Effect of smoking cessation on markers of inflammation and endothelial cell activation among individuals with high risk for cardiovascular disease

Objective. To prospectively determine the effect of smoking cessation on markers of inflammation and endothelial cell activation. Material and methods: Thirty male and 22 female smokers of >7 cigarettes daily, aged 32-64 years with cardiovascular disease (CVD) or additional risk factors to smoking, participated in a program of smoking cessation with a follow-up period of 1 year. Cessation was validated by carbon monoxide measurement in expired breath, and 41 of the patients completed the study (17 quitters and 24 non-quitters). Plasma samples were drawn at baseline and after 1 year, and inflammatory markers were analyzed by enzyme immunoassays. Peripheral blood mononuclear cells (PBMCs) were isolated at baseline and 1 year in 6 quitters and 6 smokers and mRNA levels of interleukin-8 (IL-8), tumor necrosis factor alpha (TNF alpha) and intercellular adhesion molecule 1 (ICAM-1) were analyzed by real-time quantitative RT-PCR. Results. Our main findings were: (i) While the concentration of soluble (s) ICAM-1 decreased in quitters, it increased in smokers, with a significant difference in changes between the groups (p=0.04). (ii) While there was only minor change in mRNA levels of IL-8 in smokers, those who stopped smoking showed a decrease in the gene expression of IL-8 (p<0.09; comparing difference in changes). (iii) Concentrations of the other measured parameters (E-selectin, IL-6, sCD40 ligand, TNF alpha, von Willebrand factor, and C-reactive protein) were unchanged during follow-up in both groups. Conclusion. Smoking cessation induced a reduction in ICAM-1, suggesting a novel mechanism for the rapid reduction in the risk of CVD following smoking cessation.