Regression of left ventricular mass with captopril and metoprolol, and the effects of glucose and lipid metabolism

Abstract

Objective: Angiotensin II and insulin have been suggested to promote the development of hypertensive left ventricular (LV) hypertrophy. We compared the effects of captopril and metoprolol on the regression of LV mass and the relation to insulin sensitivity. Design: 51 previously untreated non-diabetic hypertensive patients (mean age 51 ± 8 years, body mass index, BMI 25.9 ± 3.2 kg/m2, office blood pressure, 158/102 mmHg) were randomized to captopril or metoprolol; a low-dose diuretic and/or a calcium cannel antagonist were added, if needed. Interventions: LV mass index (LVMI; by echo-cardiography) and 24-h ambulatory blood pressure were examined at baseline, 6 and 12 months. At baseline and 12 months, insulin sensitivity index (MI) was calculated by a hyperinsulinemic-euglycemic insulin clamp technique. Results: Blood pressures were reduced similarly in both groups. LVMI (115 ± 21 g/m2 at baseline) was reduced in both groups (p < 0.01), but more with captopril than with metoprolol (e.g. - 16 vs -7 g/m2, i.e. -13 vs -6%, at 12 months, p < 0.01). MI decreased by 6% with captopril (p = 0.05) and by 23% with metoprolol (p < 0.01), with no difference between the groups. Changes in LVMI were not related to changes in MI in the two groups, or when all patients were analyzed together. High-density lipoprotein (HDL)-cholesterol decreased (p < 0.05) by both drugs, with small effects on low-density lipoprotein (LDL), and triglycerides increased by 30% with metoprolol (p < 0.01). Conclusion: Blockade of the renin-angiotensin-aldosterone system has a role beyond that of blood pressure reduction in the regression of LV mass. There was no relationship between regression of LV mass and improvement in insulin sensitivity. We could not confirm a beneficial effect of ACE inhibition on insulin sensitivity. Thus, our results do not support the importance of insulin in the control of LV geometry.