Recent Advances in Inflammation-Associated Epicardial Adipose Tissue for Atrial Fibrillation Patients

The relationship between inflammation and atrial fibrillation (AF) has recently attracted significant research interest. Epicardial adipose tissue (EAT) contributes to the pathogenesis of AF through its inflammatory, metabolic, and electrophysiological effects and may also influence AF outcomes. Inflammatory cells within EAT release key proinflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor-α (TNF-α), which promote cardiomyocyte apoptosis and fibrosis. These changes compromise cardiac electrophysiological stability and elevate the risk of arrhythmias. Moreover, increased EAT thickness and volume have been identified as critical biomarkers for AF risk, providing new insights into AF diagnosis and treatment. However, despite compelling evidence of a strong association between EAT and AF, further studies are needed to fully elucidate the mechanisms underlying the role of EAT and assess its potential as a therapeutic target. This review aimed to explore the specific mechanisms of inflammation-related EAT in AF and evaluate the clinical potential of EAT as a biomarker and therapeutic target.