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Atherosclerosis, cigarette smoking, and endogenous fibrinolysis: Is there a direct link?

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Abstract

Acute myocardial infarction is caused by thrombotic occlusion of a coronary artery at the site of a ruptured or eroded atheromatous plaque. The maintenance and regulation of tissue perfusion critically depend upon the integrity of endothelial function and the release of potent endothelium-derived factors, such as the fibrinolytic factor tissue plasminogen activator (tPA). Atherosclerosis and cigarette smoking are associated with dysfunction of the endothelium, and in particular, appear to impair the acute local endogenous fibrinolytic activity. This provides a potential mechanism whereby atherosclerosis and cigarette smoking can markedly influence the initiation, propagation, and resolution of the acute and chronic thrombotic complications of coronary artery disease through reductions in the capacity to release tPA acutely.

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  1. Department of Cardiology, Royal Infirmary of Edinburgh, Lauriston Place, EH3 9YW, Edinburgh, United Kingdom

    Stanley Chia MB ChB, MRCP & David E. Newby DM, PhD

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  1. Stanley Chia MB ChB, MRCP
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  2. David E. Newby DM, PhD
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Chia, S., Newby, D.E. Atherosclerosis, cigarette smoking, and endogenous fibrinolysis: Is there a direct link?. Curr Atheroscler Rep 4, 143–148 (2002). https://doi.org/10.1007/s11883-002-0038-y

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  • DOI: https://doi.org/10.1007/s11883-002-0038-y

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