Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoaf062
Tilmann Kramer, Henning Weis, Merve Kural, Mira Kramer, Stephan Baldus, Alexander Drzezga, Martin Hellmich, Matthias Schmidt, Stephan Rosenkranz
{"title":"Correlation of ventilation-perfusion mismatch with hemodynamics in chronic thromboembolic pulmonary hypertension: a quantitative V/Q SPECT analysis.","authors":"Tilmann Kramer, Henning Weis, Merve Kural, Mira Kramer, Stephan Baldus, Alexander Drzezga, Martin Hellmich, Matthias Schmidt, Stephan Rosenkranz","doi":"10.1093/annalsats/aaoaf062","DOIUrl":"https://doi.org/10.1093/annalsats/aaoaf062","url":null,"abstract":"","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":"23 4","pages":"646-650"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoag033
Aravind A Menon, Gerard A Silvestri
{"title":"A pulmonary inferno: the triad of interstitial abnormalities, emphysema, and lung cancer.","authors":"Aravind A Menon, Gerard A Silvestri","doi":"10.1093/annalsats/aaoag033","DOIUrl":"10.1093/annalsats/aaoag033","url":null,"abstract":"","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":" ","pages":"492-493"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146168503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoaf071
Beatriz S Prado, Diego R Mazzotti, André Franci, Luciano M Baracioli, Karoline Razimavicius Barbado, Roberta Saretta, Roberto Kalil-Filho, Luciano F Drager
Rationale: Previous studies have shown that glucagon-like peptide-1 (GLP-1) agonists and dual GLP-1/glucose-dependent insulinotropic peptide (GIP) agonists (tirzepatide) reduced severity of sleep apnea. However, whether these medications impact incidence of new cases of physician-reported sleep apnea (PRSA) is unknown.
Objective: To determine the potential impact of GLP-1 and dual agonists on the incidence of sleep apnea reports and to explore potential treatment consequences for this sleep-disordered breathing.
Methods: We conducted a retrospective cohort study using the TriNetX Global Health Research Network through anonymized electronic medical records. We identified adult patients with obesity and/or type 2 diabetes mellitus never prescribed GLP-1 or dual agonist therapy (reference arm) and those new initiators of these medications. The index event (June 2022) was chosen to coincide with the launching of tirzepatide in the market. We excluded patients with type 1 diabetes; previous diagnosis of PRSA; previous use of GLP-1/dual agonists, orlistat, phentermine/topiramate, or bupropion/naltrexone; or previous bariatric surgery. Initiators were matched to the reference cohort using propensity score matching in a 1:1 ratio for age, sex, ethnicity, body mass index, and menopause. We used a validated algorithm to identify PRSA using International Classification of Diseases, 10th Revision codes.
Results: The follow-up time was 1044 days. After propensity score matching, a total of 1 253 188 patients were included in the reference arm and GLP-1/dual agonist comparison. Overall, GLP-1/dual agonists were associated with a 54% lower incidence of PRSA (HR, 0.46 [95% CI, 0.45-0.49]). Individually, all drugs were able to reach this outcome as compared to the reference arm: liraglutide (HR, 0.64 [95% CI, 0.51-0.80]), dulaglutide (HR, 0.32 [95% CI, 0.28-0.36]), semaglutide (HR, 0.57 [95% CI, 0.54-0.61]), and tirzepatide (HR, 0.74 [95% CI, 0.67-0.92]). Exploratory analysis revealed a 79% lower incidence of positive airway pressure reports in the GLP-1/dual agonist group as compared to controls.
Conclusions: GLP-1/dual agonists reduced the incidence of new cases of PRSA in patients with obesity and/or type 2 diabetes.
