Multiplate® analyzer

Mulitplate Analyzer

Multiplate analyzer


Platelet function testing with best-in-class predictivity

  • Blood platelets play a pivotal role in physiological hemostasis but also in the development of arterial thrombosis (myocardial infarction and stroke)
  • Platelet function testing is used to analyze inherited and acquired platelet function disorders, in the analysis of platelet function in anesthesia and intensive care as well as monitoring of platelet function antagonists
  • The Multiplate® analyzer is an easy-to-use instrument that standardizes platelet function testing in small quantities of whole blood
  • The 5 channel analyzer has a broad menu of CE marked tests
  • It has been featured by over 400 Medline-listed articles and has been reported by several groups to be useful in tailoring anti-platelet therapy as well as improving the management of bleeding complications in surgical procedures

This customer testimonial features the medical value of platelet function diagnostics with Multiplate for tailored anti-platelet therapy after coronary stenting.

Analyzer

  • Testing in low volumes (300 µL) of whole blood
  • 5 measurement positions for simultaneous measurement of different samples/agonists
  • 10 minute time to result
  • Sensitive signal detection with a large dynamic range
  • Electronic pipette with predefined pipette programs for routine tests

Test principle

  • Multiplate® analyzer provides a disposable test cuvette featuring a duplicate sensor
  • Patented twin sensor technology (Multiple Electrode Aggregometry (MEA) for reliable results and quality control
  • Whole blood testing eliminates the need for time-consuming sample preparation while maintaining the natural physiological matrix for platelet function
  • Small quantity (300µL) of whole blood required per test, permitting up to 9 tests per blood tube draw
  • Upon activation platelets aggregate on metal sensors and increase the electrical resistance
Multiplate_test_principle_and_curve

Multiplate test principle


Test portfolio
ADPtest
ADP induced platelet activation sensitive to clopidogrel, prasugrel and other ADP receptor antagonists
ASPItest
Cyclooxygenase dependent aggregation (using arachidonic acid) sensitive to Aspirin®, NSAIDs and other inhibitors of platelet cyclooxygenase
COLtest
Collagen induced aggregation
RISTOtest
vWF and GpIb dependent aggregation (using ristocetin)
TRAPtest
Platelet stimulation via the thrombin receptor (using TRAP-6), sensitive to IIbIIIa receptor antagonists
Prostaglandin E1 reagent
For the assessment of ADPtest HS (high sensitivity). For the assessment of positive (i.e. abnormal) controls of the ADPtest
ASA reagent
Inhibitor of cyclooxygenase. Addition of ASA reagent to the blood sample leads to reduced aggregation responses in ASPItest and COLtest
GpIIb/IIIa antagonist reagent
Inhibitor of the platelet GpIIb/IIIa receptor. Addition to a blood sample leads to strongly reduced aggregation in the TRAPtest
Hirudin blood tubes
Anticoagulant for platelet function analysis under physiological calcium concentrations
Liquid control set
Quality control for electrical signal in impedance aggregometry based on the analysis of an artificial liquid control material

Powerful analysis of platelet function

The Multiplate® analyzer delivers benefits in a number of key areas:

Best predictivity - for tailored antiplatelet therapy

  • Approximately 20% of patients do not respond adequately to clopidogrel
  • Patients showing a “low-response” to clopidogrel in Multiplate® analysis have shown a 5-10 fold risk for ischemic complications
  • Other more potent drugs act more consistently but increase bleeding and cost up to 15 times as much as generic clopidogrel
  • Several groups have reported successful experiences tailoring anti-platelet therapy using Multiplate® analysis

Best predictivity – for stratification of bleeding risk

  • Patients with impaired platelet function according to Multiplate® analysis have an increased risk for intra- and post-operative bleeding complications and/or transfusion requirements
  • Multiplate can help improve hemostatic management in the bleeding patient
    after surgery, thereby contributing to a better outcome and lower costs

Detection of platelet disorders

  • Platelet dysfunction can induce transient or permanent tendency to bleed
  • Multiplate detects platelet dysfunction and disorders, and determines heparin-induced platelet aggregation in whole blood
  • It detects Glanzmann thrombasthenia, Bernard-Soulier syndrome, ADP receptor defects, and other platelet disorders associated with clinically relevant symptoms

