Pro: can physiological risk factors for obstructive sleep apnea be determined by analysis of data obtained from routine polysomnography?
Pro: can physiological risk factors for obstructive sleep apnea be determined by analysis of data obtained from routine polysomnography?
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赞成：可以通过分析常规多导睡眠图获得的数据来确定阻塞性睡眠呼吸暂停的生理危险因素吗？
DOI：
10.1093/sleep/zsac310
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发表时间：
2023
期刊：
影响因子：
5.6
通讯作者：
Edwards,BradleyA
中科院分区：
文献类型：
--
作者：
Sands,ScottA;Edwards,BradleyA
以下论点是在不了解反对论点内容的情况下为回答问题而准备的。阻塞性睡眠呼吸暂停（OSA）是一种高度流行的疾病，其特点是异质性的潜在机制和异质性的不良后果。在过去的20年里，研究人员已经描述了OSA是如何表现为几个既定的生理风险因素或“内型特征”的组合：更大的咽部可吸收性，抑制咽扩张肌补偿，超反应性呼吸控制（环路增益升高）和低唤醒阈值（睡眠唤醒能力增加）。每个病理生理途径的重要作用的证据是广泛的。使用CPAP彻底改善咽部可折叠性对于解决OSA非常有效，没有可折叠咽部（临界折叠压力< 5 cmH 2 O）的个体很少表现出OSA [2，3];因此，一定水平的咽部机械脆弱性被认为是OSA的要求。然而，单独的可渗透性测量不能准确地预测OSA的存在/不存在，也就是说，对于相同水平的可渗透性，一些患者表现出严重的OSA，而另一些则没有。负责改变阻塞性睡眠呼吸暂停综合症风险的两个主要内型特征是肌肉补偿减少和回路增益升高。值得注意的是，没有OSA的肥胖个体通常表现出增强的肌肉反应[4]，并且在具有不太严重的可耐受性的OSA患者中回路增益升高[5]。较低的觉醒阈值被认为有助于在较轻的非REM和REM中参与者中更严重的OSA [6]。研究人员还探索了OSA内源性性状的个体差异是否有助于患者是否对OSA的特定干预做出反应。今天仍然高度相关的临床问题是，CPAP治疗对于许多患者是不可耐受的，并且非CPAP替代方案对于一些患者是高度有效的，但对于其他患者不是。使用复杂的过夜研究在生理实验室，韦尔曼等人。[7]使用改良的呼吸机回路，显示具有较高回路增益的患者在补充氧气的情况下显示出有希望的OSA改善，而具有低回路增益的患者则没有。随后，Edwards et al. [8]使用了一种更新的CPAP操作方法，以证明稳定的呼吸控制（补充氧气+催眠）对最不严重的呼吸困难患者最有效。同样的方法还发现，口腔矫治器治疗的有效性在环路增益较高的患者中较低[9]。虽然这些研究证明了OSA的潜在机制影响对治疗的反应的原则，但将这项工作转化为临床实践存在重大限制。值得注意的是，在许多患者中无法获得特质测量（例如，那些通过CPAP操作无法入睡的患者），并且这项工作需要专门的设备和经验丰富的研究者操作员。“精准医学”的进展，即根据潜在的疾病病理生理学明智地治疗患者亚群，由于缺乏在临床环境中估计内源性性状的手段而受到阻碍。因此，我们试图开发一种方法来估计OSA的原因，从常规的临床多导睡眠图数据，可以收集专业的生理实验室之外。2015年，Terrill et al. [10]开发了一种方法，该方法使用来自常规睡眠研究的鼻压通气信号，以及使用模型拟合估计的呼吸驱动，来计算
The following argument was prepared in response to the question without the knowledge of the contents of the opposing argument. Obstructive sleep apnea (OSA) is a highly prevalent disorder characterized by heterogeneous underlying mechanisms and heterogeneous adverse outcomes. Over the last 20 years, investigators have described how OSA is manifest as a combination of several established physiological risk factors or “endotypic traits”: greater pharyngeal collapsibility, dampened pharyngeal dilator muscle compensation, hyper-responsive ventilatory control (elevated loop gain), and a low arousal threshold (increased arousability from sleep). Evidence for important roles of each pathophysiological pathway are extensive. Profoundly improving pharyngeal collapsibility with CPAP is highly efficacious for resolving OSA, and individuals without a collapsible pharynx (critical collapsing pressure< 5 cmH2O) very rarely exhibit OSA [2, 3]; thus, a level of pharyngeal mechanical vulnerability is considered a requirement for OSA. Yet measures of collapsibility alone do not accurately predict the presence/absence of OSA, that is, for the same level of collapsibility some patients exhibit severe OSA and others do not. The two leading endotypic traits responsible for modifying OSA risk are reduced muscle compensation and elevated loop gain. Notably, obese individuals without OSA typically exhibit augmented muscle responses [4], and loop gain is elevated in OSA patients with less-severe collapsibility [5]. A lower arousal threshold is considered to contribute to more severe OSA within participants in lighter non-REM and REM [6].Investigators have also explored whether individual differences in OSA endotypic traits contribute to whether patients would respond to a particular intervention for OSA. The clinical problem, which remains highly relevant today, is that CPAP treatment is not tolerable for many patients, and non-CPAP alternatives are highly efficacious for some patients but not others. Using complex overnight studies in the physiology laboratory, Wellman et al.[7] used a modified ventilator circuit to show that patients with higher loop gain exhibited promising improvements in OSA with supplemental oxygen, whereas patients with low loop gain did not. Subsequently, Edwards et al.[8] used a newer CPAP manipulation method to show that stabilizing ventilatory control (supplemental oxygen+ hypnotic) was most efficacious in patients with the least severe collapsibility. The same method also identified that the efficacy of oral appliance therapy was lower in patients with higher loop gain [9]. While these studies provided proof of the principle that underlying mechanisms of OSA influence responses to therapies, there were major limitations to translating this work to clinical practice. Notably, trait measures could not be derived in many patients (eg those unable to sleep through CPAP manipulation), and the work required specialized equipment and experienced investigator operators. Progress towards “precision medicine”—that is, treating patient subgroups judiciously based on underlying disease pathophysiology—was hampered by the absence of a means to estimate the endotypic traits in a clinical environment. Accordingly, we sought to develop a means to estimate the causes of OSA from routine clinical polysomnographic data that could be collected outside specialized physiology laboratories. In 2015, Terrill et al.[10] developed a method that used the nasal pressure ventilation signal from a routine sleep study, and the estimated ventilatory drive using model-fitting, to calculate
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一种根据标准多导睡眠图和临床数据评估关键 OSA 内型及其对 OSA 严重程度影响的新模型。
影响因子：
8.3
作者：
R. Dutta;G. Delaney;B. Toson;A. Jordan;D. White;A. Wellman;D. Eckert
通讯作者：
D. Eckert
DOI：
10.1164/rccm.200404-510oc
发表时间：
2004-12
影响因子：
24.7
作者：
A. Wellman;A. Jordan;A. Malhotra;R. Fogel;E. Katz;K. Schory;J. Edwards;D. White
通讯作者：
A. Wellman;A. Jordan;A. Malhotra;R. Fogel;E. Katz;K. Schory;J. Edwards;D. White
影响因子：
3.3
作者：
Kirkness, Jason P.;Schwartz, Alan R.;Patil, Susheel P.
通讯作者：
Patil, Susheel P.
中风患者的生理特征和阻塞性睡眠呼吸暂停治疗的依从性。
DOI：
10.1164/rccm.201911-2203le
发表时间：
2020
影响因子：
24.7
作者：
Zinchuk,AndreyV;Redeker,NancyS;Chu,Jen-Hwa;Liang,Jiasheng;Stepnowsky,Carl;Brandt,CynthiaA;Bravata,DawnM;Wellman,Andrew;Sands,ScottA;Yaggi,HenryK
通讯作者：
Yaggi,HenryK
DOI：
10.1164/rccm.201404-0718oc
发表时间：
2014-12-01
影响因子：
24.7
作者：
Edwards, Bradley A.;Eckert, Danny J.;Malhotra, Atul
通讯作者：
Malhotra, Atul