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Published on: November 8, 2024
Serum thromboxane B2 compared to five other platelet function tests for the evaluation of aspirin effect in stable
Giselle Kidson-Gerber1, James Weaver, Rosalie Gemmell
1South Eastern Area Laboratory Services, Department of Haematology, Prince of Wales Hospital, Sydney, Australia. Giselle.Kidson-Gerber@sesiahs.health.nsw.gov.au
Insights
Serum thromboxane B(2) (TXB(2)) measurements effectively assess aspirin
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Clinical Chemistry
Background:
- Assessing antiplatelet therapy efficacy in cardiovascular disease is crucial.
- Aspirin and clopidogrel are commonly used antiplatelet agents.
- Understanding their impact on platelet function is vital for patient management.
Purpose of the Study:
- To evaluate serum thromboxane B(2) (TXB(2)) as a marker for aspirin and clopidogrel efficacy.
- To correlate TXB(2) levels with various platelet function tests.
- To identify potential markers for antiplatelet non-response.
Main Methods:
- 76 patients on aspirin, clopidogrel, or both underwent TXB(2) measurement.
- Platelet function was assessed using whole blood aggregometry (WBA), PFA-100, and Cone and Plate Analyzer.
- Clopidogrel patients also used the VerifyNow System.
Main Results:
- Serum TXB(2) levels differed significantly between aspirin, clopidogrel users, and controls.
- Moderate correlations were observed between TXB(2) and multiple platelet function assays.
- Aspirin non-response varied across tests, with higher TXB(2) in non-responders.
- Both aspirin and clopidogrel suppressed platelet pathways; fish oil intake was associated with lower TXB(2).
Conclusions:
- Serum TXB(2) is a direct, practical measure of aspirin's pharmacological effect.
- TXB(2) correlates with other platelet function tests and may serve as a sole indicator of aspirin non-response.
- Combined TXB(2) and global platelet function tests may enhance non-response prediction.
- Both aspirin and clopidogrel demonstrate broad suppression of platelet activity.
Background:
To assess the role of serum thromboxane B(2) (TXB(2)) measurements and the correlation between platelet function studies, in patients with stable cardiovascular disease on aspirin or clopidogrel.
Methods:
76 patients (47 on aspirin, 16 clopidogrel, 13 both) underwent assessment of TXB(2), whole blood aggregometry (WBA) after stimulation with (i) arachidonic acid (0.5mM), (ii) ADP (5 microM), (iii) collagen (1 and 5 microg/ml), PFA-100, and Cone and Plate Analyzer. Clopidogrel patients were additionally assessed by the VerifyNow System.
Results:
TXB(2) values ranged between 0.2 and 56.2 ng/ml, with significant separation between those taking aspirin, clopidogrel and controls (0.45 ng/ml vs 6.85 ng/ml vs 12.97 ng/ml, p<0.001). There was moderate correlation between WBA-AA and TXB(2) (r=0.487, p<0.001), PFA-100((R)) (r=0.599, p<0.001), WBA-Col1 (r=0.424, p<0.001), WBA-Col1:5 (r=0.417, p<0.001), and between TXB(2) and PFA-100((R)) (r=0.509, p<0.001). The prevalence of aspirin non-responders for WBA-AA, TXB(2), PFA-100((R)), CPA and Coll1:5 was 13.1%, 8.2%, 14.8%, 9.7% and 16.4% respectively. Individual patients were not consistently classified as aspirin non-responders in all tests. Those with inadequate aspirin response on > or =3 tests had higher TXB(2) levels (mean 1.57+/-1.66, range 0.553-4.45 vs mean 0.45+/-0.18, range 0.23-1.50) (p=0.001). Clopidogrel suppressed TXB(2) (p=0.02), WBA-AA (p<0.001), WBA-Col1 (p=0.012) and WBA-ADP (p<0.001) compared to controls. TXB(2) in patients ingesting fish oil tablets was lower compared to those without (0.4 ng/ml vs 0.52 ng/ml, p=0.004). Obesity was associated with higher TXB(2) values (0.61 vs 0.41, p=0.01).
Conclusion:
Serum TXB(2) measurements are a direct measure of the pharmacological effect of aspirin, are easily performed and correlate with other measures of platelet function. Serum TXB(2) measurements could be a useful sole measure of aspirin non-response, and may be even more predictive when performed in tandem with a global measure of platelet function. Aspirin and clopidogrel both suppressed several platelet pathways.
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