• Alan D Michelson, Andrew L Frelinger, Eugene Braunwald, William E Downey, Dominick J Angiolillo, Nicholas P Xenopoulos, Joseph A Jakubowski, Youfu Li, Sabina A Murphy, Jie Qin, Carolyn H McCabe, Elliott M Antman, Stephen D Wiviott, and TRITON-TIMI 38 Investigators.
• Department of Medicine, Children's Hospital Boston, Center for Platelet Research Studies, Division of Hematology/Oncology, Boston, MA 02115, USA. michelson@platelets.org
• Eur. Heart J. 2009 Jul 1; 30 (14): 1753-63.

AimsTo examine the extent of platelet inhibition by prasugrel vs. clopidogrel in a TRITON-TIMI 38 substudy.Methods And ResultsTRITON-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 < 0.001) and at 30 days (P < 0.001). Maximal platelet aggregation to 20 microM ADP was lower in prasugrel-treated patients than in clopidogrel-treated patients at 1-2 h (P = 0.004) and 30 days (P = 0.03). Results were similar with 5 microM ADP. Thienopyridine hyporesponsiveness, prespecified as VASP PRI >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).ConclusionsThe 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.

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