Burke et al., in pathologic studies of sudden coronary death indicate that cigarette smoke increased the risk of plaque rupture and acute thrombosis of a lipid-rich, thin-capped atheroma in men; in female smokers, the pre¬vailing mechanism was plaque erosion with superimposed thrombosis. In addition, smoking may also be a risk factor for coronary vasoplasm.
C. Genetic Predisposition
Genetic predisposition influences the development of atherosclerosis in individuals exposed to cigarette smoke. The intersubject variability in the atherosclerotic process in smokers may be partially mediated by genetic variants. Either CYP1A1 MSP polymorphism or certain endo-thelial NO synthase intron 4 polymorphisms increased the susceptibility to cigarette smoke. In vivo, cigarette smoke is associated with an increased level of multiple inflammatory markers including C-reactive protein, interleukin-6, and tumor necrosis factor alpha in both male and female smokers.
D. Platelet Dysfunction and Thrombotic Factors
Rival et al. have shown that platelets isolated from smokers exhibited an increased stimulated as well as spontaneous aggregation. A higher fibrinogen blood level found in smokers correlates with the number of cigarettes smoked. Hirohiko et al. observed only 2-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers.

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