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

Stanley Chia, David E Newby

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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.

Original languageEnglish
Pages (from-to)143-8
Number of pages6
JournalCurrent atherosclerosis reports
Volume4
Issue number2
Publication statusPublished - Mar 2002

Keywords / Materials (for Non-textual outputs)

  • Arteriosclerosis
  • Endothelium, Vascular
  • Fibrinolysis
  • Humans
  • Myocardial Infarction
  • Smoking
  • Thrombosis
  • Tissue Plasminogen Activator

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