Regression of left ventricular hypertrophy with losartan potassium therapyin patients with hypertension

Citation
E. Acarturk et al., Regression of left ventricular hypertrophy with losartan potassium therapyin patients with hypertension, CURR THER R, 59(12), 1998, pp. 819-825
Citations number
14
Categorie Soggetti
Pharmacology,"Pharmacology & Toxicology
Journal title
CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL
ISSN journal
0011393X → ACNP
Volume
59
Issue
12
Year of publication
1998
Pages
819 - 825
Database
ISI
SICI code
0011-393X(199812)59:12<819:ROLVHW>2.0.ZU;2-C
Abstract
The aim of this study was to assess the effects of losartan potassium, an a ngiotensin II receptor antagonist, on systolic blood pressure; diastolic bl ood pressure; and left ventricular dimensions, functions, and mass index (L VMI) in patients with mild-to-moderate essential hypertension. Twenty patie nts aged 40 to 65 years with either uncontrolled or previously untreated hy pertension and echocardiographically documented left ventricular hyptertrop hy (LVH) defined by LVMI >130 g/m(2) for men and >110 g/m(2) for women mere included in the study. Blood pressure measurements were taken at a-week in tervals. Blood samples were taken before treatment and after 3 months of tr eatment for determination of Lipid concentrations and other laboratory vari ables used to monitor safety, and two-dimensional M-mode and Doppler echoca rdiographic measurements were obtained. Losartan was associated with a stat istically significant reduction of mean systolic blood pressure from 173 +/ - 6 mm Hg to 135 +/- 10 mm Hg and diastolic blood pressure from 100 +/- 4 m m Hg to 82 +/- 7 mm Hg without a change in heart rate. Significant decrease s were identified in interventricular septal and left ventricular posterior wall thicknesses (from 12.5 +/- 0.8 mm to 11.5 +/- 0.8 mm and 12.1 +/- 1.0 mm to 11.1 +/- 0.8 mm, respectively). LVMI decreased from 138.8 +/- 18.7 g /m(2) to 126.0 +/- 21.8 g/m(2) after 3 months of treatment. Left ventricula r dimensions and ejection fraction did not change significantly compared wi th baseline values. The Doppler echocardiographic assessment of mitral E/A ratio, which is a marker of diastolic function, increased significantly fro m baseline. Except for a significant increase in mean serum lactate dehydro genase activity, laboratory findings (including serum lipid concentrations) remained constant. No clinical adverse effects attributable to losartan we re observed. Results of this study suggest that losartan is an effective, w ell-tolerated drug that reduces LVH, improves left ventricular diastolic fu nctions, and controls systolic and diastolic blood pressures in patients wi th mild-to-moderate essential hypertension.