Left Ventricular Ejection Index as a Marker of Early Myocardial Dysfunction in Primary Mitral Regurgitation

M itral valve prolapse (MVP) is a common disorder affect- ing 2% to 5% of the general population (7.8 million individuals in the United States and 176 million individuals worldwide), In addition to progressive MR, MVP is associated with endocarditis, heart failure, and even sudden death. In the setting of severe primary MR, the left ventricle (LV) is affected by a significant volume load leading to compensatory adaptations that vary considerably depending on the prolonged clinical course of MR. During the compensated stage of chronic MR, LV enlargement results from remodeling of the extracellular matrix with dissolution of collagen and rearrangement of myocardial fibers. oreover, new sarcomeres are added in series, and at the ventricular level, eccentric hypertrophy develops. Consequently, preload (at the sarcomere level), afterload (at the ventricular level), and LV ejection fraction (LVEF) are normal, whereas total stroke volume is increased as a result of the large enddiastolic volume. The transition to decompensated chronic MR may occur as a consequence of a progressive increase in regurgitant volume, a decrease in LV contractile function, an increase in afterload, or a combination of these factors. During this stage, LVEF typically declines to 50% to 60%. Finally, decompensated MR is characterized by substantial and progressive LV dilation, elevated LV diastolic pressure, increased systolic wall stress, and an LVEF of <50%. The decline in LVEF is a consequence of depressed myocardial contractile state, LV afterload excess, or both. Although predominantly based on mitral valve replacement data, early echocardiographic studies have demonstrated a frequent decline in LVEF post surgery, even when MR was well compensated preoperatively. This was thought to be a consequence of an increase