心房电重构是房颤发生的电学基础，晚钠电流（INaL）是心肌细胞动作电位平台期主要离子流之一，房颤时INaL增大，研究表明血浆同型半胱氨酸（HCY）水平与房颤发生发展有关。我们前期研究也证实HCY水平与房颤消融术后复发显著相关，高HCY上调大鼠心房肌细胞钠通道NaV1.5表达。据此，我们提出高HCY水平通过激活钠通道蛋白Nav1.5，增加INaL，从而引起心房电重构及促发房颤发生的假说。为证实假说，我们拟HCY作用于人单个心房肌细胞和HL-1细胞株，同时建立高HCY大鼠模型，检测INaL和钙循环、Nav1.5和CaMK-II表达，证实HCY对INaL的作用及机制；高HCY大鼠房颤的可诱发性及心房不应期等，阐明HCY诱发心房颤动的作用。从分子、细胞和动物水平多层面证实HCY是通过增大心房肌细胞INaL影响钙循环诱发房颤。从INaL这个新视点探讨HCY诱发房颤发生机制，为房颤的防治提供新思路。

Atrial electrical remodeling is the electrophysiological basis of atrial fibrillation(AF).Late sodium current(INaL),which makes a contribution to maintaining the action potential(AP) plateauin cardiomyocytes, is pathologically increased in AF. It is reported that homocystine (HCY) plasma level is related to the development and progression of AF. Our preliminary study had shown that high HCY plasma level up expressed the voltage-sodium channel NaV1.5 in atrial myocyte of rat, which indicated that HCY plasma level have significant correlation with the AF recurrence after catheter ablation.Accordingly, we assume that high HCY level induce atrial electrical remodeling that boost AF by activating voltage-sodium channel NaV1.5 protein and increasing INal.To verify the hypothesis, we intend to incubate individual human atrial myocyte and HL-1 cells with HCY and establish high HCY plasma level rat model. We detect the INaL, calciumcycle,the expression of CaMK-II and voltage-sodium channel NaV1.5 protein to certify the role of HCY to INaL and its mechanism in vitro.We investigate the occurrence and the atrial refractory period in high HCY plasma rat to demonstrate the promoting effect of HCY on AF.We confirm HCY influence the calciumcycle by increasing INaL in atrial myocytel, and then induce the development of AF in the molecular, cellular and animal levels respectively.We explore the promoting effect of HCY on AF in the novel vision of INaL, which provides new perspective in the prevention and treatment of AF.