Obesity and atrial fibrillation: from mechanisms to treatment

By 2050, it is projected that 3.8 billion people worldwide will be overweight or obese. Alongside this growing burden of obesity is a parallel rise in the incidence and prevalence of atrial fibrillation (AF). Obesity promotes the onset of AF through several pathways, including left atrial remodelling, accumulation of epicardial adipose tissue, alterations in cardiac loading, increased inflammation, and renin-angiotensin-aldosterone system activation. In parallel, obesity frequently coexists with and can contribute to comorbidities, including hypertension, type 2 diabetes, and obstructive sleep apnoea. The past decade has seen the introduction of comorbidity and risk factor treatment as the central pillar in the care of patients with AF based on studies showing that weight loss reduces the recurrence of symptomatic AF. As we move deeper into the era of pharmacological treatment for obesity, new opportunities will appear to refine the care of patients living with AF. This review summarises the existing evidence supporting obesity as a major risk factor for AF and discusses the therapeutic options to treat obesity and prevent the growing burden of AF in the community.