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PubMed1981

[The effects of digoxin administration on normal and pathological sinus node function. An electrophysiological study (author's transl)].

In 12 normal subjects (group I), in 12 subjects with asymptomatic sinus bradycardia (group II) and in 18 patients with symptomatic sick sinus syndrome (group III), sinus node cycle length (SNCL), sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), sino-atrial conduction time (SACT), have been evaluated before and after an acute digoxin administration. Mean value of SNCL lengthened significantly in all groups. Mean value of SNRT increased moderately in the first group, remarkably in the third group, whereas it showed a mild but statistically insignificant increase in the second group. Mean value of CSNRT was significantly lengthened only in the third group. Mean value of SACT showed a mild but statistically insignificant lengthening in all groups. In order to investigate the importance of the parasympathetic action induced by digitalis, in 4 normal subjects, in 4 patients with asymptomatic sinus bradycardia, and in 10 patients with symptomatic sick sinus syndrome, SNCL, CSNRT and SACT has been evaluated after an intravenously, administration of atropine, following digoxin. In the paper the intricate mechanisms by which digitalis affects the parameters of sinus nodal function especially in patients with symptomatic sick sinus syndrome, are discussed. In disagreement with the mot papers reported in the literature we think that an acute digoxin administration is able to worsen the electrophysiological parameters of sinus nodal function especially in patients with symptomatic sick sinus syndrome.

Adult↗
PubMed1993

[Non-invasive programmed transthoracic ventricular stimulation].

In 10 healthy volunteers programmed transthoracic stimulation of the ventricles was performed using two commercially available non-invasive pacemakers. The connection of the oesophageal stimulator SP-5 with the transthoracic ventricular stimulator NP-4D made it possible to obtain a two-lead ECG tracing without artefacts. The quality of the obtained tracings (surface tracing and oesophageal tracing) made it possible to assess accurately the ventriculo-atrial conduction. The examinations performed indicate the practical use of combined oesophageal and transthoracic stimulation during non-invasive diagnosis.

Adult↗
PubMed1993

[A case of mitral regurgitation treated by combined superior transseptal approach and electrophysiological examination of the sinus node function].

A 67-year-old man with mitral regurgitation underwent mitral valvoplasty and annuloplasty successfully. Combined superior transseptal approach was adopted to expose the mitral valve, because the left atrium was small. The exposure of the mitral valve was excellent. But this approach cannot avoid damaging the sinus node artery, so that why the sinus node function was examined electrophysiologically before and after the operation. Sino-atrial conduction time (SACT) and corrected sinus node recovery time (CSRT) were measured as the indices of the sinus node function. Both SNCT and CSRT after the operation was within normal range. As far as this case, combined superior transseptal approach, which gave good exposure of the mitral valve but needed to cut the sinus node artery, did not deteriorate the sinus node function.

Aged↗
PubMed1996

[Paroxysmal nocturnal dyspnea as a severe expression of the pacemaker syndrome].

Single-chamber ventricular pacing remains a frequent pacing method for symptomatic bradyarrhythmias. VVI pacing is effective in maintaining an acceptable ventricular rate, preventing severe bradycardia. However it may cause many important symptoms as a consequence of loss atrio-ventricular synchrony. Pacemaker syndrome (i.e. symptoms and signs caused by inadequate timing of atrial and ventricular contractions) may range in severity from vague pacing awareness to congestive heart failure. This event may be related more to retrograde ventricular-atrial conduction than to the absence of atrio-ventricular synchrony. We report 2 cases of VVI pacing complicated by nocturnal dyspnea (sign of congestive heart failure) as severe manifestation of pacemaker syndrome. By implantation of dual-chamber pacemaker, atrio-ventricular synchrony was restored, nocturnal dyspnea disappeared and has not recurred during clinical follow-up (12 and 4 months respectively for the first and second case.

