Inhibition of the platelet P2Y12receptor for adenosine diphosphate does not impair the capacity of platelet to synthesize thromboxane A2
Authors' conclusion
Inherited deficiency or pharmacological inhibition of P2Y12R does not affect the platelet capacity to synthesize TxA2. There is no pharmacological evidence that ACS patients may be safely treated with P2Y12R antagonists without ASA.
Study context
- Population
- Patients with inherited P2Y12 receptor (P2Y12R) deficiency, healthy subjects, and patients treated with prasugrel or placebo
- Participants
- 3 vs 33
- Comparison
- P2Y12R-deficient vs Healthy
- P2Y12R-deficientn = 3
- Healthyn = 33reference
- Outcome
- Platelet TxA2 production (serum TxB2)
Main finding
As reported in the abstract
- Serum TxB2 similar in P2Y12R-deficient patients and healthy subjects; not decreased by P2Y12R antagonists in vitro
- Serum TxB2 did not decrease in patients treated with prasugrel (10 mg q.i.d.) or placebo for 14 days
- P2Y12R antagonists inhibited arachidonic acid- and collagen-induced platelet aggregation (PA) and TxB2 production in platelet-rich plasma (PRP) in vitro, but not TxB2 production when PA was prevented (no stirring)
- P2Y1 antagonist MRS2500 had similar effects on PA and TxB2 production as P2Y12R antagonists
- Acetylsalicylic acid (ASA) inhibited TxB2 production more effectively than a P2Y12R antagonist; only ASA plus a P2Y12R antagonist inhibited PA induced by high-concentration collagen
Original publication
Inhibition of the platelet P2Y12receptor for adenosine diphosphate does not impair the capacity of platelet to synthesize thromboxane A2. Eur Heart J. Published 29 October 2015. doi:10.
Summarised from the published abstract; every number is checked against it