To see the other types of publications on this topic, follow the link: Multiplate aggregometry.
Journal articles on the topic 'Multiplate aggregometry'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Multiplate aggregometry.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Vertessen, Francine, Gerhard Mertens, Alain Gadisseur, Marc Van der Planken, and Jaimie Breugelmans. "Multiplate whole blood impedance aggregometry: A recent experience." Thrombosis and Haemostasis 100, no. 10 (2008): 725–26. http://dx.doi.org/10.1160/th08-07-0438.
Full text
2
Pedersen, Susanne B., Erik L. Grove, Helle L. Nielsen, Jette Mortensen, Steen D. Kristensen, and Anne-Mette Hvas. "Evaluation of aspirin response by Multiplate® whole blood aggregometry and light transmission aggregometry." Platelets 20, no. 6 (2009): 415–20. http://dx.doi.org/10.1080/09537100903100643.
Full text
3
Soliman, Mohamed, and Matthias Hartmann. "Multiplate® Platelet Aggregation Findings Are Dependent on Platelet Count but Can Be Corrected by Use of a Ratio." Applied Sciences 10, no. 22 (2020): 7971. http://dx.doi.org/10.3390/app10227971.
Full textAbstract:
Impedance aggregometry (Multiplate®) detects the effects of platelet aggregation inhibitors and can predict thrombotic complications after coronary and cerebrovascular stent interventions. The bedside method uses whole blood samples not corrected for platelet count. It is claimed but not proved that the findings are unrelated to platelet count in the physiological range. We therefore investigated in the experimental study: (1) whether impedance aggregometry findings and platelet count are correlated and (2) whether the aggregation/platelet count ratio expresses platelet function independent of platelet count. Following ethics committee approval, platelet-rich plasma from healthy probands was diluted with platelet-poor plasma to obtain different platelet counts. Thereafter, platelet count was measured and samples were subjected to impedance aggregometry using thrombin receptor activating peptide (TRAP) for platelet activation. In all probands, impedance aggregometry findings and platelet count were highly correlated (r = 0.88 to 0.94; p < 0.05). The combination of all experiments revealed the proportionality between impedance aggregometry findings and platelet count (n = 31, r = 0.78, p = 0.0001). In contrast, the ratio of impedance aggregometry findings and platelet count was not significantly correlated with platelet count (r = 0.017; p = 0.3) and thus constitutes a specific measure for platelet function. In conclusion, impedance aggregometry findings subsequent to the activation with TRAP are dependent on both platelet function and platelet count. Normalization of impedance aggregometry findings for platelet count can be achieved by a ratio resulting in more specific results.
4
Petrova, О. V., S. А. Shashin, and D. G. Tarasov. "Reference Values of Platelet Aggregation in Impedance Aggregometry with Adenosine Diphosphoric Acid on Aggregometer Multiplate." Sovremennye tehnologii v medicine 8, no. 3 (2016): 100–104. http://dx.doi.org/10.17691/stm2016.8.3.11.
Full text
5
Karon, Brad S., Nicole V. Tolan, Christopher D. Koch, et al. "Precision and Reliability of 5 Platelet Function Tests in Healthy Volunteers and Donors on Daily Antiplatelet Agent Therapy." Clinical Chemistry 60, no. 12 (2014): 1524–31. http://dx.doi.org/10.1373/clinchem.2014.226332.
Full textAbstract:
Abstract BACKGROUND Anticoagulation protocols used during mechanical circulatory support call for titration of antiplatelet agents. We compared the precision and reliability of 5 platelet function tests in healthy volunteers and donors on daily antiplatelet therapy to distinguish their efficacy for titrating antiplatelet therapy. METHODS We assessed arachidonic acid–induced platelet function by light transmission aggregometry (LTA), Multiplate impedance aggregometry, VerifyNow, and platelet mapping by thromboelastography (TEG PM). We assessed ADP-induced platelet function by the same methods and flow cytometry. Forty healthy volunteers and 10–13 volunteers on daily aspirin and/or clopidogrel therapy were evaluated. We compared tests for intraassay precision, interassay precision (samples from 2 separate blood draws), and reliability coefficient. RESULTS For arachidonic acid–induced platelet aggregation in healthy volunteers, intra- and interassay CVs were ≤10% for all methods. Intra- and interassay precision among donors on daily aspirin was ≤30% for all methods except LTA (38% interassay CV) and TEG PM (95% intraassay and 104% interassay CV). For ADP-induced platelet function, intra- and interassay precision was ≤10% and ≤30% for all methods. Only Multiplate demonstrated moderate or greater (R &gt; 0.40) reliability coefficients for arachidonic acid–induced platelet function among all subjects. All methods of ADP-induced platelet function, except TEG PM, demonstrated substantial or greater (R &gt; 0.60) reliability among all subjects. CONCLUSIONS TEG PM is least suited to monitor effects of antiplatelet agents. Multiplate impedance aggregometry was the only method to demonstrate an acceptable reliability coefficient among healthy volunteers and donors on both aspirin and clopidogrel therapy.
6
Hummel, Thomas, Saskia Hannah Meves, Andreas Breuer-Kaiser, et al. "Perioperative changes of response to antiplatelet medication in vascular surgery patients." PLOS ONE 15, no. 12 (2020): e0244330. http://dx.doi.org/10.1371/journal.pone.0244330.
Full textAbstract:
Introduction Reduced antiplatelet activity of aspirin (ALR) or clopidogrel (CLR) is associated with an increased risk of thromboembolic events. The reported prevalence data for low-responders vary widely and there have been few investigations in vascular surgery patients even though they are at high risk for thromb-embolic complications. The aim of this prospective observational monocentric study was to elucidate possible changes in ALR or CLR after common vascular procedures. Methods Activity of aspirin and clopidogrel was measured by impedance aggregometry using a multiple electrode aggregometer (Multiplate®). Possible risk factors for ALR or CLR were identified by demographical, clinical data and laboratory parameters. In addition, a follow-up aggregometry was performed after completion of the vascular procedure to identify changes in antiplatelet response. Results A total of 176 patients taking antiplatelet medications aspirin and/or clopidogrel with peripheral artery disease (PAD) and/or carotid stenosis (CS) were included in the study. The prevalence of ALR was 13.1% and the prevalence of CLR was 32% in the aggregometry before vascular treatment. Potential risk factors identified in the aspirin group were concomitant insulin medication (p = 0.0006) and elevated C-reactive protein (CRP) (p = 0.0021). The overall ALR increased significantly postoperatively to 27.5% (p = 0.0006); however, there was no significant change in CLR that was detected. In a subgroup analysis elevation of the platelet count was associated with a post-procedure increase of ALR incidence. Conclusion The incidence of ALR in vascular surgery patients increases after vascular procedures. An elevated platelet count was detected as a risk factor. Further studies are necessary to analyse this potential influence on patency rates of vascular reconstructions.
7
Hamouda, Khaled, Sebastian Sommer, Mehmet Özkur, Johannes Hain, Rainer Leyh, and Christoph Schimmer. "The Predictive Value of Multiple Electrode Platelet Aggregometry (Multiplate) in Adult Cardiac Surgery." Thoracic and Cardiovascular Surgeon 61, no. 08 (2013): 733–43. http://dx.doi.org/10.1055/s-0033-1333659.
Full text
8
Thalén, Simon, Ida Forsling, Jaak Eintrei, Lisbeth Söderblom, and Jovan P. Antovic. "Pneumatic tube transport affects platelet function measured by multiplate electrode aggregometry." Thrombosis Research 132, no. 1 (2013): 77–80. http://dx.doi.org/10.1016/j.thromres.2013.04.020.
Full text
9
Lee, Kurtis R., Veerle J. E. Verheyden, and Andrew D. Mumford. "Evaluation of multiple electrode aggregometry in whole blood using Multiplate® Mini Test cells." Thrombosis Research 129, no. 4 (2012): e59-e64. http://dx.doi.org/10.1016/j.thromres.2011.12.032.
Full text
10
Femia, E. A., M. Scavone, A. Lecchi, and M. Cattaneo. "Effect of platelet count on platelet aggregation measured with impedance aggregometry (Multiplate™ analyzer) and with light transmission aggregometry." Journal of Thrombosis and Haemostasis 11, no. 12 (2013): 2193–96. http://dx.doi.org/10.1111/jth.12432.
Full text
11
Stissing, Trine, Nadia P. Dridi, Sisse R. Ostrowski, Louise Bochsen, and Pär I. Johansson. "The Influence of Low Platelet Count on Whole Blood Aggregometry Assessed by Multiplate." Clinical and Applied Thrombosis/Hemostasis 17, no. 6 (2011): E211—E217. http://dx.doi.org/10.1177/1076029610397183.
Full textAbstract:
The Multiplate, a whole blood (WB) platelet function test, has shown promising results identifying patients on antiplatelet therapy at increased risk of rethrombosis. In the present study, the influence of low platelet count on platelet aggregation was analyzed and compared with aggregation results in an artificial matrix, platelet-rich plasma (PRP). Heparinized and citrated blood was diluted with autologous plasma to platelet concentrations 200 to 25 × 109/L in WB samples (n = 10) and 200 to 100 × 109/L in PRP samples (n = 7). The platelet aggregation was investigated by the ADP-, ASPI-, COL-, and TRAP-test. The WB responses decreased at platelet concentration of ≤100 × 109/L (all P < .03), except for heparin-TRAP (50 × 109/L, P = .008) and citrate-ASPI (150 × 109/L, P = .03). In general, WB samples demonstrated higher aggregation than PRP samples at platelet concentrations 200 to 100 × 109/L ( P < .05). In conclusion, platelet concentration of <150 × 109/L may influence Multiplate which should be considered in clinical settings. Furthermore, the findings emphasize the importance of evaluating haemostasis in its natural matrix, WB.
