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At least 19 recordsLinked to original sources

Chronic ventricular pacing with ventriculo-atrial conduction versus atrial pacing in three patients with symptomatic sinus bradycardia.

Three patients with symptomatic sinus bradycardia due to sick sinus syndrome were treated with permanent ventricular pacing for periods ranging from 2.5 to 4 years. All three patients had ventriculo-atrial conduction on routine electrocardiography. Although ventricular pacing was effective, they complained of fatigue, lightheadedness, and near syncope. Hemodynamic studies revealed the presence of regular cannon waves in the right atrium as well as in the pulmonary artery wedge pressure curves. Temporary atrial pacing resulted in disappearance of the cannon waves and a significant rise in cardiac output (32-48%). After normal atrio-ventricular conduction was confirmed by rapid atrial stimulation and His bundle electrocardiography, the pacing mode was changed to permanent atrial pacing on demand. The effort tolerance of the patients markedly improved, and the previously mentioned symptoms disappeared. Control hemodynamic studies 9 to 12 months after implantation of the atrial demand pacemaker showed that the improvement in cardiac performance was maintained.

Aged

Analysis of sino-atrial conduction in man using premature atrial stimulation.

Sino-atrial conduction was investigated using premature atrial depolarization in 25 patients seven of whom had sino-atrial block. The results obtained in this investigation were evaluated plotting the test cycle (expressed as difference between the basic sinus cycle and the test cycle as a percentage of the basic sinus cycle) as a function of the return cycle (expressed as difference between the return cycle and the basic cycle as a percentage of the basic sinus cycle). In normal subjects, premature atrial depolarizations elicited in the last 10-20% of the spontaneous sinus cycle, produced a progressive prolongation of the return cycle and the points correlating the return cycle index to the test cycle index fell above the diagonal of the plotting system. After earlier premature atrial depolarizations, the return cycle remained of the same length, and the points correlating the return cycle index to the test cycle index fell along a line parallel to the y-axis ('plateau'). The mean value of the returning cycles (as expressed above) corresponding to the test cycles (as evaluated above) included in the first 5% of the 'plateau' can be defined as 'the sino-atrial conduction index'. This index, the sum of conduction into and out of the sinus node, was found to range from 79 to 185 ms. By assuming similar anterograde and retrograde conduction, the sino-atrial conduction time ranged from 39.5 to 97.5 ms (mean value=70 ms). In the patients with sino-atrial block, fully compensatory pauses were observed for atrial premature depolarizations elicited up to the last 25-35% of the atrial cycle, and a slow and progressive divergence from the diagonal of the plotting system was seen instead of the 'plateau'. In these patients the sino-atrial conduction index ranged from 151 to 297 ms (mean 253 ms). By assuming similar antegrade and retrograde conduction, the sino-atrial conduction time ranged from 75.5 to 148.5 ms (mean value=126.5 ms) with a statistically significant difference with respect to normal subjects (P=0.001).

Adult

Intra-atrial conduction delay and fragmented atrial activity in patients with paroxysmal atrial fibrillation.

To examine the electrophysiologic characteristics of paroxysmal atrial fibrillation (PAF), we studied intra-atrial conduction delay and fragmented atrial activity during premature stimulation of high right atrium in the following four groups: Group I (n = 25), patients without PAF and without sick sinus syndrome (SSS); Group II (n = 22), patients with PAF but without SSS; Group III (n = 10), patients without PAF and with SSS; Group IV (n = 6), patients with PAF and SSS. Intra-atrial conduction delay was the increase in the interval (from the stimuli to the coronary sinus electrogram) observed with early premature beats greater than or equal to 20 ms compared with that of basic rhythm. Fragmented atrial activity was defined as disorganized atrial activity greater than or equal to 150% of the duration of high atrial activity of basic beats recorded. The conduction delay zone (CDZ) and fragmented atrial activity zone (FAZ) were significantly wider in Groups II, III and IV than in Group I. There were no significant differences in either CDZs or FAZs among Groups II, III and IV. Thus, the widening of CDZs and/or FAZs are characteristic of PAF and SSS. CDZ and FAZ may be good indices of development of PAF in patients without SSS.

Adolescent

Prolonged atrial conduction. A major predisposing factor for the development of atrial flutter.

