Obstructive sleep apnea
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Home / Health News / 2009 / May 2009 / May 5, 2009
Obstructive sleep apnea raises heart disease risk
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Obstructive sleep apnea raises heart disease risk

Obstructive sleep apnea, or periodic interruptions in breathing throughout the night, can increase the risk of several forms of heart and vascular disease, researchers have found.


Washington, May 5 : Obstructive sleep apnea, or periodic interruptions in breathing throughout the night, can increase the risk of several forms of heart and vascular disease, researchers have found.

What's more, the common sleep apnea thickens sufferers' blood vessels, the study published in the May 1 issue of the American Journal of Respiratory Cell and Molecular Biology claimed.

Emory researchers have found enzyme NADPH oxidase as important for the effects obstructive sleep apnea has on blood vessels in the lung.

Standard treatment for obstructive sleep apnea involves a mechanical application of air pressure. Anything that blunts sleep apnea's effects on blood vessel physiology could reduce its impact on disease risk, senior author C. Michael Hart, professor of medicine at Emory University School of Medicine and Atlanta Veterans Affairs Medical Center said.

Cyclically depriving mice of oxygen - researchers call this "chronic intermittent hypoxia" -- in a way that simulates obstructive sleep apnea gives them pulmonary hypertension. Pulmonary hypertension, which can be life threatening, is a condition in which the right side of the heart has trouble pumping blood because of resistance in the lung's blood vessels.

Chronic intermittent hypoxia forces the blood vessels in the lung to make more NADPH oxidase, Hart and his colleagues found. Mice that lack NADPH oxidase are immune to hypoxia's effects.

NADPH oxidase is a helpful enzyme because it is responsible for making superoxide, a reactive free radical that the immune system uses to kill bacteria. But superoxide also interferes with nitric oxide, a signal that allows blood vessels to relax.

Humans with mutations in genes for NADPH oxidase have recurrent bacterial infections because their ability to fight the bacteria is weakened. Therefore, according to Hart, inhibiting the NADPH oxidase enzyme in the entire body may be harmful, and he favors an indirect intervention.

"We think that strategies to lower NADPH oxidase expression induced by hypoxia may be useful in preventing hypoxia-induced pulmonary hypertension," says Hart.

ANI

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