Obesity, Metabolic Modulation, and Arrhythmias: From Adipose Tissue Dysfunction to a Modifiable Arrhythmogenic Substrate.

The obese patient with arrhythmia represents a major challenge in cardiology. In these patients, multiple mechanisms converge to create a pro-arrhythmic milieu that remains poorly understood and only partially controllable. The anatomical and functional remodeling of adipose tissue, local inflammation, metabolic alterations, and the frequent presence of associated comorbidities lead to structural, functional, and electrical cardiac changes, resulting in a pro-arrhythmic substrate. The coexistence of these multiple contributing factors may reduce the efficacy of currently available antiarrhythmic therapies in this specific population. Although these obesity-related alterations are not currently established therapeutic targets, they may represent promising targets for future interventions to improve patients' outcomes. In this narrative review, we summarize the main scientific evidence regarding the pro-arrhythmic cardiac alterations associated with obesity, focusing separately on structural and electrical remodeling and on the role of epicardial and visceral adipose tissue. We conclude by discussing recent evidence suggesting that several therapeutic strategies may reverse this pro-arrhythmic milieu, with a particular focus on established anti-obesity treatments and emerging experimental therapeutic approaches.