Consistent results

  • Standardised and fast test procedure utilizing whole blood
  • Easy to use, low blood volume/test
  • Broad menu of CE marked tests for various applications
  • 5 channel analyzer with high throughput
  • High sensitivity and dynamic range
  • Twin sensors for quality control

Medical Momentum

  • 400 Medline-listed publications with Multiplate®
  • Consensus paper of “Working Group on High-On-Treatment-Platelet-Reactivity” features Multiplate®
  • Clinical guidelines recommend platelet function testing in CABG and PCI for patients treated with clopidogrel

Bonello, L., Tantry, U.S., Marcucci, R., et al. (2010). Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate. J Am Coll Cardiol Sep 14;56(12):919-33.

Summary:
In a recent consensus opinion on the definition of high on-treatment platelet reactivity (HPR) to ADP, studies are summarized that link HPR to ischemic events based on ROC curve derived cutoffs. The best prediction of ischemic risk was associated with the Multiplate® analyzer, with an odds ratio of 12.0, while studies using other methods demonstrated odds ratios of only 1.2 - 5.8.

Sibbing, D., Braun, S., Morath, T. et al. (2009). Platelet reactivity after clopidogrel treatment assessed with point-of-care
analysis and early drug-eluting stent thrombosis. J Am Coll Cardiol (53), 849–56.

Summary:
This prospective trial evaluated if platelet reactivity to clopidogrel assessed with multiple electrode aggregometry (MEA, Multiplate®) correlates with the risk of early drug-eluting stent thrombosis (ST). With 1,608 CAD patients enrolled who were scheduled for drug eluting stent PCI, this study is among the largest ones conducted on this topic. The primary end point was definite ST at 30 days. Before PCI, all patients received 600 mg clopidogrel. Blood was obtained directly before PCI and tested with the Multiplate® ADPtest more than 2 hours after clopidogrel loading. The upper 20% of patients according to Multiplate® measurements (n = 323) were defined as clopidogrel low responders using a cut-off value of 42 U.

This study has been featured in an article in “www.theheart.org” where Sibbing stated: “We can’t say whether the MEA assay is better than other assays or not, but we are very happy with it, and we are convinced by the results we have seen in this study. It also works out at a reasonable cost for each test. When we started this study, we were not routinely measuring platelet responsiveness in the cath lab, but now we are measuring it with this device“.

Siller-Matula, J. M., Francesconi, M., Dechant, C., Jilma, B., Maurer, G., Delle-Karth, G., et al. (2013). Personalized antiplatelet treatment after percutaneous coronary intervention: The MADONNA study. International journal of cardiology, 167(5), 2018-2023

Summary:
The MADONNA study is a prospective non-randomized non-blinded study with 798 patients on clopidogrel and undergoing PCI compared two cohorts (tailored and non-tailored treatment) with a follow-up of one month. Patients in the non-tailored cohort (n=395) received only one clopidogrel loading dose of 600 mg at least 2 h before PCI. In the tailored group (n=403) clopidogrel responsiveness was repeatedly determined via ADPtest using multiple electrode aggregometry (MEA) and non-responders (≥ 50 U) received repeated loading doses of clopidogrel or prasugrel. The MADONNA study of Siller-Matula et al.2 could prove that tailored anti-platelet treatment using Multiplate® results in an improved therapeutic efficacy with an equal safety compared to the standard treatment.

Weber, C.F., Görlinger, K., Meininger, D., Herrmann, E., Bingold, T., Moritz, A., Cohn, L.H., Zacharowski, K. (2012). Point-of-Care Testing: A Prospective, Randomized Clinical Trial of Efficacy in Coagulopathic Cardiac Surgery Patients. Anesthesiology. Sep 117(3), 531-547.

