Macrophage Accumulation and Angiogenesis in Epicardial Adipose Tissue in Cardiac Patients with or without Chronic Heart Failure

Routinely measuring epicardial fat had become a novel tool for cardiovascular risk stratification. Structural changes in epicardial adipose tissue (EAT), including fat thickness, inflammation, and angiogenesis, have been described in coronary artery disease (CAD) patients. We proposed to measure EAT thickness and characterize inflammatory infiltrate and angiogenesis in epicardial adipose tissue in CAD patients with and without chronic heart failure (CHF), established by cardiac dysfunction on echocardiography (left ventricular ejection fraction, LVEF ≤ 50%) and symptoms of heart failure (New York Heart Association (NYHA) functional class II or III).The study included 15 patients with CAD (demonstrated by coronary angiography),, who underwent right atrial appendages (RAA) excision during coronary artery bypass graft (CABG). The study was performed by histopathological, immunohistochemical (IHC), and morphometrical analysis. EAT thickness was assessed by using morphometry applied on routine histological stains. Inflammatory cell infiltration and angiogenesis were investigated immunohistochemically by using antibodies against CD68 and CD34 markers. Diminished EAT thickness in the CAD patients with CHF was associated with increased macrophage infiltration and reduced angiogenesis of the EAT as compared to CAD patients without CHF. In conclusion, the present study on epicardial fat samples of the RAA suggested that high expression of CD68 appeared to be associated with severe deterioration of heart function in CAD patients who underwent myocardial revascularization consisting of CABG.