{"title":"Impact of GLP-1 and dual agonists on the incidence of new cases of physician-reported sleep apnea: a real-world study.","authors":"Beatriz S Prado, Diego R Mazzotti, André Franci, Luciano M Baracioli, Karoline Razimavicius Barbado, Roberta Saretta, Roberto Kalil-Filho, Luciano F Drager","doi":"10.1093/annalsats/aaoaf071","DOIUrl":"https://doi.org/10.1093/annalsats/aaoaf071","url":null,"abstract":"<p><strong>Rationale: </strong>Previous studies have shown that glucagon-like peptide-1 (GLP-1) agonists and dual GLP-1/glucose-dependent insulinotropic peptide (GIP) agonists (tirzepatide) reduced severity of sleep apnea. However, whether these medications impact incidence of new cases of physician-reported sleep apnea (PRSA) is unknown.</p><p><strong>Objective: </strong>To determine the potential impact of GLP-1 and dual agonists on the incidence of sleep apnea reports and to explore potential treatment consequences for this sleep-disordered breathing.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study using the TriNetX Global Health Research Network through anonymized electronic medical records. We identified adult patients with obesity and/or type 2 diabetes mellitus never prescribed GLP-1 or dual agonist therapy (reference arm) and those new initiators of these medications. The index event (June 2022) was chosen to coincide with the launching of tirzepatide in the market. We excluded patients with type 1 diabetes; previous diagnosis of PRSA; previous use of GLP-1/dual agonists, orlistat, phentermine/topiramate, or bupropion/naltrexone; or previous bariatric surgery. Initiators were matched to the reference cohort using propensity score matching in a 1:1 ratio for age, sex, ethnicity, body mass index, and menopause. We used a validated algorithm to identify PRSA using International Classification of Diseases, 10th Revision codes.</p><p><strong>Results: </strong>The follow-up time was 1044 days. After propensity score matching, a total of 1 253 188 patients were included in the reference arm and GLP-1/dual agonist comparison. Overall, GLP-1/dual agonists were associated with a 54% lower incidence of PRSA (HR, 0.46 [95% CI, 0.45-0.49]). Individually, all drugs were able to reach this outcome as compared to the reference arm: liraglutide (HR, 0.64 [95% CI, 0.51-0.80]), dulaglutide (HR, 0.32 [95% CI, 0.28-0.36]), semaglutide (HR, 0.57 [95% CI, 0.54-0.61]), and tirzepatide (HR, 0.74 [95% CI, 0.67-0.92]). Exploratory analysis revealed a 79% lower incidence of positive airway pressure reports in the GLP-1/dual agonist group as compared to controls.</p><p><strong>Conclusions: </strong>GLP-1/dual agonists reduced the incidence of new cases of PRSA in patients with obesity and/or type 2 diabetes.</p>","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":"23 4","pages":"607-613"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoag032
Emily E Moin
{"title":"To \"require ICU care\": a circular definition near the end of its life.","authors":"Emily E Moin","doi":"10.1093/annalsats/aaoag032","DOIUrl":"10.1093/annalsats/aaoag032","url":null,"abstract":"","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":" ","pages":"487-489"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146260352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1513/AnnalsATS.202507-800OC
Shelsey W Johnson, Pietro Nardelli, James C Ross, Carolyn E Come, Gonzalo Sanchez-Ferrero, Carrie L Pistenmaa, Wei Wang, Alejandro A Diaz, Michael J Wells, George R Washko, Rachel K Putman, Farbod N Rahaghi, Raúl San José Estépar
Rationale: In smokers with and without chronic obstructive pulmonary disease (COPD), the differential strengths of association between chest computed tomography (CT)-based metrics of pulmonary vascular disease and adverse outcomes are unknown.
Objectives: We aimed to quantify the differential strengths of association of CT features, from the distal pulmonary arteries to the central great vessels and cardiac chambers, with acute respiratory exacerbations (AREs) and mortality in smokers with and without COPD.
Methods: Smokers with and without COPD with pulmonary vascular morphology and outcomes data were identified in COPDGene. Negative binominal and multivariable Cox proportional hazard models were used to investigate the association of CT features, including volume of the distal pulmonary arterial vasculature or pruning (<5 mm2 normalized to total arterial blood vessel volume [aBV5/aTBV]), preacinar vessels (5-20 mm2), and pulmonary artery to aorta (PA/Ao) and right to left ventricular epicardial volume (RV/LV) ratios, with outcomes. Kaplan-Meier curves were used to describe pruning risk on mortality.
Results: A total of 3169 smokers with COPD and 2530 smokers without COPD were analyzed. Among smokers with COPD, PA/Ao was the only imaging feature significantly associated with AREs (incidence rate ratio, 1.08 [95% CI, 1.04-1.12]), even after adjusting for aBV5/aTBV. Conversely, pruning demonstrated the strongest association with mortality, even in smokers without COPD (hazard ratio, 1.22 [95% CI, 1.14-1.30] and 1.26 [95% CI, 1.11-1.42], respectively). The association of preacinar vessels with mortality in smokers with COPD and in those without COPD, but with significant emphysema on imaging (≥5%), was novel.
Conclusions: Pruning is significantly associated with mortality risk in smokers with and without COPD; however, PA/Ao selectively associates with AREs in COPD, even when accounting for distal vasculopathy.
