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• W165120782 endingPage "1163" @default.
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• W165120782 abstract "The discovery of coronary thrombosis as the underlying cause of myocardial infarction (MI) was first reported by Parkinson and Bedford in 1928.1 However, it was not for another 50 years that the broad acceptance of this notion led to the treatment of patients with acute MI and unstable angina by directly targeting the thrombotic process. With better understanding of the molecular mechanisms of thrombosis, therapeutic targets to inhibit this process have emerged, including thrombin inhibitors, fibrinolytics, and platelet antagonists (Fig. 62-1). Among the latter class of agents, aspirin was the first to show significant clinical benefit in treatment of patients with acute MI (see Chapter 60). A remarkable 19% reduction in mortality was observed with aspirin in the International Study of Infarct Survival-2 trial.2 This significant benefit from aspirin, a relatively weak antiplatelet agent, provided a clear impetus to target platelets with more potent and specific drugs to treat patients with coronary syndromes. Advancement in the basic understanding of platelet aggregation provided the field with such targets. Although many agonists are able to activate platelets and induce their aggregation, the final common pathway underlying platelet aggregation is binding of an adhesive protein set, primarily fibrinogen or von Willebrand factor (VWF), to the platelet surface.3-5 The demonstration that integrin αIIbβ3 (glycoprotein [GP] IIb-IIIa) served as the fibrinogen receptor on the platelet surface and blockade of this interaction inhibited platelet aggregation6 defined this specific membrane protein as a target of antithrombotic therapy. However, complete abrogation of platelet aggregation, although attractive in the treatment of the thrombotic state, raised major safety concerns. Would such blockade lead to major, and ultimately unacceptable, bleeding complications? The reports that natural mutations in αIIbβ3 in patients with Glanzmann thrombasthenia7-9 (see Chapter 57) lead to only sporadic and minor bleeding tendencies and rarely to major internal bleeding provided some comfort, and efforts proceeded throughout the pharmaceutical and biotechnology sectors to develop potent, specific, and safe αIIbβ3 antagonists. These efforts led to development of the first clinically acceptable antagonist of αIIbβ3, abciximab (ReoPro), for clinical use.10 After extensive animal studies,11-14 including in primates,15 to establish efficacy and safety, the clinical benefit of abciximab was first tested in preventing thrombotic complications in patients undergoing percutaneous coronary intervention (PCI) in the Evaluation of c7E3 for Prevention of Ischemic Complications (EPIC) trial.16 In 1994, the results of the EPIC trial demonstrated the efficacy of αIIbβ3 blockade in reducing thrombotic complications. Within the next 5 years, more than 40,000 patients were randomized in studies, which demonstrated the clinical efficacy, and ultimately U.S. Food and Drug Administration (FDA) approval, of three intravenous αIIbβ3 antagonists in the reduction of thrombotic complications in patients undergoing PCI or in the medical management of patients with acute coronary syndromes (ACS)." @default.
• W165120782 created "2016-06-24" @default.
• W165120782 creator A5029768994 @default.
• W165120782 creator A5042974889 @default.
• W165120782 creator A5081920546 @default.
• W165120782 date "2007-01-01" @default.
• W165120782 modified "2023-09-23" @default.
• W165120782 title "αIIbβ3 (GPIIb-IIIa) Antagonists" @default.
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