The article reviews the role of epicardial adipose tissue (EAT) in heart failure (HF) and its potential as a therapeutic target. EAT, located between the myocardium and visceral pericardium, is anatomically and functionally connected to the heart. It secretes inflammatory cytokines and releases excessive fatty acids, increasing mechanical load on the myocardium and leading to myocardial remodeling. EAT plays a significant role in both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In HFrEF, EAT volume is reduced, while in HFpEF, EAT volume is associated with worse biomarker and hemodynamic profiles. Recent studies using sodium glucose cotransporter 2 (SGLT2) inhibitors have shown potential in reducing EAT volume, but further research is needed to determine the clinical implications. EAT's role in HF is multifaceted, including its inflammatory, metabolic, and mechanical effects. EAT volume is a significant factor in HF pathophysiology and can be assessed using various imaging modalities. The article also discusses the therapeutic potential of EAT, highlighting the effects of SGLT2 inhibitors and glucagon-like peptide-1 receptor agonists (GLP-1RAs) on EAT volume and clinical outcomes in HF. Overall, EAT is a promising biomarker and therapeutic target for HF management.The article reviews the role of epicardial adipose tissue (EAT) in heart failure (HF) and its potential as a therapeutic target. EAT, located between the myocardium and visceral pericardium, is anatomically and functionally connected to the heart. It secretes inflammatory cytokines and releases excessive fatty acids, increasing mechanical load on the myocardium and leading to myocardial remodeling. EAT plays a significant role in both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In HFrEF, EAT volume is reduced, while in HFpEF, EAT volume is associated with worse biomarker and hemodynamic profiles. Recent studies using sodium glucose cotransporter 2 (SGLT2) inhibitors have shown potential in reducing EAT volume, but further research is needed to determine the clinical implications. EAT's role in HF is multifaceted, including its inflammatory, metabolic, and mechanical effects. EAT volume is a significant factor in HF pathophysiology and can be assessed using various imaging modalities. The article also discusses the therapeutic potential of EAT, highlighting the effects of SGLT2 inhibitors and glucagon-like peptide-1 receptor agonists (GLP-1RAs) on EAT volume and clinical outcomes in HF. Overall, EAT is a promising biomarker and therapeutic target for HF management.