Key result
Epicardial adipose tissue is significantly higher in HFpEF compared to controls, but not HFrEF.
Why the study?
Epicardial adipose tissue (EAT) has emerged as a potential biomarker and therapeutic target in heart failure, but its relationship across HF phenotypes remains incompletely characterized.
Does epicardial adipose tissue differ across heart failure phenotypes compared to controls?
Meta-Analysis (n=4,037)
Does epicardial adipose tissue differ across heart failure phenotypes compared to controls?
Standardized Mean Difference: 1.17 (95% CI 0.76–1.59)
p-value: p=<0.0001
Epicardial adipose tissue is uniquely elevated in HFpEF compared to HFrEF and HFmrEF, suggesting it may serve as a phenotype-specific biomarker and therapeutic target for metabolic HFpEF.
May inform HFpEF phenotyping and risk stratification; extends meta-analytic evidence for adipose tissue's phenotype-specific role in heart failure.
Introduction: Epicardial adipose tissue (EAT) has emerged as a potential biomarker and therapeutic target in heart failure, but its relationship across HF phenotypes remains incompletely characterized. Hypothesis: We hypothesized that EAT differs across HFpEF, HFrEF, and HFmrEF phenotypes, reflecting distinct pathophysiological roles. Aim: To update the Wu et al. 2023 meta-analysis examining EAT across HF phenotypes with newly published data. Methods: We searched PubMed, Embase, and Scopus till October 2025). Observational studies comparing EAT between HF patients and controls were included, stratified by phenotype. Random-effects meta-analysis with Hartung-Knapp adjustment was performed with subgroup analyses by imaging modality and temporal trends. Results: Thirty-one studies (4,037 HF patients) were analyzed. EAT was significantly elevated in HFpEF versus controls (SMD 1.17; 95% CI: 0.76-1.59; p<0.0001; k=22) but not in HFrEF (SMD -0.36; p=0.18) or HFmrEF (SMD -0.21; p=0.69). EAT correlated negatively with function in HFpEF (r=-0.55) but positively in HFrEF (r=+0.57). Echocardiography yielded larger effects than CMR (p=0.0007). Findings persisted after trim-and-fill adjustment (SMD 0.74; 95% CI: 0.24-1.23). Conclusion: EAT is phenotype-specifically elevated in HFpEF with divergent functional correlations across phenotypes, supporting EAT as a biomarker and therapeutic target for metabolic HFpEF.
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Biswas et al. (2026) conducted a meta-analysis in Heart Failure (n=4,037). Epicardial adipose tissue vs. Controls was evaluated on EAT levels in HFpEF versus controls (SMD 1.17, 95% CI 0.76-1.59, p=<0.0001). Epicardial adipose tissue was significantly elevated in HFpEF compared to controls (SMD 1.17; 95% CI 0.76-1.59; p<0.0001), but not in HFrEF or HFmrEF phenotypes.
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