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

• Main Authors: Kumar Haraprasad Misra, Mangala Charana Das, Y Roja Ramani
• Format: Article
• Language: English
• Published: JCDR Research and Publications Private Limited 2013-07-01
• Series: Journal of Clinical and Diagnostic Research
• Subjects: left ventricular hypertrophy; hypertension; telmisartan
• Online Access: https://jcdr.net/articles/PDF/3127/22%20-%205416_PF1(M)_E(C)_F(T)_PF1(M)_PF1(T)_PF1(PUH)_PFA(H)_PF3(PM)_uPF3(PP)_u(P).pdf
• ISSN: 2249-782X; 0973-709X

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 β1 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 Department of Cardiology, MKCG Medical College Hospital, Brahmapur, India. The data were analysed by using the Student’s ‘t’ test. Results: In the cases of Left Ventricular Mass Index (LVMI), which is a better indicator of LVH, in the Atenolol group, the mean value changed from 143.93 ± 2.44 gm/m2 to 130.16 ± 2.88 gm/m2 (t=5.83,p<0.01 versus baseline).In the Telmisartan group, the mean value changed from 184.67 ± 7.14 gm/m2 to 133.41 ± 4.24 gm/m2 (t=12.12, p<0.001 versus baseline). On comparing Telmisartan with Atenolol, Telmisartan was found to produce a greater (27.49%) reduction than Atenolol (9.68%). In the Telmisartan group, 13 patients out of 26 patients achieved a target value of LVMI that was <134 gm/m2 in males and <110 gm/m2 in females (50%). In the Atenolol group, only 9 patients out of 22 patients achieved a target value (40.90%). Conclusion: Thus, Telmisartan a selective AT1 antagonist, possesses pharmacological effects beyond a blood pressure reduction in which the blockade of the AT1 receptor may lead to attenuation of the growth promoting action of Ang II. From this study, it is clear that Telmisartan is superior to Atenolol in achieving a regression of LVH, which is a better indicator of the cardiovascular morbidity and mortality.