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Life sciences · Journal article
Frontiers in Endocrinology · October 9, 2026
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Obesity-related heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF) often coexist, but the contribution of epicardial adipose tissue (EAT) to their overlap remains uncertain. EAT is anatomically contiguous with the myocardium and can undergo inflammatory, profibrotic and metabolic remodeling in obesity. In HFpEF, greater EAT burden is associated with higher filling pressures and findings compatible with external cardiac restraint; in AF, regional peri-atrial fat is associated with abnormal conduction, fibrosis and ablation outcomes. Human EAT experiments demonstrate local profibrotic signaling, while autonomic interventions involving epicardial fat pads provide procedural evidence that does not isolate adipocyte effects. Recent invasive observations in patients with AF also link CT-defined EAT to atrial pressures and obesity-related HFpEF. Exercise, weight loss and metabolic therapies can change measured cardiac fat, although the relevant compartments and responses vary. CT attenuation is not a direct or uniformly directional measure of EAT inflammation. EAT is therefore a measurable phenotype at the HFpEF–AF interface, with stronger local experimental evidence in AF than in HFpEF. Whether changing EAT itself contributes to clinical benefit beyond systemic weight loss or other treatment effects requires longitudinal studies in patients with both conditions.