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Clinical Citations: Does obstructive sleep apnea contribute to atherosclerosis?

Publication
Article
The Journal of Respiratory DiseasesThe Journal of Respiratory Diseases Vol 6 No 1
Volume 6
Issue 1

Obstructive sleep apnea (OSA) has been associated with cardiovascular disease, but the causal mechanisms are only partially understood. Researchers in São Paulo, Brazil, who investigated whether OSA contributes to atherosclerosis progression, observed that middle-aged patients with OSA who did not have overt cardiovascular disease demonstrated early signs of atherosclerosis.

Obstructive sleep apnea (OSA) has been associated with cardiovascular disease, but the causal mechanisms are only partially understood. Researchers in São Paulo, Brazil, who investigated whether OSA contributes to atherosclerosis progression, observed that middle-aged patients with OSA who did not have overt cardiovascular disease demonstrated early signs of atherosclerosis.

The study included 15 patients with severe OSA, 15 with mild to moderate OSA, and 12 controls matched for age, sex, and body mass index. None had hypertension or diabetes, were smokers, or took any medication, and none of the patients with OSA had received treatment. The study participants underwent standard overnight polysomnography. In addition, a noninvasive automatic device was used to measure carotid-femoral pulse wave velocity, and an echo-tracking device was used to measure intima-media thickness, diameter, and distensibility.

Results revealed significant differences in apnea-hypopnea index, pulse wave velocity, intima-media thickness, and carotid diameter between controls and patients with mild to moderate or severe OSA (Table). Multivariate analyses showed that the apnea-hypopnea index correlated independently with pulse wave velocity and intima-media thickness, and that minimal oxygen saturation correlated with the carotid diameter.

All vascular abnormalities were significantly correlated with OSA severity. These findings support the suggestion that OSA plays an independent role in the progression of atherosclerosis.

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