Atrioventricular Conduction Properties Research Articles

Atrial pacing site and atrioventricular conduction in patients paced for sinus node disease.

Unnecessary ventricular pacing in sinus node disease (SND) must be avoided. To test the hypothesis that in SND, with or without 1st degree atrioventricular (AV) block, cumulative percent ventricular pacing (cum%VP) can be limited by low right atrial septal (LRAS) instead of right atrial appendage (RAA) pacing. We studied 102 dual-chamber pacemaker recipients with SND. The PQ interval on 12-lead electrocardiogram and the atrial paced to ventricular sensed interval (Ap-Vs) during LRAS and RAA pacing were measured and compared at implantation, 3 months and 1 year of follow-up. Group 1 included 62 patients with baseline PQ interval <200milliseconds during LRAS (n = 28) versus RAA (n = 34) pacing. Group 2 included 40 patients with baseline PQ ≥200 milliseconds during LRAS (n = 20) versus RAA (n = 20) pacing. cum%VP were measured at 3 months and 1 year. The characteristics and AV conduction properties were similar and the Ap-Vs interval was significantly shorter in the LRAS than in the RAA pacing group up to 1 year (193 ± 32 milliseconds vs. 220 ± 27 milliseconds in Group 1; P = 0.003, 222 ± 41 milliseconds vs. 281 ± 30 milliseconds in Group 2; P < 0.001). While cumulative percent atrial pacing was consistently similar, cum%VP was significantly smaller during LRAS than RAA pacing (1 ± 1% vs. 8 ± 18% in Group 1; P = 0.03, 7 ± 10% vs. 48 ± 38% in Group 2; P < 0.001). Similar observations were made with or without left atrial (LA) enlargement. Compared with RAA, LRAS pacing showed shorter AV interval in SND patients with or without 1st degree AV block and LA enlargement. This beneficial effect persisted through 1-year follow-up, and decreased cum%VP significantly.

Atrioventricular conduction properties in patients with prolonged pauses undergoing ablation of longstanding persistent atrial fibrillation: do pauses during atrial fibrillation matter?

Atrioventricular (AV) conduction disturbances have often been considered as an etiology of prolonged pauses during atrial fibrillation (AF). We aimed to test whether there was a significant difference in the AV conduction properties between patients with and without clinically significant pauses who underwent ablation of longstanding persistent AF. Ninety-nine patients undergoing ablation of longstanding persistent AF were divided into three groups according to the extent of pauses documented on the ambulatory electrocardiogram during AF; patients without pauses (n = 25), with pauses of <3 s (n = 52), and with pauses of ≥3 s (n = 22). The AV conduction properties, heart rate variability, and bradycardia-related symptoms after conversion to sinus rhythm were compared across the three groups plus a control group (n = 35). Sinus conversion was achieved in all patients after ablation. No differences were found across the groups in the AV conduction properties including the AH and HV intervals, AV nodal effective refractory period, or Wenckebach point. A male gender (β = 0.32; p = 0.0016), structural heart disease (β = 0.24; p = 0.02), and the AA interval right after ablation (β = 0.35; p = 0.0014), rather than the AV conduction properties, were independent determinants of the longest normal RR interval during AF. No patients experienced any bradycardia-related symptoms after ablation. No AV conduction abnormalities were necessarily identified after the ablation even among the patients suspected of having an AV conduction disturbance during AF.

Clinical and electrophysiologic characteristics of left septal atrial tachycardia