背景:在患有和不患有COPD的吸烟者中,基于胸部计算机断层扫描(CT)的肺血管疾病指标与不良结局之间的差异强度相关性尚不清楚。目的:量化从肺动脉远端到中央大血管和心腔的CT特征与有和无COPD吸烟者急性呼吸事件(ARE)和死亡率的相关性的差异强度。方法:在COPDGene中识别有和没有COPD的吸烟者的肺血管形态和结局数据。采用负二项和多变量cox比例风险模型来研究CT特征与预后的关系,包括远端肺动脉血管体积或剪切量(< 5mm2归一化到总动脉血管体积(aBV5/aTBV)、腺泡前扩张(5-20mm2)、肺动脉与主动脉(PA/Ao)和右心室与左心室心外膜体积(RV/LV))比。Kaplan-Meier曲线用于描述修剪对死亡率的影响。结果:分析了31369名慢性阻塞性肺病吸烟者和2530名非慢性阻塞性肺病吸烟者。在COPD吸烟者中,PA/Ao是唯一与ARE显著相关的影像学特征(发生率比(IRR) 1.08, 95% CI 1.04, 1.12),即使在调整aBV5/aTBV后也是如此。相反,即使在没有COPD的吸烟者中,剪枝也显示出与死亡率的最强关联(危险比(HR) 1.22, 95% CI 1.14, 1.30;HR 1.26, 95% CI 1.11, 1.42)。在有慢性阻塞性肺病的吸烟者和没有慢性阻塞性肺病但影像学上有明显肺气肿的吸烟者中,腺泡前扩张与死亡率的关联(5%)是新的。结论:在有或没有COPD的吸烟者中,剪枝与死亡风险显著相关,然而PA/Ao选择性地与COPD中的ARE相关,即使考虑到远端血管病变。
{"title":"Pulmonary vascular features on chest computed tomography differentially associate with adverse outcomes in smokers in COPDGene.","authors":"Shelsey W Johnson, Pietro Nardelli, James C Ross, Carolyn E Come, Gonzalo Sanchez-Ferrero, Carrie L Pistenmaa, Wei Wang, Alejandro A Diaz, Michael J Wells, George R Washko, Rachel K Putman, Farbod N Rahaghi, Raúl San José Estépar","doi":"10.1513/AnnalsATS.202507-800OC","DOIUrl":"10.1513/AnnalsATS.202507-800OC","url":null,"abstract":"<p><strong>Rationale: </strong>In smokers with and without chronic obstructive pulmonary disease (COPD), the differential strengths of association between chest computed tomography (CT)-based metrics of pulmonary vascular disease and adverse outcomes are unknown.</p><p><strong>Objectives: </strong>We aimed to quantify the differential strengths of association of CT features, from the distal pulmonary arteries to the central great vessels and cardiac chambers, with acute respiratory exacerbations (AREs) and mortality in smokers with and without COPD.</p><p><strong>Methods: </strong>Smokers with and without COPD with pulmonary vascular morphology and outcomes data were identified in COPDGene. Negative binominal and multivariable Cox proportional hazard models were used to investigate the association of CT features, including volume of the distal pulmonary arterial vasculature or pruning (<5 mm2 normalized to total arterial blood vessel volume [aBV5/aTBV]), preacinar vessels (5-20 mm2), and pulmonary artery to aorta (PA/Ao) and right to left ventricular epicardial volume (RV/LV) ratios, with outcomes. Kaplan-Meier curves were used to describe pruning risk on mortality.</p><p><strong>Results: </strong>A total of 3169 smokers with COPD and 2530 smokers without COPD were analyzed. Among smokers with COPD, PA/Ao was the only imaging feature significantly associated with AREs (incidence rate ratio, 1.08 [95% CI, 1.04-1.12]), even after adjusting for aBV5/aTBV. Conversely, pruning demonstrated the strongest association with mortality, even in smokers without COPD (hazard ratio, 1.22 [95% CI, 1.14-1.30] and 1.26 [95% CI, 1.11-1.42], respectively). The association of preacinar vessels with mortality in smokers with COPD and in those without COPD, but with significant emphysema on imaging (≥5%), was novel.</p><p><strong>Conclusions: </strong>Pruning is significantly associated with mortality risk in smokers with and without COPD; however, PA/Ao selectively associates with AREs in COPD, even when accounting for distal vasculopathy.</p>","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":" ","pages":"527-535"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145395660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1513/AnnalsATS.202508-862OC
Andrew M Courtwright, Joshua M Diamond, Hilary J Goldberg
Rationale: There are limited longer-term follow-up data on bronchiolitis obliterans (BOS)- and retransplant-free survival among patients who underwent lung transplantation for COVID-related lung disease.
Objectives: To evaluate overall, retransplant-free, and BOS- and retransplant-free survival in a national cohort of COVID lung transplant recipients (LTRs).
Methods: We identified all US adult LTRs in the Scientific Registry of Transplant Recipients who underwent transplant for COVID-related lung disease between August 2020 and February 2025. We used propensity score matching (PSM) to construct balanced cohorts of COVID LTRs and non-COVID group D (restrictive lung disease) LTRs, comparing overall, transplant-free, and BOS- and retransplant-free survival in the 2 populations.
