Key result
CAD is linked to ~44% higher epicardial adipose tissue CD3 positivity and elevated UCP-1.
Why the study?
The relationship between epicardial adipose tissue immunohistochemical features and imaging-derived volume remains unclear.
Does epicardial adipose tissue exhibit different immunohistochemical features and volume in patients with coronary artery disease compared to those without?
Observational (n=50)
Does epicardial adipose tissue exhibit different immunohistochemical features and volume in patients with coronary artery disease compared to those without?
Epicardial adipose tissue in CAD patients exhibits increased T-cell infiltration and UCP-1 expression, suggesting an inflammatory yet metabolically active profile, despite no difference in total EAT volume compared to non-CAD patients.
May implicate epicardial adipose inflammation in CAD; leaves open causal role and therapeutic implications.
Background: Epicardial adipose tissue (EAT) is a visceral fat depot surrounding the myocardium. It contributes to coronary artery disease (CAD) through local inflammation, while its metabolic activity, including the expression of uncoupling protein-1 (UCP-1) and incretin receptors (GLP-1R, GIPR), may exert protective effects. The relationship between EAT immunohistochemical features and imaging-derived volume remains unclear. Methods: We prospectively studied 50 patients undergoing cardiac surgery: 25 with CAD undergoing coronary artery bypass grafting and 25 without CAD undergoing valve replacement. EAT samples were immunohistochemically stained for CD3, CD68, MPO, UCP-1, GLP-1R, and GIPR. Preoperative CT was used to quantify EAT volume. Results: Patients with CAD more frequently had higher CD3 immunopositivity compared to the control group (84.0 vs. 58.3%, p = 0.047), with no difference in MPO and CD68 immunoexpression. UCP-1 expression was elevated in CAD patients (p = 0.004), whereas GLP-1R and GIPR immunopositivity were similar. EAT volume did not differ between CAD and non-CAD patients (102.87 cm3 vs. 99.38 cm3, p = 0.964) but correlated modestly with BMI (rs = 0.325, p = 0.021). UCP-1 and GLP-1R immunopositivity, as well as larger LVEDD (left ventricular end-diastolic diameter), were positively associated with greater EAT volume. Conclusions: EAT in CAD exhibits increased T-cell infiltration and elevated UCP-1 expression, indicating an inflammatory yet metabolically active profile. Larger EAT volume was associated with UCP-1 and GLP-1R expression, underscoring the immunometabolic role of EAT in CAD.
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Furtula et al. (2025) conducted an observational in Coronary Artery Disease (n=50). Coronary artery disease vs. No coronary artery disease was evaluated on CD3 immunopositivity (p=0.047). Coronary artery disease was associated with higher epicardial adipose tissue CD3 immunopositivity compared to controls (84.0% vs. 58.3%, p=0.047) and elevated UCP-1 expression (p=0.004).
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