This article refers to 'Impact of epicardial adipose tissue on cardiovascular haemodynamics, metabolic profile, and prognosis in heart failure' by N.R. Pugliese et al., published in this issue on pages 1858-1871.The (patho)physiological role of epicardial adipose tissue (EAT) in heart failure (HF) is increasingly recognized. 1 EAT shares a common microcirculation with the heart, 2 and can serve as a source of adipocytokines through its anatomical intimacy with the myocardium, contributing to focal and systemic inflammation. 2 Previous studies have highlighted the importance of EAT in HF. [3][4][5][6][7][8][9] Increased EAT was associated with incident HF in the general population, especially with HF and preserved ejection fraction (HFpEF). 9 In patients with prevalent HFpEF, EAT was increased compared to people without HF in four 4-7 out of five studies, 4-8 and associated with increased cardiac filling pressures and inflammatory cytokine concentrations. [4][5][6]8 In contrast, a single study in patients with prevalent HF and reduced ejection fraction (HFrEF) suggested that EAT was reduced compared to people without HF. 3 Unfortunately, most previous studies included patients with HFrEF 3 or HFpEF, 4,5,8 and few have investigated the role of EAT across the ejection fraction spectrum. 6,7 In this issue of the Journal, the study by Pugliese et al. 10 significantly extends prior knowledge on the role of EAT in HF by studying the association of EAT with clinical biomarkers and outcomes in patients with HFrEF and HFpEF. The authors measured EAT thickness on echocardiography in a total of 393 patients with HF (48% HFpEF) and 44 controls. The HF diagnosis in participants was corroborated by objective signs and symptoms of HF, a reduced ejection fraction or increased natriuretic peptides. All participants underwent comprehensive exercise testing with measurement of peak oxygen consumption (VO 2 max) and arterial-venous oxygen content difference (AVO 2 diff) and were followed up forThe opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.