Contemporary Approach to Aortic and Mitral Regurgitation

Abstract

Hemodynamically severe aortic regurgitation (AR) and mitral regurgitation (MR) are among the most predictable causes of heart failure (HF) and sudden death (SD). During the past 4 decades, surgery has become the primary intervention for patients with these diseases. However, timing of operation is a “moving target”: surgical techniques have improved dramatically; noninvasive methods have developed for objective interrogation of cardiac size and function, continually enhancing knowledge of natural history and its predictors, and an increasing array of nonsurgical treatments show potential to beneficially alter the natural course of disease. Consequently, the benefit-to-risk relation underlying management decisions changes continually. Simultaneously, the myocardial cellular and molecular pathophysiology of valvular regurgitation is being progressively elucidated, promising new clinical evaluation strategies and novel treatments. The net result of these factors has been progressively earlier application of valve surgery and continuing discussion about the correct mix of drugs, surgery, and watchful waiting. Guidelines for management of patients with valvular heart diseases were developed by the American College of Cardiology and American Heart Association 5 years ago1 and generally remain applicable, but new information mandates periodic review. Disease prevalence is not known precisely. However, extrapolation from natural history data suggests that >5 000 000 persons have moderate to severe valvular regurgitation in the United States alone. Prevalence has grown steadily for many years. New York’s State-Wide Planning and Research Cooperative System (SPARCS) database, a compulsory hospital reporting system, indicates that AR and MR discharge diagnoses increased almost 4-fold during the past 20 years, whereas total hospitalizations declined by 20% (Figure 1).2 Several factors may account for the increase, including a shift in distribution of disease etiology from acquired (eg, rheumatic) to genetically determined (now predominant in all age groups)3–6; the strong tendency of the latter for slow anatomic/functional progression (delaying …