Extensive Preferential Pathway Ablation for the Elimination of Premature Ventricular Contractions Arising from the Right Ventricular Outflow Tract

A 76 y/o women presented with 2 different types of premature ventricular contractions (VPCs 1 and 2) arising from the right ventricular outflow tract (RVOT). Catheter ablation (CA) eliminated PVC1 at the earliest activation site (EAS), but thereafter another PVC morphology (PVC3) appeared. Small potentials preceding the local potential were broadly exhibited from the RVOT’s supero-anterior region to the EAS during PVC3. Point CA targeting such prepotentials failed. Transverse-linear CA with a line connecting sites with such pre-potentials eliminated both PVCs 3 and 2. In cases with broadly spreading preferential pathways, extensive CA might be needed to eliminate the PVCs

Cardiac fibrosis as a determinant of ventricular tachyarrhythmias

Animal and emerging clinical studies have demonstrated that increased ventricular fibrosis in a setting of reduced repolarization reserve promotes early afterdepolarizations (EADs) and triggered activity that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF). Increased ventricular fibrosis plays a key facilitatory role in allowing oxidative and metabolic stress-induced EADs to manifest as triggered activity causing VT/VF. The lack of such an arrhythmogenic effect by the same stressors in normal non-fibrotic hearts highlights the importance of fibrosis in the initiation of VT/VF. These findings suggest that antifibrotic therapy combined with therapy designed to increase ventricular repolarization reserve may act synergistically to reduce the risk of sudden cardiac death

Electrophysiological and anatomical background of the fusion configuration of diastolic and presystolic Purkinje potentials in patients with verapamil-sensitive idiopathic left ventricular tachycardia

Background: It is unclear whether false tendons (FTs) are a substantial part of the reentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT). This study aimed to prove the association between FTs and the slow conduction zone by evaluating the electro-anatomical relationship between the so-called diastolic Purkinje (Pd) potentials and FTs using an electro-anatomical mapping (EAM) system (CARTO). Methods: The 1st protocol evaluated the spatial distribution of Pd and presystolic Purkinje (Pp) potentials in 6 IVLT patients using a conventional CARTO system. In the remaining 2 patients (2nd protocol), the electro-anatomical relationship between the Pd–Pp fusion potential and the septal connection of the FT was evaluated using an EAM system incorporating an intra-cardiac echo (CARTO-Sound). Results: Pd potentials were observed in the posterior–posteroseptal region of the LV and had a slow conduction property, whereas Pp potentials were widely distributed in the interventricular (IV) septum. At the intersection of the 2 regions, which was located in the mid-posteroseptal area, both Pd and Pp potentials were closely spaced and often had a fused configuration. In the latter 2 patients (2nd protocol), it was confirmed that the intra-cardiac points at which the Pd–Pp fusion potential was recorded were located in the vicinity of the attachment site of the FT to the IV septum. In all patients, ILVTs were successfully eliminated by the application of radiofrequency at those points. Conclusion: FTs may at least partly contribute to the formation of the Pd potential, and thus form a critical part of the reentry circuit of ILVT

The role of Purkinje fibers in the emergence of an incessant form of polymorphic ventricular tachycardia or ventricular fibrillation associated with ischemic heart disease

Background: The clinical and electrophysiological characteristic of ventricular premature contractions (VPCs) which trigger the incessant form of polymorphic ventricular tachycardia (VT), so-called “electrical storm” associated with ischemic heart disease, remains unclarified. The aim of this study was to evaluate those matters and the possible role of the Purkinje network in the emergence of an electrical storm. Methods and results: We experienced 5 patients (68 ± 5 years, mean LVEF: 29%) with electrical storms which occurred during the acute phase of an infarction in 3 patients and the remote phase in 2. The triggering VPCs were multifocal in 3 patients and monofocal in the remaining 2. Radiofrequency (RF) catheter ablation was performed for a goal of eliminating the triggering VPCs. A total of 9 different kinds of VPCs differentiated by their morphology were successfully eliminated by the RF deliveries targeting the VPCs’ foci. At the successful ablation sites, Purkinje potentials preceded the QRS onset of the VPC by 67 ± 23 ms, suggesting the VPCs originated in the surviving Purkinje fibers. Moreover, the extensive RF deliveries applied at the surviving Purkinje network rendered the polymorphic VT unable to be induced by programmed stimulation which reproducibly induced it before the ablation in 2 patients. Conclusion: A surviving Purkinje network might contribute not only to the initiation of the repetitive form of lethal ventricular arrhythmias, but also to the perpetuation of the arrhythmias in patients with ischemic heart disease

Nationwide survey of catheter ablation for atrial fibrillation: The Japanese catheter ablation registry of atrial fibrillation (J-CARAF)–A report on periprocedural oral anticoagulants

Background: Catheter ablation has become an established therapy for the treatment of atrial fibrillation (AF). To obtain a perspective on the current status of this therapy in Japan, the Japanese Heart Rhythm Society (JHRS) conducted a nationwide survey, the Japanese Catheter Ablation Registry of Atrial Fibrillation (J-CARAF). In this study, we focused on whether periprocedural use of novel oral anticoagulants (NOACs) was related with excessive thromboembolic or bleeding complications. Methods: Using an online questionnaire, JHRS requested electrophysiology centers in Japan to register the data of patients who underwent AF ablations in September 2011, March 2012, and September 2012. We compared the clinical profiles and ablation data, including the incidence of complications among patients in whom warfarin, a NOAC or neither was used as a periprocedural anticoagulant. Results: A total of 179 centers submitted data relating to 3373 patients (62.2±10.6 years). Paroxysmal atrial fibrillation (PAF) was observed in 64.4% of patients. Warfarin, as a periprocedural oral anticoagulant, was used by 53.6% (1808/3373) of patients. A NOAC was given to 541 subjects (dabigatran: 504 [16.1%], rivaroxaban: 37 [1.1%]). In the remaining 1024 patients (30.4%), no periprocedural oral anticoagulants (OACs) were used. The proportion of PAF in warfarin-treated patients (61.1%) was significantly lower than that in NOAC-treated patients (70.1%, p<0.01) or in patients not treated with an OAC (67.4%, p<0.01). Patients treated with uninterrupted warfarin therapy were associated with significantly higher CHA2DS2-VASc scores. A total of 158 complications occurred in 151 subjects (4.5%). The incidence of complications in NOAC-treated patients (14/541 [2.6%]) was lower than that in patients receiving uninterrupted warfarin therapy (4.8%, p<0.05). The incidence of pericardial effusion in NOAC-treated patients (0.7%) was lower than in warfarin-treated patients (2.6%, p<0.05). The difference in the periprocedural anticoagulant strategy was not related to the frequency of other bleeding events. Cerebral infarction occurred in one patient from each patient group. Conclusions: Our results suggest that NOACs are safe for use as substitutes for warfarin without causing excessive increases in the rates of thromboembolic or bleeding complications