Thrombelastographic measures of clot propagation: a comparison of alpha with the maximum rate of thrombus generation

Ellis, Truitt C.; Nielsen, Vance G.; Marques, Marisa B.; Kirklin, James K.

doi:10.1097/mbc.0b013e3280111a8e

Cited by 42 publications

(35 citation statements)

References 11 publications

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“…We found two additional studies using the same methodology we used and reporting on reference normal values. Ellis et al (33), investigating clot propagation, reported on 33 normal individuals ranging in age from 18 to 65 years and using both plasma and whole blood. Another study by Chan et al (34) reported normal values in a pediatric population of 100 children undergoing surgery.…”

Section: Discussionmentioning

confidence: 99%

Normal range values for thromboelastography in healthy adult volunteers

Scarpelini¹,

Rhind²,

Nascimento³

et al. 2009

Braz J Med Biol Res

153

140

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Section: Discussionmentioning

confidence: 99%

Normal range values for thromboelastography in healthy adult volunteers

Scarpelini¹,

Rhind²,

Nascimento³

et al. 2009

Braz J Med Biol Res

153

140

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“…and maximum clot firmness with new dynamic parameters such as maximum velocity of clot formation and the time to maximum velocity of clot formation [8,13].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of coagulation kinetics using thromboelastometry—methodologic influence of activator and test medium

et al. 2010

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Introduction: Renewed interest has arisen in the use of thromboelastography/thromboelastometry in evaluating coagulation kinetics. The test medium, type of activator and its concentration may influence the interpretation of coagulation kinetics. This study aimed to investigate methodological influences of activator and test medium on thromboelastometric parameters of coagulation kinetics. Methods: Dynamic clot formation was evaluated by thromboelastometry using whole blood (WB), platelet rich plasma or platelet poor plasma employing different concentrations of extrinsic (tissue factor) and contact activator (synthasil) and with variable concentrations of phospholipids. Results: Plasma samples displayed prolonged clot initiation and enhanced clot propagation compared to WB. Clot firmness was markedly reduced in platelet poor plasma as compared to platelet rich plasma and whole blood. Increasing concentration of activator shortened the clot initiation and increased the velocity of clot propagation whereas terminal clot firmness remained unaffected. Platelets accelerated clot propagation and raised clot firmness. Phospholipids shortened the time of clot initiation and increased velocity of propagation, while clot firmness remained unchanged. Conclusion: Our results demonstrate that evaluation of coagulation kinetics using thromboelastometry vary according to the composition of the test medium, type-and concentration of activator, as well as the presence and concentration of phospholipids in the test reagent.Response to Reviewers: Response to reviewers.First and foremost, thank you very much for the positive and constructive review. We have tried our best to answer all questions and revised the manuscript accordingly.Reviewer #1: This is a nice methodological paper about the ROTEM device, which is well written by an experienced group.Minor comments 1) P3 , line 41: physiologically -corrected 2) P4, line 28: significantly -corrected 3) Please indicate molar concentrations of synthasil and Innovin, if possible Unfortunately, it is not possible to use molar concentrations. We are working on a detailed (including molar concentrations and activity) examination of various tissue factor sources, however that reached beyond the scope of the present study. 4) P9: followed -corrected 5) P11, line 38: please add . "in vitro [33] as well as coagulation activation in vivo, when the blood is only re-calcified [PMID: 16420574]" Thank you for this excellent point, we have added accordingly. 6) I am not sure whether I could reproduce the phospholipid preparation, maybe a graphical scheme could be helpfulWe have slightly rephrased 7) As many users of the ROTEM probably will not have the extra software, please consider providing graphical presentations of the CT and /or alpha angle in addition to MaxVel, which is a derived variable CT has been included. We found it too excessive to also show alpha. 8) Refs 21 and 26 appear identical to meWe have corrected the reference list accordingly Reviewer #2: The paper by Sorensen et ...

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“…In contrast to conventional TEG parameters, it also has the advantage of measuring the functionally relevant 133,134 clot resistance directly. 135 We also note a number of approaches to the development of coagulometry based on the measurement of the passive electrical properties of the sample, [136][137][138][139][140][141][142] a strategy that we ourselves have found useful, 143 with radio-frequency measurements of cellular properties having a particular value. [144][145][146][147] Finally, fibrin scatters light much more than does fibrinogen such that turbidimetry is often used to detect its formation (e.g.…”

Section: The Clot Lifespan Modelmentioning

confidence: 99%

The simultaneous occurrence of both hypercoagulability and hypofibrinolysis in blood and serum during systemic inflammation, and the roles of iron and fibrin(ogen)

Kell

Pretorius

2014

Integrative Biology

127

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Although the two phenomena are usually studied separately, we summarise a considerable body of literature to the effect that a great many diseases involve (or are accompanied by) both an increased tendency for blood to clot (hypercoagulability) and the resistance of the clots so formed (hypofibrinolysis) to the typical, 'healthy' or physiological lysis. We concentrate here on the terminal stages of fibrin formation from fibrinogen, as catalysed by thrombin. Hypercoagulability goes hand in hand with inflammation, and is strongly influenced by the fibrinogen concentration (and vice versa); this can be mediated via interleukin-6. Poorly liganded iron is a significant feature of inflammatory diseases, and hypofibrinolysis may change as a result of changes in the structure and morphology of the clot, which may be mimicked in vitro, and may be caused in vivo, by the presence of unliganded iron interacting with fibrin(ogen) during clot formation. Many of these phenomena are probably caused by electrostatic changes in the iron-fibrinogen system, though hydroxyl radical (OH ) formation can also contribute under both acute and (more especially) chronic conditions. Many substances are known to affect the nature of fibrin polymerised from fibrinogen, such that this might be seen as a kind of bellwether for human or plasma health. Overall, our analysis demonstrates the commonalities underpinning a variety of pathologies as seen in both hypercoagulability and hypofibrinolysis, and offers opportunities for both diagnostics and therapies.

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Thrombelastographic measures of clot propagation: a comparison of alpha with the maximum rate of thrombus generation

Cited by 42 publications

References 11 publications

Normal range values for thromboelastography in healthy adult volunteers

Normal range values for thromboelastography in healthy adult volunteers

Evaluation of coagulation kinetics using thromboelastometry—methodologic influence of activator and test medium

The simultaneous occurrence of both hypercoagulability and hypofibrinolysis in blood and serum during systemic inflammation, and the roles of iron and fibrin(ogen)

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