Abstract
It has been hypothesized that left ventricular(LV)function may deteriorate follOWing reduction in LV mass in treated hypertensives. We therefore assessed ventricular and myocardial function follOWing a substantial regression of LV mass (≥80g) after 1 year of antihypertensive treatment in 17 patients. These pts were part of a cohort of 239 undergoing echocardiography at baseline and 1 year who took part in a multicenter VA cooperative study of monotherapy in hypertension. We hypothesized that an 80 g reduction represents true LV mass regression, since it exceedS 2 standard deviations of test-retest reliability of M-mode echocardiography; such a large reduction in LV mass should allow the detection of functional changes that accompany hypertrophy regression. Circumferential stress (σc, g/cm2) vs endocardial fractional shortening (FSendo, %) relations were used to characterize LV function; ac vs midwall fractional shortening (FSmw, %) was used to define myocardial function. FSmw was derived from a two-shell model that accounts for nonuniform wall thickening, is independent of relative wall thickness (RWT) and is anatomically appropriate, since midwall fibers are oriented circumferentially. Thd and Dd are LV diastolic wall thickness and diastolic dimension (mm); SBP=systolic pressure;
Data are mean±SESBPTh dDdRWTLVMassFSendoFSmwσcbaseline153±414±156±10.50±0.03438±2639±220±195±101 year139±4*11±1*52±2*0.46±0.03326±24*36±220±1106±12**P<005 vs baseline
A significant decrease in SSP was accompanied by a substantial reduction in LV mass and a significant, albeit small, increment in aC. The increase in ac was associated with a small (p=NS) decrease in FSendo and no change in FSmw. Thus major changes in mass associated with anti-hypertensive therapy are not accompanied by a decrement in LV or myocardial function. Indeed the unchanged FSmw in the presence of increased ac suggests improved myocardial contractile function