TY - JOUR
T1 - Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction
AU - Nehme, Z.
AU - Stub, D.
AU - Bernard, S.
AU - Stephenson, M.
AU - Bray, J.E.
AU - Cameron, P.
AU - Meredith, I.T.
AU - Barger, B.
AU - Ellims, A.H.
AU - Taylor, A.J.
AU - Kaye, D.M.
AU - Smith, Karen
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 aeed 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 aeed for its aociation with cTnI/CK release using multivariable linear regreion. 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 aociated with a 1.4% (95% CI 0.6% to 2.2%, p
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 aeed 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 aeed for its aociation with cTnI/CK release using multivariable linear regreion. 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 aociated with a 1.4% (95% CI 0.6% to 2.2%, p
U2 - 10.1136/heartjnl-2015-308636
DO - 10.1136/heartjnl-2015-308636
M3 - Article
C2 - 26740484
SN - 1355-6037
VL - 102
SP - 444
EP - 451
JO - Heart
JF - Heart
IS - 6
ER -