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

Auriane C. Ernault, Veronique M. F. Meijborg, Ruben Coronel

Research output: Contribution to journalReview articleAcademicpeer-review

53 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)1730-1745
Number of pages16
JournalJournal of the American College of Cardiology
Volume78
Issue number17
DOIs
Publication statusPublished - 26 Oct 2021

Keywords

  • arrhythmias
  • cardiac electrophysiology
  • cardiovascular diseases
  • epicardial adipose tissue
  • obesity

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