Understanding the Mechanistic Links Between Mid-Wall Fibrosis and Arrhythmic Risk in Non-Ischemic DCM Using a Combined Modelling & Clinical Approach

非缺血性扩张型心肌病（NIDCM）是一种常见的结构性心脏病。它的特点是扩大心脏的腔室，拉伸和变薄的肌肉壁，造成扩张。在许多情况下，心脏组织本身的结构发生变化，在肌肉壁的中心内形成明显的纤维组织区域。这些与NIDCM相关的结构变化可以用最新的MR成像技术观察和测量。患有NIDCM的患者有非常高的机会经历心律失常和相关的心源性猝死。更具体地说，我们团队的一项高影响力研究显示，在一些NIDCM患者的心脏壁中心内发展的这些纤维区域与心律失常死亡之间存在非常明确的联系。然而，与NIDCM相关的这些结构变化和致命性心律失常之间的明确联系的原因是非常不清楚的。因此，评估患者的这种风险和计划治疗仍然是一个重大挑战。了解临床MR数据中确定的结构变化与NIDCM中心律失常的关键生理过程之间的联系，建议使用基于图像的模型来辅助机械解释。在这项研究中，我们的目标是将联合收割机临床MRI与先进的图像分析和计算建模相结合，以提高我们对心脏结构变化与心律失常之间联系的生理机制的理解。获得这些知识将有助于阐明与NIDCM相关的新的临床风险因素，并帮助临床医生计划治疗干预措施。实现我们的目标将提供更精确，更明智的决策，关于治疗特定患者心脏的最佳方式，以及患者NIDCM造成的个体心律失常风险和植入式除颤器的需求，提高NIDCM生存率并降低不必要手术的医疗服务成本。

Non-ischemic dilated cardiomyopathy (NIDCM) is a common form of structural heart disease. It is characterised by enlargement of the heart's chambers, stretching and thinning the muscle walls, causing dilation. In many cases, the structure of the heart tissue itself changes with noticeable regions of fibrous tissue developing within the centre of the muscle wall. These structural changes associated with NIDCM can be seen and measured with the latest MR imaging techniques. Patients suffering from NIDCM have a very high chance of experiencing cardiac arrhythmias and associated sudden cardiac death. More specifically, a high-impact study from our Team showed a very clear link between these fibrous regions that develop within the centre of the heart wall in some NIDCM patients and death from arrhythmias. However, the reasons underlying this clear link between these structural changes associated with NIDCM and lethal arrhythmias is extremely poorly understood. Consequently, assessing this risk in patients and planning treatments remains a significant challenge. Understanding the link between structural changes identified in clinical MR data with the key physiological processes responsible for arrhythmias in NIDCM suggests the use of an image-based model to aid mechanistic interpretation. In this study, we aim to combine clinical MRI with advanced image analysis and computational modelling to improve our physiological understanding of the mechanisms underlying the link between changes in heart structure with cardiac arrhythmias. Gaining such knowledge will help to elucidate novel clinical risk-factors associated with NIDCM and help clinicians plan therapeutic interventions. Achieving our goals will provide more precise, informed decisions regarding the optimal way to treat an particular patient's heart, as well as the individual arrhythmia risk posed by a patient's NIDCM and the need for an implantable defibrillator, improving NIDCM survival rates and reducing health-service costs on unnecessary operations.