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Biomedical subjects

A Fujiki

Publications and source records attributed to A Fujiki.

At least 37 records · Page 2Linked to original sources
PubMed1997

Electrophysiologic effects of SD-3212, a new class I antiarrhythmic drug, on canine atrial flutter and atrial action-potential characteristics.

SD-3212 (levo-semotiadil fumarate) is a newly developed compound that exhibits potent antiarrhythmic activity because of its inhibitory action on sodium and calcium channels. In animal models, SD-3212 suppressed ventricular tachyarrhythmias, but the effects of this drug on atrial tachyarrhythmias have not been reported. We investigated the electrophysiologic effects of SD-3212 on canine atrial flutter induced after placement of the intercaval obstacle and on atrial action-potential characteristics. In all seven dogs, SD-3212 (1.9 +/- 0.3 mg/kg) terminated atrial flutter after significant increase in atrial flutter cycle length from 126 +/- 5 to 166 +/- 14 ms (increase, 31 +/- 8%; p < 0.005). SD-3212 increased right atrial effective refractory period (RAERP) significantly from 126 +/- 7 to 149 +/- 11 ms at a basic cycle length of 300 ms. The increases in RAERP after SD-3212 at basic cycle lengths of 300, 200, and 150 ms did not differ (increase, 18 +/- 4%, 17 +/- 3%, and 19 +/- 3%, respectively). Interatrial conduction time (IACT) was prolonged after SD-3212 from 63 +/- 4 to 81 +/- 6 ms (increase, 31 +/- 6%) at a basic cycle length of 150 ms. Prolongation of IACT was frequency dependent. The plasma concentration of SD-3212 after the termination of atrial flutter was 187 +/- 56 ng/ml in four dogs tested. In vitro study by using standard microelectrode techniques showed SD-3212 at concentrations of 1-3 microM significantly prolonged action-potential duration at 90% repolarization. Vmax was decreased by SD-3212 in a concentration-dependent manner (0.3-3 microM), and the inhibitory effect on Vmax was greatest at the highest stimulation frequency of 3.3 Hz. These results indicate that a new antiarrhythmic drug, SD-3212, is effective in interrupting canine atrial flutter, possibly by suppressing atrial conduction, and might be effective for the treatment of clinical atrial tachyarrhythmias.

Action Potentials↗
PubMed1997

Role of sympathovagal balance in the initiation of idiopathic ventricular tachycardia originating from right ventricular outflow tract.

VT originating from the right ventricular outflow tract (RVOT) is prone to occur when sympathetic nervous activity is increased. beta-Blockade is, therefore, effective in suppressing this VT. The purpose of this study was to determine the role of sympathovagal balance assessed by heart rate variability (HRV) in the spontaneous initiation of repetitive premature ventricular contractions (PVCs) and VT (five or more consecutive PVCs) arising from RVOT in seven patients without structural heart diseases. Frequency-domain measures of HRV were determined by analyzing 24-hour Holter electrocardiographic recording with the maximum entropy method over a 1,280-second period immediately before the onset of 35 single PVCs, 26 episodes of 2-4 consecutive PVCs, and 21 episodes of VT. High frequency component (HF: 0.15-0.40 Hz) was used as an index of parasympathetic activity, and the ratio of low frequency component (LF: 0.04-0.15 Hz) to HF (LF/HF ratio), as an index of sympathovagal balance. NN50(%), a time-domain variable of parasympathetic activity, was also determined. Mean RR interval and any measures of HRV did not change significantly before single PVCs. Mean RR interval shortened and HF decreased prior to repetitive PVCs and VT. The LF/HF ratio, however, increased only before the onset of VT. NN50(%) tended to decrease before repetitive PVCs and decreased significantly before VT. With propranolol (30-60 mg/day), frequency of repetitive PVCs was suppressed from 2,048 +/- 1,201 to 746 +/- 658/day and VT was totally abolished, but frequency of single PVCs did not change significantly. In conclusion, sympathetic predominance plays an important role in the initiation of repetitive PVCs and VT originating from RVOT in patients without structural heart diseases.

Adolescent↗
PubMed1997

Essential pathway of reentry in the canine model of atrial flutter. Analysis using radiofrequency ablation.