ObjectivesIt was the purpose of this study to define the electrophysiologic (EP) identity of left septal atrial tachycardia (AT). BackgroundThe clinical and EP characteristics of this particular type of arrhythmia have not been fully described. MethodsA total of 120 patients with AT underwent invasive EP evaluation. Five patients (two men and three women; mean age 49 ± 15 years) with left septal AT were identified. Mapping of the right and left atrium was performed using conventional electrode catheters (five patients) and a three-dimensional electroanatomic mapping system (three patients) followed by radiofrequency (RF) ablation at the earliest site of local endocardial activation. ResultsFive tachycardias with a mean cycle length of 320 ± 94 ms were mapped, and the earliest endocardial electrogram occurred 22 ± 10 ms before the onset of the surface P-wave. Three left septal ATs were found to be originating from the left inferoposterior atrial septum and two from the left midseptum. During tachycardia, positive (three patients), biphasic negative-positive deflection (one patient), or isoelectric (one patient) P waves were recorded in lead V1. The inferior leads demonstrated a positive or biphasic P-wave morphology in four of five patients (80%). Four patients were given both adenosine and verapamil during AT. In three of four patients, verapamil successfully terminated AT after adenosine had failed. Adenosine successfully terminated AT in one of four patients. Successful RF ablation was performed in all patients (mean 2.2 ± 1.7 RF applications) without affecting atrioventricular conduction properties. No recurrence of AT was observed after a mean follow-up of 14 ± 8 months. ConclusionsLeft septal AT ablation is safe and effective. There was no consistent P-wave morphology associated with this particular type of AT. This arrhythmia appears to be resistant to adenosine and moderately responsive to calcium antagonists.

Electrophysiological characterization of connexin 40 deficient hearts--in vivo studies in mice

Intercellular communication is not only mediated by extracellular transmitters, but also directly by gap junction channels. One channel is composed of two hexameric hemichannels which consist of six polypeptide subunits called connexines (Cx). In the mammalian heart the following connexines have been documented: Cx37, Cx40, Cx43, Cx45, Cx46, Cx50 and Cx57. The labeling by number represents the rounded, molecular mass of the amino acid sequences given in kD. If identical connexin-isotypes form both connexons of a gap junction channel, homotypic coupling exists and a homomeric gap junction channel is formed. Different connexin-isotypes within both connexons cause form heterotypic coupling and heteromeric gap junction channels. Each channel type has specific properties regarding permeability and electrical conductance. Beside a typical age-dependent alignment of gap junction channels on the surface of the cardiac myocytes, regional distribution of the different connexins is different at distinct parts of the mouse heart. Cx40 is not found in the ventricular working myocardium of mice. In the atria as well as in the conduction system, Cx40 is the most frequently expressed. In line with the localization and the conduction properties of distinct homotypic gap junction channels, the Cx40 deficient mouse is suitable for analysis of atrial arrhythmias. Cx40-deficiency in the mouse heart results in characteristic ECG changes like first degree atrioventricular block and prolongation of the QRS duration. Thus, an impairment of the sinuatrial, intraatrial and atrioventricular conduction properties is documented in Cx40 deficient mice. These observations are associated with an increased atrial vulnerability. The Cx40 deficient mouse provides a good example of the relevance of transgenic mouse models to clarify the mechanisms of arrhythmogenesis. The clinical impact of future transgenic mouse models depends on the cooperation of geneticists, basic researchers and clinicians.

Atrioventricular conduction: a determinant for the manifestation of ventricular preexcitation in patients with Wolff-Parkinson-White syndrome.

The relation between the atrioventricular conduction properties of the atrioventricular node and the anterograde conduction ability over the accessory pathway in the Wolff-Parkinson-White syndrome has never been studied. Atrioventricular nodal characteristics were studied in 285 patients with manifest and 204 with concealed accessory pathway who underwent radiofrequency ablation, and compared with 146 controls. First and second degree atrioventricular block was observed in 13 (5%) preexcitation patients after ablation, compared with none in concealed accessory pathway (P=0.001) and control patients (P=0.006). The atrial-His intervals in preexcitation patients (88 +/- 20 ms) was significantly longer than in concealed accessory pathway (76 +/- 15 ms, P<0.0001) and control patients (77 +/- 15 ms, P=0.0007), as was PR intervals (165 +/- 25 versus 149 +/- 20 and 150 +/- 21 ms, P<0.0001, respectively) even after excluding those with atrioventricular block. Significant differences in PR and atrial-His intervals were not observed between concealed accessory pathway and control patients. More preexcitation patients had ventriculoatrial dissociation than had patients in the other groups. The results indicate that atrioventricular block is not uncommon in preexcitation patients and a relatively long atrioventricular conduction time is an electrophysiological prerequisite for the manifestation of preexcitation in the Wolff-Parkinson-White syndrome.

