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At least 19 recordsLinked to original sources
PubMed1975

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↗
PubMed1989

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↗
PubMed1978

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↗
PubMed1975

[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↗
PubMed1991

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↗
PubMed1991

[Pathological modifications of the P wave due to probable primary changes in intra-atrial conduction].

Two cases of variable changes in ECG P oscillation not due, as is usually the case, to familiar cardiac or respiratory conditions suggested a review of the literature on the subject. It is concluded that these anomalies are the result of changes in the intra-atrial conduction of the stimulus through preferential ways or to aberrant atrial conduction. These are situations of no little practical interest because they may be precursors of major rhythm disturbances such as atrial flutter or atrial fibrillation.

Electrocardiography↗
PubMed1986

Noninvasive assessment of ventriculo-atrial conduction and early experience with the tachycardia termination algorithm in pacemaker-mediated tachycardia.

Since the advent of physiologic dual chamber pacing systems, pacemaker-mediated tachycardia (PMT) has occurred and the need for invasive measurement of ventriculo-atrial conduction (VAC) has arisen. The variability in VAC and the potential for PMT often make it necessary to assess for the presence or absence of VAC at different points in time. We noninvasively evaluated 20 pacemaker patients for the presence or absence of VAC. We compared ventriculo-atrial conduction time (VACT) obtained with the atrial sense event maker with that obtained from Holter monitoring and invasive methods. The incidence of spontaneous (S) and induced (I) PMT and the efficacy of the tachycardia termination algorithm (TTA) was assessed. Fourteen of 20 had VAC with invasive or noninvasive methods. Twelve of 19 had PMT (63%); three were sustained (greater than 15 beats). We conclude that VACT assessed with the atrial sense event marker (ASEM) yielded a high correlation when compared to the Holter monitor data obtained utilizing our methodology. PMT is commonly a nonsustained (less than 15 beats) event, and the TTA is effective in sustained PMT. Myopotential sensing, atrial premature contractions and loss of atrial capture are common mechanisms in the initiation of PMT.

Adult↗
PubMed1977

Human atrial conduction with reference to heart rate and refractory periods.

Atrial conduction time (ACT) between a stimulating pacemaker electrode and an "impulse-detecting" monophasic action potential (MAP) electrode has been determined in 20 healthy males. A small increase in ACT was found with increasing paced heart rates. Using the extra stimulus technique, ACT was found to increase when the early ectopics approached the atrial effective refractory period (AERP). The degree of ACT prolongation was similar at long and short basic ACTs, indicating that the slowing of impulse propagation probably occurred near the simulating electrode and presumably within 1/2-1 cm from that electrode. The increase in ACT close to the AERP was of importance when determining the atrioventricular refractory period. In three recordings a supernormal phase of conduction was found. The small errors of the MAP recordings in detecting the time of excitation make the method sensitive enough to detect small differences in ACT.

Action Potentials↗
PubMed1978

[The effect of diphenylhydantoin on the automatism of the sinus node and on the sino-atrial conduction time in patients with and without sick sinus syndrome].

In 30 test persons (15 patients with disturbed function of the sino-auricular node, 9 of them with classical sick-sinus-syndrome as well as 15 test persons without disturbance of the sino-auricular node, of them 7 healthy ones) the influence of diphenylhydantoin on the function of the sino-auricular node was tested. By means of atrial stimulation the so-called sino-atrial conduction time, the recreation time of the sino-auricular node as well as the duration of the sinus period before and after intravenous application of 250 mg of diphenylhydantoin was estimated. The auricular stimulation was carried out either through an oesophageal electrode probe or usually through an electrode catheter directly placed in the right atrium. In the entire collective the sino-atrial conduction time did prolong itself statistically not significantly by 2 +/- 5ms (x +/- 2 s), in which cases there was not to be observed a different behaviour between test persons with a healthy rhythm and patients with disturbed function of the sino-auricular node. In 2 patients with sick-sinus-syndrome, however, after diphenylhydantoin and individual atrial stimulation in each case sino-atrial blockings of higher degree developed. The maximum absolute and corrected recovery time of the sino-auricular node prolonged itself in patients with syndrome of the sino-auricular node by on an average 1406 +/- 2120 ms or 1378 +/- 2338 ms, in which cases in 1 test person a threatening prolongation of the poststimulation pause to 10 s developed. In another patient after application of diphenylhydantoin an atrial arrest was observed. The automatism of the sino-auricular node of test persons with healthy rhythm was not influenced.

Arrhythmia, Sinus↗
PubMed1976

[Interpretation of a bundle of His electrogram (using the spike potentials of the sinus node and atrial conduction tracts in the analysis)].

