The relationship of afterload to ejection performance in chronic mitral regurgitation

Abstract

Simultaneous left ventricular micromanometry and biplane cineangiography were performed in nine control subjects (group 1), 14 patients with chronic mitral regurgitation and an ejection fraction of 57% or greater (group 2), and 13 patients with mitral regurgitation and an ejection fraction of less than 57% (group 3). End-diastolic volume index was increased in both groups with mitral regurgitation (p < .001) compared with the control group. Left ventricular end-diastolic wall thickness did not differ among the three groups, but the left ventricular muscle mass index was greater in both groups with mitral regurgitation than in controls (p < .001). End-diastolic pressure was elevated in both groups 2 and 3 compared with group 1 (p < .05), but peak systolic, mean systolic, and incisural pressure were not different among the three groups. End-diastolic stress was larger in groups 2 and 3 than in group 1 (p < .05). Muscle fiber stretch was greater in group 2 than in the control group (p < .05), whereas only the mean stress determined from aortic valve opening to closure was greater in group 2 than in the control group (p < .01). For each of the intervals, the calculated mean stress was larger in group 3 than in group 2 (p < .05). Evaluation of the end-systolic stress- and mean ejection stress-ejection fraction relationships revealed an overlap of control with group 2 data, group 3 values were downwardly displaced. The absence of an upward shift of group 2 values in the setting of an augmented preload suggests that these patients maintained only a normal level of ventricular performance with the use of preload reserve and were operating at a somewhat reduced contractile state. The downward displacement of group 3 data points in the presence of only moderately higher levels of afterload than in groups 1 and 2 implies impaired myocardial contractility. Recognition of chronic mitral regurgitation as a stress overload state may provide insight into the mechanism of myocardial injury that occurs in both volume and pressure overload.