Obesity drives atrial fibrillation pathogenesis; GLP-1R agonists and bariatric surgery show promise as disease-modifying therapies.

Atrial fibrillation (AF) is a prevalent arrhythmia with significant morbidity, and current treatments like catheter ablation often yield suboptimal long-term outcomes, particularly for persistent AF. Obesity has emerged as a major modifiable risk factor, inducing a specific atrial cardiomyopathy characterized by structural remodeling, fibrosis, epicardial adipose tissue expansion, inflammation, autonomic imbalance, and metabolic dysfunction. Understanding these mechanisms and leveraging metabolic interventions is crucial to improve AF management.

This review synthesized current evidence linking obesity to atrial fibrillation (AF), focusing on epidemiology, pathophysiological mechanisms, and therapeutic implications. The analysis was based on a structured, nonsystematic review of the literature, primarily using PubMed with 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 (BMI) 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 significantly reduces AF burden and improves rhythm control outcomes. Bariatric surgery and glucagon-like peptide-1 receptor agonists (GLP-1RAs) show promise as disease-modifying strategies. These therapies address the underlying metabolic factors, offering a novel approach to mitigate AF pathogenesis beyond traditional antiarrhythmic interventions. The review highlights that integrated management of weight and metabolic factors offers potential to improve outcomes, although direct atrial effects of metabolic therapies require further clarification.