Electrophysiological studies were performed during sinus rhythm on 21 patients who had demonstrated the spontaneous occurrence of sustained atrial flutter. The purpose was to determine if atrial conduction disease is a prediposing factor for the development of atrial flutter. Patients with atrial enlargement were excluded from the series. The control group consisted of 11 age-matched patients with normal electrocardiograms and electrophysiology studies. The flutter group showed prolongation of the mean right intra-atrial conduction time at 50 msec (control of 37 msec, P less than 0.05), the mean interatrial conduction time at 92 msec (control of 44 msec, P less than 0.001) and the mean P wave duration at 132 msec (control of 112 msec, P less than 0.01). The flutter group also demonstrated a higher incidence of sinus node dysfunction and ventricular conduction disease compared to the control group. These data indicate that patients who develop atrial flutter have atrial conduction disease. Atrial conduction disease appears to be 1) a major prediposing factor for the development of atrial flutter and 2) a part of the fibro-degenerative conduction disease spectrum.

Arrhythmia, Sinus

[The effect of drugs on "sino-atrial conduction time" and on sinus-node automaticity in man].

The effect of atropine, propafenone, and disopyramide on sinus node automaticity and "sino-atrial conduction" was tested in normal patients and patients with the sick sinus-syndrome. "Sino-atrial conduction time" was estimated indirectly by the extrastimulus technique. Atropine (n = 11) caused a significant increase in heart rate in all patients. The sinus node recovery time was shortened in 10 patients. "Sino-atrial conduction time" decreased on an average 35% (P less than 0.01). Three patients with a sick sinus-syndrome demonstrated a change of the pattern of the postextrasystolic pauses indicating great improvement in sino-atrial conduction. Propafenone (n = 10) led to a significant prolongation of the sinus node recovery time by 17% and of the "sino-atrial conduction time" by 27%. Disopyramide (n = 8) had no significant influence on heart rate and "sino-atrial conduction time". Sinus node recovery time was not changed in 6 patients. However, in two patients with a sick sinus-syndrome a dangerous prolongation of the sinus node recovery time after application of disopyramide occurred. The results indicate that atropine enhances sinus node function and sino-atrial conduction. On the other hand, propafenone and disopyramide exert either a depressant influence on sinus node automaticity or on sino-atrial conduction.

Atropine

Ventriculo-atrial conduction in patients with normal and impaired atrio-ventricular conduction.

Ventriculo-atrial (VA) conduction was studied in 133 patients with various kinds of arrhythmias using intracardiac electrograms and programmed stimulation. One-to-one VA conduction was observed during RV pacing at the rate just above the sinus rate in 6 of 31 patients (19.4%) with advanced AV block, in 7 of 26 patients (26.9%) with impaired AV nodal conduction, in 25 of 71 patients (35.2%) with normal AV nodal conduction and 3 of 5 patients (60%) with enhanced AV nodal conduction. However, the differences between these groups were not significant. There was no significant difference in either the AH block rate during RA pacing or the antegrade functional refractory period (FRP) of the AV node in patients with or without VA conduction, and the VA block rate during RV pacing was not significantly correlated with the AH block rate or the FRP of the AV node. VA conduction time (S-HRA) also showed no significant differences between these groups. The mean VA conduction time during RV pacing at rates of 60 to 80 bpm was 208 +/- 87 msec, ranging from 100 to 395 msec. In conclusion, AV conduction disturbances may influence VA conduction, but VA conduction cannot be predicted from antegrade conductivity.

Arrhythmias, Cardiac

Localization of the accessory pathway in the Wolff-Parkinson-White syndrome from the ventriculo-atrial conduction time of right ventricular apical extrasystoles.

