Aortic Stenosis

Stenosis of the aortic orifice is now the commonest valvular disease; it is seen predominantly among the elderly. The term "valvular aortic stenosis" denotes stenosis caused by a stiffened valve and is distinguished from narrowing below or above the aortic valve, occasionally seen as a variety of congenital heart disease.

There are two principal ways in which the aortic valve may become stenotic—fusion of the three valve leaflets, due to adhesion among them, or stiffening and calcification of the leaflets, which may keep the valve from fully opening, leaving a greatly reduced orifice during systole (see fig. 32, p. 130). In addition, aortic stenosis may be present since birth, as a congenital defect in which the three leaflets have grown together, leaving open a small central orifice that can still function normally during diastole.

Acquired fusion of the leaflets by adhesions among them is almost always the result of rheumatic fever and, as in mitral stenosis, takes decades to develop. Rheumatic aortic stenosis, however, is now relatively uncommon. Today most cases are considered a type of "calcific aortic stenosis," a gradual fibrotic thickening of the leaflets in which the deposition of calcium can eventually make the valve leaflets as hard as bone. Normal leaflets, paper-thin, open wide in systole, permitting easy flow of blood through the aortic orifice. The slightest deviation from the norm may alter the flow patterns through the valve and in time cause minor damage to the valve. This damage may then produce fibrosis and eventually the deposition of calcium. A common cause of calcific aortic stenosis is a minor congenital malformation, namely an aortic valve consisting of two rather than three leaflets. Such a valve functions normally, and its presence is seldom recognized. But any minor change in the shape of the orifice may initiate the process that can produce aortic stenosis after a period of sixty to seventy years.

Thus aortic stenosis is a disease of old age, with most patients in their sixties, seventies, or eighties. This process progresses slowly, so that many years usually elapse from the time aortic stenosis is first detected until it becomes severe enough to cause symptoms. The normal aortic orifice during systole measures 3–5 cm.² When it reaches about one-half of its normal size, turbulent flow produces a heart murmur. However, the overload on the left ventricle does not develop until the orifice is reduced to less than 1.5 cm.² In moderate aortic stenosis the orifice has narrowed to 0.7–1.0 cm² ; in severe aortic stenosis the orifice may be as small as 0.4 cm.² The degree of hypertrophy of the left ventricle depends on the severity of stenosis; hence the first manifestation of left ventricular failure may become apparent only once the stenosis is severe. The patient then is likely to become aware of shortness of breath during exercise. Before the onset of left ventricular failure, however, some patients develop symptoms unique to aortic stenosis, related to the extreme pressure in the left ventricle and the slow ejection of blood through the stenotic aortic orifice. Certain reflexes originating in the left ventricle may interfere with the regulation of blood pressure and produce sudden loss of consciousness (syncope); furthermore, blood flow through the coronary arteries may be affected by aortic stenosis, producing anginalike chest pain unrelated to coronary

disease. Children with congenital aortic stenosis usually tolerate it well, although sometimes unusually severe aortic stenosis may bring about emergencies in infancy.

Aortic stenosis can be detected on physical examination by the characteristic heart murmur and a peculiarity of the pulse. The electrocardiogram will disclose left ventricular hypertrophy, which, though a nonspecific finding, usually indicates that aortic stenosis is at least of moderate severity. In older patients a chest X ray may show calcification of the aortic valve. An echocardiogram can display more directly the narrowing of the aortic orifice, the severity of which can be estimated by the Doppler technique. The size of the aortic orifice can be calculated more accurately from data obtained through cardiac catheterization, which reveals the magnitude of the pressure gradient between the left ventricle and the aorta and the volume of blood flow. In older patients cardiac catheterization is usually combined with coronary angiography. Chest pain, if present, may be caused in these patients by aortic stenosis alone or by coexisting coronary-artery disease—an important distinction when deciding on the proper medical or surgical management of the patient.

In contrast to mitral stenosis, where complications play a major role in its course, there are relatively few complications in aortic stenosis. Atrial and ventricular arrhythmias occasionally develop but are relatively rare. Patients with mitral stenosis are susceptible to infective endocarditis, and preventive measures should be taken. Those with advanced aortic stenosis are at higher risk of sudden cardiac death than those with other valvular diseases.

Treatment of aortic stenosis is almost entirely surgical. Relief of the condition represents one of the most spectacular accomplishments of cardiac surgery and is usually effective even in the most advanced cases. There are several approaches, depending on the type of aortic stenosis. Aortic commissurotomy , surgical separation of adherent leaflets through open-heart surgery, is mainly performed on children and adolescents with congenital aortic stenosis. The results are moderately satisfactory, although secondary changes may develop later in life requiring reoperation. Aortic-valve replacement is the standard treatment of aortic stenosis. It is the second most frequently performed cardiac operation (after coronary bypass surgery), and its successes are often brilliant: function of the left

ventricle, if impaired, returns to normal, and hypertrophy of the left ventricle may regress. Percutaneous aortic balloon valvuloplasty has been available only since the mid-1980s; hence its long-range success is uncertain. The advantages of dilating the aortic orifice without surgery are obvious. However, in elderly patients with heavily calcified aortic valves the successful widening of the orifice may not last long, for restenosis is very common. Consequently, this procedure is performed mostly on patients who are poor candidates for open-heart surgery.

The prevailing view is that patients with symptoms clearly related to aortic stenosis should undergo surgery. In the case of an aortic stenosis, even severe, that permits the patient a symptom-free, active life, surgery is usually postponed. Following valve replacement most patients can lead a normal, unrestricted life. Further treatment consists of preventive measures against endocarditis and, in patients with nonbiological valves, anticoagulant therapy. Successful operations are being performed on patients even in their eighties or nineties.