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M Fukatani

Publications and source records attributed to M Fukatani.

At least 19 recordsLinked to original sources
PubMed1994

Mechanism of the suppression of repetitive atrial firing by isoproterenol--comparison with disopyramide.

To investigate whether isoproterenol (Iso) could suppress the initiation of repetitive atrial firing (RAF), we investigated its effect on RAF in comparison with that of disopyramide (Diso). Extrastimuli at a basic cycle length of 500 ms were delivered from the high right atrium in 49 patients who received an intravenous infusion of Iso (0.01 microgram/kg per min) and in 39 patients given intravenous Diso (2 mg/kg per 10 min). Induction of RAF, the atrial effective refractory period (A-ERP), and the maximum conduction delay (MCD) were measured. Iso abolished the induction of RAF in 13/19 (68%) patients, while Diso did so in 13/22 (59%) patients. Thirty-four of the 41 patients with RAF in the baseline study had an A-ERP < 250 ms and an MCD > 40 ms. Iso significantly decreased the A-ERP from 205 +/- 26 to 194 +/- 23 ms (P < 0.01) and significantly decreased the MCD from 67 +/- 24 to 39 +/- 16 ms (P < 0.0001) in 19 patients with RAF. On the other hand, Diso significantly increased the A-ERP from 203 +/- 31 to 235 +/- 36 ms (P < 0.0001), and significantly diminished the MCD from 68 +/- 31 to 55 +/- 30 ms (P < 0.01) in 22 patients with RAF. In patients with new RAF (n = 7) or re-induced RAF (n = 14) during Iso or after Diso, the MCD was more than 40 ms. Our results suggest that there are two different modes of RAF suppression, i.e. shortening or lengthening of the A-ERP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of intravenous verapamil on atrial vulnerability.

To investigate the effects of verapamil on indicators of atrial vulnerability, we examined 30 patients with paroxysmal supraventricular tachycardia who received intravenous verapamil during an electrophysiologic study. Single atrial extrastimuli were given before and after intravenous administration of verapamil to induce repetitive atrial firing (RAF) or atrial fibrillation, and to examine the maximum A2/A1, which was defined as the maximum ratio of the duration of the atrial electrogram resulting from premature stimulation (A2) to that resulting from the basic drive beat (A1). The maximum A2/A1 increased from 145 +/- 20% to 154 +/- 25% (p < 0.02) after verapamil administration. The maximum A2/A1 in patients in whom neither RAF nor atrial fibrillation were induced both before and after verapamil were smaller than those in patients in whom RAF was induced only after verapamil (before; 138 +/- 20% vs 165 +/- 15%, p < 0.02. after; 144 +/- 22% vs 172 +/- 17%, p < 0.05). RAF or atrial fibrillation was induced only after verapamil in 6 patients, who showed a maximum A2/A1 before verapamil of 150% or more. These data suggest that verapamil may induce repetitive atrial firing and possibly atrial fibrillation in some predisposed patients, especially in those that have a greater maximum A2/A1, which may be an indicator of local intraatrial conduction delay before drug infusion.

Adolescent↗
PubMed1993

Anterograde and retrograde decremental conduction over left-sided accessory atrioventricular pathways in the Wolff-Parkinson-White syndrome.

