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Arterial remodelling in smokers and in patients with small airway disease and COPD: implications for lung physiology and early origins of pulmonary hypertension

Citation

Bhattarai, P and Lu, W and Gaikwad, AV and Dey, S and Chia, C and Larby, J and Haug, G and Hardikar, A and Williams, A and Singhera, GK and Hackett, T-L and Eapen, MS and Sohal, SS, Arterial remodelling in smokers and in patients with small airway disease and COPD: implications for lung physiology and early origins of pulmonary hypertension, ERJ Open Research, 8, (4) Article 00254-2022. ISSN 2312-0541 (2022) [Refereed Article]


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DOI: doi:10.1183/23120541.00254-2022

Abstract

Introduction: Pulmonary vascular remodelling in chronic obstructive pulmonary disease (COPD) has detrimental consequences for lung physiology. The aim of our study was to provide a comprehensive size-based morphometric quantification of pulmonary arterial remodelling in smokers and in patients with small airway disease (SAD) or COPD.

Method: pentachrome staining was performed on lung resections for 46 subjects: 12 never-smoker normal controls (NC), six normal lung function smokers (NLFS), nine patients with SAD, nine patients with mild-to-moderate COPD who were current smokers (COPD-CS) and 10 patients with mild-to-moderate COPD who were ex-smokers (COPD-ES). Following a size-based classification of pulmonary arteries, image analysis software was used to measure their number, total wall thickness, individual layer thickness and elastin percentage.

Results: All pathological groups showed decreased numbers of pulmonary arteries compared with the NC group in all artery sizes. Arterial wall thickness was greater in NLFS and COPD-CS than in NC. Thickness in COPD-ES was decreased compared with COPD-CS. Intimal thickness was greater in all pathological groups in all arterial sizes than in the NC group. Medial thickness was also greater in small and medium arteries. Intimal thickness of larger arteries in COPD-CS correlated negatively to forced expiratory volume in 1 s/forced vital capacity (FVC) % and forced expiratory flow at 25-75% of FVC. Elastin deposition in small arteries was greatest in COPD-CS. Intimal elastin deposition had a more negative correlation with intimal thickness in NLFS and SAD than in COPD-CS.

Conclusion: Smoking, SAD and mild-to-moderate COPD are associated with pruning and a decrease in the number of pulmonary arteries, increased wall thickness and variable elastin deposition. These changes were associated with worse airway obstruction.

Item Details

Item Type:Refereed Article
Keywords:remodelling, extracellular matrix, pulmonary hypertension, COPD, smoking, Fibroblasts, Collagen, Fibrosis
Research Division:Biomedical and Clinical Sciences
Research Group:Cardiovascular medicine and haematology
Research Field:Cardiology (incl. cardiovascular diseases)
Objective Division:Health
Objective Group:Clinical health
Objective Field:Diagnosis of human diseases and conditions
UTAS Author:Bhattarai, P (Mr Prem Bhattarai)
UTAS Author:Lu, W (Dr Monica Lu)
UTAS Author:Gaikwad, AV (Ms Archana Gaikwad)
UTAS Author:Dey, S (Mr Surajit Dey)
UTAS Author:Larby, J (Dr Josie Larby)
UTAS Author:Haug, G (Dr Greg Haug)
UTAS Author:Hardikar, A (Dr Ashutosh Hardikar)
UTAS Author:Williams, A (Associate Professor Andrew Williams)
UTAS Author:Eapen, MS (Dr Mathew Eapen)
UTAS Author:Sohal, SS (Dr Sukhwinder Sohal)
ID Code:154938
Year Published:2022
Deposited By:Health Sciences
Deposited On:2023-01-20
Last Modified:2023-01-20
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