Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome

Miyazaki, Toshihisa; Mitamura, Hideo; Miyoshi, Shunichiro; Soejima, Kyoko; Aizawa, Yoshifusa; Ogawa, Satoshi

doi:10.1016/0735-1097(95)00613-3

Cited by 681 publications

(430 citation statements)

References 20 publications

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“…[7][8][9]13,14 Several studies have demonstrated that the ECG in patients with BS changes dynamically. 8,9,11,13 The configuration and degree of ST-segment elevation in the precordial leads change from day to day.…”

Section: Circulation Journal Vol70 July 2006mentioning

confidence: 99%

“…11 Other clinical studies also suggest that an increase in vagal activity and a withdrawal of sympathetic activity might play an important role in the ST elevation and arrhythmogenesis in BS. 5,7,14,15 Experimental studies suggest that a transient outward current (Ito)-mediated action potential notch and loss of the action potential dome at the epicardium, but not at the endocardium, creates a transmural voltage gradient that might be responsible for the ST-segment elevation of BS. 2,4 Acetylcholine facilitates loss of the action potential dome by suppressing ICa and/or augmenting the potassium current, leading to accentuation of ST-segment elevation.…”

Section: Circulation Journal Vol70 July 2006mentioning

confidence: 99%

“…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.…”

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confidence: 99%

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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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Section: Circulation Journal Vol70 July 2006mentioning

confidence: 99%

Section: Circulation Journal Vol70 July 2006mentioning

confidence: 99%

mentioning

confidence: 99%

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Bradycardia-Dependent ECG Changes in Brugada Syndrome

Mizumaki

Fujiki

Nishida

et al. 2006

Circ J

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“…The ST-segment elevation may also display a saddleback appearance, 11 and the VT in rare cases may be monomorphic. 12 ST-segment elevation is associated with a wide variety of benign, as well as malignant, pathophysiologic conditions.…”

Section: Discussionmentioning

confidence: 99%

Magnetic Dispersion of the Late Repolarization in Brugada Syndrome

Joung

Kim

Lee

et al. 2008

Circ J

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Background Magnetocardiography (MCG) is a new noninvasive modality for recording cardiac depolarization and repolarization and was used in the present study to evaluate abnormalities in patients with Brugada syndrome (BS). Methods and ResultsThe MCG findings of 10 BS, 21 right bundle branch block (RBBB), and 34 normal patients were compared. On the horizontal spatiotemporal activation graph (STAG), the r' waves were more frequently located on the right side in the RBBB than in the normal (p=0.001) or BS groups (p=0.001). The maximum current angles of the r' wave fell into the northwest axis in all BS patients as compared to having a right axis deviation in 19 of 21 RBBB patients (90.4%, p=0.001). In the magnetic field and current density vector maps during late repolarization, the BS group had a non-dipole pattern more frequently and a higher number of poles compared with the normal (p=0.001) and RBBB groups (p=0.001). Conclusions During depolarization, the horizontal STAG location and maximum current angle of the r' wave were beneficial in differentiating BS from RBBB and normal. The magnetic dispersion was a more frequently observed finding in BS patients than in RBBB and normal patients during late repolarization. (Circ J 2008; 72: 94 -101)

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“…Therefore, the proband suffered from two apparently distinct conditions: NMS and Brugada syndrome. The autonomic nervous system has been implicated in both diseases 12,13 , and several case reports have described patients exhibiting clinical phenotypes of both NMS and Brugada syndrome [3][4][5] .…”

Section: Discussionmentioning

confidence: 99%