Hiroshi Furushima

Unsuccessful internal defibrillation in Brugada syndrome: focus on refractoriness and ventricular fibrillation cycle length.

Introduction: In patients with Brugada syndrome, implantable cardioverter defibrillator (ICD) is the only reliable treatment to prevent sudden death though, in some cases, internal defibrillation may be unsuccessful. The aim of this study was to examine the determinants of defibrillation failure, with a focus on electrophysiologic characteristics.

Incidence and Initial Characteristics of Pilsicainide-Induced Ventricular Arrhythmias in Patients With Brugada Syndrome

Background: In patients with Brugada syndrome, class I antiarrhythmic drugs can trigger ventricular arrhythmias (VA). The incidence and initial characteristics of VA that developed after pilsicainide was examined in 28 patients with Brugada‐type electrocardiographic (ECG) abnormalities and with a positive response in the pilsicainide test. The clinical outcome was also compared between patients with and without pilsicainide‐induced VA.

Arrhythmogenesis of T wave alternans associated with surface QRS complex alternans and the role of ventricular prematurity: observations from a canine model of LQT3 syndrome.

Intramural TWA and Its Arrhythmogenesis. Introduction: T wave alternans (TWA) is characterized by cycle‐to‐cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin‐A model of long QT syndrome.

Ventricular Fibrillation and Ventricular Tachycardia Triggered by Late‐Coupled Ventricular Extrasystoles in a Brugada Syndrome Patient

Premature ventricular complexes (PVC) falling after the end of the T wave triggered ventricular fibrillation (VF) at night and monomorphic ventricular tachycardia (MVT) during daytime, in a recipient of implantable cardioverter defibrillator with Brugada syndrome. Treatment with bepridil (1) decreased the height of ST segment elevation in leads V1‐V3, (2) completely eliminated VF, and (3) markedly decreased the incidence of PVC and MVT. Albeit rare, VF can be triggered by late‐coupled PVC, due to a mechanism other than phase 2 reentry in some patients with Brugada syndrome. (PACE 2011; e1–e5)

Pilsicainide-Induced ST Segment Elevation and ST Segment Depression in Two Patients with Variant Forms of Brugada-Type Electrocardiographic Abnormalities

In two patients with variant forms of Brugada electrocardiographic abnormalities, ST segment elevation, and reciprocal ST segment depression developed during intravenous administration of pilsicainide. In one patient, pilsicainide accentuated the ST segment elevation in leads I, aVL, and V1–V3 and caused ST segment depression in leads II, III, and aVF. Coronary angiograms at the time of ST segment elevation were normal. In the other patient, pilsicainide accentuated the coved‐type ST segment elevation in leads II, III, and aVF and caused ST segment depression in leads I, aVL, and V2–V5. Frequent premature ventricular complexes (PVCs) with two different left bundle branch block patterns developed during ST segment elevation. Intravenous isoproterenol returned the ST segment to baseline in both patients and suppressed the PVCs in the second patient. We hypothesize that a wide area of epicardial myocardium with large Ito current might explain the reciprocal ST segment depression observed at the time of accentuated ST segment elevation.

Multiple premature beats triggered ventricular arrhythmias during pilsicainide infusion in a patient with inferior ST-segment elevation.

A 17‐year‐old man was referred to our hospital for treatment of common paroxysmal atrial flutter. His electrocardiogram at rest showed subtle ST‐segment elevation in leads II, III, and aVF. Intravenous pilsicainide caused further ST‐segment elevation in the inferior leads, new ST‐segment depression in leads V2–V6, two distinct forms of premature ventricular complexes (PVCs) triggering short runs of polymorphic ventricular tachycardia (VT). An infusion of isoproterenol suppressed these arrhythmias and normalized the ST‐segment. Pilsicainide may induce PVCs and polymorphic VT in atypical Brugada syndrome.

Suppression of Storms of Ventricular Tachycardia by Epicardial Ablation of Isolated Delayed Potential in Noncompaction Cardiomyopathy.

A 65‐year‐old recipient of an implantable cardioverter defibrillator suffering from ventricular noncompaction developed storms of ventricular tachycardia (VT). Epicardial voltage mapping revealed the presence of a large low‐voltage area in the left ventricular apical and inferoposterior wall, and isolated delayed potential was recorded over 1.5 cm in the posterior border between low and normal myocardial voltage. Pacemapping at the delayed potential recording site produced two different QRS depending on pacing output strength, and these two QRS morphologies were similar to clinically documented VTs. During one of the VTs, a mid‐diastolic potential was recorded from the site with the delayed potential, and rapid pacing produced concealed entrainment. After epicardial radiofrequency ablation of the isolated delayed potential, VTs were noninducible and the VT storm was suppressed.

Ventricular Fibrillation Triggered during and after Radiofrequency Energy Delivery to the Site of Origin of Idiopathic Right Ventricular Outflow Tract Arrhythmia

We observed a case of idiopathic ventricular arrhythmias originating from the right ventricular outflow tract (RVOT). The origin of target premature ventricular contraction (PVC) and nonsustained ventricular tachycardia (VT) was within a wide low‐voltage area around the RVOT. During radiofrequency (RF) application to the site of arrhythmia origin, polymorphic VT and ventricular fibrillation were repeatedly triggered by new PVC that had developed near the site of ablation. This electrical storm persisted >30 minutes after cessation of RF current delivery, and was suppressed by additional RF applications to the site of origin of the new PVC.

Effects of Bepridil Versus E-4031 on Transmural Ventricular Repolarization and Inducibility of Ventricular Tachyarrhythmias in the Dog

Background: Bepridil (a multiple channel blocker) may markedly prolong the QT interval and induce polymorphic ventricular tachyarrhythmias (VTA). We compared the transmural ventricular repolarization characteristics and inducibility of polymorphic VTA after administration of bepridil versus the pure IKr blocker, E‐4031, each administered to five open‐chest dogs.

Early Repolarization and Its Modification by Preexcitation in Two Patients with Intermittent Wolff‐Parkinson‐White Syndrome

We report two cases of intermittent Wolff‐Parkinson‐White (WPW) syndrome. In one patient, early repolarization (ER) was masked during preexcitation whereas in the other, J wave‐like notches were observed in the right precordial leads only during preexcitation. The clinical significance of ER is not apparent in WPW syndrome but some possible mechanisms are discussed.