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Ticagrelor Not Found Superior to Prasugrel in Reducing Platelet Reactivity
Study findings have shown that ticagrelor is not superior to prasugrel in reducing platelet reactivity during the first 24 hours in patients with STEMI undergoing primary PCI.
Researchers conducted the prospective, single-center, single blind study of 55 of 117 (47%) screened consecutive patients with STEMI undergoing primary PCI. Patients were randomly assigned to ticagrelor (Brilinta, AstraZeneca) 180 mg loading, followed by 90 mg twice daily, or prasugrel (Effient, Daiichi Sankyo/Eli Lilly) 60 mg loading, followed by 10 mg once daily for 5 days. Platelet reactivity was assessed at 0, 1, 2, 6 and 24 hours and 5 days.
Platelet reactivity at 1 hour, the study’s primary endpoint, did not differ significantly between the two drugs (ticagrelor: 257.3 P2Y12 reaction unit [PRU]; 95% CI, 230.8-283.8 vs. prasugrel: 231.3 PRU; 95% CI, 205.3-257.4). Platelet reactivity did not differ at 2, 6 and 24 hours, although at day 5 it was lower with ticagrelor than prasugrel (25.6 PRU; 95% CI, 12.3-38.9 vs. 50.3 PRU; 95% CI, 36.4-64.1).
At hour 2, high on-treatment platelet reactivity rates (cutoff: 208 PRU) were 46.2% for ticagrelor and 34.6% for prasugrel, and decreased significantly thereafter. Of note, these rates did not differ significantly between the two agents at any time point of the study.
Perspective
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The main finding of this study is that approximately half of the patients receiving a loading dose of ticagrelor or prasugrel in the setting of primary PCI for STEMI do not have appropriate platelet aggregation inhibition at 2 hours. As a consequence, half of patients receiving infarct artery stenting do not receive an effective antithrombotic adjunctive therapy, which carries an increased risk of acute stent thrombosis. This finding is not completely surprising considering that in the setting of STEMI, gastrointestinal absorption of the drugs may be limited by vomiting, low output, vasoconstriction and analgesic drugs — which is different when compared with the setting of stable CAD. If these findings are confirmed by future studies, the routine use of glycoprotein IIb/IIIa inhibitors in the setting of primary PCI for STEMI should be reconsidered.