Results: There were 605 LTRs with COVID lung disease and 8809 with non-COVID group D diagnoses. Among patients with at least a 3-year follow-up time, survival was 79.1% in COVID LTRs and 73.7% in non-COVID LTRs. In a PSM cohort of 451 matched pairs, overall survival (LTR; hazard ratio [HR], 0.81; 95% CI, 0.60-1.10; P = .17) and retransplant-free survival (HR, 0.81; 95% CI, 0.60-1.09; P = .16) did not differ between the groups. Among non-COVID LTRs, 51 (16.0%) developed BOS, and 56 (16.3%) COVID LTRs developed BOS. Overall, 122 (33.7%) non-COVID LTRs died, were retransplanted, or developed BOS, and 110 (29.1%) COVID LTRs died, were retransplanted, or developed BOS. COVID LTRs had improved retransplant- and BOS-free survival compared to non-COVID LTRs (HR, 0.76; 95% CI, 0.58-0.98; P = .04), driven by 8 fewer deaths in the COVID LTR cohort. COVID acute respiratory distress syndrome LTRs had similar overall, retransplant-free, and BOS- and retransplant survival as COVID fibrosis LTRs.
Conclusions: In this national cohort study, there was no significant difference in overall and retransplant-free survival for COVID LTRs compared to non-COVID, restrictive lung disease LTRs at a median follow-up time of 2.5 years. COVID LTRs, however, had slightly lower hazard for BOS- and retransplant-free survival.
{"title":"Retransplant- and bronchiolitis obliterans syndrome-free survival among COVID lung transplant recipients: a national cohort study.","authors":"Andrew M Courtwright, Joshua M Diamond, Hilary J Goldberg","doi":"10.1513/AnnalsATS.202508-862OC","DOIUrl":"10.1513/AnnalsATS.202508-862OC","url":null,"abstract":"<p><strong>Rationale: </strong>There are limited longer-term follow-up data on bronchiolitis obliterans (BOS)- and retransplant-free survival among patients who underwent lung transplantation for COVID-related lung disease.</p><p><strong>Objectives: </strong>To evaluate overall, retransplant-free, and BOS- and retransplant-free survival in a national cohort of COVID lung transplant recipients (LTRs).</p><p><strong>Methods: </strong>We identified all US adult LTRs in the Scientific Registry of Transplant Recipients who underwent transplant for COVID-related lung disease between August 2020 and February 2025. We used propensity score matching (PSM) to construct balanced cohorts of COVID LTRs and non-COVID group D (restrictive lung disease) LTRs, comparing overall, transplant-free, and BOS- and retransplant-free survival in the 2 populations.</p><p><strong>Results: </strong>There were 605 LTRs with COVID lung disease and 8809 with non-COVID group D diagnoses. Among patients with at least a 3-year follow-up time, survival was 79.1% in COVID LTRs and 73.7% in non-COVID LTRs. In a PSM cohort of 451 matched pairs, overall survival (LTR; hazard ratio [HR], 0.81; 95% CI, 0.60-1.10; P = .17) and retransplant-free survival (HR, 0.81; 95% CI, 0.60-1.09; P = .16) did not differ between the groups. Among non-COVID LTRs, 51 (16.0%) developed BOS, and 56 (16.3%) COVID LTRs developed BOS. Overall, 122 (33.7%) non-COVID LTRs died, were retransplanted, or developed BOS, and 110 (29.1%) COVID LTRs died, were retransplanted, or developed BOS. COVID LTRs had improved retransplant- and BOS-free survival compared to non-COVID LTRs (HR, 0.76; 95% CI, 0.58-0.98; P = .04), driven by 8 fewer deaths in the COVID LTR cohort. COVID acute respiratory distress syndrome LTRs had similar overall, retransplant-free, and BOS- and retransplant survival as COVID fibrosis LTRs.</p><p><strong>Conclusions: </strong>In this national cohort study, there was no significant difference in overall and retransplant-free survival for COVID LTRs compared to non-COVID, restrictive lung disease LTRs at a median follow-up time of 2.5 years. COVID LTRs, however, had slightly lower hazard for BOS- and retransplant-free survival.</p>","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":" ","pages":"558-564"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1513/AnnalsATS.202503-260OC
Lucia Cilloni, Raeesa Docrat, Carlos Haring, Suzanne M Marks, David Dowdy, Sourya Shrestha
Rationale: The United States experienced a considerable decline in tuberculosis (TB) incidence in 2020 following the COVID-19 pandemic.
Objectives: While TB rates have since returned to near prepandemic levels, analyzing the pandemic's impact offers insight into TB epidemiology in the United States.
Methods: Focusing on California, Florida, New York, and Texas-the 4 states with the highest TB incidence-we explored 3 potential mechanisms of pandemic-related disruption on TB epidemiology: (1) reduced immigration, (2) reduced Mtb transmission (through social distancing and other behavior changes), and (3) delays in care-seeking. We used data on the volume of nonimmigrant arrivals and new permanent residents, Google mobility and US transit data, and data on the volume of emergency department visits and cancer screenings to inform the magnitude of these effects at the state level, adapting previously developed state-specific transmission models. We then estimated the impact of each mechanism and projected future TB incidence through 2032.
