Cross talk: Fat and the arrhythmogenic substrate

The classical view that scarred, fibrotic myocardium in patients with myocardial infarction (MI) is the basis for ventricular tachycardia by producing a critical activation delay in surviving myocardial strands 1 Stevenson W.G. Khan H. Sager P. et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation. 1993; 88: 1647-1670 Crossref PubMed Scopus (788) Google Scholar was recently challenged by Sung et al. 2 Sung E. Prakosa A. Zhou S. et al. Fat infiltration in the infarcted heart as a paradigm for ventricular arrhythmias. Nat Cardiovasc Res. 2022; 1: 933-945 Crossref PubMed Scopus (9) Google Scholar They quantified the volume of epicardial adipose tissue in patients with MI in combination with a personalized computer simulation study and came to the conclusion that infiltrating adipose tissue is more predictive of the occurrence of ventricular arrhythmia (VA) than scar. Association of epicardial and intramyocardial fat with ventricular arrhythmiasHeart RhythmVol. 20Issue 12PreviewAmong patients with ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM), myocardial fibrosis is associated with an increased risk for ventricular arrhythmia (VA). Growing evidence suggests that myocardial fat contributes to ventricular arrhythmogenesis. However, little is known about the volume and distribution of epicardial adipose tissue and intramyocardial fat and their relationship with VAs. Full-Text PDF