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Vol. 24, No. 1, 2007   

Free Abstract     Article (Fulltext)     Article (PDF 298 KB)     

Original Paper

Variable Platelet Response to Aspirin in Patients with Ischemic Stroke
Thomas Hohlfelda, Artur-Aron Webera, Ulrich Junghansb, Marc Schumachera, Marc Boucherb, Karsten Schröra, Mario Sieblerb

aInstitut für Pharmakologie und Klinische Pharmakologie und
bNeurologische Klinik, Heinrich-Heine-Universität, Düsseldorf, Deutschland

Address of Corresponding Author

Cerebrovasc Dis 2007;24:43-50 (DOI: 10.1159/000103115)


 goto top of page Key Words

  • Aspirin
  • Stroke
  • Platelets
  • Aggregation
  • Thromboxane

 goto top of page Abstract

Background: A large number of patients experience ischemic stroke despite treatment with aspirin (acetylsalicylic acid, ASA). It is not clear whether all of these patients with ischemic stroke respond normally to ASA or are hyporesponsive as assessed by inhibition of aggregation and thromboxane (TX) synthesis. Methods: We studied the effect of ASA given orally and ASA in vitro on collagen- and arachidonic-acid-induced TX formation and aggregation in platelet-rich plasma of 90 patients with ischemic stroke and 25 healthy control subjects. Results: Thirty-seven patients were being treated with ASA at the time of stroke. Arachidonic-acid-induced TX formation was not depressed below a predefined threshold of 25 ng/ml in 9 patients. Eight of these however exhibited a normal platelet sensitivity to ASA in vitro, suggesting poor compliance or a pharmacokinetic mechanism of nonresponse. The addition of ASA in vitro did not inhibit arachidonic-acid-induced TX formation below the above threshold in 6 patients (11%) in the group of 53 stroke patients not receiving oral ASA, indicating an impaired response to ASA at the platelet level. Moreover, platelets from stroke patients showed an increased collagen-induced, TX-independent aggregation as compared with those of healthy individuals. Conclusion: Different categories of ASA nonresponders can be distinguished in patients with ischemic stroke. These include patients with poor bioavailability or noncompliance, an impaired platelet response to ASA in vitro and an increased, TX-independent hyperreactivity to collagen.

Copyright © 2007 S. Karger AG, Basel


 goto top of page Author Contacts

Dr. Thomas Hohlfeld
Institut für Pharmakologie und Klinische Pharmakologie
Universitätsklinikum, Heinrich-Heine-Universität, Moorenstrasse 5
DE-40225 Düsseldorf (Germany)
Tel. +49 211 811 2500, Fax +49 211 811 4781, E-Mail hohlfeld@uni-duesseldorf.de


 goto top of page Article Information

Received: February 3, 2006
Accepted: December 20, 2006
Published online: May 22, 2007
Number of Print Pages : 8
Number of Figures : 6, Number of Tables : 2, Number of References : 39

 
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