Epicardial Fat and HF with Preserved Ejection Fraction in Coronary Artery Disease

Patient in hospital bed. Critical care needed.
A study was conducted to determine the relationship between epicardial adipose tissue in patients with CAD and the development of HFpEF.

Epicardial adipose tissue (EAT) thickness is linked with heart failure with preserved ejection fraction (HFpEF) in patients with coronary artery disease, according to study findings published in the International Journal of Cardiology.

Investigators sought to examine if EAT as the source of inflammation and the change in EAT over time is associated with the progression of HFpEF in patients with coronary artery disease. EAT thickness was defined as space between the myocardium and the pericardium that was indexed [EATi] by body surface area.

They conducted a retrospective study that includes 379 patients (aged 65.2±11.7 years, 29.8% women) with coronary artery disease but no baseline heart failure. These patients had received echocardiographic and clinical assessment from 2010 to 2013 and were assessed again from 2014 to 2018. Change in EATi was represented by the difference in measurement between baseline and follow-up (median follow-up time, 4.3 years).

Investigators found that 37.5% of patients developed HFpEF within the follow-up period. These patients exhibit higher EATi at baseline (2.4±1.3 vs 1.9±0.9 mm/m2; P =.001), and EATi associated with the onset of HFpEF (1.25 [1.01–1.54]; P =.04). Independent of additional risks and baseline EATi, the onset of HFpEF correlates with an increase in EATi over time (1.39 [1.04–1.87]; P =.03). Baseline b-type natriuretic peptide (BNP) levels are not associated with EATi (2.24 [-0.27 to 4.76]; P =.08), however a clear association exists between EATi and follow-up BNP levels (4.31 [0.58–8.05]; P =.024).

According to investigators, study limitations include the retrospective design leading to selection and information bias and the inability to establish a causal relationship between HFpEF onset and epicardial fat accumulation. Also, the method used of quantification of epicardial fat does not allow for precise localization of epicardial fat.

Researchers concluded that the onset and development of HFpEF is linked with EATi and its change over time, and they noted, “The finding of changes in EATi altering the risk of HFpEF manifestation support the rationale for further research on epicardial fat modulation as a treatment target for HFpEF.”


Mahabadi AA, Anapliotis V, Dykun I, et al. Epicardial fat and incident heart failure with preserved ejection fraction in patients with coronary artery disease. Int J Cardiol. Published online April 5, 2022. doi:10.1016/j.ijcard.2022.04.009