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阻塞性睡眠呼吸暂停作为动脉粥样硬化的一个风险因素——对预防和个体化治疗的启示。

Obstructive sleep apnoea as a risk factor for atherosclerosis - implication for preventive and personalised treatment.

机构信息

University of Bonn, Bonn, Germany.

出版信息

EPMA J. 2011 Mar;2(1):39-47. doi: 10.1007/s13167-011-0070-5. Epub 2011 Mar 26.

DOI:10.1007/s13167-011-0070-5
PMID:23199125
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3405376/
Abstract

Atherosclerosis with its manifestations and associated diseases is a main cause of morbidity and mortality in industrial countries. The pathomechanisms underlying atherosclerosis are complex and comprise exogenous factors as well as genetic predisposition. Beyond the well-defined risk factors for the development of atherosclerosis, obstructive sleep apnoea (OSA) merits more and more attention. A growing body of evidence has associated OSA with vascular pathologies. Although the exact mechanisms involved are not known, the occurrence of intermittent hypoxia typical for OSA may lead to oxidative stress, inflammation, metabolic and neural changes which in turn are responsible for vessel dysfunction underlying atherosclerosis. It has been demonstrated that therapy with continuous positive airway pressure (CPAP) plays a vasoprotective role. This review summarises data resulting from epidemiological and clinical studies with emphasis on the possible mechanisms linking OSA with atherosclerosis, predictive biomarkers helping identify OSA patients at high cardiovascular risk and personalised treatment approaches.

摘要

动脉粥样硬化及其表现和相关疾病是工业化国家发病率和死亡率的主要原因。动脉粥样硬化的发病机制很复杂,包括外源性因素和遗传易感性。除了明确的动脉粥样硬化发展的危险因素外,阻塞性睡眠呼吸暂停(OSA)越来越受到关注。越来越多的证据将 OSA 与血管病理学联系起来。尽管确切的机制尚不清楚,但 OSA 典型的间歇性缺氧可能导致氧化应激、炎症、代谢和神经变化,进而导致动脉粥样硬化的血管功能障碍。已经证明,持续气道正压通气(CPAP)治疗具有血管保护作用。这篇综述总结了来自流行病学和临床研究的数据,重点介绍了将 OSA 与动脉粥样硬化联系起来的可能机制、有助于识别心血管风险高的 OSA 患者的预测生物标志物以及个性化治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/c3712cdb1c94/13167_2011_70_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/c7138201b735/13167_2011_70_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/26e6d5fcaa77/13167_2011_70_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/c3712cdb1c94/13167_2011_70_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/c7138201b735/13167_2011_70_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/26e6d5fcaa77/13167_2011_70_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db72/3405376/c3712cdb1c94/13167_2011_70_Fig3_HTML.jpg

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