Key result
Most antiarrhythmics and ablation fail to control KCNJ2 mutation arrhythmias, though flecainide reduces PVCs.
Why the study?
Polymorphic ventricular tachycardia without structural heart disease has a genetic foundation in cardiac ion channel mutations, but clinical presentation and management of KCNJ2 variants remain to be better characterized.
Do antiarrhythmic drugs, specifically flecainide, reduce ventricular arrhythmias in pediatric patients with polymorphic ventricular tachycardia and KCNJ2 mutations?
Population
Two patients with polymorphic VT harboring KCNJ2 gene mutations
Design
Case report
Authors
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KCNJ2 mutations may underlie select polymorphic VT cases; extends genetic associations but leaves screening implications open.
Case Report (n=2)
Do antiarrhythmic drugs, specifically flecainide, reduce ventricular arrhythmias in pediatric patients with polymorphic ventricular tachycardia and KCNJ2 mutations?
Flecainide may be a promising therapeutic option for polymorphic ventricular tachycardia associated with KCNJ2 mutations, which otherwise respond poorly to conventional antiarrhythmic drugs and ablation.
Zhou et al. (2026) conducted a case report in Polymorphic ventricular tachycardia with KCNJ2 mutation (n=2). Antiarrhythmic medications and radiofrequency catheter ablation was evaluated on Arrhythmia burden and clinical symptoms. Arrhythmias associated with KCNJ2 mutations responded poorly to most antiarrhythmic drugs and catheter ablation, although flecainide successfully reduced the premature ventricular contraction burden in one patient.
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