Epicardial Adipose Tissue as a Potential Modulator of Atrial and Ventricular Arrhythmogenesis: Mechanistic Insights and Clinical Implications

Epicardial adipose tissue (EAT) has emerged as a highly active endocrine organ and a potential modulator of cardiac arrhythmogenesis. Under cardiometabolic stress, EAT undergoes a pro-inflammatory phenotypic transition. Its anatomical contiguity with the myocardium facilitates direct fibro-fatty infiltration and the continuous release of a profibrotic secretome. This process is associated with structural remodeling, connexin lateralization, and ion channel modulation, potentially creating a highly anisotropic and vulnerable substrate for both atrial and ventricular arrhythmias. Clinically, high-density electroanatomical mapping reveals that regional EAT accumulation correlates directly with low-voltage zones and fractionated electrograms, suggesting a role as both an arrhythmogenic contributor and a biophysical confounder during catheter ablation. Furthermore, non-invasive imaging (CT, CMR, TTE) and surface electrical markers, including spatial vectorcardiographic parameters, allow for advanced risk stratification. Current evidence suggests EAT may act as an active participant rather than a mere passive bystander. Targeted pharmacological interventions, such as SGLT2 inhibitors, are associated with reverse electrical remodeling alongside a reduction in EAT burden, highlighting its potential as a dynamic therapeutic target.