Reduçäo da hipertrofia ventricular esquerda em pacientes com hipertensäo arterial com uso de inalapril, losartan ou a associaçäo enalapril + losartan / Reduction in left ventricualr hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enapril and losartan

ABSTRACT

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 arte-rial 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=1 effective in reducing blood pressure and left ventricular mass index (LVMI, g/m2) 141ñ3.9 to 123ñ3.6 in the enalapril group (p<0.05), from 147ñ3.8 to 133ñ2.8 in the losartan group (p<0.05), and from 146ñ3.0 to5) 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 116ñ4.0 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 (20.5ñ5.0 per cent) than in enalapril (12.4ñ3.2 per cent) and the losartan (9.1ñ2.1 per cent) groups. Normalization of LVMI was obtained in 10 out of the 16 patients who reinhibitor 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. (Au)ceived enalapril+ losartan, in 6 out of the 15 patients who received only enalapril and in 4 out of the 15patients 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.