VIRTUAL TOOLS FOR CARDIAC VENTRICULAR REMODELING SURGERY

7.项目摘要/摘要 目前有500万美国人被诊断为心力衰竭(HF)，每年新增55万例。 现在大多数心衰病例是由心肌梗死(MI)引起的左心室(LV)引起的。 改建。由于缺乏一种公认的有效治疗方法，导致了不断扩大的 心衰患者姑息治疗的内科和外科选择。使用我们的心肌材料属性软件 工具(MMPST；在最初的资助期开发和验证)和MI的绵羊模型，我们有 为心脏科医生和心脏外科医生提供了对心肌梗死所致心力衰竭机制的新见解 将他们的注意力集中在紧邻的正常灌流心肌中发生的变化 MI(边界地带)。我们的MMPST表明，边界地带(BZ)心肌的收缩能力是 与远离MI的LV区域相比显著降低。《公约》的总体目标 建议的研究是为了验证我们的MMPST的临床应用，并展示出强大的临床应用 局部心肌收缩能力与疾病状态的相关性。它有五个具体目标：(1)使用 我们的MMPST，在心脏移植前测量患者体内局部心肌收缩能力；(2) 从被研究的心脏获得的去皮纤维制剂中测量体外局部心肌收缩能力 在目标1中，我们将使用这些直接主动力测量来验证我们的MMPST的临床应用； (3)使用弥散磁共振成像(DMRI)，测量目标1中研究的心脏的体外局部肌纤维取向， 以及正常人和有心肌梗塞的人的心脏。如果这些临床上相关的测量是 没有显著差异(正如我们之前在正常和梗塞的绵羊心脏中发现的那样)，然后是临床 我们的MMPST的应用不需要体内dMRI；(4)测量体内局部心肌收缩能力 并比较心肌梗死后左、右室远端心肌的收缩功能。如果这些临床测量 也表现出明显的BZ收缩能力下降，然后程序设计恢复了更正常 LV几何构型在重构过程的后期可能无效(正如我们在修复的绵羊身上也发现的那样 (5)测量正常人的在体局部心肌收缩能力并比较 这些测量结果与Aim#1和Aim#4中的结果一致。如果这些临床测量能够 与疾病状态和治疗干预的潜在效果相关，然后是心脏病界 将能够在其关于病人护理方案的医疗设备中增加一种重要的新方法。

7. Project Summary/Abstract There are currently 5 million Americans with diagnosed heart failure (HF), and 550,000 new cases every year. The majority of HF cases is now the result of myocardial infarction (MI)-induced left ventricular (LV) remodeling. The lack of a well-established effective treatment has lead to a continually expanding list of medical and surgical options for the palliation of HF patients. Using our Myocardial Material Property Software Tool (MMPST; developed and validated during the initial funding period) and an ovine model of MI, we have provided cardiologists and cardiac surgeons with new insights into the mechanism of MI-induced HF by focusing their attention on changes that occur in the normally perfused myocardium immediately adjacent to the MI (the borderzone). Our MMPST demonstrates that borderzone (BZ) myocardial contractility is substantially reduced in comparison to that in LV regions remote from the MI. The overall goals of the proposed research are to validate clinical application of our MMPST and demonstrate a strong clinical correlation between regional myocardial contractility and disease state. There are five specific aims: (1) Using our MMPST, measure in-vivo regional myocardial contractility in patients before heart transplantation; (2) Measure ex-vivo regional myocardial contractility in skinned fiber preparation obtained from the hearts studied in Aim #1. We will use these direct active force measurements to validate clinical application of our MMPST; (3) Using diffusion MRI (dMRI), measure ex-vivo regional myofiber orientation in the hearts studied in Aim #1, as well as in normal human hearts and human hearts with an MI. If these clinically relevant measurements are not significantly different (as we previously discovered in normal versus infarcted sheep hearts), then clinical application of our MMPST does not require in-vivo dMRI; (4) Measure in-vivo regional myocardial contractility in patients after MI and compare BZ contractility with that in remote LV regions. If these clinical measurements also demonstrate significantly depressed BZ contractility, then procedures designed to restore a more normal LV geometry late in the remodeling process may be ineffective (as we also discovered in sheep with repaired LV aneurysm); (5) Measure in-vivo regional myocardial contractility in normal human subjects and compare these measurements with those obtained in Aim #1 and Aim #4. If these clinical measurements can be correlated to disease state and the potential effect of therapeutic intervention, then the cardiology community will be able to add a significant new methodology to its armamentarium regarding patient care protocols.