TY - JOUR T1 - Central airway and peripheral lung structures in airway disease dominant COPD JF - ERJ Open Research JO - erjor DO - 10.1183/23120541.00672-2020 SP - 00672-2020 AU - Naoya Tanabe AU - Kaoruko Shimizu AU - Kunihiko Terada AU - Susumu Sato AU - Masaru Suzuki AU - Hiroshi Shima AU - Akira Oguma AU - Tsuyoshi Oguma AU - Satoshi Konno AU - Masaharu Nishimura AU - Toyohiro Hirai Y1 - 2021/01/01 UR - http://openres.ersjournals.com/content/early/2021/01/14/23120541.00672-2020.abstract N2 - The concept that the small airway is a primary pathological site for all COPD phenotypes has been challenged by recent findings that the disease starts from the central airways in COPD subgroups and that a smaller central airway tree increases COPD risk. This study aimed to examine whether the computed tomography (CT)-based airway disease-dominant (AD) subtype, defined using the central airway dimension, was less associated with small airway dysfunction (SAD) on CT, compared to the emphysema-dominant (ED) subtype.COPD patients were categorised into mild, AD, ED, and mixed groups based on wall area percent (WA%) of the segmental airways and low attenuation volume percent in the Kyoto-Himeji (n=189) and Hokkaido COPD cohorts (n=93). The volume percent of SAD regions (SAD%) was obtained by nonrigidly registering inspiratory and expiratory CT.The AD group had a lower SAD% than the ED group and similar SAD% to the mild group. The AD group had a smaller lumen size of airways proximal to the segmental airways and more frequent asthma history before age 40 years than the ED group. In multivariable analyses, while the AD and ED groups were similarly associated with greater airflow limitation, the ED, but not the AD group, was associated with greater SAD%, whereas the AD, but not the ED group, was associated with a smaller central airway size.The CT-based AD COPD subtype might be associated with a smaller central airway tree and asthma history, but not with peripheral lung pathologies including small airway disease, unlike the ED subtype.FootnotesThis manuscript has recently been accepted for publication in the ERJ Open Research. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJOR online. Please open or download the PDF to view this article.Conflict of interest: Dr. Tanabe reports grants from FUJIFILM, during the conduct of the study; personal fees from AstraZeneka, personal fees from Nippon Boehringer Ingelheim, personal fees from GlaxoSmithKline, outside the submitted work;.Conflict of interest: Dr. Shimizu has nothing to disclose.Conflict of interest: Dr. Terada has nothing to disclose.Conflict of interest: Dr. Sato has nothing to disclose.Conflict of interest: M. Suzuki reports grants and lecture fees from AstraZeneca and Novartis, and lecture fees from Boehringer Ingelheim and GlaxoSmithKline, outside the submitted work.Conflict of interest: Dr. Shima has nothing to disclose.Conflict of interest: Dr. Oguma has nothing to disclose.Conflict of interest: T. Oguma reports joint research with FUJIFILM during the conduct of the study and lecture fees from AstraZeneca, Boehringer Ingelheim and GlaxoSmithKline outside the submitted work.Conflict of interest: Dr. Konnno reports grants from Astra-Zeneca, grants from Novartis, grants from Boeringer-ingerheim, grants from Kyorin, outside the submitted work;.Conflict of interest: Dr. Nishimura reports grants from Nippon Boehringer Ingelheim, grants from Pfizer Japan, during the conduct of the study;.Conflict of interest: Dr. Hirai reports grants from FUJIFILM, during the conduct of the study;. ER -