# Epicardial Adipose Tissue as a Cardiometabolic Target in Atrial Fibrillation: Implications for Ablation Strategies and Emerging Metabolic Therapies

## TL;DR

This review explores how epicardial fat contributes to atrial fibrillation and how targeting it might improve treatment strategies.

## Contribution

The paper highlights EAT as a novel therapeutic and diagnostic target in AF management.

## Key findings

- Increased EAT volume and inflammation are linked to atrial fibrosis and AF persistence.
- Higher EAT burden correlates with AF recurrence after ablation, especially in persistent AF.
- Metabolic therapies like GLP-1 agonists may reduce EAT and inflammation, but their impact on AF outcomes is still unclear.

## Abstract

Background: Atrial fibrillation (AF) is a prevalent arrhythmia closely associated with cardiometabolic disorders and systemic inflammation. Epicardial adipose tissue (EAT), located in direct contact with the atrial myocardium, has emerged as a biologically active tissue involved in atrial remodeling through inflammatory, fibrotic, and electrophysiological mechanisms. The objective of this review is to summarize current translational and clinical evidence on the role of EAT in AF pathophysiology and to discuss its implications for diagnostic assessment, interventional management, and cardiometabolic therapeutic strategies. Methods: A narrative, structured review of experimental, translational, and clinical studies was conducted using major biomedical databases. The literature was evaluated with a focus on mechanisms linking EAT to atrial remodeling, noninvasive imaging techniques for EAT characterization, echocardiographic and electroanatomical markers of atrial disease, outcomes of catheter ablation strategies, and pharmacological interventions targeting metabolic and inflammatory pathways. Results: The available evidence indicates that increased EAT volume and altered inflammatory activity are associated with atrial fibrosis, conduction abnormalities, and impaired atrial function, contributing to AF initiation and persistence. Multimodality imaging, including cardiac computed tomography and cardiac magnetic resonance, enables quantitative and qualitative assessment of EAT and supports clinical phenotyping. Clinical studies report an association between higher EAT burden and increased AF recurrence after pulmonary vein isolation, particularly in patients with persistent AF. Emerging cardiometabolic therapies, such as glucagon-like peptide-1 receptor agonists and dual GIP/GLP-1 agonists, have been shown to reduce EAT volume and inflammatory markers, although direct evidence linking these interventions to improved AF outcomes remains limited. Conclusions: EAT represents a relevant pathophysiological interface between metabolic disease and AF with potential clinical implications. Incorporating EAT assessment into routine evaluation may enhance risk stratification and support personalized AF management. Further prospective studies are required to define its role as a therapeutic target in clinical practice.