Annals of the American Thoracic Society最新文献

Rationale: Little is known about the long-term impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on children with asthma. Objectives: To determine whether SARS-CoV-2 infection affects symptom control and lung function in children with asthma. Methods: Using data from clinical registries and the electronic health record, we conducted a prospective case-control study of children with asthma aged 6-21 years who had (cases) or did not have (control subjects) SARS-CoV-2 infection, comparing baseline and follow-up asthma symptom control and spirometry within an ∼18-month time frame and, for cases, within 18 months of acute coronavirus disease (COVID-19). Results: A total of 171 cases had baseline and follow-up asthma symptom data, and 114 cases had baseline and follow-up spirometry measurements. There were no significant differences in asthma symptom control (P = 0.50), forced expiratory volume in 1 second (P = 0.47), forced vital capacity (P = 0.43), forced expiratory volume in 1 second/forced vital capacity (P = 0.43), or forced expiratory flow, midexpiratory phase (P = 0.62), after SARS-CoV-2 infection. Compared with control subjects (113 with symptom data and 237 with spirometry data), there were no significant differences in follow-up asthma symptom control or lung function. A similar proportion of cases and control subjects had poorer asthma symptom control (17.5% vs. 9.7%; P = 0.07) or worse lung function (29.0% vs. 32.5%; P = 0.50) at follow-up. Patients whose asthma control worsened after COVID-19 had a shorter time to follow-up (3.5 [1.5-7.5] vs. 6.1 [3.1-9.8] mo; P = 0.007) and were more likely to have presented with an asthma exacerbation during COVID-19 (46% vs. 26%; P = 0.04) than those without worse control. Conclusions: We found no significant differences in asthma symptom control or lung function in youth with asthma up to 18 months after acute COVID-19, suggesting that COVID-19 does not affect long-term asthma severity or control in the pediatric population.

Rationale: Sleep abnormalities are very frequent in critically ill patients during and after intensive care unit (ICU) stays. Their mechanisms are poorly understood. The odds ratio product (ORP) is a continuous metric (range, 0.0-2.5) of sleep depth measured in 3-second intervals and derived from the relationship of powers of different electroencephalographic frequencies to one another. When expressed as the percentage of epochs within 10 ORP deciles covering the entire ORP range, it provides information about the mechanism(s) of abnormal sleep. Objectives: To determine ORP architecture types in critically ill patients and survivors of critical illness who had previously undergone sleep studies. Methods: Nocturnal polysomnograms from 47 unsedated critically ill patients and 23 survivors of critical illness at hospital discharge were analyzed. Twelve critically ill patients were monitored also during the day, and 15 survivors underwent subsequent polysomnography 6 months after hospital discharge. In all polysomnograms, each 30-second epoch was characterized by the mean ORP of the 10 3-second epochs. The number of 30-second epochs with mean ORP within each of 10 ORP deciles covering the entire ORP range (0.0-2.5) was calculated and expressed as a percentage of total recording time. Thereafter, each polysomnogram was characterized using a two-digit ORP type, with the first digit (range, 1-3) reflecting increasing degrees of deep sleep (ORP < 0.5, deciles 1 and 2) and the second digit (range, 1-3) reflecting increasing degrees of full wakefulness (ORP > 2.25, decile 10). Results from patients were compared with those from 831 age- and gender-matched community dwellers free of sleep disorders. Results: In critically ill patients, types 1,1 and 1,2 (little deep sleep and little or average full wakefulness) dominated (46% of patients). In the community, these types are uncommon (<15%) and seen primarily in disorders that preclude progression to deep sleep (e.g., very severe obstructive sleep apnea). Next in frequency (22%) was type 1,3, consistent with hyperarousal. Day ORP sleep architecture was similar to night results. Survivors had similar patterns, with little improvement after 6 months. Conclusions: Sleep abnormalities in critically ill patients and survivors of critical illness result primarily from stimuli that preclude progression to deep sleep or from the presence of a hyperarousal state.

Rationale: Recent studies have shown that sleep apnea-specific intermittent hypoxemia quantified by the hypoxic burden (HB) predicted cardiovascular disease (CVD)-related mortality in community-based and clinical cohorts. Calculation of HB is based on manual scoring of hypopneas and apneas, which is time-consuming and prone to interscorer variability. Objective: To validate a novel method to quantify the HB that is based on automatically scored desaturations. Methods: The sample included 5,655 middle-aged or older adults from the Sleep Heart Health Study (52.8% women; age, 63.2 ± 11.3 yr). The original HB method was based on a subject-specific search window obtained from an ensemble average of oxygen saturation signals (as measured by pulse oximetry) and synchronized with respect to the termination of scored respiratory events. In this study, however, the search window was obtained from ensemble average of oxygen saturation signals that synchronized with respect to the minimum of all automatically identified desaturations (⩾2% and other thresholds, including 3% and 4%, in sensitivity analyses). The time interval between the two maxima around the minimum saturation was defined as the search window. The oximetry-derived HB (HB_Oxi) was defined as the total area under all desaturation curves (restricted by the search window) divided by the total sleep time. Logistic and Cox regression models assessed the adjusted odds ratio (aOR)/hazard ratio of excessive daytime sleepiness (EDS), hypertension (HTN), and CVD mortality per 1-standard deviation increase in HB_Oxi after adjusting for several covariates and confounders. Results: The Spearman's rank correlation between HB (median [interquartile range], 34.4 [18.4-59.8] % min/h) and HB_Oxi (median [interquartile range], 34.5 [21.6-53.8] % min/h) was 0.81 (P < 0.001). Similar to HB, HB_Oxi was significantly associated with EDS (aOR [95% confidence interval (CI)], 1.17 [1.09-1.26] per standard deviation), HTN (aOR [95% CI], 1.13 [1.05-1.21]), and CVD mortality (adjusted hazard ratio [95% CI], 1.15 [1.01-1.30]) in fully adjusted models. Conclusions: The HB_Oxi was highly correlated with the HB based on manually scored apneas and hypopneas and was associated with EDS, HTN, and CVD mortality with similar effect sizes as previously reported. This method could be incorporated into wearable technology that accurately records oxygen saturation signals.

