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Updated: Apr 3, 2026
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke
Cyrielle Coignion1, Mathilde Poli, Sharmila Sagnier
1Universitx00E9; de Bordeaux, Hx00F4;pital Pellegrin, CHU de Bordeaux, Bordeaux, France.
Insights
Platelet function testing is not useful for determining stroke causes in patients on antiplatelet drugs (APDs). However, high rates of APD resistance are linked to inflammation and stroke severity.
Area of Science:
- Neurology
- Cardiology
- Hematology
Background:
- Stroke recurrence is common even with antiplatelet drug (APD) therapy.
- Evaluating platelet aggregation testing's role in identifying stroke etiology is crucial.
Purpose of the Study:
- To assess the relevance of platelet aggregation testing in identifying stroke etiology in patients on APDs.
- To investigate the influence of APD functional status on stroke severity and resistance determinants.
Main Methods:
- Prospective inclusion of acute ischemic stroke patients on APDs (aspirin/clopidogrel).
- APD efficacy assessed via Multiplate™ assay and confirmed with light transmission aggregometry.
- Stroke mechanism classified using TOAST and ASCO criteria.
Main Results:
- Antiplatelet drug resistance observed in 18.5% of patients.
- No significant difference in stroke mechanism based on APD efficacy.
- APD resistance associated with poorer diabetes control and higher inflammation (CRP levels).
- Patients sensitive to APDs had less severe initial stroke.
Conclusions:
- Platelet function testing does not help determine stroke mechanisms in patients previously treated with APDs.
- High prevalence of APD resistance confirmed, linked to inflammation and stroke severity.
Background:
Stroke occurrence despite chronic antiplatelet drug (APD) treatment is frequent. We aimed at evaluating the relevance of platelet aggregation testing in the identification of stroke etiology in this context.
Methods:
Patients admitted for a suspected acute ischemic stroke, while under APD (aspirin and/or clopidogrel), were prospectively included. The efficacy of the APD was evaluated using a Multiplate™ assay. Resistance was confirmed using light transmission aggregometry. A standardized diagnostic work-up was performed to identify stroke mechanism according to the TOAST and the ASCO classifications. We evaluated the influence of APD functional status on stroke severity and identified potential determinants of resistance.
Results:
APD resistance was observed in 53 of the 287 patients (18.5%). No difference in stroke mechanism depending on APD efficacy was observed. Patients sensitive to APD had less severe initial stroke severity (mean National Institutes of Health Stroke Scale 3.9 ± 5.6 vs. 7.2 ± 6.8; p < 0.01). Main determinants for APD resistance were a worse control of the diabetes and higher baseline levels of inflammation (mean CRP 26.4 ± 56.0 vs. 9.3 ± 21.0; p < 0.01).
Conclusions:
Platelet function testing does not provide orientation concerning stroke mechanism in patients who were previously on APDs. However, the high frequency of APD resistance and its association with inflammation and stroke severity are confirmed.
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