Because we collected blood specimens with the addition of PG E 1 (to prevent post-sampling artefacts) we could verify that, in spite of the presence of this inhibitor, dual agonist-induced activation still caused an enhancement of activation markers, and the difference between normal controls and patients with stable coronary artery disease receiving anti-platelet drugs remained highly significant.
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Comparison of VerifyNow-P2Y12 test and Flow Cytometry for monitoring individual platelet response to clopidogrel. What is the cut-off value for identifying patients who are low responders to clopidogrel therapy?
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