Mechanisms of fever-induced QT prolongation and torsades de pointes in patients with KCNH2 mutation.

Keisuke Usuda Kenshi Hayashi Tadashi NakajimaYasutaka KurataShihe CuiTakashi KusayamaToyonobu TsudaHayato Tada Takeshi KatoKenji SakataSoichiro Usui Noboru Fujino Yoshihiro TanakaYoshiaki KanekoMasahiko Kurabayashi Shoichi Tange Takekatsu Saito Kunio OhtaMasakazu YamagishiMasayuki Takamura

Published in: Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology (2023)

These findings indicate that KCNH2 G584S, D609G, and T613M in the S5-pore region reduce the temperature-dependent increase in TCDs through an enhanced inactivation, resulting in QT prolongation and TdP at a febrile state in patients with LQT2.

Keyphrases

drug induced
amyotrophic lateral sclerosis
oxidative stress