Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data.
To investigate whether acute liver failure (ALF) leads to secondary acute myocardial injury, 100 ALF patients that were retrospectively identified in a single center based on ICD 10 codes and 8 rats from an experimental study that died early after bile duct ligation (BDL) were examined. Creatine kin...
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oai:doaj.org-article:d8b8f4270f9c41118c876f97a5fe48bf2021-12-02T20:19:21ZAcute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data.1932-620310.1371/journal.pone.0256790https://doaj.org/article/d8b8f4270f9c41118c876f97a5fe48bf2021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0256790https://doaj.org/toc/1932-6203To investigate whether acute liver failure (ALF) leads to secondary acute myocardial injury, 100 ALF patients that were retrospectively identified in a single center based on ICD 10 codes and 8 rats from an experimental study that died early after bile duct ligation (BDL) were examined. Creatine kinase (CK), creatine kinase-MB isoenzyme (CKMB) and cardiac troponin-I (cTnI) were analyzed as markers of myocardial injury. For histological analysis, hematoxylin-eosin (HE), elastic Van Gieson (EVG), CD41 and myeloperoxidase were used to stain rat hearts. Major adverse cardiac events (MACEs) were a critical factor for mortality (p = 0.037) in human ALF. Deceased patients exhibited higher levels of CKMB than survivors (p = 0.023). CKMB was a predictor of mortality in ALF (p = 0.013). Animals that died early after BDL exhibited increased cTnI, CKMB, tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) levels compared to controls (cTnI: p = 0.011, CKMB: p = 0.008, TNFα: p = 0.003, IL-6: p = 0.006). These animals showed perivascular lesions and wavy fibers, microthrombi and neutrophilic infiltration in the heart. MACEs are decisive for mortality in human ALF, and elevated CKMB values indicate that this might be due to structural myocardial damage. Accordingly, CKMB was found to have predictive value for mortality in ALF. The results are substantiated by data from a rat BDL model demonstrating diffuse myocardial injury.Moritz UhligMarc HeinMoriz A HabigtRené H TolbaTill BraunschweigMarius J HelmedagUwe KlingeAlexander KochChristian TrautweinMare MechelinckPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 8, p e0256790 (2021) |
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Medicine R Science Q Moritz Uhlig Marc Hein Moriz A Habigt René H Tolba Till Braunschweig Marius J Helmedag Uwe Klinge Alexander Koch Christian Trautwein Mare Mechelinck Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data. |
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To investigate whether acute liver failure (ALF) leads to secondary acute myocardial injury, 100 ALF patients that were retrospectively identified in a single center based on ICD 10 codes and 8 rats from an experimental study that died early after bile duct ligation (BDL) were examined. Creatine kinase (CK), creatine kinase-MB isoenzyme (CKMB) and cardiac troponin-I (cTnI) were analyzed as markers of myocardial injury. For histological analysis, hematoxylin-eosin (HE), elastic Van Gieson (EVG), CD41 and myeloperoxidase were used to stain rat hearts. Major adverse cardiac events (MACEs) were a critical factor for mortality (p = 0.037) in human ALF. Deceased patients exhibited higher levels of CKMB than survivors (p = 0.023). CKMB was a predictor of mortality in ALF (p = 0.013). Animals that died early after BDL exhibited increased cTnI, CKMB, tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) levels compared to controls (cTnI: p = 0.011, CKMB: p = 0.008, TNFα: p = 0.003, IL-6: p = 0.006). These animals showed perivascular lesions and wavy fibers, microthrombi and neutrophilic infiltration in the heart. MACEs are decisive for mortality in human ALF, and elevated CKMB values indicate that this might be due to structural myocardial damage. Accordingly, CKMB was found to have predictive value for mortality in ALF. The results are substantiated by data from a rat BDL model demonstrating diffuse myocardial injury. |
format |
article |
author |
Moritz Uhlig Marc Hein Moriz A Habigt René H Tolba Till Braunschweig Marius J Helmedag Uwe Klinge Alexander Koch Christian Trautwein Mare Mechelinck |
author_facet |
Moritz Uhlig Marc Hein Moriz A Habigt René H Tolba Till Braunschweig Marius J Helmedag Uwe Klinge Alexander Koch Christian Trautwein Mare Mechelinck |
author_sort |
Moritz Uhlig |
title |
Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data. |
title_short |
Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data. |
title_full |
Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data. |
title_fullStr |
Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data. |
title_full_unstemmed |
Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data. |
title_sort |
acute myocardial injury secondary to severe acute liver failure: a retrospective analysis supported by animal data. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2021 |
url |
https://doaj.org/article/d8b8f4270f9c41118c876f97a5fe48bf |
work_keys_str_mv |
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