Imaging Core

开发成像核心是为了支持心力衰竭运动不耐症的机制 保留射血分数：基于患者特异性病理生理学计划的“精确”治疗 通过监督所有MR成像协议的采集和分析，获得项目资助（PPG）。这将是一个共享的 作为整个计划的资源，他将在制定一个高效、高绩效的计划中发挥重要作用。 为了实现这一目标，我们组建了一个多学科团队，以满足每个项目的成像需求： （项目1），骨骼肌（项目2），自主神经生理学（项目3）和肺（项目4）。基于 根据整个计划项目的需要，成像核心有三个具体目标：目标1。执行 全面的心脏磁共振成像，以确定病理生理机制， 射血分数保留性心力衰竭（HFpEF）患者的中枢运动限制。（项目1）。到 为了实现目标1，患者和对照组将接受深入全面的心脏MRI， 心脏应力和对比增强，以评估心脏形态、功能、灌注和 纤维化目标2.在休息时、运动期间对骨骼肌进行全面的、非侵入性的代谢评估， 动态运动和运动后循环停止期间（项目2和3）。为了实现目标2，患者和 对照组将在我们最先进的7 T临床研究扫描仪中进行动态下肢运动，以评估 乳酸，肉毒碱和乙酰肉毒碱动力学的1H-磁共振波谱（MRS），和ATP- 通过31 P-MRS测定磷酸肌酸（PCr）交换动力学。进行定量肺水成像，以确定 导致HFpEF劳力性呼吸困难的病理生理机制（项目4）。标志之一 HFpEF的特征是在运动期间心脏充盈压的快速和显著升高。这种现象 增加毛细血管静水压力，并可导致肺动脉和肺泡内液体积聚; 扩大气体交换屏障。因此，区域性肺积水可能是一种主要机制 用力时呼吸困难。我们将结合项目4，通过测量肺水来验证这一假设， 动态锻炼后。这些新颖和创新的数据将共同为我们的 对HFpEF运动不耐受的机械理解。

The Imaging Core was developed in order to support the Mechanisms of Exercise Intolerance in Heart Failure with Preserved Ejection Fraction: `Precision' Therapy Based on Patient Specific Pathophysiology Program Project Grant (PPG) by overseeing the acquisition and analysis of all MR imaging protocols. This will be a shared resource of the entire Program and will play an essential role in developing an efficient, high performing Program. To accomplish this, we have assembled a multidisciplinary team to serve the imaging needs of each project: cardiac (Project 1), skeletal muscle (Project 2), autonomic neurophysiology (Project 3) and pulmonary (Project 4). Based on the needs of the overall Program Project, the Imaging Core has three specific aims: Aim 1. Perform comprehensive cardiac magnetic resonance imaging to define the pathophysiological mechanisms contributing to central limitations of exercise in Heart Failure with Preserved Ejection Fraction (HFpEF). (Project 1). To accomplish Aim 1, patients and controls will undergo an in-depth comprehensive cardiac MRI complete with cardiac stress and contrast-enhancement, in order to assess cardiac morphology, function, perfusion and fibrosis. Aim 2. Perform comprehensive, non-invasive, metabolic assessment of skeletal muscle at rest, during dynamic exercise, and during post-exercise circulatory arrest (Projects 2 and 3). To accomplish Aim 2, patients and controls will perform dynamic lower limb exercise in our state-of-the-art 7T clinical research scanner in order to assess lactate, carnitine and acetylcarnitine dynamics by 1H-magnetic resonance spectroscopy (MRS), and ATP- phosphocreatine (PCr) exchange kinetics by 31P-MRS. Aim 3. Perform quantitative lung water imaging to define the pathophysiological mechanisms contributing to dyspnea on exertion in HFpEF (Project 4). One of the hallmark features of HFpEF is a rapid and pronounced rise in cardiac filling pressures during exercise. This phenomenon increases the capillary hydrostatic pressure and can lead to an accumulation of fluid in the lung interstitium and alveoli; widening the gas exchange barrier. Regional lung water accumulation may therefore represent a principle mechanism driving dyspnea on exertion. We will integrate with Project 4 to test this hypothesis by measuring lung water before and after dynamic exercise. Together, these novel and innovative data will contribute significantly to our mechanistic understanding of exercise intolerance in HFpEF.