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- W2093517943 abstract "Thrombus formation on a disrupted atherosclerotic plaque is the main pathogenetic mechanism for the acute coronary syndromes of myocardial infarction and unstable angina. Myocardial infarction results from an acute total occlusion of the artery, while unstable angina is secondary in most cases to mural thrombus formation. Thrombus formation has also been implicated in chronic atherosclerotic disease progression, and in restenosis following coronary angioplasty. Therapeutic measures to treat thrombus rely on the ability of drugs either to prevent thrombus extension, to dissolve its fibrin component, or to prevent further platelet aggregation.Following arterial vessel wall injury, platelets adhere to the subendothelial collagen. Glycoprotein Ib on the platelet membrane is the primary receptor for this single layer of platelets, and it binds von Willebrand factor as its extracellular ligand. Platelet aggregation involves activation of several different pathways leading to exposure of the glycoprotein IIb/IIIa receptor on the platelet. These receptors bind either fibrinogen or von Willebrand factor, leading to platelet‐ platelet interaction and the formation of a white platelet thrombus. The luminal component of thrombus is a mixture of platelets and fibrin. The occlusive tail of the thrombus is composed of red blood cells and fibrin (red thrombus).Both plaque disruption and erosion of a plaque involve the presence of an inflammatory process at the site of thrombus formation. This inflammatory process consists primarily of activated macrophages and T lymphocytes.Thrombus formation depends on at least three factors: (i) the depth of vessel wall injury and the thrombogenicity of the exposed plaque; (ii) the prothrombotic state; and (iii) haemodynamic factors that promote vasoconstriction and stasis of blood flow.Traditionally, plaque rupture has been considered to result mainly from the physical pressure exerted upon the plaque surface. The plaque's vulnerability to rupture depends upon the size and consistency of its atheromatous core. Davies …" @default.
- W2093517943 created "2016-06-24" @default.
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- W2093517943 date "2001-04-01" @default.
- W2093517943 modified "2023-09-24" @default.
- W2093517943 title "Current trends in the management of thromboembolic events" @default.
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- W2093517943 doi "https://doi.org/10.1093/qjmed/94.4.179" @default.
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