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Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning
OBJECTIVE: This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. METHODS: We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible pat...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6726774/ https://www.ncbi.nlm.nih.gov/pubmed/31234690 http://dx.doi.org/10.1177/0300060519856750 |
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author | Zhou, Hong-mei Ling, Xiao-yan Ni, Yun-jian Wu, Cheng Zhu, Zhi-peng |
author_facet | Zhou, Hong-mei Ling, Xiao-yan Ni, Yun-jian Wu, Cheng Zhu, Zhi-peng |
author_sort | Zhou, Hong-mei |
collection | PubMed |
description | OBJECTIVE: This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. METHODS: We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible patients were divided into two groups based on whether DEX was infused. DEX infusion was permitted only between intubation and the beginning of cardiopulmonary bypass (CPB). Sevoflurane was inhaled via the standard postconditioning procedure starting at aortic declamping. The cardiac troponin I (cTnI) level was measured at different time points. The postoperative outcomes and complications were also analyzed. RESULTS: One hundred patients were included in the study (DEX group, n = 53; non-DEX group, n = 47). Increased cTnI levels were significantly correlated with the New York Heart Association classification, CPB time, and DEX use. DEX use and the CPB time were potential independent factors contributing to changes in the cTnI level. The cTnI level at 6, 12, and 24 hours postoperatively was remarkably lower in the DEX than non-DEX group by 1.14, 7.83, and 5.86 ng/mL, respectively. CONCLUSIONS: DEX decreased the cTnI level after CPB when sevoflurane postconditioning was used, especially at 6, 12, and 24 hours postoperatively. |
format | Online Article Text |
id | pubmed-6726774 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-67267742019-09-13 Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning Zhou, Hong-mei Ling, Xiao-yan Ni, Yun-jian Wu, Cheng Zhu, Zhi-peng J Int Med Res Clinical Research Reports OBJECTIVE: This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. METHODS: We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible patients were divided into two groups based on whether DEX was infused. DEX infusion was permitted only between intubation and the beginning of cardiopulmonary bypass (CPB). Sevoflurane was inhaled via the standard postconditioning procedure starting at aortic declamping. The cardiac troponin I (cTnI) level was measured at different time points. The postoperative outcomes and complications were also analyzed. RESULTS: One hundred patients were included in the study (DEX group, n = 53; non-DEX group, n = 47). Increased cTnI levels were significantly correlated with the New York Heart Association classification, CPB time, and DEX use. DEX use and the CPB time were potential independent factors contributing to changes in the cTnI level. The cTnI level at 6, 12, and 24 hours postoperatively was remarkably lower in the DEX than non-DEX group by 1.14, 7.83, and 5.86 ng/mL, respectively. CONCLUSIONS: DEX decreased the cTnI level after CPB when sevoflurane postconditioning was used, especially at 6, 12, and 24 hours postoperatively. SAGE Publications 2019-06-24 2019-08 /pmc/articles/PMC6726774/ /pubmed/31234690 http://dx.doi.org/10.1177/0300060519856750 Text en © The Author(s) 2019 http://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Clinical Research Reports Zhou, Hong-mei Ling, Xiao-yan Ni, Yun-jian Wu, Cheng Zhu, Zhi-peng Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning |
title | Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning |
title_full | Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning |
title_fullStr | Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning |
title_full_unstemmed | Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning |
title_short | Pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin I level following cardiac surgery with sevoflurane postconditioning |
title_sort | pre-cardiopulmonary bypass administration of dexmedetomidine decreases cardiac troponin i level following cardiac surgery with sevoflurane postconditioning |
topic | Clinical Research Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6726774/ https://www.ncbi.nlm.nih.gov/pubmed/31234690 http://dx.doi.org/10.1177/0300060519856750 |
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