Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension
Vascular wall stiffness and hemodynamic parameters are potential biomechanical markers for detecting pulmonary arterial hypertension (PAH). Previous computational analyses, however, have not considered the interaction between blood flow and wall deformation. Here, we applied an established computati...
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Frontiers Media S.A.
2021-01-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fbioe.2020.611149/full |
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author | Byron A. Zambrano Nathan McLean Xiaodan Zhao Ju-Le Tan Liang Zhong Liang Zhong C. Alberto Figueroa Lik Chuan Lee Seungik Baek |
author_facet | Byron A. Zambrano Nathan McLean Xiaodan Zhao Ju-Le Tan Liang Zhong Liang Zhong C. Alberto Figueroa Lik Chuan Lee Seungik Baek |
author_sort | Byron A. Zambrano |
collection | DOAJ |
description | Vascular wall stiffness and hemodynamic parameters are potential biomechanical markers for detecting pulmonary arterial hypertension (PAH). Previous computational analyses, however, have not considered the interaction between blood flow and wall deformation. Here, we applied an established computational framework that utilizes patient-specific measurements of hemodynamics and wall deformation to analyze the coupled fluid–vessel wall interaction in the proximal pulmonary arteries (PA) of six PAH patients and five control subjects. Specifically, we quantified the linearized stiffness (E), relative area change (RAC), diastolic diameter (D), regurgitant flow, and time-averaged wall shear stress (TAWSS) of the proximal PA, as well as the total arterial resistance (Rt) and compliance (Ct) at the distal pulmonary vasculature. Results found that the average proximal PA was stiffer [median: 297 kPa, interquartile range (IQR): 202 kPa vs. median: 75 kPa, IQR: 5 kPa; P = 0.007] with a larger diameter (median: 32 mm, IQR: 5.25 mm vs. median: 25 mm, IQR: 2 mm; P = 0.015) and a reduced RAC (median: 0.22, IQR: 0.10 vs. median: 0.42, IQR: 0.04; P = 0.004) in PAH compared to our control group. Also, higher total resistance (Rt; median: 6.89 mmHg × min/l, IQR: 2.16 mmHg × min/l vs. median: 3.99 mmHg × min/l, IQR: 1.15 mmHg × min/l; P = 0.002) and lower total compliance (Ct; median: 0.13 ml/mmHg, IQR: 0.15 ml/mmHg vs. median: 0.85 ml/mmHg, IQR: 0.51 ml/mmHg; P = 0.041) were observed in the PAH group. Furthermore, lower TAWSS values were seen at the main PA arteries (MPAs) of PAH patients (median: 0.81 Pa, IQR: 0.47 Pa vs. median: 1.56 Pa, IQR: 0.89 Pa; P = 0.026) compared to controls. Correlation analysis within the PAH group found that E was directly correlated to the PA regurgitant flow (r = 0.84, P = 0.018) and inversely related to TAWSS (r = −0.72, P = 0.051). Results suggest that the estimated elastic modulus E may be closely related to PAH hemodynamic changes in pulmonary arteries. |
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spelling | doaj.art-e4a82b1e8f9b4e6b8b4c6d20c7a97a4e2022-12-21T19:52:50ZengFrontiers Media S.A.Frontiers in Bioengineering and Biotechnology2296-41852021-01-01810.3389/fbioe.2020.611149611149Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial HypertensionByron A. Zambrano0Nathan McLean1Xiaodan Zhao2Ju-Le Tan3Liang Zhong4Liang Zhong5C. Alberto Figueroa6Lik Chuan Lee7Seungik Baek8J. Mike Walker '66 Department of Mechanical Engineering, Texas A&M University, College Station, TX, United StatesDepartment of Mechanical Engineering, Michigan State University, East Lansing, MI, United StatesNational Heart Centre Singapore, Singapore, SingaporeNational Heart Centre Singapore, Singapore, SingaporeNational Heart Centre Singapore, Singapore, SingaporeDuke-National University of Singapore, Singapore, SingaporeDepartments of Biomedical Engineering and Surgery, University of Michigan, Ann Arbor, MI, United StatesDepartment of Mechanical Engineering, Michigan State University, East Lansing, MI, United StatesDepartment of Mechanical Engineering, Michigan State University, East Lansing, MI, United StatesVascular wall stiffness and hemodynamic parameters are potential biomechanical markers for detecting pulmonary arterial hypertension (PAH). Previous computational analyses, however, have not considered the interaction between blood flow and wall deformation. Here, we applied an established computational framework that utilizes patient-specific measurements of hemodynamics and wall deformation to analyze the coupled fluid–vessel wall interaction in the proximal pulmonary arteries (PA) of six PAH patients and five control subjects. Specifically, we quantified the linearized stiffness (E), relative area change (RAC), diastolic diameter (D), regurgitant flow, and time-averaged wall shear stress (TAWSS) of the proximal PA, as well as the total arterial resistance (Rt) and compliance (Ct) at the distal pulmonary vasculature. Results found that the average proximal PA was stiffer [median: 297 kPa, interquartile range (IQR): 202 kPa vs. median: 75 kPa, IQR: 5 kPa; P = 0.007] with a larger diameter (median: 32 mm, IQR: 5.25 mm vs. median: 25 mm, IQR: 2 mm; P = 0.015) and a reduced RAC (median: 0.22, IQR: 0.10 vs. median: 0.42, IQR: 0.04; P = 0.004) in PAH compared to our control group. Also, higher total resistance (Rt; median: 6.89 mmHg × min/l, IQR: 2.16 mmHg × min/l vs. median: 3.99 mmHg × min/l, IQR: 1.15 mmHg × min/l; P = 0.002) and lower total compliance (Ct; median: 0.13 ml/mmHg, IQR: 0.15 ml/mmHg vs. median: 0.85 ml/mmHg, IQR: 0.51 ml/mmHg; P = 0.041) were observed in the PAH group. Furthermore, lower TAWSS values were seen at the main PA arteries (MPAs) of PAH patients (median: 0.81 Pa, IQR: 0.47 Pa vs. median: 1.56 Pa, IQR: 0.89 Pa; P = 0.026) compared to controls. Correlation analysis within the PAH group found that E was directly correlated to the PA regurgitant flow (r = 0.84, P = 0.018) and inversely related to TAWSS (r = −0.72, P = 0.051). Results suggest that the estimated elastic modulus E may be closely related to PAH hemodynamic changes in pulmonary arteries.https://www.frontiersin.org/articles/10.3389/fbioe.2020.611149/fullpulmonary arterial hypertensionfluid structure interactionhemodynamicspulmonary stiffnessbiomechanics metrics |
spellingShingle | Byron A. Zambrano Nathan McLean Xiaodan Zhao Ju-Le Tan Liang Zhong Liang Zhong C. Alberto Figueroa Lik Chuan Lee Seungik Baek Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension Frontiers in Bioengineering and Biotechnology pulmonary arterial hypertension fluid structure interaction hemodynamics pulmonary stiffness biomechanics metrics |
title | Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension |
title_full | Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension |
title_fullStr | Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension |
title_full_unstemmed | Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension |
title_short | Patient-Specific Computational Analysis of Hemodynamics and Wall Mechanics and Their Interactions in Pulmonary Arterial Hypertension |
title_sort | patient specific computational analysis of hemodynamics and wall mechanics and their interactions in pulmonary arterial hypertension |
topic | pulmonary arterial hypertension fluid structure interaction hemodynamics pulmonary stiffness biomechanics metrics |
url | https://www.frontiersin.org/articles/10.3389/fbioe.2020.611149/full |
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