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

Abstract

Supplemental oxygen exposure in the first 12 h after STEMI was associated with a clinically significant increase in cTnI and CK release.

Effects of supplemental oxygen therapy in patients with suspected acute myocardial infarction: a meta-analysis of randomised clinical trials

“…The study showed no additional benefit and evidence of increased myocardial injury with supplemental oxygen therapy in normoxaemic patients with ST elevation myocardial infarction (STEMI). A substudy of the AVOID trial reported a 17%–21% increase in the myocardial infarct size (measured by the creatine kinase and cardiac troponin levels) with exposure to 6 L/min of oxygen via face mask 20. A prior meta-analysis (five trials, 1173 participants) showed a lack of mortality benefit for using supplemental O 2 in patients with ACS who were not hypoxic at presentation, although the evidence was of very low quality and could not rule out potential harmful effects 21.…”

Supplemental oxygen therapy does not affect the systemic inflammatory response to acute myocardial infarction

“…In a recent randomized controlled trial of oxygen therapy in patients with STEMI, the Air Versus Oxygen in Myocardial Infarction (AVOID) study, the authors reported a significant increase in mean peak creatine kinase (CK) in the oxygen treatment group but no difference in cTnI during the first 72 h . However, in a subgroup analysis, the same authors showed a time‐ and dose‐dependent effect, that is a higher concentration and longer duration of supplemental oxygen was associated with a significant increase in cTnI and CK release . These previous findings have thus fuelled the discussion on the risk‐benefit relationship of routine oxygen therapy .…”

Oxygen supplementation for critically ill patients—A protocol for a systematic review

“…The rationale for administering supplemental oxygen to patients with acute myocardial infarction may be that increasing the tissue oxygenation in the ischemic myocardium reduce both pain and infarct size; however, hyperoxaemic vasoconstriction may impose the contrary. 14,15 Mild hypoxia is common in people with acute stroke and may have significant adverse effects on the ischemic brain after stroke. In clinical practice, administration of supplemental oxygen is generally started instantly after stroke onset because it is simple to administer, 16 however, the impact of hyperoxaemic vasoconstriction or generation of reactive oxygen species may adversely affect the benefits of oxygen supplementation.…”