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Biomedical subjects

K Mizumaki

Publications and source records attributed to K Mizumaki.

13 recordsLinked to original sources
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↗
PubMed1992

Effects of chronotropic responsive cardiac pacing on ventilatory response to exercise in patients with complete AV block.

To identify the effect of chronotropic responsive cardiac pacing on the ventilatory response to exercise, ten selected patients with complete atrioventricular block underwent paired cardiopulmonary exercise tests in fixed rate ventricular (VVI) and dual chamber (DDD) or rate responsive ventricular (VVIR) pacing modes. Compared to VVI pacing, DDD or VVIR pacing increased peak oxygen uptake (P < 0.005) and augmented anaerobic threshold (P < 0.001). In eight patients, dyspnea was the major symptom limiting exercise with VVI pacing and this was markedly attenuated with DDD or VVIR pacing. In all patients, ventilation (VE) and the ratio of ventilation to CO2 production (VE/VCO2) were consistently higher with VVI pacing during exercise. To compare the response of the two pacing modes at the same workloads in an aerobic condition, we measured ventilatory variables 1 minute prior to the anaerobic threshold obtained with VVI pacing. When DDD or VVIR pacing was compared with VVI pacing, VE and VE/VCO2 significantly decreased from 20.5 +/- 5.3 L/min to 18.3 +/- 5.0 L/min (P < 0.005) and from 35.9 +/- 5.8 to 31.9 +/- 5.0 (P < 0.001), respectively. Respiratory frequency rose significantly more with VVI pacing (P < 0.001) despite an unchanged tidal volume. Although peak VE did not differ between the two pacing modes, VE/VCO2 at the peak exercise increased significantly more with VVI pacing (P < 0.005). Respiratory frequency also rose more with VVI pacing (P < 0.005) and tidal volume did not change. This study suggests that chronotropic responsive cardiac pacing attenuates the exertional dyspnea by improving the ventilatory response to exercise as well as increasing the cardiac output in patients with complete atrioventricular block.

Anaerobic Threshold↗
PubMed1992

Two different reentrant circuits of ventricular tachycardia in a patient with an extensive anterior infarction: evaluation using electrical catheter ablation techniques.

Two morphologically distinct sustained ventricular tachycardias were initiated by programmed stimulation during attempted catheter ablation in a patient with an old anterior myocardial infarction. Right bundle branch block configuration of ventricular tachycardia, which was identical to the spontaneously occurring tachycardia, was initiated and displayed fragmented mid-diastolic potential at the apicolateral left ventricular site. Evidence of a critical slow conduction area was observed during delivery of electrical stimuli to this area. Following a 150-joule electrical shock delivered to this area, right bundle branch block pattern of ventricular tachycardia was no longer inducible but a new sustained monomorphic ventricular tachycardia with left bundle branch block pattern was initiated. The mid-diastolic fragmented activity at the ablation site became electrical activation of bystander area that was not participating in the left bundle branch block type of the ventricular tachycardia circuit. The critical slow conduction area was identified at the apicoseptal left ventricular site that was separated more than 5 cm from the ablation site. We speculate that two morphologically distinct sustained monomorphic ventricular tachycardias may be due to two different reentrant circuits and not the different expression of the same circuit.

Aged↗
PubMed1992

[Effects of chronotropic responsive cardiac pacing on ventilatory response to exercise in patients with bradycardia].

To identify the effect of chronotropic responsive cardiac pacing on ventilatory responses to exercise, 9 patients with chronotropic incompetence underwent paired cardiopulmonary exercise tests with fixed demand rates (AAI, VVI) and chronotropic responsive (AAIR, VVIR, DDD) pacing modes. Compared with fixed rate pacing, chronotropic responsive pacing increased peak oxygen uptake and delayed the attainment of the anaerobic threshold (AT) with a higher level of oxygen consumption (p < 0.01). Dyspnea was a major symptom that limited exercise time in 7 patients with fixed rate pacing, which was prominent with chronotropic responsive pacing. Ventilation (VE) and the ratio of ventilation to CO2 production (VE/VCO2) were consistently higher with fixed rate pacing during exercise. To compare the responses between the 2 pacing modes with the same work loads under aerobic conditions, we measured ventilatory variables one min prior to the AT as obtained with fixed rate pacing. When switching the pacing mode from fixed rate pacing to chronotropic responsive pacing, VE and VE/VCO2 decreased significantly from 22.0 +/- 7.8 to 19.8 +/- 6.8 l/min, and from 37.4 +/- 5.4 to 33.6 +/- 5.2, respectively. Tidal volume did not change, but respiratory frequency decreased more with chronotropic responsive pacing (p < 0.05). Although peak VE did not differ between the 2 pacing modes, VE/VCO2 decreased more with chronotropic responsive pacing (p < 0.01). Respiratory frequency decreased and tidal volume increased more with chronotropic responsive pacing (p < 0.05). This study suggests that chronotropic responsive cardiac pacing attenuates exertional dyspnea by improving ventilatory responses to exercise as well as increasing the cardiac output in patients with chronotropic incompetence.

