Research Progress on Molecular Mechanism of Epicardial Adipose Tissue and Atrial Fibrillation

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Recently, rather than general fat distribution, epicardial adipose tissue (EAT) gains a growing concern. EAT is the local adipose deposition between myocardium and pericardium. Accumulated evidence revealed several distinguishing characteristics of EAT. It lies contiguously with the myocardium and could infiltrate into myocardium, actively secrets cytokines and adipokines mediating inflammation or remodeling, and contains abundant ganglionated plexi. It is suggested that EAT is associated with the initiation, perpetuation and recurrence of AF, but the precise role of EAT in AF pathogenesis is not completely elucidated. Mechanisms involve adipocyte infiltration, profibrotic and pro-inflammatory paracrine effects, oxidative stress, neural mechanisms and genetic factors. This article reviews the characteristics of EAT, the relationship between imaging parameters and AF, the latest progress of molecular mechanism and treatment strategy in the occurrence and development of AF.