应激性心肌病是交感神经系统激活所致，易于出现室性心律失常，而T波电交替是其重要预测因子。新近研究指出，该类患者出现T波电交替的原因可能是晚钠电流的增强，但其分子机制尚未有深入研究。我们的前期研究发现，对于应激性心肌病发生的T波电交替，给予晚钠电流抑制剂治疗后，T波电交替引起的恶性室性心律失常消失。因此，我们假设晚钠电流增强是应激性心肌病发生T波电交替的重要机制。本课题用基因检测、基因转染、膜片钳及楔形组织块技术，重点对SCN5A基因进行检测，找到突变基因，并转染突变基因，评估通道功能，另一方面，诱发应激性心肌病T波电交替动物模型，用楔形组织块技术对晚钠电流的作用进行评估。通过上述方法，可以发现SCN5A基因突变是否参与了应激性心肌病患者恶性心律失常的发生，并验证晚钠电流抑制剂是应激性心肌病患者合并T波电交替的重要治疗药物，这为揭示应激性心肌病T波电交替的分子机制奠定了重要的实验基础。

Stress Cardiomyopathy is caused by activation of the sympathetic nervous system.Ventricualr arrythmias are easy to be found in this kind of disease,and T wave alternation is an important predictor for the arrythmias.The latest research found that T wave alternation in this kind of patients was caused by enhanced late sodium current potently.Recently,in our work, we gave late sodium current inhibitor for treatment of this kind of patients with T wave alternation induced malignant ventricular arrhythmia，and then,the arrhythmia was disappeared. Therefore, we hypothesise that late sodium current mediates T wave alternation in Stress Cardiomyopathy. Our study will use gene detection, gene transfection, patch clamp technique and wedge-shape technique, focusing on the SCN5A gene to find the mutation genes, and then transfect the mutantion genes, evaluate the channeles function ; On the other hand, make the Stress Cardiomyopathy T wave alternation animal model, evaluating late sodium current with wedge-shape technique. Through the above methods, we can know whether SCN5A mutations take part in malignant arrythmia in Stress Cardiomyopathy or not,and we can also verify that using late sodium current inhabitor for the Stress Cardiomyopathy with T wave alternation is an important treatment.The above work can reveal the molecular mechanism of T wave alternation in the Stress Cardiomyopathy and provide new ideas for the basis lab work.