阻塞性睡眠呼吸暂停低通气综合征30例

目的探讨阻塞性睡眠呼吸暂停低通气综合征的临床特点及治疗方法。方法30例OSAHS患儿均在局麻下行扁桃体切除术和(或)腺样体切除术。结果随访0.6～2.0年。治愈27例(90%),好转2例(6.67%),无效1例(3.33%)。结论儿童鼾症多因扁桃体、腺样体肥大引起,确诊后应尽早手术治疗。扁桃体切除术和(或)腺样体切除术是治疗OSAHS有效的方法。鼻部疾患或颅面畸形将影响其疗效,对颅面畸形者可考虑持续气道正压通气治疗。     

睡眠呼吸暂停综合征与代谢综合征

目的OSAS与MS关系密切,本文就OSAHS与MS各组分关系的进展进行综述。方法Coughlin等对61例男性OSAS患者进行研究,发现正常对照组MS的患病率仅为35%,OSAS患者组MS的患病率却高达87%。结果OSAS与MS密切相关,二者均是心血管疾病的危险因素,并认为OSAS与MS独立相关。结论长期睡眠呼吸暂停的存在可能导致或加重MS的发生,而MS又是引发心血管疾病的重要危险因素。所以在实际工作中,早期发现并干预治疗OSAS患者,可有助于避免或减少MS及随之的心血管疾病的发生。     

等离子射频消融治疗阻塞性睡眠呼吸暂停综合症规范化护理

我科自2005年以来,有选择性地为42名睡眠呼吸暂停综合症的病人行低湿等离子消融手术,均获得成功,现将护理体会加以总结。     

阻塞性睡眠呼吸暂停综合征相关维生素D受体蛋白基因的生物信息学分析

目的分析维生素D受体蛋白(vitamin D receptor protein,VDR)的理化性质、分子结构和蛋白的相互作用,及其在阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)中的功能及作用机制。方法利用NCBI、ExPASy、Protscale、SignalP 4. 0 Server、TMHMM Server v. 2. 0、PSORTⅡ、SOPMA、Conserved Domain、SWISS-MODEL、NetNGlyc 1. 0 Sever、NetOGlyc 4. 0 Server、Netphos 2. 0 Server、STRING等生物信息学软件对VDR进行结构、性质方面的系统分析。结果 VDR是一种酸性不稳定的亲水性蛋白,无信号肽形成区域,无跨膜结构,广泛定位于细胞核,是一种非分泌型蛋白。VDR的主要二级结构为无规卷曲,是NR-LBD超家族及NR-DBD样超家族的成员之一,可与RXRG、RXRB、EP300等蛋白发生理化相互作用。结论 VDR不仅参与甲状腺激素信号通路、脂肪细胞因子信号通路...     

睡眠呼吸暂停综合征病人的健康教育

目的 探讨健康教育对睡眠呼吸暂停综合征(SAS)病人的重要作用。方法 通过系统讲解和个别指导的方法对SAS病人进行健康教育。结果 10例病人均对本病有了正确认识,并树立合理生活习惯,戒烟忌酒者6例。接受手术治疗者2例。结论 接受健康教育的病人均对本病有了正确认识,建立了科学合理的生活习惯,病情不同程度得到改善。     

阻塞性睡眠呼吸暂停综合征患者手术治疗前后血压和血糖的比较

本文分析了笔者所在医院40例阻塞性睡眠呼吸暂停综合症合并糖尿病、高血压病人的术前、术后血糖、血压变化及用药变化情况。     

拜耳模克隆~:关爱睡眠呼吸暂停综合症患者

由于呼吸问题，睡眠呼吸暂停综合症患者的健康及生活质量受到了影响。透过使用鼻罩，在患者睡眠时将空气轻轻吹人患者的喉咙，是一种简单、有效的治疗方法。最近，全球医疗设备开发商及制造商瑞思迈公司与拜耳材料科技强强联手，采用拜耳的模克隆聚碳酸酯为原料生产这种鼻罩。     

