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

Abstract

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.

Keywords: atrial fibrillation (AF); biomarker; epicardial adipose tissue (EAT); inflammation.

Fig. 1.

Imaging features of EAT and the impact of inflammation in EAT on atrial fibrillation. AF is a common arrhythmia associated with multiple factors. The figure depicts the role of EAT in AF. The imaging features of EAT can be evaluated using computed tomography or cardiac magnetic resonance imaging, which reveals the thickening of the adipose layer. EAT releases inflammatory cytokines such as IL-6, IL-1, and TNF-$\alpha$, which are associated with myocardial fibrosis. Myocardial fibrosis is a key pathological basis for AF, potentially leading to alterations in cardiac electrophysiological properties, thereby promoting the onset of atrial fibrillation. Moreover, the inflammatory cytokines in EAT may directly affect cardiac electrical activity, contributing to the characteristic electrocardiographic patterns seen in atrial fibrillation. Figure created using BioRender.com.