Epicardial adipose tissue (EAT) is a visceral fat layer surrounding the heart, closely connected to the myocardium. It plays a significant role in heart failure (HF) by secreting inflammatory cytokines and fatty acids, which can lead to myocardial remodeling. EAT is associated with both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In HFrEF, EAT volume is reduced, while in HFpEF, increased EAT is linked to worse biomarker and hemodynamic profiles. EAT is easily assessed using imaging techniques like echocardiography, cardiac MRI, and CT. Recent studies suggest that SGLT2 inhibitors may reduce EAT volume, potentially improving HF outcomes. EAT is also a therapeutic target, with GLP-1 receptor agonists showing promise in reducing EAT thickness. Further research is needed to fully understand EAT's role in HF and its therapeutic potential.Epicardial adipose tissue (EAT) is a visceral fat layer surrounding the heart, closely connected to the myocardium. It plays a significant role in heart failure (HF) by secreting inflammatory cytokines and fatty acids, which can lead to myocardial remodeling. EAT is associated with both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In HFrEF, EAT volume is reduced, while in HFpEF, increased EAT is linked to worse biomarker and hemodynamic profiles. EAT is easily assessed using imaging techniques like echocardiography, cardiac MRI, and CT. Recent studies suggest that SGLT2 inhibitors may reduce EAT volume, potentially improving HF outcomes. EAT is also a therapeutic target, with GLP-1 receptor agonists showing promise in reducing EAT thickness. Further research is needed to fully understand EAT's role in HF and its therapeutic potential.