12
Braun, Siegmund, Stefan Jawansky, Wolfgang Vogt, et al. "Assessment of ADP-induced platelet aggregation with light transmission aggregometry and multiple electrode platelet aggregometry before and after clopidogrel treatment." Thrombosis and Haemostasis 99, no. 01 (2008): 121–26. http://dx.doi.org/10.1160/th07-07-0478.
Full textAbstract:
SummaryThe level of platelet aggregation, measured with light transmission aggregometry (LTA) in platelet rich plasma (PRP), has been shown to predict outcomes after percutaneous coronary intervention (PCI). However, measuring parameters of platelet function with LTA is time consuming and weakly standardized. Thus, a fast and standardized method to assess platelet function after clopidogrel treatment would be of great value for clinical practice. A new method, multiple electrode platelet aggregometry (MEA), to rapidly measure platelet aggregation in whole blood has recently been developed. The aim of this study was to assess parameters of platelet function with MEA and LTA before and after administration of 600 mg clopidogrel. Blood samples from 149 patients scheduled for coronary angiography were taken after clopidogrel treatment; in addition, in 60 of the patients samples were available before clopidogrel treatment. ADP-induced platelet aggregation was measured with LTA and simultaneously in whole blood with MEA on the Multiplate analyzer. Platelet aggregation measured with MEA decreased significantly after clopidogrel treatment (P<0.0001). ADP-induced platelet aggregation assessed with MEA and LTA correlated significantly (Spearman rank correlation coefficient=0.71; P<0.0001).The results of MEA, a fast and standardized method to assess the platelet response to ADP prior to and after clopidogrel treatment, correlate well with LTA.
13
VALARCHE, V., C. DESCONCLOIS, T. BOUTEKEDJIRET, M. DREYFUS, and V. PROULLE. "Multiplate whole blood impedance aggregometry: a new tool for von Willebrand disease." Journal of Thrombosis and Haemostasis 9, no. 8 (2011): 1645–47. http://dx.doi.org/10.1111/j.1538-7836.2011.04400.x.
Full text
14
Mărginean, Alina, Valeriu Moldovan, and Mihai Mărginean. "High-on-Aspirin Residual Platelet Reactivity Evaluated Using the Multiplate® Point-of-Care Device." Acta Medica Marisiensis 62, no. 1 (2016): 101–5. http://dx.doi.org/10.1515/amma-2015-0124.
Full textAbstract:
AbstractObjective: The aim of this study was to evaluate the prevalence of aspirin non-responsiveness using whole blood multiple electrode aggregometry and to investigate the role of different clinical and laboratory variables associated with the lack of response. Methods: The present study included 116 aspirin treated patients presented with acute coronary syndromes or stroke. Response to aspirin was assessed by impedance aggregometry using arachidonic acid as agonist, in a final concentration of 0.5 mM (ASPI test). Results: In our data set 81% (n=94) were responders and 19% (n=22) non-responders showing high-on-aspirin platelet reactivity. Correlation analysis showed that the ward of admittance, low-density lipoproteins (LDL), concomitant antibiotic treatment, beta-adrenergic receptor blockers, history of myocardial infarction as well as PCI performed on Cardiology patients have different degrees of association with aspirin response. Conclusion: Concomitant treatment with beta-adrenergic receptor inhibitors, history of myocardial infarction and Cardiology ward admittance significantly increased the chance of responding to aspirin treatment whereas antibiotic therapy and low-density lipoproteins cholesterol seemed to increase the risk of high-on-aspirin residual platelet reactivity.
15
Spannagl, Michael, and Csilla Jambor. "Baseline Platelet Reactivity as Determined by TRAP-6 Induced Aggregation in Whole Blood Is Related to the Rate of Non-Responsiveness to Clopidogrel." Blood 112, no. 11 (2008): 5362. http://dx.doi.org/10.1182/blood.v112.11.5362.5362.
Full textAbstract:
Abstract Background: Platelet inhibition by clopidogrel is often determined using ADP induced aggregometry. TRAP-6 stimulates platelets via the PAR receptors and is influenced to a much lesser extend by aspirin or clopidogrel. The value of the determination of TRAP-6 induced aggregometry in patients treated with clopidogrel is unknown. We evaluated the relation of clopidogrel non-responsiveness as determined by multiple electrode aggregometry (MEA) (1) vs. TRAP-6 induced aggregation. MEA provides a measurement of platelet aggregation in whole blood by monitoring changes in electrical impedance via disposable test cells each containing two pairs of electrodes (1). Methods: Following IRB approval hirudin-anticoagulated blood (Dynabyte, Munich, Germany) was sampled from 993 patients. Aggregation induced by arachidonic acid (0.5 mM), ADP (6.4 μM) or TRAP-6 (32μM) was determined in whole blood using a new generation impedance aggregometer. The device is called Multiplate analyzer (Dynabyte, Munich, Germany), indicating the multiplicity of channels and sensors per channel of the device. After dilution (1:2 with 0.9% NaCl solution) of hirudin-anticoagulated whole blood and stirring for three minutes in the test cuvettes at 37°C, the activator was added and aggregation was continuously recorded for six minutes. The increase of impedance due to the attachment of platelets to the electrodes is detected for each sensor unit separately and transformed to arbitrary aggregation units. The aggregation is quantified as area under the curve (AUC). Results: 618 patients were on chronic therapy with 100 mg aspirin/d, 295 patients on clopidogrel 75 mg/d (237 on dual therapy). Aspirin therapy had no influence on TRAP-6- induced aggregation (112+−260 vs. 110+−25; mean +− sd; aspirin vs. no aspirin, p&gt; 0.05 Mann-Whitney U-test). In contrast clopidogrel induced a minor but significant reduction of TRAP6-induced aggregation (107+− 277 vs. 113+−246; p&lt;0.05). Patients on clopidogrel had a significantly lower ADP induced aggregation (41+−30 vs. 86 +−33) compared to controls (p&lt;0.05), and patients on aspirin had a significantly lower arachidonic acid induced aggregation compared to controls (23+−28 vs. 94 +− 35, p&lt;0.05). 89 of 295 patients (30%) were stratified as clopidogrel non-responders based on the cut-off presented in (2). Patients were divided into 4 quartiles (q1-4) depending on their TRAP-6 induced aggregation. The rate of non-responsiveness in Q1 was 8.1%, in Q2 20%, in Q3 38% and 54% in Q4. ADPinduced aggregation was significantly higher in Q4 than in any other quartile (p&lt;0.05). Conclusion: A high TRAP-6 induced aggregation is associated with an increased rate of clopidogrel non-responsiveness as determined by multiple electrode aggregometry. TRAP-6 induced aggregometry seems to indicate the global platelet potential and might allow a prediction of clopidogrel responsiveness before the induction of therapy.
16
Bélanger, Jean-Christophe, Fabio Luiz Bandeira Ferreira, Mélanie Welman, et al. "Head-to-Head Comparison of Consensus-Recommended Platelet Function Tests to Assess P2Y12 Inhibition—Insights for Multi-Center Trials." Journal of Clinical Medicine 9, no. 2 (2020): 332. http://dx.doi.org/10.3390/jcm9020332.
Full textAbstract:
The vasodilator-associated stimulated phosphoprotein (VASP) phosphorylation level is a highly specific method to assess P2Y12 receptor inhibition. Traditionally, VASP phosphorylation is analyzed by flow cytometry, which is laborious and restricted to specialized laboratories. Recently, a simple ELISA kit has been commercialized. The primary objective of this study was to compare the performance of VASP assessment by ELISA and flow cytometry in relation to functional platelet aggregation testing by Multiplate® whole-blood aggregometry. Blood from 24 healthy volunteers was incubated with increasing concentration of a P2Y12 receptor inhibitor (AR-C 66096). Platelet function testing was carried out simultaneously by Multiplate® aggregometry and by VASP assessment through ELISA and flow cytometry. As expected, increasing concentrations of the P2Y12 receptor inhibitor induced a proportional inhibition of platelet aggregation and P2Y12 receptor activation across the modalities. Platelet reactivity index values of both ELISA- and flow cytometry-based VASP assessment methods correlated strongly (r = 0.87, p < 0.0001) and showed minimal bias (1.05%). Correlation with Multiplate® was slightly higher for the flow cytometry-based VASP assay (r = 0.79, p < 0.0001) than for the ELISA-based assay (r = 0.69, p < 0.0001). Intraclass correlation (ICC) was moderate for all the assays tested (ICC between 0.62 and 0.84). However, categorization into low, optimal, or high platelet reactivity based on these assays was strongly concordant (κ between 0.86 and 0.92). In conclusion, the consensus-recommended assays with their standardized cut-offs should not be used interchangeably in multi-center clinical studies but, rather, they should be standardized throughout sites.
17
Antic, Ana, Zoran Stanojkovic, Miodrag Vucic, Milan Lazarevic, and Nebojsa Vacic. "Comparison of farmacodynamic properties of three different aspirin formualtions in patients with stable coronary disease." Vojnosanitetski pregled 76, no. 6 (2019): 628–34. http://dx.doi.org/10.2298/vsp180110034a.
