Left Ventricular Response to Mitral Regurgitation

Abstract

Mitral regurgitation (MR) burdens the left ventricle with a volume load that leads to a series of left ventricular (LV) compensatory adaptations and adjustments that vary considerably during the prolonged clinical course of MR.1–4 The early compensatory changes observed in acute MR (ie, utilization of the Frank-Starling mechanism) are gradually replaced by a chronic remodeling process with enlargement of the LV chamber. Eventually, these compensatory adaptations fail, LV dysfunction develops, and transition to a decompensated phase of chronic MR occurs (Table). In the present report, the LV response to MR will be described, the evolution from a compensated to a decompensated state will be discussed, and the therapeutic implications of these events will be considered. Published guidelines provide detailed recommendations for the evaluation and treatment of patients with MR, including those with a variety of comorbidities.5,6 The present review is limited to a discussion of the changes in LV size and function that develop as a result of degenerative disease of the mitral valve (recognized clinically as severe mitral valve prolapse with or without partial flail leaflet) or, less commonly, rheumatic mitral valve disease. Our primary goal is to review the rationale for the use of measurements of LV size and function as guides to the management of patients with MR. View this table: Table. LV Structure and Function in the 3 Stages of Chronic MR The clinical impact of MR is determined by the magnitude of the regurgitant leak (ie, the regurgitant volume) and the time course of development of the regurgitation. Patients with the abrupt onset of severe MR generally present with markedly elevated pulmonary venous pressure, whereas those with chronic MR exhibit prominent ventricular enlargement with increased chamber compliance and lower pulmonary venous pressure.2,7 In this section, the determinants of regurgitant flow will be defined and the …