Platelet function testing in transient ischaemic attack and ischaemic stroke: A comprehensive systematic review of the literature

Lim, Soon Tjin; Coughlan, Catherine A.; Murphy, Stephen J.; Fernández-Cadenas, Israel; Montaner, Joan; Thijs, Vincent; Marquardt, Lars; McCabe, Dominick J. H.

doi:10.3109/09537104.2015.1049139

Cited by 45 publications

(44 citation statements)

References 117 publications

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“…However, the incidence of HTPR to antiplatelet medication has been reported to show a very high range between 3 and 62% [11]. Additionally, evidence associating laboratory response to antiplatelet medication and clinical outcome is unclear.…”

Section: Discussionmentioning

confidence: 99%

“…This might be a reason for the high variability in incidence of HTPR to antiplatelet medication [2,11]. Frequently used tests to evaluate platelet function in whole blood are the VerifyNow®, the Multiplate® and the PFA-100® assay [11]. Especially the VerifyNow® and the Multiplate® assay are available bedside and are easy to handle.…”

Section: Discussionmentioning

confidence: 99%

“…Many different tests are available to measure the pharmacodynamic response to antiplatelet medication. This might be a reason for the high variability in incidence of HTPR to antiplatelet medication [2,11]. Frequently used tests to evaluate platelet function in whole blood are the VerifyNow®, the Multiplate® and the PFA-100® assay [11].…”

Section: Discussionmentioning

confidence: 99%

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Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Mohring

Piayda²,

Dannenberg³

et al. 2017

Pharmacology

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Platelet inhibition by aspirin is indispensable in the secondary prevention of cardiovascular events. Nevertheless, impaired aspirin antiplatelet effects (high on-treatment platelet reactivity [HTPR]) are frequent. This is associated with an enhanced risk of cardiovascular events. The current gold standard to evaluate platelet hyper-reactivity despite aspirin intake is the light-transmittance aggregometry (LTA). However, pharmacologically, the most specific test is the measurement of arachidonic acid (AA)-induced thromboxane (TX) B2 formation. Currently, the optimal cut-off to define HTPR to aspirin by inhibition of TX formation is not known. Therefore, in this pilot study, we aimed to calculate a TX formation cut-off value to detect HTPR defined by the current gold standard LTA. We measured platelet function in 2,507 samples. AA-induced TX formation by ELISA and AA-induced LTA were used to measure aspirin antiplatelet effects. TX formation correlated nonlinearly with the maximum of aggregation in the AA-induced LTA (Spearman's rho R = 0.7396; 95% CI 0.7208-0.7573, p < 0.0001). Receiver operating characteristic analysis and Youden's J statistics revealed 209.8 ng/mL as the optimal cut-off value to detect HTPR to aspirin with the TX ELISA (area under the curve: 0.92, p < 0.0001, sensitivity of 82.7%, specificity of 90.3%). In summary, TX formation ELISA is reliable in detecting HTPR to aspirin. The calculated cut-off level needs to be tested in trials with clinical end points.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Mohring

Piayda²,

Dannenberg³

et al. 2017

Pharmacology

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“…One easy point-of-care technique is the VerifyNow® System (http://www.itcmed.com/products/verifynow-system-platelet-reactivity-test) that assesses platelet reactivity to antiplatelet medications such as aspirin, clopidogrel, and GP IIb/IIIa inhibitors [21][22][23] . However, in a recent study, it was noted that large, adequately-sized, prospective multicentre collaborative studies are urgently needed to determine whether the comprehensive assessment of antiplatelet therapy improves the ability to predict the risk of recurrent vascular events in cardiovascular patients, including ischaemic stroke patients 22) . Although this technique may be employed in an individualized patient-orientated approach, we propose a more comprehensive approach, which focuses not only on platelet function.…”

Section: Pathogenesis Of Thrombo-embolic Ischaemic Strokementioning

confidence: 99%

Novel Diagnostic and Monitoring Tools in Stroke: an Individualized Patient-Centered Precision Medicine Approach

