Acquired aortic valvular stenosis. Its diagnosis by conventional radiological study.

Abstract

Stenosis of the aortic valve may be of congenital or acquired origin. Among the congenital malformations of the heart and great vessels, aortic stenosis is not an uncommon lesion. It may occur as stenosis of the valve itself or as a localized area of constriction in the ascending aorta above the valve, so-called supravalvular stenosis. Congenital constriction of the outflow tract of the left ventricle is a well recognized entity, but since it does not involve the aorta per se, the lesion hardly deserves the oft applied designation of subaortic stenosis. In the average general practice of radiology, the acquired form of aortic valvular stenosis is much more frequently encountered than is the congenital type, and it is to the consideration of acquired constriction that the present communication will be limited. The etiology of acquired aortic stenosis has been the subject of considerable study. Two principal causes have been propounded: namely, aortic sclerosis or fibrosis and rheumatic valvulitis. Kiloh (1) and others (2, 3) have suggested that nonrheumatic sclerosis is the main cause of pure aortic stenosis. A different opinion is held by most authorities, as Wood (4) and McGinn and White (5), who believe that the disease is principally due to rheumatic involvement of the aortic cusps. Dry and Willius (6) and Karsner and Koletsky (7) have produced strong support for a rheumatic basis of acquired aortic stenosis. As in rheumatic mitral valvulitis, however, a definite history of rheumatic fever or its equivalent is not infrequently lacking. A rheumatic history has been variously recorded as ranging from 14 to 44 per cent (4, 8–11). It is well known that rheumatic involvement of the aortic valve may produce either stenosis or valvular incompetency, or varying combinations of the two. While it is not uncommon for dominant aortic stenosis to be accompanied by some element of aortic regurgitation, it is also well established that acquired stenosis does exist in “pure” form, unassociated with any aortic valvular insufficiency. The principal effect of aortic stenosis is to increase the work load of the left ventricle and, under conditions where this chamber is no longer able to compensate for the overwork, cardiac output falls below normal. Hemodynamically significant aortic stenosis results in a difference in systolic pressure between the left ventricle and the ascending aorta, a so-called left ventricular-aortic systolic pressure gradient. When this gradient of pressure exceeds 10 mm. of mercury, it is considered that aortic stenosis is present. The normal aperture of the aortic valve in human adults is approximately 3.0 sq. cm. The aperture (aortic valve area) can be estimated with reasonable accuracy by combined catheterization of both the right and left sides of the heart, with determinations of left ventricular and aortic pressures and of cardiac output, provided there is no aortic regurgitation.