Idiopathic ventricular fibrillation and bradycardia-dependent intraventricular block

Aizawa, Yoshifusa; Tamura, Makoto; Chinushi, Masaomi; Naitoh, Naoki; Uchiyama, Hirohide; Kusano, Yoriko; Hosono, Hiroyuki; Shibata, Akira

doi:10.1016/0002-8703(93)90550-s

Cited by 169 publications

(80 citation statements)

References 9 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%

“…2,4 During the night, the augmentation of ST elevation, along with an increase in vagal tone, could be explained, at least in part, by prolongation of the RR interval. 2,9,11,12,14,16 It has been noted that the amplitude of the J wave or the ST segment in the right precordial leads is dependent on the preceding RR interval and is augmented following longer RR intervals. 9,14 An augmentation of the J wave following a long pause after a PVC is suggested to be caused by bradycardia-dependent intraventricular block.…”

Section: Circulation Journal Vol70 July 2006mentioning

confidence: 99%

“…2,9,11,12,14,16 It has been noted that the amplitude of the J wave or the ST segment in the right precordial leads is dependent on the preceding RR interval and is augmented following longer RR intervals. 9,14 An augmentation of the J wave following a long pause after a PVC is suggested to be caused by bradycardia-dependent intraventricular block. 14 Recent experimental studies have also demonstrated a rate dependence of both the J-wave amplitude and ST-segment elevation.…”

Section: Circulation Journal Vol70 July 2006mentioning

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%

Section: Circulation Journal Vol70 July 2006mentioning

confidence: 99%

Section: Circulation Journal Vol70 July 2006mentioning

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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“…Early repolarization has been found in patients with idiopathic ventricular fibrillation (IVF) [120,121], these IVF associated with early repolarization was also called early repolarization syndrome (ERS). Mutations in the LTCC genes, including CACNA1C and CACNB2b , have been found to associate with both diseases.…”

Section: Other Cardiac Arrhythmiasmentioning

confidence: 99%

Mutations in voltage-gated L-type calcium channel: implications in cardiac arrhythmia

et al. 2018

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The voltage-gated L-type calcium channel (LTCC) is essential for multiple cellular processes. In the heart, calcium influx through LTCC plays an important role in cardiac electrical excitation. Mutations in LTCC genes, including CACNA1C, CACNA1D, CACNB2 and CACNA2D, will induce the dysfunctions of calcium channels, which result in the abnormal excitations of cardiomyocytes, and finally lead to cardiac arrhythmias. Nevertheless, the newly found mutations in LTCC and their functions are continuously being elucidated. This review summarizes recent findings on the mutations of LTCC, which are associated with long QT syndromes, Timothy syndromes, Brugada syndromes, short QT syndromes, and some other cardiac arrhythmias. Indeed, we describe the gain/loss-of-functions of these mutations in LTCC, which can give an explanation for the phenotypes of cardiac arrhythmias. Moreover, we present several challenges in the field at present, and propose some diagnostic or therapeutic approaches to these mutation-associated cardiac diseases in the future.

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