The electrophysiologic properties of left-sided accessory pathways (APs) were examined by cardiac stimulation in 55 patients with Wolff-Parkinson-White syndrome. Atrioventricular and ventriculoatrial conduction times were assessed at the coronary sinus level nearest to the AP and then plotted graphically as a function of coupling interval (for atrial and ventricular refractory period determinations). Of 29 patients with anterograde conduction over the AP, 10 (34%) exhibited decremental conduction. However, only two (7%) had a maximal decrement equal to or more than 30 msec. In the other eight (27%) patients the maximal decrement ranged from 10 to 20 msec. The longest coupling interval at which anterograde decremental conduction was demonstrated ranged from 260 to 440 msec (346 +/- 52 msec). The shortest coupling interval ranged from 240 to 320 msec (265 +/- 24 msec). The anterograde decremental conduction zone was 91 +/- 55 msec. Of 51 patients with retrograde conduction over the AP, 23 (45%) exhibited decremental conduction. However, only eight (15%) had a maximal decrement equal to or greater than 30 msec. In the other 15 (29%) patients the maximal decrement ranged from 10 to 25 msec. The longest coupling interval was 338 +/- 70 msec. The shortest coupling interval was 275 +/- 42 msec. The retrograde decremental conduction zone was 72 +/- 47 msec. There was a significant inverse correlation between the AP effective refractory period and the maximal decrement (r = -0.42; p < 0.05). The comparison of maximal ventriculoatrial conduction time with the maximal decrement revealed a positive correlation (r = 0.63; p < 0.01). These data reveal that minimal decremental conduction over left-sided APs is not an uncommon finding and stress that care should be taken in evaluation of conduction over these connections.

Adolescent↗
PubMed1993

Electrophysiological effects of a new class III antiarrhythmic agent (E-4031) on the conduction and refractoriness of the in vivo human atrium.

OBJECTIVE: The aim was to test the efficacy of a new class III drug, E-4031, on human atrial muscle in vivo. METHODS: Electrophysiological measurements were performed in 10 patients, age 54(SD 11) years, before and during the continuous infusion of E-4031 (0.15 microgram.kg-1.min-1) which followed an initial dose of 9 micrograms.kg-1 x 5 min-1. Extrastimuli at 500 ms were delivered from the right atrial appendage, high lateral right atrium, and low lateral right atrium. The effective refractory period, repetitive atrial firing zone, and fragmented atrial activity zone were assessed at three sites in the right atrium. The conduction delay zone from the stimulus artefact to the distal electrode pair at the coronary sinus was also measured. RESULTS: E-4031 caused a significant increase in overall right atrial effective refractory period from 210(SD 29) to 232(26) ms (p < 0.001, n = 30 sites). There were significant decreases in the incidence of repetitive atrial firing (67% to 37%: p < 0.005), in the repetitive atrial firing zone [23(20) to 11(22) ms: p < 0.01], and in the fragmented atrial activity zone [15(22) to 3(8) ms: p < 0.005], but no significant change in the conduction delay zone. However, E-4031 significantly prolonged the longest coupling interval that elicited conduction delay, from 249(31) ms to 267(28) ms (p < 0.01). E-4031 had no effect on the conduction time except at coupling intervals close to the atrial effective refractory period. CONCLUSION: These results suggest that E-4031 has a potential effect in the treatment of human paroxysmal atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMed1993

Electrophysiologic effects of a new class III antiarrhythmic agent, E-4031, on atrial flutter, atrial refractoriness, and conduction delay in a canine sterile pericarditis model.

Numerous studies have shown that E-4031 generally prolongs the atrial effective refractory period (AERP) without affecting cardiac conduction. The effects of E-4031 on AERP and cardiac conduction at short cycle lengths (CLs) close to the AERP were measured in 12 dogs with sterile pericarditis. Three pairs of electrodes were sutured at three sites in the atria 4 days after the model was created. We measured AERP and maximum conduction delay (MCD) after 8 beats train at CLs of 400, 300, 200 and 150 ms before and during continuous infusion of E-4031 (0.1 microgram/kg/min) that followed an initial dose of 10 micrograms/kg/min/5 min. E-4031 interrupted sustained atrial flutter (AF) (> or = 10 min) in 4 of 5 episodes and atrial fibrillation (> or = 10 min) in 4 of 4. The CL of AF defined as a rapid atrial rhythm (rate > or = 240 beats/min) in five episodes studied in the sterile pericarditis model was significantly (p < 0.005) prolonged from 120 +/- 8 to 160 +/- 17 ms. There were significant (p < 0.005) increases in AERP at each CL, and prolongation of AERP was 39 +/- 18, 31 +/- 14, 23 +/- 14, and 16 +/- 14 ms at CL 400, 300, 200, and 150 ms, respectively. E-4031 produced less prolongation of AERP at short pacing CLs and had no effect on conduction time during atrial rapid pacing at CLs > 150 ms. E-4031 did not prolong MCD at CL 400 ms, but did prolong MCD at CLs of 300, 200, and 150 ms, despite prolongation of AERP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Relationship between atrial conduction defects and fractionated atrial endocardial electrograms in patients with sick sinus syndrome.

