Key result
Endocardial mapping in 17 patients with Brugada syndrome revealed low-amplitude fragmented and delayed potentials at the RVOT in 10 patients, suggesting slow conduction contributes to VF induction.
Why the study?
Does slow conduction at the right ventricular outflow tract contribute to the induction of ventricular fibrillation by programmed ventricular stimulation in patients with Brugada syndrome?
Observational (n=17)
Does slow conduction at the right ventricular outflow tract contribute to the induction of ventricular fibrillation by programmed ventricular stimulation in patients with Brugada syndrome?
Abnormal delayed and fragmented potentials in the right ventricular outflow tract may play an important role in the initiation of ventricular fibrillation in patients with Brugada syndrome.
May support RVOT conduction slowing in Brugada VF; leaves open therapeutic or risk-stratification roles pending larger studies.
BACKGROUND: The pathogenesis of Brugada syndrome (BS) is reported to be phase 2 reentry resulting from shortening of the action potential duration at the epicardial site of the right ventricular outflow tract (RVOT). However, several reports have shown a high incidence of ventricular late potentials (LPs) and a high rate of induction of ventricular fibrillation (VF) by programmed ventricular stimulation (PVS) among patients with BS. The aim of this study was to investigate the role of slow conduction for the initiation of VF by PVS in these patients. METHODS AND RESULTS: Endocardial mapping of the RVOT was conducted in 17 patients in whom VF was induced by PVS from the RV apex or RVOT; 11 patients had a positive LP. In 10 patients, RV mapping showed that low-amplitude fragmented and delayed potentials (DPs) were recorded at the RVOT below the pulmonary valve (PV) or between the PV and His bundle electrogram recording site. Electrograms recorded after PVS showed a high incidence of fractionated and disorganized DPs that lead to VF. CONCLUSIONS: Slow conduction at the RVOT may contribute to the induction of VF by PVS. However, the role of slow conduction in spontaneous VF remains controversial.
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Ohkubo et al. (2007) conducted an observational in Brugada syndrome (n=17). Endocardial mapping and programmed ventricular stimulation was evaluated on Presence of delayed potentials and slow conduction at the right ventricular outflow tract. Endocardial mapping in 17 patients with Brugada syndrome revealed low-amplitude fragmented and delayed potentials at the RVOT in 10 patients, suggesting slow conduction contributes to VF induction.
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