What is the clinical evidence from this study?

Study design: Other. Population: Platelet aggregation. Intervention: ADP and P2Y12 antagonists. Primary outcome: Platelet aggregation in response to thrombin receptor activator peptide.

What question did this study set out to answer?

To determine whether adenosine derived from ADP metabolism inhibits platelet aggregation when P2Y12 receptor signaling is blocked.

November 25, 2010Arteriosclerosis Thrombosis and Vascular Biology

Adenosine Derived From ADP Can Contribute to Inhibition of Platelet Aggregation in the Presence of a P2Y 12 Antagonist

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Key result

ADP inhibits platelet aggregation in the presence of a P2Y12 antagonist through conversion to adenosine in platelet-rich plasma, but not in whole blood unless adenosine uptake is inhibited.

Why the study?

Does ADP-derived adenosine inhibit platelet aggregation in the presence of P2Y12 antagonists?

Population

Platelet-rich plasma (PRP) and whole blood samples

Comparison

ADP and P2Y12 antagonists with or without… vs Control conditions

Design

Preclinical

Authors

DIDavid IyúGrupo Español de Trasplante Hematopoyético y Terapia Celular JGJackie R. GlennUniversity of Nottingham AWAnn E. WhiteUniversity of Nottingham

Discussion

Member takes

Implication

Findings limited to platelet-rich plasma; leaves open adenosine's role in P2Y12 antagonist efficacy in vivo.

Key Points

To determine whether adenosine derived from ADP metabolism inhibits platelet aggregation when P2Y12 receptor signaling is blocked.
Measured TRAP-induced platelet aggregation via platelet counting in both platelet-rich plasma (PRP) and whole blood.
Treated samples with ADP alongside P2Y12 antagonists (cangrelor, prasugrel active metabolite, ticagrelor), with or without adenosine deaminase or dipyridamole.
Quantified cyclic AMP pathway activity through vasodilator-stimulated phosphoprotein (VASP) phosphorylation.
In the presence of any tested P2Y12 antagonist, ADP preincubation inhibited platelet aggregation in PRP, an effect completely reversed by adenosine deaminase.
Platelet aggregation was not inhibited in whole blood unless dipyridamole was co-administered to block adenosine uptake into erythrocytes.
Inhibitory responses were mirrored by exogenous adenosine, directly correlated with VASP phosphorylation, and did not differ among the three P2Y12 antagonists.

Structured PICO

Does ADP-derived adenosine inhibit platelet aggregation in the presence of P2Y12 antagonists?

Population

Platelet-rich plasma (PRP) and whole blood samples

Intervention

ADP and P2Y12 antagonists (cangrelor, prasugrel active metabolite, and ticagrelor) with or without dipyridamole

Comparator

Control conditions (e.g., without adenosine deaminase or dipyridamole)

Outcome

Platelet aggregation in response to thrombin receptor activator peptidesurrogate

ADP inhibits platelet aggregation in the presence of P2Y12 antagonists through conversion to adenosine, an effect dependent on inhibiting adenosine uptake in whole blood.

Cite This Study

Iyú et al. (2010) studied Platelet aggregation. ADP and P2Y12 antagonists was evaluated on Platelet aggregation in response to thrombin receptor activator peptide. ADP inhibits platelet aggregation in the presence of a P2Y12 antagonist through conversion to adenosine in platelet-rich plasma, but not in whole blood unless adenosine uptake is inhibited.

synapsesocial.com/papers/6a86f5b3540b033b21bf00b2 https://doi.org/10.1161/atvbaha.110.219501

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Adenosine Derived From ADP Can Contribute to Inhibition of Platelet Aggregation in the Presence of a P2Y 12 Antagonist

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Adenosine Derived From ADP Can Contribute to Inhibition of Platelet Aggregation in the Presence of a P2Y 12 Antagonist

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider