Detection of Atrial Remodeling by MRI: Validation and Emerging Significance

描述（由申请人提供）：压力和容量超负荷引起的心房牵张有助于心室功能障碍（如二尖瓣返流或充血性心力衰竭）患者发生心房纤维化。心房结构重构（包括纤维化）是心房颤动（AF）发生和发展的主要组成部分。存在减少牵张介导的心房重构的预防性治疗，并将使患者受益，但患者的适当选择尚不清楚，因为心房结构重构难以临床评估。这项工作介绍了一种新的方法，它依赖于心血管磁共振（CMR）的几个创新的想法。我们建议在心律失常或RR变异性存在的情况下，使用顺序采集顺序（具有可接受的脂肪抑制）和REPAIR脉冲（旨在减少1RR LGE采集中的伪影）来增加晚期钆增强（LGE）的稳健性和可靠性。此外，我们建议量化心房胶原分数，通过适当调整T1映射方法，以这种高分辨率的应用，与黑暗的血液准备。基于T1标测的细胞外体积分数（ECV）将是胶原蛋白存在的更精确测量。将使用液体和脂肪抑制的T2标测方法研究炎症。我们还将评价3D心房应变。由于心房的薄壁，这种心房应变测量对于传统的标记方法将是非常具有挑战性的。然而，我们将开发3D电影心房成像，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，我们将在二尖瓣返流的动物模型和二尖瓣疾病患者中研究这些方法。我们将验证我们的体内LGE和ECV测量与动物组织学，并在心脏移植受体的心脏移植。二尖瓣返流是bohAF和心房纤维化发展的主要危险因素。我们将检验一个主要假设，即通过应变测量测量的异常心房牵张（低或高）会产生炎症，并在随后的时间点产生心房纤维化。该项目通过可能允许在有心房纤维化相关AF风险的适当患者中使用抗纤维化药物或干预措施进行早期治疗，为广泛的患者带来健康益处。

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.