Surface ECG Characteristics of Ventricular Tachyarrhythmias Before Degeneration Into Ventricular Fibrillation in Patients With Brugada-Type ECG

Abstract

SummaryThis study was designed to evaluate whether the right ventricular outflow tract (RVOT) is the arrhythmogenic focus in Brugada syndrome. We enrolled 45 patients with Brugadatype ECG who underwent programmed ventricular stimulation and inducible ventricular fibrillation (VF). In 25 of these 32 patients, repetitive VT was observed before degeneration into VF. The QRS morphology of surface ECG and intracardiac electrograms were evaluated to determine the origin of the ventricular tachycardia (VT) that degenerated into VF. The VT morphology was a left bundle branch block pattern with an inferior axis in 22 of 28 VTs and the intracardiac conduction sequence during VT revealed activation from the RVOT to the RV apex in these 22 VTs. The majority of the patients with Brugada syndrome showed repetitive VT originating from the RVOT that degenerated into VF. The RVOT may be an arrhythmogenic focus in patients with Brugada syndrome. (Int Heart J 2009; 50: 477-487)

Abnormal Action Potential Duration Restitution Property in the Right Ventricular Outflow Tract in Brugada Syndrome

“…22 Previously, we recorded low-amplitude fragmented and delayed potentials at the RVOT in BS patients with inducible VF, 23 and we found that a majority of patients with BS showed repetitive VT originating from the RVOT that degenerated into VF. 17 Moreover Park et al reported that the maximum slope of the APD restitution curve in BS patients with inducible VF was 2.1 at the RVOT and significantly greater than that at the RVA (1.1). 24 To our knowledge, we provide the first description of the detailed APD restitution properties in BS.…”

“…5,6, 29 We assessed the repolarization restitution property and showed that the maximum restitution slope in the RVOT of BS patients with inducible VF is significantly steeper than that of control patients, which indicates that the RVOT region may play an important role in the degeneration into sustained VF in patients with BS. Previous studies have also revealed the importance of the RVOT in the development of VF in BS, based on the presence of delayed potentials in the RVOT, 30 the presence of initial repetitive VT originating from the RVOT before degeneration into VF, 17 and development of spontaneous premature contractions triggering VF mainly in the RVOT. 31 Transmural dispersion of repolarization in the RVOT has been shown to contribute to initial repetitive excitation during VT in experimental BS models.…”

“…15, 16 However, we showed repetitive ventricular tachycardia (VT) originating from the RVOT and degenerating into VF in a majority of patients with BS. 17 We also reported a case in which monophasic action potentials (MAPs) recorded from the RVOT at a basic cycle length (CL) of 400 ms showed MAP alternans, and VF was induced only when extrastimuli were applied after a decrease in the MAP duration (MAPD) of the alternans. 18 Thus we hypothesized that the RVOT contributes to RV Action Potential Restitution in BS the inducibility of VF in patients with BS undergoing programmed ventricular stimulation.…”

Right Ventricular Histological Substrate and Conduction Delay in Patients With Brugada Syndrome

“…37) The electrical abnormality is localized in the free wall of the RVOT, as suggested by the frequent origin or induction of ventricular arrhythmia from this region, [38][39][40][41] and Haissaguerre, et al 42) showed the importance of focal premature ventricular beats, originating mainly from the RVOT, in triggering VF in patients with Brugada syndrome. Several studies based on noninvasive techniques have shown right ventricular abnormalities in patients with the clinical phenotype of Brugada syndrome.…”

Non-Contact Mapping of the Origin of Provoked Ventricular Tachycardia in Brugada Syndrome

“…Two principal mechanisms are thought to be responsible for Brugada syndrome (BrS): right ventricular (RV) conduction delay 1,2) and RV subepicardial action potential shortening 3,4) . We have reported endocardial conduction delay in the RV outflow tract 5) (RVOT) that provoked ventricular tachycardia (VT), which degenerated into programmed ventricular stimulation (PVS)-inducible ventricular fibrillation (VF) with a left bundle branch block morphology 6) . However, only a few reports have described the site of origin of the provoked VT 7,8) .…”