Endocardial Electrograms From the Right Ventricular Outflow Tract After Induced Ventricular Fibrillation in Patients With Brugada Syndrome

Ohkubo, Kimie; Watanabe, Ichiro; Takagi, Yasuhiro; Okumura, Yasuo; Ashino, Sonoko; Kofune, Masayoshi; Kofune, Tatsuya; Shindo, Atsushi; Sugimura, Hidezou; Nakai, Toshiko; Kunimoto, Satoshi; Kasamaki, Yuji; Saito, Satoshi; Hirayama, Atsushi

doi:10.1253/circj.71.1258

Cited by 15 publications

(14 citation statements)

References 31 publications

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“…Our study revealed that low-voltage, relatively wide, and more intensively fractionated electrograms issue from the RVOT of patients with Brugada syndrome. Depolarization properties in Brugada syndrome: We know that SCN5A mutations occur in only about 20% of patients with Brugada syndrome, 22) and the consistent identification of RVOT conduction delay in our previous study 10) and the present study suggests that the particular features of Brugada syndrome arise from several factors leading to conduction block rather than to a single sodium channelopathy. As Coronel, et al suggested, the fundamental problem in Brugada syndrome may be secondary to conduction delay arising from genetic, structural, or pharmacological causes.…”

Section: Discussionsupporting

confidence: 82%

“…5,6) However, recent studies suggested that conduction delay in the right ventricle is related to arrhythmias associated with Brugada syndrome (depolarization disorder). [7][8][9][10][11][12][13][14][15] Furthermore, structural abnormalities in the right ventricle are reported in Brugada syndrome. [16][17][18] We conducted a single-center case-control electroanatomic mapping study in patients with and without Brugada syndrome to identify the arrhythmogenic substrates in Brugada syndrome.…”

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confidence: 99%

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Clarifying the Arrhythmogenic Substrate for Brugada Syndrome Electroanatomic Mapping Study of the Right Ventricle

et al. 2011

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SummaryThe right ventricular outflow tract (RVOT) is considered the arrhythmogenic region that gives rise to Brugada syndrome. To obtain a better understanding of this substrate, we performed electroanatomic mapping of the right ventricle (RV) in patients with Brugada syndrome.The RV was mapped electroanatomically with the CARTO system in 11 patients with asymptomatic Brugada syndrome but in whom ventricular fibrillation was induced by programmed ventricular stimulation, and in 5 control patients. The low voltage zone area (< 1.5 mV) was larger (16.1% versus 7.8%, P < 0.01) and the bipolar electrogram duration was greater (81.6 ± 7.8 ms versus 53.4 ± 5.6 ms, P < 0.01) in the patients with Brugada syndrome versus the control patients; the bipolar electrogram duration was greater in the septal portion and free wall of the RVOT.Our data suggest that regional endocardial conduction slowing based on structural abnormalities exists at the RVOT in Brugada syndrome. (Int Heart J 2011; 52: 290-294)

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Section: Discussionsupporting

confidence: 82%

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confidence: 99%

Clarifying the Arrhythmogenic Substrate for Brugada Syndrome Electroanatomic Mapping Study of the Right Ventricle

et al. 2011

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“…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.…”

Section: Mechanism Of Vf In Bsmentioning

confidence: 99%

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

Ashino

Watanabe

Kofune

et al. 2010

Circ J

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Background: Although patients with Brugada syndrome (BS) are at risk of ventricular fibrillation (VF) and ensuing death, the action potential duration (APD) restitution properties of the right ventricular outflow tract (RVOT) in patients with BS remain undetermined. Methods and Results:Endocardial monophasic action potentials (MAPs) were obtained from 16 patients with BS and 17 control patients. MAPs were recorded from the RVOT in all patients. The MAP duration at 90% repolarization (MAPD90), effective refractory period (ERP), and maximum slope of the APD restitution curve were obtained. VF was induced with up to 3 extrastimuli from the RV apex or RVOT. There was no difference in MAPD90 between the 2 groups, but the ERP was significantly shorter in patients with BS than in control patients (210.7±10.5 vs 223.8±13.4 ms, P=0.008). MAPD at the shortest diastolic interval was significantly shorter in patients with BS than in control patients (149.9±19.9 vs 179.8±13.7 ms, P<0.001). The maximum slope of the APD restitution curve was steeper in patients with BS than in control patients (2.90±1.29 vs 1.38±0.41, P<0.001). Conclusions:The shorter ERP, shorter MAPD at the shortest diastolic interval and steeply sloped APD restitution curve in the RVOT appear to be related to the inducibility of VF in patients with BS. (Circ J 2010; 74: 664 - 670)

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“…[7][8][9][10] However, the existence of a conduction delay at the RVOT has been suggested in many reports. [11][12][13][14] In addition, several clinical studies have also suggested that spontaneous episodes of VF are triggered by premature ventricular contractions (PVCs) originating mainly from the RVOT. [15][16][17] We previously reported that low-amplitude fragmented and delayed potentials were recorded in the RVOT in patients with Brugada syndrome and that these electrograms showed more fractionation and disorganization with programmed ventricular stimulation that led to VF.…”

Section: Discussionmentioning

confidence: 99%

“…[15][16][17] We previously reported that low-amplitude fragmented and delayed potentials were recorded in the RVOT in patients with Brugada syndrome and that these electrograms showed more fractionation and disorganization with programmed ventricular stimulation that led to VF. 14) In addition, several reports have shown a high incidence of ventricular late potentials, 18,19) high rate of induction of ventricular fibrillation (VF) by programmed ventricular stimulation, [20][21][22][23][24] and that inducibility of VF is increased more by programmed stimulation from the RVOT than from the RV apex in Brugada syndrome. 25,26) The aim of this study was to investigate the characteristics of the induced ventricular tachycardia (VT) that degenerates to VF to evaluate whether the RVOT is the arrhythmogenic focus in Brugada syndrome in a retrospective manner.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2009

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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)

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Endocardial Electrograms From the Right Ventricular Outflow Tract After Induced Ventricular Fibrillation in Patients With Brugada Syndrome

Cited by 15 publications

References 31 publications

Clarifying the Arrhythmogenic Substrate for Brugada Syndrome Electroanatomic Mapping Study of the Right Ventricle

Clarifying the Arrhythmogenic Substrate for Brugada Syndrome Electroanatomic Mapping Study of the Right Ventricle

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

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

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