急性心肌梗死患者心电图改变与其并发心律失常及死亡的相关性分析

目的 探讨急性心肌梗死患者心电图改变与其并发心律失常及死亡的相关性。方法 抽取选择于2007年3月至2009年6月来我院就诊的急性心肌梗死患者80例。通过心电图检查,观察其心电图表现特征,并对急性心肌梗死患者心电图改变与并发室性心律失常及死亡的相关性进行分析。结果 80例急性心肌梗死患者中,典型心电图表现者42例,占52.5%;不典型心电图表现者38例,占47.5%;急性心肌梗死ST段抬高57例,占71.3%;非ST段抬高性心肌梗死17例,占30.0%。ST段抬高性与非ST段抬高心肌梗死患者与室性心律失常发生的相关性存在统计学差异(P<0.05),与心肌梗死患者的病死率的相关性,并不存在统计学差异(P>0.05)。结论 急性心肌梗死患者心电图表现为急性ST段抬高合并室性心律失常的发生率高于非ST段抬高的患者。     

预激综合征合并快速心律失常的治疗体会

目的观察不同药物治疗预激综合征合并心房纤颤(Af)病人的疗效。方法观察预激综合征合并快速心律失常病人25例,回顾性分析不同治疗方法的效果。结果胺碘酮、心律平的疗效稳定,药物复律时应选用心律平或胺碘酮。     

Severe Obstructive Sleep Apnea Disrupts Vigilance-State-Dependent Metabolism

The direct pathophysiological effects of obstructive sleep apnea (OSA) have been well described. However, the systemic and metabolic consequences of OSA are less well understood. The aim of this secondary analysis was to translate recent findings in healthy subjects on vigilance-state-dependent metabolism into the context of OSA patients and answer the question of how symptomatic OSA influences metabolism and whether these changes might explain metabolic and cardiovascular consequences of OSA. Patients with suspected OSA were assigned according to their oxygen desaturation index (ODI) and Epworth Sleepiness Scale (ESS) score into symptomatic OSA and controls. Vigilance-state-dependent breath metabolites assessed by high-resolution mass spectrometry were used to test for a difference in both groups. In total, 44 patients were eligible, of whom 18 (40.9%) were assigned to the symptomatic OSA group. Symptomatic OSA patients with a median [25%, 75% quartiles] ODI of 40.5 [35.0, 58.8] events/h and an ESS of 14.0 [11.2, 15.8] showed moderate to strong evidence for differences in 18 vigilance-state-dependent breath compounds compared to controls. These identified metabolites are part of major metabolic pathways in carbohydrate, amino acid, and lipid metabolism. Thus, beyond hypoxia per se, we hypothesize that disturbed sleep in OSA patients persists as disturbed sleep-dependent metabolite levels during daytime.     

A Narrative Review of the Association between Obstructive Sleep Apnea and Glaucoma in Adults

Background: Obstructive sleep apnea (OSA) is a sleep disorder, primarily of the upper airway, which not only has a significant impact on quality of life but is also associated with various systemic diseases. Several ophthalmological diseases are also associated with OSA, especially glaucoma. The purpose of this review is to take a closer look at the causality and mutual influence. Methods: A systematic literature search was conducted using PubMed. A total of 19 studies with 316,178 adult participants were included. Results: Eleven of the sixteen studies concentrating on the prevalence of glaucoma in patients with OSA showed an association of both entities. One paper found a higher risk for progression of glaucoma in OSA patients. Five of the sixteen included studies failed to show a correlation between OSA and glaucoma. One study out of three surveying specific ophthalmological parameters showed an influence of OSA therapy on retinal nerve fiber layer (RNFL) thinning and vision. One study showed a rise in intraocular pressure (IOP), while two other studies showed no increase under continuous positive airway pressure (CPAP). Conclusions: Our findings suggest an association between OSA and glaucoma and, especially, between OSA and thinning of RNFL. CPAP therapy appears to be also suitable for patients with comorbid glaucoma.     

Sensorimotor Cortical Activity during Respiratory Arousals in Obstructive Sleep Apnea

Intensity of respiratory cortical arousals (RCA) is a pathophysiologic trait in obstructive sleep apnea (OSA) patients. We investigated the brain oscillatory features related to respiratory arousals in moderate and severe OSA. Raw electroencephalography (EEG) data recorded during polysomnography (PSG) of 102 OSA patients (32 females, mean age 51.6 ± 12 years) were retrospectively analyzed. Among all patients, 47 had moderate (respiratory distress index, RDI = 15–30/h) and 55 had severe (RDI > 30/h) OSA. Twenty RCA per sleep stage in each patient were randomly selected and a total of 10131 RCAs were analyzed. EEG signals obtained during, five seconds before and after the occurrence of each arousal were analyzed. The entropy (approximate (ApEn) and spectral (SpEn)) during each sleep stage (N1, N2 and REM) and area under the curve (AUC) of the EEG signal during the RCA was computed. Severe OSA compared to moderate OSA patients showed a significant decrease (p < 0.0001) in the AUC of the EEG signal during the RCA. Similarly, a significant decrease in spectral entropy, both before and after the RCA was observed, was observed in severe OSA patients when compared to moderate OSA patients. Contrarily, the approximate entropy showed an inverse pattern. The highest increase in approximate entropy was found in sleep stage N1. In conclusion, the dynamic range of sensorimotor cortical activity during respiratory arousals is sleep-stage specific, dependent on the frequency of respiratory events and uncoupled from autonomic activation. These findings could be useful for differential diagnosis of severe OSA from moderate OSA.     

