Abstract 2364: Bivalirudin With And Without Eptifibatide For Elective Stenting: A Pharmacodynamic Study Of Platelet Reactivity And Its Relation To Periprocedural Myocardial Infarction.
Background: It has been demonstrated that heparin and eptifibatide produced superior platelet inhibition and less myocardial necrosis than heparin alone in patients treated with clopidogrel (CLP) at the time of stenting. The primary objectives were to compare the effect of bivalirudin (B) + eptifibatide (E) vs. B alone on platelet reactivity and study the relation of platelet reactivity to myocardial necrosis following elective stenting.
Methods: The study will enroll 200 patients; at this time 170 have been randomly treated with B vs. B+E; all received CLP and aspirin; Serial measurements of platelet reactivity to multiple agonists by aggregometry and cardiac markers by ELISA were performed over 24 hours.
Results: B+E compared to B produced superior relative inhibition of platelet aggregation induced by 5uM ADP, 20uM ADP, 15uM TRAP, 25uM TRAP, collagen (p< 0.01 for all, see Table 1⇓). B+E was associated with less myocardial infarction (9% vs. 4%). Platelet reactivity was higher in patients with myocardial infarction: 46±21 % vs. 28±17% (5 μM ADP); 52±22% vs.33±19% (20 μM ADP).
Conclusions: Eptifibatide + bivalirudin produces superior platelet inhibition irrespective of the stimulating agonist. Our results suggest that a relation exists between platelet reactivity and post-stent infarction; eptifibatide + bivalirudin may reduce necrosis marker release as compared to bivalirudin therapy alone in selected patients with high platelet reactivity. Triage of patients for adjunctive GPIIb/IIIa blockade may be enhanced by platelet function measurements that requires investigation in larger studies. RPI = 100 × (baseline aggregation -post-treatment aggregation)/baseline aggregation.