Prasugrel resulted in significantly lower VASP platelet reactivity index compared to clopidogrel at 1-2 hours and 30 days post-PCI (P<0.001).
RCT (n=125)
Yes
p-value: p=<0.001
AIMS: To examine the extent of platelet inhibition by prasugrel vs. clopidogrel in a TRITON-TIMI 38 substudy. METHODS AND RESULTS: TRITON-TIMI 38 randomized acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) to prasugrel or standard dose clopidogrel. Selected sites prospectively enrolled TRITON-TIMI 38 patients to evaluate adenosine diphosphate (ADP)-attenuated phosphorylation of platelet vasodilator-stimulated phosphoprotein (VASP) (n = 125 patients) and, in a subset (n = 31 patients), ADP-stimulated platelet aggregation. VASP platelet reactivity index (PRI) was lower in prasugrel-treated patients than in clopidogrel-treated patients at 1-2 h post-PCI (>or=1 h after loading dose) (P 50%, was more frequent in clopidogrel-treated patients than in prasugrel-treated patients at 1-2 h (P < 0.001) and 30 days (P = 0.03). CONCLUSIONS: 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.
Michelson et al. (Tue,) conducted a rct in Acute coronary syndrome (ACS) (n=125). Prasugrel vs. Standard dose clopidogrel was evaluated on VASP platelet reactivity index (PRI) at 1-2 hours and 30 days (p=<0.001). Prasugrel resulted in significantly lower VASP platelet reactivity index compared to clopidogrel at 1-2 hours and 30 days post-PCI (P<0.001).