Abstract
Mitral regurgitation (MR) creates a unique hemodynamic stress by inducing a low pressure form of volume overload due to ejection into the left atrium, without the pressure component that accompanies aortic regurgitation. Chronic therapy with vasodilators has been shown to reduce left ventricular wall stress, and thereby delay or obviate the need for valve replacement in aortic regurgitation; however, no data are currently available in patients with chronic MR using standard vasodilators or agents that block renin-angiotensin system (RAS) components. Studies in a clinically relevant dog model of experimentally induced MR demonstrate upregulation of the cardiac RAS. However, RAS blockade fails to improve left ventricular remodeling and function, whereas beta-adrenergic blockade results in restoration of left ventricular chamber and myocyte function.
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