Mechanism of Mitral Regurgitation in Dilated Cardiomyopathy

Dilated cardiomyopathy is a condition characterized by chamber dilatation and impaired systolic function, resulting in the clinical manifestations of congestive heart failure. Mitral regurgitation occurs with varying frequency in dilated cardiomyopathy, and its detection depends on the diagnostic modality utilized. The presence of mitral regurgitation imposes an additional burden on the failing ventricle, and appears to be an independent prognostic indicator of mortality. The mechanism of mitral regurgitation in dilated cardiomyopathy is complex, controversial, and incompletely understood. The mitral apparatus consists of the left atrial wall, mitral annulus, mitral leaflets, chordae tendineae, papillary muscles, and left ventricular wall, and each of these components and the intimate interrelationship between these structures may contribute to the development of mitral regurgitation. Left atrial enlargement, reduced left atrial contractility, mitral leaflet retraction, abnormal vector of chordal tendineae pull, papillary muscle dysfunction (either asynergic contraction or malalignment), mitral annular dilatation, and changes in the size, shape, and function of the left ventricle have been suggested as possible mechanisms for the development of mitral regurgitation in dilated cardiomyopathy. The primary event in the development of mitral regurgitation appears to be left ventricular dilatation and dysfunction. Controversy persists as to whether the associated mechanism is annular dilatation, papillary muscle or free left ventricular wall dysfunction, or a combination of all, but recent echo‐Doppler studies reviewed in this article support the notion that annular dilatation is the predominant mechanism. Improved understanding of the mechanism of mitral regurgitation in dilated cardiomyopathy may lead to a more aggressive approach with regard to pharmacological therapy, thus impacting on survival in this group of patients. (ECHOCARDIOGRAPHY, Volume 8, March 1991)