End-systolic wall stress as a predictor of regression of left ventricular hypertrophy during antihypertensive therapy

Abstract

Background Hypertensio-induced left ventricular hypertrophy and its regression under the influence of antihypertensive therapy depend on a variety of factors.
Methods A group of 14 hypertensives over 60 years of age with left ventricular hypertrophy (LVMI > 134 g/m2 was receiving nifedipine in a mean dose of 45.2 mg/day. After 4 years of theraphy 2D and M-mode echocardiography revealed regression of left ventricular hypertrophy in 8 patients (group I), and further increase of left ventricular mass in 6 patients (group II).
Results Initial systolic (SBP) and diastolic blood pressure (DBP) and left ventricular mass index (LVMI) did not show significant unter-group differences. After 4 years of nifedipine therapy blood pressure decrease was similar in both groups. LVMI decreased in group I in contrast to group II, where it showed further increase. In group I initially significantly higher end-systolic wall stress decreased significantly after therapy; ejection fraction showed a significant increase. In group II end-systolic wall stress and ejection fraction did not change significaantly.
Conclusions Despite a comparable hypotensive effect after 4-year nifedipine therapy regression of left ventricular hypertrophy was observed only in the patients with higher initial end-systolic wall stress. Regression of left ventricular hypertrophy in the elderly was associated with improved systolic function. The present findings imply that the magnitude of end-systolic wall stress may be predictor of hypotensive effect.