Objective:

To explore the historical context and current understanding of Brugada syndrome (BrS) and its future directions.

Approach:

• Historical Foundations: Discusses the early recognition of BrS and its electrocardiographic characteristics, paralleling the discovery of Wolff–Parkinson–White syndrome.
• Current Understanding: Examines recent advances in recognizing the arrhythmogenic substrate of BrS and the implications for diagnosis and treatment.
• Therapeutic Advances: Highlights the success of epicardial substrate ablation in symptomatic patients and its impact on ECG normalization.
• Genetic Understanding: Addresses challenges in genetic testing and the limited specificity of ECG phenotypes in asymptomatic individuals.
• Risk Stratification Models: Explores contemporary risk stratification models that integrate various clinical and genetic factors.

Key Findings:

• BrS was historically defined by its ECG phenotype, lacking a clearly identifiable substrate.
• Recent studies have identified abnormal electrograms in the right ventricular outflow tract as the arrhythmogenic substrate.
• Epicardial substrate ablation has shown success in reducing ventricular arrhythmias and normalizing ECG patterns.
• Current risk stratification models remain inconsistent, particularly for asymptomatic patients.

Interpretation:

Understanding of BrS has evolved from a focus on electrocardiographic features to recognizing the significance of the underlying arrhythmogenic substrate.

Limitations:

• Risk stratification in asymptomatic individuals remains challenging due to limited specificity of ECG phenotypes.
• Genetic testing yields pathogenic variants in only a minority of patients.

Conclusion:

Ongoing research is essential to refine diagnostic criteria and enhance risk stratification in BrS.