Atrial fibrillation and epicardial adipose tissue: A bidirectional relationship

Epicardial adipose tissue (EAT) has an established role as a predictor of atrial fibrillation (AF). As a dynamic visceral fat depot overlying the myocardium, EAT shifts between a protective thermogenic state and a pro-inflammatory, pro-fibrotic phenotype that promotes local electromechanical disruption. While EAT has been studied predominantly as a predictor of incident AF and post-ablation recurrence, emerging clinical evidence suggests a bidirectional relationship in which AF itself modulates EAT. Several observational studies evaluating EAT before and after catheter ablation for AF have demonstrated significant reductions in total and left atrial EAT volume independent of changes in body mass index. The most plausible mechanism is sinus rhythm restoration with consequent reversal of atrial myopathy through cross-talk between the underlying myocardium and peri-atrial EAT. Direct thermal effects and microvascular disruption from ablation may contribute additional mechanisms. Several important questions remain unresolved. The confounding effect of weight loss on post-ablation EAT changes has not been adequately separated from rhythm control effects. The impact of pulsed field ablation on EAT remains unknown. Finally, EAT attenuation on computed tomography, a marker of adipose tissue inflammation, may offer complementary insights beyond volume alone. Standardised imaging definitions for EAT analysis are needed to advance our understanding of this potential bidirectional relationship.