Objective Metabolic syndrome (MS) is associated with an increased risk of coronary artery disease (CAD) and type 2 diabetes mellitus (DM). In MS, adipose tissue has been shown to function as a paracrine and an endocrine organ secreting various adipocytokines. In the current study, adiponectin, tumor necrosis factor-α (TNF-α) and leptin gene expressions in the epicardial adipose tissue (EAT), paracardial adipose tissue (PAT) and subcutaneous adipose tissue (SAT) were investigated in MS patients with CAD and in non-MS patients without CAD. Methods and ResultsThirty-seven patients with MS undergoing coronary artery bypass grafting due to CAD (MS group) and twenty-three non-MS patients without CAD undergoing heart valve surgery (control group) were recruited prospectively to the study. Relative gene expressions of adiponectin, TNF-α and leptin in EAT, PAT and SAT were compared between two groups of patients. Adiponectin gene expression in EAT and PAT were significantly lower in MS group compared to the control group (p<0.0001, p=0.04, respectively) while SAT adiponectin gene expression did not differ significantly (p=0.64). TNF-α and leptin gene expressions were found to be statistically significantly higher in EAT, PAT and SAT of the MS group (p< 0.0001, for all). Conclusion Our results demonstrate that TNF-α and leptin gene expressions increase prominently in the EAT, PAT and SAT while adiponectin gene expression decreases significantly in EAT and PAT in MS patients with CAD. These findings suggest that disturbances in expression of adiponectin, TNF-α and leptin in EAT, PAT and SAT might play an important role in MS patients with CAD.

BackgroundVisceral fat deposition and its associated atherogenic complications are mediated by glucocorticoids. Cardiac visceral fat comprises mediastinal adipose tissue (MAT) and epicardial adipose tissue (EAT), and MAT is a potential biomarker of risk for obese patients.AimOur objective was to evaluate the role of EAT and MAT 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) and glucocorticoid receptor (GCR) expression in comparison with subcutaneous adipose tissue (SAT) in the development of coronary atherosclerosis in obese patients with coronary artery disease (CAD), and to assess their correlations with CD68 and fatty acids from these tissues.Methods and resultsExpression of 11β-HSD-1 and GCR was measured by qRT-PCR in EAT, MAT and SAT of thirty-one obese patients undergoing coronary artery bypass grafting due to CAD (obese CAD group) and sixteen obese patients without CAD undergoing heart valve surgery (controls). 11β-HSD-1 and GCR expression in MAT were found to be significantly increased in the obese CAD group compared with controls (p < 0.05). In the obese CAD group, 11β-HSD-1 and GCR mRNA levels were strongly correlated in MAT. Stearidonic acid was significantly increased in EAT and MAT of the obese CAD group and arachidonic acid was significantly expressed in MAT of the obese male CAD group (p < 0.05).ConclusionsWe report for the first time the increased expression of 11β-HSD-1 and GCR in MAT compared with EAT and SAT, and also describe the interrelated effects of stearidonic acid, HOMA-IR, plasma cortisol and GCR mRNA levels, explaining 40.2% of the variance in 11β-HSD-1 mRNA levels in MAT of obese CAD patients. These findings support the hypothesis that MAT contributes locally to the development of coronary atherosclerosis via glucocorticoid action.

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Intracoronary bolus application of tirofiban was not associated with reduction in MACE rates compared to intravenous administration in patients with STEMI who underwent primary PCI. Future prospective trials with higher bolus doses of IC tirofiban should addressed to clarify this issue.