Late I Na Blocker GS967 Supresses Polymorphic Ventricular Tachycardia in a Transgenic Rabbit Model of Long QT Type 2

Long QT syndrome has been associated with sudden cardiac death likely caused by early afterdepolarizations (EADs) and polymorphic ventricular tachycardias (PVTs). Suppressing the late sodium current (I ) may counterbalance the reduced repolarization reserve in long QT syndrome and prevent EADs and P...

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Veröffentlicht in:	Circulation. Arrhythmia and electrophysiology 2020-08, Vol.13 (8), p.e006875
Hauptverfasser:	Hwang, Jungmin, Kim, Tae Yun, Terentyev, Dmitry, Zhong, Mingwang, Kabakov, Anatoli Y, Bronk, Peter, Arunachalam, Karuppiah, Belardinelli, Luiz, Rajamani, Sridharan, Kunitomo, Yukiko, Pfeiffer, Zachary, Lu, Yichun, Peng, Xuwen, Odening, Katja E, Qu, Zhilin, Karma, Alain, Koren, Gideon, Choi, Bum-Rak
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - drug effects Animals Animals, Genetically Modified Anti-Arrhythmia Agents - pharmacology Calcium Signaling - drug effects Computer Simulation Delayed Rectifier Potassium Channels - metabolism Disease Models, Animal Female Heart Rate - drug effects Long QT Syndrome - drug therapy Long QT Syndrome - genetics Long QT Syndrome - metabolism Long QT Syndrome - physiopathology Male Models, Cardiovascular Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Pyridines - pharmacology Rabbits Sodium Channel Blockers - pharmacology Sodium Channels - drug effects Sodium Channels - metabolism Sodium-Calcium Exchanger - metabolism Tachycardia, Ventricular - genetics Tachycardia, Ventricular - metabolism Tachycardia, Ventricular - physiopathology Tachycardia, Ventricular - prevention & control Time Factors Triazoles - pharmacology Ventricular Fibrillation - genetics Ventricular Fibrillation - metabolism Ventricular Fibrillation - physiopathology Ventricular Fibrillation - prevention & control
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