Masahiko Fukatani

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 calheter mapping of the right atrium and the afrial 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 (he 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, H (38%) patients ha d 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 eJectrograms in sinus rhythm within the right atrium have: (1) a significantly longer P wave duration: (2) a significantly longer intraatrial and interafrial conduction time of sinus impulses; and (3) a significantly greater sinus node dysfunction and higher incidence of induction of sustained atriai 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.

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 < 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 < 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.

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.

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.

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)

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

Abstract E-4031 is classified as a class III antiarrhythmic agent of the Vaughan Williams classification. Most class III agents have other antiarrhythmic effects in addition to the potassium channel-blocking action.1–3 In contrast, E-4031 could be considered as the selective blocker of the potassium channel responsible for prolonging the action potential duration without affecting the conduction time.4–6 From several experimental studies, it is believed that E-4031 suppresses reentrant tachyarrhythmias due to prolongation of the effective refractory period.7–12 However, the effects of E-4031 on electrophysiologic properties of the heart in humans are unknown. The present report investigates the electrophysiologic effects and toxicity of E-4031 in humans by means of electrophysiologic studies.

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)

Double Response of the Ventricle During Transient Entrainment in a Common Atrioventricular Nodal Reentrant Tachycardia

We report a patient with slow‐fast atrioventricuiar (AV)nodal reentrant tachycardia, in which double ventricuJar 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.