[Diagnosis of and therapy for arrhythmia (discussion)].
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Biomedical subjects
Publications and source records attributed to Yuji Nakazato.
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BACKGROUND: Bepridil hydrochloride (Bpd) has attracted attention as an effective drug for atrial fibrillation (AF) and atrial flutter (AFL). However, serious adverse effects, including torsade de pointes (Tdp), have been reported. METHODS AND RESULTS: Adverse effects of Bpd requiring discontinuation of treatment were evaluated. Bpd was administered to 459 patients (361 males, 63+/-12 years old) comprising 378 AF and 81 AFL cases. Mean left ventricular ejection fraction and atrial dimension (LAD) were 66+/-11% and 40+/-6 mm, respectively. Adverse effects were observed in 19 patients (4%) during an average follow-up of 20 months. There was marked QT prolongation greater than 0.55 s in 13 patients, bradycardia less than 40 beats/min in 6 patients, dizziness and general fatigue in 1 patient each. In 4 of 13 patients with QT prolongation, Tdp occurred. The major triggering factors of Tdp were hypokalemia and sudden decrease in heart rate. There were no differences in the clinical backgrounds of the patients with and without Tdp other than LAD and age, which were larger and older in the patients with Tdp. CONCLUSION: Careful observation of serum potassium concentration and the ECG should always be done during Bpd administration, particularly in elderly patients.
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BACKGROUND: Bepridil has multiple ion-channel blocking effects similar to amiodarone and is expected to have anti-arrhythmic effects that are useful for the management of atrial fibrillation (AF). The aim of this study was to clarify the conversion of persistent AF and maintenance of sinus rhythm (SR) by oral bepridil. METHODS AND RESULTS: Oral bepridil was administered to 112 patients (83 males, 29 females; age: 59.0+/-10.8 years) with persistent AF lasting an average of 5 months. The conversion effects and maintenance of SR after pharmacological or direct current (DC) cardioversion, as well as the incidence of adverse complications, were evaluated. In 65 of 112 (58%) patients, SR was restored within 6 months (average: 2.1 months) following bepridil administration. DC cardioversion was carried out for 21 of the remaining 47 patients with unsuccessful pharmacological conversion, and all had restoration of SR. Eventually, of the 86 patients in total who were restored to SR by either bepridil or DC cardioversion, 70 (81%) patients maintained SR after a mean follow-up of 18 months. No serious adverse complications were observed, except for marked QT prolongation in 2 cases. CONCLUSION: Bepridil showed favorable conversion effects in patients with persistent AF and was highly effective for maintaining SR after pharmacological or electrical cardioversion. However, careful follow-up is necessary for the prevention of torsade de pointes caused by QT prolongation.
BACKGROUND: A genetic correlation between Brugada syndrome (BS) and sinus node dysfunction (SND) has been proposed, although the clinical and electrophysiologic characteristics of this concomitant condition are unknown. METHODS AND RESULTS: The study comprised 5 patients with symptomatic BS (4 with spontaneous episodes of ventricular fibrillation (VF) and 1 with syncope) of whom 3 had a documented sinus pause > 3 s (a 42- and 62-year-old man, and a 49-year-old woman). Only 1 of them had a family history of sudden death; 2 of them had also had an episode of atrial fibrillation or flutter. Electrophysiologic study demonstrated prolonged sinus node recovery time in 2 patients (2.6 s and > 5 s), in whom a cardiac pacemaker had been implanted before the diagnosis of BS was made after episodes of VF. Finally, all 3 patients received an implantable cardioverter defibrillator, including 2 upgrades from pacemaker. CONCLUSIONS: SND is not a rare concomitant disorder in BS and there is a possible genetic connection.
A 14-year-old boy was admitted for the evaluation of recurrent syncope. His ECG on admission revealed a sinus rhythm with an undetermined QRS axis, T wave inversion at leads V3, V4 and abnormal q at leads I, aVL, V5 and V6. However, no underlying disease could be detected by any morphological examination. Programmed ventricular stimulation also induced no ventricular tachycardia or fibrillation (VF). Only signal-averaged ECG showed ventricular late potential and the cause of syncope was not clarified. As his brother with a similar ECG had died suddenly, he was prophylactically treated with an ICD. However, 14 months later he died suddenly after playing a video game. The ICD recorded VF, which was not converted despite 6 cardioversion attempts by the ICD. Progression of myocardial damages and/or elevation of defibrillation threshold may have been the cause of unsuccessful cardioversion.
A 28-year-old man developed severe infundibular pulmonary stenosis (PS), coronary artery stenosis with sustained ventricular tachycardia (VT) 24 years after mediastinal irradiation (total amount of 40 Gray) for non-Hodgkin's lymphoma. Repair of right ventricular outflow tract and coronary artery bypass graft procedure were performed. Infundibular PS was successfully relieved after operation and VT was also controlled by medication. Mediastinal irradiation often causes various cardiac complications after a latent period. Therefore, continuous careful observation is mandatory in patients with the history of mediastinal irradiation.