Measurements and main results: Disruptions to migration and care-seeking across all 4 states were considerable but short-lasting, with 70% to 90% reductions in the first 4 months of the pandemic that returned to prepandemic levels by 2021. In contrast, transmission disruptions were moderate but more prolonged, with mobility still 10% to 20% lower than prepandemic in 2022. No statistical evidence was identified to favor models emphasizing immigration and transmission vs access to care.
Conclusions: Revised projections for pandemic-related disruptions did not substantially differ from prepandemic projections beyond 2024. Future declines in TB incidence in the 4 states are likely to be small without additional interventions.
{"title":"Impact of the COVID-19 pandemic on tuberculosis epidemiology in California, Florida, New York, and Texas.","authors":"Lucia Cilloni, Raeesa Docrat, Carlos Haring, Suzanne M Marks, David Dowdy, Sourya Shrestha","doi":"10.1513/AnnalsATS.202503-260OC","DOIUrl":"10.1513/AnnalsATS.202503-260OC","url":null,"abstract":"<p><strong>Rationale: </strong>The United States experienced a considerable decline in tuberculosis (TB) incidence in 2020 following the COVID-19 pandemic.</p><p><strong>Objectives: </strong>While TB rates have since returned to near prepandemic levels, analyzing the pandemic's impact offers insight into TB epidemiology in the United States.</p><p><strong>Methods: </strong>Focusing on California, Florida, New York, and Texas-the 4 states with the highest TB incidence-we explored 3 potential mechanisms of pandemic-related disruption on TB epidemiology: (1) reduced immigration, (2) reduced Mtb transmission (through social distancing and other behavior changes), and (3) delays in care-seeking. We used data on the volume of nonimmigrant arrivals and new permanent residents, Google mobility and US transit data, and data on the volume of emergency department visits and cancer screenings to inform the magnitude of these effects at the state level, adapting previously developed state-specific transmission models. We then estimated the impact of each mechanism and projected future TB incidence through 2032.</p><p><strong>Measurements and main results: </strong>Disruptions to migration and care-seeking across all 4 states were considerable but short-lasting, with 70% to 90% reductions in the first 4 months of the pandemic that returned to prepandemic levels by 2021. In contrast, transmission disruptions were moderate but more prolonged, with mobility still 10% to 20% lower than prepandemic in 2022. No statistical evidence was identified to favor models emphasizing immigration and transmission vs access to care.</p><p><strong>Conclusions: </strong>Revised projections for pandemic-related disruptions did not substantially differ from prepandemic projections beyond 2024. Future declines in TB incidence in the 4 states are likely to be small without additional interventions.</p>","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":" ","pages":"516-526"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoaf048
Chad H Hochberg, Li Yan, M Elizabeth Card, Stephen A Berry, Daniel Brodie, Leo Rotello, Amirali Nader, Souvik Chatterjee, Sarina K Sahetya, Theodore J Iwashyna, David N Hager
Background: Hypertensive emergency is characterized by end-organ dysfunction due to markedly elevated blood pressure. Although guidelines recommend rapid blood pressure lowering with intravenous antihypertensives and continuous monitoring in an intensive care unit (ICU), many patients are managed in intermediate care (IMC) settings. In this study, we compare outcomes of hypertensive emergency patients admitted to ICU vs IMC settings.
Methods: Adult patients in the emergency departments of 3 hospitals were included if they had 2 or more systolic blood pressure measurements greater than 180 mm Hg within 12 hours of one another, were treated with continuous intravenous antihypertensive medications, and were subsequently admitted to an ICU or IMC setting. We excluded patients receiving mechanical ventilation in the emergency department and those presenting with acute coronary syndrome, aortic dissection, or acute cerebrovascular accident. The primary outcome was hospital length of stay (LOS) penalized for death and adjusted for baseline patient features. Secondary outcomes included ICU and IMC LOS and hospital mortality. Process outcomes included arterial line usage, frequency of blood pressure measurements in the first 24 hours, and escalations of care. Lastly, we report the proportion of patients reaching blood pressure targets and/or episodes of hypotension in each setting.
Results: Intensive care unit patients (n = 649) were younger, with a male predominance, more frequently received noninvasive respiratory support and were dialysis dependent than IMC patients (n = 629). In an adjusted analysis, there was no difference in time to hospital discharge between patients admitted to ICU vs IMC settings (absolute difference: +0.29 days; 95% CI, -0.07 to 0.70). Similarly, there was no difference in ICU vs IMC LOS, hospital readmission rate, or hospital mortality. Blood pressures were more frequently measured in the ICU, but there was no difference in time to target blood pressure goal. Any hypotensive episode in the first 24 hours was more common in the ICU.
Conclusions: In this retrospective observational study of patients with hypertensive emergency, we did not observe significantly different LOS outcomes between patients admitted to ICU vs IMC settings or detect a signal of harm among those admitted to IMC. Intermediate care settings may be a reasonable alternative to ICU admission for select patients with hypertensive emergency.
