Ventricular Arrhythmia Mechanisms in Brugada Syndrome Syncope
Brugada syndrome syncopal episodes typically result from polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF), not monomorphic VT, and when VF occurs it does not self-terminate—it requires electrical termination. 1
Primary Arrhythmic Mechanisms
The characteristic life-threatening arrhythmias in Brugada syndrome are polymorphic VT and VF, with VF being the hallmark arrhythmia that leads to sudden cardiac death. 1 Arrhythmic syncope in Brugada syndrome results from self-terminating sustained ventricular tachycardia or paroxysmal ventricular fibrillation. 2
Critical Distinction About VF Self-Termination
When true VF occurs in Brugada syndrome, it necessitates electrical termination and does not spontaneously convert. 3 Evidence from ICD data demonstrates that:
- Asymptomatic Brugada patients who received ICDs had 7-13% appropriate ICD shocks over long-term follow-up, indicating these were life-threatening arrhythmias requiring device intervention. 3, 4
- One documented death occurred from inappropriate shock-induced ventricular fibrillation in an ICD patient, demonstrating that once VF is triggered, it does not self-terminate. 3, 4
- Patients with inducible ventricular arrhythmias had a 28% incidence of spontaneous ventricular fibrillation in early observational studies, and these events required intervention. 3, 4
Syncope vs. Cardiac Arrest
The key distinction is that syncope represents self-terminating polymorphic VT, while cardiac arrest represents sustained VF requiring intervention. 2 The annual incidence of arrhythmic events varies by presentation:
- 7.7% per year in patients with aborted sudden cardiac death 4
- 1.9% per year in patients with syncope 4
- 0.5% per year in asymptomatic patients 4
Patients with syncope and spontaneous type 1 ECG pattern have a 6-fold higher risk of cardiac arrest compared to asymptomatic patients with spontaneous ECG pattern. 4, 1
Monomorphic VT: A Rare Exception
While your question focuses on VT converting to sinus rhythm or devolving to VF, monomorphic VT is actually rare in Brugada syndrome. 5, 6 Recent ICD data from 793 Brugada patients showed:
- Only 54 patients (6.8%) met criteria for documented ventricular arrhythmias on ICD recordings 5
- Among these, 47 episodes were VF and only 27 were monomorphic VT 5
- Patients with monomorphic VT were older at first event (47.7 vs 40.7 years), had higher QRS duration, and had broader epicardial substrate abnormalities 5
- Monomorphic VT showed later onset and later recurrences after ICD implantation compared to VF 5
Electrophysiologic Substrate
The cellular mechanism involves loss of the action potential dome in right ventricular epicardium but not endocardium, creating electrical heterogeneity that leads to closely coupled premature ventricular contractions via a phase 2 reentrant mechanism that precipitates VT/VF. 7
Inducibility and Risk Stratification
The role of electrophysiologic study remains controversial. 4 In a meta-analysis of 1,036 patients where 54% had VT or ventricular fibrillation induced by premature ventricular stimulation, no difference in outcome was observed at 34 months follow-up. 4 However, the induction of polymorphic VT or ventricular fibrillation in patients with Brugada syndrome may be considered diagnostic. 4
Clinical Implications
ICD implantation is mandatory (Class I recommendation) for survivors of aborted cardiac arrest because the first VF episode would have been fatal without intervention. 3, 4 For patients with spontaneous type 1 ECG pattern and syncope, ICD should be considered (Class IIa recommendation). 3, 8
Common Pitfall
The critical error is assuming that VF in Brugada syndrome can self-terminate like polymorphic VT. Syncope represents self-terminating polymorphic VT, not VF. 2 Once true VF develops, it requires electrical termination—this is why ICD therapy is the only proven effective therapy in preventing sudden death. 7, 4