Key result
GS967 reduces inducible VF by ~86% in a transgenic rabbit model of LQT2.
Why the study?
Long QT syndrome is linked to sudden cardiac death caused by early afterdepolarizations and polymorphic ventricular tachycardias, and suppressing late sodium current may counterbalance reduced repolarization reserve.
Does GS967 prevent early afterdepolarizations and polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 2?
Does GS967 prevent early afterdepolarizations and polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 2?
Absolute Event Rate: 7.7% vs 53.8%
p-value: p=<0.05
Selective INaL blockade by GS967 prevents early afterdepolarizations and abolishes polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 2.
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Supports INaL blockade as antiarrhythmic strategy in LQT2 models; leaves open clinical translation and human trials.
Hwang et al. (2020) studied Long QT syndrome type 2 (LQT2) (n=21). GS967 vs. Vehicle (DMSO) was evaluated on Ventricular fibrillation induction during ramp pacing (p=<0.05). The selective late sodium current blocker GS967 reduced the incidence of ventricular fibrillation induction from 53.8% to 7.7% in a transgenic rabbit model of Long QT syndrome type 2.
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