In humans, the isthmus in the low right atrium between the tricuspid annulus and the inferior vena cava or the coronary sinus ostium is a well-established target of catheter ablation of common atrial flutter. In the canine model of atrial flutter with a Y-shaped incision, the tricuspid annulus was thought to constitute the essential reentrant pathway. The present study was designed to determine whether the supravalvular tissue around the tricuspid annulus is essential to atrial flutter in the canine model with an intercaval obstacle on the basis of the results of radiofrequency ablation. Epicardial approach of radiofrequency ablation was tested in 4 groups of dogs. Group A (5 dogs): Single application of radiofrequency energy (20 W) for 5 sec to the mid right atrial free wall. Group B (9 dogs): One to two applications to the tricuspid annulus. A ligature was also placed encircling the tricuspid annulus from the supravalvular atrial tissue to the subvalvular ventricular tissue. Group C (9 dogs): Linear transverse applications to the mid right atrial free wall between the tricuspid annulus and the intercaval obstacle. Group D (10 dogs): The isthmus between the inferior vena cava and the tricuspid annulus was ablated. After the experiment, the heart was excised for anatomical and histological studies. Atrial flutter was never abolished in all dogs in Groups A and B. A ligature encircling the tricuspid annulus also failed to terminate atrial flutter in 2 dogs tested. In contrast, atrial flutter was successfully abolished in 6 dogs (67%) of Group C and in 7 dogs (70%) of Group D. Total energy delivered was significantly higher in Group C than in Group D (364 +/- 133 versus 139 +/- 65 joules, p < 0.003). The total energy required for successful ablation was related to the cross sectional area of the ablation site (r = 0.55, p < 0.05). These results indicate that the tricuspid annulus is not an essential part of the reentrant pathway in the canine model of atrial flutter with an intercaval obstacle. The entire atrial tissue between the anatomical barriers could be involved in the reentrant pathway, and should therefore be ablated transmurally for successful ablation.

Animals↗
PubMed1996

Electrophysiologic mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline, pilsicainide, disopyramide, procainamide) in induction of atrioventricular re-entrant tachycardia.

We evaluated the electrophysiological mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline in seven patients, pilsicainide in two, and disopyramide in two, and procainamide in three) in the induction of orthodromic atrioventricular re-entrant tachycardia (AVRT). In 14 patients (10 males, 4 females; mean age 37 +/- 18 years) who had inducible AVRT despite the administration of class I drugs, electrophysiological effects of class I antiarrhythmic drugs were evaluated using programmed electrical stimulation techniques. In 4 out of 6 patients with a manifest accessory pathway, class I drugs induced unidirectional conduction block of the accessory pathway (antegrade conduction block associated with preserved retrograde conduction) and enhanced the induction of AVRT with atrial extrastimulation. In eight patients with a concealed accessory pathway, the outward or inward expansion of the tachycardia induction zone was observed in patients who had greater prolongation of the conduction time than the refractory period of the retrograde accessory pathway after class I drugs. During ventricular extrastimulation, the induction of bundle branch re-entry after class I drugs initiated the AVRT in patients with either manifest or concealed accessory pathways. We conclude that the adverse effects of class I drugs are mainly due to induction of unidirectional retrograde conduction of the manifest accessory pathway and the greater prolongation of the retrograde conduction time of the concealed accessory pathway than the refractory period, regardless of the sub-classification of class I drugs.

Adolescent↗
PubMed1995

Left ventricular dimensions and autonomic balance during head-up tilt differ between patients with isoproterenol-dependent and isoproterenol-independent neurally mediated syncope.

OBJECTIVES: This study sought to elucidate differences in mechanisms of neurally mediated syncope between patients with syncope induced by head-up tilt alone and those requiring isoproterenol infusion to induce syncope during head-up tilt. BACKGROUND: Some patients with neurally mediated syncope require isoproterenol to induce syncope during head-up tilt (isoproterenol dependent), and others do not (isoproterenol independent). Differences in mechanisms between these two groups have not been well elucidated. METHODS: A 60 degrees head-up tilt test was performed in 13 patients with isoproterenol-independent syncope (Group I, mean [+/- SD] age 28 +/- 12 years), 14 patients with isoproterenol-dependent syncope (Group II, mean age 34 +/- 14 years) and 20 control subjects without syncope (Group III, mean age 32 +/- 12 years). Left ventricular size and contractility were determined by echocardiography, and sympathovagal balance was determined with power spectral analysis of heart rate variability using a maximal entropy method. RESULTS: Group I patients had smaller left ventricular dimensions than Group II and III during baseline tilt. During head-up tilt with isoproterenol infusion (0.01 to 0.04 microgram/kg body weight per min), left ventricular dimensions decreased to the same extent in Groups II and III, but fractional shortening was greater in Group II than in Group III at the end of the tilt. The ratio of low (0.05 to 0.15 Hz) to high frequency (0.15 to 1.0 Hz) component became greater in Group I than in Groups II and III during the last period of baseline tilt. However, the ratio was greater in Group II than in Group III during the last period of the tilt with isoproterenol. CONCLUSIONS: Patients with isoproterenol-independent syncope had an exaggerated decrease in left ventricular size and sympathetic predominance preceding syncope during head-up tilt. In contrast, in patients with isoproterenol-dependent syncope, similar changes in autonomic nervous balance were evident only during isoproterenol infusion in addition to head-up tilt.

