Author + information
- Received June 19, 2019
- Revision received August 13, 2019
- Accepted September 4, 2019
- Published online February 17, 2020.
- Stefan K. James, MD, PhDa,b,
- David Erlinge, MD, PhDc,
- Johan Herlitz, MD, PhDd,
- Joakim Alfredsson, MD, PhDe,
- Sasha Koul, MD, PhDc,
- Ole Fröbert, MD, PhDf,
- Thomas Kellerth, MDf,
- Annica Ravn-Fischer, MD, PhDg,
- Patrik Alström, MDh,
- Ollie Östlund, PhDb,
- Tomas Jernberg, MD, PhDi,
- Bertil Lindahl, MD, PhDa,b,
- Robin Hofmann, MD, PhDh,∗ (, )
- for the DETO2X-SWEDEHEART Investigators
- aDepartment of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden
- bUppsala Clinical Research Center, Uppsala University, Uppsala, Sweden
- cDepartment of Clinical Sciences, Cardiology, Lund University, Lund, Sweden
- dDepartment of Health Sciences, University of Borås, Borås, Sweden
- eDepartment of Medical and Health Sciences and Department of Cardiology, Linköping University, Linköping, Sweden
- fDepartment of Cardiology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden
- gDepartment of Molecular and Clinical Medicine and Sahlgrenska University Hospital, Department of Cardiology, University of Gothenburg, Gothenburg, Sweden
- hDepartment of Clinical Science and Education, Division of Cardiology, Karolinska Institutet, Södersjukhuset, Stockholm, Sweden
- iDepartment of Clinical Sciences, Cardiology, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden
- ↵∗Address for correspondence:
Dr. Robin Hofmann, Karolinska Institutet, Department of Clinical Science and Education, Division of Cardiology, Södersjukhuset, Sjukhusbacken 10, 11883 Stockholm, Sweden.
Objectives The aim of this study was to determine the effect of supplemental oxygen in patients with myocardial infarction (MI) on the composite of all-cause death, rehospitalization with MI, or heart failure related to baseline oxygen saturation. A secondary objective was to investigate outcomes in patients developing hypoxemia.
Background In the DETO2X-AMI (Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction) trial, 6,629 normoxemic patients with suspected MI were randomized to oxygen at 6 l/min for 6 to 12 h or ambient air.
Methods The study population of 5,010 patients with confirmed MI was divided by baseline oxygen saturation into a low-normal (90% to 94%) and a high-normal (95% to 100%) cohort. Outcomes are reported within 1 year. To increase power, all follow-up time (between 1 and 4 years) was included post hoc, and interaction analyses were performed with oxygen saturation as a continuous covariate.
Results The composite endpoint of all-cause death, rehospitalization with MI, or heart failure occurred significantly more often in patients in the low-normal cohort (17.3%) compared with those in the high-normal cohort (9.5%) (p < 0.001), and most often in patients developing hypoxemia (23.6%). Oxygen therapy compared with ambient air was not associated with improved outcomes regardless of baseline oxygen saturation (interaction p values: composite endpoint, p = 0.79; all-cause death, p = 0.33; rehospitalization with MI, p = 0.86; hospitalization for heart failure, p = 0.35).
Conclusions Irrespective of oxygen saturation at baseline, we found no clinically relevant beneficial effect of routine oxygen therapy in normoxemic patients with MI regarding cardiovascular outcomes. Low-normal baseline oxygen saturation or development of hypoxemia was identified as an independent marker of poor prognosis. (An Efficacy and Outcome Study of Supplemental Oxygen Treatment in Patients With Suspected Myocardial Infarction; NCT01787110)
- cardiovascular outcomes
- myocardial infarction
- oxygen therapy
- randomized clinical trial
- reactive oxygen species
This work was supported by the Swedish Research Council (grant VR20130307), the Swedish Heart-Lung Foundation (grant HLF20130262, HLF20160688), and the Swedish Foundation for Strategic Research (grant SSF KF10-0024). Drs. Hofmann and Östlund have received grants from the Swedish Research Council and the Swedish Heart-Lung Foundation. Dr. Hofmann was supported by the Stockholm County Council (clinical postdoctoral appointment). The funding agencies had no access to the study data and no role in trial design, implementation, or reporting. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received June 19, 2019.
- Revision received August 13, 2019.
- Accepted September 4, 2019.
- 2020 American College of Cardiology Foundation