Summary:
This trial aimed to study the efficacy of hemostatic therapy guided either by conventional coagulation analyses (platelet count, hemoglobin concentration, fibrinogen concentration, INR, aPTT) or point-of-care (POC) testing via Rotem® and Multiplate® in coagulopathic patients undergoing complex cardiac surgery. In this prospective study 100 patients with diffuse bleeding after heparin reversal or increased blood loss during the first 24 postoperative hours were randomized either to the conventional laboratory testing group (N=50) or POC-guided group (N=50).
Hemostatic therapy algorithms guided by the POC testing not only reduced patient exposure to allogenic blood products and decreased number of transfused units of packed erythrocytes but also lowered fresh frozen plasma and platelet concentrate usage. Further, POC-guided algorithm significantly improved clinical outcome and provided significant costs benefits compared to the standard treatment.

The challenge of adequate platelet inhibition

Clinical management of patients at high risk of arterial thrombosis, for example, after stent placement or in the event of acute coronary syndrome (ACS), presents a great challenge. In this case, it is imperative to achieve adequate platelet inhibition. Multiplate® analyses have established that some 20 percent of patients do not respond adequately to clopidogrel after PCI1. Patients who respond poorly to clopidogrel have been shown to have a fivefold to tenfold greater risk of ischemic complications1-4. Conversely, the risk of major bleeding is 2.6 times greater in patients who are high responders to clopidogrel5. Early major bleeding after elective and urgent PCI is associated with > 4 fold increased risk of mortality at 1 year.6

More powerful but costly and risky

Novel P2Y12 receptor antagonists with more potent and consistent action than clopidogrel have been introduced. However, they cost up to 15 times as much as clopidogrel7. The more effective action also comes at a human cost - a higher risk of major bleeding including fatal bleeding (prasugrel)8 and of non-CABG related major bleedings and dyspnea (ticagrelor)9.

More effective treatment with Multiplate®

Real life studies with more than 2,000 PCI patients support the clinical benefit and cost-effectiveness of Multiplate®-guided anti-platelet therapy algorithms.10-13 It provides the guidance physicians need to tailor treatment. The ability to monitor and control anti-platelet therapy with Multiplate® is also a tremendous asset because it enables the treating physician to confirm patient compliance.

Consensus paper supporting best-in-class predictivity of Multiplate®

In a recent consensus opinion on the definition of high on-treatment platelet reactivity (HPR) to ADP, studies are summarized that link HPR to ischemic events based on ROC curve derived cutoffs.1 The best prediction of ischemic risk was associated with the Multiplate® analyzer, with an odds ratio of 12.0, while studies using other methods demonstrated odds ratios of only 1.2 - 5.8.

Personalized anti-platelet therapy algorithm in PCI

According to Christ et al.15,16 Multiplate® can be used for the management of anti-platelet therapy in patients undergoing PCI. The investigators concluded that routine tailoring of antiplatelet therapy is capable to prevent early definite stent thrombosis in PCI.15

Evidence of improved outcome after tailored anti-platelet therapy

Growing evidence is available that routine tailoring of anti-platelet therapy using Multiplate® ADPtest has the potential to significantly reduce the incidence of major adverse ischemic complications post PCI.

A study in 542 PCI patients investigated if Multiplate® tailored anti-platelet therapy with prasugrel in patients displaying high platelet reactivity while on clopidogrel treatment reduces the incidence of stent thrombosis after PCI.16 The authors concluded that “Routine platelet function testing [Multiplate®] is useful for guidance of tailored antiplatelet treatment and switching to prasugrel markedly reduces ST risk in HPR patients on clopidogrel.”

In a prospective study of 798 patients with coronary artery disease undergoing PCI, “Personalized antiplatelet treatment according to the platelet function testing with MEA [Multiplate®] resulted in an improved efficacy with an equal safety compared to the standard treatment” with clopidogrel.17

Therapeutic window

Sibbing et al. (2010)18 aimed to explore a potential therapeutic window with 2533 patients undergoing PCI. The study provides an evidence for the existence of a so-called therapeutic window or a “sweet spot” of P2Y12-receptor inhibition, as patients with platelet aggregation values within the “normal range” (189 - 467 AU•min) have a low risk for both adverse events, ST and major bleeding.

Guidelines

PFT is supported by a Class IIb recommendation in the 2012 American College of Cardiology Foundation PCI guidelines on UA/NSTE-ACS patients.19

Tailoring anti-platelet therapy in clinical routine

In these movies Dr. Daniel Aradi from the State Heart Center in Balatonfured, Hungary, summarizes the medical value of platelet function diagnostics with Multiplate for tailored anti-platelet therapy after coronary stenting.