Adolescent↗
PubMed1995

[A transient sinus arrest after right stellate ganglion block--assessment of autonomic function by heart rate spectral analysis].

We experienced a case of sinus arrest probably induced by right stellate ganglion block (SGB). A healthy medical student volunteered in our study of the cardiac autonomic nervous system and received the SGB. After the Holter ECG had been attached, the SGB was performed with mepivacaine 8 ml. Horner's sign was observed after about 3 minutes. A transient (15 s) sinus arrest occurred suddenly after about 6 minutes of the tilt test probably due to a vasovagal reflex, and the subject lost consciousness. From spectral analysis of the Holter ECG recording, the right SGB may be closely involved in the induction of the sinus arrest. Our present case suggests that sinus arrest may occur if a patient stands up after right SGB.

Adult↗
PubMed1995

Long-term outcome of operative treatment of focal atrial tachycardia.

BACKGROUND: This study examined the long-term clinical outcome of patients with focal atrial tachycardia who were treated surgically. Focal atrial tachycardia is a relatively rare arrhythmia that is often difficult to control with conventional medical therapy. Therapeutic modalities are not well defined because of the scarcity of long-term data of treated patients, including pathologic findings. STUDY DESIGN: Nine patients, six men and three women, ranging in age from 16 to 50 years (mean of 34 +/- 14 years), underwent operative treatment for focal atrial tachycardia. The average rate of tachycardia was 167 +/- 22 beats per minute. All patients were treated with antiarrhythmic drugs (mean 2.9 drugs per patient). Concomitant operative procedures were performed upon four patients, including division of the accessory atrioventricular pathway for the Wolff-Parkinson-White syndrome in two patients, plication of the right atrium for idiopathic right atrial dilatation in one patient, and a closure of the atrial septal defect in one patient. Focal ablation was performed in all instances. RESULTS: There was no early or late death nor postoperative complications. Atrial tachycardia disappeared and there were no episodes of recurrent tachycardia postoperatively during the mean follow-up period of 67 +/- 38 months. Histopathologic findings from four patients revealed a sinus node-like structure, diffuse chronic epimyocarditis, focal myocarditis, and fascicular disarray lesions. CONCLUSIONS: Excellent long-term result were obtained in patients with focal atrial tachycardia who were treated operatively. Early operative intervention is preferable before the occurrence of impaired ventricular function. From the histopathologic findings, operative therapy should be selected in patients with diffuse atrial lesions.

Adolescent↗
PubMed1995

[Usefulness of body surface potential maps to determine ablation site in patients with WPW syndrome].

We studied body surface potential maps (BSPM) in patients with WPW syndrome before surgical ablation. These BSPM were compared with computerized epicardial mapping using sock and snap electrode. In most patients the location of minima in the early delta wave was a simple and accurate index of the site of accessory pathway. In 4 patients BSPM was useful for the diagnosis of presence of bilateral accessory pathways. We conclude that BSPM may be also useful to determine ablation site of radiofrequency catheter ablation.

Body Surface Potential Mapping↗
PubMed1994

Electrophysiologic effects of intravenous E-4031, a novel class III antiarrhythmic agent, in patients with supraventricular tachyarrhythmias.

