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The following is a summary of “Exploring the impact of metabolic comorbidities on epicardial adipose tissue in heart failure with preserved ejection fraction,” published in the March 2025 issue of the Journal of the Cardiovascular Diabetology by Menghoum et al.

Heart failure with preserved ejection fraction (HFpEF) is becoming increasingly prevalent worldwide, driven by an aging population and a growing burden of comorbidities. Epicardial adipose tissue (EAT), which accumulates preferentially in individuals with diabetes and obesity, has been implicated in the pathophysiology of HFpEF and is emerging as a potential therapeutic target. This study aimed to investigate the relationship between ventricular EAT, metabolic factors, and imaging characteristics in patients with varying degrees of heart failure, including controls, patients with pre-HF, and those diagnosed with HFpEF. Patients were recruited from a Belgian cohort between December 2015 and June 2017 and were stratified into three groups: pre-HF (n = 16), HFpEF (n = 104), and matched controls (n = 26). 

Additionally, findings were compared to a larger pre-HF cohort (n = 191) from the Beta3-LVH study. EAT volume was quantified using CMR imaging from end-diastolic short-axis cine stacks. In the Belgian cohort, associations between EAT, heart failure severity, and various biological and imaging markers were evaluated, while clinical outcomes were assessed using a composite endpoint of mortality or first HF hospitalization in the HFpEF group. EAT volumes were significantly elevated in patients with HFpEF compared to both pre-HF and control groups (72.4 ± 20.8 ml/m² vs. 55.0 ± 11.8 ml/m² and 48.0 ± 8.9 ml/m², respectively; p < 0.001) and were similarly higher when compared to the Beta3-LVH pre-HF cohort (52.0 ± 15.0 ml/m², p < 0.001). Within the Belgian cohort, EAT levels exhibited moderate correlations with key markers of HFpEF severity, including the H2FPEF score (r = 0.41, p = 0.003), body mass index (r = 0.30, p < 0.001), high-sensitivity troponin T (r = 0.41, p < 0.001), N-terminal pro-B-type natriuretic peptide (NT-proBNP) (r = 0.37, p < 0.001), soluble suppression of tumorigenicity-2 (sST2) (r = 0.30, p < 0.001), E/e’ ratio (r = 0.33, p < 0.001), and left ventricular global longitudinal strain (r = 0.35, p < 0.001). 

In patients with HFpEF, elevated EAT was independently associated with diabetes, ischemic cardiomyopathy, and increased sST2 levels, suggesting a distinct metabolic and inflammatory phenotype. However, unlike diabetes and BMI, higher EAT was not predictive of clinical prognosis. Multivariable logistic regression and random forest classification identified EAT, NT-proBNP, and the H₂FPEF score as the strongest predictors of HFpEF status. These findings demonstrate that EAT, as assessed by CMR, is significantly increased in patients with HFpEF, independent of traditional metabolic risk factors such as diabetes and obesity. The moderate association between EAT and HFpEF suggests that epicardial fat plays a contributory role in disease progression, potentially mediated through metabolic and inflammatory pathways. Given these findings, therapies targeting EAT may represent a novel approach to HFpEF management, warranting further investigation into pharmacologic and interventional strategies aimed at modulating epicardial fat accumulation and its deleterious effects on cardiac function.

Source: cardiab.biomedcentral.com/articles/10.1186/s12933-025-02688-7