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Review
. 2021 Jun;35(6):492-498.
doi: 10.1038/s41371-021-00503-w. Epub 2021 Mar 5.

Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

R Nadarajah  1 , P A Patel  1 , M H Tayebjee  2
Affiliations
Review

Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

R Nadarajah et al. J Hum Hypertens. 2021 Jun.

Abstract

Sudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Postulated mechanisms underpinning ventricular arrhythmias in hypertensive left ventricular hypertrophy.
ECM Extracellular matrix, CAD Coronary artery disease.
See this image and copyright information in PMC

References

    1. Singh S, Shankar R, Singh GP. Prevalence and associated risk factors of hypertension: a cross-sectional study in Urban Varanasi. Int J Hypertens. 2017;2017:5491838. doi: 10.1155/2017/5491838. - DOI - PMC - PubMed
    1. Verdecchia P, Angeli F, Cavallini C, Aita A, Turturiello D, De Fano M, et al. Sudden cardiac death in hypertensive patients. Hypertension. 2019;73:1071–8. doi: 10.1161/HYPERTENSIONAHA.119.12684. - DOI - PubMed
    1. Zheng Z-J, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation. 2001;104:2158–63. - PubMed
    1. Lee SW, Schwartz A, Adams RJ, Yamori Y, Whitmer K, Lane LK, et al. Decrease in Na+,K+-ATPase activity and [3H]ouabain binding sites in sarcolemma prepared from hearts of spontaneously hypertensive rats. Hypertension. 1979;5:682–8. - PubMed
    1. Cerbai E, Barbieri M, Mugelli A. Characterization of the hyperpolarization-activated current, I(f), in ventricular myocytes isolated from hypertensive rats. J Physiol. 1994;481:585–91. doi: 10.1113/jphysiol.1994.sp020465. - DOI - PMC - PubMed