Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma

Charles E Wade; Nena Matijevic; Yao-Wei W Wang; Erika G Rodriguez; Ernesto Lopez; Sisse R Ostrowski; Jessica C Cardenas; Lisa A Baer; Tzu-An Chen; Jeffrey S Tomasek; Hanne H Henriksen; Jakob Stensballe; Bryan A Cotton; John B Holcomb; Pär I Johansson

doi:10.1097/SHK.0000000000001149

Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma

Charles E Wade, Nena Matijevic, Yao-Wei W Wang, Erika G Rodriguez, Ernesto Lopez, Sisse R Ostrowski, Jessica C Cardenas, Lisa A Baer, Tzu-An Chen, Jeffrey S Tomasek, Hanne H Henriksen, Jakob Stensballe, Bryan A Cotton, John B Holcomb, Pär I Johansson

Department of Clinical Medicine

3 Citations (Scopus)

Abstract

Introduction:Severe trauma is accompanied by endothelial glycocalyx disruption, which drives coagulopathy, increasing transfusion requirements and death. This syndrome has been termed endotheliopathy of trauma (EOT). Some have suggested EOT results from endothelial cellular damage and apoptosis. Endothelial microvesicles (EMVs) represent cellular damage. We hypothesized that EOT is associated with endothelial damage and apoptosis resulting in an increase in circulating EMVs.Methods:Prospective, observational study enrolling severely injured patients. Twelve patients with EOT, based on elevated Syndecan-1 levels, were matched with 12 patients with lower levels, based on Injury Severity Score (ISS), abbreviated injury scale profile, and age. Thrombelastography and plasma levels of biomarkers indicative of cellular damage were measured from blood samples collected on admission. EMVs were determined by flow cytometry using varied monoclonal antibodies associated with endothelial cells. Significance was set at P < 0.05.Results:Admission physiology and ISS (29 vs. 28) were similar between groups. Patients with EOT had higher Syndecan-1, 230 (158, 293) vs. 19 (14, 25) ng/mL, epinephrine, and soluble thrombomodulin levels. Based on thrombelastography, EOT had reductions in clot initiation, amplification, propagation and strength, and a greater frequency of transfusion, 92% vs. 33%. There were no differences in EMVs irrespective of the antibody used. Plasma norepinephrine, sE-selectin, sVE-cadherin, and histone-complexed DNA fragments levels were similar.Conclusion:In trauma patients presenting with EOT, endothelial cellular damage or apoptosis does not seem to occur based on the absence of an increase in EMVs and other biomarkers. Thus, this suggests endothelial glycocalyx disruption is the underlying primary cause of EOT.

Original language	English
Journal	Shock
Volume	51
Issue number	2
Pages (from-to)	180-184
ISSN	1073-2322
DOIs	https://doi.org/10.1097/SHK.0000000000001149
Publication status	Published - 2019

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Wade, C. E., Matijevic, N., Wang, Y.-W. W., Rodriguez, E. G., Lopez, E., Ostrowski, S. R., Cardenas, J. C., Baer, L. A., Chen, T.-A., Tomasek, J. S., Henriksen, H. H., Stensballe, J., Cotton, B. A., Holcomb, J. B., & Johansson, P. I. (2019). Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma. Shock, 51(2), 180-184. https://doi.org/10.1097/SHK.0000000000001149

Wade, CE, Matijevic, N, Wang, Y-WW, Rodriguez, EG, Lopez, E, Ostrowski, SR, Cardenas, JC, Baer, LA, Chen, T-A, Tomasek, JS, Henriksen, HH, Stensballe, J, Cotton, BA, Holcomb, JB & Johansson, PI 2019, 'Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma', Shock, vol. 51, no. 2, pp. 180-184. https://doi.org/10.1097/SHK.0000000000001149

@article{911b2c720c6b4a1f8cdd1e7cbe2a1e79,

title = "Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma",

abstract = "Introduction:Severe trauma is accompanied by endothelial glycocalyx disruption, which drives coagulopathy, increasing transfusion requirements and death. This syndrome has been termed endotheliopathy of trauma (EOT). Some have suggested EOT results from endothelial cellular damage and apoptosis. Endothelial microvesicles (EMVs) represent cellular damage. We hypothesized that EOT is associated with endothelial damage and apoptosis resulting in an increase in circulating EMVs.Methods:Prospective, observational study enrolling severely injured patients. Twelve patients with EOT, based on elevated Syndecan-1 levels, were matched with 12 patients with lower levels, based on Injury Severity Score (ISS), abbreviated injury scale profile, and age. Thrombelastography and plasma levels of biomarkers indicative of cellular damage were measured from blood samples collected on admission. EMVs were determined by flow cytometry using varied monoclonal antibodies associated with endothelial cells. Significance was set at P < 0.05.Results:Admission physiology and ISS (29 vs. 28) were similar between groups. Patients with EOT had higher Syndecan-1, 230 (158, 293) vs. 19 (14, 25) ng/mL, epinephrine, and soluble thrombomodulin levels. Based on thrombelastography, EOT had reductions in clot initiation, amplification, propagation and strength, and a greater frequency of transfusion, 92% vs. 33%. There were no differences in EMVs irrespective of the antibody used. Plasma norepinephrine, sE-selectin, sVE-cadherin, and histone-complexed DNA fragments levels were similar.Conclusion:In trauma patients presenting with EOT, endothelial cellular damage or apoptosis does not seem to occur based on the absence of an increase in EMVs and other biomarkers. Thus, this suggests endothelial glycocalyx disruption is the underlying primary cause of EOT.",