Ca(+) waves have been implicated in Ca(2+) overload-induced cardiac arrhythmias. To deepen understanding of the behavior of Ca(2+) waves in a multicellular system, consecutive two-dimensional Ca(2+) images were obtained with a confocal microscope from surface cells of guinea pig ventricular papillary muscles loaded with fluo 3 or rhod 2. In intact muscles, no Ca(2+) waves were detected under the resting condition, whereas they were frequently observed during the rest immediately after high-frequency stimulations where cytoplasmic Ca(2+) concentration and Ca(2+) stored in the sarcoplasmic reticulum (SR) were gradually decreasing. The intervals of Ca(2+) waves increased as they occurred later, their amplitudes and velocities remaining unchanged. A SERCA inhibitor reversibly prolonged the wave intervals. In Na(+)-free/Ca(2+)-free medium where neither Ca(2+) influx nor Na(+)/Ca(2+) exchange took place, recurrent Ca(2+) waves emerged at constant intervals in each cell. These results are consistent with the conclusion that the loading level of the SR is critical for induction of Ca(2+) waves. Each cell independently exhibited its own regular rhythm of Ca(2+) wave with a distinct interval. These waves propagated in either direction along the longitudinal axis within a muscle cell, but seldom beyond the cell boundary. In contrast, in partially damaged muscles that showed spontaneous Ca(2+) waves at rest in normal Krebs solution, their propagation often was unidirectional, decreasing in frequency. In these cases, however, Ca(2+) waves rarely moved beyond the cellular boundary. The gradient of the cytoplasmic Ca(2+) concentration was suggested to be the cause of the one-way propagation.
A 49-year-old woman experienced syncope 10 months after DDD pacemaker implantation for sick sinus syndrome. ECG revealed abnormal ST elevation in leads V1 to V3 during a paced rhythm. Multifocal premature ventricular contractions followed by ventricular fibrillation were documented. Saddleback-type ST elevation was confirmed after a mode change to AAI. The diagnosis of Brugada syndrome was made, and the DDD pacemaker was upgraded to an implantable cardioverter defibrillator. Brugada syndrome can be easily overlooked if the classic ECG findings are not initially noted but may be observed even during pacing therapy.
Dislodgment of an atrial screw-in pacing lead is quite rare. This report describes a rare case of an atrial screw-in lead dislodgment 10 years after implantation. Although it is an uncommon complication, very late dislodgment can occur postoperatively, and careful follow-up is necessary.
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Isoproterenol is widely used as a provocative medium for vasovagal responses during tilt testing. Dose of isoproterenol infusion is generally titrated empirically by increase in resting heart rate before tilt up. To determine the optimal increase in resting heart rate with isoproterenol for tilt-induced vasovagal responses, we studied 97 consecutive patients with unexplained syncope. After the end of a negative baseline tilt (80 degrees for 30 min), the isoproterenol tilt was performed using one of two protocols: two-stage isoproterenol-tilt protocol, with doses of 0.01 and 0.02 microg/kg per min for 10 min each, or one-stage isoproterenol-tilt protocol, with a dose of 1 or 2 microg/min for 10 min. The resting heart rate increase was defined as a percentage increase in the resting heart rate after isoproterenol infusion, compared to the baseline heart rate before the tilt test. In 117 tilt procedures, 28 (93%) of the 30 positive responses occurred with a resting heart rate increase of > or = 21%. With the resting heart rate increase of 60 and 100%, 18 (60%) and 27 (90%) positive responses were observed, respectively. In conclusion, the minimum resting heart rate increase of > or = 21% was required to provoke a vasovagal response during subsequent isoproterenol-tilt (80 degrees for 10 min). Preferably, heart rate should be increased to 60-100% by isoproterenol titration before tilting.
A 70-year-old Japanese woman was admitted to our hospital because of transient second degree atrioventricular (AV) block. An electrophysiologic study (EPS) was performed, and Mobitz type II infra-Hisian block during atrial pacing at a rate of 130/min was noted. An AV nodal reentrant tachycardia (AVNRT) was induced by ventricular pacing at a rate of 180/min, and 2:1-3:1 infra-Hisian block during AVNRT was observed. The AV block and AVNRT rarely occurred in the clinical setting, and the patient did not complain of any symptoms related to these arrhythmias. Therefore, the patient refused permanent pacemaker implantation, although she continued to be followed in our outpatient clinic. However, the patient was re-admitted one year later because of palpitations and dyspnea upon exertion related to the AV block. The 12-lead ECG showed high degree AV block with narrow QRS complexes. The patient underwent pacemaker implantation during the subsequent hospitalization, and her symptoms improved postoperation. AV block during AVNRT is sometimes observed, and it has been considered as a functional AV block. In the present case, a pathologic conduction disturbance in the His-Purkinje system caused the high degree AV block during AVNRT. The high degree AV block during AVNRT may indicate the existence of a conduction disturbance in the His-Purkinje system in some of these types of cases.
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