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Vol. 36, No. 1, 2007/2008
Issue release date: March 2008
Section title: Original Paper
Pathophysiol Haemos Thromb 2007–08;36:40–44
(DOI:10.1159/000112638)

Reverse Effect of Aspirin: Is the Prothrombotic Effect after Aspirin Discontinuation Mediated by Cyclooxygenase 2 Inhibition?

Doutremepuich C. · Aguejouf O. · Eizayaga F.X. · Desplat V.
aLaboratoire d’Hématologie, UFR des Sciences Pharmaceutiques, Université Victor Segalen Bordeaux 2, Bordeaux, France; bCEBBAD, Facultad de Medicina, Universidad Maimónides, Buenos Aires, Argentina

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 6/26/2007
Accepted: 11/26/2007
Published online: 3/6/2008

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 1

ISSN: 1424-8832 (Print)
eISSN: 1424-8840 (Online)

For additional information: http://www.karger.com/PHT

Abstract

Background: While aspirin is the drug most often used to prevent cardiovascular complications, its discontinuation induces an increased risk of acute coronary syndrome and ischemic stroke in some patients. Objectives: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways. Methods and Results: We studied the effects of ultra-low-dose aspirin (ULDA) as well as those of sc-560 and ns-398, specific COX-1 and COX-2 inhibitors, on induced hemorrhagic time and in a model of laser-induced thrombosis in rats. In the laser-induced thrombosis model, ULDA treatment increased the number of emboli and the duration of embolization, thereby confirming its prothrombotic effect described in previous publications. This effect was also observed in rats pretreated with sc-560 but not in those pretreated with ns-398. Conclusions: We demonstrated that ULDA induced a prothrombotic effect in the rats studied. This strongly suggests that a very small amount of aspirin could remain in the patient’s blood after aspirin therapy, leading to cardiovascular complications. This effect may be mediated by the COX-2 pathway.


  

Author Contacts

Prof. Christian Doutremepuich, Laboratoire d’Hématologie
UFR des Sciences Pharmaceutiques, Université Victor Segalen Bordeaux 2
146, rue Léo Saignat, FR–33076 Bordeaux Cedex (France)
Tel. +33 5 57 57 12 53, Fax +33 5 56 98 79 70
E-Mail Christian.Doutremepuich@heph.u-bordeaux2.fr

  

Article Information

Received: June 26, 2007
Accepted after revision: November 26, 2007
Published online: March 06, 2008
Number of Print Pages : 5
Number of Figures : 2, Number of Tables : 1, Number of References : 15

  

Publication Details

Pathophysiology of Haemostasis and Thrombosis

Vol. 36, No. 1, Year 2007/2008 (Cover Date: March 2008)

Journal Editor: Rosing J. (Maastricht)
ISSN: 1424–8832 (Print), eISSN: 1424–8840 (Online)

For additional information: http://www.karger.com/PHT


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 6/26/2007
Accepted: 11/26/2007
Published online: 3/6/2008

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 1

ISSN: 1424-8832 (Print)
eISSN: 1424-8840 (Online)

For additional information: http://www.karger.com/PHT


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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