Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Objective Supplemental oxygen therapy may increase myocardial injury following ST-elevation myocardial infarction (STEMI). In this study, we aimed to evaluate the effect of the dose and duration of oxygen exposure on myocardial injury after STEMI. Methods Descriptive analysis of data from a multicentre, prospective, randomised, controlled trial of 441 patients with STEMI randomised to supplemental oxygen therapy or room air breathing. The primary endpoint was myocardial infarct size as assessed by cardiac biomarkers, troponin (cTnI) and creatine kinase (CK). Oxygen therapy was commenced by paramedics, and continued for up to 12 h postintervention in hospital. Supplemental oxygen exposure was calculated as the area under the dose×time curve for oxygen administration over the first 12 h, and then assessed for its association with cTnI/CK release using multivariable linear regression. Results The median supplemental oxygen exposure was 1746 L (IQR: 960–2858). After adjustment for potential confounders, every 100 L increase in oxygen exposure in the first 12 h was associated with a 1.4% (95% CI 0.6% to 2.2%, p<0.001) and 1.2% (95% CI 0.7% to 1.8%, p<0.001) increase in the mean peak cTnI and CK, respectively. Excluding patients who developed cardiogenic shock, recurrent myocardial infarction or desaturations (SpO2<94%) during admission, every 100 L increase in oxygen exposure was associated with a 1.2% (95% CI 0.2% to 2.1%, p=0.01) and 1.0% (95% CI 0.3% to 1.7%, p=0.003) increase in the mean peak cTnI and CK, respectively. The median supplemental oxygen exposure of 1746 L would result in a 21% (95% CI 3% to 37%) increase in infarct size according to the cTnI profile. Conclusions Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinically significant increase in cTnI and CK release.
Original languageEnglish
Pages (from-to)444-451
Number of pages8
JournalHeart
Volume102
Issue number6
DOIs
Publication statusPublished - Mar 2016

Cite this

@article{6652eec09e244a98b305683d4dd3582a,
title = "Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction",
abstract = "Objective Supplemental oxygen therapy may increase myocardial injury following ST-elevation myocardial infarction (STEMI). In this study, we aimed to evaluate the effect of the dose and duration of oxygen exposure on myocardial injury after STEMI. Methods Descriptive analysis of data from a multicentre, prospective, randomised, controlled trial of 441 patients with STEMI randomised to supplemental oxygen therapy or room air breathing. The primary endpoint was myocardial infarct size as assessed by cardiac biomarkers, troponin (cTnI) and creatine kinase (CK). Oxygen therapy was commenced by paramedics, and continued for up to 12 h postintervention in hospital. Supplemental oxygen exposure was calculated as the area under the dose×time curve for oxygen administration over the first 12 h, and then assessed for its association with cTnI/CK release using multivariable linear regression. Results The median supplemental oxygen exposure was 1746 L (IQR: 960–2858). After adjustment for potential confounders, every 100 L increase in oxygen exposure in the first 12 h was associated with a 1.4{\%} (95{\%} CI 0.6{\%} to 2.2{\%}, p<0.001) and 1.2{\%} (95{\%} CI 0.7{\%} to 1.8{\%}, p<0.001) increase in the mean peak cTnI and CK, respectively. Excluding patients who developed cardiogenic shock, recurrent myocardial infarction or desaturations (SpO2<94{\%}) during admission, every 100 L increase in oxygen exposure was associated with a 1.2{\%} (95{\%} CI 0.2{\%} to 2.1{\%}, p=0.01) and 1.0{\%} (95{\%} CI 0.3{\%} to 1.7{\%}, p=0.003) increase in the mean peak cTnI and CK, respectively. The median supplemental oxygen exposure of 1746 L would result in a 21{\%} (95{\%} CI 3{\%} to 37{\%}) increase in infarct size according to the cTnI profile. Conclusions Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinically significant increase in cTnI and CK release.",
author = "Ziad Nehme and Dion Stub and Stephen Bernard and Michael Stephenson and Bray, {Janet E.} and Peter Cameron and Meredith, {Ian T} and Bill Barger and Ellims, {Andris H} and Taylor, {Andrew J} and Kaye, {David M} and Karen Smith and {AVOID Investigators}",
note = "Export Date: 20 July 2016",
year = "2016",
month = "3",
doi = "10.1136/heartjnl-2015-308636",
language = "English",
volume = "102",
pages = "444--451",
journal = "Heart",
issn = "1355-6037",
publisher = "BMJ Publishing Group",
number = "6",

}

Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction. / Nehme, Ziad; Stub, Dion; Bernard, Stephen; Stephenson, Michael; Bray, Janet E.; Cameron, Peter; Meredith, Ian T; Barger, Bill; Ellims, Andris H; Taylor, Andrew J; Kaye, David M; Smith, Karen; AVOID Investigators.

