Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot located between the myocardium and visceral pericardium, characterized by direct microvascular, paracrine, and vasocrine continuity with the heart. Under physiological conditions, EAT exhibits beige- and brown-fat-like features that support myocardial energy homeostasis, thermoregulation, and local cardioprotection. In obesity, diabetes, and aging, EAT undergoes pathological remodeling toward a pro-inflammatory and profibrotic phenotype. Accumulating evidence implicates excess and dysfunctional EAT in the pathophysiology of multiple cardiovascular diseases, including coronary artery disease, coronary microvascular dysfunction (CMD), vasospastic angina, atrial fibrillation, and heart failure. Through inflammatory signaling, immune activation, extracellular matrix remodeling, autonomic dysregulation, and mechanical pericardial restraint, EAT contributes to myocardial fibrosis, impaired diastolic function, CMD, and reduced exercise capacity. This review focuses on the biological characteristics of EAT, current imaging approaches for its detection and quantification using echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging, and the relationship between EAT, CMD, and other cardiovascular pathologies. We also summarize therapeutic strategies targeting EAT, including pharmacological interventions with established cardiometabolic benefit, such as glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, intensive lipid-lowering therapies, and lifestyle interventions. Finally, we highlight ongoing clinical studies investigating EAT as an imaging biomarker and a potential therapeutic target in cardiometabolic cardiovascular disease.
Gašpárková et al. (Sat,) studied this question.