Obesity and Atrial Fibrillation: From Mechanisms to Treatment
Date
2025
Authors
Dziano, J.K.
Ariyaratnam, J.P.
Middeldorp, M.E.
Sanders, P.
Elliott, A.D.
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Journal article
Citation
Heart Lung and Circulation, 2025; 34(10):1021-1032
Statement of Responsibility
Jenelle K. Dziano, Jonathan P. Ariyaratnam, Melissa E. Middeldorp, Prashanthan Sanders, Adrian D. Elliott
Conference Name
Abstract
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.
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© 2025 The Author(s). Published by Elsevier B.V. on behalf of Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).