ESC-Symposium 2013 
“Monitoring of platelet function in PCI patients in clinical routine”

At this year’s ESC congress Roche organized a Satellite symposium on the topic “Monitoring of platelet function in PCI patients in clinical routine”.  It comprises the following speeches:

Routine monitoring in ACS patients improves outcomes: experiences from a national program in Hungary.
Dr. Daniel Aradi, State Heart Center Balatonfured, Hungary

Management of anti-platelet therapy using multiple electrode aggregometry: study results and future options.
PD Dr. Dirk Sibbing, Ludwig-Maximilians University Munich, Germany

Summary and discussion: monitoring of platelet function in PCI patients in clinical routine.
Prof. Dr. Julinda Mehilli, Ludwig-Maximilians University Munich, Germany 

You can watch the whole Symposium here

References
  1. Giorgi, M. A., Di Girolamo, G., & Gonzalez, C. D. (2010). Nonresponders to clopidogrel: pharmacokinetics and interactions involved. [Review]. Expert opinion on pharmacotherapy, 11(14): 2391-2403.
  2. Sibbing, D., Braun, S., Morath, T., Mehilli, J., Vogt, W., Schömig, A., Kastrati, A., von Beckerath, N. (2009). Platelet reactivity after clopidogrel treatment assessed with point-of-care analysis and early drug-eluting stent thrombosis. J Am Coll Cardiol. Mar10;53(10): 849-56.
  3. Schulz, S. et al. (2010). Platelet response to clopidogrel and restenosis in patients treated predominantly with drug-eluting stents. Am Heart J. Aug;160(2): 355-61.
  4. Siller-Matula, J.M. et al. (2010). Multiple electrode aggregometry predicts stent thrombosis better than the vasodilator-stimulated phosphoprotein phosphorylation assay. J Thromb Haemost. Feb;8(2): 351-9.
  5. Sibbing, D., Schulz, S., Braun, S., Morath, T., Stegherr, J., Mehilli, J., Schömig, A., von Beckerath, N., Kastrati, A. (2010). Antiplatelet effects of clopidogrel and bleeding in patients undergoing coronary stent placement. J Thromb Haemost Feb;8(2): 250-6.
  6. Mehran, R. et al. (2011). Impact of bleeding on mortality after percutaneous coronary intervention results from a patient-level pooled analysis of the REPLACE-2 (randomized evaluation of PCI linking angiomax to reduced clinical events), ACUITY (acute catheterization and urgent intervention triage strategy), and HORIZONS-AMI (harmonizing outcomes with revascularization and stents in acute myocardial infarction) trials. JACC Cardiovasc Interv; Jun;4(6):654-64.
  7. NHS - New drug evaluation: No 109, 01 (2011). Regional Drug and Therapeutics Centre, www.nyrdtc.nhs.uk.
  8. Wiviott, S.D., et al. (2007). Prasugrel versus clopidogrel in patients with acute coronary syndromes. The New England journal of medicine. 357(20): p. 2001-15.
  9. Wallentin, L., et al. (2009). Ticagrelor versus clopidogrel in patients with acute coronary syndromes. The New England journal of medicine. 361(11): p. 1045-57.
  10. Siller-Matula, J.M., Francesconi, M., Dechant, C., Jilma, B., Maurer, G., Delle-Karth, G., Gouya, G., Ruzicka, K., Podczeck-Schweighofer, A., Christ, G. (2012). Personalized antiplatelet treatment after percutaneous coronary intervention: The MADONNA study. Int JCardiol. May 30. [Epub ahead of print]
  11. Aradi, D., Pinter, T., Magyari, B., Konyi, A., Vorobcsuk, A., Horvath, I. G., et al. (2013). Optimizing P2Y12-Receptor Inhibition in Acute Coronary Syndrome Patients after PCI Using Platelet Function Testing: Impact of Prasugrel versus High-Dose Clopidogrel. J Am Coll Cardiol, 61(10): E1922.
  12. Mayer, K., Schulz, S., Bernlochner, I., Morath, T., Braun, S., Hausleiter, J., et al. (2013). The impact of personalized antiplatelet treatment on early adverse events in PCI-treated patients with high on-clopidogrel platelet reactivity: results of the ISAR-HPR registry. European Heart Journal, 34 (Abstract Supplement), 888-889, P4872.
  13. Straub, N., Beivers, A., Lenk, E., Aradi, D., Sibbing, D. (2013) A model-based analysis of the clinical and economic impact of personalising P2Y12-receptor inhibition with platelet function testing in acute coronary syndrome patients. Thromb Haemost. Oct 24;111(2). [Epub ahead of print]
  14. Bonello, L. et al. (2010). J Am Coll Cardiol; 56 (12):919-33.
  15. Christ, G. et al. (2011). Eurointervention Vol 7; Suppl M, May 17.
  16. Sibbing, D. et al. (2012). J Am Coll Cardiol; 59;E265.
  17. Siller-Matula, JM. et al. (2012) Int J Cardiol; doi:10.1016/j.ijcard.2012.05.040
  18. Siller-Matula, JM. et al. (2012) Int J Cardiol; doi:10.1016/j.ijcard.2012.05.040
  19. Jneid, H. et al. (2012). Circulation. Aug 14;126(7): 875-910.