The relationship between abnormal atrial electrograms (AAE) recorded during sinus rhythm by endocardial catheter mapping of the right atrium and the atrial conduction defects of sinus impulses or single atrial extrastimuli was investigated in 44 patients with sick sinus syndrome. The patients were divided into two groups on the basis of the presence (n = 29) or absence (n = 15) of AAE recorded during sinus rhythm. The P wave duration in the AAE (+) Group patients was 137 +/- 14 msec, and 125 +/- 15 msec in the AAE (-) Group; P < 0.02. The intraatrial conduction time of sinus impulses in the AAE (+) Group was 54 +/- 12 msec, and 39 +/- 9 msec in the AAE (-) Group; P < 0.001. The interatrial conduction time in the AAE (+) Group was 101 +/- 14 msec, and 78 +/- 16 msec in the AAE (-) Group; P < 0.001. In the AAE (+) Group, 11 (38%) patients had a sinus node recovery time > 4 seconds, whereas in the AAE (-) Group there was only one (6%) patient; P < 0.03. AAE showed a specificity of 93% and a positive predictive accuracy of 91% in predicting inducibility of atrial fibrillation. The sensitivity was 35% and the negative predictive accuracy was 42%. Sustained atrial fibrillation was induced in ten (35%) patients of the AAE (+) Group, and in one (7%) patient of the AAE (-) Group; P < 0.05. These data suggest that in patients with sick sinus syndrome who possess abnormal endocardial electrograms in sinus rhythm within the right atrium have: (1) a significantly longer P wave duration; (2) a significantly longer intraatrial and interatrial conduction time of sinus impulses; and (3) a significantly greater sinus node dysfunction and higher incidence of induction of sustained atrial fibrillation. It is concluded that there are significantly greater atrial conduction defects in patients with sick sinus syndrome who possess AAE within the right atrium during sinus rhythm.

Adult↗
PubMed1993

Double response of the ventricle during transient entrainment in a common atrioventricular nodal reentrant tachycardia.

We report a patient with slow-fast atrioventricular (AV) nodal reentrant tachycardia, in which double ventricular response was demonstrated during rapid pacing at cycle length of 300 msec or less from the high right atrium. The determinants of double ventricular response during transient entrainment in the present case were: (1) a crucial conduction delay in the slow pathway; (2) the collision between the activation via the antegrade fast pathway (antidromically) of the last paced beat and the activation via the antegrade slow pathway (orthodromically) of the previous paced beat, instead of the unidirectional block in the slow pathway; and (3) the enhanced AV nodal conduction over the antegrade fast pathway.

Adult↗
PubMed1992

Electrophysiological abnormalities of the atrial muscle in patients with sinus node dysfunction without tachyarrhythmias.

