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Structural abnormalities within the right ventricular outflow tract (RVOT) can present similarly to Brugada syndrome. A 34-year-old woman with no medical history presented with polymorphic ventricular tachycardia/ventricular fibrillation cardiac arrest and initial electrocardiogram showed type I Brugada pattern. Cardiac magnetic resonance imaging revealed prominent tissue thickening at the RVOT with late gadolinium enhancement.

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Background: Brugada syndrome (BrS) is a genetic heart disease that predisposes individuals to ventricular arrhythmias and sudden cardiac death. Although implantable cardioverter-defibrillators (ICDs) and quinidine are primary treatments, recurrent BrS-triggered ventricular arrhythmias can persist. In this setting, epicardial substrate ablation has emerged as a promising alternative for symptomatic patients.

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Introduction: Brugada Syndrome (BrS) is an inherited arrhythmia syndrome characterised by ST-segment elevation in the right precordial ECG leads and is associated with an increased risk of sudden cardiac death. We identify and characterise a novel SCN3B variant encoding the regulatory β3-subunit of the cardiac voltage-gated sodium channel, Na1.5.

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Background: Brugada syndrome (BrS) is an inherited channelopathy characterized by right precordial ST-segment elevation. This study investigates the clinical and genetic characteristics of children with BrS in Hong Kong.

Methods: A retrospective review was conducted at the only tertiary pediatric cardiology center in Hong Kong from 2002 to 2022, including all pediatric BrS patients under 18 years old.

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