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 furosemide daily, 115 patients with either controlled or uncontrolled hypertension and left ventricular hypertrophy were randomized in a double-blind manner to receive either placebo (n = 40), 1.25 mg (low dose, n = 38), or 5 mg (regular dose, n = 37) ramipril daily for 6 months. Treatment with furosemide was continued unchanged during this phase. The main outcome measured was left ventricular hypertrophy regression as assessed from central blind reading of echocardiograms recorded at randomization and after 6 months. No significant differences were observed for changes in casual or ambulatory blood pressure between the three groups. Left ventricular mass index was found to be significantly reduced in patients receiving 5 mg ramipril compared with those receiving placebo (-10.8 plus/minus 3.7 versus +4.1 plus/minus 4.0 g/m2, P = .008); in patients receiving 1.25 mg ramipril, the difference was close to borderline significance compared with placebo (-7.0 plus/minus 4.3 g/m2, P = .06). Similar results were observed for changes in left ventricular mass (-20.3 plus/minus 6.6 and -13.0 plus/minus 7.8 g in the 5- and 1.25-mg ramipril groups, respectively, versus +9.1 plus/minus 7.2 g in the placebo group; P = .004 and .04, respectively). In a multiple 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 ambulatory or casual systolic and diastolic blood pressures were not predictive of changes in left ventricular mass (P = .15 and .16, respectively). Ramipril at 1.25 and 5 mg daily for 6 months can induce left ventricular hypertrophy regression, independent of changes in blood pressure, in patients under furosemide (20 mg/d) antihypertensive therapy. The implications of this regression for cardiovascular morbidity and mortality in hypertensive patients should now be assessed. (Hypertension. 1995;25:92-97.)