Key result
Intracoronary hyperoxemic reperfusion fails to reduce infarct size or 30-day MACE after PCI for AMI.
Why the study?
Hyperbaric oxygen reduces myocardial injury and improves ventricular function during ischemia-reperfusion, but the effect of hyperoxemic reperfusion with aqueous oxygen after PCI for AMI was unknown.
Does intracoronary hyperoxemic reperfusion improve infarct size, ST-segment resolution, and regional wall motion in patients with acute anterior or large inferior AMI undergoing PCI?
RCT (n=269)
Randomly assigned
Yes
Does intracoronary hyperoxemic reperfusion improve infarct size, ST-segment resolution, and regional wall motion in patients with acute anterior or large inferior AMI undergoing PCI?
Intracoronary hyperoxemic reperfusion after PCI for AMI is safe but does not improve infarct size or ventricular function recovery overall.
Should not change AMI reperfusion practice; leaves open hypothesis-generating benefit in early anterior MI for confirmatory RCTs.
OBJECTIVES: This study sought to determine whether hyperoxemic reperfusion with aqueous oxygen (AO) improves recovery of ventricular function after percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). BACKGROUND: Hyperbaric oxygen reduces myocardial injury and improves ventricular function when administered during ischemia-reperfusion. METHODS: In a prospective, multicenter study, 269 patients with acute anterior or large inferior AMI undergoing primary or rescue PCI (<24 h from symptom onset) were randomly assigned after successful PCI to receive hyperoxemic reperfusion (treatment group) or normoxemic blood autoreperfusion (control group). Hyperoxemic reperfusion was performed for 90 min using intracoronary AO. The primary end points were final infarct size at 14 days, ST-segment resolution, and delta regional wall motion score index of the infarct zone at 3 months. RESULTS: At 30 days, the incidence of major adverse cardiac events was similar between the control and AO groups (5.2% vs. 6.7%, p = 0.62). There was no significant difference in the incidence of the primary end points between the study groups. In post-hoc analysis, anterior AMI patients reperfused <6 h who were treated with AO had a greater improvement in regional wall motion (delta wall motion score index = 0.54 in control group vs. 0.75 in AO group, p = 0.03), smaller infarct size (23% of left ventricle in control group vs. 9% of left ventricle in AO group, p = 0.04), and improved ST-segment resolution compared with normoxemic controls. CONCLUSIONS: Intracoronary hyperoxemic reperfusion was safe and well tolerated after PCI for AMI, but did not improve regional wall motion, ST-segment resolution, or final infarct size. A possible treatment effect was observed in anterior AMI patients reperfused <6 h of symptom onset.
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O’Neill et al. (2007) conducted an RCT in Acute myocardial infarction (AMI) (n=269). Hyperoxemic reperfusion with aqueous oxygen (AO) vs. Normoxemic blood autoreperfusion was evaluated on Final infarct size at 14 days, ST-segment resolution, and delta regional wall motion score index of the infarct zone at 3 months. Intracoronary hyperoxemic reperfusion after PCI for AMI did not improve primary endpoints and resulted in similar 30-day major adverse cardiac events compared to control (6.7% vs 5.2%; p=0.62).
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