Adult↗
PubMed1992

[Mechanisms of vasovagal syncope elucidated by upright-tilt with isoproterenol infusion].

To elucidate the role of increased basal vagal activity in vasovagal syncope, we compared patients with bradyarrhythmia due to increased vagal tone and patients with vasovagal syncope using an upright-tilt (60 degrees) positioning test with isoproterenol infusion. Eight patients with unexplained recurrent syncope after clinical and electrophysiological investigations and 5 patients without syncope who had bradyarrhythmias due to increased vagal tone were studied. All 8 patients with recurrent syncope had some prodrome suggestive of vasovagal syncope. The upright-tilting test was considered positive if syncope developed in association with hypotension or bradycardia, or both. If 10 min of control tilting was negative, the patient was lowered to the supine position. Upright-tilting was then repeated during continuous intravenous isoproterenol infusion at successive incremental doses of 0.01 to 0.03 microgram/kg/min. During the control upright-tilting test, none of the patients had positive responses. During the upright-tilting with isoproterenol infusions, all patients with vasovagal syncope had positive responses; whereas, all patients with bradyarrhythmia due to increased vagal tone had negative responses. In patients with vasovagal syncope, the heart rate (HR) and the mean blood pressure (mBP) were higher at the time of supine positioning than at the time of syncope (HR: 109 +/- 16-->88 +/- 16 bpm, p < 0.05) (mBP: 86 +/- 5-->53 +/- 6 mmHg, p < 0.01). However, in patients with bradyarrhythmia there was no significant change in HR and mBP between the supine and 10 min of the upright-tilting with isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Quantification of human concealed atrioventricular nodal conduction: relation to ventricular response during atrial fibrillation.

We studied the relation between a new quantitative index of concealed atrioventricular nodal (AVN) conduction and the variability of ventricular response during atrial fibrillation in 12 patients without preexcitation. The second atrial extrastimulus (A3) was introduced following the first extrastimulus (A2), which was fixed at a coupling interval 20 to 40 msec longer than the AVN effective refractory period (ERP) during a basic atrial drive (A1) cycle length of 400 to 750 msec. The AVNERP of conducted A2 defined as the longest A2A3 interval at which A3 was not conducted to the His bundle was determined. This pacing sequence was repeated, whereas A2 was fixed at a coupling interval 20 to 40 msec shorter than the AVNERP, which means A2 was concealed within the AVN. Thus AVNERP of blocked A2, defined as the longest A2A3 interval at which A3 was not conducted to the His bundle, was measured. Concealment index (AVNERP of blocked A2/AVNERP of conducted A2) was developed to quantitate the magnitude of concealed penetration into the AVN by A2. During atrial fibrillation induced by premature or rapid atrial stimulation, the coefficient of variation (SD/mean) of R-R intervals and the maximum R-R/minimum R-R interval were significantly correlated with the concealment index (r = 0.838, p less than 0.001; r = 0.678, p less than 0.05). However, neither of these parameters was correlated with AVNERP. Both the minimum R-R and the mean R-R interval were related to the AVNERP (r = 0.946, r = 0.823, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1990

Pacemaker syndrome evaluated by cardiopulmonary exercise testing.

Two patients who presented with dyspnea on effort, persisting after insertion of a fixed rate ventricular demand pacemaker (VVI) for sick sinus syndrome, were evaluated by cardiopulmonary exercise testing. During VVI pacing a heightened ventilatory response to exercise and a fluctuation of ventilation occurred. The high ventilatory equivalent for CO2 throughout exercise with VVI pacing suggests that the patients had ventilation-perfusion mismatching due to an increase in the pulmonary capillary wedge pressure caused by 1:1 ventriculoatrial conduction. Rate responsive ventricular (VVIR) pacing associated with intact 1:1 ventriculoatrial conduction exaggerated the exertional dyspnea, while rate responsive atrial (AAIR) pacing improved the ventilatory response to exercise. We suggest that a heightened ventilatory response to exercise due to ventilation-perfusion mismatching may be an important factor causing the pacemaker syndrome, and that cardiopulmonary exercise testing is useful in identifying the exercise-induced symptoms with ventricular pacing.

