SURGERY FOR ACUTE MYOCARDIAL INFARCTION

该提案旨在开发新的外科手术程序， 了解左心室（LV）力学、材料变化 急性心肌梗死（AMI）的性质和几何形状 不同的特定心室位置 该项目测试了一个中央 假设：手术干预可以有利地改变心室 心肌梗死后重塑或重塑的影响。 该项目的重点是 缺血性二尖瓣返流（MR）、左心室前尖部动脉瘤和大 前尖部AMI 拟议的工作将利用我们成熟的绵羊模型， 心尖部心肌梗死占LV质量的22%和30%; 22% 产生缺血性MR的梗死，涉及前部或 后乳头肌; 30%梗死后急性重度MR;和 不产生动脉瘤或MR的后壁梗死。 使用四种技术成像;声测微阵列定位（SAL）， 定量超声心动图、连续心室造影和电影磁共振 共振成像 梗死区、边缘区和 远端心肌将使用我们的双轴应力-伸展进行评估 设备. 二尖瓣亚单位相互关系的变化（即，环， 乳头肌，邻近心室壁） 闭塞产生缺血性MR;瓣膜本身的组件不会 改变（例如，小叶、腱索）。 我们将使用SAL来跟踪这些变化 并设计修复手术来逆转这些变化并恢复二尖瓣 瓣膜功能 我们将使用多种成像技术，双轴应力-伸展研究， 和不同的梗死模型，以描述重塑过程后， 特定大小和位置的LV梗死。 我们的目标是量化 区域应变，计算区域应力，并观察这些 在重塑过程中重新分布。 我们将评估左心室力学并将其与血流动力学相关联 折叠或修补前尖部LV动脉瘤后的测量值。 我们 将评估一个惰性的，感觉补丁和一个补丁的可行， 未受刺激的骨骼肌 我们将尝试修改前尖左心室的材料特性 减少心室变形和改善心室 通过改变梗塞的材料性质来改善性能， 再灌注，血管紧张素转换酶抑制剂，并通过直接 注射硬化材料。 心脏是一个泵。 这些研究旨在开发外科手术 干预以改善术后早期和长期心室性能 AMI。

This proposal seeks to develop new surgical procedures based upon knowledge of changes in left ventricular (LV) mechanics, material properties and geometric shape for acute myocardial infarctions (AMI) of different, specific ventricular locations. The project tests a central hypothesis: that surgical interventions can favorably alter ventricular remodeling or the effects of remodeling after AMI. The project focuses on ischemic mitral regurgitation (MR), antero-apical LV aneurysm and large antero-apical AMI. The proposed work will utilize our well-developed sheep models of antero- apical myocardial infarctions of 22 and 30% of the LV mass; 22% infarctions that produce ischemic MR involving either the anterior or posterior papillary muscle; acute, severe MR after 30% infarctions; and posterior infarctions that do not produce aneurysm or MR. The LV will be imaged using four techniques; sonomicrometry array localization (SAL), quantitative echocardiography, serial ventriculography and cine magnetic resonance imaging. Material properties of infarcted, border zone and remote myocardium will be assessed using our biaxial stress-extension apparatus. Changes in the interrelationships of mitral valve subunits (i.e., annulus, papillary muscle, adjacent ventricular wall) after coronary artery occlusion produces ischemic MR; the components of the valve itself do not change (e.g., leaflets, chordae). We will use SAL to track these changes and devise reparative operations to reverse the changes and restore mitral valvular competence. We will use multiple imaging techniques, biaxial stress-extension studies, and different infarction models to describe the remodeling process after LV infarctions of specific size and location. Our goal is to quantitate regional strains, calculate regional stresses, and to observe how these are redistributed during remodeling. We will assess LV mechanics and correlate these with hemodynamic measurements after plication or patching antero-apical LV aneurysms. We will evaluate both an inert, felt patch and a patch of viable, nonstimulated skeletal muscle. We will attempt to modify the material properties of antero-apical LV infarcts to reduce ventricular deformation and to improve ventricular performance by modifying the material properties of the infarct by reperfusion, an angiotensin converting enzyme inhibitor, and by direct injection of a stiffening material. The heart is a pump. These studies are designed to develop surgical interventions to improve early and long-term ventricular performance after AMI.