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Impact of Obstructive Sleep Apnea Syndrome on Endothelial Function, Arterial Stiffening, and Serum Inflammatory Markers: An Updated Meta‐analysis and Metaregression of 18 Studies

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) has been indicated to contribute to the development of cardiovascular disease; however, the underlying mechanism remains unclear. This study aimed to test the hypothesis that OSAS may be associated with cardiovascular disease by elevating serum lev...

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Detalles Bibliográficos
Autores principales: Wang, Jiayang, Yu, Wenyuan, Gao, Mingxin, Zhang, Fan, Gu, Chengxiong, Yu, Yang, Wei, Yongxiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4845236/
https://www.ncbi.nlm.nih.gov/pubmed/26567373
http://dx.doi.org/10.1161/JAHA.115.002454
Descripción
Sumario:BACKGROUND: Obstructive sleep apnea syndrome (OSAS) has been indicated to contribute to the development of cardiovascular disease; however, the underlying mechanism remains unclear. This study aimed to test the hypothesis that OSAS may be associated with cardiovascular disease by elevating serum levels of inflammatory markers and causing arterial stiffening and endothelial dysfunction. METHODS AND RESULTS: Related scientific reports published from January 1, 2006, to June 30, 2015, were searched in the following electronic literature databases: PubMed, Excerpta Medica Database, ISI Web of Science, Directory of Open Access Journals, and the Cochrane Library. The association of OSAS with serum levels of inflammatory markers, endothelial dysfunction, and arterial stiffening were investigated. Overall, 18 eligible articles containing 736 patients with OSAS and 424 healthy persons were included in this meta‐analysis. Flow‐mediated dilation in patients with moderate–severe OSAS was significantly lower than that in controls (standardized mean difference −1.02, 95% CI −1.31 to −0.73, P<0.0001). Carotid‐femoral pulse wave velocity (standardized mean difference 0.45, 95% CI 0.21–0.69, P<0.0001), augmentation index (standardized mean difference 0.57, 95% CI 0.25–0.90, P<0.0001), and serum levels of high‐sensitivity C‐reactive protein and C‐reactive protein (standardized mean difference 0.58, 95% CI 0.42–0.73, P<0.0001) were significantly higher in patients with OSAS than in controls. CONCLUSION: OSAS, particularly moderate–severe OSAS, appeared to reduce endothelial function, increase arterial stiffness, and cause chronic inflammation, leading to the development of cardiovascular disease.