Sleep apnea, a disorder characterized by the temporary cessation of breathing during sleep, displays the same cellular and biochemical changes that are found in atherosclerosis, a disease in which the walls of the arteries thicken, harden, and lose elasticity, resulting in impaired blood circulation.

The study explains why those who suffer from sleep apnea -- which affects as many as 18 million people in the United States alone, particularly men over age 35 -- also have cardiovascular problems.

The findings of the study, led by biochemist Lena Lavie of the Faculty of Medicine at the Technion-Israel Institute of Technology, are published in the American Journal of Respiratory and Critical Care Medicine (April 1, 2002).

"We found that white blood cells of sleep apnea patients show a large increase in the amount of adhesion molecules that appear on the surface of the cells. These molecules are responsible for the atherogenic processes that thicken artery walls," said Dr. Lavie, who headed the study with colleagues Larissa Dyugovskaya and Peretz Lavie. "We also saw these white blood cells produced more free radicals, which damage the endothelial cells lining the vessel walls, which, in turn, play a crucial role in maintaining healthy blood vessels, and therefore also contribute to the formation of atherosclerosis."

Dr. David White, director of the Sleep Disorders Program at Brigham and Women's Hospital in Boston and associate professor of medicine at Harvard Medical School, praised the study.

"This study is an important step forward because the Technion researchers have put together the components needed to explain at least some of the predisposition of apnea patients to vascular disease at the cellular level," said Dr. White.

"There are good data indicating that obstructive sleep apnea leads to adverse cardiovascular outcomes including stroke, congestive heart failure and probably myocardial infarction," he added.

To examine the clinical significance of the changes in apnea sufferers' white blood cells, Dr. Lavie's team added white blood cells from sleep apnea patients to a medium containing cultured human endothelial cells, and studied the interactions between the two types of cells. After one hour, the white blood cells attached themselves firmly to the endothelial cells in the medium. Dr. Lavie attributed this to an abundance of adhesion molecules.

When white blood cells of normal controls were added to the medium, the researchers did not find comparable changes. They also found that there was no increase in the number of adhesion molecules on the white blood cells of sleep apnea sufferers who were effectively treated with continuous positive air pressure, or CPAP, which delivers air into patients' airways through specially designed nasal masks.

"If the firm binding of white blood cells to endothelial cells in the test tube is what happens in the blood of sleep apnea patients every night, then this may be significant evidence that sleep apnea is associated with an active process of atherosclerosis that inflicts damage on the endothelial cells and may lead to increased risk for cardiovascular diseases," Dr. Lavie explained.

The next step, she said, is to examine whether effective treatment of sleep apnea can abort or even reverse this process and thereby reduce the risk of cardiovascular diseases in sleep apnea patients.