The duration and the number of fragmented deflections of the right atrial electrograms were assessed and quantitatively measured in 74 patients who underwent endocardial catheter mapping during sinus rhythm. The bipolar electrograms were recorded at 12 sites in the right atrium. An abnormal atrial electrogram was defined as a duration of 100 ms or longer, and/or 8 or more fragmented deflections, according to our previous criteria. The patients were divided into two groups. The control group consisted of 41 age-matched patients with normal sinus node function and without paroxysmal atrial fibrillation. The study group comprised 33 patients with sinus node dysfunction but without tachyarrhythmias. Abnormal atrial electrograms were observed in 8 (19.5%) control patients, and in 16 (48.5%) sinus node dysfunction patients; p < 0.02. The total number of abnormal electrograms was 14 (2.89%) of 483 atrial electrograms in controls, and 36 (9.38%) of 384 in the study group; p < 0.0002. The mean duration (75.6 +/- 17) and the mean number of fragmented deflections (4.1 +/- 2) of the total atrial electrograms in the sinus node dysfunction group was significantly greater than that in controls (70.9 +/- 11 and 3.6 +/- 1, respectively); p < 0.01. The mean number of abnormal electrograms per patient in the study group (1.06 +/- 1.8) was significantly higher than that in the control group (0.3 +/- 0.8); p < 0.05. These data suggest that: (1) there is a significantly greater electrophysiological abnormality of the atrial muscle in patients with sinus node dysfunction but without paroxysmal atrial fibrillation than in age-matched controls, and (2) not only the sinus node but also the atrial muscle is electrophysiologically altered in patients with sinus node dysfunction but without tachyarrhythmias.

Adult↗
PubMed1992

Electrophysiological abnormalities of the atrial muscle in patients with manifest Wolff-Parkinson-White syndrome associated with paroxysmal atrial fibrillation.

We investigated the electrophysiological properties of the atrial muscle in 33 patients with manifest Wolff-Parkinson-White syndrome. Group I consisted of 13 patients with paroxysmal atrial fibrillation and group II consisted of 20 patients without paroxysmal atrial fibrillation. The anterograde and retrograde effective refractory periods of the accessory pathway and the inducibility of atrioventricular reciprocating tachycardia were not significantly different between the two groups. Endocardial electrograms, obtained by right atrial catheter mapping, were recorded during sinus rhythm from 12 sites of the right atrium in 12 of the 13 group I patients and in all group II patients. An abnormal atrial electrogram was defined as 100 msec or longer in duration, and/or the occurrence of eight or more deflections. Ten (83%) of the 12 group I patients had abnormal atrial electrograms, while only two (10%) of the 20 group II patients had abnormal atrial electrograms, and the difference was significant (P less than 0.01). Thirty-six (26%) of the total 139 electrograms obtained from 12 group I patients and two (1%) of the total 199 electrograms obtained from 20 group II patients fulfilled the criteria for an abnormal atrial electrogram, and the difference was significant (P less than 0.01). The fragmented atrial activity zone, interatrial conduction delay zone, and repetitive atrial firing zone obtained by right atrial extrastimulation were significantly wider in group I than in group II, respectively. It was concluded that electrical abnormalities of the atrial muscle may play an important role in the occurrence of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome.

Adult↗
PubMed1992

Different distribution of abnormal endocardial electrograms within the right atrium in patients with sick sinus syndrome.

BACKGROUND: Prolonged and fractionated right atrial endocardial electrograms are characteristic of paroxysmal atrial fibrillation (idiopathic or associated with sick sinus syndrome). The distribution of these abnormal atrial electrograms within the right atrium and the way it is related to the likelihood that patients with sick sinus syndrome will develop paroxysmal atrial fibrillation was studied. METHODS: Endocardial catheter mapping of the right atrium during sinus rhythm was performed in 41 control patients with normal sinus node function and without paroxysmal atrial fibrillation, in 33 patients with sick sinus syndrome but without tachycardia, and in 27 patients with sick sinus syndrome and paroxysmal atrial fibrillation (group 3). The bipolar electrograms were recorded at 12 sites in the right atrium and an abnormal atrial electrogram was defined as lasting > or = 100 ms and/or showing eight or more fragmented deflections. RESULTS: 1195 atrial endocardial electrograms were assessed and quantitatively measured. In patients with sick sinus syndrome and paroxysmal atrial fibrillation 54% of the abnormal atrial electrograms were recorded from the high right atrium, 28% from the mild right atrium, and 18% from the low right atrium. However, in patients with sick sinus syndrome without tachycardia 78% of the abnormal atrial electrograms were recorded from the high right atrium and 22% from the mid right atrium. No abnormal electrograms were recorded from the low right atrium. CONCLUSIONS: In patients with sick sinus syndrome without tachycardia abnormal atrial electrograms generally came from the high right atrium but in patients with sick sinus syndrome and paroxysmal atrial fibrillation abnormal atrial electrograms were more widely distributed in the right atrium. In patients with sick sinus syndrome the greater the extent of the compromised atrial muscle, the greater the likelihood that paroxysmal atrial fibrillation will develop.

