Jisho Kojima

Bepridil prevents paroxysmal atrial fibrillation by a class III antiarrhythmic drug effect.

YOSHIDA, T., et al.: Bepridil Prevents Paroxysmal Atrial Fibrillation by a Class III Antiarrhythmic Drug Effect. Background: Bepridil, a multiple ion‐channel blocker, has been reported to prevent paroxysmal atrial fibrillation (PAF). The f‐f interval of PAF during treatment with bepridil versus class Ic antiarrhythmic drugs was compared. Methods: Fifty‐two patients with PAF were randomized to bepridil, 200 mg/day (n = 14) versus flecainide, 100 to 200 mg/day (n = 15) or pilsicainide, 75 to 150 mg/day (n = 23) . The drug was considered effective when symptomatic episodes of PAF were decreased to < 50% during a follow‐up of 2 to 6 months. The f‐f interval was measured in 12‐lead ECGs of initial PAF episodes. Results: Bepridil and Ic were effective in 10 of 14 (71.4%) and 24 of 38 patients (63.2%), respectively (ns). In the Ic group, the f‐f interval was longer in successfully (114 ± 48  ms) than in unsuccessfully (68 ± 25  ms) treated patients (P = 0.002) . In the bepridil group, the f‐f interval was shorter in successfully (84 ± 27  ms) than unsuccessfully (155 ± 68  ms) treated patients (P = 0.015) . When comparing unsuccessfully treated patients, the f‐f interval in the bepridil group was significantly longer than in the Ic group (P = 0.007) . Conclusions: Bepridil was as effective as Ic drugs in the prevention of PAF. Because it was more effective in smaller (functional) than larger (anatomical) reentrant circuits, the effect of bepridil was considered to be mainly attributable to a class III antiarrhythmic action. (PACE 2003; 26[Pt. II]:314–317)

Verapamil Suppresses the Inhomogeneity of Electrical Remodeling in a Canine Long‐Term Rapid Atrial Stimulation Model

Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short‐term atrial pacing, although the effect of a long‐term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmanns bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 ± 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 ± 4 ms in the control group and was larger than that in the verapamil group (31 ± 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (−19 ± 3 vs −5 ± 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged. (PACE 2003; 26:2072–2082)

Measurement of body surface energy leakage of defibrillation shock by an implantable cardioverter defibrillator.

NIWANO, S., et al.: Measurement of Body Surface Energy Leakage of Defibrillation Shock by an Implantable Cardioverter Defibrillator. Leakage of electrical current from the body surface during a defibrillation shock delivery by an ICD device was evaluated in 27 patients with life‐threatening ventricular tachyarrhythmias. All patients underwent the implantation of the Medtronic Jewel Plus ICD system, and the defibrillation shocks were delivered between the active can implanted in the left subclavicular region and the endocardial lead placed in the right ventricle. At the time of measurement of the effect of electrical energy delivery for defibrillation, the shocks were delivered in a biphasic form at the energy level of 20 or 30 J. During each delivery of the defibrillation shock, the electrical current to the body surface was measured through large skin electrodes (6.2 cm2) that were pasted at the following positions: (1) parallel position: the electrodes were placed at the left shoulder and the right low‐chest, and the direction of the electrode vector was parallel to the direction of the defibrillation energy flow, and (2) cross position: the electrodes were placed at the right shoulder and the left low‐chest, and the vector of the electrodes was roughly perpendicular to the direction of the energy flow. The energy leakages were measured in 80 defibrillation shocks. The peak leakage current during the shock delivery at energy of 30 J was 48 ± 26 mA at the parallel position and 19 ± 15 mA at the cross position (P = 0.0002). The energy leakage at a 30‐J shock was 7.4 ± 7.2 mJ at the parallel position and 1.4 ± 2.3 mJ at the cross position (P = 0.0002). The actual maximum energy leakage was 105 mA, 29 mJ, and 106 V that appeared at the parallel position. The body surface leakage of the defibrillation energy of the ICD device was evaluated. The power of the energy leakage strongly depended on the angle between the alignment of the recording electrodes and the direction of the energy flow. The highest current leakage to the body surface reached a considerable level, but the energy leakage was small because of the short duration of the defibrillation shock.