Document Type

Article

Publication Date

2-4-2026

Comments

This article is the author’s final published version in Cardiology Discovery, 2026.

The published version is available at https://doi.org/10.1097/CD9.0000000000000184. Copyright © 2026 The Chinese Medical Association, published by Wolters Kluwer Health, Inc..

 

Abstract

Abstract – Heart failure (HF) is a complex, multifactorial clinical syndrome with diverse etiologies and phenotypic manifestations, affecting millions of people globally. HF is broadly classified into 3 subtypes: HF with reduced ejection fraction, HF with mildly reduced ejection fraction, and HF with preserved ejection fraction. Each subtype exhibits distinct pathophysiological mechanisms, clinical trajectories, and therapeutic responses, posing significant challenges in terms of diagnosis and management. Epicardial adipose tissue (EAT), a metabolically active visceral fat depot situated in close proximity to the myocardium, plays a dual role in physiological and pathological states, offering potential utility as a biomarker and therapeutic target. Despite its unique anatomical and functional characteristics, the EAT has been largely overlooked in both clinical practice and basic research. This review aims to elucidate the mechanisms by which dysfunctional EAT contributes to HF progression, particularly through the promotion of proinflammatory and profibrotic phenotypes. Specific attention is given to the effects of EAT-derived extracellular vesicles, altered adipokine secretion, and immune modulation on myocardial metabolism, endothelial function, and immune cell activity. These pathways contribute to cardiomyocyte injury, myocardial fibrosis, and adverse remodeling, which are hallmarks of HF pathogenesis. Furthermore, the review highlights the distinct and potentially divergent roles of EAT across HF subtypes, including HF with reduced ejection fraction, HF with preserved ejection fraction, and the intermediate phenotype HF with mildly reduced ejection fraction, with special attention to the emerging evidence of EAT involvement in the transitional pathophysiological characteristics of HF with mildly reduced ejection fraction. Finally, this review synthesizes current insights into the pathogenic role of EAT in HF and evaluates its potential as a biomarker for disease severity and progression, as well as a target for novel therapeutic interventions. Advances in imaging modalities and molecular profiling techniques may enhance the precision of EAT characterization and facilitate the development of personalized strategies for the diagnosis, risk stratification, and management of HF in the future.

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Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Language

English

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