Mitigating complications, maximizing patient management

Platelet function plays a pivotal role in hemostasis during surgery and following traumatic injuries. Dysfunction can trigger complications that require increased blood transfusions and renewed exploratory surgery. Anti-platelet drugs are associated with increased risk of bleeding and reoperation. European and US guidelines suggest discontinuation of ADP receptor antagonists (clopidogrel, prasugrel, ticagrelor) 3-7 days before major surgery.1,2. Several studies attest to the Multiplate® analyzer’s ability to detect a higher risk of bleeding and the need for increased transfusions in patients during surgery3-7.

From insight to impact

The ability to assess platelet function before, during and after major surgical procedures helps improve hemostatic patient management. This insight is a positive force that can help reduce hospitalization time, exposure to allogenic blood products and, by extension, costs8. The savings potential is considerable.

Prediction of peri-operative bleeding risk in cardiac surgery with Multiplate®

Patients on dual anti-platelet therapy with impaired platelet function before surgery are at increased risk of massive bleeding and transfusion requirements9:

  • 3.7 fold higher risk of massive bleeding in patients with Multiplate® ADPtest ≤ 30 U. 9
  • 2.5 fold higher risk for platelet transfusion in patients with Multiplate® ADPtest ≤ 30 U. 9

Reduced blood loss and improved outcome in cardiac surgery with POC guided hemostatic therapy

Weber et al.10 investigated the efficacy of hemostatic therapy guided either by conventional coagulation analyses (platelet count, hemoglobin concentration, fibrinogen concentration, INR, aPTT) or point-of-care (POC) testing via Multiplate® and ROTEM® in 100 coagulopathic patients undergoing complex cardiac surgery.

Results showed that the use of hemostatic therapy algorithms based on POC testing was associated with decreased bleedings and significantly reduced perioperative exposure to allogenic blood products. Improved clinical outcome was observed for the POC group, driven by a significantly lower incidence of composite adverse events (acute renal failure, sepsis, thrombotic complications and allergic reactions) and decreased 6-month mortality. The POC group also had reduced hospital costs.

Guidelines

The Society of Thoracic Surgeons recommends perioperative assessment of platelet function in their 2012 update guideline on use of anti-platelet drugs in patients having cardiac and noncardiac operations11. Platelet function analysis with Multiplate® is recommended for surgical patients on dual anti-platelet therapy, to limit blood transfusion (Class IIb) and for making decisions about surgical timing “rather than arbitrary use of a specified period of surgical delay” (Class IIa).