Aged↗
PubMed1991

Conduction in bullfrog atrial strands: simulations of the role of disc and extracellular resistance.

A number of fundamental properties of intercellular conduction in simulated cylindrical strands of cardiac tissue are examined. The paper is based on recent biophysical information describing the transmembrane ionic currents in bullfrog atrial cells as well as anatomical data on the structures (gap junctions) responsible for the coupling between cells in that tissue. A mathematical model of the single bullfrog atrial cell based on suction microelectrode single-cell voltage clamp data is employed, as well as a modified version of the well-known model of Heppner and Plonsey, to characterized the resistive connections between adjacent cells in a cardiac strand. In addition, the simulated cellular strand is assumed to be encased in a cylindrical, resistive endothelial sheath, thus forming an idealized atrial trabeculum; the trabeculum is immersed in an extensive volume conductor. It is possible to simulate both uniform and discontinuous conduction in this atrial strand model by appropriately changing the resistance of the intercalated discs that occur at cell boundaries. The conduction velocity achieved in the normal or control case is within the range of conduction velocities that have been measured for bullfrog atrial trabeculae using optical methods. Extracellular resistance is shown to have a significant effect on both conduction velocity and the critical value of disc resistance at which discontinuous conduction first occurs. Since the atrial cell model employed in this study is based on experimental data and can accurately simulate the atrial action potential, the transmembrane ionic currents generated by the model are capable of providing detailed information concerning the mechanisms of intercellular current spread, particularly in the region of the intercalated disc.

Animals↗
PubMed1997

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter.

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.

Adolescent↗
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↗
PubMed1979

Conduction disturbances after surgical correction of ventricular septal defect by the atrial approach.

Conduction disturbances have been documented after correction of ventricular septal defects by the ventricular route. Recently, repair of the ventricular septal defect has been through the right atrium to overcome damage to the conduction system and a right ventriculotomy. Thirty-nine children with ventricular septal defects under the age of 5 years were operated upon by the atrial route (group 1). The incidence of conduction disturbances in this group was compared with that occurring in 19 children of comparable age with a ventricular septal defect repaired via a right ventriculotomy (group 2). Complete right bundle-branch block developed in 13 of 39 children (33.3%) in group 1, compared with 15 of 19 children (78.9%) in group 2. This was a statistically significant reduction in complete right bundle-branch block in group 1. The incidence of left axis deviation occurring with complete right bundle-branch block was similarly statistically reduced. Transient complete heart block and arrhythmias were not statistically different in the two groups. The atrial approach to the repair of the ventricular septal defect significantly reduced the incidence of complete right bundle-branch block alone and occurring with left axis deviation.

Aortic Coarctation↗
PubMed1999

Sick sinus syndrome with and without atrial fibrillation: atrial refractoriness and conduction characteristics.

