## 4 Discussion  
Identifying the patients with risk of developing cardiac ischemia subsequently to cardiac surgery would result in the prevention of undesired clinical consequences associated with CAD (6). In this paper, we studied the known CV risk factors in association with EAT on RAA samples following open-heart surgery. The commonest risk factors identified in our patients that are likely to be significant predictors of CAD progression were male sex, obesity, and dyslipidemia. Previously, [PERSON] et al. [17] and [PERSON] et al. [18] identified EAT thickness as a CV risk factor in patients with or without preoperative heart failure, operated with standard CABG technique.  
Epicardial fats visceral fat between the myocardial surface and the visceral layer of the pericardium. Scarce evidence is available on EAT measurement and the association of EAT and the severity of cardiac ischemia in CAD patients who underwent CABG surgery.  
Large evidence showed that the severity of CAD was associated with EAT thickness [19; 20]. [PERSON] et al. [21] revealed that epicardial fat was associated with lower ejection fraction. Other studies have suggested that epicardial tissue could serve as a predictor of CAD, and EAT values >2.4 mm can predict the presence of significant (>50% diameter) CAD [7; 22].  
In the current study, we noticed a non-significant reduction of EAT thickness in patients with CHF as compared to those without CHF, associated to EAT fibrous tissue remodeling. According to [PERSON] et al. [17], the EAT amount is an independent CAD risk factor and is related to other CV risk factors. In concordance with previous studies [23; 24], we consider that EAT thickness, measured by imaging techniques, may serve as a tool in the follow-up assessment of the CAD patients.  
In our previous study [6], we noticed extracellular matrix alterations in EAT of CAD patients due to a great number of collagen deposits. By assessing the adipocyte size in EAT, we noticed that fibrosis could limit the adipocyte expandability [25]. We [3] showed that the adipocyte size in EAT had no significant difference between non-CAD individuals and CAD patients. According to [PERSON] et al. [26], these data indicated that the increased EAT thickness in CAD patients may not be due to adipocyte hypertrophy because fibrosis might restrict the extension of EAT by limiting adipocyte hypertrophy. A notable finding of this study was the presence of the EAT inflammatory foci, including macrophages, which may act to stimulate angiogenesis in the adipose tissue. Both [PERSON] et al. [27] and [PERSON] et al. [14], consider that epicardial fat is a source of inflammatory cells in CAD.  
The particularity of our CABG patient series is that patients with CHF were obese. Our histologic analysis suggests that in obese cardiac patients with CHF, epicardial adipose tissue changes were increased inflammation and decreased thickness as compared to non-obese patients without CHF. Several studies reported that EAT thickness measured post-mortem [28] or clinically by echocardiography, computed tomography (CT), or magnetic resonance imaging (MRI) was lower in patients with CHF [11; 12; 24]. The diminished epicardial fat could explain the increased inflammation by a reduction in the local secretion of protective anti-inflammatory adipokines [24; 29].  
The current results, which are consistent with previous studies [1; 30], revealed angiogenesis as another morphological hallmark of the EAT in CAD patients. Angiogenesis was of about three times greater in our CAD patients without CHF (of about 65 microvessels/um2) than in CAD patients with CHF (23 microvessels/um2) on coronary arteries [3; 23; 31].  
The reduced number of participants was a limitation of our study. Another limitation is that immunohistochemistry can only measure one or two markers per sample, and it may not completely reflect the complex mechanisms involved in epicardial adipose tissue thickening.