2003Hunan Medical JournalRequires access

Therapeutic Efficacy of Valsartan for Treatment of Left Ventricular Hypertrophy and Its Effects on Vascular Active Substances in Hypertension

Jun Yang

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Abstract

ObjectiveTo study the effects of valsartan on reversion of left ventricular hypertrophy(LVH) and vascular active substances in patients with hypertension.Methods Fifty patients with hypertensive LVH were randomly divided into two groups: 26 patients were treated with valsartan(80mg,qd); 24 patients treated with enalapril(10mg,qd) served as control group. Before and 8 weeks after treatment, their blood pressures(BP)were measured by 24 h ambulatory monitoring and levels of plasma rennin activity(PRA),angiotensionⅡ(AngⅡ),aldosterone(ALD) were estimated. Before and 16 weeks after treatment, echocardiography was performed in all patients to monitor indices of LVH and cardiac functions.ResultsBetween two groups, BP decreased obviously after treatment, but the valley peak ratio in valsartan group was better than that of control group(P0.01).Sixteen weeks after treatment ,their diastolic interventricular septum thickness(IVST),left ventricle posterior wall thickness(LVPWT)and left ventricle weight measuring index(LVMI)all decreased significantly(P0.01);there were no statistical differences between two groups. A distinct decline of ALD levels and mild elevation of PRA were observed in both groups. Enalapril caused a decrease of AngⅡlevels, while valsartan raised its levels. This might be related to effective inhibition of AngⅡ receptor by its inhibitor(ARI) in renin angiotensin system. ConclusionsValsartan can decrease 24 h BP steadily, produce a significant regression of LVH, improve the plasma levels of PRA, AngⅡ and ALD, as well as suppress the activity of renin angiotensin system for protecting the target organs.

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ObjectiveTo study the effects of valsartan on reversion of left ventricular hypertrophy(LVH) and vascular active substances in patients with hypertension.Methods Fifty patients with hypertensive LVH were randomly divided into two groups: 26 patients were treated with valsartan(80mg,qd); 24 patients treated with enalapril(10mg,qd) served as control group. Before and 8 weeks after treatment, their blood pressures(BP)were measured by 24 h ambulatory monitoring and levels of plasma rennin activity(PRA),angiotensionⅡ(AngⅡ),aldosterone(ALD) were estimated. Before and 16 weeks after treatment, echocardiography was performed in all patients to monitor indices of LVH and cardiac functions.ResultsBetween two groups, BP decreased obviously after treatment, but the valley peak ratio in valsartan group was better than that of control group(P0.01).Sixteen weeks after treatment ,their diastolic interventricular septum thickness(IVST),left ventricle posterior wall thickness(LVPWT)and left ventricle weight measuring index(LVMI)all decreased significantly(P0.01);there were no statistical differences between two groups. A distinct decline of ALD levels and mild elevation of PRA were observed in both groups. Enalapril caused a decrease of AngⅡlevels, while valsartan raised its levels. This might be related to effective inhibition of AngⅡ receptor by its inhibitor(ARI) in renin angiotensin system. ConclusionsValsartan can decrease 24 h BP steadily, produce a significant regression of LVH, improve the plasma levels of PRA, AngⅡ and ALD, as well as suppress the activity of renin angiotensin system for protecting the target organs.

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Available abstract

ObjectiveTo study the effects of valsartan on reversion of left ventricular hypertrophy(LVH) and vascular active substances in patients with hypertension.Methods Fifty patients with hypertensive LVH were randomly divided into two groups: 26 patients were treated with valsartan(80mg,qd); 24 patients treated with enalapril(10mg,qd) served as control group. Before and 8 weeks after treatment, their blood pressures(BP)were measured by 24 h ambulatory monitoring and levels of plasma rennin activity(PRA),angiotensionⅡ(AngⅡ),aldosterone(ALD) were estimated. Before and 16 weeks after treatment, echocardiography was performed in all patients to monitor indices of LVH and cardiac functions.ResultsBetween two groups, BP decreased obviously after treatment, but the valley peak ratio in valsartan group was better than that of control group(P0.01).Sixteen weeks after treatment ,their diastolic interventricular septum thickness(IVST),left ventricle posterior wall thickness(LVPWT)and left ventricle weight measuring index(LVMI)all decreased significantly(P0.01);there were no statistical differences between two groups. A distinct decline of ALD levels and mild elevation of PRA were observed in both groups. Enalapril caused a decrease of AngⅡlevels, while valsartan raised its levels. This might be related to effective inhibition of AngⅡ receptor by its inhibitor(ARI) in renin angiotensin system. ConclusionsValsartan can decrease 24 h BP steadily, produce a significant regression of LVH, improve the plasma levels of PRA, AngⅡ and ALD, as well as suppress the activity of renin angiotensin system for protecting the target organs.

Key concepts: Valsartan, Medicine, Left ventricular hypertrophy, Enalapril, Ventricle, Internal medicine, Cardiology, Interventricular septum

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