- 作者列表："Van Steenkiste T","Groenendaal W","Dreesen P","Lee S","Klerkx S","De Francisco R","Deschrijver D","Dhaene T
:Sleep apnea is one of the most common sleep-related breathing disorders. It is diagnosed through an overnight sleep study in a specialized sleep clinic. This setup is expensive and the number of beds and staff are limited, leading to a long waiting time. To enable more patients to be tested, and repeated monitoring for diagnosed patients, portable sleep monitoring devices are being developed. These devices automatically detect sleep apnea events in one or more respiration-related signals. There are multiple methods to measure respiration, with varying levels of signal quality and comfort for the patient. In this study, the potential of using the bio-impedance (bioZ) of the chest as a respiratory surrogate is analyzed. A novel portable device is presented, combined with a two-phase Long Short-Term Memory (LSTM) deep learning algorithm for automated event detection. The setup is benchmarked using simultaneous recordings of the device and the traditional polysomnography in 25 patients. The results demonstrate that using only the bioZ, an area under the precision-recall curve of 46.9% can be achieved, which is on par with automatic scoring using a polysomnography respiration channel. The sensitivity, specificity and accuracy are 58.4%, 76.2% and 72.8% respectively. This confirms the potential of using the bioZ device and deep learning algorithm for automatically detecting sleep respiration events during the night, in a portable and comfortable setup.
: 睡眠呼吸暂停是最常见的睡眠相关呼吸障碍之一。它是通过在专门的睡眠诊所进行夜间睡眠研究来诊断的。这种设置是昂贵的，床和工作人员的数量是有限的，导致很长的等待时间。为了使更多的患者能够接受测试，并对确诊患者进行重复监测，便携式睡眠监测设备正在开发中。这些设备自动检测一个或多个呼吸相关信号中的睡眠呼吸暂停事件。有多种方法来测量呼吸，具有不同水平的信号质量和患者的舒适度。在这项研究中，分析了使用胸部的生物阻抗 (bioZ) 作为呼吸替代物的潜力。提出了一种新型便携式设备，结合两阶段长短期记忆 (LSTM) 深度学习算法，用于自动事件检测。在 25 例患者中，使用设备和传统多导睡眠图的同时记录对设置进行基准。结果表明，仅使用 bioZ，可获得 46.9% 的准确率-召回曲线下面积，与使用多导睡眠监测呼吸通道的自动评分相当。其敏感性、特异性和准确性分别为 58.4% 、 76.2% 和 72.8%。这证实了在便携式和舒适的设置中使用 bioZ 设备和深度学习算法自动检测夜间睡眠呼吸事件的潜力。
METHODS:OBJECTIVE:The functions and molecular regulatory mechanisms of miR-193a-3p in cardiac injury induced by obstructive sleep apnea (OSA) are poorly understood. This study aimed to explore the role of miR-193a-3p in intermittent hypoxia(IH)-induced human umbilical vein endothelial cells (HUVECs) injury. RESULTS:In this study, we found that IH significantly decreased viability but enhanced cell apoptosis. Concurrently, the miR-193a-3p expression level was increased in HUVECs after IH. Subsequent experiments showed that IH-induced injury was ameliorated through miR-193a-3p silence. Fas apoptotic inhibitory molecule 2 (FAIM2) was predicted by bioinformatics analysis and further identified as a direct target gene of miR-193a-3p. Interestingly, the effect of miR-193a-3p inhibition under IH could be reversed by down-regulating FAIM2 expression. CONCLUSION:In conclusion, our study first revealed that miR-193a-3p inhibition could protect HUVECs against intermittent hypoxia-induced damage by negatively regulating FAIM2. These findings could advance our understanding of the underlying mechanisms for OSA-related cardiac injury. METHODS:We exposed HUVECs to IH condition; the expression levels of miR-193a-3p were detected by RT-qPCR. Cell viability, and the expressions of apoptosis-associated proteins were examined via CCK-8, and western blotting, respectively. Target genes of miR-193a-3p were confirmed by dual-luciferase reporter assay.
