Intravenous Administration of Class I Antiarrhythmic Drug Induced T Wave Alternans in an Asymptomatic Brugada Syndrome Patient

Ohkubo, Kimie; Watanabe, Ichiro; Okumura, Yasuo; Yamada, Takeshi; Masaki, Riko; Kofune, Tatsuya; Oshikawa, Naohiro; Kasamaki, Yuji; Saito, Satoshi; Ozawa, Yukio; Kanmatsuse, Katsuo

doi:10.1046/j.1460-9592.2003.00288.x

Cited by 22 publications

(19 citation statements)

References 25 publications

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“…[15][16][17] Takagi et al demonstrated that pilsicainide induced T-wave alternans, increased the frequency of multiform premature ventricular contractions, and eventually VF developed. 16 Morita et al demonstrated in an invitro canine tissue model of BS that T-wave alternans was caused by adjacent regions having action potentials (APs) with longer duration and larger domes or without domes coexisting simultaneously in the epicardium, and compared with the shallow T waves, deep T waves were associated with epicardial APs having longer durations and larger domes.…”

Section: Discussionmentioning

confidence: 99%

“…[2][3][4][5][6][7][8][9][10][11][12][13][14] Furthermore, several reports demonstrate T-wave alternans in the 12-lead ECG after administration of class Ic antiarrhythmic drugs. [14][15][16][17][18] This case report describes a patient with asymptomatic BS in whom monophasic action potentials (MAPs) recorded from the RVOT demonstrated alternans and VF was induced only when the extrastimuli were applied after a shorter MAP of the alternans. …”

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confidence: 99%

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Action Potential Alternans in the Right Ventricular Outflow Tract in a Patient With Asymptomatic Brugada Syndrome

Kofune

Watanabe

Ashino

et al. 2009

Circ J

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Circ J 2009; 73: 580 -583 n both experimental and clinical studies, the pathogenesis of Brugada syndrome (BS) has been reported as depression or loss of the action potential dome in the right ventricular (RV) epicardium, which creates a transmural voltage gradient that may be responsible for the ST-segment elevation and also induce extrasystolic activity because of phase 2 reentry. 1-4 However, several reports show a high induction rate of ventricular fibrillation (VF) by programmed ventricular stimulation 5-8 and recent reports demonstrate that ventricular premature complexes occurring after administration of pilsicainide to unmask ST-segment elevation in the right precordial leads show left-bundle branch block and inferior axis, suggesting RV outflow tract (RVOT) origin 9-11 and increased inducibility of VF at the RVOT in BS. [2][3][4][5][6][7][8][9][10][11][12][13][14] Furthermore, several reports demonstrate T-wave alternans in the 12-lead ECG after administration of class Ic antiarrhythmic drugs. [14][15][16][17][18] This case report describes a patient with asymptomatic BS in whom monophasic action potentials (MAPs) recorded from the RVOT demonstrated alternans and VF was induced only when the extrastimuli were applied after a shorter MAP of the alternans. Case ReportA 71-year-old man who had frequent ventricular premature contractions after right hip joint surgery at the Nihon University Hospital was referred to the Cardiology Division. Twelve-lead ECG showed type II Brugada-type ECG and incomplete right bundle branch block (Figure 1). 19 The 12-lead ECG changed to type I Brugada-type ECG after administration of the class Ic antiarrhythmic drug, pilsicainide (Figure 2). He did not have a family history of sudden death or attacks of unconsciousness. Physical examination was normal and laboratory data were in the normal ranges, except for high total cholesterol level (250 mg/dl). Chest X-ray showed calcification of the aortic arch and echocardiography showed hypokinesis of the left ventricular anterior wall. The signal-averaged ECG showed border- (Received April 1, 2008; revised manuscript received April 30, 2008; accepted May 21, 2008; released online December 12, 2008 A 71-year-old man with frequent ventricular premature contractions after right hip joint surgery was referred to the Cardiology Division. Twelve-lead ECG showed type II Brugada-type ECG and signal-averaged ECG showed positive ventricular late potentials. The 12-lead ECG changed to type I Brugada-type after administration of the class Ic antiarrhythmic drug, pilsicainide. Ventricular fibrillation (VF) was reproducibly induced with double premature stimuli from the right ventricular outflow tract (RVOT) at a basic cycle length (BCL) of 400 ms. Monophasic action potentials (MAPs) recorded from the RVOT at a BCL of 400 ms showed MAP alternans and VF was only induced when extrastimuli were applied after a shorter MAP of the alternans. (Circ J 2009; 73: 580 -583)

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Action Potential Alternans in the Right Ventricular Outflow Tract in a Patient With Asymptomatic Brugada Syndrome

