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Updated: Apr 11, 2026
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet function testing in transient ischaemic attack and ischaemic stroke: A comprehensive systematic review of
Soon Tjin Lim1, Catherine A Coughlan, Stephen J X Murphy
1Department of Neurology, The Adelaide and Meath Hospital, Dublin, incorporating the National Children's Hospital , Dublin , Ireland .
Insights
Many patients with cerebrovascular disease (CVD) remain unprotected by antiplatelet therapy. Measuring platelet function ex vivo could help tailor treatments to prevent recurrent vascular events.
Area of Science:
- Cardiology
- Neurology
- Pharmacology
Background:
- Ischaemic cerebrovascular disease (CVD) patients often experience recurrent vascular events despite antiplatelet therapy.
- Personalized antiplatelet therapy requires reliable ex vivo platelet function monitoring.
Purpose of the Study:
- To systematically review data on ex vivo platelet function in CVD patients on antiplatelet therapy.
- To assess the prevalence and influencing factors of high on-treatment platelet reactivity (HTPR).
Main Methods:
- Systematic literature review of 249 articles, with 93 meeting inclusion criteria.
- Focus on whole blood platelet function analysers (PFA-100®, VerifyNow®, Multiplate®).
- Review of pharmacogenetic data influencing HTPR.
Main Results:
- Prevalence of ex vivo HTPR in CVD varies widely (3-62% aspirin, 8-61% clopidogrel).
- HTPR prevalence differs based on assay (PFA-100 vs. VerifyNow) and definition (longitudinal vs. cross-sectional).
- Limited data exist on pharmacogenetic influences, requiring validation.
Conclusions:
- A significant proportion of CVD patients exhibit ex vivo HTPR on standard antiplatelet regimens.
- Assay and definition choice significantly impact HTPR prevalence estimates.
- Large prospective studies are needed to validate HTPR assessment and pharmacogenetics for predicting recurrent events and optimizing secondary prevention.
Abstract:
The majority of patients with ischaemic cerebrovascular disease (CVD) are not protected from further vascular events with antiplatelet therapy. Measurement of inhibition of platelet function ex vivo on antiplatelet therapy, using laboratory tests that correlate with the clinical effectiveness of these agents, would potentially enable physicians to tailor antiplatelet therapy to suit individuals. A systematic review of the literature was performed to collate all available data on ex vivo platelet function/reactivity in CVD patients, especially those treated with aspirin, dipyridamole or clopidogrel. Particular emphasis was paid to information from commonly available whole blood platelet function analysers (PFA-100®, VerifyNow® and Multiplate®). Data on pharmacogenetic mechanisms potentially influencing high on-treatment platelet reactivity (HTPR) on antiplatelet therapy in CVD were reviewed. Two-hundred forty-nine potentially relevant articles were identified; 93 manuscripts met criteria for inclusion. The prevalence of ex vivo HTPR in CVD varies between 3-62% with aspirin monotherapy, 8-61% with clopidogrel monotherapy and 56-59% when dipyridamole is added to aspirin in the early, subacute or late phases after TIA/stroke onset. The prevalence of HTPR on aspirin was higher on the PFA-100 than on the VerifyNow in one study (p < 0.001). Furthermore, the prevalence of HTPR on aspirin was lower when one used 'novel longitudinal' rather than 'cross-sectional, case-control' definitions of HTPR on the PFA early after TIA or stroke (p = 0.003; 1 study). Studies assessing the influence of genetic polymorphisms on HTPR in CVD patients are limited, and need validation in large multicentre studies. Available data illustrate that an important proportion of CVD patients have ex vivo HTPR on their prescribed antiplatelet regimen, and that the prevalence varies depending on the definition and assay used. Large, adequately-sized, prospective multicentre collaborative studies are urgently needed to determine whether comprehensive assessment of HTPR at high and low shear stress with a range of user-friendly whole blood platelet function testing platforms, in conjunction with pharmacogenetic data, improves our ability to predict the risk of recurrent vascular events in CVD patients, and thus enhance secondary prevention following TIA or ischaemic stroke.