The electrophysiologic effects of intravenous (i.v.) E-4031, a new class III antiarrhythmic drug, were evaluated in 15 patients with supraventricular tachyarrhythmias [11 men, 4 women; mean age 41 +/- 19 (SD) years]. Eleven patients had accessory atrioventricular (AV) pathways, and 4 patients with no accessory pathway had paroxysmal atrial fibrillation. Electrophysiologic studies were performed before and after E-4031 administration (loading infusion 9 micrograms/kg for 5 min + maintenance infusion 0.15 microgram/kg/min). QT and QTc intervals were significantly prolonged by E-4031 from 0.40 +/- 0.03 (mean +/- SD) to 0.46 +/- 0.03 s (p < 0.0001) and from 0.43 +/- 0.03 to 0.49 +/- 0.04 s (p < 0.0001), respectively. No effect was observed on RR interval, PR interval, QRS duration, or AH and HV intervals. The effective refractory periods (ERPs) of the right atrium and ventricle were significantly prolonged from 219 +/- 27 to 236 +/- 26 ms (p < 0.001) and from 230 +/- 12 to 249 +/- 11 ms (p < 0.001), respectively. The ERP of the AV node did not change significantly after E-4031 administration. In patients with ventricular preexcitation, E-4031 significantly prolonged the ERP of the antegrade accessory pathway conduction from 340 +/- 101 to 362 +/- 106 ms (p < 0.001), but not retrograde accessory pathway conduction. AV reentrant tachycardia was induced in 3 of 11 patients with an accessory pathway, and repetitive atrial firing was induced in 3 of 4 patients with paroxysmal atrial fibrillation. E-4031 could prevent repetitive atrial firing in only 1 patient and could not prevent induction of AV reentrant tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Transient terminal U wave inversion as a more specific marker for myocardial ischemia.

Transient U wave inversion can be caused either by regional myocardial ischemia or by an elevation of systemic blood pressure. The characteristics of U wave inversion during chest pain attacks in 21 patients with variant angina were compared with those observed in 38 patients with hypertension without apparent ischemic heart disease. Differentiation was possible according to the ECG phase in which U wave inversion appeared. U wave inversion was considered to be significant if there was a discrete negative deflection of more than 0.05 mV within the TP segment. U wave inversion proceeded to positive deflection of U wave in patients with hypertension without ischemic heart disease (initial U wave inversion). In contrast, inverted U wave occurred after positive U wave deflection during attacks in patients with variant angina (terminal U wave inversion). When cold pressor test was performed in patients with variant angina during treatment with calcium entry blockers, no patient had either anginal attacks or ischemic ST-segment deviation, but 9 of 21 patients (43%) had transient initial U wave inversion, which was followed by positive U wave deflection. U wave inversion can be classified as initial U wave inversion and terminal U wave inversion according to the phasic relationship to positive U wave deflection; the latter is observed in association with regional myocardial ischemia. The former seems to be related to elevated blood pressure rather than to myocardial ischemia.

Adult↗
PubMed1993

Effects of diltiazem on concealed atrioventricular nodal conduction in relation to ventricular response during atrial fibrillation in anesthetized dogs.

By means of a new quantitative index for concealed conduction, we evaluated the effects of diltiazem on atrioventricular (AV) node concealment and correlated this index with the variability of the ventricular response during atrial fibrillation in 16 anesthetized mongrel dogs. After determination of the atrial effective refractory period (ERP), AV nodal ERP (AVNERP), concealment zone, and concealment index (AVNERP of blocked atrial extrasystole/AVNERP of conducted atrial extrasystole), the R-R intervals during atrial fibrillation induced by electrical stimulation were measured. Both low (0.1 mg/kg) and medium (0.2 to 0.4 mg/kg) doses of diltiazem prolonged the AVNERP and increased the mean R-R interval during atrial fibrillation. Only medium doses of diltiazem increased the degree of concealed conduction in the AV node and accentuated the variability of R-R intervals. There was a good positive correlation between the variability of the ventricular response during atrial fibrillation and the concealment index. In conclusion, medium doses of diltiazem are more effective in reducing heart rate during atrial fibrillation than a low dose. However, medium doses also increase the degree of concealed conduction in the AV node and enhance the irregularity of the ventricular response during atrial fibrillation. Measurement of the concealment index is useful for quantitating the degree of concealed conduction in the AV node, which is actually an important determinant of the ventricular response during atrial fibrillation.

Animals↗
PubMed1993

Effects of acute ischemia on anisotropic conduction in canine ventricular muscle.

