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Chronic smoking is associated with a marked incidence of cardiovascuclar morbidity and mortality. Although the impact of cigarette smoke on vascular disease is probably predetermined by patients’ phenotype status, smoking-induced vascular disease is strongly believed to be secondary to oxidative stress. It has been demonstrated that chronic smoking is associated with high level of plasma cholesterol, vasoreactivity dysregulation, platelet aggregation disorder, and atherosclerotic plaque formation. Although the precise mechanism by which chronic smoking induces vascular disease is not completely understood, growing evidence shows that impairment of endothelial morphology and function plays a crucial role in pathogenesis of vascular disease. Oxidants, delivered by cigarette and deposited in pulmonary vessels through the sys-temic vasculature, activate superoxide producing enzymes within the vascular wall via oxidative stress, and might be the cause of endothelial dysfunction and dysregulation of endothelial barrier.
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