Full textAbstract:
Background/Aim. The platelet aggregation, as a laboratory test for assessment of platelet function, is very efficient for optimal antiplatelet treatment and also to identify individuals who have suboptimal response to antiplatelet drugs, such as aspirin and clopidogrel. The aim of this study was to determine the level of inhibition of platelet aggregation using impedance aggregometry in the patients receiving different preparations of acetylsalicylic acid (ASA) in a dose of 100 mg per day. Methods. The examination included 215 patients (110 men and 105 women), treated with one of three different ASA preparations after acute myocardial infarction, as a single therapy or with clopidogrel. Among them, 89 patients were on Aspirin protect? (Bayer, Germany) ? Group 1 and 66 patients were on Cardiopirin? (GL Pharma GMBH, Austria) ? Group 2, while 60 patients were taking Andol? (Pliva, Croatia) ? Group 3. The groups were equal in the presence of factors that can influence platelet aggregation (age, gender, smoking, diabetes, taking other drugs). The platelet function was measured using the impedance aggregometer Multiplate (Multiplate Platelet Function Analyzer, Roche) in the blood samples with heparin for the platelet aggregation activated by the arachidonic acid (ASPI) and by thrombin (TRAP) tests [the area under the aggregation curve (AUC) was used to express the aggregation response over the measured time (AU*min)]. Results. Efficacy of ASA preparations showed statistically significant differences among the three investigated groups (?KW2 = 46.279; p < 0.001), and it was also observed separately in the patients undergoing single therapy (?KW2 = 26.344; p < 0.001) and dual therapy (?KW2 = 23.498; p < 0.001). It was found that the patients who were taking Aspirin protect? obtained significantly better antiplatelet efficiency compared to the patients receiving Cardiopirin? (Z = 5.472; p < 0.001) and Andol? (Z = 5.387; p = 0.022). There is reduced efficiency of all ASA preparations in smokers, while patients receiving Aspirin protect? were 10.5 times more likely to be responders. Conclusion. Different ASA preparations observed in this study showed different efficiency on the platelet function as measured by the method of impedance aggregometry.
18
Dugan, Greg, Lisa O’Donnell, David B. Hanbury, J. Mark Cline, and David L. Caudell. "Assessment of Multiplate platelet aggregometry using citrate, heparin or hirudin in Rhesus macaques." Platelets 26, no. 8 (2014): 730–35. http://dx.doi.org/10.3109/09537104.2014.988694.
Full text
19
Cabañas, Valentin, Juan Jose Cerezo-Manchado, Faustino Garcia-Candel, et al. "Decrease of Aggregation By Platelet Impedance Aggregometry ( MULTIPLATE ) in Patients Treated with Dabigatran." Blood 128, no. 22 (2016): 5022. http://dx.doi.org/10.1182/blood.v128.22.5022.5022.
Full textAbstract:
Abstract Introduction: Dabigatran is a direct oral anticoagulant (DOAC) that has been proved effective and safe in preventing thromboembolic events experienced by patients with non-valvular atrial fibrillation (AF). This drug acts directly inhibiting thrombin and particularly affects the intrinsic and the final coagulation pathways. Thrombin is a platelet agonist therefore dabigatran could be involved in altering the aggregation. However, it is not well known whether they modify the platelet function. We conducted an initial study in our hospital to assess platelet aggregation in patients treated with dabigatran. Methods: An observational study was conducted in 17 randomly selected patients who had started dabigatran in the last year in our center. The results were compared with 8 healthy platelet donors randomly selected from our database. Platelet aggregation was quantified in patients and controls using MEA (Multiplate, Roche Diagnostics, Switzerland). The indication and dosing of dabigatran was performed as clinically indicated. The main variables investigated were: aggregation time with four agonists: thrombin, ADP, collagen, ristocetin, APTT, INR addition, D Dimer, kidney and liver function and the usual demographic parameters. Statistical analysis were performed using SPSS 21.0 (SPSS Inc., Chicago, IL). Results: All patients had AF as an indication for treatment with dabigatran. Dabigatran doses were 110 mg in 7 patients (41%) and 150 mg in 10 patients (58%). No patient was on any antiplatelet agent. Platelet aggregation induced by TRAP measured by MEA was not significantly different in patients compared to controls: 121 RI (94-127) vs. RI 122 (108-137) units (p = 0.711). Aggregation using collagen and ristocetin as agonists was significantly decreased compared to that of controls: RI 48 (32-63) vs. 83 RI (69-110) (p = 0.05) and 76 RI (71-32) vs. 120 RI (97-142) units (p <0.01). There were no differences in the aggregation depending on the dose of dabigatran. Conclusion: Despite the limitations of the study we observed a change in the aggregation of patients treated with dabigatran measured by MEA, compared with healthy controls. Contrary to what one might expect, it was not dependent on the thrombin pathway unless the ristocetin and collagen agonists. These findings must be confirmed in more powerful studies designed for this purpose because others studies, with the same characteristics than our work, have shown TRAP-induced platelet aggregation enhance in patients treated with dabigatran.1 1 TRAP-induced platelet aggregation is enhanced in cardiovascular patients receiving dabigatran. Christoph B. Olivier et al. Thrombosis Research Thromb Res. 2016 Feb;138:63-8 Disclosures Blanquer Blanquer: Pfizer: Research Funding.
20
Calatzis, Andreas, Franz Theisen, Armin J. Reininger, and Michael Spannagl. "Monitoring of Clopidogrel Using Multiple Electrode Aggregometry." Blood 108, no. 11 (2006): 883. http://dx.doi.org/10.1182/blood.v108.11.883.883.
Full textAbstract:
Abstract A control of clopidogrel response is one proposed strategy for an improvement of anti-platelet therapy. Different methods have been evaluated for this indication. We assessed ADP induced aggregation in whole blood in healthy blood donors and patients treated with clopidogrel 75 mg qd using a new monitoring method. Methods: Platelet function was determined using multiple electrode aggregometry (MEA) on the Multiplate analyzer (Dynabyte, Munich, Germany). This device uses a single use test cell with two separate impedance sensors, consisting of a total of 4 electrodes and has 5 channels for parallel tests. Aggregation was triggered using ADP (6.4 μM, ADPtest, Dynabyte) and using a combination of ADP (6.4 μM) and prostaglandin E1 (20 nM) (ADPtest high sensitivity = ADPtest HS, Dynabyte). The combination of ADP + prostaglandin E1 (PGE1) is used to enhance sensitivity for the effects of clopidogrel onto ADP induced platelet activation. PGE1 reduces intracellular calcium mobilisation and therefore platelet activation and acts thus synergistical to the effect of clopidogrel. For the analysis 300 μl of blood are analyzed with the addition of 300 μl of saline. Aggregation was quantified by the area under the curve in arbitrary U (1 U corresponds to 10 AU*min). Following IRB approval venous blood was collected from 120 blood donors without anamnestic intake of platelet inhibitors in the 2 weeks before the analysis and 160 patients taking clopidogrel 75 mg qd using the direct thrombin inhibitor Melagatran in a final concentration of 15 μg/ml as the anticoagulant. Results: The distribution of the aggregation values is shown in Fig. 1. The median (min-max) was 83 (36–143) for the blood donors in the ADPtest and 68 (1–130) in the ADPtest HS. In the patient group the median (mix–max) was 30 (2–147) in the ADPtest and 10 (0–108) in the ADPtest HS. If a non-response rate of 25% is assumed, the cut-off between clopidogrel responders and non-responders would be 51 for the ADPtest and 21 for ADPtest HS. Discussion: The comparison of the results of clopidogrel-treated patients and healthy controls (blood donors) reveals a higher sensitivity of ADPtest HS vs. ADPtest for the effects of clopidogrel onto ADP induced aggregation in whole blood. Due to the use of a direct thrombin inhibitor as the anticoagulant in our study platelet function was determined under physiological levels of ionized calcium. For both test methods a significant proportion of patients does not show adequate reductions in their vitro platelet aggregation. Prospective trials are required to show whether a clopidogrel-non-response in this particular method is associated with an increased occurrence of arterial thromboembolism. Fig. 1 Fig. 1.
21
Khadim, Murad A., Hasan A. Farhan, Muthanna ., and Muthanna H. Al-Quraishi. "Clopidogrel Responsiveness in Patients Undergoing Percutaneous Coronary Intervention using Multiplate Analyzer: Frequency and Outcomes." INTERNATIONAL JOURNAL OF DRUG DELIVERY TECHNOLOGY 13, no. 03 (2023): 1112–16. http://dx.doi.org/10.25258/ijddt.13.3.53.