Villiers

Swanepoel

Bester

et al. 2016

J Atheroscler Thromb

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Central to the pathogenesis of ischaemic stroke are the normally protective processes of platelet adhesion and activation. Experimental evidence has shown that the ligand-receptor interactions in ischaemic stroke represent a thrombo-inflammatory cascade, which presents research opportunities into new treatment. However, as anti-platelet drugs have the potential to cause severe side effects in ischaemic stroke patients (as well as other vascular disease patients), it is important to carefully monitor the risk of bleeding and risk of thrombus in patients receiving treatment. Because thrombo-embolic ischaemic stroke is a major health issue, we suggest that the answer to adequate treatment is based on an individualized patient-centered approach, inline with the latest NIH precision medicine approach. A combination of viscoelastic methodologies may be used in a personalized patient-centered regime, including thromboelastography (TEG®) and the lesser used scanning electron microscopy approach (SEM). Thromboelastography provides a dynamic measure of clot formation, strength, and lysis, whereas SEM is a visual structural tool to study patient fibrin structure in great detail. Therefore, we consider the evidence for TEG® and SEM as unique means to confirm stroke diagnosis, screen at-risk patients, and monitor treatment efficacy. Here we argue that the current approach to stroke treatment needs to be restructured and new innovative thought patterns need to be applied, as even approved therapies require close patient monitoring to determine efficacy, match treatment regimens to each patient's individual needs, and assess the risk of dangerous adverse effects. TEG® and SEM have the potential to be a useful tool and could potentially alter the clinical approach to managing ischaemic stroke. As envisaged in the NIH precision medicine approach, this will involve a number of role players and innovative new research ideas, with benefits that will ultimately only be realized in a few years. Therefore, with this ultimate goal in mind, we suggest that an individualized patient-orientated approach is now available and therefore already within our ability to use. J Atheroscler Thromb, 2016; 23: 493-504.

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“…Dual antiplatelet therapy with clopidogrel and aspirin has become an effective therapeutic strategy in patients with ACS [2], but there is inevitably individual variability in platelet aggregation, resulting in different clinical outcomes [3-6]. The reasons for these phenotypic differences in platelet reactivity are not completely known, but genetic factors may make crucial contributions to such variability [7-9]. …”

Section: Introductionmentioning

confidence: 99%

Study of the Association of PEAR1, P2Y12, and UGT2A1 Polymorphisms with Platelet Reactivity in Response to Dual Antiplatelet Therapy in Chinese Patients

Zhang

Zhu

et al. 2018

Cardiology

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Objectives: Genetic variation is thought to contribute to considerable interindividual variability in platelet function, and there is a pressing need to identify genetic markers that can be used to predict the response to treatment. Our study investigated whether PEAR1, P2Y12, and UGT2A1 polymorphisms were associated with platelet reactivity in response to dual antiplatelet therapy in Chinese patients with acute coronary syndrome. Methods: Patients with inhibition of platelet aggregation (IPA) < 30% after treatment were classified as the high platelet reactivity (HPR) group. Patients with IPA > 30% were classified as the normal platelet reactivity (NPR) group. ADP-induced platelet aggregation was measured by thromboelastography (TEG) platelet-mapping assay. Thirteen single nucleotide polymorphisms (SNPs) of PEAR1, P2Y12 and UGT2A1 were genotyped using the MassARRAY platform. Results: Seven SNPs were significantly associated with ADP-induced platelet aggregation by univariate analysis. Major allele G at rs12041331, minor allele G at rs2644592, minor allele C at rs11264580, and minor allele C at rs11249454 were significantly associated with HPR, whereas minor allele T at rs57731889, minor allele A at rs16863356, and minor allele T at rs7634096 were significantly associated with NPR. The mean IPA was significantly lower in patients suffering recurrent ischemic events than in patients without recurrent events in our study (p = 0.048). Conclusions: Our findings suggest that PEAR1, P2Y12, and UGT2A1 genetic variants may be potential biomarkers that can be used to guide clinical applications of clopidogrel and aspirin in Chinese patients.

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Platelet function testing in transient ischaemic attack and ischaemic stroke: A comprehensive systematic review of the literature

Cited by 45 publications

References 117 publications

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin

Novel Diagnostic and Monitoring Tools in Stroke: an Individualized Patient-Centered Precision Medicine Approach

Study of the Association of <b><i>PEAR1</i></b>,<b><i> P2Y12</i></b>, and <b><i>UGT2A1</i></b> Polymorphisms with Platelet Reactivity in Response to Dual Antiplatelet Therapy in Chinese Patients

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