INFLUENCE OF THE ANGIOTENSIN-II ANTAGONIST VALSARTAN ON LEFT-VENTRICULAR HYPERTROPHY IN PATIENTS WITH ESSENTIAL-HYPERTENSION

Citation
Pa. Thurmann et al., INFLUENCE OF THE ANGIOTENSIN-II ANTAGONIST VALSARTAN ON LEFT-VENTRICULAR HYPERTROPHY IN PATIENTS WITH ESSENTIAL-HYPERTENSION, Circulation, 98(19), 1998, pp. 2037-2042
Citations number
37
Categorie Soggetti
Peripheal Vascular Diseas",Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097322
Volume
98
Issue
19
Year of publication
1998
Pages
2037 - 2042
Database
ISI
SICI code
0009-7322(1998)98:19<2037:IOTAAV>2.0.ZU;2-D
Abstract
Background-Left ventricular hypertrophy (LVH) represents an independen t risk factor in patients with essential hypertension. Because reversa l of LVH may be associated with an improvement of prognosis, the influ ence of new antihypertensive compounds, such as angiotensin II AT(1) r eceptor antagonists, on LVH should be determined. Methods and Results- In a randomized, double-blind trial, 69 predominantly previously untre ated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m(2) in men and >110 g/m(2) in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Ech ocardiographic data of 58 patients were available. After 8 months of v alsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/ m(2) (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/ -25 to 117+/-27 g/m(2) (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m(2) under valsarta n and only to 10 g/m(2) under atenolol (R=0.91; 90% CI, 0.85 to 0.97 v ersus atenolol). Baseline mean blood pressure values were determined t o be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/- 14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatmen t, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsart an and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the va lsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide. Conclusions-Antihypertensive tre atment with the angiotensin II antagonist valsartan for 8 months produ ced a significant regression of LVH in predominantly previously untrea ted patients with essential hypertension. The drug may be safely admin istered in this subset of hypertensive patients; however, the long-ter m benefit in terms of risk reduction has still to be evaluated in furt her trials.