Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.

<h4>Background</h4>Elevated cardiac troponin I (cTnI) is frequently observed in patients with severe sepsis and septic shock. However, the mechanisms underlying cTnI release in these patients are still unknown. To date no data regarding coagulation disturbances as a possible mechanism fo...

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Autores principales:	David R Altmann, Wolfgang Korte, Micha T Maeder, Thomas Fehr, Philipp Haager, Hans Rickli, Gian-Reto Kleger, Regulo Rodriguez, Peter Ammann
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/addde58007f54a05af569b4a57c0e5ba
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spelling	oai:doaj.org-article:addde58007f54a05af569b4a57c0e5ba2021-11-25T06:26:10ZElevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.1932-620310.1371/journal.pone.0009017https://doaj.org/article/addde58007f54a05af569b4a57c0e5ba2010-02-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20140242/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Elevated cardiac troponin I (cTnI) is frequently observed in patients with severe sepsis and septic shock. However, the mechanisms underlying cTnI release in these patients are still unknown. To date no data regarding coagulation disturbances as a possible mechanism for cTnI release during sepsis are available.<h4>Methodology/principal findings</h4>Consecutive patients with systemic inflammatory response syndrome (SIRS), sepsis or septic shock without evidence of an acute coronary syndrome were analyzed. Coagulation parameters (clotting time (CT), clot formation time (CFT), maximum clot firmness (MCF), alpha-angle) were assessed in native whole blood samples, and using specific activators to evaluate the extrinsic and intrinsic as well as the fibrin component of the coagulation pathway with the use of rotational thrombelastometry (ROTEM). Thirty-eight patients were included and 22 (58%) were cTnI-positive. Baseline characteristics between TnI-positive and -negative patients were similar. The CT, CFT, MCF and the alpha-angle were similar between the groups with trends towards shorter CT in the extrinsic and fibrin activation.<h4>Conclusions/significance</h4>We found no differences in coagulation parameters analyzed with rotational thrombelastometry between cTnI-positive and -negative patients with SIRS, severe sepsis, and septic shock. These findings suggest that pathophysiological mechanisms other than thrombus-associated myocardial damage might play a major role, including reversible myocardial membrane leakage and/or cytokine mediated apoptosis in these patients.David R AltmannWolfgang KorteMicha T MaederThomas FehrPhilipp HaagerHans RickliGian-Reto KlegerRegulo RodriguezPeter AmmannPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 2, p e9017 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q David R Altmann Wolfgang Korte Micha T Maeder Thomas Fehr Philipp Haager Hans Rickli Gian-Reto Kleger Regulo Rodriguez Peter Ammann Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
description	<h4>Background</h4>Elevated cardiac troponin I (cTnI) is frequently observed in patients with severe sepsis and septic shock. However, the mechanisms underlying cTnI release in these patients are still unknown. To date no data regarding coagulation disturbances as a possible mechanism for cTnI release during sepsis are available.<h4>Methodology/principal findings</h4>Consecutive patients with systemic inflammatory response syndrome (SIRS), sepsis or septic shock without evidence of an acute coronary syndrome were analyzed. Coagulation parameters (clotting time (CT), clot formation time (CFT), maximum clot firmness (MCF), alpha-angle) were assessed in native whole blood samples, and using specific activators to evaluate the extrinsic and intrinsic as well as the fibrin component of the coagulation pathway with the use of rotational thrombelastometry (ROTEM). Thirty-eight patients were included and 22 (58%) were cTnI-positive. Baseline characteristics between TnI-positive and -negative patients were similar. The CT, CFT, MCF and the alpha-angle were similar between the groups with trends towards shorter CT in the extrinsic and fibrin activation.<h4>Conclusions/significance</h4>We found no differences in coagulation parameters analyzed with rotational thrombelastometry between cTnI-positive and -negative patients with SIRS, severe sepsis, and septic shock. These findings suggest that pathophysiological mechanisms other than thrombus-associated myocardial damage might play a major role, including reversible myocardial membrane leakage and/or cytokine mediated apoptosis in these patients.
format	article
author	David R Altmann Wolfgang Korte Micha T Maeder Thomas Fehr Philipp Haager Hans Rickli Gian-Reto Kleger Regulo Rodriguez Peter Ammann
author_facet	David R Altmann Wolfgang Korte Micha T Maeder Thomas Fehr Philipp Haager Hans Rickli Gian-Reto Kleger Regulo Rodriguez Peter Ammann
author_sort	David R Altmann
title	Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
title_short	Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
title_full	Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
title_fullStr	Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
title_full_unstemmed	Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
title_sort	elevated cardiac troponin i in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/addde58007f54a05af569b4a57c0e5ba
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Elevated cardiac troponin I in sepsis and septic shock: no evidence for thrombus associated myocardial necrosis.

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