Gender Differences in the Electrophysiological Characteristics of Atrioventricular Conduction System and their Clinical Implications

Objective - The underlying mechanisms of the differences in sex distribution of patients with atrioventricular (AV) nodal re-entrant tachycardia and Wolff-Parkinson-White syndrome are poorly understood. The objective of this study was to determine potential gender differences in the electrophysiological properties of the normal AV conduction system that may be attributable to differences in sex distribution. Design - The AV conduction properties were studied in 96 patients (52 men and 44 women) who underwent electrophysiological testing, 32 patients with atrial tachycardia, 39 with idiopathic ventricular tachycardia and 25 with unexplained palpitations or syncope. Results - The AH (83 - 15 ms) and His-ventricular intervals in men (42 - 6 ms) were significantly longer than in women (78 - 14, 38 - 6 ms, p < 0.05, respectively), as was the PR interval (160 - 17 vs 152 - 13 ms, p = 0.02). The effective refractory period of AV node in men (349 - 75 ms) was longer than in women (297 - 45 ms, p = 0.03). However, no significant difference was observed between men and women with respect to the incidence of AV nodal dual pathway and the maximum AH interval achieved during premature stimulation or incremental pacing. The AV block cycle length was significantly longer in men (371 - 76 ms) than in women (330 - 52 ms, p = 0.02). A longer ventriculoatrial block cycle length was also found in men than in women although not at a significant level (436 - 107 vs 384 - 90 ms, p = 0.08). In addition, men (23%) were twice as likely to have ventriculoatrial dissociation during ventricular pacing as women were (11%, p = 0.2). Conclusion - The data show that gender-related differences in AV conduction properties may be responsible for the differences in sex distribution observed in patients with AV nodal re-entrant tachycardia and those with ventricular pre-excitation.

Cardiac arrhythmias in targeted connexin deficient mice: significance for the arrhythmia field

Intercellular communication can be mediated by gap junction channels. One channel is composed of two hexameric hemichannels which consist of six polypeptide subunits called connexines (Cx). Three different connexines were documented in the cardiac myocytes: Cx40, Cx43 and Cx45. The labeling by number represents the rounded, molecular mass of the amino acid sequences given in kD. Identical connexons form homotypic channels different connexons can form heterotypic channels. Each channel type has specific properties regarding permeability and electrical conductance. Beside a typical age-dependent alignment of gap junction channels on the surface of the cardiac myocytes, regional distribution of the different connexins is different at distinct parts of the mouse heart. The ventricular working myocardium is characterized by Cx43, whereas Cx40 and Cx45 were not found in this region. In the atria as well as in the conduction system, Cx40 is the most frequently expressed. Cx45 appears to form a border zone between conductive and the surrounding working myocardium. In line with the localization and the conduction properties of distinct homotypic gap junction channels, the Cx43 deficient mouse is suitable for analysis of ventricular arrhythmias and the Cx40 deficient mouse primarily for studies of atrial arrhythmias. Increased ventricular conduction velocity and increased ventricular vulnerability were observed in the presence of a decreased number and density of Cx43 gap junction channels. This observation, however, is controversially discussed. Cx40 deficiency induces an impairment of the sinuatrial, intraatrial and atrioventricular conduction properties and is associated with an increased atrial vulnerability. Transgenic mouse models and new mapping techniques for detection of the electrical wavefront propagation provide new insights into the mechanisms of arrhythmogenesis. Geneticists, clinicians and basic researchers need to collaborate in order to explore the clinical relevance of the new mouse models and their use for molecular medicine.

Conduction disturbances and increased atrial vulnerability in Connexin40-deficient mice analyzed by transesophageal stimulation.

Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. Fifty-two mice (18 Cx40(+/+), 15 Cx40(+/-), and 19 Cx40(-/-) mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40(-/-) mice compared with Cx40(+/-) and Cx40(+/+) mice (287.8+/-109.0 vs 211.1+/-61.8 vs 204.4+/-60.9 ms; P<0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40(-/-) mice than in Cx40(+/-) or Cx40(+/+) mice (93. 3+/-11.8 vs 83.9+/-9.7 vs 82.8+/-8.0 ms, P<0.05). Analysis of 27 Cx40(-/-) mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40(+/-) and 31 wild-type (Cx40(+/+)) mice. Furthermore, in Cx40(-/-) mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis.

Circadian Rhythms of Atrioventricular Conduction Properties in Chronic Atrial Fibrillation With and Without Heart Failure

Objectives. We examined the circadian variations in atrioventricular (AV) conduction properties during atrial fibrillation (AF) by a technique based on the Lorenz plot of successive ventricular response (VR) intervals and analyzed their relations with clinical features.Background. The VR interval in chronic AF shows circadian variation, which is attenuated in patients with an increased risk of death. Although the VR interval is determined by the dynamic processes in the AV node randomly stimulated by rapid atrial activity, the circadian variations of the AV conduction properties related to this mechanism are unknown.Methods. In 48 patients with chronic AF, Lorenz plots were generated on overlapping sequential segments of 512 VR intervals in 24-h ambulatory electrocardiograms. For each scatter plot, the 1.0-s intercept of the lower envelope (LE1.0) of the plot and the degree of scatter above the envelope (root mean square difference from the envelope [scattering index]) were measured for estimating AV node refractoriness and concealed AV conduction, respectively.Results. In all patients, a significant circadian rhythm was observed for the average VR interval, LE1.0and scattering index, with an acrophase occurring at night. The mesor, amplitude and acrophase of LE1.0and the scattering index closely and independently correlated with the corresponding rhythm variables of the average VR interval (partial r20.98, 0.86 and 0.68 for LE1.0and 0.98, 0.92 and 0.92 for scattering index). The amplitudes of these measures were lower in patients with congestive heart failure (CHF) even after adjustment for the effects of age, duration of AF, medications, left atrial diameter and blood pressure (p < 0.01 for all).Conclusions. These results suggest that 1) both AV node refractoriness and the degree of concealed AV conduction during AF may show a circadian rhythm; 2) the circadian rhythms of these properties may independently contribute to the circadian variation of the VR interval; and 3) these circadian rhythms may be attenuated in patients with CHF.

Different effects of flecainide on atrioventricular conduction properties in the adult and immature rabbit heart.

The influence of flecainide (0.1, 0.5, 1.0, and 2.0 micrograms/mL) on atrioventricular (AV) conduction was studied in neonatal and adult perfused rabbit hearts using extracellular bipolar surface electrograms and premature atrial and ventricular pacing. Flecainide produced a concentration and rate-related increase in the steady-state nodal conduction (AHmin) and an increase in slow AH conduction (AHmax) in both age groups. The drug produced significant increases in the refractory periods of the atrium, AV node, His-Purkinje system, and ventricular myocardium. The neonatal refractory periods were significantly greater at lower or the same drug concentrations than those of the adult. The neonatal Wenckebach cycle length was significantly greater with a lower concentration of drug (0.5 microgram/mL) than was the adult Wenckebach cycle length. The His-Purkinje system steady-state conduction time (HVmin) was increased by a lower concentration of drug in the neonate (0.5 microgram/mL) as compared with 2.0 micrograms/mL in the adult. These data show that across a wide range of AV conduction parameters, the neonatal preparations responded to a lower concentration of flecainide than did the adult preparations. These findings may, in part, be the basis for the reported greater efficacy of the drug in children than in adults.

Invasive electrophysiological evaluation of patients with sleep apnoea-associated ventricular asystole-methods and preliminary results.

