Comparison of platelet aggregation using light transmission and multiple electrode aggregometry in Glanzmann thrombasthenia

Awidi, Abdalla; Maqablah, Ahmad; Dweik, Manar; Bsoul, Nazzal; Abu‐Khader, Ahmad

doi:10.1080/09537100903006246

Cited by 37 publications

(23 citation statements)

References 27 publications

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“…Platelet aggregation was measured with MEA as previously described [10,17]. For each of the three samples, the tests ADP, ASPI, TRAP and COL were used.…”

Section: Analysesmentioning

confidence: 99%

In vitroassessment of platelet concentrates with multiple electrode aggregometry

et al. 2014

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Storage impairs platelet function. It was hypothesized that multiple electrode aggregometry in vitro could be used to follow aggregability in platelet concentrates over time and that the results predict the efficacy of platelet transfusion in an ex vivo transfusion model. In vitro platelet aggregability was assessed in apheresis and pooled buffy coat platelet concentrates (BCs) (n = 13 each) using multiple electrode aggregometry with different agonists 1, 3, 5 and 7 days after preparation. In the ex vivo transfusion model, whole blood samples from nine healthy volunteers were collected every second day. The samples were supplemented with stored platelets (+146 × 10(9) × l(-1)) from the same unit 1, 3, 5 and 7 days after preparation. Platelet aggregability was assessed in the concentrate and in the whole blood samples before and after platelet supplementation. There was a continuous reduction in in vitro platelet aggregability over time in both apheresis and pooled BCs. The same pattern was observed after ex vivo addition of apheresis and pooled BCs to whole blood samples. The best correlation between in vitro aggregability and changes in aggregation after addition was achieved with collagen as agonist (r = 0.67, p < 0.001). In conclusion, multiple electrode aggregometry can be used to follow aggregability in platelet concentrates in vitro, and the results predict with moderate accuracy changes in aggregation after addition of platelet concentrate to whole blood samples.

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“…Platelet aggregation was measured with MEA as previously described [10,17]. For each of the three samples, the tests ADP, ASPI, TRAP and COL were used.…”

Section: Analysesmentioning

confidence: 99%

In vitroassessment of platelet concentrates with multiple electrode aggregometry

et al. 2014

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“…The role of PGE 2 in human atherosclerotic plaque 163 to glycoprotein Ib [27,28], it could not be excluded by these measurements that PGE 2 influences platelet adhesion and thrombus formation under flow conditions. To address this possibility, we performed flow experiments, simulating flow conditions in moderately stenosed coronary arteries.…”

Section: Discussionmentioning

confidence: 89%

The role of PGE2 in human atherosclerotic plaque on platelet EP3 and EP4 receptor activation and platelet function in whole blood

Schober

Khandoga

Dwivedi

et al. 2011

J Thromb Thrombolysis

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Atherosclerosis has an important inflammatory component. Macrophages accumulating in atherosclerotic arteries produce prostaglandin E(2) (PGE(2)), a main inflammatory mediator. Platelets express inhibitory receptors (EP(2), EP(4)) and a stimulatory receptor (EP(3)) for this prostanoid. Recently, it has been reported in ApoE(-/-) mice that PGE(2) accumulating in inflammatory atherosclerotic lesions might contribute to atherothrombosis after plaque rupture by activating platelet EP(3), and EP(3) blockade has been proposed to be a promising new approach in anti-thrombotic therapy. The aim of our investigation was to study the role of PGE(2) in human atherosclerotic plaques on human platelet function and thrombus formation. Plaque PGE(2) might either activate or inhibit platelets depending on stimulation of either EP(3) or EP(4), respectively. We found that the two EP(3)-antagonists AE5-599 (300 nM) and AE3-240 (300 nM) specifically and completely inhibited the synergistic effect of the EP(3)-agonist sulprostone on U46619-induced platelet aggregation in blood. However, these two EP(3)-antagonists neither inhibited atherosclerotic plaque-induced platelet aggregation, GPIIb/IIIa exposure, dense and alpha granule secretion in blood nor reduced plaque-induced platelet thrombus formation under arterial flow. The EP(4)-antagonist AE3-208 (1-3 μM) potentiated in combination with PGE(2) (1 μM) ADP-induced aggregation, demonstrating that PGE(2) enhances platelet aggregation when the inhibitory EP(4)-receptor is inactivated. However, plaque-induced platelet aggregation was not augmented after platelet pre-treatment with AE3-208, indicating that plaque PGE(2) does not stimulate the EP(4)-receptor. We found that PGE(2) was present in plaques only at very low levels (15 pg PGE(2)/mg plaque). We conclude that PGE(2) in human atherosclerotic lesions does not modulate (i.e. stimulate or inhibit) atherothrombosis in blood after plaque rupture.

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“…For example, MEA was used to investigate the inherited bleeding disorder Glanzmann's thrombasthenia where markedly reduced responses to a number of platelet-aggregating agents were evident, in the same way as seen with LTA [22,23]. The approach also proved as useful as LTA for measuring the degree of inhibition of platelet aggregation by the antiplatelet agents aspirin and clopidogrel in preoperative patients scheduled for elective cardiac surgery [24].…”

Section: Multiplate Electrode Aggregometrymentioning

confidence: 99%

Novel Strategies for Assessing Platelet Reactivity

Algahtani

Heptinstall

2016

Future Cardiol.

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There are many approaches to assessing platelet reactivity and many uses for such measurements. Initially, measurements were based on the ability of platelets separated from other blood cells to aggregate together following activation with an appropriate 'aggregating agent'. Later, measurements of platelet aggregation in blood itself were performed, and this led to a point-of-care approach to platelet function testing. Measurement of secretory activity through the appearance of the activation marker Pselectin on platelets now provides an alternative approach, which enables remote testing. Measurement of vasodilator-stimulated phosphoprotein phosphorylation is also moving toward application in situations remote from the testing laboratory. Here we provide an overview of the various approaches that are now available, assess their advantages and disadvantages, and describe some of the clinical situations in which they are being used. Keywordsaspirin, flow cytometry, light transmission aggregometry (LTA), multiplate electrode aggregometry (MEA), P-selectin, P2Y12 antagonists, platelet aggregation, platelet reactivity, VASP phosphorylation, VerifyNow Platelet reactivity is a broad term indicating the degree of the response of blood platelets to an external stimulus, usually an 'aggregating agent'. Platelet reactivity can be measured in many different ways and the purpose of this review is to summarize the approaches, with an emphasis on the newer approaches that are becoming available.Platelets play an important role in the hemostatic process [1,2]. They contribute to the formation of a hemostatic plug that serves to prevent blood loss from injured blood vessels. The hemostatic plug contains thousands of platelets that have aggregated together within a network of fibrin. However, platelets also contribute to the generation of a thrombotic mass in a coronary or cerebral artery or in an artificial stent leading to blockage and resulting in conditions such as heart attack, stroke and stent thrombosis [3,4]. A thrombus is also composed of platelet aggregates within a fibrin network. So thrombus formation can thus be considered to be hemostasis in the wrong place.

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Comparison of platelet aggregation using light transmission and multiple electrode aggregometry in Glanzmann thrombasthenia

Cited by 37 publications

References 27 publications

In vitroassessment of platelet concentrates with multiple electrode aggregometry

In vitroassessment of platelet concentrates with multiple electrode aggregometry

The role of PGE2 in human atherosclerotic plaque on platelet EP3 and EP4 receptor activation and platelet function in whole blood

Novel Strategies for Assessing Platelet Reactivity

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