Scholarlink

Purpose <p>Vascular remodelling is increasingly recognised as a key pathological feature in Chronic Obstructive Pulmonary Disease (COPD), with changes in pulmonary blood flow offering early biomarkers of disease. However, computational models capable of capturing the evolution of pulmonary haemodynamics across COPD severity stages are lacking. This study presents an anatomically based in silico model of the pulmonary circulation designed to investigate haemodynamic changes in response to vascular remodelling and parenchymal destruction in smokers without COPD and in patients with varying stages of COPD.</p> Methods <p>A one-dimensional, steady-state model of pulmonary blood flow was adapted to simulate extra-acinar arterial remodelling and intra-acinar capillary pruning consistent with emphysema. The model was parameterised using morphometric and clinical haemodynamic data at rest and during exercise across GOLD stages 1–4.</p> Results <p>Model-predicted mean pulmonary arterial pressure (mPAP) increased progressively from 13.5&#xa0;mmHg (baseline) to 16.1&#xa0;mmHg (GOLD 2), 21.2&#xa0;mmHg (GOLD 3), and 25.9&#xa0;mmHg (GOLD 4), with increasing vascular remodelling, matching clinical data within reported error bounds. In the most severe COPD case, GOLD 4, 70% of arterial vessels and 35% of acinar units were modified to represent disease. Height-dependent flow and pressure gradients were markedly altered in GOLD 4 indicating significant redistribution and increased heterogeneity of pulmonary blood flow.</p> Conclusion <p>This model reproduces clinically measured mPAP and pulmonary vascular resistance values across COPD stages and quantifies how specific degrees of remodelling and pruning drive haemodynamic deterioration. This model provides a tool for hypothesis testing, patient stratification, and evaluation of potential targeted therapies in obstructive lung disease.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Vascular Remodelling in COPD: An In Silico Tool to Represent Pulmonary Haemodynamics in Obstructive Lung Disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月31日

查看全文
  • B. Allen,
  • B. S. Ebrahimi,
  • A. R. Clark,
  • M. H. Tawhai,
  • Kelly S. Burrowes

摘要

Purpose

Vascular remodelling is increasingly recognised as a key pathological feature in Chronic Obstructive Pulmonary Disease (COPD), with changes in pulmonary blood flow offering early biomarkers of disease. However, computational models capable of capturing the evolution of pulmonary haemodynamics across COPD severity stages are lacking. This study presents an anatomically based in silico model of the pulmonary circulation designed to investigate haemodynamic changes in response to vascular remodelling and parenchymal destruction in smokers without COPD and in patients with varying stages of COPD.

Methods

A one-dimensional, steady-state model of pulmonary blood flow was adapted to simulate extra-acinar arterial remodelling and intra-acinar capillary pruning consistent with emphysema. The model was parameterised using morphometric and clinical haemodynamic data at rest and during exercise across GOLD stages 1–4.

Results

Model-predicted mean pulmonary arterial pressure (mPAP) increased progressively from 13.5 mmHg (baseline) to 16.1 mmHg (GOLD 2), 21.2 mmHg (GOLD 3), and 25.9 mmHg (GOLD 4), with increasing vascular remodelling, matching clinical data within reported error bounds. In the most severe COPD case, GOLD 4, 70% of arterial vessels and 35% of acinar units were modified to represent disease. Height-dependent flow and pressure gradients were markedly altered in GOLD 4 indicating significant redistribution and increased heterogeneity of pulmonary blood flow.

Conclusion

This model reproduces clinically measured mPAP and pulmonary vascular resistance values across COPD stages and quantifies how specific degrees of remodelling and pruning drive haemodynamic deterioration. This model provides a tool for hypothesis testing, patient stratification, and evaluation of potential targeted therapies in obstructive lung disease.