Last Updated: 2008-12-05 17:08:29 -0400 (Reuters Health)

Postsleep carbon monoxide (CO) level correlates with obstructive sleep apnea (OSA) severity, according to a report in the November issue of Chest.

Circulating CO level has been shown to be a marker for cardiovascular risk, the authors explain, and heme oxygenase (HO)-1, which catalyzes the degradation of heme to endogenous CO, is upregulated by hypoxia, oxidative stress, and other factors.

Dr. Yoshiaki Ishigatsubo from Yokohama City University Graduate School of Medicine, Yokohama, Japan, and colleagues investigated venous CO levels presleep and postsleep in 35 OSA patients, including 7 who were reexamined during treatment with continuous positive airway pressure (CPAP).

Postsleep CO levels were significantly higher than presleep CO levels in OSA patients, but not in healthy controls, the authors report.

The increase in CO level correlated with the apnea/hypopnea index and with hypoxia duration as a percentage of total sleep time, the report indicates.

CPAP therapy and its associated improvement in the apnea/hypopnea index "was associated with the normalization of morning CO levels," the researchers note.

OSA patients also had significantly higher presleep-to-postsleep changes in indirect bilirubin levels compared to controls, the investigators say, but there was no difference between patients and controls in postsleep HO-1.

"Increased levels of circulating CO increased hypoxia during sleep in OSA patients and were helpful in assessing the clinical severity," the authors conclude. "Moreover, the normalization of venous CO levels by CPAP therapy can potentially reduce the risk of disease associated cardiovascular events, which is most critical for patients with OSA."

"The induction of the HO system and the generation of CO is likely a protective response to the stress of OSA, rather than a causative mechanism of cardiovascular morbidity," according to a related editorial by Dr. Robert L. Owens and colleagues from Brigham and Women’s Hospital, Boston, Massachusetts.

"[This study] is important because it suggests the functional involvement of HO in OSA, and provides a basis for CO as a marker of OSA stress," the editorialists write.

Chest 2008;134:895-896,904-910.