Cigarette smoking and hemostatic function

Altered hemostatic function, either as a direct result of smoking or caused by smoking-induced vascular damage, may account for the more rapidly reversible component of cardiovascular risk observed in chronic smokers.

Abstract

Epidemiologic studies clearly link cigarette smoking with vasoocclusive cardiovascular disease. Postmortem studies provide evidence of accelerated atherogenesis in asymptomatic smokers. However, the rapid regression of cardiovascular risk within the first year of quitting smoking is difficult to explain solely in terms of vascular disease. Recent evidence indicates that plasma fibrinogen, which has been prospectively associated with the risk of ischemic heart disease, is elevated in smokers. Similarly, results from studies investigating thromboxane metabolite excretion in urine confirm those involving radiolabeled platelet turnover, suggesting that platelets are activated in the circulation of chronic smokers. Altered hemostatic function, either as a direct result of smoking or caused by smoking-induced vascular damage, may account for the more rapidly reversible component of cardiovascular risk observed in chronic smokers.