Journal
JOURNAL OF THROMBOSIS AND HAEMOSTASIS
Volume 4, Issue 4, Pages 813-819Publisher
WILEY
DOI: 10.1111/j.1538-7836.2006.01867.x
Keywords
aspirin; clopidogrel; genetics; platelets; resistance
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Background: Some data suggest that biological 'resistance' to aspirin or clopidogrel may influence clinical outcome. Objective: The aim of this study was to evaluate the relationship between aspirin and clopidogrel responsiveness in healthy subjects. Methods: Ninety-six healthy subjects were randomly assigned to receive a 1-week course of aspirin 100 mg day(-1) followed by a 1-week course of clopidogrel (300 mg on day 1, then 75 mg day(-1)), or the reverse sequence, separated by a 2-week wash-out period. The drug effects were assessed by means of serum TxB(2) assay, platelet aggregation tests, and the PFA -100 (R) and Ultegra RPFA -Verify Now (R) methods. Results: Only one subject had true aspirin resistance, defined as a serum TxB(2) level > 80 pg mu L-1 at the end of aspirin administration and confirmed by platelet incubation with aspirin. PFA-100 (R) values were normal in 29% of the subjects after aspirin intake, despite a drastic reduction in TxB(2) production; these subjects were considered to have aspirin pseudo-resistance. Clopidogrel responsiveness was not related to aspirin pseudo-resistance. Selected polymorphisms of platelet receptor genes were not associated with either aspirin or clopidogrel responsiveness. Conclusions: In healthy subjects, true aspirin resistance is rare and aspirin pseudo-resistance is not related to clopidogrel responsiveness.
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