Rationale: Subjects with preserved ratio impaired spirometry (PRISm) experience increased respiratory symptoms, although they present heterogeneous characteristics. However, the longitudinal changes in these symptoms and respiratory function are not well known. Objectives: To investigate PRISm from the viewpoint of respiratory symptoms in a longitudinal, large-scale general population study. Methods: The Nagahama study included 9,789 inhabitants, and a follow-up evaluation was conducted after 5 years. Spirometry and self-administered questionnaires regarding respiratory symptoms, including prolonged cough, sputum and dyspnea, and comorbidities were conducted. Results: In total, 9,760 subjects were analyzed, and 438 subjects had PRISm. Among the subjects with PRISm, 53% presented with respiratory symptoms; dyspnea was independently associated with PRISm. Follow-up assessment revealed that 73% of the subjects with PRISm with respiratory symptoms were consistently symptomatic, whereas 39% of the asymptomatic subjects with PRISm developed respiratory symptoms within 5 years. In addition, among subjects with respiratory symptoms without airflow limitation at baseline, PRISm was a risk factor for the development of airflow limitation independent of smoking history and comorbidities. Conclusions: This study demonstrated that 53% of the subjects with PRISm had respiratory symptoms; dyspnea was a distinct characteristic of PRISm. Approximately three-fourths of the symptomatic subjects with PRISm consistently complained of respiratory symptoms within 5 years. Together with our result that PRISm itself is an independent risk factor for the development of chronic obstructive pulmonary disease among subjects with respiratory symptoms, the clinical course of subjects with PRISm with symptoms requires careful monitoring.

Patients with interstitial lung diseases (ILD) often have hypoxemia at rest and/or with exertion, for which supplemental oxygen is commonly prescribed. The number of patients with ILD who require supplemental oxygen is unknown, although estimates suggest it could be as much as 40%; many of these patients may require high-flow support (>4 L/min). Despite its frequent use, there is limited evidence for the impact of supplemental oxygen on clinical outcomes in ILD, with recommendations for its use primarily based on older studies in patients with chronic obstructive pulmonary disease. Oxygen use in ILD is rarely included as an outcome in clinical trials. Available evidence suggests that supplemental oxygen in ILD may improve quality of life and some exercise parameters in patients whose hypoxemia is a limiting factor; however, oxygen therapy also places new burdens and barriers on some patients that may counter its beneficial effects. The cost of supplemental oxygen in ILD is also unknown but likely represents a significant portion of overall healthcare costs in these patients. Current Centers for Medicare and Medicaid reimbursement policies provide only a modest increase in payment for high oxygen flows, which may negatively impact access to oxygen services and equipment for some patients with ILD. Future studies should examine clinical and quality-of-life outcomes for oxygen use in ILD. In the meantime, given the current limited evidence for supplemental oxygen and considering cost factors and other barriers, providers should take a patient-focused approach when considering supplemental oxygen prescriptions in patients with ILD.

Rationale: Intimate partner violence and child maltreatment have been separately associated with asthma in adults. No study has concurrently examined of adulthood adverse events (including, but not limited to, intimate partner violence) and child maltreatment on asthma in adults. Objectives: To concurrently examine of adulthood adverse events and child maltreatment on asthma in adults. Methods: This was a cross-sectional study of adulthood adverse events and child maltreatment on current asthma in 87,891 adults 40-69 years old who participated in the UK Biobank. Adulthood adverse events were assessed using questions adapted from a national crime survey. Child maltreatment was ascertained using the Childhood Trauma Screener questionnaire. Current asthma was defined as physician-diagnosed asthma and current wheeze and was further classified as noneosinophilic or eosinophilic according to eosinophil count (<300 vs. ⩾300 cells per microliter). Results: In a multivariable analysis, participants who reported two or more types of adulthood adverse events had 1.19-1.45 times significantly higher odds of asthma than those who did not, whereas participants who reported two or more types of child maltreatment had 1.25-1.59 significantly higher odds of asthma than those who reported no child maltreatment. After stratification by sex, similar results were obtained for child maltreatment in women and men, whereas adulthood adverse events were only significantly associated with asthma in women. Similar findings were observed in analyses that were restricted to never-smokers and former smokers with <10 pack-years of smoking and in analyses of noneosinophilic and eosinophilic asthma. Conclusions: In a cohort of British adults, child maltreatment was associated with current asthma in men and women, whereas adulthood adverse events were associated with current asthma in women only. This was independent of cigarette smoking or eosinophil count.

