Aspirin Resistance: Detection, Mechanisms and Clinical Implications

Author(s): Matthew D. Linden, A. L. Frelinger III, Karin Przyklenk, Mark I. Furman, Alan D. Michelson

Journal Name: Current Cardiology Reviews

Volume 1 , Issue 3 , 2005

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Aspirin, the most widely used antiplatelet agent, irreversibly acetylates the enzyme cyclooxygenase 1 (COX-1), thereby inhibiting platelet thromboxane synthesis and subsequent platelet aggregation. Although aspirin has been demonstrated to reduce the odds of serious atherothrombotic events and death in high-risk patients by 25%, subsets of patients fail to respond to therapy and continue to suffer atherothrombotic events. This aspirin treatment failure may be due to sub-optimal bioavailability (e.g. because of non-compliance or under-dosing) or may be a consequence of the as yet poorly understood phenomenon of aspirin resistance. In this review, we summarize the current laboratory methods used to identify aspirin-resistant patients, outline the cellular mechanisms that may contribute to aspirin resistance, and discuss the clinical implications of this important issue.

Keywords: aspirin, aspirin resistance, thromboxane, cyclooxygenase 1, polymorphisms, treatment failure, antiplatelet therapy

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Article Details

Year: 2005
Page: [203 - 211]
Pages: 9
DOI: 10.2174/157340305774574134
Price: $65

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