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

Abstract

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 x (TNFx) 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, TNFx, 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.