Whole Blood Multiple Electrode Aggregometry Is a Reliable Point-of-Care Test of Aspirin-Induced Platelet Dysfunction

2009 ◽  
Vol 109 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Csilla Jámbor ◽  
Christian F. Weber ◽  
Konstanze Gerhardt ◽  
Wulf Dietrich ◽  
Michael Spannagl ◽  
...  
Author(s):  
Alexander Kutz ◽  
Pierre Hausfater ◽  
Michael Oppert ◽  
Murat Alan ◽  
Eva Grolimund ◽  
...  

AbstractProcalcitonin (PCT) is increasingly being used for the diagnostic and prognostic work up of patients with suspected infections in the emergency department (ED). Recently, B·R·A·H·M·S PCT direct, the first high sensitive point-of-care test (POCT), has been developed for fast PCT measurement on capillary or venous blood samples.This is a prospective, international comparison study conducted in three European EDs. Consecutive patients with suspicion of bacterial infection were included. Duplicate determination of PCT was performed in capillary (fingertip) and venous whole blood (EDTA), and compared to the reference method. The diagnostic accuracy was evaluated by correlation and concordance analyses.Three hundred and three patients were included over a 6-month period (60.4% male, median age 65.2 years). The correlation between capillary or venous whole blood and the reference method was excellent: rThis study found a high diagnostic accuracy and a faster time to result of B·R·A·H·M·S PCT direct in the ED setting, allowing shortening time to therapy and a more wide-spread use of PCT.


Author(s):  
Evangelos Giannitsis ◽  
Hannsjörg Baum ◽  
Thomas Bertsch ◽  
Martin Juchum ◽  
Margit Müller-Bardorff ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5362-5362 ◽  
Author(s):  
Michael Spannagl ◽  
Csilla Jambor

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> 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<0.05). Patients on clopidogrel had a significantly lower ADP induced aggregation (41+−30 vs. 86 +−33) compared to controls (p<0.05), and patients on aspirin had a significantly lower arachidonic acid induced aggregation compared to controls (23+−28 vs. 94 +− 35, p<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<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.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1105-1105
Author(s):  
Vassiliki Galea ◽  
Grigoris T Gerotziafas ◽  
Mouna Sassi ◽  
Jawed Fareed ◽  
Jeanine M. Walenga ◽  
...  

Abstract Abstract 1105 Introduction: Heparin induced thrombocytopenia (HIT) is the major complication of heparin treatment but is less frequent in patients treated with low molecular weight heparins (LMWHs) than with unfractionated heparin (UFH). Cross immunological reactions of LMWHs with HIT antibodies from patients treated with UFH is a common finding. The immunological profile is among the criteria for similarity of a generic LMWHs. The cross reactivity of generic LMWHs with HIT antibodies has yet to be compared with the innovator product. Aim: To compare the profile of platelet aggregation induced by HIT antibodies in the presence of Lovenoxâ or seven generic enoxaparins. Methods: Platelet activation by HIT antibodies in the presence of UFH (Héparine Choay, France), branded enoxaparin (Lovenox®) and 7 generics (Novex®, Enoxa®, Dilutol®, Versa®, Cutenox®, Loparin®, Fibrinox®) was assessed by Multiple Electrode Aggregometry (MEA, Multiplate, Dynabyte, Germany) according to previously published assay1. Briefly, whole blood (340 μl) from 5 individual healthy donors was incubated with pooled platelet poor plasma (200 μl) from well characterised HIT positive patients and 40 μl of UFH or Lovenox® or generic enoxaparins yielding a final concentration of 1 anti-Xa IU/ml. Platelet aggregation was recorded over 15 min and the area under the curve (AUC, AU*min) was determined. Results: UFH and branded enoxaparin showed high cross reactivity with HIT antibodies in 4 out of 5 experiments. All of the 7 generic enoxaparins gave also a high positive cross-reactivity but the intensity of platelet aggregation varied. The magnitude of the response was classified as follows: Versa® > Enoxa® > Lovenox® > Novex® > Fibrinox® > Cutenox® > Loparin® > Dilutol®. In one experiment Lovenox® showed border-line cross-reactivity with HIT antibodies. Among generic enoxaparins Versa® showed the same extent of cross reactivity as that of Lovenox®. The other generic enoxaparins did not cross react with HIT antibodies. Conclusions: This is the first study that provides key data on the comparison of in vitro cross reactivity with HIT antibodies of generic enoxaparins versus Lovenox®. In the presence of a cross-reactivity of the originator enoxaparin with heparin-PF4-IgG immune complex, there is also a cross-reactivity of the 7 studied generic enoxaparins. The intensity of cross-reactivity is an additional criterion for comparison of generic LMWHs and the originator one. The differences on the intensity of cross reactivity follow the same pattern in the case of border line cross reactivity of the originator enoxaparin. References 1. I. Elalamy, V. Galea, M. Hatmi, G. Gerotziafas. Heparin-Induced Multiple Electrode Aggregometry: A potential tool for improvement of Heparin-Induced Thrombocytopenia diagnosis. JTH 2009;7:1932-4. Figure 1. Cross-reactivity of branded and generic forms of enoxaparin. Whole blood platelet aggregation of a HIT positive patient with 4 different blood donors. Values of AUC are expressed as mean ± sd. *p<0.05 versus Lovenox®. Disclosures: No relevant conflicts of interest to declare.


2018 ◽  
Vol 12 (8) ◽  
pp. e0006536 ◽  
Author(s):  
Joseph Lykins ◽  
Xuan Li ◽  
Pauline Levigne ◽  
Ying Zhou ◽  
Kamal El Bissati ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document