Obesity and Atrial Fibrillation: Weighing the Evidence
- 1Victorian Heart Institute and Victorian Heart Hospital, Monash Health, Monash University, 631 Blackburn Road, Clayton, VIC 3168, Australia
Abstract
Obesity is a major, modifiable risk factor for atrial fibrillation (AF). Potential mechanisms include haemodynamic and metabolic changes, inflammation, changes in epicardial adipose tissue (EAT) composition and cardiovascular–kidney–metabolic (CKM) syndrome. EAT is increasingly recognised as a dynamic, pro-arrhythmic fat depot with a possible bidirectional relationship with AF, whereby AF itself may modulate EAT independent of weight change. CKM syndrome also underlies the complex interplay between obesity and AF. Despite guideline recommendations for at least 10% weight reduction in obese patients with AF, recent randomised trials focusing on weight reduction have largely failed to demonstrate clinically meaningful improvements in AF outcomes compared with catheter ablation or usual care. Incretin-based therapies including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are a promising therapy offering sustained weight loss alongside broader cardiometabolic benefits, although randomised trials with AF as a primary endpoint are lacking. Comprehensive multidisciplinary lifestyle risk factor modification (LRFM) clinics that address cardiometabolic risk factors, AF education and medication adherence have shown benefit beyond weight reduction alone, although their delivery has been heterogeneous. This narrative review examines the evolving relationship between obesity and AF including a multidimensional cardiometabolic lens, EAT characterisation, contemporary randomised trials of weight reduction, and the emerging role of incretin-based therapies and LRFM clinics.
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BibTeX
@article{ha2026obesity,
title = {{Obesity and Atrial Fibrillation: Weighing the Evidence}},
author = {Francis J. Ha and Jit Yoei Tang and Shaun Khanna and Adam J. Brown and Emily Kotschet and Nitesh Nerlekar},
journal = {Journal of Clinical Medicine},
year = {2026},
month = oct,
doi = {10.3390/jcm15208101},
url = {https://www.mdpi.com/2077-0383/15/20/8101},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Obesity and Atrial Fibrillation: Weighing the Evidence
AU - Francis J. Ha
AU - Jit Yoei Tang
AU - Shaun Khanna
AU - Adam J. Brown
AU - Emily Kotschet
AU - Nitesh Nerlekar
PY - 2026
DA - 2026/10/19
JO - Journal of Clinical Medicine
DO - 10.3390/jcm15208101
UR - https://www.mdpi.com/2077-0383/15/20/8101
AB - Obesity is a major, modifiable risk factor for atrial fibrillation (AF). Potential mechanisms include haemodynamic and metabolic changes, inflammation, changes in epicardial adipose tissue (EAT) composition and cardiovascular–kidney–metabolic (CKM) syndrome. EAT is increasingly recognised as a dynamic, pro-arrhythmic fat depot with a possible bidirectional relationship with AF, whereby AF itself may modulate EAT independent of weight change. CKM syndrome also underlies the complex interplay between obesity and AF. Despite guideline recommendations for at least 10% weight reduction in obese patients with AF, recent randomised trials focusing on weight reduction have largely failed to demonstrate clinically meaningful improvements in AF outcomes compared with catheter ablation or usual care. Incretin-based therapies including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are a promising therapy offering sustained weight loss alongside broader cardiometabolic benefits, although randomised trials with AF as a primary endpoint are lacking. Comprehensive multidisciplinary lifestyle risk factor modification (LRFM) clinics that address cardiometabolic risk factors, AF education and medication adherence have shown benefit beyond weight reduction alone, although their delivery has been heterogeneous. This narrative review examines the evolving relationship between obesity and AF including a multidimensional cardiometabolic lens, EAT characterisation, contemporary randomised trials of weight reduction, and the emerging role of incretin-based therapies and LRFM clinics.
SN - 2077-0383
ER -