Smoking, Platelet Reactivity and Fibrinogen
It is universally accepted that smoking constitutes a major independent risk factor for the development of atherosclerosis as well as arterial thrombosis formation and its most serious consequences, i.e., coronary artery disease/acute myocardial infarction and stroke (A Report of the Surgeon General, 1983). Likewise, it is well recognized that platelets play an important role in the development of occlusive arterial disease (Schafer and Handin, 1979); there is indeed substantial evidence to suggest that abnormal platelet/vessel wall interaction is involved in the pathogenesis of the atherosclerotic lesion itself (Weksler and Nachman, 1981; Hoak, 1988). Also, a strong association between plasma fibrinogen concentration and platelet aggregability was reported by Meade et al. (1985). In atherosclerosis, lipids and fibrinogen accumulate in the subintimal layers of the arterial wall. Fibrinogen is an acute phase protein and plasma concentrations rise as a result of a wide range of stimuli many of which are of a non-specific nature, e.g., chronic inflammatory disorders, after surgery, in malignant disease and during pregnancy. Indeed, atheroma displays some of the characteristics of an inflammatory response. The present article attempts to review some of the concepts as to how smoking relates to platelet reactivity and plasma fibrinogen concentration, and thereby to arterial vascular disease.
KeywordsPlatelet Aggregation Bleeding Time Platelet Reactivity Plasma Fibrinogen Habitual Smoker
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