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Regression of the Left Ventricular Hypertrophy in Patients with Essential Hypertension on Standard Drug Therapy

DISCOVERIES (ISSN 2359-7232), 2020, July-September issue

CITATION: 

Ahmed SN, Jhaj R, Sadasivam B, Joshi R. Regression of the Left Ventricular Hypertrophy in Patients with Essential Hypertension on Standard Drug Therapy. Discoveries 2020, 8(3): e115. DOI: 10.15190/d.2020.12


Submitted: August 3, 2020; Revision: September 4, 2020; Accepted: September 10, 2020; Published: September 30, 2020; 

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Regression of the Left Ventricular Hypertrophy in Patients with Essential Hypertension on Standard Drug Therapy

Shah Newaz Ahmed (1, *), Ratinder Jhaj (1), Balakrishnan Sadasivam (1), Rajnish Joshi (2)

(1) Department of Pharmacology, All India Institute of Medical Sciences Bhopal, Madhya Pradesh, India

(2) Department of General Medicine, All India Institute of Medical Sciences Bhopal, Madhya Pradesh, India


*Corresponding author: Dr Shah Newaz Ahmed, Department of Pharmacology, All India Institute of Medical Sciences Bhopal, Bhopal, Madhya Pradesh, India; Phone: 91-9903857789; Email: shahnewazpharmacology@gmail.com

Abstract

Purpose: The American College of Cardiology/ American Heart Association 2017 and European Society of Cardiology/European Society of Hypertension 2018 guidelines were a paradigm shift in hypertension management in contemporary medicine. Lowering of blood pressure to less than 130 (systolic) and 80 (diastolic) mm of Hg irrespective of cardiovascular risk is recommended. While intensive blood pressure control is commonly achievable with rational pharmacotherapy, the magnitude of left ventricular hypertrophy regression is an independent factor in improvement in cardiovascular health. The regression of left ventricular hypertrophy has been adjudged as a clinically useful surrogate marker that reflects the efficacy of hypertension treatment. Though angiotensin converting enzyme inhibitors/ angiotensin receptor blockers (ACEI/ARB) are the preferred initial drug for greater regression of left ventricular mass, the choice of add-on therapy, if required, is still debatable. Therefore, in our observational study, we sought to compare the reduction in left ventricular mass index in hypertensives with left ventricular hypertrophy on standard ACEI/ARB based drug therapy.

Materials and Methods: The cohort (n=217) comprised of patients with uncontrolled hypertension (blood pressure>140/90 mm of Hg) and left ventricular hypertrophy (left ventricular mass index>115 and 95 gram/square meter in males and females respectively). The add-on drug in ACEI/ARB therapy was either thiazide diuretics (TD) or calcium channel blockers (CCB). Four sub-cohorts were constituted: mono-therapy - group A (n=70, ACEI/ARB), dual-therapy - group B (n=48, ACEI/ARB+TD) and  group C (n=51, ACEI/ ARB+CCB), triple therapy - group D (n=48, ACEI/ ARB+TD+CCB). Left ventricular mass index was determined using echocardiography at baseline and after 24 weeks of therapy.

Results: There was no significant difference in baseline clinical or demographic variables between group B and group C. Baseline blood pressure and duration of hypertension was greater in group D compared to group A (P<0.001). The reduction in left ventricular mass index (mean ±SD) in the four groups (A to D) was 16.7±18.7, 21.0±20.8, 20.5±15.5  and 29.1±21.5 g/m2  respectively (D>A, P=0.011, B versus C, P=1.00). The corresponding change in blood pressure (systolic/diastolic) was 18.5±13.6/8.9±11.2, 27.5±19.2/12.2±9.3, 23.4±16.7/ 5.4±10.1, 26.6±19.5/10.7±12.8 mm of Hg respectively (systolic, B>A, P=0.027, D>A, P=0.048) (diastolic, B>C, P=0.013).

Conclusion: Anti-hypertensive treatment with angiotensin converting enzyme inhibitors/angiotensin receptor blockers-based therapy produced graded regression of left ventricular hypertrophy with monotherapy, dual therapy and triple therapy.  In dual therapy, add-on of either thiazide diuretics or calcium channel blockers to angiotensin converting enzyme inhibitors/angiotensin receptor blockers showed equal efficacy in regression of left ventricular hypertrophy independent of blood pressure reduction.


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