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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.
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.
The analysis revealed that flow-mediated dilation(FMD) in patients with OSAS was significantly lower than that in controls (standardized mean difference(SMD) 1.21, 95% CI 1.60 to 0.83, P<0.0001). Subgroup analysis of moderate–severe OSAS (AHI ≥15) showed that patients with moderate–severe OSAS had significantly lower FMD than controls (SMD 1.02, 95% CI1.31 to 0.73, P<0.0001) without significant study heterogeneity (Q statistic P=0.154, I2=42.9%) and publication bias (P=0.243). In contrast to FMD, nitroglycerin(NTG)-induced dilation was similar in the OSAS and control groups (SMD 0.11, 95% CI 0.22 to 0.44, P=0.306) without significant heterogeneity (Q statistic P=0.164, I2 =44.7%) and publication bias (P=0.856).Carotid-femoral pulse wave velocity (SMD 0.45, 95% CI 0.21–0.69, P<0.0001), augmentation index (SMD 0.57, 95% CI 0.25–0.90, P<0.0001). Similarly, subgroup analysis also demonstrated significantly higher carotid-femoral PWV in patients with moderate–severe OSAS(SMD 0.55, 95% CI 0.27–0.84, P<0.0001) without significant study heterogeneity (I2=46.4%, P=0.133)Consistently, Augmentation index (AIx), which also indicates arterial stiffness, was significantly higher in patients with OSAS than in controls (SMD 0.57, 95% CI 0.25–0.90, P<0.0001) without study heterogeneity (I2=0.0%, P=0.826).Serum levels of high-sensitivity C-reactive protein and C-reactive protein (SMD 0.58, 95% CI 0.42–0.73, P<0.0001) were significantly higher in patients with OSAS than in controls.
To the best of our knowledge, this meta-analysis is the first to investigate the impact of OSAS, per se, on endothelial function and arterial stiffening. We demonstrate that OSAS, particularly moderate–severe OSAS, appeared to reduce endothelial function, increase arterial stiffness, and cause chronic inflammation, leading to the development of cardiovascular disease.