Research explains why those with obstructive sleep apnea are at higher risk for cardiovascular disease

Jun 3 2007

Researchers have found that patients with obstructive sleep apnea (OSA) have higher levels of a type of dead cells (apoptotic cells) from the lining (endothelium) of their blood vessels circulating in their bloodstream than people who do not have OSA.

The finding may help explain why those with OSA are at higher risk for cardiovascular disease (CVD).

According to the researchers, “levels of apoptotic endothelial cells are correlated with abnormal endothelial vasorelaxation, a precursor of atherosclerosis-related events,” and that treatment with nasal continuous positive airway pressure (nasal CPAP) can reduce levels of circulating apoptotic endothelial cells in OSA patients.

These findings appear in the June 1 issue of the American Journal of Respiratory and Critical Care Medicine , a publication of the American Thoracic Society.

Lead researcher Ali El Sohl, M.D., M.P.H., said the study was done “to explain why patients with OSA had a higher risk of cardiovascular morbidity and mortality.” He added that “the increased levels of circulating apoptotic endothelial cells would mean less production of nitric oxide that is crucial to artery vasodilatation. The less nitric oxide, the higher potentially is the risk of hypertension and acute heart attack. CPAP treatment would likely restore the physiologic function of the lining of the blood vessels.”

For the study, 14 men with OSA were recruited from the Sleep Clinic at the Erie County Medical Center, a hospital affiliated with the University of Buffalo, in New York. The patients were nonsmokers without any coexisting diseases, and they did not use medications. Ten healthy nonsmokers were recruited from a wellness clinic at the same hospital to serve as controls.

The OSA patients were given polysomnographic testing to verify the diagnosis. This involved evaluating brain waves, electrical activity of muscles, eye movements, breathing rates, blood pressure, blood oxygen saturation and heart rhythm, as well as direct observation of patients during sleep.

The men were comparable in age, blood pressure and metabolic profiles, but the OSA patients had a higher body–mass index, though the difference was not statistically significant. The OSA patients also had more apoptotic cells circulating in their bloodstreams and had vasomotor dysfunction.

The OSA patients were given nasal CPAP treatment for eight weeks. Use of CPAP ranged from four to seven hours per night. At the end of the study, the patients' vascular reactivity and circulating endothelial apoptotic cells were reevaluated and compared to the controls.

There were no significant differences in body measurements and metabolism in the men from baseline, but most of the patients who received CPAP had reduced circulating endothelial apoptotic cells and had marked improvements in brachial artery vascular reactivity.

The study had some limitations. Women were excluded to keep the study population homogeneous. Said Dr. El Sohl, “a follow-up study would be required to look at this phenomenon in women and in particular the hormonal effect on apoptosis in OSA.” The researchers “did not perform a thorough assessment for excluding coronary disease.”

More research is needed before these results can be applied clinically, according to Dr. El Sohl. While CPAP is currently used to treat OSA, looking for circulating apoptotic endothelial cells as a marker to fine-tune the therapy is one potential application. This may potentially reduce OSA patients' risk of CVD. Dr. El Sohl mentioned that statins, angiotensin converting enzyme inhibitors, and vitamin C reduce enthothelial apoptosis, but it is not known if these agents could help patients with OSA.

According to Dr. El Sohl, further research will investigate if the improvements in vascular function correlate with actual improvements in the sleep patterns of patients with OSA.

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