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Coronary artery disease
Original article
Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction
  1. Ziad Nehme1,2,
  2. Dion Stub2,3,4,5,
  3. Stephen Bernard1,2,3,
  4. Michael Stephenson1,
  5. Janet E Bray2,3,
  6. Peter Cameron2,3,
  7. Ian T Meredith6,
  8. Bill Barger1,
  9. Andris H Ellims3,4,
  10. Andrew J Taylor3,4,
  11. David M Kaye2,3,4,
  12. Karen Smith1,2,7
  13. for the AVOID Investigators
  1. 1Department of Research and Evaluation, Ambulance Victoria, Melbourne, Australia
  2. 2Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia
  3. 3Department of Cardiology, Alfred Hospital, Melbourne, Australia
  4. 4Hypertension and Cardiac Disease Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
  5. 5Department of Cardiology, Western Health, Melbourne, Australia
  6. 6Monash Heart, Monash Medical Centre, Melbourne, Australia
  7. 7Discipline of Emergency Medicine, University of Western Australia, Western Australia, Australia
  1. Correspondence to Ziad Nehme, Department of Research and Evaluation, Ambulance Victoria, 31 Joseph Street, Blackburn North, VIC 3130, Australia; ziad.nehme{at}ambulance.vic.gov.au

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.

https://doi.org/10.1136/heartjnl-2015-308636

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