REGIONAL MECHANICS OF LEFT VENTRICULAR ANEURYSM

以左心衰为特征的整体左心功能不全 室壁瘤(LVA)与肌肉拉伸有关 邻近非梗死区(交界区)的纤维 等容收缩。这种区域功能障碍的机制是 知之甚少，但很可能涉及心肌梗死减少 交界区心肌收缩功能和心肌应力增加 在等容收缩时。这项拟议的研究调查了 心肌材料特性和应力在局部心肌损伤中的作用 LVA实验动物模型的机械功能障碍。 这项研究的长期目标是使用实验和 为动脉瘤修复开发新手术的理论模型。 本研究的实验模型为前根尖。 绵羊动脉瘤模型(穿壁性脑梗塞后10周)。第一, 使用磁共振成像组织标记，心肌 变形将在整个过程中以正交集的图像进行测量 活体心脏的室壁；有或没有LVA。下一首, 梗死区、交界区和偏远地区的材料特性 LVA心脏停搏后的非梗死区 在隔离的正常心脏中相应区域的那些，将 使用我们的机械测试新方法来确定 (“心外膜抽吸”)，使室壁完好无损， 中引入了一种复杂的(弯曲和剪切)变形模式 感兴趣的区域。那么，这些被动的材料属性将是 在现有最先进的有限元模型中用于 计算三维跳动脑室的力学问题 心肌在整个室壁的应力和变形 活体心脏；有无LVA。活体测量 将使用心肌变形来验证收缩物质 模型的属性。最后，第一个现实的模型 传统的动脉瘤修补术和最新的动脉瘤修补术 将通过修改几何图形和边界来进行此修复 打浆力学有限元模型的建立条件 脑室有LVA。这些模型将被用来预测影响 对三维心肌应力和应变的修复 分配。这项研究将：1)确定潜在的机制 与LVA相关的局部机械功能障碍；2) 提供客观评估修改的方法 传统的动脉瘤修复和开发新的手术，可能 基于心肌成形术或“心脏补片”的改进 从心肌组织培养中产生。

The global left ventricular dysfunction that is characteristic of left ventricular aneurysm (LVA) is associated with stretching of muscle fibers in the adjacent noninfarcted (border zone) region during isovolumic systole. The mechanism of this regional dysfunction is poorly understood, but it likely involves reduced myocardial contractility and increased myocardial stress in the border zone region during isovolumic systole. This proposed research investigates the role that myocardial material properties and stress play in the regional mechanical dysfunction of an experimental animal model of LVA. The long-term goal of this research is to use experimental and theoretical models to develop new operations for aneurysm repair. The experimental model for the proposed research is the anterioapical sheep aneurysm model (10 weeks after transmural infarction). First, using magnetic resonance imaging tissue tagging, myocardial deformation will be measured in orthogonal sets of images throughout the ventricular walls of in vivo hearts; with and without LVA. Next, the material properties of infarcted, border zone, and remote noninfarcted regions in isolated arrested hearts with LVA, as well as those of corresponding regions in isolated arrested normal hearts, will be determined using our novel approach to mechanical testing ("epicardial suction"), which leaves the ventricular walls intact and introduces a complex (bending and shearing) mode of deformation in the region of interest. Then, these passive material properties will be used in an existing state-of-the-art finite element model for the mechanics of the beating ventricles to compute three-dimensional myocardial stress and deformation throughout the ventricular walls of in vivo hearts; with and without LVA. The measurements of in vivo myocardial deformation will be used to validate the systolic material properties of the model. Finally, the first realistic models of the conventional aneurysm repair and the state-of-the-art modification of this repair will be developed by modifying the geometry and boundary conditions of the finite element model for the mechanics of the beating ventricles with LVA. These models will be used to predict the effects of these repairs on three-dimensional myocardial stress and strain distributions. This study will: 1) determine the mechanism underlying the regional mechanical dysfunction associated with LVA; and 2) provide the means to objectively evaluate modifications of conventional aneurysm repair and to develop new operations, possibly based on modifications of cardiomyoplasty or on "heart patches" produced from myocardial tissue cultures.