Key result
Abundant epicardial adipose tissue linked to higher mortality and hospitalizations in HF patients.
Why the study?
Emerging evidence suggests epicardial adipose tissue plays a significant role in the pathophysiology and prognosis of heart failure across different LVEF phenotypes.
Effect estimate: HR (exact values not provided)
Epicardial adipose tissue emerges as a promising imaging-derived biomarker for risk stratification in heart failure, with increased volume consistently predicting adverse outcomes in HFpEF and HFmrEF independent of systemic obesity.
Supports EAT quantification for HF risk stratification; extends evidence to HFpEF and HFmrEF independent of systemic obesity.
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.
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Nowakowski et al. (2026) studied Heart Failure. In heart failure patients, more abundant epicardial adipose tissue was consistently associated with adverse clinical outcomes, including higher rates of heart failure hospitalizations and mortality across various phenotypes.
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