Nagase Satoshi, Kusano Kengo Fukushima, Yoshida Masashi, Ohe Tohru
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Heart Rhythm. 2007 Apr;4(4):512-5. doi: 10.1016/j.hrthm.2006.10.030. Epub 2006 Nov 10.
We report the first case of a patient with Andersen syndrome in whom electrophysiologic study was performed. The patient was a 19-year-old woman with familial periodic paralysis, abnormal QT-U complex, and nonsustained ventricular tachycardia. Mutation analysis revealed a missense mutation in KCNJ2, a component of Kir2.1. Monophasic action potential recordings showed a delayed afterdepolarization (DAD)-like hump in the left ventricle. Initiation of epinephrine-induced premature ventricular contractions always coincided with both the exaggerated DAD-like hump and the U wave. These findings suggest that reduced Kir2.1 current contributes to the development of DAD and ventricular arrhythmias in Andersen syndrome.
我们报告了首例接受电生理研究的安德森综合征患者。该患者为一名19岁女性,患有家族性周期性麻痹、异常QT-U复合波和非持续性室性心动过速。突变分析显示,作为Kir2.1组成部分的KCNJ2存在错义突变。单相动作电位记录显示左心室有延迟后去极化(DAD)样驼峰。肾上腺素诱发的室性早搏的起始总是与夸张的DAD样驼峰和U波同时出现。这些发现表明,Kir2.1电流减少促成了安德森综合征中DAD和室性心律失常的发生。