Aortic Regurgitation

There are several causes of incompetence of the aortic valve:

rheumatic damage to the leaflets

perforation of leaflets in infective endocarditis

disease of the aortic root (the initial portion of the aorta just above the valve)

congenital deformity (either combined with other malformations or as a sole lesion)

trauma producing detachment of a leaflet

Two basic mechanisms produce aortic regurgitation—abnormality of the leaflet and dilatation of the root of the aorta (the ring to which the valve is attached becomes widened and the orifice too large for healthy valves to cover it).

Given a comparable volume of blood regurgitating through an incompetent left-sided cardiac valve, aortic regurgitation imposes a greater overload on the left ventricle than does mitral regurgitation. Blood leaking through an incompetent mitral valve into the atrium raises the left ventricular workload mildly; blood returning to the left ventricle through an incompetent aortic valve has to be ejected again into the aorta, steeply increasing the workload. This difference results in a more pronounced hypertrophy of the left ventricle in aortic regurgitation. Furthermore, the large volume of blood handled by the left ventricle dilates it. The dilated, volume-overloaded left ventricle characteristic of aortic regurgitation works less efficiently than the nondilated, pressure-overloaded left ventricle in aortic stenosis.

In the past, chronic aortic regurgitation was caused frequently by rheumatic fever, with or without coexisting mitral stenosis. With the decline in the prevalence of rheumatic heart disease in the West, the commonest cause of chronic aortic regurgitation has become disease of the aortic root, a variety of aortitis affecting the portion of the aorta immediately above the aortic valve (see chap. 14). Syphilitic aortitis was once common, often affecting the aortic valve, but today it is a rarity. Nowadays aortitis may be associated with certain varieties of rheumatoid arthritis or may develop as a result of atherosclerotic disease of the aorta in the elderly.

On physical examination aortic regurgitation displays a characteristic heart murmur. The severity of the regurgitation can be estimated by abnormalities of the arterial pulse and unusually low diastolic blood pressure. Aortic insufficiency cannot be quantified, but a more accurate estimation of regurgitant volume is possible by echocardiography, using the Doppler principle. As a rule, cardiac catheterization contributes little to the diagnosis.

The consequences of aortic regurgitation depend on whether the

lesion develops gradually or abruptly. The increased workload acute aortic regurgitation imposes on a normal left ventricle, if severe, may produce life-threatening heart failure requiring emergency valvular surgery. Chronic aortic regurgitation, by contrast, permits adaptive hypertrophy of the ventricle and is generally well tolerated; patients with severe aortic regurgitation may lead an unrestricted active life for many years. Eventually the left ventricle reaches the limit of its adaptative capacity, leading to cardiac failure. But in aortic regurgitation, more than in other valvular diseases, the onset of the first symptoms (usually dyspnea produced by activity) may develop so late that relief of the overload by valve replacement may no longer restore good left ventricular function. To avert this problem, in aortic regurgitation early deterioration of left ventricular function is occasionally considered an indication for surgery even in asymptomatic patients. When symptoms suggestive of heart failure are present, surgery is mandatory.

The major complication of aortic regurgitation is infective endocarditis. Atrial fibrillation is rare; ventricular arrhythmias may appear during late stages. The prolonged asymptomatic course of aortic regurgitation usually makes medical treatment unnecessary except to prevent endocarditis.