Chronic Aortic Regurgitation

Long-standing retrograde blood flow through an incompetent aortic valve into the left ventricle during ventricular diastole.

Chronic aortic regurgitation may be caused by disease of the aortic valve leaflets (due to congenital or rheumatic heart disease, myxomatous degeneration, or infective endocarditis) or by aortic annular root dilation or ascending aortic disease (eg, as occurs in syphilis, rheumatoid spondylitis, Marfan's syndrome, ascending aortic aneurysm, aortic dissection, and various types of aortitis).

Pathophysiology

The regurgitant volume increases the left ventricular end-diastolic volume. If the left ventricular end-diastolic volume increases gradually, eccentric hypertrophy (hypertrophy with dilation) of the left ventricle results; ie, the ventricle enlarges so that it can accommodate the increased left ventricular end-diastolic volume without an increase in left ventricular filling pressure. Left ventricular stroke volume increases sufficiently to maintain a normal aortic forward effective stroke volume and to accommodate the regurgitant volume. With the increased stroke volume, systolic aortic pressure and runoff into the left ventricle are increased, and diastolic pressure is decreased, increasing pulse pressure.

The enlarged ventricle and increased left ventricular systolic pressure increases myocardial oxygen demand, and the low diastolic aortic pressure limits subendocardial blood flow. Consequently, myocardial ischemia and its complications occur, usually late in the course of the disorder.

Symptoms, Signs, and Diagnosis

Most often, mild to moderate aortic regurgitation produces no symptoms for many years, and exercise tolerance is preserved.

Rheumatic aortic regurgitation, which occurs predominantly in men, often produces no symptoms, even in old age. A short, soft basal diastolic murmur is characteristic and may be accentuated by hypertension. Syphilitic aortic regurgitation is more severe, and the prognosis is worse, often because of an associated aortic aneurysm or coronary ostial involvement. A long, loud decrescendo basal diastolic murmur, often with a short basal systolic ejection murmur, is characteristic of hemodynamically severe aortic regurgitation. Because left ventricular stroke volume is increased, the systolic ejection murmur can be loud and long, sounding like that of aortic valve stenosis. The peripheral signs of severe aortic regurgitation distinguish predominant aortic regurgitation from predominant aortic valve stenosis.

Effort intolerance and dyspnea may develop and may progress to heart failure. Chest pain is often due to associated coronary atherosclerosis but can be due to myocardial ischemia. Usually, palpitations are not due to arrhythmias but to the forceful ejection of blood.

The findings of severe regurgitation include bounding peripheral arterial pulses, a wide pulse pressure, and a hyperactive precordium with a rocking motion. Occasionally, a bisferious pulse (pulsus bisferiens) is present. The high-pitched diastolic murmur is best heard at the cardiac base. It is louder at the upper right sternal border in aortic root disease and is more prominent along the left sternal border in aortic valve leaflet disease. An associated diastolic thrill and a systolic murmur of increased aortic outflow may be heard. Third and fourth heart sounds and an apical diastolic rumble (Austin Flint murmur) are common. If the femoral artery is compressed over the groin with the bell of a stethoscope, a to-and-fro diastolic bruit (Duroziez's murmur) can be heard because there is retrograde flow of blood across the compressed artery during diastole.

Chest x-ray shows characteristic cardiac enlargement with a dilated aorta. Occasionally, an ascending aortic aneurysm is seen. Linear calcification of the ascending aorta is typical in syphilitic aortic regurgitation; in contrast, calcification in aortic atherosclerosis is patchy and frequently denser and thicker. The ECG shows left ventricular hypertrophy. The echocardiogram shows an enlarged left ventricular cavity, often with early diastolic fluttering of the anterior mitral valve leaflet. Doppler echocardiography can be used to estimate the severity of aortic regurgitation.

Treatment

Patients with left ventricular failure and severe chronic aortic regurgitation should be stabilized medically even if the valve is to be replaced. Patients with heart failure are treated with a diuretic, an angiotensin-converting enzyme (ACE) inhibitor, and digoxin before valve replacement. Asymptomatic patients with moderate to severe aortic regurgitation and good left ventricular function should receive an ACE inhibitor, a vasodilating calcium channel blocker, or hydralazine to reduce afterload. Afterload reduction can slow progression of left ventricular dilation and even postpone the onset of symptoms that warrant valve replacement. Drugs that cause bradycardia should be avoided, because relative diastolic prolongation can increase regurgitation and accentuate symptoms.

Patients who have left ventricular failure, even if they become asymptomatic with medical management, and patients who remain symptomatic after receiving optimal medical therapy should be considered for aortic valve replacement, preferably with bioprosthetic valves. However, because these patients commonly have severe underlying ventricular dysfunction, the results are less satisfactory than those for patients with aortic valve stenosis. Because decreasing myocardial contractility is manifested by a decreasing ability to eject a large stroke volume, a progressive increase in left ventricular end-diastolic and end-systolic dimensions with a decreasing left ventricular ejection fraction (detected by echocardiography or radionuclide angiography) is an indication for aortic valve replacement. Most patients become symptomatic before these changes occur.