Abstract
Antiplatelet effects of aspirin vary with level of P2Y₁₂ receptor blockade supplied by either ticagrelor or prasugrel.
Highlights
ÔDual antiplatelet therapyÕ, comprising aspirin and a P2Y12 receptor inhibitor, is firmly established for the secondary prevention of thrombotic events with the rationale that they inhibit thromboxane A2- (TxA2) and ADP-P2Y12-dependent pathways of platelet activation, respectively
Additional methodological details are provided as online supplementary information. Using this approach we determined the inhibitory potencies of ticagrelor, PAM and aspirin against aggregations induced by ADP (0.625–20 lmol L)1), the thromboxane-mimetic U46619 (0.1–30 lmol L)1) and arachidonic acid (0.1–1 mmol L)1)
Ticagrelor and PAM, but not aspirin, produced complete, concentration-dependent inhibition of platelet aggregations induced by U46619 (Fig. S2)
Summary
ÔDual antiplatelet therapyÕ, comprising aspirin and a P2Y12 receptor inhibitor, is firmly established for the secondary prevention of thrombotic events with the rationale that they inhibit thromboxane A2- (TxA2) and ADP-P2Y12-dependent pathways of platelet activation, respectively. Ticagrelor and PAM, but not aspirin, produced complete, concentration-dependent inhibition of platelet aggregations induced by U46619 (Fig. S2)
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