The combination of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) is associated with substantial morbidity and mortality. We hypothesized that predictors of OSA among patients with COPD may be distinct from OSA in the general population. Therefore, we investigated associations between traditional OSA risk factors (e.g. age), and sleep questionnaires [e.g. Epworth Sleepiness Scale] in 44 patients with advanced COPD. As a second aim we proposed a pilot, simplified screening test for OSA in patients with COPD. In a prospective, observational study of patients enrolled in the UCSD Pulmonary Rehabilitation Program we collected baseline characteristics, cardiovascular events (e.g. atrial fibrillation), and sleep questionnaires [e.g. Pittsburgh Sleep Quality Index (PSQI)]. For the pilot questionnaire, a BMI ≥25 kg/m2 and the presence of cardiovascular disease were used to construct the pilot screening test. Male: 59%; OSA 66%. FEV1 (mean ± SD) = 41.0±18.2% pred., FEV1/FVC = 41.5±12.7%]. Male gender, older age, and large neck circumference were not associated with OSA. Also, Epworth Sleepiness Scale and the STOP-Bang questionnaire were not associated with OSA in univariate logistic regression. In contrast, BMI ≥25 kg/m2 (OR = 3.94, p = 0.04) and diagnosis of cardiovascular disease (OR = 5.06, p = 0.03) were significantly associated with OSA [area under curve (AUC) = 0.74]. The pilot COPD-OSA test (OR = 5.28, p = 0.05) and STOP-Bang questionnaire (OR = 5.13, p = 0.03) were both associated with OSA in Receiver Operating Characteristics (ROC) analysis. The COPD-OSA test had the best AUC (0.74), sensitivity (92%), and specificity (83%). A ten-fold cross-validation validated our results.We found that traditional OSA predictors (e.g. gender, Epworth score) did not perform well in patients with more advanced COPD. Our pilot test may be an easy to implement instrument to screen for OSA. However, a larger validation study is necessary before further clinical implementation is warranted.
Obstructive sleep apnea (OSA) is a common sleep disorder with serious associated morbidities. Although several treatment options are currently available, variable efficacy and adherence result in many patients either not being treated or receiving inadequate treatment long term. Personalized treatment based on relevant patient characteristics may improve adherence to treatment and long-term clinical outcomes. Four key traits of upper airway anatomy and neuromuscular control interact to varying degrees within individuals to cause OSA. These are: (1) the pharyngeal critical closing pressure, (2) the stability of ventilator chemoreflex feedback control (loop gain), (3) the negative intraesophageal pressure that triggers arousal (arousal threshold), and (4) the level of stimulus required to activated upper airway dilator muscles (upper airway recruitment threshold). Simplified diagnostic methods are being developed to assess these pathophysiological traits, potentially allowing prediction of which treatment would best suit each patient. In contrast to current practice of using various treatment modes alone, model predictions and pilot clinical trials show improved outcomes by combining several treatments targeted to each patient's pathophysiology profile. These developments could theoretically improve efficacy and adherence to treatment and in turn reduce the social and economic health burden of OSA and the associated life-threatening morbidities. This article reviews OSA pathophysiology and identifies currently available and investigational treatments that may be combined in the future to optimize therapy based on individual profiles of key patient pathophysiological traits.
BACKGROUND: COPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the relationship between subjective sleep quality and risk of COPD exacerbations. METHODS: Data were obtained from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study. Participants with COPD who had completed 18 months of follow-up were included. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI) and a three-factor analysis. Symptom-based (dyspnea or sputum change $ 48 h) and eventbased (symptoms plus medication or unscheduled health services use) exacerbations were assessed. Association of PSQI with exacerbation rate was assessed by using negative binomial regression. Exacerbation-free survival was also assessed. RESULTS: A total of 480 participants with COPD were studied, including 185 with one or more exacerbations during follow-up and 203 with poor baseline sleep quality (PSQI score > 5). Participants with subsequent symptom-based exacerbations had higher median baseline PSQI scores than those without (6.0 [interquartile range, 3.0-8.0] vs 5.0 [interquartile range, 2.0-7.0]; P ¼ .01), and they were more likely to have baseline PSQI scores > 5 (50.3% vs 37.3%; P ¼ .01). Higher PSQI scores were associated with increased symptombased exacerbation risk (adjusted rate ratio, 1.09; 95% CI, 1.01-1.18; P ¼ .02) and event-based exacerbation risk (adjusted rate ratio, 1.10; 95% CI, 1.00-1.21; P ¼ .048). The association occurred mainly in those with undiagnosed COPD. Strongest associations were with Factor 3 (sleep disturbances and daytime dysfunction). Time to symptom-based exacerbation was shorter in participants with poor sleep quality (adjusted hazard ratio, 1.49; 95% CI, 1.09-2.03). CONCLUSIONS: Higher baseline PSQI scores were associated with increased risk of COPD exacerbation over 18 months' prospective follow-up.
ClinicalTrials.Gov; Title: The Impact of Sleep Apnea Treatment on Physiology Traits in Chinese Patients With Obstructive Sleep Apnea; Identifier: NCT02696629; URL: https://clinicaltrials.gov/show/NCT02696629.
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