Estimating pulmonary arterial remodeling via an animal-specific computational model of pulmonary artery stenosis.

Autor: Kozitza CJ; Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI, USA., Colebank MJ; Edwards Lifesciences Foundation Cardiovascular Innovation and Research Center, and Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA., Gonzalez-Pereira JP; Pediatrics, Division of Cardiology, University of Wisconsin-Madison, Madison, WI, USA., Chesler NC; Edwards Lifesciences Foundation Cardiovascular Innovation and Research Center, and Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA., Lamers L; Pediatrics, Division of Cardiology, University of Wisconsin-Madison, Madison, WI, USA., Roldán-Alzate A; Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI, USA.; Department of Mechanical Engineering, University of Wisconsin-Madison, Madison, WI, USA.; Department of Radiology, University of Wisconsin-Madison, Madison, WI, USA., Witzenburg CM; Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI, USA. witzenburg@wisc.edu.
Jazyk: angličtina
Zdroj: Biomechanics and modeling in mechanobiology [Biomech Model Mechanobiol] 2024 Oct; Vol. 23 (5), pp. 1469-1490. Date of Electronic Publication: 2024 Jun 25.
DOI: 10.1007/s10237-024-01850-6
Abstrakt: Pulmonary artery stenosis (PAS) often presents in children with congenital heart disease, altering blood flow and pressure during critical periods of growth and development. Variability in stenosis onset, duration, and severity result in variable growth and remodeling of the pulmonary vasculature. Computational fluid dynamics (CFD) models enable investigation into the hemodynamic impact and altered mechanics associated with PAS. In this study, a one-dimensional (1D) fluid dynamics model was used to simulate hemodynamics throughout the pulmonary arteries of individual animals. The geometry of the large pulmonary arteries was prescribed by animal-specific imaging, whereas the distal vasculature was simulated by a three-element Windkessel model at each terminal vessel outlet. Remodeling of the pulmonary vasculature, which cannot be measured in vivo, was estimated via model-fitted parameters. The large artery stiffness was significantly higher on the left side of the vasculature in the left pulmonary artery (LPA) stenosis group, but neither side differed from the sham group. The sham group exhibited a balanced distribution of total distal vascular resistance, whereas the left side was generally larger in the LPA stenosis group, with no significant differences between groups. In contrast, the peripheral compliance on the right side of the LPA stenosis group was significantly greater than the corresponding side of the sham group. Further analysis indicated the underperfused distal vasculature likely moderately decreased in radius with little change in stiffness given the increase in thickness observed with histology. Ultimately, our model enables greater understanding of pulmonary arterial adaptation due to LPA stenosis and has potential for use as a tool to noninvasively estimate remodeling of the pulmonary vasculature.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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