Tsuji Yukiomi
Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.
J Electrocardiol. 2011 Nov-Dec;44(6):725-9. doi: 10.1016/j.jelectrocard.2011.07.022.
Electrical storm (ES), characterized by recurrent ventricular tachycardia/fibrillation, is a serious condition, adversely affecting prognosis in patients with implantable cardioverter/defibrillators. Electrical storm patients often die of progressive heart failure, but the underlying molecular basis is poorly understood. We have recently created an animal model of ES that features repetitive implantable cardioverter/defibrillator firing for recurrent ventricular fibrillation and found that ES events cause striking activation of Ca(2+)/calmodulin-dependent protein kinase II and prominent alteration of Ca(2+)-handling protein phosphorylation, possibly explaining mechanical dysfunction and arrhythmia promotion that characterize ES. Here, the pathophysiology and potential therapeutic strategies for ES, based on experimental and clinical studies by us and others, are described.
电风暴（ES）以反复发作的室性心动过速/心室颤动为特征，是一种严重病症，会对植入式心脏复律除颤器患者的预后产生不利影响。电风暴患者常死于进行性心力衰竭，但其潜在的分子基础尚不清楚。我们最近创建了一种电风暴动物模型，其特征是植入式心脏复律除颤器因反复发作的心室颤动而反复放电，并且发现电风暴事件会导致钙/钙调蛋白依赖性蛋白激酶II显著激活以及钙处理蛋白磷酸化发生显著改变，这可能解释了电风暴所特有的机械功能障碍和心律失常加重现象。在此，我们将基于我们自己以及其他人的实验和临床研究，描述电风暴的病理生理学及潜在治疗策略。
