Key result
Patients with Brugada syndrome demonstrated a significant right ventricular longitudinal conduction delay compared to controls (P=0.027), which became non-significant with isoproterenol.
Why the study?
The mechanism of Brugada syndrome remains unclear between repolarization and depolarization hypotheses, and prolonged longitudinal activation time has been verified in only a small number of human right ventricles.
Do patients with Brugada syndrome exhibit right ventricular longitudinal conduction delay compared to controls?
Case-Control (n=21)
Do patients with Brugada syndrome exhibit right ventricular longitudinal conduction delay compared to controls?
Patients with Brugada syndrome exhibit right ventricular longitudinal conduction delay, supporting the depolarization hypothesis of the disease mechanism.
RV conduction delays shown in small BrS cohort; leaves open depolarization hypothesis and requires larger prospective studies before any clinical application.
BACKGROUND: The mechanism of Brugada syndrome (BrS) is still unclear, with different researchers favoring either the repolarization or depolarization hypothesis. Prolonged longitudinal activation time has been verified in only a small number of human right ventricles (RVs). The purpose of the present study was to demonstrate RV conduction delays in BrS. METHODS: The RV outflow tract (RVOT)-to-RV apex (RVA) and RVA-to-RVOT conduction times were measured by endocardial stimulation and mapping in 7 patients with BrS and 14 controls. The difference in longitudinal conduction time was not significant when isoproterenol was administered. CONCLUSION: The patients with BrS showed an RV longitudinal conduction delay obviously. These findings suggest that RV conduction delay might contribute to generate the BrS phenotype.
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Yoon et al. (2021) conducted a case-control in Brugada Syndrome (n=21). Brugada syndrome vs. Controls was evaluated on Right ventricular longitudinal conduction time (RVOT-to-RVA and RVA-to-RVOT) (p=0.027). Patients with Brugada syndrome demonstrated a significant right ventricular longitudinal conduction delay compared to controls (P=0.027), which became non-significant with isoproterenol.
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