Assessment of noninvasive markers in identifying patients at risk in the brugada syndrome: insight into risk stratification

Ikeda, Takanori; Sakurada, Harumizu; Sakabe, Koichi; Saruta, Takao; Takami, Mitsuru; Tezuka, Naoki; Nakae, Takeshi; Noro, Mahito; Enjoji, Yoshihisa; Tejima, Tamotsu; Sugi, Kaoru; Yamaguchi, Tetsu

doi:10.1016/s0735-1097(01)01197-4

Cited by 202 publications

(84 citation statements)

References 26 publications

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“…Clinically, late potentials are consistently found in signalaveraged ECGs. 7,16 -20 They have a higher prevalence in Brugada syndrome patients, 17 are associated with malign (covedtype) ST elevations, 20 and are exacerbated by flecainide. 19 They and other markers of slow conduction are associated with stronger inducibility of ventricular tachyarrhythmias.…”

Section: Tukkie Et Al Activation Delay In Brugada Syndrome 1275mentioning

confidence: 99%

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

et al. 2004

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Background-Although Brugada syndrome revolves around reduced net depolarizing force, the electrophysiological mechanisms of its defining features (right precordial ST-segment elevation and ventricular tachyarrhythmias) remain unresolved. Two proposed mechanisms are (1) right ventricular (RV) conduction delay and (2) selective and significant RV subepicardial action potential shortening. Both mechanisms must cause disparate contractile changes: delay in RV contraction and reduction of contractile force, respectively. We aimed to establish the electrophysiological mechanism of Brugada syndrome by studying the timing and force of RV contraction. Methods and Results-Using tissue Doppler echocardiography, we studied how these contractile variables change on induction of the characteristic ST-segment changes of Brugada syndrome by flecainide challenge. Accordingly, we studied patients in whom flecainide induced these changes (inducible) and those in whom these changes were not induced (control). We found that (1)

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Section: Tukkie Et Al Activation Delay In Brugada Syndrome 1275mentioning

confidence: 99%

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

et al. 2004

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“…8,[17][18][19] Depolarization abnormality is reflected in prolonged HV intervals, abnormal late potential and abnormal delayed potential in the epicardial region of the right ventricular outflow tract. 8,16,[20][21][22] A widening of the S wave in the right precordial leads, reflecting an underlying right ventricular conduction delay, was frequently observed in symptomatic patients and might be an important indicator of increased risk. 23 However, rate-dependent changes in the conduction abnormality have not been fully elucidated.…”

Section: Rate-dependent Changes In S Wave and Qrs Durationmentioning

confidence: 99%

Bradycardia-Dependent ECG Changes in Brugada Syndrome

Mizumaki

Fujiki

Nishida

et al. 2006

Circ J

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rugada syndrome (BS), a distinct subtype of idiopathic ventricular fibrillation (VF), is characterized by a distinctive ST segment elevation in the right precordial leads. [1][2][3] The mechanism responsible for this ST segment elevation and genesis of VF is still under investigation. Several possible mechanisms have been proposed for the ST segment elevation in BS. Among them are conduction delay, accentuation of the action potential notch and loss of the action potential dome in the right ventricular outflow epicardium. 3,4 In BS, unlike other diseases, VF and sudden death mainly occur in the resting state, predominantly during sleep. 5,6 The typical ECG changes are variable over time and are modulated by exercise or pharmacological interventions that interact with autonomic nervous activities. 5,[7][8][9] We recently reported an inadequate prolongation of the QT interval (short QT interval) at longer RR intervals 10 and an augmentation of the ST elevation through vagal activity in patients with BS. 11 The nighttime onset of VF episodes may be related to both a shorter QT interval and an enhanced ST elevation during bradycardia at night. This could be because of a slow recovery from the inactivation of prominent Ito. 12 However, it is still unclear how the RR intervals affect the ECG changes in BS and whether rate dependent changes in the ECG would be different between symptomatic and asymptomatic patients. The present study was therefore designed to examine the effects of the RR intervals on ECG changes during an electrophysiologic study (EPS) in both symptomatic and asymptomatic patients. Methods Study PopulationTwenty-one consecutive male patients with BS were studied: 9 were symptomatic with either documented VF or episodes of unexplained syncope, and the other 12 were asymptomatic without either spontaneous VF or inducible VF during the EPS. The study protocol was approved by the institutional review board and written informed consent was given by all patients before participation. We diagnosed BS in accordance with recently established ECG criteria. 3 Patients with coved-type ST elevation accompanied by Jwave amplitude ≥2 mm in one of the leads V1-3 were included. 3 For patients with saddle-back-type ST elevation (type 2 or 3), coved-type ST elevation ≥2 mm induced by pilsicainide, a class Ic antiarrhythmic drug, was required. 3 In all patients, physical examination, chest X-ray, 2-dimensional-echocardiography, exercise test and thallium or 99m Tc-tetrofosmin myocardial single photon emission computed tomography failed to disclose apparent evidence of organic heart disease. Patients with diabetes mellitus, long QT syndrome or electrolyte abnormality and patients taking any drugs were excluded from the present study. EPS and Analysis of ECGsEPS was performed in all 21 patients after all antiarrhythmic drugs had been discontinued for at least 5 halflives of the drug. A steerable 6F octapolar catheter with Background In patients with Brugada syndrome (BS), ventricular fibrillation (VF) occurs mainly during ...

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“…[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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Assessment of noninvasive markers in identifying patients at risk in the brugada syndrome: insight into risk stratification

Abstract: Late potentials are a noninvasive risk stratifier in patients with Brugada syndrome. These results may support the idea that conduction disturbance per se is arrhythmogenic.

Cited by 202 publications

References 26 publications

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

Bradycardia-Dependent ECG Changes in Brugada Syndrome

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

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