» Articles » PMID: 32208439

Effect of Four Classes of Antihypertensive Drugs on Cardiac Repolarization Heterogeneity: A Double-blind Rotational Study

Overview
Journal PLoS One
Date 2020 Mar 26
PMID 32208439
Authors
Affiliations
Soon will be listed here.
Abstract

Background: T-wave area dispersion (TW-Ad) is a novel electrocardiographic (ECG) repolarization marker associated with sudden cardiac death. However, limited data is available on the clinical correlates of TW-Ad. In addition, there are no previous studies on cardiovascular drug effects on TW-Ad. In this study, we examined the relation between TW-Ad and left ventricular mass. We also studied the effects of four commonly used antihypertensive drugs on TW-Ad.

Methods: A total of 242 moderately hypertensive males (age, 51±6 years; office systolic/diastolic blood pressure during placebo, 153±14/100±8 mmHg), participating in the GENRES study, were included. Left ventricular mass index was determined by transthoracic echocardiography. Antihypertensive four-week monotherapies (a diuretic, a beta-blocker, a calcium channel blocker, and an angiotensin receptor antagonist) were administered in a randomized rotational fashion. Four-week placebo periods preceded all monotherapies. The average value of measurements (over 1700 ECGs in total) from all available placebo periods served as a reference to which measurements during each drug period were compared.

Results: Lower, i.e. risk-associated TW-Ad values correlated with a higher left ventricular mass index (r = -0.14, p = 0.03). Bisoprolol, a beta-blocker, elicited a positive change in TW-Ad (p = 1.9×10-5), but the three other drugs had no significant effect on TW-Ad.

Conclusions: Our results show that TW-Ad is correlated with left ventricular mass and can be modified favorably by the use of bisoprolol, although demonstration of any effects on clinical endpoints requires long-term prospective studies. Altogether, our results suggest that TW-Ad is an ECG repolarization measure of left ventricular arrhythmogenic substrate.

References
1.
Noseworthy P, Havulinna A, Porthan K, Lahtinen A, Jula A, Karhunen P . Common genetic variants, QT interval, and sudden cardiac death in a Finnish population-based study. Circ Cardiovasc Genet. 2011; 4(3):305-11. PMC: 3119024. DOI: 10.1161/CIRCGENETICS.110.959049. View

2.
Wellens H, Schwartz P, Lindemans F, Buxton A, Goldberger J, Hohnloser S . Risk stratification for sudden cardiac death: current status and challenges for the future. Eur Heart J. 2014; 35(25):1642-51. PMC: 4076664. DOI: 10.1093/eurheartj/ehu176. View

3.
Morganroth J, Lichstein E, Byington R . Beta-Blocker Heart Attack Trial: impact of propranolol therapy on ventricular arrhythmias. Prev Med. 1985; 14(3):346-57. DOI: 10.1016/0091-7435(85)90061-1. View

4.
Gardner R, Ripplinger C, Myles R, Habecker B . Molecular Mechanisms of Sympathetic Remodeling and Arrhythmias. Circ Arrhythm Electrophysiol. 2016; 9(2):e001359. PMC: 4730917. DOI: 10.1161/CIRCEP.115.001359. View

5.
Straus S, Kors J, De Bruin M, van der Hooft C, Hofman A, Heeringa J . Prolonged QTc interval and risk of sudden cardiac death in a population of older adults. J Am Coll Cardiol. 2006; 47(2):362-7. DOI: 10.1016/j.jacc.2005.08.067. View