Kofune

Watanabe

Ashino

et al. 2009

Circ J

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“…This large spatial dispersion in epicardial AP morphology would not be expected when electrical coupling is normal. Still, some authors suggest that ST segment and T wave alternans after class I antiarrhythmic drugs [42,112] support the repolarization disorder hypothesis; however, whether this observation truly reflects a repolarization or depolarization disorder is unresolved.…”

Section: Heterogeneity In Repolarizationmentioning

confidence: 99%

“…Accordingly, pacing provided an effective therapy against bradycardia-related VT/VF onset in a Brugada syndrome patient [122]. Yet, ST elevations may also increase at fast heart rates [42,112,123,124]. While particular circumstances may be responsible (enhanced intermediate inactivation of the mutant Na channel [123] or the use of class IC antiarrhythmic drugs with use-dependence [42,112]), this phenomenon was also described in the absence of such confounders [42,112].…”

Section: Effects Of Heart Ratementioning

confidence: 99%

Pathophysiological mechanisms of Brugada syndrome: Depolarization disorder, repolarization disorder, or more?

Meregalli¹,

Wilde²,

Tan³

2005

Cardiovascular Research

336

266

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After its recognition as a distinct clinical entity, Brugada syndrome is increasingly recognized worldwide as an important cause of sudden cardiac death. Brugada syndrome exhibits autosomal dominant inheritance with SCN5A, which encodes the cardiac sodium channel, as the only gene with a proven involvement in 20-30% of patients. Its signature feature is ST segment elevation in right precordial ECG leads and predisposition to malignant ventricular tachyarrhythmias. The pathophysiological mechanism of ST elevation and ventricular tachyarrhythmia, two phenomena strongly related, is controversial. Here, we review clinical and experimental studies as they provide evidence to support or disprove the two hypotheses on the mechanism of Brugada syndrome that currently receive the widest support: (1) nonuniform abbreviation of right ventricular epicardial action potentials ("repolarization disorder"), (2) conduction delay in the right ventricular outflow tract ("depolarization disorder"). We also propose a schematic representation of the depolarization disorder hypothesis. Moreover, we review recent evidence to suggest that other derangements may also contribute to the pathophysiology of Brugada syndrome, in particular, right ventricular structural derangements. In reviewing these studies, we conclude that, similar to most diseases, it is likely that Brugada syndrome is not fully explained by one single mechanism. Rather than adhering to the notion that Brugada syndrome is a monofactorial disease, we should aim for clarification of the contribution of various pathophysiological mechanisms in individual Brugada syndrome patients and tailor therapy considering each of these mechanisms.

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“…Ohkubo et al also described TWA in a patient with Brugada syndrome after class 1 antiarrhythmic drug (pilsicainide). TWA persisted for 15 min and was followed by microvolt TWA [19].…”

Section: T-wave Alternans In Patients With Brugada Syndromementioning

confidence: 99%

ICD Electrograms in Patients with Brugada Syndrome

Cismaru¹,

S²,

Gușetu³

et al. 2017

Interpreting Cardiac Electrograms - From Skin to Endocardium

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In patients with Brugada syndrome, implantable cardioverter-defibrillator (ICD) is the only demonstrated treatment that prevents sudden cardiac death. The progress in ICD technology improved the diagnosis and efficacy of implantable devices in the management and treatment of ventricular tachycardia (VT) and ventricular fibrillation (VF). Recording of electrical events just before and after a delivered or aborted ICD therapy permits a more accurate characterization of the rhythm but also provides information on the electrical events preceding the arrhythmia. This chapter aims to gain insight into the mechanism of initiation and termination of spontaneous VF by analyzing intracardiac electrograms (IEGM) in Brugada patients implanted with ICDs. It has two parts:(1) update on ICD electrograms in Brugada syndrome patients, where we review the medical literature on ICD electrograms and their use for detecting electrical manifestations of Brugada syndrome, and (2) examples of ICD electrograms, from our own database of patients affected by Brugada syndrome.

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Intravenous Administration of Class I Antiarrhythmic Drug Induced T Wave Alternans in an Asymptomatic Brugada Syndrome Patient

Cited by 22 publications

References 25 publications

Action Potential Alternans in the Right Ventricular Outflow Tract in a Patient With Asymptomatic Brugada Syndrome

Action Potential Alternans in the Right Ventricular Outflow Tract in a Patient With Asymptomatic Brugada Syndrome

Pathophysiological mechanisms of Brugada syndrome: Depolarization disorder, repolarization disorder, or more?

ICD Electrograms in Patients with Brugada Syndrome

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