BACKGROUND: Clinical electrophysiology has focused the attention on the electrophysiological properties of the atrial muscle in patients with atrial fibrillation: shortened and inhomogeneous refractoriness and local and regional conduction slowing, as well as prolonged intra- and interatrial conduction disturbances, are well described as electrophysiological parameters associated with the genesis of atrial fibrillation. Patients with sick sinus syndrome are variously included in these studies, but electrophysiological characteristics of patients with sick sinus syndrome alone appear less investigated, even if atrial fibrillation is part of its natural history. The aim of the present study was to define the electrophysiological characteristics of sick sinus syndrome patients with or without paroxysmal atrial fibrillation, compared to subjects without atrial fibrillation and sick sinus syndrome. METHODS: We reviewed the electrophysiological data of 39 patients with sick sinus syndrome (mean age 70 +/- 8 years), who underwent an electrophysiological study in sinus rhythm for the evaluation of the atrial substrate. In 12 patients an associated history of paroxysmal atrial fibrillation was documented. Twenty-seven patients were included in the study with a diagnosis of sinus node dysfunction alone. We also considered as control group 25 subjects (mean age 63 +/- 14 years), referred to our electrophysiological laboratory for unexplained syncope or atrioventricular disturbances. Following pharmacological wash-out and at a drive cycle of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and the latent vulnerability index (effective refractory period/A2), were measured. In addition, the P-wave duration during spontaneous sinus rhythm on the surface ECG in D II/V1 leads was measured. RESULTS: Between sick sinus syndrome patients with or without atrial fibrillation, no significant statistical differences in electrophysiological parameters were found. When compared to the control group, sick sinus syndrome patients did not show any differences in effective refractory period (239 +/- 34 vs 250 +/- 29 ms), functional refractory period (276 +/- 28 vs 280 +/- 32 ms), S1-A1 (38 +/- 16 vs 33 +/- 11 ms), and S2-A2 latency (68 +/- 25 vs 63 +/- 25 ms). In contrast, we observed remarkable differences in terms of atriogram duration A1 (60 +/- 20 vs 39 +/- 13 ms, p < 0.001), A2 (95 +/- 34 vs 57 +/- 18 ms, p < 0.001), and effective refractory period/A2 (2.8 +/- 1.2 vs 4.8 +/- 1.7 cm, p < 0.001). Also the duration of the P wave was longer (103 +/- 17 vs 94 +/- 45 ms, p < 0.05). CONCLUSIONS: In sick sinus syndrome patients with or without atrial fibrillation, electrophysiological characteristics appear homogeneous. When compared to the control group, refractoriness was quite similar. In contrast, the most important abnormalities appear based on conduction slowing disturbances, responsible for a low latent vulnerability index. This could explain, at least in part, the tendency of sick sinus syndrome to develop atrial fibrillation as a part of its natural history. At present, the influence of an altered electrophysiological substrate on pharmacological or pacing therapy in patients with sick sinus syndrome is not yet known.

Aged↗
PubMed2002

[Atrioventricular conduction and permanent atrial pacing].

UNLABELLED: The goal of the report was to evaluate changes of atrioventricular conduction in patients with sick sinus syndrome treated with permanent atrial pacing. METHODS AND RESULTS: 150 patients (82 women and 68 men) with implanted permanent atrial AAI and AAIR pacemakers were followed for 5.9 +/- 3.6 years (maximum 15 yrs). After mean 5.9 years of follow up incidence of III degrees AVB was 0.7%, II degrees AVB--2.7%, and I degree AVB--2.74%; twenty six of 150 patients showed nonphysiological increase of the SQ interval at pacing rate 120 imp/min. CONCLUSIONS: 1. Atrioventricular conduction in elderly patients with sick sinus syndrome is decreasing. 2. Continuous observation of the atrioventricular conduction is obligatory in patients with single chamber AAI pacing. 3. Upper heart rate limit in patients with single chamber atrial pacing must be programmed taking into account changes of atrioventricular conduction.

Adult↗
PubMed1999

Isoproterenol to evaluate resumption of conduction after right atrial isthmus ablation in type I atrial flutter.

BACKGROUND: After radiofrequency (RF) ablation of atrial flutter (AFL), the demonstration of bidirectional isthmus conduction (BIC) block is considered the hallmark of a successful procedure. The purpose of our study was to test the persistence of BIC block after isoproterenol administration and to evaluate the importance of this finding with regard to AFL recurrences. METHODS AND RESULTS: RF ablation of AFL was performed in 44 consecutive patients with type I AFL by linear ablation of the posterior isthmus (n=29 patients), septal isthmus (n=4 patients), or both right atrial (RA) isthmi (n=11 patients). The procedural end point was complete BIC block and noninducibility of AFL. In case of noninducibility and apparent BIC block, the pacing protocol was repeated under isoproterenol infusion (1 to 3 microgram/min). Reversal of apparent BIC block occurred in 7 (15.9%) of 44 patients. Six patients had bidirectional and 1 had unidirectional resumption of isthmus conduction. Counterclockwise AFL could be reinduced in 4 of these patients. Two to 24 (median, 4) additional RF applications were required to achieve permanent BIC block. At a mean follow-up of 7.3+/-7.6 months (range, 2 to 31 months), 2 (4.5%) of 44 patients had AFL recurrences. CONCLUSIONS: Partial linear RF ablation could possibly aggravate preexisting nonuniform anisotropic conduction in the RA isthmus, resulting in profound conduction slowing and apparent BIC block. Isoproterenol can unmask apparent BIC block, thus providing an opportunity to assess the possibility of reversal of BIC block and completeness of isthmus ablation during the same procedure. The low incidence (4.5%) of AFL recurrences at follow-up suggests that noninducibility and BIC block under isoproterenol infusion may be a better end point for successful AFL ablation.