Adult↗
PubMed1992

The influence of advancing age on the electrophysiological changes of the atrial muscle induced by programmed atrial stimulation.

The influence of advancing age on the electrophysiological changes of the atrial muscle induced by programmed atrial stimulation, such as fragmented atrial activity (FAA), interatrial conduction delay (ICD), and repetitive atrial firing (RAF), was investigated in 42 patients with neither documented episodes of paroxysmal atrial fibrillation nor sick sinus syndrome. The induction rates of FAA, ICD, and RAF were not affected by age. The zones of FAA, ICD and RAF, did not show any correlation with age. However, the longest coupling interval giving rise to FAA (longest CI-FAA) or ICD (longest CI-ICD) showed a significant correlation with age (longest CI-FAA; r = 0.428, p less than 0.01, longest CI-ICD; r = 0.398, p less than 0.01). Although the longest coupling interval giving rise to RAF did not show a direct correlation with age (r = 0.267), it was significantly longer in patients over 60 years of age than in those under 60 (p less than 0.05). These results suggest that aging affects the electrophysiological properties of the atrial muscle, which can help to explain why atrial fibrillation is seem more frequently in the elderly.

Adult↗
PubMed1991

Effects of standing on the induction of paroxysmal supraventricular tachycardia.

To evaluate the effects of standing on induction of paroxysmal supraventricular tachycardia, electrophysiologic studies were performed in both the supine and standing positions in 22 patients with atrioventricular (AV) reciprocating tachycardia and in 11 with AV node reentrant tachycardia. AV reciprocating tachycardia was induced in 9 of the 22 patients with AV reciprocating tachycardia when they were in the supine position and in 17 when standing. The effective refractory period of the AV node markedly shortened, from 275 +/- 72 to 203 +/- 30 ms (n = 16, p less than 0.005) after standing. The effective refractory period of the accessory pathway shortened slightly, from 293 +/- 75 to 278 +/- 77 ms (n = 8, p less than 0.005), after standing. AV node reentrant tachycardia was induced in 3 of the 11 patients with AV node reentrant tachycardia when they were in the supine position and in 6 when standing. The effective refractory periods of the slow pathway and fast pathway shortened markedly, from 293 +/- 72 to 216 +/- 40 ms (n = 6, p less than 0.025) and from 416 +/- 85 to 277 +/- 50 ms (n = 10, p less than 0.005), respectively, after standing. Plasma norepinephrine levels increased during standing both in patients with AV reciprocating and in those with AV node reentrant tachycardia (n = 11, p less than 0.005, n = 8, p less than 0.005, respectively). In conclusion, standing, which is associated with increased sympathetic tone, changed the electrophysiologic properties of the reentrant circuits, facilitating induction of AV reciprocating tachycardia and AV node reentrant tachycardia.

Blood Pressure↗
PubMed1991

Prolonged and fractionated right atrial electrograms during sinus rhythm in patients with paroxysmal atrial fibrillation and sick sinus node syndrome.

