Wisneski Andrew D, Matthews Peter B, Azadani Ali N, Mookhoek Aart, Chitsaz Sam, Guccione Julius M, Ge Liang, Tseng Elaine E
J Heart Valve Dis. 2014 May;23(3):377-84.
Remodeling of the pulmonary autograft upon exposure to systemic pressure can lead to progressive dilatation and aneurysmal pathology. Remodeling is driven by changes in autograft wall stress upon exposure to systemic pressure; however, the magnitude of these changes is unknown. Previously, a porcine autograft finite element model was developed to determine wall stress, but the porcine and human material properties differed significantly. Hence, the study aim was to understand human pulmonary autograft biomechanics that lead to remodeling by determining wall stress magnitudes immediately after the Ross procedure using finite element analysis (FEA).
Human pulmonary root was scanned by high-resolution microcomputed tomography to construct a realistic three-dimensional geometric mesh. Stress-strain data from biaxial stretch testing was incorporated into an Ogden hyperelastic model to describe autograft mechanical properties for an adult Ross patient. Autograft dilatation and wall stress distribution during pulmonic and systemic pressures prior to remodeling were determined using explicit FEA in LS-DYNA.
Human pulmonary autograft demonstrated non-linear material properties, being highly compliant in the low-strain region, and stiffening at high strain. The majority of dilatation occurred with < 20 mmHg pressurization. From pulmonary to systemic pressures, the increases in autograft diameter were up to 17%. Likewise, the maximal wall stress increased approximately 14.6-fold compared to diastolic pressures (from 13.0 to 190.1kPa), and six-fold compared to systolic pressures (from 48.6 to 289.6kPa).
The first finite element model of the human pulmonary autograft was developed and used to demonstrate how autograft material properties prevent significant dilatation upon initial exposure to systemic pressure. Mild dilatation was noted in the sinuses and sinotubular junction. Autograft wall stress was increased greatly when subjected to systemic pressures, and may trigger biomechanical remodeling of the autograft. Sustained exposure to higher wall stresses, coupled with inadequate remodeling, may lead to future autograft dilatation.
肺自体移植物在承受体循环压力时发生重塑，可导致渐进性扩张和动脉瘤样病变。重塑是由自体移植物壁在承受体循环压力时的应力变化驱动的；然而，这些变化的程度尚不清楚。此前，已建立了一个猪自体移植物有限元模型来确定壁应力，但猪和人的材料特性有显著差异。因此，本研究的目的是通过有限元分析（FEA）确定Ross手术后即刻的壁应力大小，以了解导致重塑的人肺自体移植物生物力学特性。
通过高分辨率微型计算机断层扫描对人肺根部进行扫描，构建逼真的三维几何网格。将双轴拉伸试验的应力-应变数据纳入Ogden超弹性模型，以描述成年Ross手术患者的自体移植物力学特性。在LS-DYNA中使用显式有限元分析确定重塑前肺动脉压和体循环压力期间自体移植物的扩张和壁应力分布。
人肺自体移植物表现出非线性材料特性，在低应变区域高度柔顺，在高应变时变硬。大部分扩张发生在压力增加<20 mmHg时。从肺动脉压到体循环压力，自体移植物直径增加高达17%。同样，最大壁应力与舒张压相比增加了约14.6倍（从13.0 kPa增加到190.1 kPa），与收缩压相比增加了6倍（从48.6 kPa增加到289.6 kPa）。
建立了首个用于人肺自体移植物的有限元模型，并用于证明自体移植物材料特性如何在初次暴露于体循环压力时防止显著扩张。在窦部和窦管交界处观察到轻度扩张。自体移植物在承受体循环压力时壁应力大幅增加，可能触发自体移植物的生物力学重塑。持续暴露于较高的壁应力，再加上重塑不足，可能导致未来自体移植物扩张。
