Epicardial electrogram of the right ventricular outflow tract in patients with the brugada syndrome

Nagase, Satoshi; Kusano, Kengo; Morita, Hiroshi; Fujimoto, Yoshihisa; Kakishita, Mikio; Nakamura, Kazufumi; Emori, Tetsuro; Matsubara, Hiromi; Ohe, Tohru

doi:10.1016/s0735-1097(02)01888-0

Cited by 197 publications

(150 citation statements)

References 10 publications

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“…The magnitude of delay in RV contraction (compared with LV contraction) on flecainide challenge in inducible patients was similar to RV contraction delay in patients with typical ST elevations at baseline (baseline positive). Interestingly, this delay was also similar to the timing of late potentials and delayed potentials from the RVOT subepicardium in Brugada patients, as reported previously, 18 suggesting that these potentials represent delayed RV activation. Our finding that conduction is more strongly impaired in RV than LV, both at baseline and after the occurrence of typical ST elevations on flecainide, corroborates previous direct and indirect observations on preferential RV involvement in Brugada syndrome.…”

Section: Rv Conduction Slowingsupporting

confidence: 88%

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: Rv Conduction Slowingsupporting

confidence: 88%

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

et al. 2004

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“…Recently, Nagase et al demonstrated an 'epicardial abnormality' in the RVOT, which may help to explain late potentials in Brugada syndrome, 16 but in the present study 9 of 11 patients who underwent SAECG had late potentials, and 5 of those 9 had an 'endocardial abnormality' on the endomyocardial biopsy. This difference in results suggests that both epicardial and endocardial abnormalities may be involved in the pathogenesis of the ST-segment elevation in the right precordial leads, an hypothesis that is supported by Coronel et al who showed that localized epicardial conduction delay in the RVOT was associated with ST-segment elevation in the right precordial leads.…”

Section: Circulation Journal Vol70 June 2006contrasting

confidence: 67%

Underlying Cardiomyopathy in Patients With ST-Segment Elevation in the Right Precordial Leads

Kim

Cho

Park

et al. 2006

Circ J

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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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Epicardial electrogram of the right ventricular outflow tract in patients with the brugada syndrome

Cited by 197 publications

References 10 publications

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

Delay in Right Ventricular Activation Contributes to Brugada Syndrome

Underlying Cardiomyopathy in Patients With ST-Segment Elevation in the Right Precordial Leads

Bradycardia-Dependent ECG Changes in Brugada Syndrome

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