Cigarette smoking and inflammatory indices in coronary artery disease

Background: Smoking-induced endothelial dysfunction may lead to inflammatory activation within a vascular wall mediated by cytokines and adhesion molecules. The aim of the study was to assess the relationship between the smoking status and serum levels of tumor necrosis factor (TNF) alpha, sTNFR 1 and 2 (soluble forms of TNF receptor), Interleukin (IL)-2, IL-10 and some selected adhesion molecules (AM): sE-selectin, sP-selectin, Vascular Cell AM-1 (sVCAM-1) and Intercellular AM-1 (sICAM-1) in patients with coronary artery disease (CAD). Methods and results: The study group consisted of 122 consecutive admissions with stable CAD (class II/III CCS): 31 current smokers (group I; mean age±S.E.M.: 53.8±1.6 years), 38 ex-smokers (group II; mean age±S.E.M.: 57.8±1.4 years) and 53 patients who have never smoked (group III; mean age±S.E.M.: 62.4±1.1 years). Serum concentration of IL-2 was higher in the group of active smokers (77.5±12.7 pg/ml) than in ex-smokers (40.0±10.6 pg/ml; P=0.017). AM determination also revealed differences between groups I and II—elevated serum sP-selectin levels in active smokers (174.7±17.1 ng/ml) than in ex-smokers (123.5±10.3 ng/ml; P=0.024). Serum sTNFR 2 level was higher in group III (2457.3±120.5 pg/ml) in comparison to group II (2018.4±121.5 pg/ml; P=0.006). There were no differences between TNFα, sTNFR 1, IL-10, sE-selectin, sICAM-1, sVCAM-1 levels in the groups examined. Conclusions: Cigarette smoking is associated with the elevation of IL-2 and sP-selectin serum levels in patients with stable CAD. CAD patients who have never smoked are characterized by delayed onset of angina and increased sTNFR 2 concentrations.