Cigarete Smoking Impact on Atherothrombosis Risk: Review of Biomarkers

In the article cigarette smoking related changes of biomarkers reflecting various mechanisms of atheropathogenesis are reviewed. Cigarette smoking and invol­untary exposure to tobacco smoke (pas­sive smoking) is a significant modifiable risk factor for cardiovascular diseases. The cardiovascular risk attributable to ciga rette smok ing in creases with the number of cigarettes smoked and with the duration of smoking. Smoking en­hances cardiovascular risk through vari­ous mechanisms including progression of atherosclerosis, vascular injury, endothe­lial dysfunction and thrombosis. Levels of inflammatory markers are increased in smokers, as well as is increased count of white blood cells and levels of vascular cellular adhesion molecule-1 and intra­cellular adhesion molecule-1. Smoking is associated with oxidative stress and smokers have higher plasma level of oxi­dized low density lipoproteins, malondialdehyde and Fg-isoprostanes. Cigarette smoke is an important source of free radicals, which have been shown to di - minish antioxidant capacity. Smoking causes uniavorable changes in the lipid profile: cigarette smoking increases total cholesterol and triglycerides, and lowers high density cholesterol. Smoking en­hances platelet aggregability and shifts the pro- and antithrombotic balance to­wards increased coagulability and blood viscosity. Insulin resistance is higher in smokers compared with nonsmokers, and smokers have higher blood levels of homocysteine than nonsmokers. Smoke exposure may influence acute as well as chronic changes of markers. Smoking cessation has been shown to restore the most of markers to the level of nonsmok­ers, except that the level of inflammatory biomarkers does not drop to levels ob­served in never-smokers.

Keywords: smoking, atherosclerosis, nicotine, biomarkers.