Liang Xie1,2, Penghao Zhen1,3, Fuchao Yu1,3, Xiaojin Yu4, Hai Qian5, Fang Yang6, Jiayi Tong7,8. 1. School of Medicine, Southeast University, Nanjing, China. 2. Jinling Hospitial, School of Medicine, Nanjing University, Nanjing, China. 3. Department of Cardiology, Zhongda Hospital, Nanjing, China. 4. School of Public Health, Southeast University, 87 Dingjiaqiao, Nanjing, China. 5. Center of Drug Discovery, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China. 6. State Key Laboratory of Bioelectronics, Jiangsu Key Laboratory for Biomaterials and Devices, School of Biomedical Sciences and Medical Engineering, Southeast University, Nanjing, China. 7. School of Medicine, Southeast University, Nanjing, China. 101007925@seu.edu.cn. 8. Department of Cardiology, Zhongda Hospital, Nanjing, China. 101007925@seu.edu.cn.
Abstract
PURPOSE: Previous studies suggest that sleep apnea hypopnea syndrome (SAHS) is an independent risk factor that contributes to certain cardiovascular events. However, there are studies arguing that patients with SAHS had lower peak troponin levels when suffering cardiovascular events compared to patients without SAHS, which indicates that there may potentially be a protective effect of SAHS. This meta-analysis aimed to assess the impact of SAHS on cardiovascular events. METHODS: Databases were searched for studies that examined cardiac biomarkers or reported angiographic data when patients with SAHS experienced cardiovascular events. The data about peak cardiac biomarkers and angiographic coronary lesion were extracted and then used to compute the pooled standardized mean difference (SMD) and 95% confidence interval (95% CI). RESULTS: Among 26 studies included in the meta-analysis, there was not a definite difference between the SAHS group and the control group for troponins (SMD, 0.05; 95% CI, [- 0.16, 0.26]), creatine kinase (SMD, - 0.08; 95% CI, [- 0.38, 0.22]), and CK-MB (SMD, - 0.11; 95% CI, [- 0.51, 0.29]). However, patients with SAHS revealed worse coronary lesion condition grading via both Gensini score (SMD, 0.63; 95% CI, [0.31, 0.95]) and SYNTAX score (SMD, 0.99; 95% CI, [0.31-1.67]). CONCLUSIONS: Ischemic preconditioning induced by the intermittent hypoxia at the early stage could generate a cardiac protection effect, which would then benefit SAHS patients encountering a major adverse cardiovascular event.
PURPOSE: Previous studies suggest that sleep apnea hypopnea syndrome (SAHS) is an independent risk factor that contributes to certain cardiovascular events. However, there are studies arguing that patients with SAHS had lower peak troponin levels when suffering cardiovascular events compared to patients without SAHS, which indicates that there may potentially be a protective effect of SAHS. This meta-analysis aimed to assess the impact of SAHS on cardiovascular events. METHODS: Databases were searched for studies that examined cardiac biomarkers or reported angiographic data when patients with SAHS experienced cardiovascular events. The data about peak cardiac biomarkers and angiographic coronary lesion were extracted and then used to compute the pooled standardized mean difference (SMD) and 95% confidence interval (95% CI). RESULTS: Among 26 studies included in the meta-analysis, there was not a definite difference between the SAHS group and the control group for troponins (SMD, 0.05; 95% CI, [- 0.16, 0.26]), creatine kinase (SMD, - 0.08; 95% CI, [- 0.38, 0.22]), and CK-MB (SMD, - 0.11; 95% CI, [- 0.51, 0.29]). However, patients with SAHS revealed worse coronary lesion condition grading via both Gensini score (SMD, 0.63; 95% CI, [0.31, 0.95]) and SYNTAX score (SMD, 0.99; 95% CI, [0.31-1.67]). CONCLUSIONS: Ischemic preconditioning induced by the intermittent hypoxia at the early stage could generate a cardiac protection effect, which would then benefit SAHS patients encountering a major adverse cardiovascular event.
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