The present study was undertaken to investigate the release of adipokines by epicardial adipose tissue (EAT) and their potential to interact with human monocytes and coronary artery endothelial cells in the context of obesity and coronary artery disease (CAD). Participants of this study were patients undergoing elective cardiac surgery (n=94), diagnosed with CAD (n=62) or not (n=32) and divided according to body mass index (BMI) ≤27 or >27 kg/m2. Results of the present study confirmed the secretion of multiple proinflammatory biomarkers by the EAT and identified several novel inflammatory mediators secreted abundantly by EAT such as growth-related oncogene-alpha, soluble intercellular adhesion molecule-1, monocyte migration inhibitory factor, and interleukin-8, both in the presence and in the absence of CAD. Release of adiponectin by EAT was suppressed both in obesity and CAD. CAD was also associated with increased regulated on activation T-cell and secreted (RANTES) release by EAT, independently of BMI. Moreover, data suggest that statins suppress cytokine release by EAT. Furthermore, in patients with obesity and CAD, epicardial adipokines could induce cell surface expression of adhesion molecules, enhance adhesion of monocytes to endothelial cells, and facilitate migration of adherent monocytes. These effects were found to be modulated by the levels of adiponectin. Thus, these results suggest a different pattern of secretion of pro- and anti-inflammatory markers by EAT in obesity and CAD.
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