Detection of Atrial Remodeling by MRI: Validation and Emerging Significance

描述（由申请人提供）：在二尖瓣反流或充血性心力衰竭等心室功能障碍患者中，由压力和容量过载引起的心房拉伸有助于心房纤维化的发展。心房结构重塑-包括纤维化-是心房颤动（AF）发生和发展的主要组成部分。减少拉伸介导的心房重构的预防性治疗是存在的，并且会使患者受益，但患者的适当选择尚不清楚，因为心房结构重构难以在临床上评估。这项工作介绍了一种新的方法，它依赖于心血管磁共振（CMR）的几个创新思想。我们建议使用可接受的脂肪抑制和修复脉冲的顺序采集顺序来增加晚期钆增强（LGE）的稳健性和可靠性，旨在减少存在心律失常或RR变异性的1RR LGE采集中的伪影。此外，我们建议量化心房胶原蛋白分数，通过适当地调整T1测绘方法来适应这种高分辨率应用，并进行暗血制备。基于T1映射的细胞外体积分数（ECV）将是对胶原存在的更精确的测量。炎症将使用液体和脂肪抑制的t2制图方法进行调查。我们还将评估三维心房劳损。由于心房壁薄，这种心房应变测量将是非常具有挑战性的传统标记方法。然而，我们将开发3D电影心房成像，可以根据我们合作者的专业知识，通过形状跟踪来估计心房应变。然后，我们将在二尖瓣反流动物模型和二尖瓣疾病患者中研究这些方法。我们将在动物和心脏移植受者的移植心脏中验证我们的活体LGE和ECV测量值与组织学的对比。二尖瓣反流是房颤和心房纤维化发展的主要危险因素。我们将检验主要的假设，即异常的心房拉伸（低或高）-通过应变测量-产生炎症，并在稍后的时间点，心房纤维化。该项目为广泛的患者带来了健康益处，可能允许抗纤维化药物的早期治疗或对有心房纤维化相关房颤风险的适当患者进行干预。

DESCRIPTION (provided by applicant): Atrial stretch, caused by pressure and volume overload, contributes to development of atrial fibrosis, in patients with ventricular dysfunction such as mitral regurgitation or congestive heart failure. Atrial structural remodeling-including fibrosis- is a major component in development and progression of atrial fibrillation (AF). Prophylactic treatments which reduce stretch-mediated atrial remodeling exist, and would benefit patients, but the appropriate selection of patients is unclear, because atrial structural remodeling is difficult to assess clinically. This work introduces a new approach, which relies on several innovative ideas in cardiovascular magnetic resonance (CMR). We propose to increase the robustness and reliability of late gadolinium enhancement (LGE) using a sequential acquisition order, with acceptable fat-suppression, and a REPAIR pulse, designed to reduce artifacts in 1RR LGE acquisitions, in the presence of arrhythmias or RR variability. Further, we propose to quantify atrial collagen fraction, by suitably adapting T1 mapping methods to this high resolution application, with dark blood preparation. Extracellular volume fraction (ECV), based on T1 mapping, will be a more precise measure of the presence of collagen. Inflammation will be investigated using a fluid and fat-suppressed T2-mapping method. We will also evaluate 3D atrial strain. This atrial strain measurement would be extraordinarily challenging with conventional tagging methods, because of the thin walls of the atrium. However, we will develop 3D cine atrial imaging which can be processed, based on the expertise of our collaborators, with shape tracking to estimate atrial strain. We will then study these methods in an animal model of mitral regurgitation, and in patients with mitral disease. We will validate our in-vivo LGE and ECV measurements vs. histology in animals, and in the explanted hearts of heart-transplant recipients. Mitral regurgitation is a major risk factor for boh AF and atrial fibrosis development. We will test the major hypothesis that abnormal atrial stretch (low or high) -measured via strain measurements-generates inflammation and, at later time-points, atrial fibrosis. The project carries a health benefit to a broad spectrum of patients, by potentially permitting early treatment with anti-fibrotic medications or interventions in appropriae patients at risk for atrial-fibrosis related AF.