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Obesity and atrial fibrillation (AF) are closely connected conditions that share many metabolic, hemodynamic, and inflammatory pathways. An increasing body mass index is linked to incident AF, AF progression, and higher recurrence rates after cardioversion or catheter ablation. Notably, obesity contributes to atrial structural and electrical remodeling through various mechanisms, including systemic inflammation, oxidative stress, epicardial adipose tissue buildup, metabolic dysregulation, and changes in calcium handling and connexin expression. These alterations create a proarrhythmic substrate that promotes AF initiation and maintenance. Sustained weight loss has been strongly associated with reverse atrial remodeling, improved hemodynamics, decreased AF burden, and lower recurrence rates. In this evolving treatment landscape, anti-obesity pharmacotherapy, particularly glucagon-like peptide-1 (GLP-1) receptor agonists, has emerged as a promising supplementary strategy. Beyond weight reduction and blood sugar control, these medications have pleiotropic cardiovascular effects, such as anti-inflammatory and antioxidant actions, hemodynamic improvements, decreases in epicardial adipose tissue, and reductions in atrial fibrosis. Several observational studies and meta-analyses suggest that GLP-1 receptor agonists lower the risk of new-onset AF and AF recurrence after cardioversion or ablation. However, most available data come from studies where AF was a secondary endpoint, involving diverse populations and relatively short follow-up periods. While anti-obesity drugs - especially GLP-1 receptor agonists - show significant potential to influence AF risk and progression, conclusive evidence requires well-powered randomized controlled trials with AF as the primary endpoint, standardized arrhythmia monitoring, and long-term follow-up.