Mounting Evidence of an Association Between OSA and Dyslipidemia

Editor's Note: This review is based on Adedayo AM, Olafiranye O, Smith D, Hill A, Zizi F, Brown C, Jean-Louis G. Obstructive sleep apnea and dyslipidemia: evidence and underlying mechanism. Sleep Breath 2012. [Epub ahead of print].

In the review article title "Obstructive sleep apnea and dyslipidemia: evidence and underlying mechanism," Adedayo and his colleagues examined mounting evidence of the association between chronic intermittent hypoxia and dyslipidemia.1 Although a clear causal relationship has not been established between obstructive sleep apnea (OSA) and cardiovascular diseases (CVD), there is increasing experimental data that suggest OSA as an important cardiovascular risk factor for incident ischemic heart disease, stroke, and CVD-caused mortality. The researchers suggest that hypersympathetic tone and oxidative stress induced by OSA may have adverse impact on cholesterol metabolism via generation of stearoyl-coenzyme A desaturase-1, reactive oxygen species, peroxidation of lipids, as well as systemic inflammation. Oxidative stress also impacts total cholesterol, triglycerides and HDL levels with implications for progressive atherosclerosis in susceptible patients.

In addition, there appears to be a dose relationship between the severity of OSA and the likelihood of vascular injury as well as atherosclerotic burden. There is evidence indicating that chronic intermittent hypoxia (CIH), a characteristic complication of OSA, is a key factor in the development of dyslipidemia, systemic inflammation, oxidative stress, impaired endothelial vasodilator response and atherosclerosis.

In a recent article, Wang and his colleagues reported down-regulation of endothelial nitric oxide synthase expression by an NF-κB dependent mechanism, secondary to CIH.2 Although the mechanism is not fully understood, this evidence supports multiple physiological perturbations triggered by CIH to interfere with normal vascular function.

Because of the immense number of OSA patients at risk, the public health burden may be large and costly. The implications for the cardiovascular specialists are significant, since the patients in their practices frequently have coexistent obstructive sleep apnea and atherosclerosis. Although basic and clinical science studies have not established a clear causal relationship between these metabolic derangements and OSA, the evidence is growing and further investigation is required.


References

  1. Adedayo AM, Olafiranye O, Smith D, Hill A, Zizi F, Brown C, Jean-Louis G. Obstructive sleep apnea and dyslipidemia: evidence and underlying mechanism. Sleep Breath 2012. [Epub ahead of print].
  2. Wang B, Yan B, Song D, Ye X, Liu S. Chronic intermittent hypoxia down-regulates endothelial nitric oxide synthase expression by an NF-κB-dependent mechanism. Sleep Medicine 2013;14:165-71.

Clinical Topics: Diabetes and Cardiometabolic Disease, Dyslipidemia, Prevention, Sleep Apnea, Stress

Keywords: Atherosclerosis, Cardiovascular Diseases, Dyslipidemias, Myocardial Ischemia, Oxidative Stress, Sleep Apnea, Obstructive, Stroke


< Back to Listings