Abstract
Sudden cardiac death is the most frequent cause of mortality in industrialized societies accounting for the majority of the over 325,000 smoking-related deaths each year in the United States1. The strong link between cigarette smoking and the platelet-modulated syndrome of sudden cardiac death2,3 implicates smoking as a cause of platelet activation. Consistent with this hypothesis of a direct activation of platelets is that platelet turnover appears to be accelerated in apparently healthy smokers4,5. However, an enhanced turnover of platelets may be the result of their increased clearance following membrane alterations after interaction with a damaged vasculature and conversely, thrombosis has been shown to occur in vivo without evidence of increased turnover6–8. Thus, an enhanced platelet turnover in smokers may not necessarily reflect a direct activation of platelets in vivo. In fact, ex vivo aggregation has been found to be either increased9,10, unchanged4,12–14 or significantly decreased15,16 in chronic smokers.
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© 1990 Plenum Press, New York
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Murray, J.J., Nowak, J., Oates, J.A., FitzGerald, G.A. (1990). Platelet — Vessel Wall Interactions in Individuals who Smoke Cigarettes. In: Diana, J.N. (eds) Tobacco Smoking and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 273. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5829-9_19
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DOI: https://doi.org/10.1007/978-1-4684-5829-9_19
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