Aged↗
PubMed1990

[Phase 3 and phase 4 block in the accessory pathway].

Pacemaker activity at a site proximal to the area of a conduction disturbance has been postulated as depressing conduction in late diastole (phase 4 block). To elucidate the correlation between the site of phase 4 depolarization and that of a conduction disturbance, we examined seven patients with intermittent Wolff-Parkinson-White syndrome who had tachycardia (phase 3) and bradycardia (phase 4) dependent on block in the accessory pathway. In each patient, antegrade conduction over the accessory pathway was absent at the sinus rate. During premature atrial stimulation a "window" of accessory pathway conduction was identified in each patient. The outer limit of the window ranged from 420 to 670 ms; the inner limit, from 330 to 620 ms. The duration of the window ranged from 20 to 160 ms. Four patients with orthodromic atrioventricular reentrant tachycardia exhibited preserved retrograde accessory pathway conduction. In one patient with unsustained orthodromic atrioventricular reentrant tachycardia, retrograde accessory pathway conduction also exhibited phase 3 and phase 4 blocks. The remaining two patients had no retrograde accessory pathway conduction. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation eliminated a phase 4 block in antegrade accessory pathway conduction. These results suggest that 1) an antegrade phase 4 block may have phase 4 depolarization in the accessory pathway and block at the ventricular insertion of the accessory pathway; 2) a retrograde phase 4 block may have a conduction disturbance at the atrial insertion of the accessory pathway; and 3) a complete retrograde block may occur at the atrial insertion of the accessory pathway.

Adolescent↗
PubMed1989

[Sinus node function evaluated by spontaneous atrial premature contractions].

Sinus node function was evaluated according to spontaneous premature atrial contractions (APC). In 33 patients, who showed evidence of more than 10 APCs in 24-hour Holter ECG, sinoatrial conduction times (SACT) were measured by the Strauss' method. Time difference between the interval preceding PP, the APC and return cycle following APC was expressed as RC-SC. Patients were categorized in three groups; CSRT less than 500 and 2SACT less than 180 msec (A), 500 less than or equal to CSRT less than 1000 and/or 180 less than or equal to 2SACT less than 250 msec (B), and CSRT greater than or equal to 1000 and or 2SACT greater than or equal to 250 msec (C). There was significant correlation between the mean RC-SC and 2SACT (r = 0.69). Mean RC-SC was greater than 2SACT in all seven patients whose CSRTs exceeded 2000 msec. The mean RC-SC was 0.15 +/- 0.03 in group A, 0.20 +/- 0.02 in group B and 0.25 +/- 0.06 (sec; mean +/- SD) in group C. The max RC-SC was 0.20 +/- 0.03 in group A, 0.28 +/- 0.03 in group B and 0.36 +/- 0.07 sec in group C. The mean RC-SC and max RC-SC differed significantly among the three groups (p less than 0.05). The standard deviation in distribution of the RC-SC was 0.033 +/- 0.008 in group A, 0.044 +/- 0.007 in group B and 0.052 +/- 0.017 sec in group C. RC-SCs equal to or longer than 0.24 sec were observed in 1% in group A, 26% in group B and 58% in group C, and that equal to or longer than 0.30 sec was found in 0, 3 and 28% in groups A, B and C, respectively. The RC-SC reflects not only SACT but sinus node automaticity, and provides more simple detection of sinus dysfunction. Sinus dysfunction may exist when the RC-SC is greater than 0.30 sec.

Adult↗
PubMed1989

[Incessant supraventricular tachycardia due to upper atrioventricular nodal reentry].

Three patients with recurrent supraventricular tachycardia were presented. Atrial cycle length unchanged during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia, the first AH interval was shorter than the subsequent one. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. Ventriculoatrial conduction was not observed in patient 1 and 2. In patient 3 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response, and the tachycardia was terminated by the ventricular stimulation without atrial capture. In patient 1, verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (180 mg/day) suppressed the tachycardia in patients 2 and 3. These findings suggest that the mechanism of the tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has a tendency to be incessant.

Adenosine Triphosphate↗
PubMed1988

Fast-slow type of atrioventricular nodal reentrant tachycardia: horizontal dissociation of the AV node during tachycardia.

Two patients with recurrent supraventricular tachycardia are presented. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. In patient 1 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response. In patient 2 the ventriculoatrial conduction was not observed. In both patients, the unchanged atrial cycle length during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia the first AH interval was shorter than the subsequent HA interval. In patient 2 verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (180 mg/day) suppressed the tachycardia in patient 1. These findings suggest that the mechanism of tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has tendency to show incessant form.

Adenosine Triphosphate↗