January 1, 2009Platelets
Ticagrelor yields consistent dose-dependent inhibition of ADP-induced platelet aggregation in patients with atherosclerotic disease regardless of genotypic variations inP2RY12, P2RY1,andITGB3
Why the study?
Do genotypic variations in P2RY12, P2RY1, and ITGB3 influence the pharmacodynamic response to ticagrelor in patients with atherosclerotic disease?
Population
151 clopidogrel-naive Caucasian patients with stable atherosclerotic disease or non-ST-segment elevation…
Design
Cohort
Follow-up
4 weeks
Authors
Discussion
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Member takes
Implication
No support for genotyping these loci to predict ticagrelor response; leaves open other genetic or population effects.
Structured PICO
Do genotypic variations in P2RY12, P2RY1, and ITGB3 influence the pharmacodynamic response to ticagrelor in patients with atherosclerotic disease?
P
Population
151 clopidogrel-naive Caucasian patients with stable atherosclerotic disease (from the DISPERSE study) or non-ST-segment elevation acute coronary syndromes (from the DISPERSE2 study)
I
Intervention
Ticagrelor
O
Outcome
Inhibition of ADP-induced platelet aggregation at 4 weekssurrogate
Ticagrelor provides consistent inhibition of platelet aggregation regardless of genetic variations in P2RY12, P2RY1, and ITGB3, highlighting a potential pharmacodynamic advantage over clopidogrel.
Cite This Study
Storey et al. (2009) studied this question.