Intraatrial catheter mapping of the right atrium was performed during sinus rhythm in 92 patients: Group I = 43 control patients without paroxysmal atrial fibrillation or sick sinus node syndrome; Group II = 31 patients with paroxysmal atrial fibrillation but without sick sinus node syndrome; and Group III = 18 patients with both paroxysmal atrial fibrillation and sick sinus node syndrome. Atrial electrograms were recorded at 12 sites in the right atrium. The duration and number of fragmented deflections of the atrial electrograms were quantitatively measured. The mean duration and number of fragmented deflections of the 516 atrial electrograms in Group I were 74 +/- 11 ms and 3.9 +/- 1.3, respectively. The criteria for an abnormal atrial electrogram were defined as a duration of greater than or equal to 100 ms or eight or more fragmented deflections, or both. Abnormal atrial electrograms were observed in 10 patients (23.3%) in Group I, 21 patients (67.7%) in Group II and 15 patients (83.3%) in Group III (Group II versus Group I, p less than 0.001; Group III versus Group I, p less than 0.001). The mean number of abnormal electrograms per patient with an abnormal electrogram was 1.3 +/- 0.7 in Group I, 2.5 +/- 1.9 in Group II and 3.5 +/- 2.5 in Group III (Group I versus Group II, p less than 0.01; Group II versus Group III, p less than 0.05). A prolonged and fractionated atrial electrogram characteristic of paroxysmal atrial fibrillation can be closely related to the vulnerability of the atrial muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Conduction properties of the antegrade fast and slow AV nodal pathways associated with AV nodal reentrant tachycardia.

To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500 msec, p less than 0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.

Adolescent↗
PubMed1990

Prediction of a fatal atrial fibrillation in patients with asymptomatic Wolff-Parkinson-White pattern.

Paroxysmal atrial fibrillation (PAF) in patients with manifest WPW syndrome can be a life-threatening arrhythmia by deterioration into ventricular fibrillation. In patients with asymptomatic WPW pattern, the first PAF may lead to ventricular fibrillation or sudden death. Therefore, the purpose of this study was to predict a fatal PAF in patients with asymptomatic WPW pattern. The patient population was divided into two groups: (1) 145 patients with manifest WPW syndrome, excluding intermittent ones (32 with an episode of PAF, 49 with AV reciprocating tachycardia alone, and 64 without any episode of paroxysmal tachyarrhythmia), and (2) mixed group of patients with and without WPW syndrome (36 with an episode of PAF and 66 without PAF). The results were as follows: (1) (a) out of 32 patients with WPW syndrome and PAF, 8 patients were observed to have both the shortest preexcited R-R interval of less than 200 msec during PAF and the shortest antegrade effective refractory period of the accessory pathway (ERP-AP) of less than 250 msec, 7 of whom had dizziness or syncope during PAF and 2 died suddenly during the follow-up period; (b) 21 (32.8%) out of 64 patients with asymptomatic WPW pattern showed the shortest antegrade ERP-AP less than 250 msec; (2) patients with PAF had a higher tendency to develop repetitive atrial firing (RAF), as well as fragmented atrial activity (FAA), which were induced using programmed atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1989

Electrophysiologic properties of atrial muscle in paroxysmal atrial fibrillation.

The electrophysiologic properties of atrial muscle were studied by programmed atrial stimulation in 42 patients with paroxysmal atrial fibrillation (PAF) and in 53 control patients without PAF. Single premature atrial stimulation was given at the right atrial appendage following 8 basic stimuli with a basic cycle length of 500 ms. Repetitive atrial firing (RAF) was defined as the occurrence of 2 or more successive premature atrial activations following single premature atrial stimulation. Fragmented atrial activity (FAA) was defined as an increase by more than 75% of the duration of the atrial electrogram in response to a single premature stimulation. Interatrial conduction delay was defined as an increase of the conduction time by more than 50 ms in response to a single premature stimulation. RAF was induced in 26 of 42 patients (61.9%) with PAF and in 14 of 53 control patients (26.4%). FAA and interatrial conduction delay were elicited in 69.0 and 80.9% of patients with PAF and in 34.0 and 56.6% of control patients, respectively. In 16 patients with PAF in whom RAF was not induced, FAA developed in 11 patients (68.8%). In 88.1% of 42 patients with PAF and in 41.5% of 53 controls, RAF or FAA, or both, were elicited by atrial premature stimulation. It is concluded that the incidence of RAF and FAA were significantly higher in patients with PAF than in the control group, and the induction of RAF or FAA, or both, was closely related to the vulnerability of the atrial muscle to atrial fibrillation.

Atrial Fibrillation↗