The European Society of Anaesthesiology recommends in their 2013 guidelines on the management of severe perioperative bleeding the preoperative platelet function testing in patients on anti-platelet therapy or with positive bleeding anamnesis (Class IIc).12

References
  1. Hamm, C.W. et al. (2011). Eur Heart J; Dec 32(23):2999-3054.
  2. Ferraris, V.A. et al. (2011). Ann Thorac Surg; Mar 91(3):944-82.
  3. Ranucci, M. et al. (2011). Ann Thorac Surg. Jan;91(1):123-9.
  4. Wang, H., Leff, J., Nair, S., Shore-Lesserson, L. (2012). Anesth Analg;114(suppl);1-94
  5. Reece, M.J. et al. (2011). Anaesthesia. Feb;66(2):97-103.
  6. Rahe-Meyer, N. et al. (2008). Anesth Analg. Dec;107(6):1791-7.
  7. Rahe-Meyer, N. et al. (2009). Acta Anaesthesiol Scand. Feb;53(2):168-75.
  8. Weber, C.F. et al. (2012). Anesthesiology. Sep;117(3): 531-547.References
  9. Ranucci, M. et al. (2011). Ann Thorac Surg; Jan 91(1):123-9.
  10. Weber, C.F. et al. (2012). Anesthesiology; Sep 117(3):531-47.
  11. Ferraris, V. A. et al. (2012). The Annals of thoracic surgery, 94(5), 1761-1781.
  12. Kozek-Langenecker, S. A., et al. (2013). Eur J Anaesthesiol. 2013 Jun;30(6): 270-382.

Detection of platelet disorders

Platelet dysfunction triggered by drugs, diseases or genetic factors may induce a transient or permanent tendency to bleed. The Multiplate® analyzer is able to detect platelet dysfunction. And that makes it an invaluable therapeutic asset for doctors who manage patients with platelet dysfunctions.

Designed to determine and distinguish

Sensitivity to platelet disorders is designed into Multiplate®. It detects Glanzmann thrombasthenia, Bernard-Soulier syndrome, ADP receptor defects1,2 and von Willebrand disease (comparable to optical aggregometry)3. It is also well-suited for the functional determination of heparin-induced thrombocytopenia in whole blood4,5.

Speed paired with efficiency

Easy to use and compact, the Multiplate® system analyzes platelet function in whole blood. Designed for speed as well as accuracy, its turnaround time is just ten minutes per test. It is equipped with five channels, so it processes up to 30 tests per hour. Each analysis requires no more than 300 μL of blood.

The Multiplate® analyzer comes with a comprehensive menu featuring six CE marked and standardized PFT procedures (ADPtest, ASPItest, TRAPtest, COLtest, RISTOtest, ADPtest HS). The system’s underlying low-shear detection principle enables the specific activation of platelet receptors or transduction pathways.

Advanced detection with sophisticated sensors

The advanced detection principle and sophisticated sensors built into Multiplate® lend it a superior dynamic range, sensitivity and signal magnitude for detecting platelet function. Each test  cell incorporates two pairs of sensors (multiple electrode aggregometry, or MEA for short) that serve as an on-board quality control device.

High sensitivity  for platelet disorders and other causes of platelet dysfunction

Multiplate is highly sensitive for:

  • The detection and differentiation of platelet disorders which are based on defined receptor defects like Glanzmann thrombasthenia, Bernard-Soulier syndrome, and ADP receptor defects.6,7
  • The monitoring of platelet function inhibitors Aspirin®8,9, clopidogrel10 and prasugrel11, across its large dynamic range.
  • The determination of platelet dysfunction before invasive procedures and the support of improved hemostatic management in bleeding patients.9,10
  • Von Willebrand disease (comparable to optical aggregometry).13
  • The functional determination of heparin induced thrombocytopenia in whole blood.14,15
  • Various animal and research models.16-20

Multiplate outperforms genotyping and other platelet phenotyping methods

The PEGASUS-PCI study by Siller-Matula et al. (2012)21 compared the diagnostic accuracy of genotyping vs. phenotyping for the prediction of ischemic events in patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) with drug-eluting stents.

ROC curve analysis demonstrated that platelet aggregation assessed by Multiplate [ADPtest and ADPtestHS] was the best predictor of stent thrombosis (ST) (c-index = 0.78 and 0.9 respectively); whereas other assays (VASP, PFA-100 and Impact-R) failed to distinguish between patients with and without ST (c-index p values n.s.). Furthermore, Multiplate demonstrated higher specificity and sensitivity than VASP, PFA-100, Impact-R, and genotyping of the CYP2C19*2 carrier status.

