Pharmacodynamic assessment of platelet inhibition by prasugrel vs. clopidogrel in the TRITON-TIMI 38 trial
Authors
Michelson, Alan D.Frelinger, Andrew L. III
Braunwald, Eugene
Downey, William E.
Angiolillo, Dominick J.
Xenopoulos, Nicholas P.
Jakubowski, Joseph A.
Li, YouFu
Murphy, Sabina A.
Qin, Jie
McCabe, Carolyn H.
Antman, Elliott M.
Wiviott, Stephen D.
UMass Chan Affiliations
Department of PediatricsDocument Type
Journal ArticlePublication Date
2009-07-01Keywords
Acute Coronary SyndromeAdenosine Diphosphate
Angioplasty, Balloon, Coronary
Cell Adhesion Molecules
Female
Humans
Male
Microfilament Proteins
Middle Aged
Myocardial Infarction
Phosphoproteins
Phosphorylation
Piperazines
Platelet Aggregation Inhibitors
Thiophenes
Ticlopidine
Hematology
Oncology
Pediatrics
Metadata
Show full item recordAbstract
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 andlt; 0.001) and at 30 days (P andlt; 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 andlt; 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.Source
Eur Heart J. 2009 Jul;30(14):1753-63. Epub 2009 May 12. doi 10.1093/eurheartj/ehp159DOI
10.1093/eurheartj/ehp159Permanent Link to this Item
http://hdl.handle.net/20.500.14038/43313PubMed ID
19435740Related Resources
Link to article in PubMedae974a485f413a2113503eed53cd6c53
10.1093/eurheartj/ehp159