scholarly journals Platelet Function Disturbance During Veno-Venous ECMO in ARDS Patients Assessed by Multiple Electrode Aggregometry—A Prospective, Observational Cohort Study

2019 ◽  
Vol 8 (7) ◽  
pp. 1056 ◽  
Author(s):  
Saskia Wand ◽  
Jan Felix Huber-Petersen ◽  
Joern Schaeper ◽  
Claudia Binder ◽  
Onnen Moerer

Extracorporeal (veno-venous) membrane oxygenation (vvECMO) has been shown to have negative effects on platelet number and function. This study aimed to gain more information about the impact of vvECMO on platelet function assessed by multiple electrode aggregometry (MEA). Twenty patients with the indication for vvECMO were included. Platelet function was analyzed using MEA (Multiplate®) before (T-1), 6 h (T0), one (T1), two (T2), three (T3), and seven (T4) days after the beginning of vvECMO. Median aggregational measurements were already below the normal reference range before vvECMO initiation. Platelet aggregation was significantly reduced 6 h after vvECMO initiation compared to T-1 and spontaneously recovered with a significant increase at T2. Platelet count dropped significantly between T-1 and T0 and continuously decreased between T0 and T4. At T4, ADP-induced platelet aggregation showed an inverse correlation with the paO2 in the oxygenator. Platelet function should be assessed by MEA before the initiation of extracorporeal circulation. Although ECMO therapy led to a further decrease in platelet aggregation after 6 h, all measurements had recovered to baseline on day two. This implies that MEA as a whole blood method might not adequately reflect the changes in platelet function in the later stages of extracorporeal circulation.

2009 ◽  
Vol 102 (08) ◽  
pp. 397-403 ◽  
Author(s):  
Jolanta Siller-Matula ◽  
Ghazaleh Gouya ◽  
Michael Wolzt ◽  
Bernd Jilma

SummarySeveral test systems exist for assessment of platelet function in patients under clopidogrel or aspirin therapy. The objective was to cross-validate the Multiple Electrode Aggregometry (MEA) with three other methods used for determining platelet reactivity under treatment with clopidogrel and aspirin. Platelet function was assessed by the MEA, Vasodilator Stimulated Phosphoprotein (VASP) phosphorylation assay, Platelet Function Analyzer-100 (PFA-100) and the Cone and Platelet Analyzer. Measurements were performed in blood from nine healthy volunteers at baseline, 2, 4, 6 and 72 hours after clopidogrel and aspirin loading. The apparent effect size for clopidogrel and aspirin was greatest for the MEA: treatment induced a 19-fold difference in the arachidonic acid-induced platelet aggregation and an 11-fold difference in the adenosine diphosphate-induced platelet aggregation before/after treatment. For comparison, aspirin and clopidogrel induced only 2.0– to 2.6 -fold changes in other tests (VASP assay, Cone and Platelet Analyzer and PFA-100). Maximal effects were seen 2 hours after aspirin loading and shorter than 72 hours after clopidogrel loading. In conclusion, aspirin and clopidogrel produce stronger signals in the MEA compared to several other methods.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Bernd Jilma ◽  
Florian B Mayr ◽  
Alexander O Spiel ◽  
Patricia G Merlino ◽  
Harold N Marsh ◽  
...  

