Pulmonary vein isolation is the electrophysiological endpoint of complete conduction block at the level of the veno-atrial junction and must be explicitly distinguished from encircling PV ablation which frequently does not result in isolation.
The prerequisites for successful PV isolation include a knowledge of the individual anatomy of the PVs and the left atrium, appropriate positioning of circular mapping catheters, and a knowledge of the electrophysiology of PV activation, in addition to effective ablation tools. Excessive ablation, and possibly complications, can be avoided by the recognition of non-PV myocardial contributions to electrograms recorded from within the PVs. The posterior wall of the left atrial appendage contributes far-field electrograms to recordings from all or nearly all left superior PVs, the low anterior left atrium to 80% of left inferior PV recordings and the superior vena cava to 23% of right superior PV recordings. Recognition of these far-field components is feasible and accurate in sinus rhythm as well as during ongoing atrial fibrillation. Finally, the creation of temporally stable PV isolation remains a currently unsolved problem although prolonged post isolation surveillance, may be helpful.

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Arrhythmogenic right venticular dysplasia/cardiomyopathy (ARVD/C) is an inherited cardiomyopathy with a very low penetrance affecting the right ventricle (RV) and presenting palpitation and syncope due to ventricular tachycardia (VT) originating from RV. The VT can degenerate into ventricular fibrillation and sudden cardiac death. The genetic background of ARVD/C has recently been found to be heterogeneous, mainly resulting from cell adhesion abnormalities due to mutations in five different genes encoding members of the desmosome complex. In Asian countries, however, the genetic aspect of the disease has not been fully studied, although the clinical features of Asian ARVD/C patients are different from those in Western countries in the penetrance of phenotypes, relation to Brugada syndrome and link to RV outflow tract ventricular tachycardia. It is of urgent need to have a registry of Asian ARVD/C patients and to conduct a more detailed genetic survey on the candidate genes, including desomosomal ones.

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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.

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Adenosine-sensitive reentrant atrial tachycardia (AT) has been recognized to originate from the confined area of either the right or left atiroventricular nodal regions. We describe a case with adenosine-sensitive focal AT which was successfully ablated at the uncommon focus located at the mitral annulus-aorta junction. The mode of AT initiation during the atrial extrastimulus suggested as the mechanism tachycardia reentry; AT was terminated by a bolus of 2 mg of adenosine 5′-triphosphate. These electrophysiological features are possibly associated with a substrate involved in the mitral annulus-aorta junction with node-like properties that is responsive to adenosine.

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Here we report a case of a 16-year old female with symptomatic nonsustained atrial tachycardia (NSAT) originating from the septal mitral annulus. NSAT was induced by atrial burst pacing after an intravenous isoproterenol (ISP) injection. The array mode of the noncontact mapping system (NCM) allowed us to quickly identify the tachycardia focus at the septal mitral annulus, where the contact bipolar voltage map revealed no low voltage area (<0.5 mV). The NSAT was eliminated by a radiofrequency energy application to the identified tachycardia focus during sinus rhythm, and the patient has been free from any symptoms during 10 months of follow-up.

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We have experienced two patients with the Brugada-type electrocardiographic abnormalities and incessant wide QRS tachycardia (presumed ventricular tachycardia) induced by intoxication of a class IC antiarrhythmic drug pilsicainide. They were elderly men with impaired renal function. Plasma concentration of pilsicainide was elevated to a toxic level in both patients. After cessation of pilsicainide, incessant wide QRS tachycardia spontaneously subsided and intraventricular conduction delay with coved type ST segment elevation in V1 and V2 disappeared. In the elderly or patients with renal dysfunction, we should be very careful regarding dose adjustment of pilsicainide or it may be better to avoid using this drug.

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A 67-year-old male with dilated cardiomyopathy and chronic renal failure who received chronic hemodialysis for 9 years admitted with pulmonary edema. Three days after admission, electrocardiogram showed transient prolongation of QT interval which was followed by macroscopic T wave alternans (TWA) and ventricular fibrillation (VF). Temporary pacing from right ventricular apex suppressed TWA and VF effectively. Combined cardiac resynchronization therapy and implantable cardioverter defibrillator device was implanted for the secondary prevention of VF. Both prolongation of QT interval and TWA disappeared for 10 days after therapy and no arrhythmic event occurred since then.

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