Epicardial adipose tissue and atrial fibrillation: guilty as charged or guilty by association?

Abstract

Abstract Background Epicardial adipose tissue (EAT) has been linked to the presence and burden of atrial fibrillation (AF). However, it is still unclear whether this relationship is causal or simply a surrogate marker of other risk factors commonly associated with AF. Purpose The purpose of this study was to assess the relationship between these factors and EAT, and to compare their performance in predicting AF recurrence after an ablation procedure. Methods We assessed 575 consecutive patients (mean age 61±11 years, 62% male) undergoing AF ablation preceded by cardiac CT in a high-volume ablation center. EAT was measured on cardiac CT using a modified simplified method. Patients were divided into 2 groups (above vs. below the median EAT volume). Cox regression was used to assess the relationship between epicardial fat, risk factors, and AF relapse. Results Patients with above-median EAT volume were older (p<0.001), more often male (OR 1.7, p=0.002), had higher body mass index, and higher prevalence of smoking, hypertension, diabetes and dyslipidemia (p<0.05). Non-paroxysmal AF was also more common in those with above-median EAT volume. During a median follow-up of 18 months, 232 patients (40.3%) suffered AF recurrence. After adjustment for BMI and other univariate predictors of relapse, three variables emerged independently associated with time to AF recurrence: non-paroxysmal AF (HR 2.1, 95% CI: 1.5–2.7, p<0.001), indexed left atrial (LA) volume (HR 1.006 per mL/m2, 95% CI: 1.002–1.011, p<0.001), and indexed epicardial fat volume (HR 1.87 per mL/m2, 95% CI: 1.66–2.1, p<0.001). None of the classic cardiovascular risk factors were an independent predictor of AF recurrence (all p>0.10). Conclusion Classic cardiovascular risk factors are more prevalent in patients with higher amounts of epicardial fat. However, unlike these risk factors, EAT is a powerful predictor of AF recurrence after ablation. These findings suggest that EAT is not merely a surrogate marker, but an important participant in the pathophysiology of AF. EAT, cvrf and AF burden Funding Acknowledgement Type of funding source: None