Modulation of Cardiac Arrhythmogenesis by Epicardial Adipose Tissue: JACC State-of-the-Art Review.

Obesity is a significant risk factor for arrhythmic cardiovascular death. Interactions between epicardial adipose tissue (EAT) and myocytes are thought to play a key role in the development of arrhythmias. In this review, the authors investigate the influence of EAT on arrhythmogenesis. First, they summarize electrocardiographic evidence showing the association between increased EAT volume and atrial and ventricular conduction delay. Second, they detail the structural cross talk between EAT and the heart and its arrhythmogenicity. Adipose tissue infiltration within the myocardium constitutes an anatomical obstacle to cardiac excitation. It causes activation delay and increases the risk of arrhythmias. Intercellular electrical coupling between cardiomyocytes and EAT can further slow conduction and increase the risk of block, favoring re-entry and arrhythmias. Finally, EAT secretes multiple substances that influence cardiomyocyte electrophysiology either by modulating ion currents and electrical coupling or by stimulating fibrosis. Thus, structural and paracrine cross talk between EAT and cardiomyocytes facilitates arrhythmias.
Competing Interests: Funding Support and Author Disclosures Dr Ernault was supported by Fondation pour la Recherche Médicale (FRM; PBR201810007613). Dr Meijborg was supported by Leducq Foundation grant (RHYTHM): 16CVD02. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)