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When Enough Isn't Enough

Steven R. Steinhubl, MD; Richard Charnigo, PhD

JAMA. 2006;295:1581-1582. Published online March 13, 2006 (doi:10.1001/jama.295.13.jed60017).

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Worldwide, more than 2 million patients will be treated with a percutaneous coronary intervention (PCI) this year, with approximately half of these performed in the United States.¹ For almost three fourths of these patients, the diagnosis necessitating the procedure will be an acute coronary syndrome (ACS)—either unstable angina or a myocardial infarction (MI).²

Inhibitors of platelet function are a critical component of peri-PCI pharmacological therapy. Aspirin, although initially viewed as a weak agent with minimal potential to prevent acute thrombotic events, has been shown in a placebo-controlled trial to decrease the incidence of Q-wave MIs by 75% compared with heparin alone during coronary angioplasty.³ However, with aspirin alone, thrombotic complications following PCI remained unacceptably high. To address this, the platelet glycoprotein (Gp) IIb/IIIa antagonists were developed as a means to effectively prevent platelet aggregation and its associated complications. Abciximab, eptifibatide, and tirofiban were . . . [Full Text of this Article]

Author Affiliations: Division of Cardiovascular Medicine, Gill Heart Institute, and Department of Statistics, University of Kentucky, Lexington.

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