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Blood, 15 March 2007, Vol. 109, No. 6, pp. 2285-2292. Prepublished online as a Blood First Edition Paper on December 5, 2006; DOI 10.1182/blood-2006-01-010645. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-01-010645v1 109/6/2285    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Undas, A. Articles by Mann, K. G. Search for Related Content PubMed PubMed Citation Articles by Undas, A. Articles by Mann, K. G. Related Collections Free Research Articles Review Articles Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW ARTICLE Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions Anetta Undas1, Kathleen E. Brummel-Ziedins2, and Kenneth G. Mann2 1 Institute of Cardiology, Jagiellonian University School of Medicine, Krakow, Poland; 2 Department of Biochemistry, University of Vermont, Colchester, VT Aspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall. Growing evidence also indicates that aspirin exerts additional antithrombotic effects, which appear to some extent unrelated to platelet thromboxane A2 production. Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation. Aspirin also acetylates lysine residues in fibrinogen resulting in increased fibrin clot permeability and enhanced clot lysis as well as directly promoting fibrinolysis with high-dose aspirin. The variable effectiveness of aspirin in terms of clinical outcomes and laboratory findings, which has been termed aspirin resistance, may be related to these additional antithrombotic effects that are altered when associated with common genetic polymorphisms such as the Leu33Pro ß3-integrin or Val34Leu factor XIII mutations. However, the clinical relevance of these observations is still unclear. Elucidation of the actual impacts of aspirin other than antiaggregation effects could be important in view of the widespread use of this drug in the prevention of thrombotic manifestations of atherosclerosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Cattaneo Laboratory detection of 'aspirin resistance': what test should we use (if any)? Eur. Heart J., July 2, 2007; 28(14): 1673 - 1675. [Full Text] [PDF]

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