背景:高血压急症以血压显著升高引起的终末器官功能障碍为特征。虽然指南建议通过静脉注射抗高血压药物快速降低血压,并在重症监护病房(ICU)持续监测,但许多患者在中间护理(IMC)环境中进行管理。在这项研究中,我们比较了ICU和IMC的高血压急诊患者的预后。方法:纳入3家医院急诊科的成年患者,如果他们在12小时内两次或两次以上收缩压测量值大于180 mm Hg,持续静脉注射降压药物治疗,并随后入住ICU或IMC。我们排除了在急诊科接受机械通气的患者以及出现急性冠状动脉综合征、主动脉夹层或急性脑血管意外的患者。主要结局是因死亡而受到惩罚的住院时间(LOS),并根据基线患者特征进行调整。次要结局包括ICU和IMC的LOS和医院死亡率。过程结局包括动脉导管使用情况、最初24小时内血压测量频率和护理升级。最后,我们报告了在每种情况下达到血压目标和/或低血压发作的患者比例。结果:重症监护病房患者(n = 649)比IMC患者(n = 629)更年轻,以男性为主,更频繁地接受无创呼吸支持,并依赖透析。在一项调整后的分析中,ICU和IMC患者在出院时间上没有差异(绝对差异:+0.29天;95% CI, -0.07至0.70)。同样,ICU与IMC的LOS、医院再入院率或医院死亡率也没有差异。在ICU更频繁地测量血压,但在达到血压目标的时间上没有差异。前24小时出现低血压发作在ICU更为常见。结论:在这项对高血压急症患者的回顾性观察研究中,我们没有观察到ICU和IMC住院患者的LOS结果有显著差异,也没有发现IMC住院患者的伤害信号。对于某些高血压急症患者,中间护理环境可能是ICU住院的合理选择。
{"title":"Outcomes of patients with hypertensive emergency managed in intensive vs intermediate care settings: a multihospital retrospective cohort study.","authors":"Chad H Hochberg, Li Yan, M Elizabeth Card, Stephen A Berry, Daniel Brodie, Leo Rotello, Amirali Nader, Souvik Chatterjee, Sarina K Sahetya, Theodore J Iwashyna, David N Hager","doi":"10.1093/annalsats/aaoaf048","DOIUrl":"10.1093/annalsats/aaoaf048","url":null,"abstract":"<p><strong>Background: </strong>Hypertensive emergency is characterized by end-organ dysfunction due to markedly elevated blood pressure. Although guidelines recommend rapid blood pressure lowering with intravenous antihypertensives and continuous monitoring in an intensive care unit (ICU), many patients are managed in intermediate care (IMC) settings. In this study, we compare outcomes of hypertensive emergency patients admitted to ICU vs IMC settings.</p><p><strong>Methods: </strong>Adult patients in the emergency departments of 3 hospitals were included if they had 2 or more systolic blood pressure measurements greater than 180 mm Hg within 12 hours of one another, were treated with continuous intravenous antihypertensive medications, and were subsequently admitted to an ICU or IMC setting. We excluded patients receiving mechanical ventilation in the emergency department and those presenting with acute coronary syndrome, aortic dissection, or acute cerebrovascular accident. The primary outcome was hospital length of stay (LOS) penalized for death and adjusted for baseline patient features. Secondary outcomes included ICU and IMC LOS and hospital mortality. Process outcomes included arterial line usage, frequency of blood pressure measurements in the first 24 hours, and escalations of care. Lastly, we report the proportion of patients reaching blood pressure targets and/or episodes of hypotension in each setting.</p><p><strong>Results: </strong>Intensive care unit patients (n = 649) were younger, with a male predominance, more frequently received noninvasive respiratory support and were dialysis dependent than IMC patients (n = 629). In an adjusted analysis, there was no difference in time to hospital discharge between patients admitted to ICU vs IMC settings (absolute difference: +0.29 days; 95% CI, -0.07 to 0.70). Similarly, there was no difference in ICU vs IMC LOS, hospital readmission rate, or hospital mortality. Blood pressures were more frequently measured in the ICU, but there was no difference in time to target blood pressure goal. Any hypotensive episode in the first 24 hours was more common in the ICU.</p><p><strong>Conclusions: </strong>In this retrospective observational study of patients with hypertensive emergency, we did not observe significantly different LOS outcomes between patients admitted to ICU vs IMC settings or detect a signal of harm among those admitted to IMC. Intermediate care settings may be a reasonable alternative to ICU admission for select patients with hypertensive emergency.</p>","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":"23 4","pages":"565-574"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13052349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoaf054
Wenli Ni, Stephanie T Grady, Nicholas Nassikas, Jaime E Hart, Petros Koutrakis, Junfeng Jim Zhang, Eric Garshick, Mary B Rice
<p><strong>Rationale: </strong>Greater ambient air temperatures may have implications for respiratory health. While prior research has primarily examined the associations of air temperature with lung health in the general population, individuals with chronic obstructive pulmonary disease (COPD) may be particularly susceptible. This study aims to assess the associations between air temperature and pulmonary function, as well as biomarkers of inflammation and oxidative stress, in this potentially susceptible population.