基于4D血流MRI成像的左心房室流场变化介导的炎症反应在房颤心肌纤维化中的始动作用及机制研究

房颤是临床最常见的严重心律失常。房颤患者治疗效果不佳以及治疗后易复发的病理基础是心房纤维化；而心室纤维化则使得房颤患者合并心衰风险大大增加。然而至今为止，房颤心肌纤维化的具体机制尚未被阐明。近年来，多个研究表明，不同类型房颤患者炎症介质水平均有不同程度升高。这些研究结果提示炎症介质可能在房颤心肌纤维化中起着重要作用。有研究已证实异常流体力学改变激活炎症反应所释放的炎症因子可促进转化生长因子（TGF-β1）表达，活化心肌纤维母细胞分泌胶原，并影响金属基质蛋白酶降解胶原。房颤后，左心房室内流体力学会发生巨大变化，但其变化与炎症介质的表达及房颤心肌纤维化形成的关系尚不清楚。因此，本研究创新性地采用先进的4D血流MRI成像研究不同房颤模型左心房室流体力学特征，并且以“左心房室流体力学变化-炎症反应-胶原分泌与降解失衡-心肌纤维化”为主线来探索房颤心肌纤维的形成机制。

Atrial fibrillation (AF) is the most common type of severe arrhythmia in clinical practice. AF patient with atrial fibrosis is associated with reduced effectiveness of therapy and susceptible to recurrence. Ventricular fibrosis increases the risk of combination of AF with heart failure. But so far, the fundamental pathogenesis of cardiac fibrosis in AF has not been clarified. Recently, several studies shows that inflammatory cytokines are overexpressed to varying degrees. These results show that inflammatory cytokine might play an important role in the pathogenesis of cardiac fibrosis in AF. Studies have confirmed that abnormal hemodynamic changes induced inflammation reactions may occur with release of inflammatory cytokines, which could activate myofibroblast by promoting the expression of transforming growth factor-β1 (TGF-β1), and influence the degrading of collagen with matrix metalloproteinase (MMP). The hemodynamic features of left heart in AF would greatly altered. But the relationship between the hemodynamic changes and inflammatory cytokine release and development of cardiac fibrosis of AF is still unclear. In this study, we innovatively use 4D flow MRI to evaluate the hemodynamic features in different AF animal models, and then to further explore the potential pathogenesis of cardiac fibrosis in AF on the hypothesis of pathway of “hemodynamic changes-inflammation-collagen deposition and degrading imbalance-cardiac fibrosis”.