Cigarette smoking promotes atherosclerotic cardiovascular disease through mechanisms involving inflammation, endothelial dysfunction, oxidative stress, increased coagulability, and insulin resistance.
What are the mechanisms and biomarkers by which cigarette smoking contributes to the development of atherosclerotic cardiovascular disease?
This review summarizes the extensive pathophysiological mechanisms, including inflammation, oxidative stress, and endothelial dysfunction, by which cigarette smoking drives atherosclerotic cardiovascular disease.
Potential mechanisms and biomarkers of atherosclerosis related to cigarette smoking - a modifiable risk factor for that disease - are discussed in this article. These include smoking-associated inflammatory markers, such as leukocytes, high-sensitivity C-reactive protein, serum amyloid A, ICAM-1 and IL-6. Other reviewed markers are indicative for smoking-related impairment of arterial endothelial function (transcapillary leakage of albumin, inhibition of endogenous nitric oxide synthase activity and reduced endothelium-dependent vasodilation) or point to oxidative stress caused by various chemicals (cholesterol oxidation, autoantibodies to oxidized low-density lipoprotein, plasma levels of malondialdehyde and F(2)-isoprostanes and reduced antioxidant capacity). Smoking enhances platelet aggregability, increases blood viscosity and shifts the pro- and antithrombotic balance towards increased coagulability (e.g., fibrinogen, von Willebrand factor, ICAM-1 and P-selectin). Insulin resistance is higher in smokers compared with nonsmokers, and hemoglobin A1c is dose-dependently elevated, as is homocysteine. Smoke exposure may influence the kinetics of markers with different response to transient or chronic changes in cigarette smoking behavior.
Unverdorben et al. (Thu,) conducted a review in Atherosclerotic Cardiovascular Disease. Cigarette smoking vs. Nonsmokers was evaluated. Cigarette smoking promotes atherosclerotic cardiovascular disease through mechanisms involving inflammation, endothelial dysfunction, oxidative stress, increased coagulability, and insulin resistance.