Dyslipidemia: another brick in the wall. A feasible link in the OSA–cardiovascular disease axis

Abstract

Obstructive sleep apnea (OSA) is a frequent and often severe clinical condition that has been linked to cardiovascular diseases and metabolic disorders among others. The underlying mechanisms initiating and aggravating cardiovascular disorders are not clearly understood yet, oxidative stress and endothelial dysfunction are considered as major factors. A frequent consequence of OSA is diminished endothelial function including decreased nitric oxide (NO)-dependent vasodilation. A very recent review summarizing current experimental information from animal models gives a deep insight in the complexity of alterations in NO production in patients with OSA

Lipoprotein Subfractions Associated with Endothelial Function in Previously Healthy Subjects with Newly Diagnosed Sleep Apnea—A Pilot Study

“…In this population, significantly lower levels of atheroprotective LDL1 and large HDL subfractions were detected as well as significantly higher levels of atherogenic small dense LDL 3–7 subfractions [ 21 ]. Our results are consistent with the findings of previously mentioned studies [ 17 , 41 , 42 , 43 , 44 , 45 ]. Among our previously healthy patients with newly diagnosed moderate-to-severe OSA, small HDL was the only significant predictor of RHI, suggesting a pro-atherogenic role of small HDL subfractions in this population.…”

“…Our study was based on a strict exclusion process, and the final sample of apparently healthy subjects of our “real-world” population with no previous history of sleep apnea had only 18 responders; at the time, this was a pilot project on the topic of the possible association of lipoprotein subfractions with endothelial function in previously healthy individuals (with newly diagnosed sleep apnea). Juházs in 2014 [ 17 ] suggested dyslipidemia as one of the possible mechanisms linking OSA with increased vascular morbidity. The same opinion was presented by Helkin et al in 2016 [ 17 , 39 ].…”

“…Juházs in 2014 [ 17 ] suggested dyslipidemia as one of the possible mechanisms linking OSA with increased vascular morbidity. The same opinion was presented by Helkin et al in 2016 [ 17 , 39 ]. LDL is generally considered to be atherogenic and HDL to be atheroprotective.…”

“…Dyslipidemia, defined as an excessive increase in total cholesterol (TC) or triacylglycerols (TAG), with or without a concomitant decrease in high-density lipoproteins (HDL), leads to the acceleration of the atherosclerotic process in predisposed individuals and is also one of the most important risk factors for vascular disease [ 15 ]. Along with increased sympathetic nervous system activity, oxidative stress, systemic inflammation, subsequent hypertension and glucose metabolism impairment [ 16 ], dyslipidemia is one of the possible mechanisms linking OSA with increased vascular morbidity [ 17 ]. The mechanisms of dyslipidemia induced by OSA include the up-regulation of lipoprotein biosynthesis, increased lipolysis, impaired clearance of lipoproteins, lipoprotein peroxidation, and HDL dysfunction [ 18 ]; this may represent a pathway by which the increase in cardiovascular risk is mediated [ 19 ].…”

The impact of sleep apnea syndrome on the altered lipid metabolism and the redox balance

“…From previously published works there is known the association between intermittent hypoxia and a wide range of pathological processes, such as endothelial dysfunction, activation of the sympathetic nervous system, systemic inflammatory response, impaired glucose and lipid metabolisms [ 5 , 6 ]. Dyslipidemia, defined as an excessive increase in total cholesterol or triacylglycerols, with or without a concomitant decrease in high-density lipoproteins (HDL), leads to an acceleration of the atherosclerotic process in predisposed individuals and is one of the most important risk factors for vascular disease [ 7 , 8 ]. Although it is not known what role OSA plays in the development of dyslipidemia, recent studies provide evidence for an independent association of intermittent hypoxia with dyslipidemia that might result in an increased risk of vascular disase in patients with OSA [ 9 , 10 ].…”