A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions

Pulmonary hypertension has multiple etiologies and so can be difficult to diagnose, prognose, and treat. Diagnosis is typically made via invasive hemodynamic measurements in the main pulmonary artery and is based on observed elevation of mean pulmonary artery pressure. This static mean pressure enab...

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Autores principales:	Behdad Shaarbaf Ebrahimi, Merryn H. Tawhai, Haribalan Kumar, Kelly S. Burrowes, Eric A. Hoffman, Margaret L. Wilsher, David Milne, Alys R. Clark
Formato:	article
Lenguaje:	EN
Publicado:	SAGE Publishing 2021
Materias:	Diseases of the circulatory (Cardiovascular) system RC666-701 Diseases of the respiratory system RC705-779
Acceso en línea:	https://doaj.org/article/6779125f93fc4416a1d12fd224f752bb
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spelling	oai:doaj.org-article:6779125f93fc4416a1d12fd224f752bb2021-11-18T23:34:58ZA computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions2045-894010.1177/20458940211056527https://doaj.org/article/6779125f93fc4416a1d12fd224f752bb2021-11-01T00:00:00Zhttps://doi.org/10.1177/20458940211056527https://doaj.org/toc/2045-8940Pulmonary hypertension has multiple etiologies and so can be difficult to diagnose, prognose, and treat. Diagnosis is typically made via invasive hemodynamic measurements in the main pulmonary artery and is based on observed elevation of mean pulmonary artery pressure. This static mean pressure enables diagnosis, but does not easily allow assessment of the severity of pulmonary hypertension, nor the etiology of the disease, which may impact treatment. Assessment of the dynamic properties of pressure and flow data obtained from catheterization potentially allows more meaningful assessment of the strain on the right heart and may help to distinguish between disease phenotypes. However, mechanistic understanding of how the distribution of disease in the lung leading to pulmonary hypertension impacts the dynamics of blood flow in the main pulmonary artery and/or the pulmonary capillaries is lacking. We present a computational model of the pulmonary vasculature, parameterized to characteristic features of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension to help understand how the two conditions differ in terms of pulmonary vascular response to disease. Our model incorporates key features known to contribute to pulmonary vascular function in health and disease, including anatomical structure and multiple contributions from gravity. The model suggests that dynamic measurements obtained from catheterization potentially distinguish between distal and proximal vasculopathy typical of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. However, the model suggests a non-linear relationship between these data and vascular structural changes typical of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension which may impede analysis of these metrics to distinguish between cohorts.Behdad Shaarbaf EbrahimiMerryn H. TawhaiHaribalan KumarKelly S. BurrowesEric A. HoffmanMargaret L. WilsherDavid MilneAlys R. ClarkSAGE PublishingarticleDiseases of the circulatory (Cardiovascular) systemRC666-701Diseases of the respiratory systemRC705-779ENPulmonary Circulation, Vol 11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Diseases of the circulatory (Cardiovascular) system RC666-701 Diseases of the respiratory system RC705-779
spellingShingle	Diseases of the circulatory (Cardiovascular) system RC666-701 Diseases of the respiratory system RC705-779 Behdad Shaarbaf Ebrahimi Merryn H. Tawhai Haribalan Kumar Kelly S. Burrowes Eric A. Hoffman Margaret L. Wilsher David Milne Alys R. Clark A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
description	Pulmonary hypertension has multiple etiologies and so can be difficult to diagnose, prognose, and treat. Diagnosis is typically made via invasive hemodynamic measurements in the main pulmonary artery and is based on observed elevation of mean pulmonary artery pressure. This static mean pressure enables diagnosis, but does not easily allow assessment of the severity of pulmonary hypertension, nor the etiology of the disease, which may impact treatment. Assessment of the dynamic properties of pressure and flow data obtained from catheterization potentially allows more meaningful assessment of the strain on the right heart and may help to distinguish between disease phenotypes. However, mechanistic understanding of how the distribution of disease in the lung leading to pulmonary hypertension impacts the dynamics of blood flow in the main pulmonary artery and/or the pulmonary capillaries is lacking. We present a computational model of the pulmonary vasculature, parameterized to characteristic features of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension to help understand how the two conditions differ in terms of pulmonary vascular response to disease. Our model incorporates key features known to contribute to pulmonary vascular function in health and disease, including anatomical structure and multiple contributions from gravity. The model suggests that dynamic measurements obtained from catheterization potentially distinguish between distal and proximal vasculopathy typical of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. However, the model suggests a non-linear relationship between these data and vascular structural changes typical of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension which may impede analysis of these metrics to distinguish between cohorts.
format	article
author	Behdad Shaarbaf Ebrahimi Merryn H. Tawhai Haribalan Kumar Kelly S. Burrowes Eric A. Hoffman Margaret L. Wilsher David Milne Alys R. Clark
author_facet	Behdad Shaarbaf Ebrahimi Merryn H. Tawhai Haribalan Kumar Kelly S. Burrowes Eric A. Hoffman Margaret L. Wilsher David Milne Alys R. Clark
author_sort	Behdad Shaarbaf Ebrahimi
title	A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
title_short	A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
title_full	A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
title_fullStr	A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
title_full_unstemmed	A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
title_sort	computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions
publisher	SAGE Publishing
publishDate	2021
url	https://doaj.org/article/6779125f93fc4416a1d12fd224f752bb
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A computational model of contributors to pulmonary hypertensive disease: impacts of whole lung and focal disease distributions

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