Rationale: Landmark studies of long-term oxygen therapy (LTOT) in patients with chronic obstructive pulmonary disease (COPD) used arterial oxygen pressure (Pa_O2) to define severe hypoxemia; however, oxygen saturation as measured by pulse oximetry (Sp_O2) is commonly used instead. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommend evaluation with arterial blood gas (ABG) analysis if Sp_O2 is ⩽92%. This recommendation has not been evaluated in stable outpatients with COPD undergoing testing for LTOT. Objectives: To evaluate the performance of Sp_O2 compared with ABG analysis of Pa_O2 and arterial oxygen saturation (Sa_O2) to detect severe resting hypoxemia in patients with COPD. Methods: Retrospective analysis of paired Sp_O2 and ABG values from stable outpatients with COPD who underwent LTOT assessment in a single center. We calculated false negatives (FNs) as an Sp_O2 >88% or >89% in the presence of pulmonary hypertension with a Pa_O2 ⩽55 mm Hg or ⩽59 mm Hg in the presence of pulmonary hypertension. Test performance was assessed using receiver operating characteristic (ROC) analysis, intraclass correlation coefficient (ICC), test bias, precision, and accuracy root-mean-square (A_rms). An adjusted multivariate analysis was used to evaluate factors affecting Sp_O2 bias. Results: Of 518 patients, the prevalence of severe resting hypoxemia was 74 (14.3%), with 52 missed by Sp_O2 (FN, 10%), including 13 (2.5%) with an Sp_O2 > 92% (occult hypoxemia). FNs and occult hypoxemia in Black patients were 9% and 1.5%, respectively, and were 13% and 5%, respectively, among active smokers. The correlation between Sp_O2 and Sa_O2 was acceptable (ICC = 0.78; 95% confidence interval, 0.74-0.81); and the bias of Sp_O2 was 0.45%, with a precision of 2.6 (-4.65 to +5.55%) and A_rms of 2.59. These measurements were similar in Black patients, but in active smokers, correlation was lower and bias showed greater overestimation of Sp_O2. ROC analysis suggests that the optimal Sp_O2 cutoff to warrant LTOT evaluation by ABG analysis is ⩽94%. Conclusions: Sp_O2 as the only measure of oxygenation carries a high FN rate in detecting severe resting hypoxemia in patients with COPD undergoing evaluation for LTOT. Reflex measurement of Pa_O2 by ABG analysis should be used as recommended by GOLD, ideally at a cutoff higher than an Sp_O2 ⩽92%, especially in active smokers.

Rationale: Acute pulmonary embolism is a leading cause of cardiovascular death. There are limited data on the national mortality trends from pulmonary embolism. Understanding these trends is crucial for addressing the mortality and associated disparities associated with pulmonary embolism. Objectives: To analyze the national mortality trends related to acute pulmonary embolism and determine the overall age-adjusted mortality rate (AAMR) per 100,000 population for the study period and assess changes in AAMR among different sexes, races, and geographic locations. Methods: We conducted a retrospective cohort analysis using mortality data of individuals aged ⩾15 years with pulmonary embolism listed as the underlying cause of death in the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research database from January 2006 to December 2019. These data are produced by the National Center for Health Statistics. Results: A total of 109,992 pulmonary embolism-related deaths were noted in this dataset nationwide between 2006 and 2019. Of these, women constituted 60,113 (54.7%). The AAMR per 100,000 was not significantly changed, from 2.84 in 2006 to 2.81 in 2019 (average annual percentage change [AAPC], 0.2; 95% confidence interval [CI], -0.1 to 0.5; P = 0.15). AAMR increased for men throughout the study period compared with women (AAPC, 0.7 for men; 95% CI, 0.3 to 1.2; P = 0.004 vs. AAPC, -0.4 for women; 95% CI, -1.1 to 0.3; P = 0.23, respectively). Similarly, AAMR for pulmonary embolism increased for Black compared with White individuals, from 5.18 to 5.26 (AAPC, 0.4; 95% CI, 0.0 to 0.7; P = 0.05) and 2.82 to 2.86 (AAPC, 0.0; 95% CI, -0.6 to 0.6; P = 0.99), respectively. Similarly, AAMR for pulmonary embolism was higher in rural areas than in micropolitan and large metropolitan areas during the study period (4.07 [95% CI, 4.02 to 4.12] vs. 3.24 [95% CI, 3.21 to 3.27] vs. 2.32 [95% CI, 2.30-2.34], respectively). Conclusions: Pulmonary embolism mortality remains high and unchanged over the past decade, and enduring sex, racial and socioeconomic disparities persist in pulmonary embolism. Targeted efforts to decrease pulmonary embolism mortality and address such disparities are needed.