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Atherosclerosis. 2010 Apr;209(2):381-6. doi: 10.1016/j.atherosclerosis.2009.10.017. Epub 2009 Oct 17.

Effect of intermittent hypoxia on atherosclerosis in apolipoprotein E-deficient mice.

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Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, United States.



Obstructive sleep apnea causes intermittent hypoxia (IH) and is associated with increased cardiovascular mortality. This increased risk may be attributable to more extensive or unstable atherosclerotic plaques in subjects with OSA. We studied the effect of chronic IH in atherosclerosis-prone mice.


Apolipoprotein E-deficient (ApoE(-/-)) mice fed a high cholesterol diet were exposed to 4 or 12 weeks of IH and compared to intermittent air-exposed controls. At 4 weeks, IH increased plaque size in the aortic sinus and the descending aorta. At 12 weeks, atherosclerosis progressed in all groups, but more rapidly in the descending aorta of IH-exposed animals. Plaque composition was similar between IH and controls. Between 4 and 12 weeks, there were progressive increases in blood pressure, with relatively stable increases in serum lipids and arterial stiffness.


IH accelerates atherosclerotic plaque growth in ApoE(-/-) mice without affecting plaque composition. The mechanisms may include non-additive increases in serum lipids, and cumulative increases in blood pressure.

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