Utility of whole blood impedance aggregometry for the assessment of clopidogrel action using the novel Multiplate® analyzer—comparison with two flow cytometric methods

Mueller, Thomas; Dieplinger, Benjamin; Poelz, Werner; Calatzis, Andreas; Haltmayer, Meinhard

doi:10.1016/j.thromres.2007.03.022

Cited by 75 publications

(45 citation statements)

References 19 publications

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“…The fluids were mixed in a measuring cuvette for 3 min at a constant temperature of 37°C (Mueller et al, 2007;Seyfert et al, 2007). To determine aspirin resistance, arachidonic acid as an inducer was added at a final concentration of 15 mM.…”

Section: Multiple Electrode Aggregometrymentioning

confidence: 99%

“…Nowadays, the so-called golden standard is platelet aggregation testing in platelet-rich plasma (PRP) using light transmission aggregometry (Cattaneo, 2007;Cattaneo et al, 2007). A novel option for determining residual platelet aggregation is the use of multiple electrode aggregometry (MEA) in whole blood (Mueller et al, 2007;Seyfert et al, 2007). It measures electrical impedance between two electrodes in hirudin-treated whole blood.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Genetic Polymorphisms of Platelet Receptors in Patients with Acute Myocardial Infarction and Resistance to Antiplatelet Therapy

Úlehlová

Slavík

Kučerová

et al. 2014

Genetic Testing and Molecular Biomarkers

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Section: Multiple Electrode Aggregometrymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphisms of Platelet Receptors in Patients with Acute Myocardial Infarction and Resistance to Antiplatelet Therapy

Úlehlová

Slavík

Kučerová

et al. 2014

Genetic Testing and Molecular Biomarkers

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“…Multiple electrode aggregometry (MEA) in whole blood is a semi-automated point-of-care device (24,25). It performs dual measurements as internal control and abolishes disadvantages of the light transmission aggregometry (26,27).…”

Section: Introductionmentioning

confidence: 99%

Multiple electrode aggregometry and vasodilator stimulated phosphoprotein-phosphorylation assay in clinical routine for prediction of postprocedural major adverse cardiovascular events

Freynhofer¹,

Brozovic²,

Bruno³

et al. 2011

Thromb Haemost

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SummaryReduced antiplatelet effect of clopidogrel assessed with multiple electrode aggregometry (MEA) and vasodilator stimulated phosphoprotein-phosphorylation (VASP-P) assay has been proven to predict major adverse cardiovascular events (MACE) after coronary stenting. So far no consecutive registry has evaluated the usefulness of different adenosine diphosphate-based platelet function tests to predict outcome in unselected patients. Hence, our objective was to determine the feasibility of MEA and VASP-P for clinical routine and whether low-response to clopidogrel as determined by MEA and/or the VASP-P assays predicts MACE in a "real-life" population undergoing coronary stenting. Threehundred consecutive patients were included in this prospective registry. Blood was sampled 6-24 hours after stenting to measure MEA and VASP-P. The use of glycoprotein-IIb/IIIa-blockers limited MEA to 196 measurements. Concerning the VASP-P assay, 300 measurements were achieved. Receiver Operating Characteristics (ROC)-curves of sensitiv- ity and specificity estimates for MACE were plotted for VASP-P assay. The area under the ROC-curve was 0.683 (p=0.014) for the platelet reactivity index (PRI) calculated from median fluorescence intensities (FI) with an optimal cut-off at 60.2% PRI. Patients above 60.2% had a significantly increased risk for MACE at six months follow-up (p=0.007). Estimating the cut-offs for the PRI from mean FI (52%) or from geometric mean FI (56.6%) led to clinically relevant differences. VASP-P assay is feasible for clinical routine to measure clopidogrel effects and to predict post-procedural MACE in unselected patients. With regard to differing cut-offs, exact standardisation of the VASP-P assay is mandatory. The use of GP-IIb/IIIa-blockers prevents MEA testing and limits its usability in unselected patients.

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“…The Multiplate whole blood platelet aggregation assay is based on measurement of impedance at low shear stress as platelets adhere to two adjacent electrodes and aggregate to one another within a cuvette [78,79]. The extent of platelet adhesion and aggregation is recorded as the area under the curve (AUC) up to 6 minutes after the addition of either arachidonic acid (AA) or ADP to measure the antiplatelet effects of aspirin or clopidogrel, respectively [78,79].…”

Section: Multiplatementioning

confidence: 99%

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

et al. 2015

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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 Õ , VerifyNow Õ and Multiplate Õ ). 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 (p50.001). 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 ¼ 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.

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Utility of whole blood impedance aggregometry for the assessment of clopidogrel action using the novel Multiplate® analyzer—comparison with two flow cytometric methods

Cited by 75 publications

References 19 publications

Genetic Polymorphisms of Platelet Receptors in Patients with Acute Myocardial Infarction and Resistance to Antiplatelet Therapy

Genetic Polymorphisms of Platelet Receptors in Patients with Acute Myocardial Infarction and Resistance to Antiplatelet Therapy

Multiple electrode aggregometry and vasodilator stimulated phosphoprotein-phosphorylation assay in clinical routine for prediction of postprocedural major adverse cardiovascular events

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

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