Elevated levels of serum chemerin in patients with obstructive sleep apnea syndrome

Context: Chemerin is implicated to be correlated with obesity and inflammation.

Objective: This study aims to investigate whether serum chemerin is associated with the presence of obstructive sleep apnea syndrome (OSAS).

Methods: A total of 132 patients with OSAS and 108 healthy subjects were enrolled in this study.

Results: Serum chemerin levels were significantly elevated in OSAS patients (120.93 ± 25.84 µg/L vs. 107.51 ± 20.41 µg/L). Multivariable logistic regression analysis revealed that serum chemerin levels were an independent determinant of the presence of OSAS (OR 1.030, 95% CI 1.016–1.045; p < 0.001). Serum chemerin levels in severe OSAS patients were significantly higher compared with those in mild and moderate OSAS patients (p = 0.015 and p = 0.020, respectively). Spearman correlation analysis indicated that serum chemerin levels were correlated with the severity of OSAS (r = 0.210, p = 0.016). Serum chemerin were positively correlated with waist circumference (r = 0.164, p = 0.008), body mass index (r = 0.158, p = 0.014), systolic blood pressure (r = 0.135, p = 0.037), homeostasis model assessment of insulin resistance (r = 0.140, p = 0.031), C-reactive protein (r = 0.202, p = 0.002), and apnea–hypopnea index (r = 0.152, p = 0.022).

Conclusion: Elevated serum chemerin levels could be an independent predicting marker of the presence and severity of OSAS.     

阻塞性睡眠呼吸暂停低通气综合征患者血脂水平的变化

探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与血脂水平的关系。方法:选取32例OSAHS患者(OSAHS组)为试验组和30例健康体检者为对照组,均经多导睡眠监测仪(PSG)检查,测定空腹血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)的含量,比较两组间的差异。结果:OSAHS组空腹时TC、TG、LDL显著高于对照组,而HDL显著低于对照组。结论:OSAHS可引起脂质代谢异常,从而促进心血管疾病的发生。     

Diagnosis of obstructive sleep apnea syndrome]

Symptoms and signs in 12 patients with severe obstructive sleep apnea (OSA) syndrome have been presented. The most common symptoms were snoring , increased motor activity during sleep and excessive daytime somnolence. The factors predisposing to OSA syndrome were obesity and anatomic abnormalities of the upper airway structure. In some cases the signs of OSA syndrome included hypertension, right heart failure, chronic alveolar hypoventilation and polycythemia. Polysomnography showed sleep fragmentation and the prevalence of light sleep stages. Obstructive sleep apneas repeated 73 +/- 23 times per hour of sleep. The mean apnea duration was 19 +/- 8 s. The mean arterial oxygen saturation during apnea was 72 +/- 14%.     

Cardiovascular changes associated with obstructive sleep apnea syndrome.

Five men free of lung or cardiovascular diseases and with severe obstructive sleep apnea participated in a study on the impact of sleep states on cardiovascular variables during sleep apneas. A total of 128 obstructive apneas [72 from stage 2 non-rapid-eye-movement (NREM) sleep and 56 from rapid-eye-movement (REM) sleep] were analyzed. Each apnea was comprised of an obstructive period (OP) followed by a hyperventilation period, which was normally associated with an arousal. Heart rate (HR), stroke volume (SV), cardiac output (CO) (determined with an electrical impedance system), radial artery blood pressures (BP), esophageal pressure nadir, and arterial O2 saturation during each OP and hyperventilation period were calculated for NREM and REM sleep. During stage 2 NREM sleep, the lowest HR always occurred during the first third of the OP, and the highest was always seen during the last third. In contrast, during REM sleep the lowest HR was always noted during the last third of the OP. There was an inverse correlation when the percentage of change in HR over the percentage of change in SV during an OP was considered. The HR and SV changes during NREM sleep allowed maintenance of a near-stable CO during OPs. During REM sleep, absence of a compensatory change in SV led to a significant drop in CO. Systolic, diastolic, and mean BP always increased during the studied OPs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Orthodontic treatment for obstructive sleep apnea syndrome

Sleep and Biological Rhythms - We report a case where obstructive sleep apnea syndrome (OSAS) was improved with orthodontic treatment. The lower dental arch was expanded, the distance between the...     

阻塞性睡眠呼吸暂停患者的心脏早期损伤

目的：评估尚无心血管症状的单纯阻塞性睡眠呼吸暂停（OSA）造成的心脏早期损害。方法：将随机纳入的92例OSA患者依照呼吸暂停低通气指数（AHI）分为轻、中、重三组（轻度25例,中度30例,中度36例）,另取正常健康者25例作为正常对照组,分析血清中脑钠肽N末端前体（NT-proBNP）、心脏型脂肪酸结合蛋白（h-FABP）及超声心动参数的变化状况来评估OSA患者的早期心脏损伤。随机选取中、重度30例（重度20例,中度10例） OSA患者予以持续正压通气（CPAP）治疗一个月,比较治疗前、后NT-proBNP、h-FABP及超声心动参数的变化。结果：与对照组比较,OSA各亚组患者的h-FABP和NT-proBNP水平均显著升高（P<0.01）,并与AHI呈正相关;OSA各组患者的Em/Am值和中、重度OSA组的E/A值均明显降低（P<0.01）;Em/Am值各组之间差异有统计学意义（P<0.01）;与治疗前对比,CPAP治疗后患者血清中的h-FABP和NT-proBNP水平均显著降低（P<0.01）,Em/Am值和E/A值均明显增加（P<0.01）。结论：OSA患者早期心脏损伤以左室舒张功能损伤和心肌早期微损伤为主,CPAP治疗可显著改善OSA患者的早期心脏损伤。     

Circulating microparticles from obstructive sleep apnea syndrome patients induce endothelin-mediated angiogenesis

Microparticles are deemed true biomarkers and vectors of biological information between cells. Depending on their origin, the composition of microparticles varies and the subsequent message transported by them, such as proteins, mRNA, or miRNA, can differ. In obstructive sleep apnea syndrome (OSAS), circulating microparticles are associated with endothelial dysfunction by reducing endothelial-derived nitric oxide production. Here, we have analyzed the potential role of circulating microparticles from OSAS patients on the regulation of angiogenesis and the involved pathway. VEGF content carried by circulating microparticles from OSAS patients was increased when compared with microparticles from non-OSAS patients. Circulating microparticles from OSAS patients induced an increase of angiogenesis that was abolished in the presence of the antagonist of endothelin-1 receptor type B. In addition, endothelin-1 secretion was increased in human endothelial cells treated by OSAS microparticles. We highlight that circulating microparticles from OSAS patients can modify the secretome of endothelial cells leading to angiogenesis.     

Sleep spindle characteristics in overweight adolescents with obstructive sleep apnea syndrome

Sleep and Biological Rhythms - Sleep spindles may display a sleep protective function. Thus, their activity is also a stable marker of sleep disturbances. We investigated whether spindle activity...     

Inflammation and oxidative stress in obstructive sleep apnea syndrome

Similar to obesity, with which it is closely associated, obstructive sleep apnea syndrome (OSAS) is rapidly becoming a worldwide epidemic. Current knowledge of its pathogenesis has been significantly enriched by numerous experimental studies that have demonstrated an important role of oxidative stress and inflammation. Furthermore, new and exciting data strongly connect these two components in the perpetuation of the condition via the overexpression of nuclear factor kappaB. Experimental data support the hypothesis that nutrition might represent a promising future approach with antioxidants currently being good candidates for the modulation of cardiovascular sequelae, although weight reduction and controlled positive airway pressure remain the only established treatments for OSAS. We discuss herein the recent literature that illustrates these new paradigms and speculate on possible implications and future scenarios.     

Caveolin-1 polymorphisms in patients with severe obstructive sleep apnea

Objective: To investigate the associations of G14713A and T29107A polymorphic variants of Caveolin-1 with severe obstructive sleep apnea (OSA).

Materials and methods: This study was performed on 86 severe OSA patients and 86 controls. Genotyping was performed to investigate the association of G14713A and T29107A polymorphisms of Caveolin-1 with severe OSA.

Results: The distribution of genotypes of T29107A was significantly different between controls and OSA patients with a higher proportion of TT carriers in the OSA group.

Conclusion: T29107A-specific genotype of Caveolin-1 may be linked with severe OSA pathogenesis.     

Cardiovascular outcomes of CPAP therapy in obstructive sleep apnea syndrome

Considerable evidence is now available of an independent association between obstructive sleep apnea syndrome (OSAS) and cardiovascular disease. The association is particularly strong for systemic arterial hypertension, but there is growing evidence of an association with ischemic heart disease and stroke. The mechanisms underlying cardiovascular disease in patients with OSAS are still poorly understood. However, the pathogenesis is likely to be a multifactorial process involving a diverse range of mechanisms, including sympathetic overactivity, selective activation of inflammatory molecular pathways, endothelial dysfunction, abnormal coagulation, and metabolic dysregulation, the latter particularly involving insulin resistance and disordered lipid metabolism. Therapy with continuous positive airway pressure (CPAP) has been associated with significant benefits to cardiovascular morbidity and mortality, both in short-term studies addressing specific aspects of morbidity, such as hypertension, and more recently in long-term studies that have evaluated major outcomes of cardiovascular morbidity and mortality. However, there is a clear need for further studies evaluating the impact of CPAP therapy on cardiovascular outcomes. Furthermore, studies on the impact of CPAP therapy have provided useful information concerning the role of basic cell and molecular mechanisms in the pathophysiology of OSAS.     

Mechanisms of breathing instability in patients with obstructive sleep apnea.

The response to chemical stimuli (chemical responsiveness) and the increases in respiratory drive required for arousal (arousal threshold) and for opening the airway without arousal (effective recruitment threshold) are important determinants of ventilatory instability and, hence, severity of obstructive apnea. We measured these variables in 21 obstructive apnea patients (apnea-hypopnea index 91 +/- 24 h(-1)) while on continuous-positive-airway pressure. During sleep, pressure was intermittently reduced (dial down) to induce severe hypopneas. Dial downs were done on room air and following approximately 30 s of breathing hypercapneic and/or hypoxic mixtures, which induced a range of ventilatory stimulation before dial down. Ventilation just before dial down and flow during dial down were measured. Chemical responsiveness, estimated as the percent increase in ventilation during the 5(th) breath following administration of 6% CO(2) combined with approximately 4% desaturation, was large (187 +/- 117%). Arousal threshold, estimated as the percent increase in ventilation associated with a 50% probability of arousal, ranged from 40% to >268% and was <120% in 12/21 patients, indicating that in many patients arousal occurs with modest changes in chemical drive. Effective recruitment threshold, estimated as percent increase in pre-dial-down ventilation associated with a significant increase in dial-down flow, ranged from zero to >174% and was <110% in 12/21 patients, indicating that in many patients reflex dilatation occurs with modest increases in drive. The two thresholds were not correlated. In most OSA patients, airway patency may be maintained with only modest increases in chemical drive, but instability results because of a low arousal threshold and a brisk increase in drive following brief reduction in alveolar ventilation.     

New insights in the management of patients with obstructive sleep apnea

Sleep and Biological Rhythms - The prevalence of patients with obstructive sleep apnea (OSA) is high and increasing. Controlling OSA is an important issue for a medical domain. OSA adversely...     

Reduced respiratory-related evoked activity in subjects with obstructive sleep apnea syndrome.

Midlatency respiratory-related evoked potentials were measured during wakefulness by using a 60-electrode array placed over the cortical region of the scalp. We studied the responses evoked by 200-ms pressure pulses at -5 and -10 cmH(2)O applied at inspiratory onset and during control tests (no pressure applied) in 14 subjects with obstructive sleep apnea syndrome (OSAS) and 18 normal subjects. Wavelet decomposition was used to smooth and dissect the respiratory-related evoked potentials in frequency and time in 8 frequency bands. After denoising, selected wavelet scales were used to reconstruct the respiratory-related evoked potentials, which were quantified by using global field power estimates. The time course of the global field power activity in OSAS subjects compared with normal subjects was significantly depressed in the period 55-70 ms poststimulus onset, a time when afferent traffic from upper airway receptors arrives in normal subjects. The reduced evoked response in subjects with OSAS suggests that these subjects receive less afferent input from upper airway mechanoreceptors. This may reflect reduced sensitivity of mechanoreceptors or reduced mechanoreceptor stimulation due to decreased upper airway compliance during wakefulness in OSAS.