European Heart Journal Advance Access originally published online on June 14, 2007
European Heart Journal 2007 28(14):1702-1708; doi:10.1093/eurheartj/ehm226
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A comparison of six major platelet function tests to determine the prevalence of aspirin resistance in patients with stable coronary artery disease
1 Faculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada
2 Research Center, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec, Canada
3 Department of Pharmacy, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec, Canada
4 Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada
5 Division of Cardiology, Hôpital du Sacré-Cœur de Montréal, 5400, boul. Gouin ouest, Montréal, Québec, Canada H4J 1C5
Received 1 March 2007; revised 26 April 2007; accepted 10 May 2007; online publish-ahead-of-print 14 June 2007.
* Corresponding author. Tel: +1 514 338 2222 ext. 3420; fax: +1 514 338 2694. E-mail address: jean.gino.diodati{at}umontreal.ca
See page 1673 for the editorial comment on this article (doi:10.1093/eurheartj/ehm232)
Aims: 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.
Methods and results: 201 patients with stable coronary artery disease receiving daily aspirin therapy (
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 µM) stimulation, (iii) whole blood aggregometry, (iv) PFA-100®, (v) VerifyNow Aspirin®; urinary 11-dehydro-thromboxane B2 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 B2 concentrations. Results from these tests showed poor correlation and agreement between themselves.
Conclusion: 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.
Key Words: Aspirin • Coronary artery disease • Platelet aggregation • Thromboxane
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