Beneficial impact of ramipril on left ventricular hypertrophy in normotensive nonalbuminuric NIDDM patients

OBJECTIVE - To evaluate the effect of the ACE inhibitor ramipril as compared with placebo on left ventricular mass index (LVMI) in normotensive, nonalbuminuric NIDDM patients with left ventricular hypertrophy (LVH). Patients with NIDDM are characterized by excessive cardiovascular morbidity and mortality, and LVH, an independent risk factor for cardiac events, is often present in NIDDM patients. RESEARCH DESIGN AND METHODS - A total of 38 normotensive, nonalbuminuric (albuminuria < 100 mg/24 h) NIDDM patients with LVH (LVMI > 131 g/m² in men and > 100 g/m² in women) were enrolled in a 6- month randomized, double-blind parallel group study to compare the effects of ramipril (5 mg/day) with placebo on LVMI (echocardiography, Vingmed CFM725, Diasonics Sonotron), QT(c) dispersion determined as the interlead variation in QT(c) interval on standard electrocardiogram (ECG), and 24-h ambulatory blood pressure (A and D TM2420, Tokyo, Japan). A total of 16 ramipril (10 men, 60 ± 9 years [mean ± SD]) and 15 placebo-treated (8 men, 55 ± 10 years) patients completed the study, and their data are presented. RESULTS - Ambulatory blood pressure was almost identical at baseline (132/76 ± 3/1 vs. 133/74 ± 5/2 mmHg [mean ± SEM]) and remained stable during follow-up (134/76 ± 3/1 vs. 136/74 ± 6/2 mmHg) in the ramipril and placebo group, respectively. LVMI was comparable at baseline (137.1 ± 7.0 vs. 129.6 ± 3.7 g/m²) in the ramipril and placebo group, respectively, and decreased significantly more in the ramipril group as compared with the placebo group (17.6 ± 3.0 vs. 5.7 ± 4.6 g/m², respectively, 11.9 [0.7-23.1] g/m², mean difference [95% CI]; P = 0.037). QT(c) dispersion was comparable at baseline (60.2 [5.5] vs. 64.1 [6.5] ms) and did not change significantly during follow-up: -2.5 [7.0] vs. -12.2 [9.5] ms; mean difference 9.8 (-14.2 to 33.8 ms) in the ramipril and placebo group, respectively. CONCLUSIONS - Ramipril induces regression of LVH in normotensive, nonalbuminuric NIDDM patients, independent of reduction in systemic blood pressure.