Platelet function measurement in elective percutaneous coronary intervention patients: exploring the concept of a P2Y₁₂ inhibitor therapeutic window.

When clopidogrel was first clinically used, the relation between the pharmacodynamic effect and thrombotic event occurrence was unknown. Moreover, when the new P2Y12 inhibitors were developed, the desired level of on-treatment platelet reactivity to adenosine diphosphate to avoid ischemic event occurrence was highly debated and some recommended that near-100% inhibition should be the target. Concern surrounding the clinical implications of aggregometrydefined poor platelet inhibition in clopidogrel-treated elective percutaneous coronary intervention (PCI) patients arose over 1 decade ago (1). In that study, approximately 30% had a 10% decrease in aggregation at 24 h after a 300-mg load; these patients were defined as resistant. It was suggested that, “further study is necessary to investigate the mechanisms of these findings and how they correlate with the occurrence of ischemic events” (1).