Left ventricular end-systolic stress-shortening and stress-length relations in humans: Normal values and sensitivity to inotropic state

Abstract

Experimental studies suggest that the extent of left ventricular (LV) fiber shortening is determined by both the wall stress at end-systole and the contractile state. To evaluate the relation between these variables assessed noninvasively, 26 normal subjects were studied by M-mode echocardiography, phonocardiography, and indirect carotid pulse tracings during infusion of methoxamine to alter load (in all 26 subjects) and infusion of dobutamine (in 10 subjects) to increase contractility. End-systolic pressure was estimated from the incisura of a calibrated carotid pulse tracing. LV end-systolic dimension and wall thickness, and percent internal dimension shortening were determined by echocardiography, and end-systolic meridional wall stress was calculated. The relation between end-systolic stress and shortening was inversely linear (r = −0.83) for 130 control points. Dobutamine infusion resulted in a higher percent fractional shortening for any end-systolic stress; all 43 stress-shortening points were more than 2 standard deviations above the mean for the regression line. The relation between stress and dimension for the control points showed wider scatter than between stress and shortening (r = 0.56). However, in individual patients dobutamine always shifted the stress-dimension lines to the right, as compared with the baseline position resulting in a smaller end-systolic dimension for any end-systolic wall stress. Thus, LV end-systolic wall stress and percent fractional shortening are inversely and linearly related and their relation can be accurately assessed by noninvasive methods. The end-systolic stress-shortening relation is highly sensitive, while the end-systolic stress-dimension relation is less sensitive to alterations in LV inotropic state.