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Previous Volume 361:1108-1111 September 10, 2009 Number 11 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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The thienopyridine clopidogrel, which irreversibly blocks the adenosine diphosphate (ADP) receptor P2Y12 on platelets, has become an essential component of therapy in patients with acute coronary syndromes, because it significantly improves the outcomes.¹ However, clopidogrel has at least three drawbacks: delayed onset of action, large interindividual variability in platelet response, and irreversibility of its inhibitory effect on platelets (Figure 1). The two-step activation process, involving a series of cytochrome P-450 (CYP) isoenzymes, is susceptible to the interference of genetic polymorphisms² and drug–drug interactions.³ Patients with a poor response to clopidogrel have an increased risk of coronary thrombosis.⁴ The . . . [Full Text of this Article]

Source Information

From the Department of Cardiology, Deutsches Herzzentrum and First Medizinische Klinik rechts der Isar, Munich, Germany.

This article (10.1056/NEJMe0906549) was published on August 30, 2009, at NEJM.org.

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