Einstein Daniel R, Del Pin Facundo, Jiao Xiangmin, Kuprat Andrew P, Carson James P, Kunzelman Karyn S, Cochran Richard P, Guccione Julius M, Ratcliffe Mark B
Biological Monitoring & Modeling, Pacific Northwest National Laboratory, Richland, WA. {
Int J Numer Methods Eng. 2010 Mar;26(3-4):348-380. doi: 10.1002/cnm.1280.
The remodeling that occurs after a posterolateral myocardial infarction can alter mitral valve function by creating conformational abnormalities in the mitral annulus and in the posteromedial papillary muscle, leading to mitral regurgitation (MR). It is generally assumed that this remodeling is caused by a volume load and is mediated by an increase in diastolic wall stress. Thus, mitral regurgitation can be both the cause and effect of an abnormal cardiac stress environment. Computational modeling of ischemic MR and its surgical correction is attractive because it enables an examination of whether a given intervention addresses the correction of regurgitation (fluid-flow) at the cost of abnormal tissue stress. This is significant because the negative effects of an increased wall stress due to the intervention will only be evident over time. However, a meaningful fluid-structure interaction model of the left heart is not trivial; it requires a careful characterization of the in-vivo cardiac geometry, tissue parameterization though inverse analysis, a robust coupled solver that handles collapsing Lagrangian interfaces, automatic grid-generation algorithms that are capable of accurately discretizing the cardiac geometry, innovations in image analysis, competent and efficient constitutive models and an understanding of the spatial organization of tissue microstructure. In this manuscript, we profile our work toward a comprehensive fluid-structure interaction model of the left heart by reviewing our early work, presenting our current work and laying out our future work in four broad categories: data collection, geometry, fluid-structure interaction and validation.
后外侧心肌梗死后发生的重塑可通过在二尖瓣环和后内侧乳头肌中产生构象异常来改变二尖瓣功能,导致二尖瓣反流(MR)。通常认为这种重塑是由容量负荷引起的,并由舒张期壁应力增加介导。因此,二尖瓣反流既可以是异常心脏应力环境的原因,也可以是其结果。缺血性二尖瓣反流及其手术矫正的计算模型很有吸引力,因为它能够检查给定的干预措施是否以异常组织应力为代价来解决反流(流体流动)的矫正问题。这很重要,因为干预导致的壁应力增加的负面影响只会随着时间的推移而显现。然而,建立一个有意义的左心流固耦合模型并非易事;它需要仔细表征体内心脏几何形状,通过逆分析进行组织参数化,一个强大的耦合求解器来处理拉格朗日界面的塌陷,能够精确离散心脏几何形状的自动网格生成算法,图像分析方面的创新,合适且高效的本构模型以及对组织微观结构空间组织的理解。在本手稿中,我们通过回顾我们的早期工作、展示我们的当前工作并在四个广泛类别中阐述我们的未来工作:数据收集、几何形状、流固耦合和验证,来概述我们在建立一个全面的左心流固耦合模型方面所做的工作。