Full textAbstract:
Objectives: Over and under response to dual antiplatelet therapy (DAPT) can lead to bleeding and thrombotic events in patients undergoing coronary stent placement. The present study aimed to assess the platelet response to clopidogrel in patient undergoing percutaneous coronary intervention (PCI) using Multiplate Analyzer. The primary outcome in the present study was the short-term incidence of stent thrombosis and bleeding events. Background: Multiple electrode aggregometry is a rapid and standardized tool to for diagnosis of platelet defects and monitoring response to DAPT. Methods: A hospital-based, prospective study was conducted on 431 patients who underwent PCI from September 2016 to November 2017 and received clopidogrel therapy. The platelet aggregometry was done using a Multiplate analyzer (Dynabyte, Munich, Germany). Patients were followed for 30 days to assess the incidence of stent thrombosis and bleeding. Results: The patients’ mean age was 58 ± 6.7 years. A total of 40% of the patients were diabetic and 7.7% had chronic renal failure. The rate of clopidogrel non-responders was 10.7%, while clopidogrel over-responders were 18.3%. Patients with diabetes and chronic renal failure had significantly lower platelet responsiveness (40.1% with p < 0.05 and 7.7% with p <0.005, respectively). Smoking was significantly associated with platelet over-responsiveness (39.4%, p < 0.001). Patients with low platelet responsiveness to clopidogrel were associated with an increased risk of definite stent thrombosis (p < 0.005), while increasing bleeding risk was significantly associated with over-responsiveness to patients to clopidogrel (p <0.001). Conclusions: Antiplatelet responsiveness showing individual variability with increased risk of stent thrombosis among the cases with no response to the effect of clopidogrel and high risk of bleeding with the over-responsiveness group.
22
Taher, Qasim Mohammed, Khalid Amber, and Ahmed N. Rgeeb. "Assessment of platelet reactivity with anti platelet agent (clopidogrel) after two drugs formulation PLAVIX® and PLAGERINE." Kufa Journal for Nursing Sciences 2, no. 3 (2012): 36–42. http://dx.doi.org/10.36321/kjns.vi20123.2535.
Full textAbstract:
Cardiovascular disease remains the main cause of mortality. Antiplatelet therapy is the main drug use in the management of coronary artery disease. Several million of people received colpidogril, however the cost of the drug that might 3-4 dollars daily for the brand company Sanofi. pharmacies start to sell cheaper generic in Indian origin. assessment of platelet function after two drugs (Plavix and plagrine) by multiple electrode platelet aggregometry (MEA) shows no difference of both drugs on the multiplate activity, this is assessed by prospective cross sectional study included 28 patients randomized to receive either Plavix or plagrine, there is no significant differences regarded the effects of some risk factors in outcome in both group Plavix and plagrine.
23
Flechtenmacher, N., F. Kämmerer, R. Dittmer, et al. "Clopidogrel Resistance in Neurovascular Stenting: Correlations between Light Transmission Aggregometry, VerifyNow, and the Multiplate." American Journal of Neuroradiology 36, no. 10 (2015): 1953–58. http://dx.doi.org/10.3174/ajnr.a4388.
Full text
24
Pikta, M., L. J. Mettis, K. Rahuoja, T. Helin, S. Saulyte Trakymiene, and V. Banys. "Verification of reference values for multiplate impedance aggregometry analyzer: A call for international cooperation." Clinica Chimica Acta 558 (May 2024): 118371. http://dx.doi.org/10.1016/j.cca.2024.118371.
Full text
25
Roka-Moiia, Yana, Silvia Bozzi, Chiara Ferrari, et al. "The MICELI (MICrofluidic, ELectrical, Impedance): Prototyping a Point-of-Care Impedance Platelet Aggregometer." International Journal of Molecular Sciences 21, no. 4 (2020): 1174. http://dx.doi.org/10.3390/ijms21041174.
Full textAbstract:
As key cellular elements of hemostasis, platelets represent a primary target for thrombosis and bleeding management. Currently, therapeutic manipulations of platelet function (antithrombotic drugs) and count (platelet transfusion) are performed with limited or no real-time monitoring of the desired outcome at the point-of-care. To address the need, we have designed and fabricated an easy-to-use, accurate, and portable impedance aggregometer called “MICELI” (MICrofluidic, ELectrical, Impedance). It improves on current platelet aggregation technology by decreasing footprint, assay complexity, and time to obtain results. The current study aimed to optimize the MICELI protocol; validate sensitivity to aggregation agonists and key blood parameters, i.e., platelet count and hematocrit; and verify the MICELI operational performance as compared to commercial impedance aggregometry. We demonstrated that the MICELI aggregometer could detect platelet aggregation in 250 μL of whole blood or platelet-rich plasma, stimulated by ADP, TRAP-6, collagen, epinephrine, and calcium ionophore. Using hirudin as blood anticoagulant allowed higher aggregation values. Aggregation values obtained by the MICELI strongly correlated with platelet count and were not affected by hematocrit. The operational performance comparison of the MICELI and the Multiplate® Analyzer demonstrated strong correlation and similar interdonor distribution of aggregation values obtained between these devices. With the proven reliability of the data obtained by the MICELI aggregometer, it can be further translated into a point-of-care diagnostic device aimed at monitoring platelet function in order to guide pharmacological hemostasis management and platelet transfusions.
26
Desconclois, Celine, Vincent Valarche, Tewfik Boutekedjiret, Martine Raphael, Marie Dreyfus, and Valerie Proulle. "Whole Blood Impedance Aggregometry: A New Tool for Severe Inherited Platelet Disorder Diagnosis?" Blood 118, no. 21 (2011): 5266. http://dx.doi.org/10.1182/blood.v118.21.5266.5266.
Full textAbstract:
Abstract Abstract 5266 Diagnosis and characterization of platelet function disorders may be challenging. It requires multiple laboratory data including the assessment of platelet functions. Platelet function analysis is most commonly performed using light transmission aggregometry (LTA). LTA is a time-consuming method requiring centrifugation steps and large blood volumes. It is difficult to perform in children and in cases of thrombocytopenia. In contrast, platelet aggregation in whole blood using impedancemetry (WBI) is a fast method, allows omission of centrifugation steps and performance of platelet function studies under more physiological conditions with small samples size. It is based on the change of resistance proportional to the amount of platelets sticking to two electrodes where an alternating current is applied. Multiplate® (for “multiple electrode aggregometry”, Dynabite Medical) is a new generation of WBI aggregometer using diluted blood and single-use test cells containing twin electrodes that reduce the variation of results. We have already showed the good Multiplate® performance concerning ristocetin-induced platelet aggregation in a population of 30 patients with characterized von Willebrand disease (Valarche et al, 2011). Our aim in this ongoing study was to assess the performance of WBI in patients with inherited platelet function disorders. We tested 8 patients including 2 unrelated patients with Glanzmann Thrombasthenia (GT), 2 unrelated patients with Bernard-Soulier Syndrome (BSS), 1 patient with Gray Platelet Syndrome (GPS) and 3 patients from the same family with a platelet type von Willebrand disease (PTVWD). GT, BSS, and PTVWD diagnosis were confirmed using genotyping. BSS and GPS patients had chronic thrombocytopenia. GT, BSS, GPS and 1/3 PTVWD had platelet function tests with LTA in parallel. WBI was performed on heparinized whole blood diluted at ½ in NaCl at 37°C and triggered using high (0.77 mg/mL, WBI RH) and low (0.5 mg/mL, WBI RL) final ristocetin concentrations, ADP (6.5 Âμ Mol, WBI ADP) and collagen (3.2 Âμg/mL, WBI Coll). Results were expressed in arbitrary unit (AU) corresponding to the area under the aggregation curve observed during 6 min. Normal ranges indicated in brackets were based on the mean +/− 2 SD of 30 healthy volunteers' results. Results highlighted in grey are those out of the normal ranges (Table 1).Table 1:Results of the 8 patients with inherited platelet disorders.PatientsPlatelet count (109/L)WBI RH (AU) [>500]WBI RL (AU) [<150]WBI ADP (AU) [>550]WBI Coll (AU) [>500]GT 116923441443GT 224955417ND7BSS 134371119129BSS 230254733582GPS7916217ND42PTVWD22099493ND338PTVWD231116560ND1092PTVWD2341174168ND852 All patients except those with PTVWD had decreased results with WBI. However, as expected, patients with GT had flat traces using WBI ADP and WBI Coll but normal or only decreased curves (234 – 554 AU) using WBI RH. On the opposite, BSS patients had flat traces using WBI RH but detectable curves using WBI ADP (191 – 335 AU) despite decreased platelet count. The thrombocytopenic GPS patient has a flat trace using WBI Coll and decreased WBI RH (162 AU). Members of the PTVWD family had normal results except a slightly increased result with WBI RH in 1/3 patients. Finally, LTA results performed in 6/8 patients were all in accordance with those of the WBI. In conclusion, in 8 patients with well characterized inherited platelet disorders, WBI was able to detect all abnormalities except PTVWD. In such cases, different ristocetin concentrations use might be critical to increase sensitivity. In our hands, WBI was able to discriminate disorders involving platelet glycoprotein (GP) IIb-IIIa from GP Ib-IX-V: GT patients exhibited flat traces using WBI ADP and WBI Coll, whereas patients with BSS exhibited flat traces with ristocetin. These preliminary results need to be confirmed on a larger population of patients with various characterized platelet function disorders. They suggest that WBI using the Multiplate® analyzer, which is a fast, easy and blood-preserving test, could be a valuable extra step before or in addition to the classic LTA for the diagnosis of severe inherited platelet disorders. Disclosures: No relevant conflicts of interest to declare.
27
Schmidt, David E., Maria Bruzelius, Ammar Majeed, Jacob Odeberg, Margareta Holmström, and Anna Ågren. "Whole blood ristocetin-activated platelet impedance aggregometry (Multiplate) for the rapid detection of Von Willebrand disease." Thrombosis and Haemostasis 117, no. 08 (2017): 1528–33. http://dx.doi.org/10.1160/th17-02-0129.
