Epicardial adipose tissue (EAT), the visceral fat layer next to the myocardium, has become an important focus in heart failure with preserved ejection fraction (HFpEF). When enlarged and inflamed, EAT increases pericardial restraint, releases fibroinflammatory mediators, and disrupts myocardial energetics, thereby reproducing the high-pressure, exercise-intolerant HFpEF phenotype regardless of body mass index. Modern echocardiography, cardiac CT, and MRI, enhanced by artificial intelligence texture analytics, now enable precise depot-specific quantification, making EAT a measurable therapeutic target. Early interventional studies suggest that caloric restriction, bariatric surgery, SGLT2 inhibitors, GLP-1 receptor agonists, statins, PCSK9 antibodies, and colchicine can reduce EAT volume or alter its inflammatory profile, with concurrent improvements in haemodynamics and biomarkers. However, definitive outcome trials are still pending. Priority directions include standardising imaging cut-offs, mapping EAT immune–metabolic niches, and testing combined metabolic–inflammatory regimens to translate EAT modulation into precision therapy for HFpEF. This review aims to synthesise current mechanistic, diagnostic, and therapeutic insights on EAT in HFpEF and outline future research priorities.
Mihăilă et al. (Sat,) studied this question.