Abstract
Obstructive sleep apnea (OSA) is independently associated with dyslipidemia. Previous studies have demonstrated that sleep fragmentation can impair lipid metabolism. The present study aimed to identify whether sleep fragmentation is independently associated with dyslipidemia, in a large-scale, clinic-based consecutive OSA sample. This cross-sectional study was conducted among 2,686 patients who underwent polysomnography (PSG) for suspicion of OSA from January 2008 to January 2013 at the sleep laboratory. Multivariate regression analyses were performed to evaluate the independent associations between the microarousal index (MAI) and lipid profiles adjusting for potential confounders, including metabolic syndrome components and nocturnal intermittent hypoxia. The adjusted odds ratios (ORs) for various types of dyslipidemia according to MAI quartiles, as determined by logistic regression were also evaluated. MAI was found positively associated with low-density lipoprotein cholesterol (LDL-c) but not with total cholesterol (TC), triglyceride (TG) or high-density lipoprotein cholesterol (HDL-c). Furthermore, the adjusted ORs (95% confidence interval) for hyper-LDL cholesterolemia increased across MAI quartiles, as follows: 1 (reference), 1.3 (1.1–1.7), 1.6 (1.2–2.0), and 1.6 (1.2–2.1) (p = 0.001, linear trend). Sleep fragmentation in OSA is independently associated with hyper-LDL cholesterolemia, which may predispose patients with OSA to a higher risk of cardiovascular disease.
Highlights
Previous studies have attributed the pathophysiology of lipid metabolism disorders in Obstructive sleep apnea (OSA) mainly to chronic nocturnal intermittent hypoxia[7,8,9]
A positive dose-response relationship was observed between microarousal index (MAI) and total cholesterol (TC), low- density liproprotein cholesterol (LDL-c), and triglyceride (TG) levels, and a negative dose-response relationship was observed between MAI and high- density liproprotein cholesterol (HDL-c) levels
According to model 1, the multiple linear regression analysis showed that the MAI was significantly associated with TC, low-density lipoprotein cholesterol (LDL-c), and TG, but not with high-density lipoprotein cholesterol (HDL-c) (Table 3)
Summary
Previous studies have attributed the pathophysiology of lipid metabolism disorders in OSA mainly to chronic nocturnal intermittent hypoxia[7,8,9]. A previous study reported an association between sleep fragmentation and dyslipidemia in a population of approximately 700 OSA patients[17]. The included subjects in that studies were non-consecutive, which could have induced selection bias, and the confounding effect of intermittent hypoxia on the association between sleep fragmentation and dyslipidemia was not evaluated. In addition to these previous reports on the association between sleep fragmentation and dyslipidemia[15], studies performed in animal models showed that repeated arousal from sleep could cause impaired lipid levels[11,18]. Adjusted odds ratios (ORs) for different dyslipidemia categories in OSA patients with different levels of sleep fragmentation were calculated
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