# Epicardial adipose tissue as a determinant of heart failure prognosis: insights across ejection fraction phenotypes

## TL;DR

Epicardial fat around the heart affects heart failure outcomes differently depending on heart pumping ability, offering potential for better risk assessment and treatment.

## Contribution

This review highlights EAT as a novel imaging biomarker for heart failure prognosis across different ejection fraction phenotypes.

## Key findings

- Increased EAT is linked to worse outcomes in heart failure with preserved or mildly reduced ejection fraction.
- EAT's role in heart failure with reduced ejection fraction is complex, showing both harmful and protective effects.
- EAT contributes to arrhythmias and may influence inflammation, fibrosis, and heart tissue changes.

## Abstract

Epicardial adipose tissue (EAT) is a metabolically active fat depot located between the myocardium and visceral pericardium, directly interacting with cardiomyocytes and coronary vasculature. Emerging evidence suggests that EAT plays a significant role in the pathophysiology and prognosis of heart failure (HF) across different left ventricular ejection fraction (LVEF) phenotypes. This review summarizes current data on the prognostic role of EAT in HF, including volume, thickness, and density, measured by echocardiography, computed tomography, and cardiac magnetic resonance imaging. In HF with preserved (HFpEF) and mildly reduced ejection fraction (HFmrEF), increased EAT consistently associates with adverse outcomes, including higher rates of hospitalization and mortality, independent of systemic obesity. In HF with reduced ejection fraction (HFrEF), the relationship is more complex, with studies showing both protective and detrimental associations depending on EAT quantity, density, and spatial distribution. EAT also appears to contribute to ventricular arrhythmogenesis, particularly in patients with preserved myocardial structure. Mechanistically, EAT may promote inflammation, fibrosis, and electrophysiological remodeling, while moderate amount EAT may exert metabolic or mechanical protection. Overall, EAT emerges as a promising imaging-derived biomarker for risk stratification in HF, highlighting the need for phenotype-specific evaluation and potential therapeutic targeting. Future studies should focus on EAT quality, remodeling, and its interaction with myocardial tissue to guide individualized HF management.