Aspirin resistance: Detection, mechanisms, and clinical implications

Linden, M, Frelinger, A, Przyklenk, K, Furman, M and Michelson, A 2005, 'Aspirin resistance: Detection, mechanisms, and clinical implications', Current Cardiology Reviews, vol. 1, no. 3, pp. 203-212.


Document type: Journal Article
Collection: Journal Articles

Title Aspirin resistance: Detection, mechanisms, and clinical implications
Author(s) Linden, M
Frelinger, A
Przyklenk, K
Furman, M
Michelson, A
Year 2005
Journal name Current Cardiology Reviews
Volume number 1
Issue number 3
Start page 203
End page 212
Total pages 10
Publisher Bentham Science Publishers Ltd
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.
Subject Haematology
Keyword(s) Aspirin
aspirin resistance
thromboxane
cyclooxygenase 1
polymorphisms
treatment failure
antiplatelet therapy.
DOI - identifier 10.2174/157340305774574134
Copyright notice © 2005 Bentham Science Publishers Ltd
ISSN 1573-403X
Versions
Version Filter Type
Altmetric details:
Access Statistics: 170 Abstract Views  -  Detailed Statistics
Created: Fri, 10 Feb 2012, 11:56:00 EST by Catalyst Administrator
© 2014 RMIT Research Repository • Powered by Fez SoftwareContact us