Full textAbstract:
SummaryVon Willebrand disease (VWD) is the most common bleeding disorder, but no bedside tests specific for Von Willebrand factor are available. The objective of this study was to evaluate the diagnostic accuracy of whole blood ristocetin-induced platelet aggregometry (WB-RIPA) in VWD. WB-RIPA was performed in VWD patients (n=100) and healthy controls (n=17) using the Multiplate® platelet impedance aggregometry platform. The diagnostic properties of the test were described as sensitivity/specificity, positive and negative predictive value, and ROC area under the curve (AUC). Patients with VWD had impaired platelet aggregation by WB-RIPA. At a cut-off of 98 U, the test sensitivity and specificity of WB-RIPA for VWD was 0.95 and 0.53. A cut-off of 60 U provided a specificity of 1.00 with reduced sensitivity of 0.76. All patients with type 3 VWD and >90% of patients with type 2 VWD were accurately distinguished from the controls. Incorrect classifications were attributable to patients with type 1 VWD, showing partly overlapping WB-RIPA results with healthy controls. Remarkably, these patients had lower bleeding scores and higher VWF activity than other type 1 VWD patients. Overall, WB-RIPA discriminated VWD patients from healthy controls accurately with a ROC AUC of 0.94. These results show that WB-RIPA is a promising diagnostic test for VWD, especially when timely results are required. Depending on the chosen test threshold, WB-RIPA could be clinically used as a rule out test, or to suggest patients in whom further testing for VWD is warranted.
28
Blomqvist, L., A. Strandell, F. Baghaei, and M. Hellgren. "P-034: Multiple impedance aggregometry (Multiplate®) in healthy women during normal pregnancy – a prospective and longitudinal study." Thrombosis Research 151 (March 2017): S120. http://dx.doi.org/10.1016/s0049-3848(17)30132-9.
Full text
29
Pedersen, Susanne B., Steen D. Kristensen, and Anne-Mette Hvas. "Measurement of Whole Blood Platelet Aggregation by Multiplate® Aggregometry Before and during Aspirin Treatment." Blood 110, no. 11 (2007): 3895. http://dx.doi.org/10.1182/blood.v110.11.3895.3895.
Full textAbstract:
Abstract The inhibition of platelet aggregation by aspirin (ASA) is fundamental in treatment of ischemic heart disease (IHD). Several studies report findings of normal platelet aggregation despite ASA treatment in some individuals, referred to as ASA resistance (AR). It has been hypothesized that AR increases the risk of a future ischemic event. We evaluated a new impedance method for measurement of platelet aggregation, Multiplate® aggregometry (MA), and compared this method to light aggregometry ad modum Born (OPA), with reference to repeatability and detection of AR. Blood samples from 43 IHD patients and 21 healthy individuals treated with ASA 75 mg daily were analyzed in duplicate by MA and OPA on 4 consecutive days. An additional blood sample was obtained prior to ASA treatment in the group of healthy individuals. Compliance was confirmed by measurements of thromboxane B2 in serum. MA was performed with arachidonic acid (AA) in concentrations of 0.25 mM, 0.50 mM and 0.75 mM, and with adenosine diphosphate (ADP) in concentrations of 7.5 μM and 15 μM. OPA was performed with AA-concentrations of 0.5 mM, 1.0 mM and 1.5 mM, and with ADP-concentrations of 5 μM and 10 μM. Table 1. Area under the curve (AUC) measured by MA in patients and in healthy individuals before and during ASA treatment. Agonist AUC, aggregation units · min Healthy Before ASA HealthyDuring ASA PatientsDuring ASA Median Range Median Range Median Range AA, mM 0.25 520 402–999 38 12–83 41 8–110 0.50 574 461–976 51 20–112 56 17–187 0.75 551 434–889 68 21–333 98 18–418 ADP, μM 7.5 474 272–859 422 195–816 472 126–720 15 503 328–922 479 262–995 525 172–834 In healthy individuals, the AA-induced AUC was reduced significantly by ASA at all concentrations (88–93%, p=0.0001). The reduction of AUC was small and insignificant when using ADP (5–11%, p≥0.06). There was a trend towards a higher median AUC measured in patients than in healthy individuals during ASA (p=0.07). Table 2. Coefficients of variation (CV) of double measurements determined by MA and OPA in healthy individuals prior to ASA treatment and during ASA treatment. AA, mM MA AA, mM OPA CVBefore ASA, % CVDuring ASA, % CVBefore ASA, % CVDuring ASA, % 0.25 8 46 0.5 48 25 0.50 10 40 1.0 5 20 0.75 12 41 1.5 5 21 The CV of OPA was generally lower. The reference method was OPA with AA 1.0 mM and AR was defined as a residual platelet aggregation ≥ 20%. According to this definition 7 participants (16%) had AR. A receiver operating characteristics (ROC) analysis showed a sensitivity of MA using AA 0.75 mM of 100% at an AUC cut-point of 94 aggregation units (AU) · min, 71% at 135 AU · min and 29% at 212 AU · min. The specificity was 60, 81 and 93%, respectively. The area under the ROC-curve was 0.79 (95% CI 0.66–0.92). In conclusion, the large ASA-induced reduction in AUC of healthy individuals indicated that MA measures the effect of ASA efficiently when using AA. ADP seems less suitable, as the AUC was only slightly reduced by ASA. The CV of MA was high during ASA treatment, indicating that platelet aggregation during ASA was low and difficult to measure precisely with MA. The area under the ROC-curve was moderately satisfying, but of uncertain correctness due to the rather small number of observations.
30
Minde, Jan-Wighard, and Reinhard Mischke. "Influence of sample storage on impedance aggregometry measured using the Multiplate® analyser in dogs." Comparative Clinical Pathology 23, no. 5 (2013): 1403–7. http://dx.doi.org/10.1007/s00580-013-1797-2.
Full text
31
Kuliczkowski, Wiktor, Dan Atar, Victor Serebruany, and Dániel Aradi. "Inter-patient variability and impact of proton pump inhibitors on platelet reactivity after prasugrel." Thrombosis and Haemostasis 107, no. 02 (2012): 338–45. http://dx.doi.org/10.1160/th11-09-0622.
Full textAbstract:
SummaryAlthough there is considerable variability of platelet reactivity among patients treated with clopidogrel, little is known about inter-individual differences and possible role of proton pump inhibitors (PPIs) after prasugrel. We defined the extent of inter-patient variability, and evaluated the impact of PPI interaction in prasugrel-treated patients with acute coronary syndrome (ACS). Between January 2010 and May 2011, 104 prospective, high-risk patients with ACS were recruited into this multicentre, prospective, observational study. Twelve to 24 hours after receiving 60 mg loading dose of prasugrel, light transmission aggregometry (LTA) and whole blood impedance aggregometry (Multiplate) were used to assess platelet activity. Platelet function measurements were repeated during maintenance phase on reduced (5 mg) or on conventional (10 mg) doses of prasugrel. High platelet reactivity (HPR) was defined according to the consensus document of the Working Group on High On-Treatment Platelet Reactivity (LTA:>46%; Multiplate:>47U). Compared to maintenance doses, 60 mg loading dose of prasugrel provided significantly greater platelet reactivity inhibition (p<0.05). There were no significant differences between the conventional and reduced maintenance doses. Notably, a remarkable inter-patient variability was present in platelet reactivity after all doses of prasugrel, and the prevalence of HPR was significantly higher during the maintenance doses (p<0.05). Although median platelet reactivity values were consistently higher when prasugrel was used in combination with PPIs, these differences were not significant (p≥0.17). Despite potent platelet inhibition, inter-patient variability is present after all tested doses of prasugrel. The 60 mg loading dose is superior to conventional and reduced maintenance doses in terms of platelet reactivity inhibition and regarding the prevention of HPR.
32
Larsen, Sanne, Erik Grove, Steen Kristensen, Søs Neergaard-Petersen, and Anne-Mette Hvas. "Increased platelet aggregation and serum thromboxane levels in aspirin-treated patients with prior myocardial infarction." Thrombosis and Haemostasis 108, no. 07 (2012): 140–47. http://dx.doi.org/10.1160/th12-01-0026.
Full textAbstract:
SummaryThe antiplatelet effect of aspirin displays considerable inter-individual variability. We investigated the antiplatelet effect of aspirin in patients with coronary artery disease on aspirin mono-therapy with and without prior myocardial infarction (MI). Further, we investigated whether the effect of aspirin differed between patients with and without aspirin use at the time of MI onset. We performed a study on 231 patients, including 171 with prior MI. Among patients with only one prior MI (116 patients), 59 patients were on aspirin at the time of MI onset. All patients received 75 mg aspirin as mono-therapy. Platelet aggregation was assessed by multiple electrode aggregometry (Multiplate®) and Verify -Now®, and platelet activation was evaluated by soluble P-selectin. Furthermore, we measured serum thromboxane B2. MI patients had higher median platelet aggregation levels than patients without prior MI when evaluated by Multiplate® (parachidonic acid<0.0001, pcollagen=0.20). This was not supported by VerifyNow®. Furthermore, MI patients had higher median serum thromboxane B2 levels than patients without prior MI (p=0.01). Patients on aspirin before MI onset had significantly higher median aggregation levels compared with MI patients not on aspirin when evaluated by Multiplate® (pcollagen=0.02) and VerifyNow® (p<0.0001). In conclusion, patients with prior MI had higher platelet aggregation levels than patients without prior MI when evaluated by Multiplate®, despite same aspirin dose and optimal compliance. Serum thromboxane B2 levels were higher in MI patients than in patients without prior MI. Finally, patients on aspirin before MI onset had higher aggregation levels compared with patients not on aspirin.
