Hyperbaric oxygen therapy for acute coronary syndrome
Michael H Bennett, Jan P Lehm, Nigel Jepson
m.bennett@unsw.edu.au.

Editorial group: Cochrane Heart Group.
Publication status and date: Edited (no change to conclusions), published in Issue 1, 2009.

Citation:
Bennett MH, Lehm JP, Jepson N. Hyperbaric oxygen therapy for acute coronary syndrome. Cochrane Database of Systematic Reviews 2011, Issue 8. Art. No.: CD004818.

Background
Acute coronary syndrome (ACS) includes acute myocardial infarction and unstable angina. ACS 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 will perish. The addition of HBOT to the standard treatment may reduce death rate and other major adverse outcomes.

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

Search strategy
We searched the following from inception to June 2007: the Cochrane Central Register of Controlled Trials (CENTRAL),MEDLINE, EMBASE, CINAHL, DORCTHIM, and references from selected articles. Relevant journals were handsearched and researchers in the field contacted.

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

Data collection and analysis
Three reviewers independently evaluated the quality of trials using the guidelines of the Cochrane Reviewer’s Handbook and extracted data from included trials.

Main results
Five trials with 536 participants contributed to this review.
There was a trend towards, but no significant decrease in, the risk of death with HBOT (relative risk [RR] 0.63, 95% CI 0.38 to 1.03, P=0.07).
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, 95% CI 0.02 to 0.85, P=0.03; NNT 4, 95% CI 3 to 10) and some dysrhythmias following HBOT (RR 0.59, 95% CI 0.39 to 0.89, P=0.01; NNT 6, 95% CI 3 to 24), and the time to relief of pain was reduced with HBOT (MD 353 minutes shorter, 95% CI 219 to 488, P<0.00001).
One trial suggested a significant incidence of claustrophobia in single occupancy chambers of 15% (RR of claustrophobia with HBOT 31.6, 95%CI 1.92 to 521, P=0.02).

Authors’ conclusions
For people with ACS, there is some evidence from small trials to suggest that HBOT is associated with a reduction in the volume of damaged muscle, the risk of MACE and time to relief from ischaemic pain, but does not reduce mortality. 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.


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