Fontan手术是治疗复杂紫绀型先天性心脏病重要手术之一。术后房性心动过速（房速）作为其主要并发症之一，严重影响预后，与术后死亡率密切相关。目前，Fontan术后房速发生的确切机制尚不明确。研究发现：触发机制引起的局灶性房速起了重要作用。而触发机制主要由钙调控异常引起。据此，我们推测钙调控异常在Fontan术后房速发生中起了重要作用，且目前尚无Fontan术后房速与钙调控异常相关的研究报道。我们前期已成功建立犬的Fontan模型，并通过钙释放实验检测发现在Fanton模型中心房肌细胞钙离子释放异常，且存在自发电活动。由此，本项目拟在现有研究基础上进一步探讨钙离子在Fanton术后房速发生中的作用，及术后容量和压力负荷改变导致的心房肌重塑对钙离子调控异常的具体机制。此研究的成功将为减少Fontan术后房速的发生和预防复发提供新的处理策略。

The Fontan operation is a well-established surgical technique used for palliation of complex cyanotic congenital heart disease such as tricuspid atresia, double-inlet ventricle, or single ventricle defect. Atrial tachyarrhythmia (AT) is one of the most common complications in Fontan patients . Previous studies have recognized that AT contributes to ongoing morbidity and mortality in patients with a Fontan circulation. However, the exact mechanisms of postoperative AT in Fontan patients are not well defined. There is evidence that focal drivers and triggered activity play a role in Fontan operation-related AT. At the cellular level, triggered activity can be caused by abnormal calcium handling. However, there are no published descriptions of atrial calcium handling in Fontan patients or relevant animal models. The Fontan canine model was successfully established by our team, and the spontaneous sarcoplasmic reticulum Ca2+ release events and triggered activities were observed. This project is proposed to explore the role of calcium handling in post-Fanton AT. The success of this study will provide a theoretical basis for establishing new therapeutic strategies and new drug targets.