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Updated: Apr 29, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Multi-parameter assessment of platelet inhibition and its stability during aspirin and clopidogrel therapy
A Anil Timur1, Gurunathan Murugesan1, Li Zhang2
1Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, OH, USA.
Insights
Platelet inhibition from aspirin and clopidogrel is stable over time. Clopidogrel function assays show better agreement than aspirin assays, aiding in assessing antiplatelet drug response.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Clinical Chemistry
Background:
- Poor response to antiplatelet drugs like aspirin and clopidogrel is linked to adverse cardiovascular outcomes.
- Assessing platelet inhibition is crucial for managing patients undergoing percutaneous coronary intervention (PCI).
Purpose of the Study:
- To evaluate the stability of platelet inhibition and the correlation/agreement between various platelet function assays in patients on dual antiplatelet therapy.
- To compare the performance of different assays in identifying poor responders to aspirin and clopidogrel.
Main Methods:
- Peripheral blood was collected from 58 patients post-PCI at two time points (discharge and 30-90 days).
- Platelet function was measured using light transmission aggregometry (LTA), VerifyNow®, ex vivo thromboxane B2 (TxB2), urinary 11dhTxB2, and VASP phosphorylation index (PRI) assays.
- Patients were classified as poor responders based on established assay-specific cutoffs for aspirin and clopidogrel.
Main Results:
- Aspirin poor response ranged from 3-33%, and clopidogrel poor response from 10-35%.
- Measures of clopidogrel response demonstrated good correlation and agreement between the two visits.
- The VerifyNow® P2Y12 assay and VASP assay showed the highest correlation and agreement for assessing clopidogrel inhibition.
Conclusions:
- Platelet inhibition remains stable during treatment with aspirin and clopidogrel.
- Clopidogrel-response assays exhibit better inter-assay correlation and agreement compared to aspirin-response assays.
- These findings support the use of specific assays for reliable monitoring of antiplatelet therapy effectiveness.
Introduction:
Poor response to antiplatelet drugs is associated with adverse outcomes. We assessed platelet inhibition and its stability and tested correlation and agreement between platelet function assays.
Methods:
Peripheral blood from 58 patients on both aspirin and clopidogrel who underwent percutaneous coronary intervention (PCI) was collected at hospital discharge (visit-1) and at 30-90 days (visit-2). Platelet function was measured using light transmission aggregometry (LTA-AA and LTA-ADP), VerifyNow® (Aspirin; ARU and P2Y12; PRU), ex vivo TxB2, urinary 11dhTxB2, and VASP (PRI) assays. Data were analyzed as continuous, quartiles and binary. Patients were defined as aspirin poor responder (PR) with ARU ≥ 550, LTA-AA maximum ≥ 20%, TxB2 ≥ 1 ng/mL or 11dhTxB2 ≥ 1,500 pg/mg of creatinine and as clopidogrel PR with PRU ≥ 240, PRU ≥ 208, LTA-ADP maximum ≥ 40%, PRI ≥ 50%, or PRI ≥66%.
Results:
Aspirin PR was 3-33% and clopidogrel PR was 10-35% in visit-1. LTA-AA, 11dhTxB2, and all clopidogrel-response measures showed correlation and agreement between visit-1 and visit-2. The highest agreement between two visits was revealed by PRU ≥ 240 and PRI ≥ 66% (PRU-κ=0.7, 95% CI=0.47, 0.93; PRI-κ=0.69, 95% CI=0.42, 0.95, p-values<0.001). Comparison of platelet function assays in a single visit (visit-1) revealed a poor correlation between LTA-AA and 11dhTxB2 assays and no agreement among aspirin-response assays. The highest correlation and agreement were obtained between VerifyNow® P2Y12 and VASP assays (rho=0.7, p-value<0.001 and PRU ≥ 208-PRI-κ=0.41-0.42, 95% CI=0.13, 0.69, p-values<0.001).
Conclusions:
Platelet inhibition is stable during aspirin and clopidogrel treatment. Clopidogrel-response assays correlate and agree with each other better than aspirin-response assays.
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