Atherosclerosis, cigarette smoking, and endogenous fibrinolysis: is there a direct link?
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.
Chia
Stanley
S
Department of Cardiology, Royal Infirmary of Edinburgh, Lauriston Place, Edinburgh EH3 9YW, United Kingdom. schia@ed.ac.uk
Newby
David E
DE
D001161:Arteriosclerosis / Q000150:complications*; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000503:physiopathology; D005342:Fibrinolysis; D006801:Humans; D009203:Myocardial Infarction / Q000209:etiology / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects* / Q000503:physiopathology; D013927:Thrombosis / Q000209:etiology / Q000503:physiopathology; D010959:Tissue Plasminogen Activator / Q000378:metabolism*
D010959:Tissue Plasminogen Activator