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- History: angina, dyspnea, syncope.
- Physical examination: midsystolic murmur; small and slow rising carotid pulse contour (parvus et tardus).
- Echocardiography: thickened immobile aortic valve leaflets; increased peak transaortic jet velocity and mean gradient; reduced valve area.
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Over the past century, there has been a linear climb in record life expectancy and an overall aging of the human race. Therefore, we are faced with an epidemic of aging and age-associated disease, not the least of which is valvular heart disease. Aortic stenosis, the narrowing of the aortic valve orifice caused by failure of the leaflets to open normally, is now the most common indication for valve replacement in North America and Europe.
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The pathogenesis of aortic stenosis is most commonly progressive calcification and degeneration of a trileaflet or congenitally bicuspid valve. Although once thought to be a degenerative process, it is now recognized that calcific aortic stenosis is in fact an active disease process that shares similarities to atherosclerosis where there is inflammation, lipid accumulation, and calcification of the leaflets. The mechanisms by which some valves degenerate and become stenotic while others remain relatively normal are unknown but are probably related to genetic polymorphisms. Those with end-stage renal disease, Paget disease, or severe familial hypercholesterolemia may present with calcific aortic stenosis at a younger age and are susceptible to more rapid progression of stenosis severity.
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Rheumatic valve disease is a rare cause of aortic stenosis in industrialized nations. However, for indigenous populations within these countries as well as in developing countries, there remains a significant prevalence of rheumatic valve disease. In contrast to calcific aortic valve stenosis, the rheumatic valve shows adhesion, leaflet retraction, and commissural fusion. Along or just a few millimeters away from the free margins of the valve leaflets, small sessile nodules develop that also contribute to leaflet malcoaptation. Therefore, the rheumatic aortic valve invariably will leak. Rheumatic aortic valve disease is almost never present in isolation, and there is invariably concomitant mitral valve disease. A patient with aortic stenosis and a perfectly normal mitral valve should be considered as having another cause for their disease. Other rare causes of aortic stenosis include those associated with connective tissues diseases such as systemic lupus erythematosus and ochronosis.
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Those with acquired aortic stenosis generally have a long latent period before the onset of the salient clinical manifestations of the disease: effort-related dyspnea (heart failure), angina, and syncope. The most common initial clinical manifestations are a gradual decline in functional capacity and effort-related dyspnea. Regardless of the initial presenting symptom(s), it is imperative to ensure that the pathophysiologic mechanism is attributed to valve disease and not another mechanism such as concomitant coronary artery or lung disease because the onset of even mild symptoms attributed to aortic stenosis heralds a dramatic increase in the mortality rate for these patients if the valve is not replaced. Symptoms are therefore the guidepost for intervention, and ...