Hluchanova Alzbeta, Kollar Branislav, Klobucnikova Katarina, Hardonova Miroslava, Poddany Michal, Zitnanova Ingrid, Dvorakova Monika, Konarikova Katarina, Tedla Miroslav, Urik Milan, Klail Pavel, Skopek Petr, Turcani Peter, Siarnik Pavel
Department of Neurology, University Hospital Bratislava, 85107 Bratislava, Slovakia.
1st Department of Neurology, Faculty of Medicine, Comenius University, University Hospital, 81499 Bratislava, Slovakia.
Life (Basel). 2023 Feb 4;13(2):441. doi: 10.3390/life13020441.
Obstructive sleep apnea (OSA) activates several pathophysiological mechanisms which can lead to the development of vascular diseases. Endothelial dysfunction (ED) is an initial step in the development of atherosclerosis. The association between ED and OSA has been described in several studies, even in previously healthy subjects. High-density lipoproteins (HDL) were generally considered to be atheroprotective, and low-density lipoprotein (LDL) to be an atherogenic component of lipoproteins. However, recent findings suggest a pro-atherogenic role of small HDL subfractions (8-10) and LDL subfractions (3-7). This study aimed to evaluate the relationship between endothelial function and lipid subfractions in previously healthy OSA subjects.
We prospectively enrolled 205 subjects with sleep monitoring. Plasma levels of triacylglycerols, total cholesterol, LDL, HDL, and their subfractions were assessed. Endothelial function was determined using peripheral arterial tonometry, and reperfusion hyperemia index (RHI) was assessed.
Plasma levels of small and intermediate HDL subfractions have statistically significant pro-atherogenic correlations with endothelial function ( = 0.015 and = 0.019). In other lipoprotein levels, no other significant correlation was found with RHI. In stepwise multiple linear regression analysis, small HDL (beta = -0.507, = 0.032) was the only significant contributor in the model predicting RHI.
In our studied sample, a pro-atherogenic role of small HDL subfractions in previously healthy subjects with moderate-to-severe OSA was proven.
阻塞性睡眠呼吸暂停(OSA)会激活多种病理生理机制,这些机制可导致血管疾病的发生。内皮功能障碍(ED)是动脉粥样硬化发展的起始步骤。多项研究已描述了ED与OSA之间的关联,即使在既往健康的受试者中也是如此。高密度脂蛋白(HDL)通常被认为具有抗动脉粥样硬化作用,而低密度脂蛋白(LDL)则被认为是脂蛋白的致动脉粥样硬化成分。然而,最近的研究结果表明,小HDL亚组分(8 - 10)和LDL亚组分(3 - 7)具有促动脉粥样硬化作用。本研究旨在评估既往健康的OSA受试者内皮功能与脂质亚组分之间的关系。
我们前瞻性纳入了205名进行睡眠监测的受试者。评估了血浆甘油三酯、总胆固醇、LDL、HDL及其亚组分的水平。使用外周动脉张力测量法测定内皮功能,并评估再灌注充血指数(RHI)。
小和中等HDL亚组分的血浆水平与内皮功能具有统计学上显著的促动脉粥样硬化相关性( = 0.015和 = 0.019)。在其他脂蛋白水平中,未发现与RHI有其他显著相关性。在逐步多元线性回归分析中,小HDL(β = -0.507, = 0.032)是预测RHI模型中唯一的显著贡献因素。
在我们的研究样本中,已证实小HDL亚组分在既往健康的中重度OSA受试者中具有促动脉粥样硬化作用。