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- W42181749 abstract "Plaque rupture and vascular thrombosis are key initiating factors in the pathogenesis of ischemic complications of percutaneous coronary revascularization (1,2). The central role of platelet activity in this setting is highlighted by the unequivocal benefit of aspirin in preventing death or myocardial infarction among patients undergoing coronary intervention (3). Newer strategies for more potent inhibition of platelet activity at the injured coronary plaque focus on the integrin glycoprotein (GP) IIb/IIIa receptor on the platelet surface membrane, which binds circulating fibrinogen or von Willebrand factor and crosslinks adjacent platelets as the final common pathway to platelet aggregation (4). Pharmacologic compounds directed against GPIIb/IIIa block this receptor, prevent binding of circulating adhesion molecules, and potently inhibit platelet aggregation." @default.
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- W42181749 date "2003-01-01" @default.
- W42181749 modified "2023-09-23" @default.
- W42181749 title "Overview of the Glycoprotein IIb/IIIa Interventional Trials" @default.
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- W42181749 doi "https://doi.org/10.1007/978-1-59259-376-7_8" @default.
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