4.6 Article

Response to aspirin in healthy individuals Cross-comparison of light transmission aggregometry, VerifyNow system, platelet count drop, thromboelastography (TEG) and urinary 11-dehydrothromboxane B2

Journal

THROMBOSIS AND HAEMOSTASIS
Volume 102, Issue 2, Pages 404-411

Publisher

SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN
DOI: 10.1160/TH09-02-0126

Keywords

Agregometry; aspirin; thromboelastography; thromboxane; VerifyNow

Funding

  1. Fondation de l'Hopital du Sacre-Coeur de Montreal, Montreal, Canada
  2. Fonds de recherche en sante du Quebec

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Variable biological effect of aspirin is suggested to be related to pharmacological resistance. The incidence of this so-called resistant state varies with the study population and the assay used. We determined performance features of five assays used to assess aspirin effects in non-smoking healthy volunteers not taking any drug known to interfere with platelet function. Blood and urine samples were obtained immediately before and after 8-10 days of aspirin 80 mg intake. Forty-five participants 19-59 years old were enrolled. The sensitivity (SE), specificity (SP), and optimal cut-off (CO) value to detect the effect of aspirin were: light transmission aggregometry (LTA) with 1.6 mM arachidonic acid (AA) - SE 100%, SP 95.9%, CO 20%; LTA with adenosine diphosphate (ADP) 10 mu M - SE 84.4%, SP 77.8%, CO 70%;VerifyNow(R) Aspirin - SE 100%, SP 95.6%, CO 550 ARU; platelet count drop - SE 82.2%, SP 86,7%, CO 55%;TEG(R) - SE 82,9%, SP 75,8%, CO 90%; and urinary 11-dehydrothromboxane B-2 levels (11-dHTB(2)) - SE 62.2%, SP 82.2%, CO 60 pg/ml. AA-induced LTA and the VerifyNow(R) assay reliably detected aspirin intake in all subjects; there was wide overlap in pre- and post-aspirin results with ADP-induced LTA, platelet count drop,TEG(R) and urinary 11-dHTB(2) assays. These results suggest that some of the variability in the reported incidence of aspirin resistance is unrelated to aspirin intake but related to inherent limitations of some assays to detect aspirin mediated effects or to underlying platelet reactivity variability independent of aspirin-mediated cyclooxygenase-1 inhibition.

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