33
Kam, P. C. A., J. P. C. Liou, and K. X. F. Yang. "In Vitro Evaluation of the Effect of Haemodilution with Dextran 40 on Coagulation Profile as Measured by Thromboelastometry and Multiple Electrode Aggregometry." Anaesthesia and Intensive Care 45, no. 5 (2017): 562–68. http://dx.doi.org/10.1177/0310057x1704500506.
Full textAbstract:
We evaluated the effects of haemodilution with either dextran 40 or 0.9% normal saline on coagulation in vitro using rotational thromboelastometry (ROTEM®, Pentapharm Co., Munich, Germany) and multiple electrode aggregometry (Multiplate® Platelet Function Analyser, Dynabyte, Munich, Germany). Venous blood samples obtained from 20 healthy volunteers were diluted in vitro with dextran 40 or normal saline by 5%, 10% and 15%. Fibrinogen concentration, ROTEM-EXTEM® (screening test for the extrinsic coagulation pathway), FIBTEM® (an EXTEM-based assay of the fibrin component of clot) parameters including coagulation time, clot formation time, alpha angle, maximum clot firmness and lysis index were measured in the undiluted sample and at each level of haemodilution. Dextran 40 at 15% haemodilution significantly prolonged coagulation time, clot formation time and significantly decreased the alpha angle and maximal clot firmness (EXTEM amplitude at five minutes [A5] and ten minutes [A10]) compared with normal saline. The FIBTEM assay (maximal clot firmness and FIBTEM A5 and A10) showed a marked decrease in maximal clot firmness at all dilutions suggesting impaired fibrinogen activity and a risk of bleeding. Multiple electrode aggregometry did not demonstrate any platelet dysfunction. Haemodilution with dextran 40 causes significant impairment in clot formation and strength compared to saline haemodilution and undiluted blood. At the levels of in vitro haemodilution designed to reflect the clinical use of dextran infusions, no significant fibrinolysis or platelet inhibition was observed.
34
Spannagl, Michael, Andrea Dick, and Andreas Calatzis. "Comprehensive Quality Management of Multiple Electrode Platelet Aggregometry." Blood 114, no. 22 (2009): 4463. http://dx.doi.org/10.1182/blood.v114.22.4463.4463.
Full textAbstract:
Abstract Abstract 4463 Platelet function analysis provides quantitative results which may reveal platelet disorders, platelet inhibition during anti-platelet therapy or anti-platelet drug resistance. The results may have important consequences on patients therapy. As in all laboratory methods, a comprehensive quality management approach is crucial and increasingly demanded by regulatory authorities. In platelet function methods quality control is hampered by the fact that platelets are not stable over longer time periods and loose their functional activities after freezing and freeze-drying. Therefore for most platelet function tests no control materials are available. When no biological quality control material is available, it is even more important to install and maintain a quality management approach, which covers as many influence factors and sources of error as possible. Here we present the quality management procedures of Multiple Electrode Aggregometry (MEA) a relative new platelet function test based on the analysis of whole blood (Multiplate analyzer, Dynabyte medical, Munich, Germany). In the MEA device temperature of the measurement system is controlled by the analyser and can be verified by an external QC kit. The signal reaction of this method is based on the rise of electrical resistance induced by the adhesion and aggregation of activated blood platelets on metal sensor electrodes in a disposable test cell. In order to control possible sensor inconsistencies and improve precision, the test cell incorporates two independent sensor units, each consisting of 2 silver-coated highly conductive wires. The duplicate sensors thus serve as an internal control. During each measurement Pearson's correlation coefficient of single measurements of the curves assessed by the two electrode pairs and the difference of the two AUCs are calculated automatically by the analyzer's software. The result is flagged if the values are outside of the acceptance range (correlation coefficient <0.98, difference to the mean curve >20%). The instrument has an integrated procedure for an electronic control which checks the function of the electronic amplifier in the analyzer. In addition liquid controls are available, based on solutions with different ional strength. Using these solutions the instrument, pipettor and test cells are controlled. Using blood from a healthy individual, users can control qualitatively all aspects of the analysis (instrument, test cells, reagents, pipettor). Abnormal control reagents are available, containing either aspirin, a GpIIbIIIa antagonist or prostaglandin E1, which can produce an abnormal result when added to a normal blood sample before the analysis. The instrument provides an electronic pipettor with interactive software-guided operation procedures, which help standardise the analysis and minimize user-related errors. Using artificial liquid control materials a pilot external QC was performed in 6 individual centers and the results were centrally analyzed. Level I control was determined as 125+-6 aggregation units (AU, mean+-sd), level II control was 64+-5 AU. Coefficients of variation of all determinations were 4.6% and 7.3% respectively. In conclusion it is shown that while a stable biological control material for platelet function analysis is not available, it is possible to perform quality controls covering many parts of the analytical procedure. Manufacturers and users of platelet function tests should try to implement control procedures that cover as many aspects of the technology they apply as possible to ensure correct performance of the tests over the lifetime of the instrument, test cells and reagents. As long as stable biological quality control materials for platelet function analysis are not available, qualitative biological controls using normal blood or plasma should be combined with artificial control materials or electronic test procedures according to the analytical reaction which is performed. If the biological reaction cannot be quantitatively controlled, then at least the physical process leading to the signal of the respective test procedure should be verified (measurement of pressure, optical density or electrical impedance). Using a step by step approach comprehensive quality management of platelet function analysis is feasible and should be implemented in routine. Disclosures: Calatzis: Dynabyte Medical : Equity Ownership, Patents & Royalties.
35
Krekels, Joyce P. M., Paul W. M. Verhezen, and Yvonne M. C. Henskens. "Platelet Aggregation in Healthy Participants is Not Affected by Smoking, Drinking Coffee, Consuming a High-Fat Meal, or Performing Physical Exercise." Clinical and Applied Thrombosis/Hemostasis 25 (June 19, 2018): 107602961878244. http://dx.doi.org/10.1177/1076029618782445.
Full textAbstract:
Platelet aggregation can be measured using optical aggregation (light transmission aggregometry, LTA) as well as by impedance (Multiplate analyzer). The LTA (the gold standard method) can be influenced by many preanalytical variables. Several guidelines differ in recommendations for the duration patients should refrain from smoking, coffee, fatty meals, and physical exercise prior to blood collection for performing platelet function tests. In this pilot study, the influence of smoking, coffee, high-fat meal, or physical exercise on platelet aggregation was investigated to improve patient friendliness and laboratory logistics in platelet function diagnostics. Standardized blood collection was performed when participants were fasting and after each parameter (n=5 per group). As a control for diurnal fluctuations, participants (n=6) were fasting during both blood collections. Platelet aggregation was executed using standardized methods for LTA and Multiplate analyzer. Statistical analysis of the results using Wilcoxon signed-rank test did not show any significant differences in platelet aggregation in healthy participants under different preanalytical variables. Therefore, these variables are not expected to adversely affect testing, which can avoid canceling tests for those patients who inevitably did.
36
Campello, Elena, Luca Spiezia, Eva Zabeo, Sara Maggiolo, Roberto Vettor, and Paolo Simioni. "Hypercoagulability detected by whole blood thromboelastometry (ROTEM®) and impedance aggregometry (MULTIPLATE®) in obese patients." Thrombosis Research 135, no. 3 (2015): 548–53. http://dx.doi.org/10.1016/j.thromres.2015.01.003.
Full text
37
Jastrzębska, Maria, Kornel Chełstowski, Aneta Wódecka, Aldona Siennicka, Jeremy Clark, and Przemysław Nowacki. "Factors influencing Multiplate whole blood Impedance Platelet Aggregometry measurements, during aspirin treatment in acute ischemic stroke." Blood Coagulation & Fibrinolysis 24, no. 8 (2013): 830–38. http://dx.doi.org/10.1097/mbc.0b013e3283655640.
Full text
38
Seyfert, Ulrich Theo, Hannelore Haubelt, Anette Vogt, and Peter Hellstern. "Variables influencing Multiplate™ whole blood impedance platelet aggregometry and turbidimetric platelet aggregation in healthy individuals." Platelets 18, no. 3 (2007): 199–206. http://dx.doi.org/10.1080/09537100600944277.
Full text
39
Scaravilli, Vittorio, Luca Di Girolamo, Eleonora Scotti, et al. "Effects of sodium citrate, citric acid and lactic acid on human blood coagulation." Perfusion 33, no. 7 (2018): 577–83. http://dx.doi.org/10.1177/0267659118777441.
Full textAbstract:
Introduction: Citric acid infusion in extracorporeal blood may allow concurrent regional anticoagulation and enhancement of extracorporeal CO2 removal. Effects of citric acid on human blood thromboelastography and aggregometry have never been tested before. Methods: In this in vitro study, citric acid, sodium citrate and lactic acid were added to venous blood from seven healthy donors, obtaining concentrations of 9 mEq/L, 12 mEq/L and 15 mEq/L. We measured gas analyses, ionized calcium (iCa++) concentration, activated clotting time (ACT), thromboelastography and multiplate aggregometry. Repeated measure analysis of variance was used to compare the acidifying and anticoagulant properties of the three compounds. Results: Sodium citrate did not affect the blood gas analysis. Increasing doses of citric and lactic acid progressively reduced pH and HCO3− and increased pCO2 (p<0.001). Sodium citrate and citric acid similarly reduced iCa++, from 0.39 (0.36-0.39) and 0.35 (0.33-0.36) mmol/L, respectively, at 9 mEq/L to 0.20 (0.20-0.21) and 0.21 (0.20-0.23) mmol/L at 15 mEq/L (p<0.001). Lactic acid did not affect iCa++ (p=0.07). Sodium citrate and citric acid similarly incremented the ACT, from 234 (208-296) and 202 (178-238) sec, respectively, at 9 mEq/L, to >600 sec at 15 mEq/L (p<0.001). Lactic acid did not affect the ACT values (p=0.486). Sodium citrate and citric acid similarly incremented R-time and reduced α-angle and maximum amplitude (MA) (p<0.001), leading to flat-line thromboelastograms at 15 mEq/L. Platelet aggregometry was not altered by any of the three compounds. Conclusions: Citric acid infusions determine acidification and anticoagulation of blood similar to lactic acid and sodium citrate, respectively.
