A comparison of six major platelet function tests to determine the prevalence of aspirin resistance in patients with stable coronary artery disease

Faculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada.
European Heart Journal (Impact Factor: 14.72). 08/2007; 28(14):1702-8. DOI: 10.1093/eurheartj/ehm226
Source: PubMed

ABSTRACT We sought to compare the results obtained from six major platelet function tests in the assessment of the prevalence of aspirin resistance in patients with stable coronary artery disease.
201 patients with stable coronary artery disease receiving daily aspirin therapy (> or =80 mg) were recruited. Platelet aggregation was measured by: (i) light transmission aggregometry (LTA) after stimulation with 1.6 mM of arachidonic acid (AA), (ii) LTA after adenosine diphosphate (ADP) (5, 10, and 20 microM) stimulation, (iii) whole blood aggregometry, (iv) PFA-100, (v) VerifyNow Aspirin; urinary 11-dehydro-thromboxane B(2) concentrations were also measured. Eight patients (4%, 95% CI 0.01-0.07) were deemed resistant to aspirin by LTA and AA. The prevalence of aspirin resistance varied according to the assay used: 10.3-51.7% for LTA using ADP as the agonist, 18.0% for whole blood aggregometry, 59.5% for PFA-100, 6.7% for VerifyNow Aspirin, and finally, 22.9% by measuring urinary 11-dehydro-thromboxane B(2) concentrations. Results from these tests showed poor correlation and agreement between themselves.
Platelet function tests are not equally effective in measuring aspirin's antiplatelet effect and correlate poorly amongst themselves. The clinical usefulness of the different assays to classify correctly patients as aspirin resistant remains undetermined.

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Available from: Marie Lordkipanidzé, Jun 02, 2014
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    • "Depuis quelques années, le phénomène de « résistance biologique » aux antiplaquettaires a été décrit [1] [2], puis associé à une incidence plus importante de récidives d'événements cardiovasculaires . La définition de cette « résistance biologique » est difficile à établir car elle est dépendante de la technique utilisée pour la mettre en évidence [3] [4]. La première technique utilisée a été le test d'agrégation plaquettaire par transmission lumineuse en plasma riche en plaquettes en réponse à des agonistes spécifiques (l'ADP pour la réponse au clopidogrel et l' "
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    • "Multiple assays of platelet function exist but correlate poorly with regard to positive predictive value. Application of the assays in a single population resulted in a variance of diagnosis of aspirin resistance between 4 and 60% (Lordkipanidzé et al., 2007). The lack of a reproducible, cheap, and accurate test has hampered clinical utility. "
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    • "Due to the instability of TxA 2 , it is rapidly converted to stable and inactive thromboxane B 2 (TxB 2 ), the metabolite of which can be measured in urine, 11-dehydro thromboxane B 2 (11-dehydroTxB 2 ). A myriad of tests are currently available to assess the anti-platelet effect of aspirin, but these tests are not equally effective and correlate poorly amongst themselves [8] [9]. ARA-induced platelet aggregation and measurement of TxB 2 are two of the most sensitive methods [10]. "
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