Statins May Reduce Heart Risks Associated With Sleep Apnea, Study Suggests

By Dr Deepu

The NPR (1/7, Chen) “Shots” blog reports that a study (1/7) published in Science Translational Medicine “suggests that cholesterol...plays a special role in raising risk for people with sleep apnea.” The research also “hint[s] that...statins could limit the damage sleep apnea does to blood vessels.” Investigators thought “there might be something happening to the cells lining our blood vessels since they would be the first to experience the particular rise and fall in oxygen afflicting sleep apnea patients.”
        STAT (1/7, Boodman) reports that the investigators “extracted these cells from the arms of 76 patients with obstructive sleep apnea and 52 others who” did not have OSA. Sleep apnea patients were found to have higher CD59 levels. The researchers found that “the CD59 of people with sleep apnea had been pulled inside the cell, instead of guarding the cell’s surface, leaving the cell vulnerable to attacks from the immune system.” The “damaged cells, in turn, would be more likely to obstruct blood flow – the first such cellular explanation of how apnea may cause heart problems.” The investigators found, however, that patients with OSA who were taking statins did not exhibit “these abnormal CD59 effects.”
        HealthDay (1/7, Haelle) reports, “How much protein the cells pulled inside them depended on how much cholesterol...was present.” The researchers found that “statins stopped the cells from bringing the protein inside them.”

Obstructive sleep apnea is a common medical condition characterized by intermittent cessation of breathing during sleep, which results in intermittent hypoxia. It greatly increases patients’ risk of cardiovascular disease, and now Emin et al. provide a mechanism, which helps to explain this correlation. The authors discovered that intermittent hypoxia causes internalization of CD59, a protein that is normally found on the membrane of endothelial cells and protects them from being injured by circulating complement. After internalization, CD59 could no longer protect the cells, resulting in damage to the vascular walls. In contrast, statins stabilized CD59 on the endothelial cell surface and protected them from injury, revealing yet another mechanism by which these versatile drugs protect against cardiovascular disease.

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