Elevated Monocytic Interleukin-8 Expression under Intermittent Hypoxia Condition and in Obstructive Sleep Apnea Patients

Obstructive sleep apnea (OSA) is a disease with great cardiovascular risk. Interleukin-8 (IL-8), an important chemokine for monocyte chemotactic migration, was studied under intermittent hypoxia condition and in OSA patients. Monocytic THP-1 cells were used to investigate the effect of intermittent hypoxia on the regulation of IL-8 by an intermittent hypoxic culture system. The secreted protein and mRNA levels were studied by means of enzyme-linked immunosorbent assay and RT/real-time PCR. The chemotactic migration of monocytes toward a conditioned medium containing IL-8 was performed by means of the transwell filter migration assay. Peripheral venous blood was collected from 31 adult OSA patients and RNA was extracted from the monocytes for the analysis of IL-8 expression. The result revealed that intermittent hypoxia enhanced the monocytic THP-1 cells to actively express IL-8 at both the secreted protein and mRNA levels, which subsequently increased the migration ability of monocytes toward IL-8. The ERK, PI3K and PKC pathways were demonstrated to contribute to the activation of IL-8 expression by intermittent hypoxia. In addition, increased monocytic IL-8 expression was found in OSA patients, with disease severity dependence and diurnal changes. This study concluded the monocytic IL-8 gene expression can be activated by intermittent hypoxia and increased in OSA patients.     

Obstructive Sleep Apnea Syndrome In Vitro Model: Controlled Intermittent Hypoxia Stimulation of Human Stem Cells-Derived Cardiomyocytes

Cardiovascular morbidity is the leading cause of death of obstructive sleep apnea (OSA) syndrome patients. Nocturnal airway obstruction is associated with intermittent hypoxia (IH). In our previous work with cell lines, incubation with sera from OSA patients induced changes in cell morphology, NF-κB activation and decreased viability. A decrease in beating rate, contraction amplitude and a reduction in intracellular calcium signaling was also observed in human cardiomyocytes differentiated from human embryonic stem cells (hESC-CMs). We expanded these observations using a new controlled IH in vitro system on beating hESC-CMs. The Oxy-Cycler system was programed to generate IH cycles. Following IH, we detected the activation of Hif-1α as an indicator of hypoxia and nuclear NF-κB p65 and p50 subunits, representing pro-inflammatory activity. We also detected the secretion of inflammatory cytokines, such as MIF, PAI-1, MCP-1 and CXCL1, and demonstrated a decrease in beating rate of hESC-CMs following IH. IH induces the co-activation of inflammatory features together with cardiomyocyte alterations which are consistent with myocardial damage in OSA. This study provides an innovative approach for in vitro studies of OSA cardiovascular morbidity and supports the search for new pharmacological agents and molecular targets to improve diagnosis and treatment of patients.     

Disruption of Circadian Rhythm Genes in Obstructive Sleep Apnea Patients—Possible Mechanisms Involved and Clinical Implication

Obstructive sleep apnea (OSA) is a chronic condition characterized by recurrent pauses in breathing caused by the collapse of the upper airways, which results in intermittent hypoxia and arousals during the night. The disorder is associated with a vast number of comorbidities affecting different systems, including cardiovascular, metabolic, psychiatric, and neurological complications. Due to abnormal sleep architecture, OSA patients are at high risk of circadian clock disruption, as has been reported in several recent studies. The circadian clock affects almost all daily behavioral patterns, as well as a plethora of physiological processes, and might be one of the key factors contributing to OSA complications. An intricate interaction between the circadian clock and hypoxia may further affect these processes, which has a strong foundation on the molecular level. Recent studies revealed an interaction between hypoxia-inducible factor 1 (HIF-1), a key regulator of oxygen metabolism, and elements of circadian clocks. This relationship has a strong base in the structure of involved elements, as HIF-1 as well as PER, CLOCK, and BMAL, belong to the same Per-Arnt-Sim domain family. Therefore, this review summarizes the available knowledge on the molecular mechanism of circadian clock disruption and its influence on the development and progression of OSA comorbidities.     

