Epicardial adipose tissue predicts early-stage atrial fibrillation in heart failure with preserved ejection fraction

Background/Introduction While myocardial fibrosis is a hallmark of established structural remodeling, the drivers of early-stage atrial fibrillation (AF) in heart failure with preserved ejection fraction (HFpEF) are less understood. Specifically, the relative contributions of pro-inflammatory epicardial adipose tissue (EAT) versus diffuse fibrosis (extracellular volume, ECV) in predicting new-onset AF remain unclear. Purpose To determine whether EAT or ECV predicts new-onset AF in HFpEF patients. Methods From a perspective cohort of 228 patients with HFpEF, we enrolled 195 subjects to investigate the early pathophysiology of AF. To ensure a strict baseline of sinus rhythm, all participants underwent long-term ambulatory ECG monitoring to confirm the absence of paroxysmal AF. Patients were then assessed by cardiac magnetic resonance (CMR) imaging to quantify EAT and ECV. Multivariable Cox proportional hazards models were used to investigate the association between myocardial adiposity, fibrosis, and the incidence of new-onset AF. Results After 72-month follow-up, 45 patients (23.1%) developed AF. Patients with AF had higher EAT (45.5±21.7 vs 34.3±18.2 g/m², p=0.001) and NT-proBNP (1367±2145 vs 314±668 pg/mL, p0.001). There was no significant different of ECV (28.1±4.1% vs 27.7±4.8%, p=0.67). EAT independently predicted atrial fibrillation (hazard ratio 1.028, 95% confidence interval 1.011-1.045, p0.001), whereas ECV did not (hazard ratio 1.040, 95% confidence interval 0.969-1.116). Kaplan-Meier analysis revealed higher AF incidence with elevated EAT (p=0.027). Conclusion(s) In patients with HFpEF, epicardial adiposity (EAT), rather than diffuse fibrosis (ECV), independently predicts new-onset AF in patients with HFpEF. This suggests that epicardial fat-mediated mechanisms may predominate over diffuse fibrosis in early-stage AF pathogenesis.Visual abstractEAT quantification