The effects of acute ischemia on conduction velocities in the longitudinal (theta L) and transverse (theta T) fiber axis were determined from epicardial activation patterns, recorded with 48 bipolar electrodes (plaque electrode, 25 x 35 mm) on the left anterior ventricular wall of eight dogs and the posterior wall of seven dogs. During left ventricular stimulation (cycle length = 300 msec) in the center of the plaque electrode, theta L, theta T, and the ratio of longitudinal to transverse conduction velocities (theta L/T) were measured before and 2 to 5 minutes after occlusion of the left anterior descending coronary artery or the left circumflex coronary artery. During the control state theta L was greater than theta T demonstrating anisotropic properties of cardiac muscle, not only in the anterior but also in the posterior wall. During acute ischemia theta L and theta T were decreased from the control value and theta T was decreased by a greater extent than theta L resulting in an increase in theta L/T from 1.83 +/- 0.31 (mean +/- SD) to 2.19 +/- 0.36 in the anterior wall and from 1.58 +/- 0.17 to 1.92 +/- 0.28 in the posterior wall. During ventricular fibrillation some lines of conduction block were parallel to the long axis of epicardial muscle fiber bundle and the others were perpendicular. In conclusion, acute ischemia increased anisotropic conduction (theta L/T) in the epicardial ventricular muscle mainly due to greater reduction in theta T, in the anterior and the posterior wall. This augmented anisotropic ventricular conduction may have some relation to the initiation of ventricular fibrillation during acute ischemia.

Animals↗
PubMed1992

Rate-dependent accessory pathway conduction due to phase 3 and phase 4 block. Antegrade and retrograde conduction properties.

Six patients who had antegrade phase 3 and phase 4 block in the accessory pathway were examined. In each patient, antegrade conduction over the accessory pathway was absent both at the sinus rate and at slower heart rates. During premature atrial stimulation a "window" of accessory pathway conduction was identified in all patients. The outer limits of the window ranged from 480 ms to 670 ms. The inner limits ranged from 410 ms to 620 ms. The durations of the window ranged from 20 ms to 160 ms. Three patients with orthodromic atrioventricular reentrant tachycardia showed preserved retrograde accessory pathway conduction. The remaining three patients had impaired retrograde accessory pathway conduction. One of the patients showed retrograde phase 4 block in the accessory pathway. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation prolonged the outer limit of the window in the antegrade accessory pathway conduction. These findings suggest that the mechanism of antegrade phase 3 and phase 4 block in the accessory pathway may be spontaneous diastolic depolarization in the accessory pathway and conduction disturbance at the ventricular and/or atrial insertion of the accessory pathway.

Adult↗
PubMed1992

Electrophysiologic effects and efficacy of cibenzoline in patients with supraventricular tachycardia.

Electrophysiologic effects of intravenous (i.v.) cibenzoline were evaluated in 18 patients with accessory pathways or dual atrioventricular (AV) nodal pathways (12 men and 6 women with a mean age of 44 +/- 18 years). Twelve patients had accessory AV pathways, including 6 patients with a manifest accessory pathway. Six patients had AV nodal reentrant tachycardia (AVNRT). Electrophysiologic studies were performed before and after cibenzoline (1.4 mg/kg i.v.) infusion for 5 min. Sinus cycle length did not change significantly after cibenzoline administration. Cibenzoline increased both the AH (85 +/- 20 vs. 91 +/- 21 ms, p less than 0.05) and HV intervals (41 +/- 10 ms vs. 53 +/- 11 ms, p less than 0.001). Neither the atrial nor ventricular effective refractory period (ERP) was altered by cibenzoline. Complete block in the accessory pathway occurred antegradely in 4 patients and retrogradely in 1 patient. Cibenzoline prevented induction of AV reentrant tachycardia (AVRT) in 3 of 8 patients with sustained orthodromic AVRT by abolishing retrograde accessory pathway conduction or prolonging the retrograde accessory pathway ERP. Of 5 patients who continued to have inducible AVRT before and after cibenzoline administration, the tachycardia cycle length was increased in 3, mainly due to the increase in retrograde accessory pathway conduction time. Cibenzoline prevented induction of sustained AVNRT in 4 of 5 patients by prolonging the minimum pacing cycle length, maintaining 1:1 ventriculoatrial (VA) conduction through the retrograde fast AVN pathway or shortening the antegrade fast AVN pathway ERP equal to the slow AVN pathway. In one patient who had an uncommon type of AVNRT, sustained tachycardia was induced by cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