Proteomic Biomarkers of the Apnea Hypopnea Index and Obstructive Sleep Apnea: Insights into the Pathophysiology of Presence,Severity, and Treatment Response

Obstructive sleep apnea (OSA), a disease associated with excessive sleepiness and increased cardiovascular risk, affects an estimated 1 billion people worldwide. The present study examined proteomic biomarkers indicative of presence, severity, and treatment response in OSA. Participants (n = 1391) of the Stanford Technology Analytics and Genomics in Sleep study had blood collected and completed an overnight polysomnography for scoring the apnea–hypopnea index (AHI). A highly multiplexed aptamer-based array (SomaScan) was used to quantify 5000 proteins in all plasma samples. Two separate intervention-based cohorts with sleep apnea (n = 41) provided samples pre- and post-continuous/positive airway pressure (CPAP/PAP). Multivariate analyses identified 84 proteins (47 positively, 37 negatively) associated with AHI after correction for multiple testing. Of the top 15 features from a machine learning classifier for AHI ≥ 15 vs. AHI < 15 (Area Under the Curve (AUC) = 0.74), 8 were significant markers of both AHI and OSA from multivariate analyses. Exploration of pre- and post-intervention analysis identified 5 of the 84 proteins to be significantly decreased following CPAP/PAP treatment, with pathways involving endothelial function, blood coagulation, and inflammatory response. The present study identified PAI-1, tPA, and sE-Selectin as key biomarkers and suggests that endothelial dysfunction and increased coagulopathy are important consequences of OSA, which may explain the association with cardiovascular disease and stroke.     

Reconstitution of Monocyte Subsets and PD-L1 Expression but Not T Cell PD-1 Expression in Obstructive Sleep Apnea Patients upon PAP Therapy

Obstructive sleep apnea (OSA) is characterized by nocturnal breathing intermissions resulting in oxidative stress and eventually, a low-grade systemic inflammation. The study aimed to investigate the impact of positive airway pressure (PAP) therapy on the inflammatory milieu as measured by monocyte and T cell phenotypic alterations. Participants were assessed for their OSA severity before PAP therapy and about six months later, including patient-reported outcome and therapy usage by telemetry readout. The distributions of the CD14/CD16-characterized monocyte subsets as well as the CD4/CD8-characterized effector T cell subsets with regard to their PD-1 and PD-L1 expression were analyzed by flow cytometry from blood samples. Data of 25 patients revealed a significant reconstitution of the monocyte subset distribution and a decrease in PD-L1 expression on pan-monocytes and CD8⁺ T cells without an association to initial AHI and overweight. The PD-1 expression was still increased on T cell subsets, especially on CD4⁺ TH17/22 cells. We conclude that PAP therapy might have a rapid effect on the monocyte phenotype and overall PD-L1 expression levels. However, T cell immune alterations especially on TH17/22 cells persist longer, indicating an ongoing disturbance of the adaptive immune system.     

The Effect of Sera from Children with Obstructive Sleep Apnea Syndrome (OSAS) on Human Cardiomyocytes Differentiated from Human Embryonic Stem Cells

Obstructive sleep apnea syndrome (OSAS) patients suffer from cardiovascular morbidity, which is the leading cause of death in this disease. Based on our previous work with transformed cell lines and primary rat cardiomyocytes, we determined that upon incubation with sera from pediatric OSAS patients, the cell’s morphology changes, NF-κB pathway is activated, and their beating rate and viability decreases. These results suggest an important link between OSAS, systemic inflammatory signals and end-organ cardiovascular diseases. In this work, we confirmed and expanded these observations on a new in vitro system of beating human cardiomyocytes (CM) differentiated from human embryonic stem cells (hES). Our results show that incubation with pediatric OSAS sera, in contrast to sera from healthy children, induces over-expression of NF-κB p50 and p65 subunits, marked reduction in CMs beating rate, contraction amplitude and a strong reduction in intracellular calcium signal. The use of human CM cells derived from embryonic stem cells has not been previously reported in OSAS research. The results further support the hypothesis that NF-κB dependent inflammatory pathways play an important role in the evolution of cardiovascular morbidity in OSAS. This study uncovers a new model to investigate molecular and functional aspects of cardiovascular pathology in OSAS.