RAMIPRIL-INDUCED REGRESSION OF LEFT-VENTRICULAR HYPERTROPHY IN TREATED HYPERTENSIVE INDIVIDUALS

Citation
M. Lievre et al., RAMIPRIL-INDUCED REGRESSION OF LEFT-VENTRICULAR HYPERTROPHY IN TREATED HYPERTENSIVE INDIVIDUALS, Hypertension, 25(1), 1995, pp. 92-97
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
25
Issue
1
Year of publication
1995
Pages
92 - 97
Database
ISI
SICI code
0194-911X(1995)25:1<92:RROLHI>2.0.ZU;2-4
Abstract
The objective of this trial was to assess the effects of 6-month daily treatment with two doses of ramipril on left ventricular mass and the dependence of this on blood pressure changes in hypertensive patients with left ventricular hypertrophy. After a selection phase of 4 to 6 weeks with patients under antihypertensive therapy with 20 mg furosemi de daily, 115 patients with either controlled or uncontrolled hyperten sion and left ventricular hypertrophy were randomized in a double-blin d manner to receive either placebo (n=40), 1.25 mg (low dose, n=38), o r 5 mg (regular dose, n=37) ramipril daily for 6 months. Treatment wit h furosemide was continued unchanged during this phase. The main outco me measured was left ventricular hypertrophy regression as assessed fr om central blind reading of echocardiograms recorded at randomization and after 6 months. No significant differences were observed for chang es in casual or ambulatory blood pressure between the three groups. Le ft ventricular mass index was found to be significantly reduced in pat ients receiving 5 mg ramipril compared with those receiving placebo (- 10.8+/-3.7 versus +4.1+/-4.0 g/m(2), P=.O08); in patients receiving 1. 25 mg ramipril, the difference was close to borderline significance co mpared with placebo (-7.0+/-3.3 g/m(2), P=.06). Similar results were o bserved for changes in left ventricular mass (-20.3+/-6.6 and -13.0+/- 7.8 g in the 5- and 1.25-mg ramipril groups, respectively, versus +9.1 +/-7.2 g in the placebo group; P=.004 and .04, respectively). In a mul tiple regression model testing 10 potential explicative variables, we found that this reduction was correlated with treatment, both 1.25 and 5.0 mg ramipril (P=.03 and .01, respectively), and with the baseline value of the left ventricular mass index (P=.005). Changes in ambulato ry or casual systolic and diastolic blood pressures were not predictiv e of changes in left ventricular mass (P=.15 and .16, respectively). R amipril at 1.25 and 5 mg daily for 6 months can induce left ventricula r hypertrophy regression, independent of changes in blood pressure, in patients under furosemide (20 mg/d) antihypertensive therapy. The imp lications of this regression for cardiovascular morbidity and mortalit y in hypertensive patients should now be assessed.