Efficacy of exercise, losartan, enalapril, atenolol and rilmenidine in subjects with blood pressure hyperreactivity at treadmill stress test and left ventricular hypertrophy.

High levels of activity of the renin-angiotensin system (RAS) and sympathetic nervous system (SNS) are related to left ventricular hypertrophy (LVH). A percentage of subjects with hyperactivity to treadmill stress test show LVH to echocardiogram. This paper aims at evaluating neurohumoral influence over these subjects by comparing drugs that block both the RAS and the SNS. In a 1-year open protocol, 195 normotensive subjects, with hyperactivity to treadmill stress test and LVH, were randomly assigned to supervised physical exercise, rilmenidine 1 mg day(-1), atenolol 50 mg day(-1), enalapril 10 mg day(-1) or losartan 50 mg day(-1). Changes in left ventricular mass index (LVMI), measured by means of echocardiogram, were the primary end point. Changes in systolic blood pressure (SBP) at rest and peak effort were also evaluated. Enalapril significantly brought LVMI down in relation to the basal value (28.2%; n=36) similarly to losartan (26.9%; n=42); P>0.05. However, both were more efficient than physical exercise (2.9%; n=39), rilmenidine (5.1%; n=38) and atenolol (7.2%; n=40); P<0.001. There was no significant difference in SBP reduction at rest and peak effort in groups assigned to atenolol, enalapril and losartan; P>0.05. In such groups, reduction was greater than in groups assigned to physical exercise and rimenidine; P<0.001. In conclusion, drugs that block RAS were more efficient in reducing LVH than physical exercise and drugs that block SNS, and such reduction took place regardless of SBP level reduction at rest and peak effort.

Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan.

OBJECTIVE: To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses. METHODS: Patients of both sexes with moderate hypertension confirmed by ambulatory monitoring of arterial blood pressure and with left ventricular hypertrophy on echocardiogram were assigned to three groups: enalapril (35 mg/day, n=15), losartan (175 mg/day, n=15) and enalapril losartan (15 mg+100 mg/day, n=16). The patients received the drugs for 10 months. RESULTS: The three therapeutic regimens were equally effective in reducing blood pressure and left ventricular mass index (LVMI, g/m2): 141+/-3.9 to 123+/-3.6 in the enalapril group (p<0.05), from 147+/-3.8 to 133+/-2.8 in the losartan group (p<0.05), and from 146+/-3.0 to 116+/-4.0 in the enalapril+losartan group (p<0.05). However, the percent reduction of LVMI was significantly greater (p<0.01) in the enalapril+losartan group (20.5+/-5.0%) than in enalapril (12.4+/-3.2%) and the losartan (9.1+/-2.1%) groups. Normalization of LVMI was obtained in 10 out of the 16 patients who received enalapril+ losartan, in 6 out of the 15 patients who received only enalapril and in 4 out of the 15 patients treated with losartan. CONCLUSION: The combination of an angiotensin-converting enzyme inhibitor and an angiotensin II receptor antagonist (AT1 receptor antagonist) in patients produced an additional effect on the reduction of left ventricular hypertrophy. This finding may depend on a more complete inhibition of the cardiac renin-angiotensin.