</p><p><strong>Methods: </strong>We conducted a study of 166 participants with COPD (either a former or no history of smoking) from eastern Massachusetts, United States, who completed up to 4 visits over 12 months at the VA Boston Healthcare System between 2012 and 2017, yielding 620 observations. Daily mean temperature exposures, at a spatial resolution of 4 × 4 km, were assigned to geocoded home addresses. We used generalized additive mixed models to investigate associations of short-term temperature exposures at 0- to 1-day, 2- to 6-day, 0- to 6-day, and 0- to 13-day moving averages with repeated lung function measurements, blood biomarkers of systemic inflammation (high-sensitivity C-reactive protein [hsCRP], interleukin 6, soluble vascular cell adhesion molecule 1), and urinary biomarkers of oxidative stress (8-hydroxy-2'-deoxyguanosine, malondialdehyde), adjusting for confounders (eg, air conditioner usage and season). We performed mediation analyses to determine if temperature-lung function relationships were mediated by inflammatory or oxidative stress pathways.</p><p><strong>Results: </strong>The population was 97.0% male, mean (SD) age = 72.8 (8.4) years, mean (SD) percent predicted forced expiratory volume in 1 second (FEV1%) = 66.2 (21.8), and mean (SD) temperature = 10.2 °C (10.4 °C). Higher temperature exposures at all moving averages were associated with lower FEV1. For example, per 5 °C increase in temperature at lags of 0 to 1 and 0 to 13 days, FEV1 decreased by (mL, 95% CI) 12.06 (-23.14 to -0.98) and 16.24 (-29.23 to -3.25), respectively. Similarly, higher temperature exposures were associated with lower forced expiratory volume in 1 second/forced vital capacity. There were positive associations between higher temperature across all moving averages and higher hsCRP. For instance, a 5 °C increase in temperature at lags of 0 to 1 days and 0 to 13 days was associated with percent increases in hsCRP of 6.37 (95% CI, 1.05-11.97) and 9.40 (95% CI, 3.02-16.16), respectively. hsCRP did not mediate the temperature-lung function relationship. Associations were similar, adjusting for indoor and outdoor air pollution. No associations were observed with forced vital capacity or other inflammatory or oxidative stress biomarkers.</p><p><strong>Conclusion: </strong>Short-term exposures to higher air temperatures were associated with lower lung function and higher hsCRP concentrations among individuals with COPD, suggesting that ri
{"title":"Associations of daily air temperature with lung function and biomarkers of inflammation and oxidative stress in chronic obstructive pulmonary disease.","authors":"Wenli Ni, Stephanie T Grady, Nicholas Nassikas, Jaime E Hart, Petros Koutrakis, Junfeng Jim Zhang, Eric Garshick, Mary B Rice","doi":"10.1093/annalsats/aaoaf054","DOIUrl":"10.1093/annalsats/aaoaf054","url":null,"abstract":"<p><strong>Rationale: </strong>Greater ambient air temperatures may have implications for respiratory health. While prior research has primarily examined the associations of air temperature with lung health in the general population, individuals with chronic obstructive pulmonary disease (COPD) may be particularly susceptible. This study aims to assess the associations between air temperature and pulmonary function, as well as biomarkers of inflammation and oxidative stress, in this potentially susceptible population.</p><p><strong>Methods: </strong>We conducted a study of 166 participants with COPD (either a former or no history of smoking) from eastern Massachusetts, United States, who completed up to 4 visits over 12 months at the VA Boston Healthcare System between 2012 and 2017, yielding 620 observations. Daily mean temperature exposures, at a spatial resolution of 4 × 4 km, were assigned to geocoded home addresses. We used generalized additive mixed models to investigate associations of short-term temperature exposures at 0- to 1-day, 2- to 6-day, 0- to 6-day, and 0- to 13-day moving averages with repeated lung function measurements, blood biomarkers of systemic inflammation (high-sensitivity C-reactive protein [hsCRP], interleukin 6, soluble vascular cell adhesion molecule 1), and urinary biomarkers of oxidative stress (8-hydroxy-2'-deoxyguanosine, malondialdehyde), adjusting for confounders (eg, air conditioner usage and season). We performed mediation analyses to determine if temperature-lung function relationships were mediated by inflammatory or oxidative stress pathways.</p><p><strong>Results: </strong>The population was 97.0% male, mean (SD) age = 72.8 (8.4) years, mean (SD) percent predicted forced expiratory volume in 1 second (FEV1%) = 66.2 (21.8), and mean (SD) temperature = 10.2 °C (10.4 °C). Higher temperature exposures at all moving averages were associated with lower FEV1. For example, per 5 °C increase in temperature at lags of 0 to 1 and 0 to 13 days, FEV1 decreased by (mL, 95% CI) 12.06 (-23.14 to -0.98) and 16.24 (-29.23 to -3.25), respectively. Similarly, higher temperature exposures were associated with lower forced expiratory volume in 1 second/forced vital capacity. There were positive associations between higher temperature across all moving averages and higher hsCRP. For instance, a 5 °C increase in temperature at lags of 0 to 1 days and 0 to 13 days was associated with percent increases in hsCRP of 6.37 (95% CI, 1.05-11.97) and 9.40 (95% CI, 3.02-16.16), respectively. hsCRP did not mediate the temperature-lung function relationship. Associations were similar, adjusting for indoor and outdoor air pollution. No associations were observed with forced vital capacity or other inflammatory or oxidative stress biomarkers.</p><p><strong>Conclusion: </strong>Short-term exposures to higher air temperatures were associated with lower lung function and higher hsCRP concentrations among individuals with COPD, suggesting that ri","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":"23 4","pages":"506-515"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01DOI: 10.1093/annalsats/aaoaf043
