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Variation in thromboxane B2 concentrations in serum and plasma in patients taking regular aspirin before and after
Richard I S Good1, Anne McGarrity, Rory Sheehan
1BHF Glasgow Cardiovascular Research Centre, University of Glasgow , Glasgow , UK .
Insights
Dual antiplatelet therapy with aspirin and P2Y12 antagonists is common. This study found that P2Y12 antagonists do not affect aspirin
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Biochemistry
Background:
- Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 antagonist is standard for preventing thrombotic events after acute coronary syndrome or percutaneous coronary intervention (PCI).
- Inter-individual variability in antiplatelet drug response is recognized, with recent data suggesting P2Y12 antagonists may influence aspirin's efficacy.
- Measuring thromboxane B2 (TxB2) generation in serum minus plasma ([TxB2]S-P) offers a direct assessment of aspirin's effect on platelets, avoiding confounding factors.
Purpose of the Study:
- To analyze [TxB2]S-P as a measure of aspirin response in patients undergoing elective PCI before and after clopidogrel introduction.
- To compare [TxB2]S-P with VerifyNow Aspirin for assessing aspirin response in patients on aspirin alone.
- To determine if P2Y12 antagonists impact aspirin's antiplatelet effect as measured by thromboxane generation.
Main Methods:
- Analysis of serum and plasma thromboxane B2 ([TxB2]S-P) in 123 patients undergoing elective PCI, before and after clopidogrel initiation.
- Comparison of [TxB2]S-P and VerifyNow Aspirin in a subgroup of 40 patients taking aspirin monotherapy.
- Assessment of TxB2 generation as a direct indicator of aspirin's effect on platelet function.
Main Results:
- A wide variation in TxB2 levels was observed, but few patients (3.5%) had residual serum TxB2 > 10 ng/ml.
- Strong correlation between pre- and post-clopidogrel TxB2 levels (r ≥ 0.78; p = 0.001) with no significant change in [TxB2]S-P.
- No correlation found between clopidogrel response magnitude and thromboxane B2 generation; poor correlation between [TxB2]S-P and VerifyNow Aspirin.
Conclusions:
- P2Y12 antagonist use does not influence aspirin's effect on platelet thromboxane generation.
- Measurement of [TxB2]S-P is a valid method to assess aspirin response in patients on dual antiplatelet therapy.
- The [TxB2]S-P assay provides a reliable assessment of aspirin's antiplatelet activity, independent of P2Y12 inhibition.
Abstract:
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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