author = "Wade, {Charles E} and Nena Matijevic and Wang, {Yao-Wei W} and Rodriguez, {Erika G} and Ernesto Lopez and Ostrowski, {Sisse R} and Cardenas, {Jessica C} and Baer, {Lisa A} and Tzu-An Chen and Tomasek, {Jeffrey S} and Henriksen, {Hanne H} and Jakob Stensballe and Cotton, {Bryan A} and Holcomb, {John B} and Johansson, {P{\"a}r I}",

year = "2019",

doi = "10.1097/SHK.0000000000001149",

language = "English",

volume = "51",

pages = "180--184",

journal = "Shock",

issn = "1073-2322",

publisher = "Lippincott Williams & Wilkins",

number = "2",

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TY - JOUR

T1 - Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma

AU - Wade, Charles E

AU - Matijevic, Nena

AU - Wang, Yao-Wei W

AU - Rodriguez, Erika G

AU - Lopez, Ernesto

AU - Ostrowski, Sisse R

AU - Cardenas, Jessica C

AU - Baer, Lisa A

AU - Chen, Tzu-An

AU - Tomasek, Jeffrey S

AU - Henriksen, Hanne H

AU - Stensballe, Jakob

AU - Cotton, Bryan A

AU - Holcomb, John B

AU - Johansson, Pär I

PY - 2019

Y1 - 2019

N2 - Introduction:Severe trauma is accompanied by endothelial glycocalyx disruption, which drives coagulopathy, increasing transfusion requirements and death. This syndrome has been termed endotheliopathy of trauma (EOT). Some have suggested EOT results from endothelial cellular damage and apoptosis. Endothelial microvesicles (EMVs) represent cellular damage. We hypothesized that EOT is associated with endothelial damage and apoptosis resulting in an increase in circulating EMVs.Methods:Prospective, observational study enrolling severely injured patients. Twelve patients with EOT, based on elevated Syndecan-1 levels, were matched with 12 patients with lower levels, based on Injury Severity Score (ISS), abbreviated injury scale profile, and age. Thrombelastography and plasma levels of biomarkers indicative of cellular damage were measured from blood samples collected on admission. EMVs were determined by flow cytometry using varied monoclonal antibodies associated with endothelial cells. Significance was set at P < 0.05.Results:Admission physiology and ISS (29 vs. 28) were similar between groups. Patients with EOT had higher Syndecan-1, 230 (158, 293) vs. 19 (14, 25) ng/mL, epinephrine, and soluble thrombomodulin levels. Based on thrombelastography, EOT had reductions in clot initiation, amplification, propagation and strength, and a greater frequency of transfusion, 92% vs. 33%. There were no differences in EMVs irrespective of the antibody used. Plasma norepinephrine, sE-selectin, sVE-cadherin, and histone-complexed DNA fragments levels were similar.Conclusion:In trauma patients presenting with EOT, endothelial cellular damage or apoptosis does not seem to occur based on the absence of an increase in EMVs and other biomarkers. Thus, this suggests endothelial glycocalyx disruption is the underlying primary cause of EOT.

AB - Introduction:Severe trauma is accompanied by endothelial glycocalyx disruption, which drives coagulopathy, increasing transfusion requirements and death. This syndrome has been termed endotheliopathy of trauma (EOT). Some have suggested EOT results from endothelial cellular damage and apoptosis. Endothelial microvesicles (EMVs) represent cellular damage. We hypothesized that EOT is associated with endothelial damage and apoptosis resulting in an increase in circulating EMVs.Methods:Prospective, observational study enrolling severely injured patients. Twelve patients with EOT, based on elevated Syndecan-1 levels, were matched with 12 patients with lower levels, based on Injury Severity Score (ISS), abbreviated injury scale profile, and age. Thrombelastography and plasma levels of biomarkers indicative of cellular damage were measured from blood samples collected on admission. EMVs were determined by flow cytometry using varied monoclonal antibodies associated with endothelial cells. Significance was set at P < 0.05.Results:Admission physiology and ISS (29 vs. 28) were similar between groups. Patients with EOT had higher Syndecan-1, 230 (158, 293) vs. 19 (14, 25) ng/mL, epinephrine, and soluble thrombomodulin levels. Based on thrombelastography, EOT had reductions in clot initiation, amplification, propagation and strength, and a greater frequency of transfusion, 92% vs. 33%. There were no differences in EMVs irrespective of the antibody used. Plasma norepinephrine, sE-selectin, sVE-cadherin, and histone-complexed DNA fragments levels were similar.Conclusion:In trauma patients presenting with EOT, endothelial cellular damage or apoptosis does not seem to occur based on the absence of an increase in EMVs and other biomarkers. Thus, this suggests endothelial glycocalyx disruption is the underlying primary cause of EOT.

U2 - 10.1097/SHK.0000000000001149

DO - 10.1097/SHK.0000000000001149

M3 - Journal article

C2 - 29621120

SN - 1073-2322

VL - 51

SP - 180

EP - 184

JO - Shock

JF - Shock

IS - 2

ER -

Absences of Endothelial Microvesicle Changes in the Presence of the Endotheliopathy of Trauma

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