RT Book, Section A1 Bashore, Thomas M. A1 Granger, Christopher B. A1 Jackson, Kevin P. A1 Patel, Manesh R. A2 Papadakis, Maxine A. A2 McPhee, Stephen J. A2 Rabow, Michael W. A2 McQuaid, Kenneth R. SR Print(0) ID 1184695134 T1 Valvular Heart Disease T2 Current Medical Diagnosis & Treatment 2022 YR 2022 FD 2022 PB McGraw-Hill Education PP New York, NY SN 9781264269389 LK accessmedicine.mhmedical.com/content.aspx?aid=1184695134 RD 2024/03/28 AB 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 the elderly, "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 10–28 and 10–29). 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. 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.