40
Jaitner, Juliane, Julia Stegherr, Tanja Morath, et al. "Stability of the high on-treatment platelet reactivity phenotype over time in clopidogrel-treated patients." Thrombosis and Haemostasis 105, no. 01 (2011): 107–12. http://dx.doi.org/10.1160/th10-07-0440.
Full textAbstract:
SummaryInterindividual response variability to clopidogrel treatment is a well established phenomenon. In recent studies and ongoing large-scale trials where patients with high on-treatment platelet reactivity (HPR) to clopidogrel are being randomised to an intensified antiplatelet treatment, confirmation of the HPR phenotype is based on one single platelet function assessment. The stability of the HPR phenotype over time has never been investigated but should be considered crucial for justification of intensified antiplatelet treatment regimens beyond clinical trials. The goal of this study was to test for the stability of the HPR phenotype over time in clopidogrel-treated patients. Patients (n=31) under chronic clopidogrel treatment (75 mg/day) were investigated by serial adenosine diphosphate (ADP)-induced platelet aggregation assessment with multiple electrode aggregometry (MEA) on a Multiplate analyser and light transmission aggregometry (LTA) at three different time points (once per week) during monitored antiplatelet treatment. On the basis of a cut-off level approach (468 AU*min for MEA, 53% for LTA) patients were classified into patients with (n=27) or without (n=4) HPR. For MEA, the phenotype was stable in 93.5% (n=29) of patients whereas 6.5% (n=2) crossed the cut-off level. For LTA, the phenotype was stable in 68% (n=21) of patients whereas 32% (n=10) patients crossed the cut-off level (chi-square P=0.01 for comparison of pheno-type stability between both assays). In conclusion, the HPR phenotype is stable over time in the majority of clopidogrel-treated patients. Comparative assessment of phenotype stability across available platelet function assays warrants further investigation.
41
Sut, Agnieszka, Marcin Różalski, Jacek Golański, Maria Pytel, and Marek Zadrożny. "A polyphenol-rich diet is associated with decreased platelet aggregation in breast cancer patients." Diagnostyka Laboratoryjna 54, no. 2 (2019): 81–84. http://dx.doi.org/10.5604/01.3001.0013.7683.
Full textAbstract:
It is well documented that plant polyphenols have both anti-cancer and anti-platelet effects. Hence, the aim of this work was to investigate a relationship between dietary intake of polyphenols and platelet aggregation in newly-diagnosed breast cancer patients. The nutritional value of a diet, including dietary intake of plant polyphenols was estimated. Platelet aggregation was induced with arachidonic acid (0.5 mmol/l), collagen (3.2 μg/ml) or ADP (6.4 μmol/l) and measured using multiple electrode aggregometry (Multiplate<sup>®</sup>) in whole blood. It was found that platelet aggregation was significantly higher in the low polyphenol intake group than the high intake group: the respective values (area under the aggregation curve recorded in units; U) were arachidonic acid: 84.8 vs. 65.3, P=0.003; ADP: 76.5 vs. 67.8, P=0.006; collagen 79.5 vs. 64.3, p=0.024 respectively. The study indicates, for the first time, an association between diet rich in polyphenols and reduced platelet reactivity in breast cancer patients.
42
Rother, Daniel, Andreas Böning, and Johannes Gehron. "Der Einfluss der moderaten Hypothermie bei 28 °C auf die Gerinnungs- und Thrombozytenfunktion – Untersuchung in einem In-vitro-Chandler-Loop-Modell." Kardiotechnik 30, no. 2 (2021): 60–67. http://dx.doi.org/10.47624/kt.030.060.
Full textAbstract:
In the use of hypothermia in cardiac surgery an increased risk of bleeding is noticeable intra- and postoperatively. So far, the effects on coagulation and platelets caused by complex interactions between the extracorporeal circulation (ECC), surgical trauma and the effects of hypothermia prevent a clinical investigation of the cause of hypothermia associated bleeding in cardiac surgery. Methods: Using a Chandler-Loop blood flow model the effects of hypothermia could be studied under in-vitro conditions isolated from other competing factors. In the experimental group blood samples of three adult probands were cooled down from 37 °C to 28 °C and reheated at standardized temperature and flow conditions. During the measurements blood samples were taken at four checkpoints from the Chandler-Loops. A normothermic series of measurements served as a control group. Coagulation was examined using thrombelastometry and platelet function using impedance aggregometry. Results: Hypothermia irregularly caused a reduced coagulation; however, the platelet function seemed to be unaffected or only reversibly affected. Therefore, a decreased platelet function associated to hypothermia could not be detected via impedance aggregometry. In both groups the effects caused by the circulation in the Chandler-Loops on coagulation and platelet function were more pronounced than the effects caused by hypothermia. Discussion: The effects of hypothermia on coagulation seem to be not as pronounced and uniform as in other studies described. It is instead to assume that only specific components are impaired by cooling whereas the rotation in the Chandler-Loops always leads to measurable contact reactions. The results of the thrombelastomtry indicate that the cause for an impaired coagulation under hypothermia are reduced protein kinetics and a decreased platelet function. The reversible effects of hypothermia on platelets may account for the lack of measurable alterations in platelet function when using the Multiplate method. This being the case hypothermia caused impairment of platelet function could not be detected using the Multiplate method under clinical conditions.
43
Pronko, T. P., V. A. Snezhitskiy, and A. V. Kapytski. "Platelet reactivity clinical and biochemical markers when taking acetylsalicylic acid as part of dual antiplatelet therapy in the myocardial infarction subacute period." Rational Pharmacotherapy in Cardiology 20, no. 6 (2024): 618–24. https://doi.org/10.20996/1819-6446-2024-3037.
Full textAbstract:
Aim. To study markers that determine residual platelet reactivity in the subacute period of myocardial infarction (MI) during the administration of acetylsalicylic acid (ASA) as part of dual antiplatelet therapy.Material and methods. 405 patients with MI (79.5% men and 20.5% women, average age 58.0 years) were divided into groups based on aggregometry results. Group 1 — 11 patients with low residual platelet reactivity, group 2 — 236 patients with optimal platelet reactivity, group 3 — 158 patients with high residual platelet reactivity (HRPR). All studies were performed on days 12-14 after MI: aggregometry on a Multiplate aggregometer (Germany) with several aggregation inducers, a blood test and a study of platelet indices, determination of endothelin-1, von Willebrand factor, sP-selectin and soluble CD40 ligand levels.Results. Parameters influencing the ASPItest value according to univariate linear regression analysis: body mass index (β=0.53, 95% CI: 0.11-0.96; p=0.013); waist circumference (β=0.31, 95% CI: 0.14-0.49; p=0.0004); erythrocyte sedimentation rate (β=0.27, 95% CI: 0.12-0.42; p=0.0004); white blood cells count (β=1.47, 95% CI: 0.51-2.42; p=0.0027); platelets count (β=0.042, 95% CI: 0.019-0.064; p=0.00025); thrombocrit (β=36.8, 95% CI: 14.6-59.1; p=0.0012); mean platelet volume (β=1.94, 95% CI: 0.06-3.84; p=0.043); platelet distribution width (β=1.36, 95% CI: 0.22-2.51; p=0.02); creatinine (β=0.11, 95% CI: 0.011-0.21; p=0.03); C-reactive protein (β=0.18, 95% CI: 0.05-0.32; p=0.007); TRAP-test (β=0.18, 95% CI: 0.11-0.24; p=0.000001); fibrinogen (β=2.6, 95% CI: 1.17-4.02; p=0.0004). The binary logistic regression model to calculate the probability of developing HRPR to ASA included the following factors: platelet count, percentage of large platelet volume (PLCR), fibrinogen, endothelin-1 and von Willebrand factor. With a probability cutoff p₀=0.5412 for this model: sensitivity — 81.08%, specificity — 73.21%, classification accuracy — 76.34%, area under the ROC curve — 0.79 (CI: 0.696 - 0.883).Conclusion. There are 2.7% of patients with an excessive response to ASA and 39.0% with an insufficient response to ASA on days 12-14 of MI. Clinical and biochemical markers of HRPR to ASA in the subacute period of MI are the number of platelets, PLCR, fibrinogen, endothelin-1 and von Willebrand factor.
44
Ankri, Annick, Isabelle Martin-Toutain, Anne Baranger, Marie-Claude Couty, Jean Philippe Collet, and Gilles Montalescot. "Evaluation of Residual Platelet Reactivity in Patients Treated with Aspirin and or Clopidogrel: Comparison of Results Obtained On Multiplate®, PFA-100TM and Classical Light Transmission Aggregometry." Blood 114, no. 22 (2009): 3129. http://dx.doi.org/10.1182/blood.v114.22.3129.3129.
