evaluation with echocardiography: