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IntroductionWe aimed to assess, in patients with Parkinson's disease (PD), the association between obstructive sleep apnea (OSA), progression of motor dysfunction and the effect of OSA treatment.MethodsData were analysed from a prospective cohort study of idiopathic PD patients from a movement disorders clinic. Patients found to have OSA on polysomnography (apnea-hypopnea index [AHI] ≥15 events/h, OSA+) were offered treatment using continuous positive airway pressure (CPAP). CPAP+ was defined as an average ≥ 2 h/night use at each follow-up. Motor symptoms were assessed using the motor section of the Movement Disorder Society Unified Parkinson's Disease Rating Scale (mUPDRS) and the Timed-Up-And-Go (TUG). Follow-up times were 3, 6 and 12 months. Mixed models were constructed, adjusting for age, sex, body mass index, levodopa equivalent dose and comorbidities.ResultsWe studied 67 individuals (61.2% male) of mean age 64.7 years (SD = 10.1). Baseline mUPDRS was higher in OSA+ compared to OSA- (24.5 [13.6] vs. 16.2 [7.2], p < 0.001). Motor dysfunction increased at comparable rates in OSA- and OSA+CPAP-. However, in OSA+CPAP+, mUPDRS change was significantly lower compared to OSA- (β = −0.01 vs. 0.61, p = 0.03; p = 0.12 vs. OSA+CPAP- [β = 0.39]) and TUG change was lower compared to OSA+CPAP- (β = −0.01 vs. 0.13, p = 0.002; p = 0.05 vs. OSA- [β = 0.02]).ConclusionsIn this PD cohort, OSA was associated with higher baseline mUPDRS. In those with OSA, CPAP use was associated with stabilization of motor function (mUPDRS and TUG) over 12 months. These observations support further research to clarify the role of OSA in PD pathophysiology and motor dysfunction.  相似文献   
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目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)CYP3A4基因的多态性,了解其对芬太尼类药物的敏感性及不同基因型的人群分布特征,指导临床个体化用药。方法对50例OSAHS患者进行CYP3A4基因的多态性检测,采静脉血,通过DNA抽提-PCR扩增-焦磷酸测序方法检测CYP3A4基因。结果野生纯合型型34例(68%),突变杂合型15例(30%),突变纯合型型1例(2%)。结论OSAHS患者中约2%为AA型,该型对芬太尼类药物极其敏感,术后有易发生窒息的风险,应高度警惕芬太尼类药物呼吸抑制的潜在风险。  相似文献   
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BackgroundIdentifying electroencephalogram (EEG) cortical arousals are crucial in scoring hypopneas and respiratory efforts related arousals (RERAs) during a polysomnogram. As children have high arousal threshold, many of the flow limited breaths or hypopneas may not be associated with visual EEG arousals, hence this may lead to potential underestimation of the degree of sleep disordered breathing. Pulse wave amplitude (PWA) is a signal obtained from finger photoplethysmography which correlates directly to finger blood flow. The drop in PWA has been shown to be a sensitive marker for subcortical/autonomic and cortical arousals. Our aim was to use the drop in PWA as a surrogate for arousals to guide scoring of respiratory events in pediatric patients.MethodsTen polysomnograms for patients between the ages of 5–15 years who had obstructive apnea-hypopnea indices between 1 and 5 events/hour were identified. Patients with syndromes were excluded. A drop in PWA signal of at least 30% that lasted for 3 s was needed to identify subcortical/autonomic arousals. Arousals were rescored based on this criteria and subsequently respiratory events were rescored. Paired t-tests were employed to compare PSG indices scored with or without PWA incorporation.ResultsThe sample of 10 children included 2 females, and the average age was 9.8 ± 3.1 years. Overall, polysomnography revealed an average total sleep time of 464.1 ± 25 min, sleep efficiency of 92% +/−4.2, sleep latency of 19.6 ± 17.0 min, rapid eye movement (REM) latency 143 ± 66 min, N1 3.9% +/−2.0, N2 50.3% +/−12.0, N3 28.2% +/−9.1, REM 16.7% +/−4.0, and wakefulness after sleep onset (WASO) 18.1 ± 7.5 min. Including arousals from PWA changes, respiratory indices significantly increased including total AHI (2.3 ± 0.7 vs 5.7 ± 2.1, p < 0.001), obstructive AHI (1.45 ± 0.7 vs 4.8 ± 1.8, p < 0.001), and RDI (2.36 ± 0.7 vs 7.6 ± 2.0, p < 0.001). Likewise, total arousal index was significantly higher (8.7 ± 2.3 vs 29.4 ± 6.5, p < 0.001).ConclusionsThe drop in pulse wave amplitude signal is a useful marker to guide scoring arousals that are not otherwise easily identified in pediatric polysomnography and subsequently helped in scoring respiratory events that otherwise would not be scored. Further studies are needed to delineate if such methodology would affect clinical outcome.  相似文献   
