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Cigarette Smoking Increases Plasma Concentrations of Vascular Cell Adhesion Molecule-1 in Patients with Coronary Artery Disease

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey, yukselc{at}ogu.edu.tr

Bilgin Timuralp, MD

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Tercan Us, MD

Department of Microbiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Yurdanur Akgün, MD

Department of Microbiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Gulmira Kudaiberdieva, MD

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Bulent Gorenek, MD

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Ahmet Unalr, MD

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Omer Goktekin, MD

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Necmi Ata, MD

Department of Cardiology, Faculty of Medicine, Osmangazi University, Eskisehir, Turkey

Cigarette smoking adversely affects endothelial function and increases risk of coronary artery disease (CAD). The pathogenesis of coronary atherosclerosis is currently thought to involve interactions between inflammatory cells and vascular endothelium. Adhesion molecules play a pivotal role in the accumulation of inflammatory cells at the endothelium. Little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. The aim of this study was to evaluate the effects of cigarette smoking on the plasma concentrations of soluble vascular cell adhesion molecule-1 (VCAM-1) in patients with CAD. The soluble VCAM-1 level was quantified in smoking CAD patients (n=19) in comparison to those from patients with CAD alone (n=10). Plasma concentrations of soluble VCAM-1 were measured by enzyme-linked immunosorbent assay. The soluble VCAM-1 level was found significantly higher in smokers than in nonsmokers (32.1279 ±21.6421 vs 9.4570 ±7.8138 ng/mL, p<0.01), and in patients with previous myocardial infarction (MI) than in those without previous MI, but not significant statistically (27.7279 ±22.8813 vs 17.8170 ±15.9172 ng/mL, p>0.05). No significant difference was observed for soluble VCAM-1 levels between hypertensive and nonhypertensive patients, multivessel and one-vessel disease, or anterior and inferior MI localizations. The present study suggests that in patients with CAD, smoking leads to elevated levels of soluble VCAM-1 that may clarify one of the mechanisms of its accelerating effect on the atherosclerotic process.

Angiology, Vol. 55, No. 4, 397-402 (2004)
DOI: 10.1177/000331970405500406


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