Obesity and Atrial Fibrillation: Epidemiology, Mechanisms, and Therapeutic Implications in the Era of Metabolic Therapies

Obesity has become a major modifiable risk factor for atrial fibrillation (AF) and contributes significantly to its rising global prevalence. Beyond epidemiological associations, obesity induces a specific form of atrial cardiomyopathy characterized by structural remodeling, fibrosis, expansion of epicardial adipose tissue, inflammation, autonomic imbalance, and metabolic dysfunction, all of which promote AF initiation and progression. This review synthesizes current evidence linking obesity to AF, focusing on epidemiology, pathophysiological mechanisms, and therapeutic implications, including catheter ablation, bariatric surgery, and metabolic pharmacotherapies. The analysis is based on a structured, nonsystematic review of the literature, with studies identified primarily through PubMed using keywords related to obesity and AF. Priority was given to large population-based cohorts, mechanistic investigations, randomized controlled trials, and recent high-impact publications, with additional references identified through manual screening. Evidence consistently demonstrates a graded relationship between increasing body mass index and the incidence, progression, and recurrence of AF. Mechanistically, obesity contributes to atrial remodeling through fibrosis, inflammation, dysregulated adipose signaling, autonomic dysfunction, and metabolic disturbances. Interventional studies indicate that sustained weight loss reduces AF burden and improves rhythm control outcomes, while bariatric surgery and glucagon-like peptide-1 receptor agonists show promise as disease-modifying strategies. Overall, obesity plays a central role in AF pathogenesis and represents a key therapeutic target, with integrated management of weight and metabolic factors offering potential to improve outcomes, although further research is needed to clarify the direct atrial effects of metabolic therapies.