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Observational study reveals increased platelet reactivity and elevated acute phase proteins in chronic smokers, indicating smoking accelerates vascular inflammation and prothrombotic risk.
Blood samples were obtained on four different occasions from 18 cigarette smoking and 34 non-smoking healthy men (age 40-69) and analyzed to assess age- and smoking-associated changes in plasma proteins, blood coagulation and platelet functions. Collagen-induced platelet aggregation was significantly increased with aging in non-smokers. Significant changes in chronic smokers were increases in platelet count and fibrinogen in plasma; elevation of platelet factor-3 (PF-3) activity in platelet-poor plasma (PPP); increase in serum levels of alpha 1-antitrypsin, orosomucoid, haptoglobin and properdin factor B; and shortening of the lag period of collagen-induced platelet aggregation. Filtration of PPP through Millipore filters removed PF-3 membranes. The differences in PF-3 activities in filtered plasma were no longer significant between smokers and non-smokers. Results suggest that chronic smokers have higher levels of acute phase proteins reflecting underlying inflammatory processes, and higher levels of PF-3 activity in plasma due to liberation of PF-3 membranes from platelets.
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Chao et al. (1982) studied this question.
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