Computational fluid dynamics of small airway disease in chronic obstructive pulmonary disease.
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Ошибки и ограничения
История · было → стало
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Mohamady Yousry K, Geudens Vincent, De Fays Charlotte, Zapata Marta, Hagrass Omar, Aversa Lucia, Vermant Marie, Jin Xin, Willems Lynn, Gyselinck Iwein, Hooft Charlotte, Vermaut Astrid, Beeckmans Hanne, Kerckhof Pieterjan, Aerts Gitte, Aelbrecht Celine, Verhaegen Janne, Higham Andrew, Coudyzer Walter, Cortesi Emanuela E, Vanstapel Arno, McDonough John E, Carlon Marianne S, Quarck Rozenn, Boone Matthieu N, Dupont Lieven, Everaerts Stephanie, Van Raemdonck Dirk E, Ceulemans Laurens J, Hackett Tillie-Louise, Vos Robin, Abuouf Yasser, Jacob Joseph, Wuyts Wim A, Hogg James C, Filoche Marcel, Gayan-Ramirez Ghislaine, Janssens Wim, Vanaudenaerde Bart M
Аннотация
METHODS: We performed computational fluid dynamics (CFD) simulations of inspiratory airflow in three lung groups: control non-used donor lungs (no smoking/emphysema history), non-used donor lungs with a smoking history and emphysema, and explanted end-stage COPD lungs. Each group included four lungs, with two tissue cylinders. Micro-CT-scanned small airways were segmented into 3D models for CFD simulations to quantify pressure, resistance, and shear stress. CFD results were benchmarked against simplified linear and Weibel models.
FINDINGS: CFD simulations showed higher pressures in COPD vs. controls (p = 0.0091) and smokers (p = 0.015), along with increased resistance (p = 0.0057 vs. controls; p = 0.0083 vs. smokers) and up to a tenfold rise in shear stress (p = 0.010 vs. controls). Narrowing and occlusion were shown to independently increase pressure, resistance, and shear stress, which were validated through segmentation corrections. Pressures and resistance assessed with simplified models were up to seven-fold higher for smokers and even 72 higher for COPD compared with CFD values.
INTERPRETATION: These findings show that increased airflow parameters can explain the association between small airway disease and airflow limitation in COPD, underscoring small airway vulnerability. Additionally, they highlight the limitations of theoretical models in accurately capturing small airway disease.
FUNDING: Supported by the KU Leuven (C16/19/005).