Epicardial adipose tissue (EAT)

Epicardial adipose tissue (EAT) is a unique visceral fat depot located between the myocardium and the visceral layer of the serous pericardium, sharing a common microcirculation with the heart [PMID: 31548128]. Under physiological conditions, EAT serves as a metabolically active organ that provides mechanical protection, local thermogenesis, and immediate fatty acid energy to the myocardium [PMID: 29467597]. However, in pathological states like obesity or metabolic syndrome, EAT expands and undergoes a phenotypic shift, becoming a source of pro-inflammatory and profibrotic cytokines that contribute to coronary artery disease and atrial fibrillation through paracrine signaling [PMID: 30043133]. While EAT is an anatomical tissue rather than a single molecular receptor, it is a significant therapeutic focus in cardiovascular medicine. Drugs such as sodium-glucose cotransporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists have been shown to reduce EAT volume and improve its inflammatory profile, thereby mitigating its cardiotoxic effects [PMID: 33734035].

Other names

Epicardial fatSubepicardial fatVisceral fat of the heart

Drugs targeting this tissue typically work by reducing adipose volume, decreasing the secretion of pro-inflammatory adipokines (e.g., TNF-alpha, IL-6), and promoting a transition to a more brown-like or anti-inflammatory (e.g., adiponectin-secreting) phenotype.