METHODS:RATIONALE:Obstructive sleep apnea-hypopnea syndrome, a sleep breathing disorder in which chronic intermittent hypoxia (CIH) is the primary pathology, is associated with multiple cardiovascular diseases. However, whether and how CIH may affect cardiac remodeling following myocardial infarction (MI) remains unknown. OBJECTIVE:To determine whether CIH exposure at different periods of MI may exacerbate post-MI heart failure and to identify the mechanisms underlying CIH-exacerbated post-MI remodeling. METHODS AND RESULTS:Adult male mice were subjected to MI (4 weeks) with and without CIH (4 or 8 weeks). CIH before MI (CIH+MI) had no significant effect on post-MI remodeling. However, double CIH exposure (CIH+MI+CIH) or CIH only during the MI period (MI+CIH) significantly exacerbated pathological remodeling and reduced survival rate. Mechanistically, CIH activated TGF-β (tumor growth factor-β)/Smad (homologs of both the Drosophila protein MAD and the C. elegans protein SMA) signaling and enhanced cardiac epithelial to mesenchymal transition, markedly increasing post-MI cardiac fibrosis. Transcriptome analysis revealed that, among 15 genes significantly downregulated (MI+CIH versus MI), Ctrp9 (a novel cardioprotective cardiokine) was one of the most significantly inhibited genes. Real-time polymerase chain reaction/Western analysis confirmed that cardiomyocyte CTRP9 expression was significantly reduced in MI+CIH mice. RNA-sequencing, real-time polymerase chain reaction, and dual-luciferase reporter assays identified that microRNA-214-3p is a novel Ctrp9 targeting miRNA. Its upregulation is responsible for Ctrp9 gene suppression in MI+CIH. Finally, AAV9 (adeno-associated virus 9)-mediated cardiac-specific CTRP9 overexpression or rCTRP9 (recombinated CTRP9) administration inhibited TGF-β/Smad and Wnt/β-catenin pathways, attenuated interstitial fibrosis, improved cardiac function, and enhanced survival rate in MI+CIH animals. CONCLUSIONS:This study provides the first evidence that MI+CIH upregulates miR-214-3p, suppresses cardiac CTRP9 (C1q tumor necrosis factor-related protein-9) expression, and exacerbates cardiac remodeling, suggesting that CTRP9 may be a novel therapeutic target against pathological remodeling in MI patients with obstructive sleep apnea-hypopnea syndrome.
METHODS:STUDY OBJECTIVES:Sleep apnea (SA) is prevalent among patients with coronary artery disease (CAD) and increases cardiovascular risk. A previous study showed that 1 month of cardiac rehabilitation (CR) reduced severity of SA in patients with CAD by reducing fluid accumulation in the legs during the day and the amount of fluid shifting rostrally into the neck overnight. The aim of this study was to evaluate whether CR will lead to longer-term attenuation of SA in patients with CAD. METHODS:Fifteen patients with CAD and SA who had participated in a 1-month randomized trial of the effects of exercise training on SA were followed up until they completed 6 months of CR (age: 65 ± 10 years; body mass index: 27.0 ± 3.9 kg/m²; apnea-hypopnea index [AHI]: 39.0 ± 16.7). The AHI was evaluated at baseline by polysomnography and then at 6 months by portable monitoring at home. Cardiorespiratory fitness (VO2peak) was evaluated via a graded cardiopulmonary exercise test at baseline and 6 months later. The 6-month CR program included once weekly, 90-minute, in-facility exercise sessions, and 4 days per week at-home exercise sessions. RESULTS:After 6 months of CR, there was a 54% reduction in the AHI (30.5 ± 15.2 to 14.1 ± 7.5, P < .001). Body mass index remained unchanged, but VO2peak increased by 27% (20.0 ± 6.1 to 26.0 ± 8.9 mL/kg/min, P = .04). CONCLUSIONS:Participation in CR is associated with a significant long-term decrease in the severity of SA. This finding suggests that attenuation of SA by exercise could be a mechanism underlying reduced mortality following participation in CR in patients with CAD and SA. CLINICAL TRIAL REGISTRATION:This study is registered at www.controlled-trials.com with identifier number ISRCTN50108373.