Mutation N588K in KCNH2 causes an increase in net repolarizing current.[6] In addition, recent studies have revealed a significant association between early repolarization and SQT in clinical phenotype.[14], [15] Because of the high prevalence of early repolarization detected in SQT, it is thought that enhancement of repolarization is a common mechanism underlying arryhthmogenicity in early repolarization and SQT.[14] Since QT interval is affected by other ion channels and cardiac enlargement, QT interval of HF patients with ventricular tachyarrhythmia in this study was not short. This evidence concerns the gene KCNH2 and hydrops fetalis.