Antiplatelet effects of aspirin vary with level of P2Y12 receptor blockade supplied by either ticagrelor or prasugrel

Kirkby, Nicholas S.; Leadbeater, P. D. M.; Chan, Melissa; Nylander, Sven; Mitchell, Jane A.; Warner, Timothy D.

doi:10.1111/j.1538-7836.2011.04453.x

Cited by 70 publications

(48 citation statements)

References 8 publications

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“…The majority of this work concerns the characterization of platelet reactivity in the presence of antiplatelet therapies such as GPIIb/IIIa inhibitors (16,23) or dual anti-platelet therapy with ADP P2Y 12 antagonists plus aspirin (10–13,17,21,22,25,26). Using these techniques, it is possible to produce concentration-response curves which can be used to evaluate the pharmacological action of these therapies.…”

Section: -Well Plate Aggregationmentioning

confidence: 99%

96-well plate-based aggregometry

2018

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While there are many bench and bedside tests to assess platelet reactivity, ex vivo light transmission aggregometry (LTA) remains the gold standard. LTA, however, is expensive, time-consuming and requires dedicated equipment and staff, making it impractical in many situations. In addition, there is significant variability between data generated at different testing sites meaning that tests often need to be repeated if a patient is transferred to the care of a different hospital. As such, there is clearly an unmet need for standardization of platelet testing.Using the principles of LTA, aggregometry can be conducted in 96-well plates with readings being made in a standard plate reader. This approach allows for the assessment of multiple concentrations of agonists, since the volume of platelets required for each test is significantly lower than for LTA. Furthermore, the lyophilization of a set panel of agonists to a 96-well plate to produce a stable assay substrate allows the production of portable, standardized plates that can be used to generate reproducible tests at multiple sites.In this review, we will discuss the methods and uses of 96-well plate aggregometry for both research and the clinic.

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Section: -Well Plate Aggregationmentioning

confidence: 99%

96-well plate-based aggregometry

2018

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“…In addition, data from the CHARISMA study have suggested that levels of urinary 11-dehydro-TxB2 are not influenced by the addition of clopidogrel to regular low dose aspirin [18]. However, there are data to suggest that ADP contributes to the response of platelets to thromboxane [19], P2Y 12 inhibition influences thromboxane A2 (TxA2) production and the addition of aspirin augments the antiplatelet effects of partial P2Y 12 inhibition [20,21].…”

Section: Introductionmentioning

confidence: 97%

Variation in thromboxane B2 concentrations in serum and plasma in patients taking regular aspirin before and after clopidogrel therapy

et al. 2014

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Dual antiplatelet therapy with aspirin and a P2Y12 antagonist is widely prescribed for the prevention of thrombotic events in patients with an acute coronary syndrome or undergoing percutaneous coronary intervention (PCI). It is recognised that there is inter-individual variation in the antiplatelet effects of both drugs. Recent data also suggest that P2Y12 antagonists can affect the response to aspirin. A direct indicator of the effect of aspirin on platelets is their ability to generate thromboxane, which if measured as the difference between the level of thromboxane B2 in serum and plasma ([TxB2]S-P) avoids the confounding effect of endogenous TxB2 production from other cells. We therefore analysed [TxB2]S-P as a measure of aspirin response in a group of 123 patients undergoing elective PCI before and after the introduction of clopidogrel. In a subgroup of 40 patients taking aspirin alone, we compared [TxB2]S-P and VerifyNow Aspirin for the assessment of aspirin response. There was a wide variation in plasma and serum TxB2 concentrations both before and after clopidogrel therapy but only 3.5% of patients had residual serum concentration of TxB2 > 10 ng/ml. There was a strong correlation between the pre and post clopidogrel levels of TxB2 (r ≥ 0.78; p = 0.001) and no significant difference in [TxB2]S-P. There was no correlation between the magnitude of response to clopidogrel response and the generation of thromboxane B2. Correlation between [TxB2]S-P and VerifyNow Aspirin was poor. We conclude that the use of a P2Y12 antagonist does not influence the effect of aspirin on the ability of platelets to generate thromboxane. Therefore, measurement of TxB2 levels in serum, after subtracting the contribution from plasma, provides a measure of the response to aspirin in patients taking dual antiplatelet therapy.

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“…These agents have also been shown to block thromboxane-mediated pathways, which calls into question whether aspirin is even needed in conjunction with these antiplatelets [54]. Several pharmacodynamics studies have shown that aspirin provides little additional antiplatelet effect when used with potent P2Y 12 Optimal aspirin dose in acute coronary syndromes: an emerging consensus REviEW future science group www.futuremedicine.com inhibitors [55][56][57]. At this time, no clinical trial has tested the impact of aspirin in the presence of strong P2Y 12 receptor blockade.…”

Section: Newer P2y 12 Receptor Antagonists (Prasugrel and Ticagrelor)mentioning

confidence: 96%

Optimal Aspirin Dose in Acute Coronary Syndromes: an Emerging Consensus

et al. 2014

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Numerous clinical trials testing the efficacy of aspirin for the secondary prevention of cardiovascular disease have been published. We reviewed the literature pertaining to aspirin dose in acute coronary syndrome patients. Clinical trials assessing the comparative efficacy of different doses of aspirin are scarce. This complex antiplatelet therapy landscape makes it difficult to identify the best aspirin dose for optimizing efficacy and minimizing risk of adverse events, while complying with the various guidelines and recommendations. Despite this fact, current evidence suggests that aspirin doses of 75-100 mg/day may offer the optimal benefit:risk ratio in acute coronary syndrome patients.

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Antiplatelet effects of aspirin vary with level of P2Y12 receptor blockade supplied by either ticagrelor or prasugrel

Cited by 70 publications

References 8 publications

96-well plate-based aggregometry

96-well plate-based aggregometry

Variation in thromboxane B2 concentrations in serum and plasma in patients taking regular aspirin before and after clopidogrel therapy

Optimal Aspirin Dose in Acute Coronary Syndromes: an Emerging Consensus

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