Muneo Tanigawa

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)

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.

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.

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)