Adult↗
PubMed2002

Ablation of atrial flutter: block (isthmus conduction) or not a block, that is the question?

It is important to identify residual slow conduction and minimize the chance of resumption of conduction after right atrial isthmus ablation to reduce the chance of recurrence of atrial flutter (AFL). The aim of this article is to discuss the best possible way of confirming a bi-directional isthmus conduction (BIC) block after ablation of an isthmus-dependent AFL. A combination of activation and double potential mapping seems to be the most practical way of acutely confirming the BIC block.

Journal Article↗
PubMed1991

A model of slow conduction in bullfrog atrial trabeculae.

The success or failure of the propagation of electrical activity in cardiac tissue is dependent on both cellular membrane characteristics and intercellular coupling properties. This paper considers a linear arrangement of individual bullfrog atrial cells that are resistively coupled end to end to form a cylindrical strand. The strand, in turn, is encased by an endothelial sheath that provides a restricted extracellular space and an ion diffusion barrier to the outer bathing medium. This encased strand serves as an idealized model of an atrial trabeculum. Excitable membrane characteristics of the atrial cell are specified in terms of a Hodgkin-Huxley type of model that is quantitatively based on single-microelectrode voltage clamp data from bullfrog atrial myocytes. This membrane model can simulate the behavior of normal cells as well as of ischemic cells that exhibit depressed electrophysiological behavior (e.g., decreased resting potential, upstroke velocity, peak height, and action potential duration). Depressed activity can be easily simulated with variation of a single model parameter, the gain of the Na+/K+ pump current (INaK). Intercellular coupling properties are specified in terms of a lumped resistive T-type network between adjacent cells. The atrial strand model provides a means for studying the theoretical aspects of slow conduction in a "hybrid" strand that consists of a central region of cells having abnormal membrane or coupling properties, flanked on either side by normal atrial cells. Both uniform and discontinuous conduction are simulated by means of appropriate changes in the coupling resistance between cells. In addition, by varying either the degree of depressed electrical activity or the intercalated disc resistance in the central zone of the strand, slow conduction or complete conduction block in that region is demonstrated. Since the cellular model used in this study is based on experimental data and closely mimics both the atrial action potential and the underlying membrane currents, it has the potential to (1) accurately represent the current and voltage wave-forms occurring in the region of intercalated discs and (2) provide detailed information regarding the mechanisms in intercellular current spread in the region of slow conduction.

Animals↗
PubMed1983

["Supernormal" A-V conduction during chaotic atrial rhythm. A case report].

We describe the electrocardiogram of a patient who had a chaotic atrial rhythm with partial A-V block. Only the late P waves (R-P greater than 1 sec.), and the early ones (with one R-P interval between 44 and 52 hundredths of a second) were conducted to the ventricle. On the contrary, no P waves with coupling intervals between 52 and 100 hundredths of a second reached the ventricles. Careful analysis of the tracing showed that the conduction of the early P waves could not depend upon the atrial pacemaker site, or upon concealed conduction of preceding atrial impulses. The existence of a "gap" phenomenon although unlikely, could not be excluded. Supernormal A-V conduction, or early diastolic decrease of the vagal tone due to hemodynamic mechanism could be responsible for the early ventricular captures observed in this patient.

