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At one time, most cases of valvular disease in the United States were due to rheumatic heart disease. While this is still true in many developing countries, other causes are much more common in the developed world. In older adults, "degenerative" calcific aortic valvular disease is believed to be due to a process similar to that which produces atherosclerosis; studies have suggested that up to 25% of adults over age 65 have some thickening of their aortic valve (aortic sclerosis) while 2–3% have frank aortic stenosis (eFigures 10–23 and 10–24). Aortic sclerosis alone is a marker for future cardiovascular events and death. There is also increasing information that genetic markers associated with aortic stenosis play a role in the expression of this disease. Lipoprotein (a) in particular has a growing body of data supporting a role in the development and progression of calcific aortic valve stenosis. Calcium deposition may also occur in the mitral annulus creating enough dysfunction of the valve that either stenosis or regurgitation (or both) results. Mitral valve prolapse is still frequently seen and rarely may be associated with the hyperadrenergic syndrome in younger patients. AV valvular regurgitation may be due to LV dysfunction and papillary muscle displacement (functional mitral regurgitation) or RV dysfunction (tricuspid regurgitation). Low-flow, low-gradient aortic stenosis is recognized as occurring with both a normal LVEF as well as an abnormal LVEF. Both entities carry significant morbidity and mortality.
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The typical findings of each native valve lesion are described in Table 10–2. Table 10–3 outlines bedside maneuvers to distinguish among the various systolic murmurs. Echocardiography yields key information about valve morphology, LV mass and function, and atrial and ventricular chamber size. Doppler ultrasound provides quantitative measurements of transvalvular ...