Pharmacodynamic assessment of platelet inhibition by prasugrel vs. clopidogrel in the TRITON-TIMI 38 trial

Abstract

The TRITON-TIMI 38 platelet substudy shows that prasugrel results in greater inhibition of ADP-mediated platelet function in ACS patients than clopidogrel, supporting the hypothesis that greater platelet inhibition leads to a lower incidence of ischaemic events and more bleeding both early and late following PCI.

Prasugrel overcomes high on-clopidogrel platelet reactivity in the acute phase of acute coronary syndrome and maintains its antiplatelet potency at 30-day follow-up

“…Similarly, we expected that additional administration of 30 mg of prasugrel in HTPR patients who had received a 600 mg loading dose of clopidogrel would decrease PRI to a value comparable with that observed in clopidogrel-naive patients after treatment with a 60 mg loading dose of prasugrel (34.3 ± 23.1%) [19]. Additionally, we anticipated in our prasugrel-treated patients to obtain PRI values at 30 days comparable to these observed in the TRITON-TIMI 38 platelet substudy at this time point (33.6 ± 2.9%) [20]. Bearing in mind these results and assuming a 2-sided alpha value of 0.05, we calculated, using the t-test for dependent variables, that enrolment of 46 HTPR patients would provide a 99.9% power to demonstrate significant reductions in PRI associated with the implementation of prasugrel-based antiplatelet regimen between its baseline value and both values at 24 h and 30 days.…”

2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST‐Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 2007 Focused Update)

“…(Prasugrel has a higher level of inhibition of platelet aggregation than clopidogrel and a more rapid onset of action. 55 Its metabolism is not affected by the 2C19 allele variant. 56 ).…”

High residual platelet reactivity during dual antiplatelet therapy, found by optical aggregometry and the rate of atherothrombotic complications after coronary artery stenting in patients with ischemic heart disease in clinical practice

“…Вы-явление взаимосвязи между недостаточным ингиби-рованием ФАТ (ВОРТ) на фоне ААТ и неблагоприятными исходами (НС, ИМ, тромбозом стента) позволяет об-суждать вопрос о возможной модификации ААТ, исходя из показателей ФАТ [25,26]. Среди возможных вари-антов можно обсуждать увеличение дозы клопидогрела [27], либо его замену на другие блокаторы P2Y 12 ре-цепторов (тикагрелор или прасугрел) [28][29][30].…”