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《Cor et vasa》2015,57(3):e157-e162
IntroductionObstructive sleep apnea (OSA) is often connected with arterial hypertension and it could also be a cause of secondary hypertension. Treatment of arterial hypertension and optimal blood pressure level are important for prevention of cardiovascular complications. It is not well known how to treat patients with OSA and arterial hypertension. Also many patients with OSA suffer from metabolic syndrome which worsen their prognosis.AimThe aim of our study was to assess arterial hypertension compensation in patients with metabolic syndrome and moderate to severe OSA and to analyze used pharmacotherapy.Materials and methods85 hypertensive patients (75 men) with metabolic syndrome, average age 53.6 ± 9.3 years, were evaluated using overnight sleep study with diagnosis of OSA, average apnea–hypopnea index (AHI) 56.3 ± 23. Patients underwent 24 h ambulatory blood pressure monitoring (ABPM) and their current pharmacotherapy data were obtained. Appropriate combinations of antihypertensive drugs (patients with metabolic syndrome) were derived from ESH/ESC 2013 guidelines.ResultsArterial hypertension was well compensated in only 11.8% of the patients. 24.7% patients were treated according to current guidelines. Fisher's exact test with analysis of adjusted residues has found higher rate of blood pressure subcompensation in patients treated with triple+ combination of drugs (p = 0.035, 51.4% vs 10%).ConclusionOnly a small number of patients had optimal blood pressure level and were treated according to current ESH/ESC guidelines. We have to constantly appeal to all physicians to perform ABPM in patients with OSA.  相似文献   
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BackgroundThe peripheral level of matrix metalloproteinase (MMP)-9 and polymorphism of MMP9 -1562C>T in patients with obstructive sleep apnea (OSA) remains controversial. Therefore, the aims of this systemic review and meta-analysis are to assess the MMP9 level in OSA patients and identify the relationship between MMP9 -1562C>T and OSA susceptibility.MethodsThis systematic review was performed following the PRISMA guideline. We searched for studies in major databases, identifying those indexed from inception to July 3, 2019 which related to MMP9 level, MMP9 -1562C>T and OSA. The pooled standardized mean differences (SMDs) and 95% confidence interval (CI) of MMP9 levels were calculated. In addition, the relationship between MMP9 -1562C>T and OSA susceptibility was assessed by three genetic models. The heterogeneity analysis and calculation of the pooled odds ratio (OR) were also performed, followed by quality assessment using the Newcastle-Ottawa Scale (NOS).ResultsIn sum, our review included 15 eligible studies regarding MMP9 level and three regarding MMP9 -1562C>T. The pooled results showed that peripheral level of MMP9 was increased in OSA patients (SMD = 1.37; 95% CI = 1.15–1.59). Furthermore, significant difference of MMP9 level can be found between severe and mild-to-moderate OSA patients (SMD = 28.17; 95% CI = 4.23–52.11) or between moderate-severe and mild OSA (SMD = 36.62; 95% CI = 12.19–61.04). However, no relationship was observed between MMP9 -1562C>T and OSA susceptibility in three genetic models (Homozygote model, OR = 1.37; 95% CI = 0.87–2.18); (Recessive model, OR = 1.42; 95% CI = 0.83–2.42); (Allele model, OR = 1.07; 95% CI = 0.96–1.18).ConclusionsThis systemic review and meta-analysis indicated that the level of MMP9 was increased in patients with OSA and this increase is relevant to OSA severity. Moreover, the relationship between MMP9 -1562 C>T and OSA susceptibility has currently not been proven by current merging values. Further analyses with larger sample size are required to verify these associations.  相似文献   
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目的:运用软硬腭前移的手术方法扩大鼻咽下口,改善因鼻咽部狭小致阻塞性睡眠呼吸暂停综合征患者的呼吸暂停症状。方法:手术切除硬腭后份使其缩短、悬雍垂软腭成形并将软腭拉向前,扩大鼻咽下口。结果:患者术后自觉症状及客观评价疗效满意。结论:软硬腭前移鼻咽下口扩大显著改善鼻咽下口狭小导致的阻塞性睡眠呼吸暂停患者的症状。  相似文献   
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