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Life sciences · Journal article
Journal of Clinical Medicine · October 19, 2026
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Obesity is a major, modifiable risk factor for atrial fibrillation (AF). Potential mechanisms include haemodynamic and metabolic changes, inflammation, changes in epicardial adipose tissue (EAT) composition and cardiovascular–kidney–metabolic (CKM) syndrome. EAT is increasingly recognised as a dynamic, pro-arrhythmic fat depot with a possible bidirectional relationship with AF, whereby AF itself may modulate EAT independent of weight change. CKM syndrome also underlies the complex interplay between obesity and AF. Despite guideline recommendations for at least 10% weight reduction in obese patients with AF, recent randomised trials focusing on weight reduction have largely failed to demonstrate clinically meaningful improvements in AF outcomes compared with catheter ablation or usual care. Incretin-based therapies including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are a promising therapy offering sustained weight loss alongside broader cardiometabolic benefits, although randomised trials with AF as a primary endpoint are lacking. Comprehensive multidisciplinary lifestyle risk factor modification (LRFM) clinics that address cardiometabolic risk factors, AF education and medication adherence have shown benefit beyond weight reduction alone, although their delivery has been heterogeneous. This narrative review examines the evolving relationship between obesity and AF including a multidimensional cardiometabolic lens, EAT characterisation, contemporary randomised trials of weight reduction, and the emerging role of incretin-based therapies and LRFM clinics.