Abstract 15496: Combined Effect of an Interleukin-6 Gene Variant and Smoking on Endothelial Function, Inflammatory and Thrombotic Processes and Prevalence of Coronary Artery Disease

• Published in: Circulation (New York, N.Y.) N.Y.), 2014-11, Vol.130 (suppl_2)
• Main Authors: Hatzis, George, Papageorgiou, Nikolaos, Oikonomou, Evangelos, Miliou, Antigoni, Siasos, Gerasimos, Papaioannou, Spyridon, Papaoikonomou, Stavroula, Toutouzas, Konstantinos, Antoniades, Charalambos, Stefanadis, Christodoulos, Tousoulis, Dimitris
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.130.suppl_2.15496

Abstract only Introduction: Smoking is a well known risk factor for coronary artery disease (CAD). Moreover, controversial data suggest that the -174 G/C polymorphism on Interleukin-6 (IL-6) gene promoter (rs1800795) may represent an early marker of inflammatory activation, closely related to the initiation and evolution of atherosclerosis. However, no data exist concerning a combined effect of smoking and this IL-6 genetic variant on several aspects of inflammation and thrombosis, endothelial function and the presence of CAD. Methods: 646 subjects (361 non smokers) were subjected to appropriate genotyping. Endothelial function was assessed by the flow mediated dilatation (FMD) of brachial artery. IL-6 (pg/ml), Tumor Necrosis Factor-a (TNF-a) (pg/ml), high sensitivity CRP (hsCRP) (mg/l) and D-dimers (μg/l) were measured with appropriate methods. Results: An increased incidence of CAD was found among the carriers of the allele C, compared to GG homozygotes, (OR:1.59, CI:1.26-2.93, p=0.032) in smokers, while a decreased incidence was observed in non smokers (OR:0.42, CI:0.26-0.68, p