作者: Osman Faheem , John K. Forrest
DOI: 10.1007/978-1-4471-4528-8_11
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摘要: Platelets play a pivotal role in the development of arterial thrombus formation both setting plaque rupture during ST elevation myocardial infarction (STEMI) and routine PCI through disruption previously stable coronary plaques. In acute syndromes, there are critical changes that occur within platelets promote clot formation. These include (1) platelet adhesion mediated by von Willebrand factor other adhesive proteins; (2) activation, part thromboxane A2; (3) aggregation due to fibrinogen cross-linking (Fig. 11.1). Many commonly used oral antiplatelet agents discussed subsequently work mechanisms disrupt one or more these pathways.