Hyperbaric oxygen therapy for acute coronary syndrome

Acute coronary syndrome (ACS), includes acute myocardial infarction and unstable angina, is common and may prove fatal. Hyperbaric oxygen therapy (HBOT) will improve oxygen supply to the threatened heart and may reduce the volume of heart muscle that perishes. The addition of HBOT to standard treatment may reduce death rate and other major adverse outcomes.

To assess the benefits and harms of adjunctive HBOT for treating ACS.

We updated the search of the following sources in June 2010, finding one further trial: the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, CINAHL, DORCTHIM, LILACS and checked the references from selected articles. Relevant journals were handsearched and researchers in the field contacted. No language restrictions were applied.

Randomised studies comparing the effect on ACS of regimens that include HBOT with those that exclude HBOT.

Three reviewers independently evaluated the quality of trials using the guidelines of the Cochrane Handbook and extracted data from included trials.

Six trials with 665 participants contributed to this review. There was a significant decrease in the risk of death with HBOT (risk ratio (RR) 0.58, 95% CI 0.36 to 0.92, P = 0.02). The extent of heart muscle damage was lower following HBOT, as shown by a lesser rise in muscle enzyme in the blood (mean difference (MD) 493 IU, P = 0.005) and a better LVEF (MD 5.5%, P = 0.001). There was evidence from individual trials of reductions in the risk of major adverse coronary events (MACE) (RR 0.12, P = 0.03); re-infarction (RR 0.28, P = 0.04) and dysrhythmias following HBOT (RR 0.59, P = 0.01, and the time to relief of pain was reduced with HBOT (MD 353 minutes shorter, P < 0.00001). One trial suggested a significant incidence of claustrophobia in single occupancy chambers of 15% (RR of claustrophobia with HBOT 31.6, P = 0.02).

For people with ACS, there is some evidence from small trials to suggest that HBOT is associated with a reduction in the risk of death, the volume of damaged muscle, the risk of MACE and time to relief from ischaemic pain. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously, and an appropriately powered trial of high methodological rigour is justified to define those patients (if any) who can be expected to derive most benefit from HBOT. The routine application of HBOT to these patients cannot be justified from this review.