In 18 consecutive patients with the Wolff-Parkinson-White syndrome undergoing electrophysiologic study, the ventriculo-atrial conduction time of right ventricular apical extrasystoles which advanced atrial activation during circus movement tachycardia was studied in relation to accessory pathway location. Accessory pathway location was determined by delta wave morphology during maximal pre-excitation, mapping of atrial activation during circus movement tachycardia and ventricular pacing, the effect of bundle branch block on ventriculo-atrial conduction time during circus movement tachycardia, and the effect of pacing from different sites in the atria on the stimulus-to-delta wave interval. In 7 patients with septal accessory pathways, ventriculo-atrial conduction time was similar during circus movement tachycardia and following right ventricular apical extrasystoles (mean difference 0 +/- 6 ms, range -5 to +10 ms). In contrast, in 11 patients with a left free wall accessory pathway, ventriculo-atrial conduction time increased by 46 +/- 15 ms (range 15 to 65 ms) following right ventricular apical extrasystoles. Therefore, measurement of the ventriculo-atrial conduction time of right ventricular extrasystoles during circus movement tachycardia provides an easy way to distinguish between septal and left free wall accessory pathways. This finding may be of particular use in determining the location of concealed bypass tracts.

Adolescent

Vagal effects on sinoatrial and atrial conduction studied with epicardial mapping in dogs: the influence of pacemaker shifts on the measurement of sinoatrial conduction time.

The influence of pacemaker shifts on sinoatrial conduction time (SACT) was studied by investigating the effects of vagal stimulation on SACT and atrial conduction in anesthetized open-chest dogs. Isochronal maps were drawn from unipolar electrograms simultaneously recorded at 60 epicardial sites on the right atrial free wall and the inferior and superior vena cava. Vagal stimulation caused atrial conduction velocity to increase from 0.99 +/- 0.10 m/s (mean +/- SD) to 1.23 +/- 0.23 m/s (p less than 0.01), and the pacemaker to shift to lower positions along the superior vena cava - right atrial junction. As a result of the changes, the distances and the atrial conduction times from the stimulating and recording electrodes to the pacemaker site varied, and hence, the SACT values obtained indirectly by premature atrial stimulation varied. The isochronal maps were used to measure the atrial conduction times from stimulating to recording electrodes (a), from stimulating electrode to pacemaker site (b), and from pacemaker site to recording electrode (c). Indirect SACT was lengthened by vagal stimulation from 43 +/- 16 to 64 +/- 22 ms (p less than 0.02). After correcting by subtracting the atrial conduction time (b + c - a), these values became 26 +/- 6 ms (control) and 40 +/- 11 ms (vagal stimulation) (p less than 0.01). SACT values measured directly from the electrograms were 27 +/- 7 ms (control) and 42 +/- 10 ms (vagal stimulation) (p less than 0.01). Corrected indirect SACTs were closer to direct SACTs than were the uncorrected indirect SACTs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Anterograde sinuatrial conduction evaluated by sinus node electrogram in atropine blocked retrograde atrial conduction.

Two cases are described where atropine induced the disappearance of reset zone as response to premature atrial stimulation for blocked retrograde atrial conduction. Because of this, sinuatrial conduction time could not be estimated. The sinus node electrogram allowed the direct measurement of sinuatrial conduction and showed a facilitated anterograde conduction through the perinodal fibers after administration of the drug.

Atropine

Experimental validation of sino-atrial conduction time using sinus node potential recording, right and left atrial continuous pacing method.

In an experimental study indirect sino-atrial conduction time (SACT) was measured, using continuous pacing method from right and left atrial sites, and compared with direct SACT obtained from sinus node potential recording, all the determination being done before and after autonomic blockade. The distance between the two sites of stimulation may be taken into account as a correction factor for SACT determination. The SACT obtained with sinus node potential technique is the same as the indirect SACT after autonomic blockade. These findings are valuable for SACT determination with transesophageal pacing method. Left atrial pacing, thus transesophageal pacing, is a valuable method in estimating the SACT, but a time correction and autonomic blockade is required in order to obtain a real value, eliminating the extrinsic influences.

Animals

Atrial conduction: effects of extrastimuli with and without atrial dysrhythmias.

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Retrograde (ventriculo-atrial) conduction, premature beats, pseudotricuspid regurgitation, systolic atrial sounds and pacemaker sounds observed together in two patients with ventricular pacing.

Two patients were found to have retrograde atrioventricular conduction with premature beats during permanent ventricular pacing. In both patients the auscultatory phenomena had been heard and recorded that had been described as independent signs, but all together in the same patient had not been reported before. In one of the patients pseudotricuspid regurgitation was observed with Doppler echocardiography and the other was suspected having the same. It seems that patients with these symptoms deserve high preventive care and attention.

Arrhythmias, Cardiac