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

IF 3 3区 医学 Q2 BIOPHYSICS
Callyn J. Kozitza, Mitchel J. Colebank, Juan Pablo Gonzalez-Pereira, Naomi C. Chesler, Luke Lamers, Alejandro Roldán-Alzate, Colleen M. Witzenburg
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Abstract

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.

Abstract Image

通过肺动脉狭窄的动物特异性计算模型估算肺动脉重塑。
肺动脉狭窄(PAS)常出现在患有先天性心脏病的儿童身上,会在生长发育的关键时期改变血流和血压。肺动脉狭窄的发病时间、持续时间和严重程度各不相同,因此肺血管的生长和重塑也各不相同。通过计算流体动力学(CFD)模型可以研究与 PAS 相关的血流动力学影响和力学改变。在这项研究中,我们使用一维流体动力学模型模拟了个体动物肺动脉的血流动力学。大肺动脉的几何形状由动物特定的成像确定,而远端血管则由每个末端血管出口的三元素 Windkessel 模型模拟。肺血管的重塑无法在体内测量,只能通过模型拟合参数进行估算。左肺动脉(LPA)狭窄组血管左侧的大动脉僵硬度明显较高,但两侧均与假体组不同。假体组远端血管总阻力分布均衡,而左肺动脉(LPA)狭窄组左侧血管阻力普遍较大,组间无明显差异。相反,LPA 狭窄组右侧外周顺应性明显大于假体组的相应一侧。进一步分析表明,鉴于组织学观察到的厚度增加,灌注不足的远端血管半径可能适度减小,而刚度变化不大。最终,我们的模型使人们能够更好地了解 LPA 狭窄引起的肺动脉适应性,并有可能用作一种工具,以无创方式估计肺血管的重塑情况。
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来源期刊
Biomechanics and Modeling in Mechanobiology
Biomechanics and Modeling in Mechanobiology 工程技术-工程:生物医学
CiteScore
7.10
自引率
8.60%
发文量
119
审稿时长
6 months
期刊介绍: Mechanics regulates biological processes at the molecular, cellular, tissue, organ, and organism levels. A goal of this journal is to promote basic and applied research that integrates the expanding knowledge-bases in the allied fields of biomechanics and mechanobiology. Approaches may be experimental, theoretical, or computational; they may address phenomena at the nano, micro, or macrolevels. Of particular interest are investigations that (1) quantify the mechanical environment in which cells and matrix function in health, disease, or injury, (2) identify and quantify mechanosensitive responses and their mechanisms, (3) detail inter-relations between mechanics and biological processes such as growth, remodeling, adaptation, and repair, and (4) report discoveries that advance therapeutic and diagnostic procedures. Especially encouraged are analytical and computational models based on solid mechanics, fluid mechanics, or thermomechanics, and their interactions; also encouraged are reports of new experimental methods that expand measurement capabilities and new mathematical methods that facilitate analysis.
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