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PRINCIPLE TIMI 44: Prasugrel inhibited in vivo platelet aggregation
Effects of clopidogrel and prasugrel on both in vivo and in vitro platelet aggregation compared.
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Prasugrel inhibited adenosine diphosphate–stimulated platelet-monocyte aggregates, platelet-neutrophil aggregates and P-selectin–positive platelets to a greater extent than clopidogrel while preventing in- creased myeloperoxidase.
Results from a substudy of the PRINCIPLE-TIMI 44 trial suggested that a 60- mg dose of prasugrel was similar to a 600-mg loading dose and 150-mg maintenance dose of clopidogrel (Plavix; SanofiAventis, Bristol-Myers Squibb) for inhibition of in vivo platelet aggregation. The researchers for the PRINCIPLE-TIMI 44 trial, a randomized, double blind, crossover study, enrolled 201 patients undergoing cardiac catheterization for planned percutaneous coronary intervention and assigned them to either 60 mg of prasugrel or a 600-mg loading dose and 150-mg maintenance dose of clopidogrel.
The researchers from various sites including Brigham and Women’s Hospital in Boston reported that at six hours following administration of prasugrel, patients had similar reductions in circulating platelet-monocyte aggregates (P<.05) to those treated with a 600-mg loading dose of clopidogrel.
They also reported that in patients treated with prasugrel, in vitro ADP–stimulated platelet-monocyte aggregates (P<.05), platelet-neutrophil aggregates and P-selectin–positive platelets were inhibited to a greater extent than with clopidogrel during the loading-dose and maintenance-dose phases. At six hours following the loading dose of clopidogrel, patients who were not treated with prasugrel had elevated levels of plasma myeloperoxidase (P<.05) compared with baseline.
“These results demonstrate for the first time inhibition by prasugrel for markers of in vivo platelet activation,” Andrew L. Frelinger, III, PhD, associate director of the Center for Platelet Function Studies at the University of Massachusetts Medical School in Worcester, concluded in his presentation at the American Heart Association Scientific Sessions 2008 in New Orleans. “These results extend previous findings of greater platelet inhibition by prasugrel than high-dose clopidogrel to include greater inhibition of ADP–stimulated P-selectin–positive platelets, platelet-monocyte aggregates and platelet-neutrophil aggregates, which may be mechanistically important given the high local concentrations of ADP at sites of thrombus formation.” – by Eric Raible
For more information:
- Frelinger A. #3995. Presented at: American Heart Association Scientific Sessions 2008; Nov. 8-12, 2008; New Orleans.