The clinical utility of <scp>M</scp>ultiplate analyser measurement in platelet function testing following stroke and transient ischaemic attack

Mannu, Gurdeep; Macartney, Alistair; Lambert, Jonathan; Bettencourt‐Silva, Joao H.; M, Lawn; Lyall, Hamish; Metcalf, Anthony K.; Potter, John F.; Wood, John; Clark, Allan; Baglin, Trevor; Myint, Phyo Kyaw; Bowles, Kristian M.

doi:10.1111/ejh.12406

Cited by 14 publications

(17 citation statements)

References 33 publications

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“…Second, the validity of the point of care used to determine APD efficacy is still a large source of debate and could explain the discrepancies observed between studies [19] . However, the Multiplate TM has been widely validated [19][20][21] , and we used thresholds specifically established in our hematological lab in a co- hort of healthy patients and verified resistance using specific light transmission aggregometry, which reinforce the validity of our data. Third, the absence of a control group of patients with ischemic stroke who were not on APD before is another potential limitation.…”

Section: Discussionsupporting

confidence: 61%

Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke

Coignion

Poli²,

Sagnier

et al. 2015

Eur Neurol

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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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Section: Discussionsupporting

confidence: 61%

Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke

Coignion

Poli²,

Sagnier

et al. 2015

Eur Neurol

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“…Although LTA may be considered the gold standard for the determination of platelet activity, we chose to use Multiplate® in this study because it is a standardized fully automated point-of-care test that is relatively easy to use without many of the technical limitations of the previous assays [32]. Additionally the feasibility of using Multiplate® in the context of routine hospital service has been ascertained to provide reproducible and precise results in stroke patients [33]. This potentially makes our findings easier to replicate and translate into large clinical studies to investigate clinical endpoints.…”

Section: Discussionmentioning

confidence: 99%

Assessment of platelet function in patients with stroke using multiple electrode platelet aggregometry: a prospective observational study

et al. 2016

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BackgroundThere is a link between high on-treatment platelet reactivity (HPR) and adverse vascular events in stroke. This study aimed to compare multiple electrode platelet aggregometry (MEA), in healthy subjects and ischaemic stroke patients, and between patients naive to antiplatelet drugs (AP) and those on regular low dose AP. We also aimed to determine prevalence of HPR at baseline and at 3–5 days after loading doses of aspirin.MethodsPatients with first ever ischaemic stroke were age and sex-matched to a healthy control group. Three venous blood samples were collected: on admission before any treatment given (baseline); at 24 h and 3–5 days after standard treatment. MEA was determined using a Mutliplate® analyser and agonists tested were arachidonic acid (ASPI), adenosine diphosphate (ADP) and collagen (COL).ResultsSeventy patients (mean age 73 years [SD 13]; 42 men, 28 women) were age and sex-matched to 72 healthy subjects. Thirty-three patients were on antiplatelet drugs (AP) prior to stroke onset and 37 were AP-naive. MEA results for all agonists were significantly increased in AP-naive patients compared to healthy subjects: ADP 98 ± 31 vs 81 ± 24, p < 0.005; ASPI 117 ± 31 vs 98 ± 27, p < 0.005; COL 100 ± 25 vs 82 ± 20, p < 0.005. For patients on long term AP, 33% (10/30) of patients were considered aspirin-resistant. At 3–5 days following loading doses of aspirin, only 11.1% were aspirin resistant based on an ASPI cut-off value of 40 AU*min.ConclusionsMany patients receiving low dose aspirin met the criteria of aspirin resistance but this was much lower at 3–5 days following loading doses of aspirin. Future studies are needed to establish the causes of HPR and potential benefits of individualizing AP treatment based on platelet function testing.

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“…Unfortunately, a significant minority of patients (≥35%) do not respond adequately to clopidogrel [16–25]; and a similar but lesser problem exists for aspirin [16, 18, 20, 26, 27]. A number of laboratory-based systems for measuring platelet function exist, including aggregation and commercial systems such as Multiplate and VerifyNow [27–29].…”

Section: Introductionmentioning

confidence: 99%

Remote Assessment of Platelet Function in Patients with Acute Stroke or Transient Ischaemic Attack

Bath

May

Flaherty

et al. 2017

Stroke Research and Treatment

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Background The TARDIS trial assessed the safety and efficacy of intensive versus guideline antiplatelet agents given for one month in patients with acute stroke or TIA. The aim of this substudy was to assess the effect of antiplatelet agents taken at baseline on platelet function reactivity and activation. Methods Platelet function, assessed by remotely measured surface expression of P-selectin, was assessed in patients at their time of randomisation. Data are median fluorescence values. Results The aspirin P-selectin test demonstrated that platelet expression was lower in 494 patients taking aspirin than in 162 patients not: mean 210 (SD 188) versus 570 (435), difference 360.3 (95% CI 312.2–408.4) (2p < 0.001). Aspirin did not suppress P-selectin levels below 500 units in 23 (4.7%) patients. The clopidogrel test showed that platelet reactivity was lower in 97 patients taking clopidogrel than in 585 patients not: 655 (296) versus 969 (315), difference 314.5 (95% CI 247.3–381.7) (2p < 0.001). Clopidogrel did not suppress P-selectin level below 860 units in 24 (24.7%) patients. Conclusions Aspirin and clopidogrel suppress stimulated platelet P-selectin, although one-quarter of patients on clopidogrel have high on-treatment platelet reactivity. Platelet function testing may be performed remotely in the context of a large multicentre trial. Trial registration ISRCTN47823388.

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The clinical utility of Multiplate analyser measurement in platelet function testing following stroke and transient ischaemic attack

Abstract: The Multiplate device gives reproducible, precise results in volunteers and stroke/TIA patients.

Cited by 14 publications

References 33 publications

Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke

Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke

Assessment of platelet function in patients with stroke using multiple electrode platelet aggregometry: a prospective observational study

Remote Assessment of Platelet Function in Patients with Acute Stroke or Transient Ischaemic Attack

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