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Cochrane systematic review
No current evidence that routine administration of oxygen to people with acute myocardial infarction improves pain or mortality; further conclusive trials are needed
  1. Nathan Mewton1,
  2. Kihei Yoneyama2
  1. 1Hôpital Cardiologique Louis Pradel, Hospices Civils de Lyon, Bron, France
  2. 2Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki-City, Kanagawa, Japan
  1. Correspondence to Nathan Mewton
    Centre d'Investigation Clinique, 28 Avenue Doyen Lépine, 69500 Bron, France; nmewton{at}gmail.com

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Context

Nothing much remains of the treatments and strategies that were applied 25 years ago in the clinical setting of an acute myocardial infarction (AMI). One of the few remaining treatments is oxygen therapy. This oxygen therapy is employed in a reflexive and ‘emergency-department based’ empirical manner as a reaction to a life-threatening situation. Oxygen therapy is still recommended in several international guidelines for the treatment of uncomplicated AMI, but this ‘reasonable’ recommendation has no true scientific background.1 2 It is to the credit of Cabello and colleagues to have explored the evidence or rather, in this case, the absence of evidence for the clinical effects of oxygen therapy at the acute phase of myocardial infarction.

Methods

In this study, Cabello and colleagues performed an extensive and thorough review of the literature, retrieving all randomised controlled trials of the use of inhaled oxygen at normal pressure delivered by facial mask or nasal cannula, at any concentration during AMI. Using appropriate selection criteria over all existing languages, their research wasn't limited only to bibliographic databases and also explored the knowledge of field experts through interviews. With a rigorous and clear methodology, they evaluated each potential study that could qualify. They then analysed the effect of oxygen therapy on in-hospital mortality and the use of analgesics in the selected studies.

Findings

The final result of their research, which is very unlikely to have missed relevant studies, reports only three qualifying clinical studies, the principal one having been published in the 1970s, prior to the reperfusion era.3 All of those studies had limitations and significant risks of bias because of the small number of patients, patient selection criteria, different study time periods with the consequent differences in therapeutic strategies and low rate of events. Those limitations significantly affect any valuable conclusions we could draw from this review although the ‘evidence’ suggests that oxygen may in fact be harmful for AMI patients, with an in-hospital risk of mortality multiplied by three in-patients who are given oxygen.

Commentary

The main therapy for AMI is the quick and efficient reopening of the culprit coronary artery either by primary percutaneous coronary intervention or by thrombolytic agents. The second-line pharmacologic treatments come in addition either to provide a strong antiaggregant/anticoagulant and anti-inflammatory environment within the coronary vessels or to protect the ischemic myocardium and enhance its recovery/cicatrisation. The successful application of these evidence-based strategies in the last 10 years has allowed us to reduce efficiently the mortality and morbidity of AMI.4 These strategies are constantly evolving/progressing either to improve current practice or to focus on new targets such as reperfusion injury.

What is the place for nasal oxygen in these therapeutic strategies? According to this review, it is difficult to conclude anything, and as the authors suggest, a large multicentric contemporary clinical trial would be warranted to determine the effect of oxygen therapy on AMI patients' outcome. Such a trial is very unlikely to take place considering the number of patients and the means necessary to control all potential confounding factors. The truth might come from smaller trials, using surrogate markers of clinical end points such as infarct size and precise functional parameters to assess the effect of oxygen therapy on the final myocardial damage. Small clinical studies have already been undertaken and show that supplemental oxygen significantly reduces coronary blood flow and increases coronary vascular resistance in patients with chronic ischemic disease.5 Other clinical trials in AMI patients, excluded from this review, used hyperbaric oxygen or aqueous oxygen therapy applied immediately after reperfusion and reported controversial results.6 7

Clearly, if it is not possible to conclude that there is any deleterious effect of oxygen therapy, there is even less evidence showing that it might have a beneficial one. Therefore, when faced with an AMI patient, a reasonable choice for the physician would be to use common sense and apply oxygen not because of the AMI, but because other clinical parameters (e.g. pulse oxymetry monitoring/heart failure signs) indicate it.

Acknowledgments

I am currently supported by a research grant from the French Federation of Cardiology.

References

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Footnotes

  • Competing interests None.