Molecular Cardiology in Clinical Practice
Cardiology is an area of great recent triumphs in pharmacological and surgical treatment, yet cardiovascular disease remains the leading cause of death and disability in the industrialized world. Coronary disease, heart failure, stroke and sudden arrhythm
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BASIC SCIENCE FOR THE CARDIOLOGIST
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B. Levy, A. Tedgui (eds.): Biology of the Arterial Wall. 1999 ISBN 0-7923-8458-X M.R. Sanders, J.B. Kostis (eds): Molecular Cardiology in Clinical Practice. 1999. ISBN 0-7923-8602-7 B. Swynghedauw (ed.): Molecular Cardiology for the Cardiologist. Second Edition. 1998. ISBN: 0-7923-8323-0
MOLECULAR CARDIOLOGY IN CLINICAL PRACTICE edited by
Michael R. Sanders John B. Kostis Department of Medicine University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School
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Electronic Services l+ aortic regurgitation was present
Molecular Cardiology in Clinical Practice 45 in 2% of the population while 22+ mitral regurgitation was present in 1%% (8). This is a minimal estimate: today, most common causes of valvular regurgitation involve inborn variations in connective tissue structures (mitral valve prolapse, idiopathic aortic root dilatation, etc.) for which the association with valve dysfunction (and the severity of such dysfunction) increases with age. Thus, several million Americans have regurgitant valvular abnormalities, and a large subset has hemodynamically severe and potentially clinically important disease. However, at any one time, most of these people are not clinically ill. "Decompensation" (i.e., cardiac functional and symptomatic debility) results when the mechanical loads on the left ventricle (LV) and, in the case of MR, the right ventricle (RV), exceed the capacity of the ventricles to pump blood in sufficient quantity to meet systemic demands; this situation usually is associated with, and preceded by, development of subnormal myocardial contractility ("systolic function") and compromised chamber compliance andor active relaxation ("diastolic dysfunction"). Regurgitation can result from sudden loss of valve integrity (cordal rupture, leaflet avulsion) but, more commonly, regurgitation increases slowly, associated with ventricular geometric remodeling and myocardial growth which initially retard the occurrence of decompensation but which ultimately may potentiate organ dysfunction. From the development of hemodynamically severe valvular regurgitation, many years typically intervene before objective evidence of cardiac dysfunction can be detected by any but the most sophisticated testing methods and before heart failure (CHF) becomes clinically apparent or sudden death occurs. Finally, the prevalence of these lesions, while not on a par with coronary artery disease or hypertension as a cause of CHF, nonetheless is sufficient to render valvular regurgitation a true public h
