Cardiac Remodeling Due to Aortic Regurgitation and Mitral Regurgitation
Mitral regurgitation and aortic regurgitation (MR, AR) both impose a volume overload on the left ventricle (LV). Despite this similarity, the two lesions and loads they present are quite different from one another. In MR, the extra volume pumped by the LV
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Cardiac Remodeling Due to Aortic Regurgitation and Mitral Regurgitation Blase A. Carabello
Abstract Mitral regurgitation and aortic regurgitation (MR, AR) both impose a volume overload on the left ventricle (LV). Despite this similarity, the two lesions and loads they present are quite different from one another. In MR, the extra volume pumped by the LV is ejected into the left atrium, while in AR the extra volume is delivered into the aorta where it increases pulse pressure and systolic pressure. Thus MR is a “pure” volume overload, while AR is a combined pressure and volume overload, and afterload excess plays a much greater role in AR. As a consequence, the ventricle of AR demonstrates both eccentric and concentric hypertrophy, while the MR ventricle is a thin-walled dilated chamber. These different pathologies are associated with different mechanisms of hypertrophy and different mechanisms that lead to LV dysfunction. Thus, while once MR and AR were lumped together as volume-overload lesions, their differences are considerable so that each lesion should be approached as a uniquely separate entity with differing pathophysiologies and differing clinical outcomes. Keywords Volume overload • Mitral regurgitation • Aortic regurgitation • Remodeling
B.A. Carabello, M.D. (*) Department of Medicine, Center for Heart Valve Disease, St. Luke’s Episcopal Hospital, Baylor College of Medicine, Houston, TX 77030, USA Veterans Affairs Medical Center,Medical Service (111), 2002 Holcombe Boulevard, Houston, TX 77030, USA e-mail: [email protected] B.I. Jugdutt and N.S. Dhalla (eds.), Cardiac Remodeling: Molecular Mechanisms, Advances in Biochemistry in Health and Disease 5, DOI 10.1007/978-1-4614-5930-9_13, © Springer Science+Business Media New York 2013
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Introduction
All valvular heart diseases place a hemodynamic overload upon the left and/or right ventricle, and for each valve lesion, this overload is unique. Uniqueness extends to mitral and aortic regurgitation (MR, AR). While MR and AR were once lumped together as volume-overloading lesions, it is now clear that mitral regurgitation and aortic regurgitation are actually quite different from one another, presenting the left ventricle (LV) with different hemodynamic overloads, in turn resulting in different geometric adaptation and remodeling [1]. Decades ago, Grossman et al. postulated that hemodynamic stress (s) was the progenitor of cardiac hypertrophy [2]. Laplacian stress (s) = P × r/2th where P = ventricular pressure, r = ventricular radius, and th = wall thickness. In their formulation, an increase in systolic stress, mediated by increased systolic pressure, caused the myocardium to lay down new sarcomeres in parallel, increasing myocyte thickness and thus increasing LV wall thickness. In this formulation, the increase in the pressure term in the numerator of the Laplace equation would be offset by an increase in the thickness term of the denominator, in turn normalizing systolic wall stress (afterload), an adaptation tha
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