So many of our therapeutic staples, while based on sound physiological reasoning, fail to translate into clinically important realities when empirically tested, as a recent publication by Hoffmann, et al., in the New England Journal of Medicine nicely reminds us. (2017 Aug 28. doi: 10.1056/NEJMoa1706222.)
This mammoth undertaking, entitled the DETO2X trial, randomized 6,629 adult patients over 30 presenting to 35 hospitals in Sweden with signs concerning for a myocardial infarction and ECG changes or an elevated troponin to either oxygen therapy (6L via a standard face mask) or ambient air for six to 12 hours after enrollment. If determined clinically necessary by the treating clinician, the use of supplemental oxygen was permitted outside the trial's protocol.
Using a novel registry-based, randomized design, the authors utilized the previously established SWEDEHEART registry to collect data prospectively on the patients enrolled and randomized them into the DETO2X Trial. The registry compiled data for 106 variables, including patient demographics, admission logistics, risk factors, past medical history, medical treatment prior to admission, electrocardiographic changes, biochemical markers, other clinical features and investigations, medical treatment in the hospital, interventions, hospital outcome, discharge diagnoses, and discharge medications. A follow-up visit was performed after six to 10 weeks and again after 12 to 14 months for all patients registered in SWEDEHEART.
The authors reported no difference in one-year mortality, the primary outcome, between patients randomized to oxygen therapy and those who received ambient air (5.0% vs 5.1%). Nor was there a difference in the composite endpoint of death from any cause, re-hospitalization with myocardial infarction (8.3% vs 8.0%), or 30-day mortality.
While clearly negative, DETO2X did not show any sign of harm associated with the use of supplemental oxygen, unlike past literature. This is in contrast to the previously published AVOID trial, which suggested an increase in infarct size in patients exposed to supplemental oxygen. (Circulation 2015;131:2143.) These findings were based on cardiac MR imaging, and no significant difference in clinically important outcomes was observed. Such images were not assessed in the DETO2X cohort, but the authors found no clinical signs of deleterious outcomes in patients randomized to the supplemental oxygen arm. The suggestion of harm observed in the statistically smaller AVOID trial was due to either random sampling error or was representative of a surrogate measure that does not translate into clinically important outcomes.
Supplemental oxygen has long been considered a universally beneficial intervention, applied with great enthusiasm to a vast majority of patients transported to the ED by ambulance. The authors powered their study expecting a one-year mortality of approximately 14 percent, but this is a fairly robust demonstration of oxygen's lack of utility in patients experiencing a myocardial infarction. This is yet another physiological fairy tale to add to our considerable list of therapeutically futile endeavors.
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