Full textAbstract:
Abstract Abstract 3129 Poster Board III-66 Residual platelet reactivity (RPR), despite antiplatelet therapy (AT), is currently associated with an increased risk of recurrent ischemic events and is linked to a biological resistance to AT. We determined whether whole blood impedance aggregometry using the Multiplate® (Dynabyte and IL France) detects the effects of AT as reliably as does classical light transmission aggregometry (LTA) (PAP-8, Biodis). We compared also results with those obtained on PFA-100TM (Siemens). Patients and Methods Ninety-three controls, healthy volunteers or patients without intake of AT or other drugs or pathology impairing platelet functions and 182 consecutive patients on AT were studied. Among patients, 61 received Aspirin 100mg (group A), 36 Clopidogrel 75mg (group C) and 85 the association of the two drugs. Among these 85 patients, 58 received continuously Aspirin 75mg and Clopidogrel 75mg (group AC) and 27 received a loading dose for both drugs before coronarography (group LAC). Venous blood samples were obtained on Becton Dickinson vacutainer containing citrate 0.129M. Multiplate® measures change in electrical resistance as arbitrary aggregation units (AU) over time. Aggregation is quantified as AU and area under the curve (AUC) of AU.min. On LTA, aggregation was quantified according to manufacturer's recommendations as AUC. “Resistance” to Aspirin or Aspirin RPR was determined on Multiplate® (M) using arachidonic acid at 0.5 mM (ASPITEST), in LTA with arachidonic acid at 1 mM (AA-LTA) and on PFA-100TM using the cartridge with membrane coated with epinephrine (PFA-EPI). In the same way, “resistance” to Clopidogrel was determined on M using ADP at 6.4 μM (ADPTEST), in LTA with the presence of ADP at 10 μM (ADP-LTA) and occlusion time on PFA-100TM using cartridge with membrane coated with ADP (PFA-ADP). Results All patients were tested on M, 169 on PFA-100TM and 37 with LTA. Significant correlations (p<.0001) were observed between ASPITEST and AA-LTA (r = .771), ASPITEST and PFA-EPI (r = -.42), AA-LTA and PFA-EPI (r = -.47), ADPTEST and ADP-LTA (r = .6) ADPTEST and PFA-ADP (r = -.39) and ADP-LTA and PFA-ADP (r = -.56). To define RPR on M and LTA, cut-off values (5th percentile) were determined from controls for each inducer. Treated patients presenting reactivity higher than the threshold value were considered as ‘resistant’. For PFA-100TM, results of patients under cut-off point defined by the manufacturer were considered as ‘resistant’. The frequency of “resistant” patients according to the different platelet functions tests was: a) for Aspirin: 10% on M, 4.5% with LTA and 32.8% with PFA-EPI. b) for Clopidogrel 23.1% on M 16.1% with LTA and 54.5% with PFA-ADP. A good agreement was found between ASPITEST and AA-LTA and between ADPTEST and ADP-LTA (respectively 92% and 88.7%). On the other hand, results on comparison between ASPITEST and PFA-EPI and LTA and PFA-EPI were respectively 70% and 72.6%. Results for ADPTEST and PFA-ADP were 69% and 72.3% for ADP-LTA and PFA-ADP. A significant gradation of mean AUC was observed using ASPITEST on M between all groups of subjects: controls (mean = 494±176); group A (mean = 214±186); group C (mean = 310±198); group AC (mean = 118±109); group LAC (mean = 74±45). Similar results are obtained with LTA and on PFA-100TM (except for the group C, Clopidogrel alone). Thus, a potentiating effect of Aspirin by the association with Clopidogrel may be postulated in this study. Using ADPTEST to assess the treatment response by clopidogrel, mean AUC were significantly lower for all group of patients with Clopidogrel than for controls. No gradient has been observed. Mean AUC of patients with Aspirin alone was similar to controls. In conclusion, our results confirm that Multiplate® is more effective than PFA-100TM in monitoring patients on AT. The good agreement between Multiplate® and LTA could lead to use the Multiplate® in first intention to detect RPR in these patients. Furthermore the easiness of Multiplate® use may contribute to development of new studies on biological activities of AT. Disclosures No relevant conflicts of interest to declare.
45
Ponschab, Martin, Martijn van Griensven, Stefan Heitmeier, et al. "Platelet function in baboons and humans — A comparative study of whole blood using impedance platelet aggregometry (Multiplate®)." Thrombosis Research 147 (November 2016): 115–21. http://dx.doi.org/10.1016/j.thromres.2016.10.005.
Full text
46
Halimeh, S., G. de Angelis, A. Sander, et al. "Multiplate®Whole Blood Impedance Point of Care Aggregometry: Preliminary Reference Values in Healthy Infants, Children and Adolescents." Klinische Pädiatrie 222, no. 03 (2010): 158–63. http://dx.doi.org/10.1055/s-0030-1249081.
Full text
47
Marschner, Clara B., Annemarie T. Kristensen, Eva H. Spodsberg, and Bo Wiinberg. "Evaluation of platelet aggregometry in dogs using the Multiplate platelet analyzer: impact of anticoagulant choice and assay duration." Journal of Veterinary Emergency and Critical Care 22, no. 1 (2012): 107–15. http://dx.doi.org/10.1111/j.1476-4431.2011.00709.x.
Full text
48
Petricevic, M., S. Konosic, B. Biocina, et al. "Bleeding risk assessment in patients undergoing elective cardiac surgery using ROTEM®platelet and Multiplate®impedance aggregometry." Anaesthesia 71, no. 6 (2016): 636–47. http://dx.doi.org/10.1111/anae.13303.
Full text
49
Li, JiaXin, Moo Hyun Kim, LongZhe Guo, et al. "Impact of CYP2C19 Polymorphism on Antiplatelet Potency of Prasugrel 5 and 10 mg Daily Maintenance." Cardiology 140, no. 3 (2018): 155–62. http://dx.doi.org/10.1159/000491598.
Full textAbstract:
Background: Whether genetic polymorphisms (GP) impact residual platelet aggregation (RPA) following prasugrel is unclear, especially during maintenance phase. We assessed the influence of CYP2C19 GP carriers on RPA in the prospective observational cohort study. Methods and Results: All post-stent patients (n = 206) received prasugrel 60 mg loading and either 5 or 10 mg daily maintenance with aspirin100 mg. RPA levels by light transmission aggregometry (LTA), multiplate electrode aggregometry (MEA), and VerifyNow (P2Y12 reaction units, PRU) with CYP2C19 GP were measured simultaneously. Demographics and clinical characteristics were not useful for predicting response after prasugrel. GP carriers exhibited higher RPA (PRU: p = 0.001, LTA: p = 0.001, MEA: p = 0.023) than noncarriers. CYP2C19 carriers had higher RPA for 5 mg (n = 35; LTA: p = 0.043, MEA: p = 0.023) and reached significance for 10 mg (n = 27; LTA: p = 0.001, PRU: p = 0.001) prasugrel. When divided into extensive, intermediate, and poor metabolizers, all exhibited statistical differences among the 3 groups (LTA: 14.9 ± 12.3%, 22.6 ± 14.9%, 22.9 ± 15.6%, p = 0.002; PRU: 104.1 ± 70.8%, 141.8 ± 78.0%, 151.0 ± 84.8%, p = 0.003; MEA: 19.7 ± 8.9%, 24.4 ± 12.2%, 28.1 ± 14.7%, p = 0.002). Conclusion: CYP2C19 GP impacts RPA during maintenance phase prasugrel in Korean outpatients. This effect is consistent for both of the approved prasugrel doses potentially affecting long-term outcomes including bleeding risks. However, the clinical utility of these findings is still uncertain, and requires more evidence from larger randomized trials beyond East Asians.
50
Dineva, D., Е. Doncheva, and I. Paskaleva. "Antiplatelet therapy – platelet function test for platelet response assessment." Bulgarian Cardiology 31, no. (1) (2025): 42–66. https://doi.org/10.3897/bgcardio.31.e151011.
Full textAbstract:
Dual antiplatelet therapy is the main pharmacological mechanism used to suppress platelet function in order to prevent thrombotic complications following percutaneous coronary angioplasty. Current studies show that the use of tailored antiplatelet therapy leads to significant clinical improvement after stent implantation. The need to individualize therapy is due to the presence of wide interindividual variations in platelet response and the differing pharmacodynamics of various P2Y12 inhibitors – clopidogrel, prasugrel, and ticagrelor. Assessment of ADP-induced platelet aggregation helps prevent both adverse ischemic events and the associated bleeding risk. The primary objective of our studies was initially to establish and overcome resistance to clopidogrel therapy with the aim of reducing adverse ischemic events. With the introduction of prasugrel and ticagrelor – medications that offer a stronger and more predictable antiplatelet effect – our focus shifted to identifying increased response and bleeding in the context of dual antiplatelet therapy, and to individualizing therapy to minimize bleeding. Our long-term experience shows that impedance aggregometry is a fast and reliable method for evaluating platelet function. The tests allow for the differentiation of patients with optimal, high, and low platelet reactivity to P2Y12 inhibitor therapy. The main conclusion from our studies is that individualizing therapy leads to the absence of ischemic events without an increased risk of hemorrhage, thereby achieving a balance between ischemic and hemorrhagic complications during treatment.