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Heart. 2016 Mar;102(6):444-51. doi: 10.1136/heartjnl-2015-308636. Epub 2016 Jan 6.

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

Author information

1
Department of Research and Evaluation, Ambulance Victoria, Melbourne, Australia Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
2
Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia Department of Cardiology, Alfred Hospital, Melbourne, Australia Hypertension and Cardiac Disease Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia Department of Cardiology, Western Health, Melbourne, Australia.
3
Department of Research and Evaluation, Ambulance Victoria, Melbourne, Australia Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia Department of Cardiology, Alfred Hospital, Melbourne, Australia.
4
Department of Research and Evaluation, Ambulance Victoria, Melbourne, Australia.
5
Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia Department of Cardiology, Alfred Hospital, Melbourne, Australia.
6
Monash Heart, Monash Medical Centre, Melbourne, Australia.
7
Department of Cardiology, Alfred Hospital, Melbourne, Australia Hypertension and Cardiac Disease Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
8
Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia Department of Cardiology, Alfred Hospital, Melbourne, Australia Hypertension and Cardiac Disease Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
9
Department of Research and Evaluation, Ambulance Victoria, Melbourne, Australia Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia Discipline of Emergency Medicine, University of Western Australia, Western Australia, Australia.

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 doseƗtime 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.

PMID:
26740484
DOI:
10.1136/heartjnl-2015-308636
[Indexed for MEDLINE]

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