Key result
Epicardial adipose tissue expansion is linked to HFpEF development and mortality.
Why the study?
Reducing epicardial adipose tissue expansion is a promising strategy in HFpEF, but specific treatments and a platform to reduce it are lacking.
Targeting epicardial adipose tissue expansion represents a promising but currently unavailable therapeutic strategy for HFpEF, requiring further research into mechanisms and appropriate animal models.
EAT expansion may aid HFpEF risk stratification; leaves open whether targeting it improves outcomes.
Heart failure with preserved ejection fraction (HFpEF) exhibits an inflammatory‐metabolic phenotype in association with multiple factors. Among them, epicardial adipose tissue (EAT), a type of visceral adipose tissue surrounding the heart, has been gaining attention. EAT expansion is associated with the development of HFpEF, the increased risk for heart failure–related mortality in patients with HFpEF, independent of age, body mass index, diabetes, and sex. Thus, reducing EAT expansion has been proposed as a promising therapeutic strategy for treating HFpEF. Although specific treatment for EAT expansion is unavailable, modulating the inflammatory response and systemic energy metabolism are beneficial in improving clinical symptoms or prognosis in patients with HFpEF. To further enhance our capacity in effectively treating HFpEF, this review discusses the knowledge gaps between EAT expansion and the lack of a platform to reduce EAT expansion in HFpEF, including the choices of appropriate animal models, the conceptual mechanisms of glucose and lipid metabolism in EAT expansion toward potential strategies for selective EAT‐targeted therapeutic avenues.
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Qi et al. (2026) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Epicardial adipose tissue (EAT) targeting was evaluated. Epicardial adipose tissue expansion is associated with HFpEF development and mortality, highlighting the need for targeted therapeutic strategies to modulate inflammatory and metabolic responses.
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