{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T23:03:53Z","timestamp":1776380633397,"version":"3.51.2"},"reference-count":37,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2024,3,19]],"date-time":"2024-03-19T00:00:00Z","timestamp":1710806400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institute of Heath Research","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Respiratory Health Network of the FRQS"},{"DOI":"10.13039\/501100021743","name":"Canadian Respiratory Research Network","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100021743","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000221","name":"Canadian Lung Association","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000221","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010647","name":"Canadian Thoracic Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010647","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015752","name":"British Columbia Lung Association","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100015752","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Astra Zeneca Canada Inc"},{"name":"Boehringer-Ingelheim Canada Inc"},{"name":"GlaxoSmithKline Canada Inc"},{"DOI":"10.13039\/100009009","name":"Novartis Pharma Canada","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100009009","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Nycomed Canada Inc"},{"name":"Pfizer Canada Ltd"},{"DOI":"10.13039\/501100000038","name":"Natural Sciences and Engineering Research Council","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000038","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Canada Research Chair Program"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,5,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Trachea structural abnormalities occur in patients with chronic obstructive pulmonary disease (COPD), yet there are few methods for quantifying trachea surface topology.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Purpose<\/jats:title>\n                  <jats:p>To develop a method to quantify trachea surface roughness on CT imaging and investigate the association with airflow limitation and symptoms in COPD.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Materials and Methods<\/jats:title>\n                  <jats:p>Participants from the multicenter prospective Canadian Cohort Obstructive Lung Disease study between 2009 and 2015 underwent CT imaging and analysis. Established CT measurements included: tracheal index (TI), defined as the smallest ratio of coronal-to-sagittal trachea diameter, low attenuation areas below \u2013950 HU, and wall thickness of a theoretical 10-mm airway. Trachea surface roughness shape (SRS) was calculated as the percent fraction of the measurement box filled by the surface mesh. Multivariable regression models were used to determine association for CT measurements with forced expiratory volume in 1\u2009second (FEV1) and forced vital capacity (FVC), and Medical Research Council dyspnea scale (MRC)\u22653, adjusting for covariates.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>A total of 1253 participants (mean age, 66\u2009\u00b1\u200910\u2009years; 727 men) from 9 centers were investigated: n\u2009=\u2009267 never smokers, n\u2009=\u2009369 ever smokers, n\u2009=\u2009352 mild COPD, and n\u2009=\u2009265 moderate-to-severe COPD. There were no differences between groups for age or race (P\u2009&amp;lt;\u2009.05). In models including SRS and TI, a 1-standard deviation (SD) increase in SRS was independently associated with a 0.11-SD decrease in FEV1 (\u03b2\u2009=\u2009\u20130.11; P\u2009&amp;lt;\u2009.001) and a 0.16-SD decrease in FEV1\/FVC (\u03b2\u2009=\u2009\u20130.16; P\u2009&amp;lt;\u2009.001); a 1-point increase in SRS was associated with a 13% increased likelihood of MRC\u2009\u2265\u20093 (odds ratio\u2009=\u20091.13; P\u2009=\u2009.003). In models including SRS, low attenuation areas below \u2013950 HU and wall thickness of a theoretical 10-mm airway, a 1-SD increase in SRS was associated with a 0.21-SD decrease in FEV1 (\u03b2\u2009=\u2009\u20130.21; P\u2009&amp;lt;\u2009.001) and a 0.13-SD decrease in FEV1\/FVC (\u03b2\u2009=\u2009\u20130.13; P\u2009&amp;lt;\u2009.001); a 1-point increase in SRS was associated with a 12% increased likelihood of MRC\u2009\u2265\u20093 (odds ratio\u2009=\u20091.12; P\u2009=\u2009.006).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Increased trachea surface shape roughness is independently associated with worse airflow and increased symptom burden in COPD.<\/jats:p>\n               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