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Previous Volume 350:277-280 January 15, 2004 Number 3 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Rupture or injury of an atherosclerotic coronary arterial plaque — as occurs spontaneously in patients with an acute coronary syndrome or as the result of a percutaneous coronary intervention — serves as a nidus for platelet aggregation and thrombus formation, which, in turn, may cause myocardial infarction or death. Activation of the platelet-surface glycoprotein IIb/IIIa receptor is the final common pathway in the process leading to platelet aggregation and, eventually, thrombus formation. When this receptor is activated, circulating fibrinogen binds to it and cross-links with adjacent platelets to create a platelet–fibrinogen matrix. Since platelets have a pivotal role in the . . . [Full Text of this Article]

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From the Department of Internal Medicine, Cardiovascular Division, University of Texas Southwestern Medical Center, Dallas.

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Antiplatelet Therapy for Ischemic Heart Disease
Steimle A. E., Lange R. A., Hillis L. D.
Extract | Full Text | PDF  
N Engl J Med 2004; 350:2101-2102, May 13, 2004. Correspondence

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