In: Heart, Vol. 102, No. 6, 03.2016, p. 444-451.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction

AU - Nehme, Ziad

AU - Stub, Dion

AU - Bernard, Stephen

AU - Stephenson, Michael

AU - Bray, Janet E.

AU - Cameron, Peter

AU - Meredith, Ian T

AU - Barger, Bill

AU - Ellims, Andris H

AU - Taylor, Andrew J

AU - Kaye, David M

AU - Smith, Karen

AU - AVOID Investigators

N1 - Export Date: 20 July 2016

PY - 2016/3

Y1 - 2016/3

N2 - Objective Supplemental oxygen therapy may increase myocardial injury following ST-elevation myocardial infarction (STEMI). In this study, we aimed to evaluate the effect of the dose and duration of oxygen exposure on myocardial injury after STEMI. Methods Descriptive analysis of data from a multicentre, prospective, randomised, controlled trial of 441 patients with STEMI randomised to supplemental oxygen therapy or room air breathing. The primary endpoint was myocardial infarct size as assessed by cardiac biomarkers, troponin (cTnI) and creatine kinase (CK). Oxygen therapy was commenced by paramedics, and continued for up to 12 h postintervention in hospital. Supplemental oxygen exposure was calculated as the area under the dose×time curve for oxygen administration over the first 12 h, and then assessed for its association with cTnI/CK release using multivariable linear regression. Results The median supplemental oxygen exposure was 1746 L (IQR: 960–2858). After adjustment for potential confounders, every 100 L increase in oxygen exposure in the first 12 h was associated with a 1.4% (95% CI 0.6% to 2.2%, p<0.001) and 1.2% (95% CI 0.7% to 1.8%, p<0.001) increase in the mean peak cTnI and CK, respectively. Excluding patients who developed cardiogenic shock, recurrent myocardial infarction or desaturations (SpO2<94%) during admission, every 100 L increase in oxygen exposure was associated with a 1.2% (95% CI 0.2% to 2.1%, p=0.01) and 1.0% (95% CI 0.3% to 1.7%, p=0.003) increase in the mean peak cTnI and CK, respectively. The median supplemental oxygen exposure of 1746 L would result in a 21% (95% CI 3% to 37%) increase in infarct size according to the cTnI profile. Conclusions Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinically significant increase in cTnI and CK release.

AB - Objective Supplemental oxygen therapy may increase myocardial injury following ST-elevation myocardial infarction (STEMI). In this study, we aimed to evaluate the effect of the dose and duration of oxygen exposure on myocardial injury after STEMI. Methods Descriptive analysis of data from a multicentre, prospective, randomised, controlled trial of 441 patients with STEMI randomised to supplemental oxygen therapy or room air breathing. The primary endpoint was myocardial infarct size as assessed by cardiac biomarkers, troponin (cTnI) and creatine kinase (CK). Oxygen therapy was commenced by paramedics, and continued for up to 12 h postintervention in hospital. Supplemental oxygen exposure was calculated as the area under the dose×time curve for oxygen administration over the first 12 h, and then assessed for its association with cTnI/CK release using multivariable linear regression. Results The median supplemental oxygen exposure was 1746 L (IQR: 960–2858). After adjustment for potential confounders, every 100 L increase in oxygen exposure in the first 12 h was associated with a 1.4% (95% CI 0.6% to 2.2%, p<0.001) and 1.2% (95% CI 0.7% to 1.8%, p<0.001) increase in the mean peak cTnI and CK, respectively. Excluding patients who developed cardiogenic shock, recurrent myocardial infarction or desaturations (SpO2<94%) during admission, every 100 L increase in oxygen exposure was associated with a 1.2% (95% CI 0.2% to 2.1%, p=0.01) and 1.0% (95% CI 0.3% to 1.7%, p=0.003) increase in the mean peak cTnI and CK, respectively. The median supplemental oxygen exposure of 1746 L would result in a 21% (95% CI 3% to 37%) increase in infarct size according to the cTnI profile. Conclusions Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinically significant increase in cTnI and CK release.

U2 - 10.1136/heartjnl-2015-308636

DO - 10.1136/heartjnl-2015-308636

M3 - Article

VL - 102

SP - 444

EP - 451

JO - Heart

JF - Heart

SN - 1355-6037

IS - 6

ER -