REGIONAL MECHANICS OF LEFT VENTRICULAR ANEURYSM

左室功能不全是左室功能不全的特征， 室壁瘤（LVA）与肌肉拉伸有关 纤维在相邻的非梗死（边界区）的区域， 等容收缩 这种区域功能障碍的机制是 了解不多，但它可能涉及减少心肌 边界区心肌收缩力和心肌应力增加 在等容收缩期。 这项研究调查了 心肌材料特性和应力在局部心肌缺血中的作用 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 理论模型来开发动脉瘤修复的新手术。 所提出的研究的实验模型是前根尖 绵羊动脉瘤模型（透壁梗死后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图像集进行测量 体内心脏的心室壁;有和没有LVA。 下一个是 梗死区、边缘区和远端的材料特性 LVA的离体停搏心脏的非梗死区，以及 在孤立的正常心脏中， 使用我们新颖的机械测试方法进行确定 （“心外膜抽吸”），使心室壁保持完整， 引入了一种复杂的（弯曲和剪切）变形模式， 感兴趣的区域。 然后，这些被动材料特性将被 用于现有的最先进的有限元模型， 跳动心室的力学来计算三维 整个心室壁的心肌应力和变形 体内心脏;有和无LVA。 体内的测量 心肌变形将用于验证收缩期材料 模型的属性。 最后，第一个现实的模型， 传统动脉瘤修复术和最先进的动脉瘤修复术 这种修复将通过修改几何形状和边界来开发 打浆力学有限元模型的条件 左心室肥厚 这些模型将用于预测 这些修复对三维心肌应力和应变 分布。 本研究将：1）确定潜在的机制 与LVA相关的局部机械功能障碍;以及2） 提供客观评估修改的方法 传统的动脉瘤修复术，并开发新的手术， 基于心肌成形术的改进或基于“心脏补片” 由心肌组织培养物产生。

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.