Preoperative Predictors of Response to Hypoglossal Nerve Stimulation for Obstructive Sleep Apnea.


  • 影响因子:2.23
  • DOI:10.1177/0194599820901499
  • 作者列表:"Xiao R","Trask DK","Kominsky AH
  • 发表时间:2020-01-21

OBJECTIVE:Hypoglossal nerve stimulation (HGNS) is an effective treatment for patients with obstructive sleep apnea (OSA) who fail continuous positive airway pressure (CPAP). We assessed the relationship between patient characteristics and response to HGNS. STUDY DESIGN:Retrospective cohort study. SETTING:Single tertiary care institution. SUBJECTS AND METHODS:This study included CPAP-intolerant patients with moderate to severe OSA after HGNS system implantation from November 2015 to December 2017. Patient measures, drug-induced sleep endoscopy (DISE) findings, and apnea-hypopnea indices (AHIs) were recorded. RESULTS:Forty-eight patients underwent implantation with the following median measures: age, 66 years; body mass index, 28.6; and neck circumference, 41.0 cm. Patients were classified by Friedman tongue position (II, 27%; III, 56%; IV, 17%) and Mallampati grade (I, 25%; II, 50%; III, 23%; IV, 2%). By DISE, 71% had anterior-posterior palatal collapse. Additionally, 38% had lateral oropharynx collapse; 50%, tongue base collapse; and 27%, epiglottis collapse. Following implantation, median AHI improved from 38.5 to 2.7 (P < .001), and 92% of patients had no worse than mild OSA (8% moderate). Patients with Friedman tongue position grade II/III experienced greater change in AHI as compared with grade IV (94.2% vs 73.8%, P < .001). Patients with Mallampati score I/II experienced greater improvement versus score III/IV (94.7% vs 66.5%, P < .001). No DISE findings, including any obstruction or collapse, were associated with change in AHI. CONCLUSION:This study further confirms HGNS as an effective treatment of CPAP-intolerant OSA. Office measures such as Friedman tongue position IV and Mallampati III/IV were associated with mildly decreased response. DISE findings were not associated with patient response.


目的: 舌下神经刺激 (HGNS) 是持续气道正压通气 (CPAP) 失败的阻塞性睡眠呼吸暂停 (OSA) 患者的有效治疗方法。我们评估了患者特征与 HGNS 反应之间的关系。 研究设计: 回顾性队列研究。 单位: 单一三级医疗机构。 对象和方法: 本研究纳入了 2015年11月至 2017年12月 HGNS 系统植入后 CPAP 不耐受的中重度 OSA 患者。记录患者测量、药物诱导睡眠内镜检查 (DISE) 结果和呼吸暂停低通气指数 (AHIs)。 结果: 48 例患者接受了以下中位测量: 年龄,66 岁; 体重指数,28.6; 颈围,41.0厘米。患者按 Friedman 舌位 (ⅱ,27%; ⅲ,56%; ⅳ,17%) 和 Mallampati 分级 (ⅰ,25%; ⅱ,50%;III,23%; IV,2%)。到 DISE,71% 的患者有腭前-后塌陷。此外,38% 有口咽外侧塌陷; 50%,舌根塌陷; 27%,会厌塌陷。植入后,AHI 中位数从 38.5 改善至 2.7 (P



作者列表:["Chen Q","Lin G","Huang J","Chen L","Liu Y","Huang J","Zhang S","Lin Q"]

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.

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来源期刊:Circulation research
作者列表:["Du Y","Wang X","Li L","Hao W","Zhang H","Li Y","Qin Y","Nie S","Christopher TA","Lopez BL","Lau WB","Wang Y","Ma XL","Wei Y"]

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.

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作者列表:["Mendelson M","Inami T","Lyons O","Alshaer H","Marzolini S","Oh P","Bradley TD"]

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.

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