Left ventricular stress-dimension-shortening relations before and after correction of chronic aortic and mitral regurgitation

Abstract

Mechanical characteristics of the left ventricle in chronic aortic regurgitation (AR) differ from those in chronic mitral regurgitation (MR). The differences are thought to be responsible, in part, for the changes in left ventricular (LV) function observed after surgical correction of AR or MR. To test this hypothesis, LV stress-dimension-shortening relations were determined before and after valve replacement in patients with compensated and decompensated chronic AR and MR. Echocardiographic data from 32 patients with AR and 20 patients with MR were used; preoperatively, all 52 patients had LV enlargement. Based on postoperative data, 2 subgroups were defined for each lesion: Patients in group A achieved a normal end-diastolic dimension (less than 3.3 cm/m 2) and patients in group B had persistent LV enlargement. Preoperatively, the patients in group A with AR had increased peak systolic stress, but end-systolic stress and fractional shortening were normal; the patients in group B with AR had increased peak systolic stress, increased end-systolic stress and depressed shortening. One year after aortic valve replacement the patients in group A had normal systolic wall stresses and normal shortening, whereas those in group B had persistently abnormal wall stresses and a decrease in shortening. Preoperatively, patients in group A with MR had only modest elevations of peak stress, while end-systolic stress and fractional shortening were normal; in patients in group B with MR the peak stress was similar to that seen in group A, but end-systolic stress was increased and shortening was depressed. One year after mitral valve replacement, patients in group A had no change in end-systolic stress, but peak stress fell and shortening decreased; patients in group B had persistently abnormal stress-shortening relations. Thus, in group B patients with either AR or MR, persistent elevations of systolic stress may contribute to a postoperative decrease in shortening (“afterload excess”). However, in group A patients with MR, the postoperative decrease in shortening cannot be explained on the basis of afterload excess.