Aspirin Resistance: Detection, Mechanisms and Clinical Implications

Title: Aspirin Resistance: Detection, Mechanisms and Clinical Implications

Volume: 1 Issue: 3

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

Affiliation:

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

Abstract: 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.

Cite this article as:

Linden D. Matthew, Frelinger III L. A., Przyklenk Karin, Furman I. Mark and Michelson D. Alan, Aspirin Resistance: Detection, Mechanisms and Clinical Implications, Current Cardiology Reviews 2005; 1(3) . https://dx.doi.org/10.2174/157340305774574134