Electrical Storm in Idiopathic Ventricular Fibrillation Is Associated With Early Repolarization

ObjectivesThis study sought to characterize patients with idiopathic ventricular fibrillation (IVF) who develop electrical storms.BackgroundSome IVF patients develop ventricular fibrillation (VF) storms, but the characteristics of these patients are poorly known.MethodsNinety-one IVF patients (86% male) were selected after the exclusion of structural heart diseases, primary electrical diseases, and coronary spasm. Electrocardiogram features were compared between the patients with and without electrical storms. A VF storm was defined as VF occurring ≥3 times in 24 h and J waves >0.1 mV above the isoelectric line in contiguous leads.ResultsFourteen (15.4%) patients had VF storms occurring out-of-hospital at night or in the early morning. J waves were more closely associated with VF storms compared to patients without VF storms: 92.9% versus 36.4% (p < 0.0001). VF storms were controlled by intravenous isoproterenol, which attenuated the J-wave amplitude. After the subsidence of VF storms, the J waves decreased to the nondiagnostic level during the entire follow-up period. Implantable cardioverter-defibrillator therapy was administered to all patients during follow-up. Quinidine therapy was limited, but the patients on disopyramide (n = 3), bepridil (n = 1), or isoprenaline (n = 1) were free from VF recurrence, while VF recurred in 5 of the 9 patients who were not given antiarrhythmic drugs.ConclusionsThe VF storms in the IVF patients were highly associated with J waves that showed augmentation prior to the VF onset. Isoproterenol was effective in controlling VF and attenuated the J waves, which diminished to below the diagnostic level during follow-up. VF recurred in patients followed up without antiarrhythmic agents

Radiofrequency catheter ablation of macroreentrant ventricular tachycardia after corrective surgery for tetralogy of Fallot

Ventricular tachycardia (VT) may occur in patients after corrective surgery for tetralogy of Fallot (ToF), and this can be a cause of sudden cardiac death. Macroreentrant VT is a unique mechanism in these patients, although other mechanisms are involved in VT development. Owing to advances in electrophysiological knowledge and medical technology, macroreentrant VT after corrective surgery for ToF can be treated by catheter ablation. In the macroreentrant circuit of VT, several critical isthmuses (types 1–4) could be included, and these are supported by anatomical obstacles and operative interventions in the right ventricle. Linear radiofrequency (RF) application through the critical isthmus can terminate and prevent the recurrence of macroreentrant VT. Among the critical isthmuses, the type 1 isthmus (between the right ventricular outflow scar and tricuspid annulus) is the most common, but compared with the other types of isthmuses, it is longer so and has a thicker myocardium. Therefore, higher-energy RF application using irrigation and/or large-tip ablation catheters is usually required to complete the linear conduction block. Since other isthmuses may simultaneously work as critical components of the macroreentrant circuit, detailed mapping is encouraged before starting RF application in the type 1 isthmus. Since long-term evidence of the effectiveness of catheter ablation for VT in patients after ToF repair is limited, hybrid treatment with implantable cardioverter defibrillators (ICDs) would be a reasonable strategy for secondary prevention of cardiac events, such as that in patients with other underlying heart diseases. Indications of electrophysiological study, catheter ablation, and/or ICD therapy for primary prevention of sudden cardiac death should be further examined in high-risk patients after ToF repair

Triggers of ventricular tachyarrhythmias and therapeutic effects of nicorandil in canine models of LQT2 and LQT3 syndromes

AbstractObjectivesWe sought to identify the triggers of ventricular tachyarrhythmia (VTA) in experimental models of long QT type 2 (LQT2) and long QT type 3 (LQT3) syndromes.BackgroundMost adverse cardiac events occurring in the long QT type 1 syndrome are related to sympathetic nerve activity. In contrast, various factors may trigger VTA in patients with LQT2 and LQT3.MethodsThe mode of onset of VTA and therapeutic effects of the potassium-adenosine triphosphate channel opener nicorandil were compared in canine models of LQT2 and LQT3, using three induction protocols: 1) bradycardia produced by atrioventricular block (BRADY); 2) programmed ventricular stimulation; and 3) electrical stimulation of the left stellate ganglion (left stellate stimulation [LSS]). Transmural unipolar electrograms were recorded, and the activation-recovery interval (ARI) was measured.ResultsVentricular tachyarrhythmias developed during BRADY in all six experiments in the LQT3 model, but in none of the six experiments in LQT2. Programmed ventricular stimulation induced VTA in two experiments of the LQT2 model, but in none of the LQT3 experiments. Stimulation of the left stellate ganglion induced VTA in three experiments in LQT2 and in two experiments in LQT3. Nicorandil caused greater shortening of ARI and greater attenuation of transmural ARI dispersion in the LQT2 model than in the LQT3 model. After treatment with nicorandil, a single VTA was induced in the LQT2 model by LSS, whereas in the LQT3 model, VTA remained inducible by BRADY in four experiments and LSS in one experiment.ConclusionsAn abrupt increase in sympathetic activity appeared arrhythmogenic in both models. Nicorandil attenuated the heterogeneity of ventricular repolarization and suppressed the induction of VTA in the LQT2 model, but had a limited therapeutic effect in the LQT3 model

Concomitant abnormalities in Brugada syndrome

Brugada syndrome (BS) is characterized by ST-segment elevation in the right precordial leads and is associated with sudden cardiac death secondary to polymorphic ventricular tachycardia (PVT)/ventricular fibrillation (VF) in the absence of structural heart disease. Vasospastic angina (VSA) and neurally mediated syncope (NMS) are observed occasionally in BS patients, although their associations with BS remain controversial. The incidence of concomitant VSA and BS is 11–13%, and there might be an increased risk of VF when BS and VSA coexist, as reported in several previous studies. Whether the manifestation or augmentation of a coved-type electrocardiography (ECG) pattern is associated with coronary artery vasospasm is unclear. The significance of increased coved-type ST-segment elevation and its relation to arrhythmogenesis in BS is an important issue that needs to be resolved in future studies of concomitant BS and VSA. The coexistence of BS and VSA should always be taken into account in the management of both conditions, particularly when calcium antagonists are used. Previous reports suggest a high incidence of NMS in BS patients, and it is often difficult to differentiate between NMS and high-risk syncopal episodes due to ventricular tachyarrhythmias. Therefore, the identification of a therapeutic strategy to treat syncope in BS patients is often problematic. The autonomic nervous system is involved in arrhythmogenesis and may precipitate cardiac events in BS patients. To investigate BS, it may be useful to consider VSA and NMS as concomitant abnormalities. Future studies are needed to understand the relationship between BS and the autonomic nervous system