Umeda Akira, Miyagawa Kazuya, Mochida Atsumi, Takeda Hiroshi, Takeda Kotaro, Okada Yasumasa, Gozal David
Department of Respiratory Medicine, International University of Health and Welfare Shioya Hospital, Yaita, Japan.
Department of Pharmacology, School of Pharmacy, International University of Health and Welfare, Otawara, Japan.
Front Physiol. 2020 Oct 22;11:583735. doi: 10.3389/fphys.2020.583735. eCollection 2020.
Obstructive sleep apnea (OSA) patients are at risk for increased blood pressure and carotid intima-media thickness (IMT), with pulmonary hypertension and right-sided heart failure potentially developing as well. Chronic intermittent hypoxia (IH) has been used as an OSA model in animals, but its effects on vascular beds have not been evaluated using objective unbiased tools. Previously published and current experimental data in mice exposed to IH were evaluated for IMT in aorta and pulmonary artery (PA) after IH with or without normoxic recovery using software for meta-analysis, Review Manager 5. Because IMT data reports on PA were extremely scarce, atherosclerotic area percentage from lumen data was also evaluated. IH significantly increased IMT parameters in both aorta and PA as illustrated by Forest plots ( < 0.01), which also confirmed that IMT values after normoxic recovery were within the normal range in both vascular beds. One-sided scarce lower areas in Funnel Plots were seen for both aorta and PA indicating the likelihood of significant publication bias. Forest and Funnel plots, which provide unbiased assessments of published and current data, suggest that IH exposures may induce IMT thickening that may be reversed by normoxic recovery in both aorta and PA. In light of the potential likelihood of publication bias, future studies are needed to confirm or refute the findings. In conclusion, OSA may induce IMT thickening (e.g., aorta and/or PA), but the treatment (e.g., nasal continuous positive airway pressure) will likely lead to improvements in such findings.
阻塞性睡眠呼吸暂停（OSA）患者有血压升高和颈动脉内膜中层厚度（IMT）增加的风险，还可能发展为肺动脉高压和右心衰竭。慢性间歇性缺氧（IH）已被用作动物的OSA模型，但尚未使用客观无偏倚工具评估其对血管床的影响。使用荟萃分析软件Review Manager 5，对先前发表的以及当前在暴露于IH的小鼠中的实验数据进行评估，以观察在有或没有常氧恢复的情况下，IH后主动脉和肺动脉（PA）的IMT情况。由于关于PA的IMT数据报告极为稀少，因此还评估了管腔数据中的动脉粥样硬化面积百分比。森林图显示，IH显著增加了主动脉和PA的IMT参数（<0.01），这也证实了常氧恢复后的IMT值在两个血管床中均处于正常范围内。主动脉和PA的漏斗图均出现单侧稀少的较低区域，表明存在显著发表偏倚的可能性。森林图和漏斗图对已发表和当前数据提供了无偏倚评估，表明IH暴露可能会诱导IMT增厚，而常氧恢复可能会使其逆转，在主动脉和PA中均如此。鉴于存在发表偏倚的潜在可能性，需要未来的研究来证实或反驳这些发现。总之，OSA可能会诱导IMT增厚（例如主动脉和/或PA），但治疗（例如鼻持续气道正压通气）可能会改善这些情况。
