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(Circulation. 2009;119:2625-2632.)
© 2009 American Heart Association, Inc.

New Drugs and Technologies

Bedside Evaluation of Thienopyridine Antiplatelet Therapy

Matthew J. Price, MD

From the Division of Cardiovascular Diseases, Scripps Clinic, La Jolla, Calif.

Correspondence to Matthew J. Price, MD, 10666 N Torrey Pines Rd, Mail Drop S1056, La Jolla, CA 92037. E-mail price.matthew@scrippshealth.org

Key Words: clopidogrel • platelets • prognosis • risk factors • thienopyridine

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Dual antiplatelet therapy with aspirin and a thienopyridine is a cornerstone of treatment for patients with coronary artery disease. Compared with aspirin alone, the combination of aspirin and a thienopyridine significantly improves outcomes in patients with ST-elevation myocardial infarction (MI) and non–ST-elevation acute coronary syndrome (ACS),^1,2 in stable patients after percutaneous coronary intervention (PCI),^3,4 and, by subgroup analysis, in stable patients with established atherosclerosis.⁵ The marked association between premature discontinuation of dual antiplatelet therapy and stent thrombosis further underscores the importance of prolonged treatment with aspirin and a thienopyridine in patients receiving drug-eluting stents (DES).⁶ The pharmacodynamic effect of the thienopyridine clopidogrel varies substantially between individuals despite a clinical benefit across a range of disease states. Furthermore, a growing body of data supports an association between a lack of pharmacodynamic effect and ischemic events. These observations have spurred interest in the use of point-of-care platelet function assays to identify and treat at-risk patients. This review discusses the evidence that supports platelet function screening, describes the currently available assay devices, and outlines the future developments necessary for the adoption of routine platelet function testing in clinical practice.

The molecular target of the thienopyridines is the platelet P2Y₁₂ receptor. Binding of the P2Y₁₂ receptor by its agonist, ADP, activates the G-protein inhibitor secondary messenger system, which, through a complex series of events, mediates the completion and amplification of the aggregatory response.⁷ Ticlopidine and clopidogrel are prodrugs that are converted to an active metabolite through a 2-step process mediated by the hepatic cytochrome . . . [Full Text of this Article]