Key result
Scn5a+/- mice exhibit ~5-fold higher ventricular arrhythmia susceptibility than wild-type mice during programmed electrical stimulation.
Why the study?
Relevant experimental models and electrophysiological protocols are needed to study underlying mechanisms of ventricular arrhythmias and develop new therapies in genetically engineered mouse models.
Population
Two transgenic mouse models of arrhythmia (Brugada syndrome and cardiolaminopathy) and control mice
Comparison
Programmed electrical stimulation in transgenic models vs control mice
Design
Animal experimental study
Authors
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Refines arrhythmia induction protocols in Scn5a+/- Brugada models; leaves open translation to human risk stratification.
Absolute Event Rate: 7.5% vs 1.4%
p-value: p=<0.001
A progressive programmed electrical stimulation protocol using 2-4 extrastimuli successfully characterizes ventricular arrhythmia susceptibility in murine models of Brugada syndrome and cardiolaminopathy while avoiding non-specific arrhythmia induction seen with burst pacing.
Ferrand et al. (2024) studied Ventricular arrhythmias (n=71). Progressive S2-S5 programmed electrical stimulation (PES) vs. Wild-type mice was evaluated on Cumulative arrhythmia score (CAS) (p=<0.001). A progressive programmed electrical stimulation protocol using 2-4 extrastimuli revealed a significantly higher susceptibility to ventricular arrhythmias in Scn5a+/- mice (cumulative arrhythmia score 7.5 vs 1.4, p<0.001) compared to wild-type mice.
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