{"id":"7d8ac207b69d","type":"article","url":"https://hartvaat.nl/2016/03/01/effect-van-aanvullende-zuurstoftoediening-op-myocardschade-bij-stemi/","title":"Effect van aanvullende zuurstoftoediening op myocardschade bij STEMI","title_en":"Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction.","category":"algemeen","category_label":"Algemeen","professions":["cardioloog","huisarts"],"tags":[],"journal":"Heart (British Cardiac Society)","doi":"10.1136/heartjnl-2015-308636","source_url":"https://doi.org/10.1136/heartjnl-2015-308636","authors":["Ziad Nehme","Dion Stub","Stephen Bernard","Michael Stephenson","Janet E Bray","Peter Cameron","Ian T Meredith","Bill Barger","Andris H Ellims","Andrew J Taylor","David M Kaye","Karen Smith"],"significance":7,"published":"2016-03-01","source_date":"2016-03-01","image":"","kennis":["https://hartvaat.nl/kennis/coronairlijden/stemi/","https://hartvaat.nl/kennis/diagnostiek/inspanningstest-loopband-fiets/"],"congress":"","summary_en":"This study showed that supplemental oxygen therapy may increase myocardial injury in patients with STEMI who are not hypoxemic, providing evidence for a dose-response relationship between oxygen exposure and troponin release in acute MI.","created":"2026-07-03T10:25:58Z","updated":"2026-07-03T13:25:20Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie die aantoonde dat aanvullende zuurstoftherapie de myocardschade na STEMI kan vergroten. Onderzocht de dosis-responsrelatie tussen zuurstofblootstelling en infarctgrootte, met relevantie voor ambulanceprotocollen.","abstract_original":"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."}