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Published on: December 6, 2016
HDL dysfunction in obstructive sleep apnea
Kathryn C B Tan1, Wing-Sun Chow, Jamie C M Lam
1Department of Medicine, University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong, PR China. kcbtan@hkucc.hku.hk
Insights
High-density lipoprotein (HDL) is dysfunctional in obstructive sleep apnea (OSA) patients, contributing to increased cardiovascular risk. This dysfunction impairs HDL
Area of Science:
- Cardiovascular Science
- Sleep Medicine
- Lipid Metabolism
Background:
- High-density lipoprotein (HDL) possesses anti-atherogenic and antioxidant properties.
- HDL dysfunction is observed in coronary heart disease and may be implicated in obstructive sleep apnea (OSA).
- OSA is associated with elevated oxidative stress.
Purpose of the Study:
- To investigate HDL function in patients with obstructive sleep apnea (OSA).
- To determine if HDL exhibits dysfunction in OSA, potentially contributing to cardiovascular risk.
Main Methods:
- Recruited 128 OSA patients and 82 controls.
- Assessed HDL dysfunction by measuring its ability to inhibit LDL oxidation ex vivo.
- Quantified plasma levels of oxidized LDL and 8-isoprostane.
Main Results:
- OSA subjects exhibited elevated plasma 8-isoprostane levels.
- Despite similar lipid profiles, OSA patients showed significantly greater HDL dysfunction and increased oxidized LDL.
- Apnea-hypopnea index was the primary determinant of HDL dysfunction in OSA.
Conclusions:
- HDL is dysfunctional in OSA, impairing its ability to prevent oxidized lipid formation and inactivation.
- This HDL dysfunction may contribute to the heightened cardiovascular risk observed in OSA patients.
Objective:
HDL is anti-atherogenic and has antioxidant property. HDL dysfunction has been reported in patients with coronary heart disease and we hypothesize that HDL may also be dysfunctional in obstructive sleep apnea (OSA), a condition associated with increased oxidative stress.
Methods:
128 OSA patients and 82 controls were recruited. HDL dysfunction was determined by evaluating the ability of HDL to inhibit LDL oxidation ex vivo. Plasma HDL was incubated with native LDL in the presence of dichlorofluorescein which fluoresced upon interaction with lipid oxidation products. Plasma levels of oxidized LDL and 8-isoprostane were measured by ELISA and a specific enzyme immunoassay, respectively.
Results:
Plasma total 8-isoprostane levels were elevated in OSA subjects (p<0.01). Despite having similar concentrations of plasma lipids and apolipoproteins as controls, OSA subjects had greater degree of HDL dysfunction (p<0.01) and increased oxidized LDL levels (p<0.05). The apnea-hypopnea index was the main determinant of HDL dysfunction in OSA, accounting for 30% of its variance, with oxidized LDL and apolipoprotein AI contributing to 8% and 5% of its variance respectively (p<0.001).
Conclusion:
HDL is dysfunctional in preventing the formation and inactivation of oxidized lipids in OSA subjects and may partly contribute to their increased cardiovascular risk.
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