Abstract:

Purpose: Detection of a decrease in left ventricular hypertrophy (SVH) with antihypertensive treatment is associated with a decrease in the risk of cardiovascular disease. Angiotensin receptor blockers (ARBs) are an effective agent in the deterioration of SVH associated with hypertension. We intended to investigate the impact of Olmesartan on SVH in our study. Method: We included patients with hypertension with SVH in our study. The study included 16 patients with 20 mg/day and 16 atenolol 50 mg/day. Ecocardiography was applied to all patients at the beginning, in the 1st and 6th months. The left ventricular mass index (SVKI) was calculated by the Devereux formula. Results: In Olmesartan group, the initial SVKI was 127.7 ± 21.8 gr/m2, 124.2 ± 19.7 gr/m2 in the first month and 107.3 ± 17.2 gr/m2 in the sixth month. The initial SVKI in the Atenolol group was 128.7 ± 24.2 gr/m2, 128.3 ± 24.2 gr/m2 in the first month and 123.1 ± 22.7 gr/m2 in the sixth month. There was no significant difference between the two groups at the beginning. There is no significant difference between the two groups of SVKI’s values in the first month. There was a statistically significant difference between the sixth month of the SVKI. (p = 034 and 034 ) The result: the area between the two groups that did not have the SVKI at the end of the 6th month significantly declined in the group. The reduction in the SVKI in the Olmesartan group suggests that, in addition to lowering blood pressure, ARBs have a molecular effect.

Abstract:

Objective: Detection of left ventricular hypertrophy (LVH) regression with antihypertensive treatment in hypertensive patients is associated with decreased risk of cardiovascular disease. Angiotensin receptor blockers (ARBs) that were decreased left ventricular hypertophy in hypertensive patients. In this study, we aimed to investigate the effect of olmesartan on LVH in hypertensive patients. Method: In this study we enrolled hypertensive patients whom have LVH. 16 patients received olmesartan 20 mgr/day and 16 patients received atenolol 50 mgr/day. Echocardiography was performed at the begining and in the first and sixth month. Left ventricular mass index (LVMI) were calculated using Devereux Formula. Results: In the olmesartan group, initial left ventricular mass index (LVMI) was 127.7 ± 21.8 g / m2, 124.2 ± 19.7 g / m2 in the first month and 107.3 ± 17.2 g / m2 in the sixth month. The initial LVMI in the atenolol group was 128.7 ± 24.2 g / m2, 128.3 ± 24.2 g / m2 in the first month and 123.1 ± 22.7 g / m2 in the sixth monthThere was no significant difference between LVMI in both groups at baseline and at 1 month. LVMI regressed more in the group receiving olmesartan in the sixth month ( p= 0,034). Conclusion: LVMI regressed significantly in the group receiving olmesartan at the end of the 6th month. The decrease in LVMI in Olmesartan group suggests that ARBs have molecular effect besides blood pressure decrease.

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