Effect of Telmisartan on the Regression of the Left Ventricular Hypertrophy in the Patients of Essential Hypertension

Abstract

Introduction: An increase in the Left Ventricular Mass as a result of muscle hypertrophy, has emerged as a powerful pressure independent risk factor for the cardiovascular mortality and morbidity. It is associated with a risk of death that is 3 times greater than the risk which is associated with hypertension alone. For the development of Left Ventricular Hypertrophy (LVH), in addition to a chronic increase in the pressure and/or volume overload, an elevation in the plasma ACE activity, plasma aldosterone levels, and the angiotensin-II concentrations play a major role .In this study, the effect of Telmisartan, a selective angiotension-II receptor blocker, was compared with that of Atenolol, a selective β 1 adrenergic receptor blocker, on the regression of LVH in the patients of essential hypertension. Material and Method:Essential hypertensive patients with LVH were selected for this study, as per the inclusion and exclusion criteria. This study was carried out on two groups of hypertensive patients with LVH: Group-1 : The patients who were taking telmisartan 80 mg OD. Group-2 :The patients who were taking atenolol 50 mg OD.The blood pressure was measured and echocardiography was done in both the groups, prior to the treatment and 6 months after the treatment in the

The valosin‐containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload

“…First, VCP attenuated the cardiac response to pressure overload by inhibiting the mechanical stretch‐induced reprogramming of fetal genes, which is a known mechanism of LVH. Secondly, it has been reported that AngII plays an important role in pathological cardiac hypertrophy beyond blood pressure elevation (Misra et al ., ). Our data showed that VCP was downregulated in AngII‐induced hypertrophic cardiomyocytes in a dose‐ and time‐dependent manner, whereas the overexpression of VCP prevented these AngII‐induced changes.…”

Telmisartan improves myocardial remodeling by inhibiting leptin autocrine activity and activating PPARγ

“…Telmisartan can also reverse myocardial remodeling and improve LVH in hypertension. 17–19 Moreover, our previous results suggested that telmisartan could reduce perirenal adipose tissue-derived leptin paracrine activity and exert an indirect renoprotective effect on MetS rats by restoring the balance between angiotensin II-AT1R and angiotensin-converting enzyme 2-angiotensin (1–7)-Mas axes. 20 The present study therefore investigated whether telmisartan can reverse myocardial remodeling by reducing leptin autocrine activity induced by local Ang II in rats with hypertensive LVH, and assessed the potential molecular mechanisms underlying the effects of telmisartan on hypertensive LVH.…”