Abstract 2362: Myonecrosis is Predicted by Lack of Platelet Inhibition Measured in Response to Multiple Agonists in Patients Undergoing Elective Stenting:The Risk of A Global High Platelet Reactivity Phenotype
Background: Small studies have demonstrated the relation of clopidogrel nonresponsiveness to adverse clinical events. We sought to determine:
the relation between inhibition of ADP-induced platelet aggregation and inhibition of aggregation induced by other agonists and
the relation of clopidogrel responsiveness to periprocedural myonecrosis in patients undergoing stenting treated with a 600mg clopidogrel loading dose and bivalirudin.
Methods: Platelet inhibition by low and high dose ADP, collagen and TRAP by conventional aggregometry (LTA) was determined at 2 hr and 24 hr post-stenting in 50 patients treated with aspirin, bivalirudin and 600 mg clopidogrel. Patients were stratified into low clopidogrel responders (LR)[≤10% relative platelet inhibition (RPI)], moderate responders (>10 – <30% RPI) and high responders (>30% RPI)].
Results: Inhibition measured by 5uM ADP correlated with inhibition by 20uM ADP, collagen and TRAP (r =0.98, 0.91, and 0,83, respectively, p < 0.001 for all). Myocardial marker release occurred in the LR and MR groups only. (Table⇓)
Conclusions: 600 mg clopidogrel markedly inhibits platelet reactivity to multiple agonists in selected patients who are in turn protected from periprocedural MI during elective stenting. These data suggest that low and high risk patients can be identified by platelet function testing that may enhance decision making for adjunctive antithrombotic therapy in elective stenting.