scholarly journals The assessment of platelet function using multiple electrode aggregometry in practical procedures in anaesthesia

2018 ◽  
Vol 50 (3) ◽  
pp. 210-214 ◽  
Author(s):  
Jan Pluta ◽  
Barbara Nicińska ◽  
Michał Ciurzyński ◽  
Janusz Trzebicki
Keyword(s):  
Platelet Function ◽  
Multiple Electrode Aggregometry ◽  
Multiple Electrode

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
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Extracorporeal Circulation ◽  
Inverse Correlation ◽  
Negative Effects ◽  
Multiple Electrode Aggregometry ◽  
Observational Cohort ◽  
And Function ◽  
The Impact ◽  
Multiple Electrode

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.

Prevalence of Aspirin Non-Response in Out-Patients and In-Patients as Determined by Multiple Electrode Aggregometry.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 879-879 ◽  
Author(s):  
Andreas Calatzis ◽  
Klaus-Werner von Pape ◽  
Armin J. Reininger ◽  
Franz Theisen ◽  
Michael Spannagl
Keyword(s):  
Platelet Function ◽  
Blood Donors ◽  
Venous Blood ◽  
High Sensitivity ◽  
Direct Thrombin Inhibitor ◽  
Thrombin Inhibitor ◽  
Similar Distribution ◽  
Monitoring Method ◽  
Multiple Electrode Aggregometry ◽  
Multiple Electrode

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.

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