Twelve patients (aged 48 +/- 12 y) with ventricular asystole of >3 s due to complete atrioventricular (AV) block (n = 8), sinoatrial (SA) block or sinus node arrest (n = 3) or both (n = 1) associated with obstructive sleep apnoea underwent invasive electrophysiological evaluation of sinus node function and AV conduction properties before and after administration of atropine (0.02 mg kg-1). Ventricular asystole lasted for 5.9 +/- 2.8 s (range 3.1-13 s). Sinus node function was assessed by measurement of sinus node recovery time, sinoatrial conduction time, and the response of sinus rate to atropine. Parameters of AV-conduction assessment included AH- and HV-intervals, AV- and VA-Wenckebach periods, and effective refractory period of the AV node before and after atropine. Sinus node function was normal in 11 of the 12 study patients and moderately abnormal in 1 patient. AV-nodal function was normal in 8 patients and moderately abnormal in 4 patients. A slightly prolonged HV-interval (59-63 ms) was present in 6 patients. Intra- or infra His block was not observed in any patient. In conclusion, normal or only moderately abnormal electrophysiological findings in patients with sleep apnoea-associated ventricular asystole suggest that a neurally mediated cardioinhibitory reflex may cause ventricular asystole in these patients. This sleep apnoea-triggered 'vasovagal' reflex may unmask pre-existing mild to moderate structural abnormalities of the AV conduction system.

Electrophysiologic characteristics of manifest and latent retrograde conduction in dogs

Atrioventricular (AV) nodal reentry requires intact retrograde ventriculoatrial (VA) conduction. The purpose of this study was to assess the contribution of various pacing and pharmacologic techniques to uncover VA conduction during apparent unidirectional VA block, and to evaluate the role of several biologic and electrophysiologic factors in concealment of retrograde conduction. Forty healthy dogs underwent catheter-electrophysiologic studies of AV and VA conduction. Group I (20 animals) had intact VA conduction. Group II (six animals) had VA dissociation with ventricular pacing initiated during sinus rhythm, but the presence of VA conduction was confirmed by isoproterenol infusion or by premature ventricular stimulation. In group III (14 animals), the above techniques failed to uncover VA conduction. Eight of 14 group III animals underwent thoracotomy and crushing or freezing of the sinoatrial (SA) node. Ventricular pacing initiated during sinus standstill was associated with 1:1 VA conduction in each experiment. VA conduction time and retrograde Wenckebach cycle length, both in the baseline state and during isoproterenol infusion, were significantly longer in the eight animals in group III than in those in group I. Age, gender, weight, breed, sinus cycle length, and anterograde AV conduction properties were not significantly different between groups I, II, and III. The data suggest that (1) in normal dogs, complete unidirectional VA block probably does not exist; (2) in the presence of anterograde input to the AV node, even sophisticated pacing and pharmacologic maneuvers may fail to uncover the presence of VA conduction; (3) although anterograde input is essential for concealment of VA conduction, the phenomenon is more closely associated with depressed retrograde than with anterograde AV nodal characteristics. These data may be important when analyzing the effects of various AV nodal modification procedures on the apparent elimination of VA conduction.

Pacemaker Syndrome with AAI Rate Variable Pacing: Importance of Atrioventricular Conduction Properties, Medication, and Pacemaker Programmability

A patient who received an AAI Activitrax rate variable pacemaker for treatment of symptomatic sinus bradycardia is described. disopyramide prolonged the anterograde effective refractory period of the fast conducting atrioventricular (AV) nodal pathway to such an extent, that conduction switched to the slow AV nodal pathway at low atrial pacing rates. This gave rise to symptoms of the pacemaker syndrome during moderate exercise because the paced atrial event was conducted with a long, spike to Q interval with occurrence of the paced atrial event just after the preceding QRS complex. A change of medication solved this problem. Programming a bipolar electrode configuration avoided sensing of far-field QRS signals with the associated problems of resetting the basic pacing interval as well as the upper rate interval. AAI rate variable pacing requires careful evaluation of AV conduction properties, AV conduction intervals as well as the influence of medication to be given. The use of multiprogrammable pacemakers with marker channel capability will significantly facilitate the understanding and resolution of anomalous behavior.