Test   
c-index
(95% CI)        
P   
Sensitivity %       Specificity %  Positive   predictive value %
Negative      predictive value %

Multiplate ADPtest HS (U)

0.90
(0.86-0.95)

<0.001  

90

83

13

100

Multiplate ADPtest (U)

0.78
(0.63-0.94)

0.002

70

67

7

100

VASP (% PRI)

0.62
(0.46-0.79)

0.204

70

38

3

98

PFA-100: CADP-CT(s)

0.66
(0.48-0.84)

0.084

70

61

4

98

Impact-R: ADP (SC %)

0.62
(0.47-0.76)

0.205

90

36

3

98

CYP2C19*2

0.56
(0.32-0.69)

0.950

30

71

3

93

Adapted from Siller-Matula, J.M. et al. (2012)

Kaplan-Meier curve analysis shows early separation of stent thrombosis event rates between clopidogrel poor-responders (MEA aggregation ≥ 48 U, 12.5%) compared with regular or ultra-responders (aggregation < 48 U, 0.3%; P < 0.001) for Multiplate (Fig. A) but not for CYP2C19 genotyping (Fig. B).

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Guidelines

Multiplate® analysis is included in the latest Clinical and Laboratory Standards Institute guideline on platelet function testing (H58-A).22

References

  1. Awidi, A. et al. (2009). Comparison of platelet aggregation using light transmission and multiple electrode aggregometry in Glanzmann thrombasthenia. Platelets. Aug;20(5):297-301.
  2.  Stemberger M., E. S., Al Khatib A., Spannagl M., Calatzis A., Lison S. (2012). Usefulness of Multiple Electrode Aggregometry (MEA) for the detection of inherited platelet disorders. Schattauer Hämostaseologie 1, ED12-17.
  3. Valarche, V. et al. (2011). Multiplate whole blood impedance aggregometry: a new tool for von Willebrand disease. J Thromb Haemost. Aug;9(8):1645-7.
  4. Morel-Kopp, et al. (2012). Validation of whole blood impedance aggregometry as a new diagnostic tool for HIT. J Thromb Haemost. Mar;107(3): 575-583.
  5. Galea, V., Khaterchi, A., Robert, F., Gerotziafas, G., Hatmi, M., Elalamy, I. (2012). Heparin-induced multiple lectrode aggregometry is a promising and useful functional tool for heparin-induced thrombocytopenia diagnosis: Confirmation in a prospective study. Platelets. Sep 20. [Epub ahead of print]
  6. Awidi, A. et al. (2009). Platelets. 20(5):297-301.
  7. Stemberger, M. et al. (2012). Hämostaseologie. 32 1: A2-A107 ED12-7.
  8. Jambor, C. et al. (2009). Anesth Analg;109:25–31.
  9. Siller-Matula, J.M. et al. (2009). Thromb Haemost. 102(2):397-403
  10. Bernlochner, I. et al. (2013). Thromb Haemost. 109(3):517-24.
  11. Ranucci, M. et al. (2011). Ann Thorac Surg. 41(1):123-9.
  12. Weber, C.F. et al. (2012). Anesthesiology. 117(3):531-47.
  13. Valarche, V. et al. (2011). J Thromb Haemost. 9(8):1645-7.
  14. Morel-Kopp, M.C. et al. (2012). Thromb Haemost. 107(3):575-83.
  15. Galea, V. et al. (2012). Platelets. DOI: 11.3109/09537104.2012.724736
  16. Kalbantner, K. et al. (2010). Vet J. Aug;185(2):144-51
  17. Baumgarten, A. et al. (2010). Vet Clin Pathol. Jun;39(2):149-56.
  18. Czura, C.J. et al.(2010). Shock. Jun;33(6):608-13.
  19. Kirkeby, A. et al. (2008). Thromb Haemost. Apr;99(4):720-8.
  20. Fröbert, O. et al. (2010). Thromb J. Jun 2;8:11.
  21. Siller-Matula, J.M. et al. (2012) J Thromb Haemost.Apr;10(4):529-42.
  22. Clinical and Laboratory Standards Institute (CLSI) document H58-A. (2008). Platelet Function Testing by Aggregometry; Approved Guideline. ISBN 1-56238-683-2.