Background: ARC1779 is an aptamer which blocks the A1 domain binding of the vWF A1 domain to platelet GPIb receptors that is now in development for the treatment of AMI. vWF is increased in the elderly and in the setting of AMI, as reflected in higher vWF levels in circulation and in increased shear-dependent platelet function as measured by the platelet function analyzer (PFA-100) and cone and plate analyzer (IMPACT). Conventional therapy of AMI partially reduces platelet activation and aggregation, but does not address excessive vWF activity or platelet adhesion. Methods: We studied the ex vivo dose response curves for ARC1779 on PFA-100 and IMPACT platelet function tests, agonist-induced platelet aggregation, and vWF activity (free A1 domain sites) of patients with AMI on standard treatment including aspirin and clopidogrel (n=40), young (n=20) and elderly controls (n=20). Results: ARC1779 fully blocked collagen ADP induced platelet plug formation as measured by PFA-100 with an IC100 of ~ 1–2 mcg/mL with citrate anticoagulation, and 3–5 mcg/mL with hirudin anticoagulation. ARC1779 fully blocked shear-dependent platelet adhesion measured by the IMPACT analyzer with an IC100 of ~ 1 mcg/mL with citrate anticoagulation. In contrast to GPIIb/IIIa antagonists, ARC1779 did not inhibit platelet aggregation by ADP, collagen or arachidonic acid at concentrations (10mcg/mL) that fully inhibited vWF dependent platelet function. ARC1779 fully blocked vWF activity ex vivo with an IC90 of ~ 1 mcg/mL in young controls and 6 – 8 mcg/mL in STEMI and NSTEMI patients. Conclusions: ARC1779 potently and specifically inhibits vWF activity and vWF dependent platelet function, even in the setting of AMI where vWF activity is increased. ARC1779 represents a novel therapeutic principle (vWF antagonism) and a novel therapeutic class (aptamers). Potent and specific inhibition of VWF makes ARC1779 a promising development candidate for patients with AMI. Results


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 879-879 ◽  
Author(s):  
Andreas Calatzis ◽  
Klaus-Werner von Pape ◽  
Armin J. Reininger ◽  
Franz Theisen ◽  
Michael Spannagl

Abstract A control of aspirin response is one proposed strategy for an improvement of anti-platelet therapy. Different methods have been proposed for this indication. We evaluated the prevalence of aspirin non-responsiveness in two different cohorts 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 arachidonic acid (0.16 mM, ASPItest, Dynabyte). For the analysis 300 μl of blood are analyzed with the addition of 300 μ 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 Aspirin in the 2 weeks before the analysis, in 76 outpatients taking aspirin 25–300 mg/d (mean 128 mg/d) and 341 cardiovascular in-patients on Aspirin 100 mg qd using the direct thrombin inhibitor Melagatran in a final concentration of 15 μ as the anticoagulant. Results: The distribution of the aggregation values is shown in Fig. 1. The median (min–ax) was 100 (5–159) for the blood donors, 13 (2–71) for the out-patients and 11 (0–145) for the in-patients. When a cut-off of 48 (lower end of a 95% confidence interval for the MEA results of the blood donors) is selected, then 51 of 341 in-patients (15%) would have been stratified as non-responders to the aspirin treatment and 2 of 76 out-patients (2,6%). Discussion: The comparison of the results of aspirin-treated patients and healthy controls (blood donors) reveals a high sensitivity of the new method for the effect of aspirin. 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. The results of the two aspirin-treated cohorts examined shows a similar distribution of aggregation values with an aggregation of less than 30 U in 96% of the out-patients and 80% of the in-patients. Using the cut-off of 48 U (based on the results of the blood donors) more patients would have been stratified as aspirin-resistant in the in-patients compared to the out-patients. The out-patients were members of a cardiovascular sports group and knew long in advance that their platelet function would be analyzed on the particular day. Therefore a high level of compliance in respect to the aspirin intake during the days preceeding the analysis can be expected. In addition the out-patient group was significantly healthier compared to the in-patients. In conclusion multiple electrode aggregometry showed a high sensitivity for aspirin. The rate of non-response to the treatment seems to be influenced by compliance and comorbidities. Prospective trials are required to prove that aspirin-non-response in this particular method is associated with an increased occurrence of arterial thromboembolism. Fig. 1 Fig. 1.


2014 ◽  
Vol 63 (01) ◽  
pp. 021-027 ◽  
Author(s):  
Haitham Mutlak ◽  
Christian Reyher ◽  
Patrick Meybohm ◽  
Nestoras Papadopoulos ◽  
Alexander Hanke ◽  
...  

2008 ◽  
Vol 99 (01) ◽  
pp. 121-126 ◽  
Author(s):  
Siegmund Braun ◽  
Stefan Jawansky ◽  
Wolfgang Vogt ◽  
Julinda Mehilli ◽  
Albert Schömig ◽  
...  

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.


2018 ◽  
Vol 50 (3) ◽  
pp. 210-214 ◽  
Author(s):  
Jan Pluta ◽  
Barbara Nicińska ◽  
Michał Ciurzyński ◽  
Janusz Trzebicki

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