Spike potentials of the sinus node and of the atrial conductivity pathways were recorded by way of heart microcatheterization via the subclavian vein in 40 canine experiments and in 307 patients, using the obtained data for a more precise interpretation of the bundle of His electrogramme taken in the course of these examinations. The importance of the density of the spikes for their successful recording was studied, and it was found that the onset of the atrial A--wave preceeded that of the P-wave by 10-30 ms on ECG tracings recorded from the body surface. The atrial A--complex recorded with the aid of an intracardiac unipolar electrode from the right atrium was found to consist of a slow depolarization wave of the atria and of three spike potentials (A1, A2 and A3). The A2 spike coinsides with the peak of the P-wave in the II lead and reflects the moment of the impulse's arrival at the atrioventricular node along the Bachman and Wenkebach's tract, while the A3 spike coinsides with the termination of the P-wave in the II lead being dependent on the depolarization of the Torel's tract. The P--A interval should be measured between the sinus spike and the A2 spike, while the A--H interval--between the A2 spike and the H-potential.

Action Potentials↗
PubMed1976

[Significance of spike potentials in the sinus nodes and atrial conduction system during interpretation of bundle-of-his electrography].

The article deals with the issues of the His bundle electrogram (HBE) analysis, using the spike potentials of the sinus node and the atrial conductive tracts for the interpretation of the HBE. The HBE and the atrium spike potentials have been recorded in 40 dogs and in 307 patients. According to our data the onset of the A-wave on the IcECG begins in some msec earlier than the onset of the P-wave on the standard ECG leads. The spike potentials of the sinus node have been recorded directly at the sinus node area, the onset of which begins in 20-40 msec earlier than the onset of the P-wave. By our data the atrial A-wave recorded from the right atrium on the IcECG consists of the slow wave showing summary effect of the atrium depolarization and the three spikes (A1, A2, A3). They are recorded at the beginning (A1) middle (A2) and the end (A3) of the P-wave and reflect the quick impulse spread through the atrium conductive tracts. The moment of the impulse coming to the AV nodes is reflected by the atrial spike A2. The time of the impulse spread from the sinus node to the AV node shows exactly the interval from the onset of the spike potential of the sinus node till the spike A2. The interval from the spike A2 to the H-potential (A2-H) shows the impulse spread time through the AV node. The recording of the HBE and the atrium spike potentials was performed by means of the microcatheter of own construction (with the unipolar electrodes, external diameter of which does not exceed 1 mm) after our method of the heart microcatheterization through the subclavian vein.

Action Potentials↗
PubMed1978

Multicentric origin of the atrial depolarization wave: the pacemaker complex. Relation to dynamics of atrial conduction, P-wave changes and heart rate control.

In studies to ascertain the basis of dynamic changes in the P wave, bipolar epicardial potentials were recorded from multiple atrial electrodes in dogs. One hundred to 120 activation times were displayed by a digital computer and used to construct atrial isotemporal activation sequence maps. Changes in heart rate or beat-to-beat cycle length were induced by vagal stimulation or infusion of autonomic mediating drugs. Changes in cycle length were associated with dynamic changes in the atrial activation sequence and surface P-wave. A conspicuous finding was that epicardial atrial depolarization began at three widely separated locations. These three points were consistently present in all animals and were generally located at the 12, 3, and 6 o'clock positions of the superior vena cava-right atrial junction. The dynamic changes in P waves and atrial activation sequence which accompanied the changes in cycle length were due to sudden shifts in the point of earliest activity between the three early sites. Asymmetric atrial depolarization with more rapid conduction along the crista terminalis, superior interatrial band, and pectinate muscles was present in all dogs. Although the anisotropic atrial geometry played an important role in the asymmetric conduction, the widely distributed onset of activity contributed significantly to the uneven spread. The multiple points of origin of the atrial wavefront might be explained by either a trifocal, distributed pacemaker or the epicardial exits of three specialized pathways conducting an impulse emanating from a single focus. These data explain the dynamic variation in P-wave morphology in normal hearts and also imply a relationship between the altered origin of atrial depolarization, atypical P waves, brady- or tachyarrhythmias, and heart rate control.

Action Potentials↗
PubMed1976

[Intra-atrial conduction disorders of 2d degree].

Five patients with second degree intraatrial block are presented. The first three cases had a sick sinus syndrome with sinus bradycardia, broad P waves and episodes of atrial flutter or fibrillation. In these patients a Wenckebach phenomenon could bei elicited by atrial stimulation at a critical driving rate between the stimulated site and the recording electrode. In the first patient this conduction disturbance was obtained at several right atrial stimulation sites. The block could be elicited in the other two patients only in a limited area of the right atrium respectively only by left atrial pacing. In the remaining two patients an atrial tachycardia with block was observed. The intraatrial conduction disturbance was manifested as an exit block around the ectopic pacemaker. In one patient the tachycardia was induced by digitalis intoxication. In the other patient no etiologic factor of the tachycardia could be found. While the first three patients presented intraatrial conduction disturbances already in sinus rhythm, the last two cases showed after recovery from the atrial tachycardia P waves of normal duration and configuration.

Aged↗