Jean-Louis Pepin, Eleonore Herquelot, Hélène Denis, Maxime Patout, Anne Josseran, Florent Lavergne, Aurélie Schmidt, Atul Malhotra, Peter A Cistulli, Alain Palot, Arnaud Prigent
Rationale: Coexisting chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) is known as overlap syndrome. This may represent a distinct clinical phenotype that shows different responses after being initiated on noninvasive ventilation (NIV) for hypercapnic chronic respiratory failure. However, current data remain scarce.
Objective(s): This study estimated the impact of overlap syndrome versus COPD without OSA on transitions between 3 states (without/recovery from severe exacerbation, severe exacerbation and death) in patients initiated on domiciliary NIV therapy.
Methods: Multistate model data came from the French national health insurance reimbursement system database for individuals with COPD aged ≥40 years and ≥1 NIV reimbursement in 2015-2019. Outcomes in the overlap syndrome and COPD without OSA groups were compared using a Cox model and inverse probability of treatment weighting analysis, adjusted for patient characteristics.
Results: Data from 54,545 patients were included (median age 70 years, 51.2% male). Probabilities of transitioning from severe exacerbation to death (10% vs. 22%) and without severe exacerbation to death (5% vs. 18%) were lower in the overlap syndrome versus COPD without OSA group. The rate of transition from severe exacerbation to without exacerbation/recovery was also higher in the overlap syndrome group. After NIV initiation, the mortality rate was 33% lower in people with overlap syndrome vs COPD without OSA.
Conclusions: For people with COPD started on domiciliary NIV, those with overlap syndrome might benefit from NIV to a greater extent than those without OSA. This highlights the need for OSA screening in people with COPD.
{"title":"Mortality impact of long-term home non-invasive ventilation in COPD patients with versus without obstructive sleep apnea.","authors":"Jean-Louis Pepin, Eleonore Herquelot, Hélène Denis, Maxime Patout, Anne Josseran, Florent Lavergne, Aurélie Schmidt, Atul Malhotra, Peter A Cistulli, Alain Palot, Arnaud Prigent","doi":"10.1093/annalsats/aaoaf043","DOIUrl":"10.1093/annalsats/aaoaf043","url":null,"abstract":"<p><strong>Rationale: </strong>Coexisting chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) is known as overlap syndrome. This may represent a distinct clinical phenotype that shows different responses after being initiated on noninvasive ventilation (NIV) for hypercapnic chronic respiratory failure. However, current data remain scarce.</p><p><strong>Objective(s): </strong>This study estimated the impact of overlap syndrome versus COPD without OSA on transitions between 3 states (without/recovery from severe exacerbation, severe exacerbation and death) in patients initiated on domiciliary NIV therapy.</p><p><strong>Methods: </strong>Multistate model data came from the French national health insurance reimbursement system database for individuals with COPD aged ≥40 years and ≥1 NIV reimbursement in 2015-2019. Outcomes in the overlap syndrome and COPD without OSA groups were compared using a Cox model and inverse probability of treatment weighting analysis, adjusted for patient characteristics.</p><p><strong>Results: </strong>Data from 54,545 patients were included (median age 70 years, 51.2% male). Probabilities of transitioning from severe exacerbation to death (10% vs. 22%) and without severe exacerbation to death (5% vs. 18%) were lower in the overlap syndrome versus COPD without OSA group. The rate of transition from severe exacerbation to without exacerbation/recovery was also higher in the overlap syndrome group. After NIV initiation, the mortality rate was 33% lower in people with overlap syndrome vs COPD without OSA.</p><p><strong>Conclusions: </strong>For people with COPD started on domiciliary NIV, those with overlap syndrome might benefit from NIV to a greater extent than those without OSA. This highlights the need for OSA screening in people with COPD.</p>","PeriodicalId":93876,"journal":{"name":"Annals of the American Thoracic Society","volume":"23 4","pages":"597-606"},"PeriodicalIF":5.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}