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Novel Pathogenetic Mechanisms and Structural Adaptations in Ischemic Mitral Regurgitation

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MOSBY-ELSEVIER
DOI: 10.1016/j.echo.2013.07.003

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Ischemic mitral regurgitation; Epithelial-mesenchymal transition; Papillary muscles; Mitral annulus; Left ventricular false tendons; Ventricular-valvular continuity; Atriogenic leaflet tethering; Echocardiography

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Ischemic mitral regurgitation (MR) is a common complication of myocardial infarction thought to result from leaflet tethering caused by displacement of the papillary muscles that occurs as the left ventricle remodels. The author explores the possibility that left atrial remodeling may also play a role in the pathogenesis of ischemic MR, through a novel mechanism: atriogenic leaflet tethering. When ischemic MR is hemodynamically significant, the left ventricle compensates by dilating to preserve forward output using the Starling mechanism. Left ventricular dilatation, however, worsens MR by increasing the mitral valve regurgitant orifice, leading to a vicious cycle in which MR begets more MR. The author proposes that several structural adaptations play a role in reducing ischemic MR. In contrast to the compensatory effects of left ventricular enlargement, these may reduce, rather than increase, its severity. The suggested adaptations involve the mitral valve leaflets, the papillary muscles, the mitral annulus, and the left ventricular false tendons. This review describes the potential role each may play in reducing ischemic MR. Therapies that exploit these adaptations are also discussed.

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