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arious factors have been suggested for altering the energy requirements for ventricular defibrillation in animals and humans, including underlying heart disease, changes in autonomic tone, acid -base and electrolyte imbalances, and various antiarrhythmic agents. [1][2][3][4][5][6][7] With regard to the effects of antiarrhythmic drugs on the defibrillation threshold (DFT), studies have shown that drugs which prolong the cardiac repolarization, but do not affect the conduction velocity, lower the DFT. Nifekalant hydrochloride is a pure class III antiarrhythmic drug that inhibits the rapid component of the delayed rectifier potassium current, transient outward potassium current, and inward rectifier potassium current without affecting the inward sodium current, inward calcium current, or -adrenergic activity. 8,9 A previous report demonstrated that nifekalant significantly decreased the DFT of ventricular fibrillation in canine hearts, 10 so the aim of this study was to determine whether short-term intravenous administration of nifekalant would alter the DFT in humans with paroxysmal and persistent atrial fibrillation (AF). Methods Study PopulationBetween 2003 and 2005, we enrolled a total of 42 patients with persistent and paroxysmal AF lasting longer than 24 h, and which was refractory not only to antiarrhythmic drugs, but also to external cardioversion, and who had subsequently underwent internal catheter cardioversion with and without the concomitant administration of nifekalant. The research protocol was approved by the institutional ethics committee. Patients were excluded if they were less than 18 years old, had a corrected QT interval >450 ms or QRS duration >140 ms, had third-degree atrioventricular block or a serum potassium level <3.5 mmol/L. Written informed consent was given by all patients prior to cardioversion and nifekalant administration. The average duration of paroxysmal AF was 46.8±8.2 h (ranging from 35.8 to 49.5 h). All patients were refractory to direct current cardioversion in the control state, and necessitated further therapeutic interventions, such as administration of nifekalant, in order to restore sinus rhythm (SR). Defibrillation ProcedureThe patients were placed under general anesthesia, which was maintained with ultra-rapid barbiturates. Under fluoroscopic guidance, 2 multipolar electrode catheters were introduced from the right femoral vein and positioned at the lateral wall of the right atrium and inserted into the coronary sinus (Fig 1). The internal leads were connected to a battery-operated external cardioverter-defibrillator (DVX, Tokyo, Japan) that could be preset to deliver a variable amount of energy from 5 to 100 joules in 5 J increments. The defibrillating pulse was in the form of a truncated exponen- Clinical Study of the Acute Effects of Intravenous Nifekalant on the Defibrillation Threshold in Patients With Persistent and Paroxysmal Atrial FibrillationKaoru Okishige, MD; Hiroki Uehara, MD; Naoto Miyagi, MD; Kentarou Nakamura, MD; Kouji Azegami, MD; Hirofumi Wakimoto,...

n general, ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is not associated with organic heart disease. The origin of RVOT tachycardia is almost in the anterior septum of the right ventricle. 1,2 The mechanism is mainly due to triggered activity and it is rare for there to be a reentry. A case of 2 types of reentrant VT originating from RVOT induced by electrophysiological study (EPS) in a patient with mitral regurgitation, atrial fibrillation with complete atrioventricular block and pacemaker implantation is reported. The exit of the VT reentry circuit and slow conduction zone were examined using an entrainment mapping technique and a pace mapping technique. Case ReportA 72-year-old woman with a history of mitral regurgitaCirculation Journal Vol.72, May 2008 tion, hypertension, atrial fibrillation, complete atrioventricular block and pacemaker implantation was admitted to hospital for treatment of symptomatic VT, which was recorded by Holter electrocardiogram (ECG) monitoring, and complaining of edema in the legs and dyspnea. An ECG recorded during atrial fibrillation showed a right ventricular (RV) pacing rhythm of 80 beats/min, and a chest X-ray revealed cardiac enlargement (59.9%) with slight lung congestion. Echocardiography revealed the following: decreased left ventricular (LV) wall motion, especially in the anterior septum; LV diastole/systole of 50/43 mm; ejection fraction of 36%; aorta/left atrial size of 29/55 mm; ventricular septum/posterior wall of 12/11 mm; and mitral and tricuspid regurgitation levels of IV and II, respectively (27.5 mmHg).Coronary angiography (CAG) revealed no significant stenosis. Symptoms were improved with diuretics and PDE III inhibitors after admission. A monitoring ECG recorded VT that lasted for 1 min, and this was considered to be the contributing cause of palpitation. EPS and Radiofrequency Catheter Ablation: First SessionAfter written informed consent was obtained from the patient and her family to undertake all procedures associated with this study, a standard EPS, endocardial catheter mapping and radiofrequency catheter ablation were performed. Electrode catheters were inserted percutaneously into the femoral vein and positioned in the RV apex, outflow and His bundle position. Ventricular mapping and radiofrequen- A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was desig...

We definitively demonstrated involvement of the ASOV in OT reentrant tachycardia using entrainment mapping. It may be useful for successful VT ablation to identify reentry circuit localization.

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