Background: Epicardial adipose tissue (EAT) is a visceral fat tissue that surrounds the coronary arteries and the myocardium without a distinct boundary. EAT is suggested to promote local inflammation, leading to myocardial fibrosis. We aimed to determine, whether EAT is associated with diastolic dysfunction and development of heart failure with preserved ejection fraction (HFpEF).

Methods: We retrospectively included without heart failure at baseline, undergoing clinical and echocardiographic assessment in 2010-2013 and receiving a second clinical and echocardiographic examination in 2014-2018. EAT thickness was defined as space between the myocardium and the pericardium and indexed (EATi) by body surface area. HFpEF was defined according to presence of dyspnea, elevated natriuretic peptides, and structural and/or functional alterations on echocardiography. Logistic regression analysis was performed to determine the association of EAT with onset of HFpEF. 

Results: Overall, 546 patients (mean age 65.2±12.2 years at baseline, 68% male) were included. EATi was associated with E/A- (-0.045 [-0.079 - -0.011], p=0.009) and E/e’-ratio (0.37 [0.06 - 0.68], p=0.018) as measures of diastolic function. During a follow-up of 3.7 (2.7 - 4.8) years, 193 patients developed HFpEF. EATi was higher in patients with onset of HFpEF than in those without (2.4±1.3 vs. 2.0±0.9 mm/m², p=0.002). In regression analysis, EATi was associated with onset of HFpEF (1.30 [1.11 - 1.52], p=0.001). Effect sizes were more pronounced in patients with a duration between both assessments of ≥ median (1.56 [1.22 - 1.99], p=0.0003) and remained statistically significant after adjustment for risk factors (1.38 [1.06 - 1.81], p=0.018). 

Conclusion: EAT is associated with measures of diastolic dysfunction and contributes to development of HFpEF over time. Our results support the hypothesis of a local inflammatory influence of EAT on the development of HFpEF, directing towards potential targets for therapeutic interventions.