Aged↗
PubMed2000

Factors determining clockwise and counterclockwise conduction patterns in atrial reentrant tachycardias: a rabbit model of atrial flutter.

INTRODUCTION: In the development of atrial flutter due to reentry, the crista terminalis is supposed to pose a conduction barrier, but the role of its longitudinal conduction in determining the propagation pattern of the reentrant impulse is not known. In rabbit right atrial preparations, we induced reentrant atrial tachycardias and examined the effects of transverse section of the crista terminalis on the development and conduction patterns of arrhythmias. METHODS AND RESULTS: Right atrial preparations from 12 albino rabbits were placed endocardial surface down in a chamber with an array of 48 bipolar electrodes to draw activation maps. A single premature stimulus was delivered to induce tachycardias at the free wall. In the control, five instances of tachycardia per preparation were induced and another five were induced after cutting the crista terminalis. In the control, the mean duration of tachycardia was 127.1+/-25.2 seconds. The tachycardia was counterclockwise in 39 of 60 instances, clockwise in 12, and undetermined in 4 defined as "atypical." After transverse section of the crista terminalis, the duration was prolonged to 372.6+/-30.4 seconds, but the conduction patterns were not changed. In the free wall, counterclockwise reentry had a broader wavefront and faster conduction than clockwise reentry. CONCLUSION: Longitudinal conduction block at the crista terminalis contributed to maintenance of reentrant atrial tachycardias, but had no influence on their propagation patterns. Clockwise and counterclockwise rotation of impulses in reentrant tachycardias had different paths and velocities of the wavefront in the free wall of the right atrium.

Animals↗
PubMed1996

Mechanism of ventricular rate control after radiofrequency modification of atrioventricular conduction in patients with atrial fibrillation.

BACKGROUND: Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification. METHODS AND RESULTS: Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 micrograms/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356 +/- 72 versus 371 +/- 78 ms versus 432 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/- 56 ms, P < .0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485 +/- 88 versus 533 +/- 116 ms versus 637 +/- 142 ms for mean RR, P < .0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion. CONCLUSIONS: Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.

Adult↗
PubMed2006

The superior transseptal surgical approach to mitral valve creates slow conduction.

BACKGROUND: Atrial tachycardia is very frequent after mitral valve surgery using the superior transseptal approach. METHODS: Sixteen patients operated on for mitral valve disease (superior transseptal approach = Group A, n = 9, and left atrial approach = Group B, n = 7) underwent radiofrequency catheter ablation of atrial tachycardia guided by electroanatomic mapping. Twenty-six consecutive patients without previous cardiac surgery with typical atrial flutter served as controls (Group C). RESULTS: Atrial tachycardia occurred earlier after the operation in Group A than in Group B (median 97 vs 2,159 days, P = 0.003). Typical atrial flutter was the most frequent circuit in all groups (Group A-7 patients, Group B-5 patients, Group C-26 patients). Three patients in Group A developed right atrial incisional tachycardia. Ten of 14 tachycardia circuits (typical atrial flutter, n = 7, incisional tachycardia, n = 3) in Group A depended on the corridor between the right atrial part of the atriotomy and the tricuspid annulus. Slow conduction during typical atrial flutter was detected in this corridor in Group A, but not in the corresponding region in Groups B and C (P < 0.001). The cycle length of typical atrial flutter was longer in Groups A and B than in Group C (mean 283 ms and 282 ms vs 233 ms, P = 0.003). Patients in Group B with typical atrial flutter had larger right atria than patients in Group A or Group C (mean 156 mL vs 96 mL and 113 mL, P = 0.033). CONCLUSIONS: The superior transseptal incision may predispose to atrial tachycardia by creating slow conduction between the atriotomy and the tricuspid annulus.

Adult↗