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Dissociation of the atrioventricular node in acute inferior wall myocardial infarction. 2. Longitudinal dissociation (dual atrioventricular nodal pathways).

Four cases of longitudinal dissociation of the atrioventricular node, with dual pathways developing during the acute phase of an inferior wall myocardial infarction (three cases) or during acute ischemia (one case), are presented. In all four cases, two grossly different P-R intervals were recorded, and in two cases, studies of the His bundle confirmed the location of the dissociation within the atrioventrcular node. In one case, premature atrial depolarization caused a bidirectional shifting of P-R intervals, while in the remaining three cases, premature ventricular depolarization (spontaneous or pacemaker-induced) was responsible for this phenomenon. In all cases, evidence of longitudinal dissociation of the atrioventricular node appeared during the acute phase of the infarction or ischemia, and in all of them the phenomenon was transient. This favors the assumption that this phenomenon is of a functional nature, most probably related to the ischemic lesion of the atrioventricular node.

Acute Disease↗

Incidence of complete atrioventricular block following attempted radiofrequency catheter modification of the atrioventricular node in 880 patients. Results of the Multicenter European Radiofrequency Survey (MERFS) The Working Group on Arrhythmias of the European Society of Cardiology.

UNLABELLED: The Multicenter European Radiofrequency Survey (MERFS) retrospectively analysed the incidence of procedure-related complications in 4463 patients who had undergone radiofrequency catheter ablation in 69 European institutions between 1987 and 1992. Of these 4463 patients, 880 underwent modification of the atrioventricular node to cure atrioventricular nodal reentrant tachycardia. This report presents a detailed analysis of the incidence of complete atrioventricular block with respect to the target site and the number of patients reported per institution. The most common complication of modification of the atrioventricular node was the unintended induction of complete atrioventricular block (41 of 880 patients, 4.7%). In 684 of 880 patients (78%), detailed information about the approached target site for modification of the atrioventricular node was available. Complete atrioventricular block occurred significantly more often in patients who underwent ablation of the fast pathway (19/361, 5.3%) or in whom ablation of the slow and fast pathway was attempted after failure at the initial site (4/25, 16%) than in patients who underwent slow pathway ablation (6/298, 2.0%, P < 0.05). The overall incidence of complete atrioventricular block was significantly higher (6.3%) in centres with limited experience in radiofrequency modification of the atrioventricular node ( < or = 30 patients treated; group I: n = 526) compared to centres that had treated > 30 patients (group II: n = 354; 2.3%; P < 0.05). In addition, in those patients in whom the target site was available, the incidence of complete atrioventricular block after fast pathway ablation was significantly higher in group I (n = 168 patients) when compared to group II (n = 193 patients) (7.7% vs 3.1%, P < 0.05) and also tended to be higher after slow pathway ablation in group I (2.4% in group I vs 1.5% in group II; P = ns). CONCLUSIONS: In this analysis of collaborative data, radiofrequency catheter modification of the atrioventricular node carried a risk of approximately 5% of complete atrioventricular block. The incidence of complete atrioventricular block was significantly higher in patients who underwent fast pathway ablation or fast and slow pathway ablation after failure at the initial site compared with slow pathway ablation. In addition, the results indicate that there is a learning curve, regarding the incidence of complete atrioventricular block, which is a significant complication of the procedure, when modifying the atrioventricular node. Thus, caution is recommended when performing radiofrequency modification of the atrioventricular node using the so-called anterior approach to abolish fast pathway conduction, especially when the experience of the institution or investigator/s is limited.

Atrioventricular Node↗

Comparison of exponential and hyperbolic models of conduction through the atrioventricular node.

Conduction through the atrioventricular node (AVN) is assessed during electrophysiology study by relating the output to the input generated by an atrial extrastimulus. This extrastimulus scans electrical diastole of the heart to enable output to be plotted against input. Using this technique, we compared two mathematical models of the AVN, a rectangular hyperbola and a decaying exponential, respectively. The models were compared in 40 curves from 32 patients with only one AVN transmission pathway. Standard errors of the estimate were usually (25/40 trials) less with the exponential model, suggesting this the preferred algorithm for further development.

Adolescent↗

Study of the development of the atrioventricular conduction system as a consequence of observing an extra atrioventricular node in the normal heart of a human fetus.

We have observed an extra atrioventricular node in the normal heart of a human fetus. It is located in the septal wall of the right atrium, subendocardially, and just where Todaro's tendon leaves this wall to go toward the inferior vena cava valve. In its trajectory, this tendon gives way to a remarkable prominence in the cavity of the right atrium: the sinus band. In order to explain the embryogenesis of this extra atrioventricular node, we have studied the normal development of the atrioventricular specific system and have concluded that the atrioventricular node is formed from a growth and displacement toward the atrium of the primitive atrioventricular specific material, which originates from the myocardium of the posterior wall of the atrioventricular canal. Likewise, during its development, the atrioventricular node keeps in close proximity with the Todaro's tendon. In our view, this accounts for the embryogenesis of the extra atrioventricular node, since a fragment of the atrioventricular node can remain cranial to Todaro's tendon and be displaced by it in a craniodorsal direction. This fragment would then lead to the formation of an extra atrioventricular node like the one present in the heart of the fetus we have examined.

Atrioventricular Node↗

Mesothelioma in the atrioventricular node. Case report.

A patient with complete atrioventricular block and an implanted permanent pacemaker died of colon cancer at the age of 64 years. At autopsy, a cardiac tumor in the region of the atrioventricular node (mesothelioma of the atrioventricular node) was found. The origin of this type of tumor is controversial. Histochemical findings suggested that the tumor in this case was of endodermal origin.

Atrioventricular Node↗

Interruption of the inferior extension of the compact atrioventricular node underlies successful radio frequency ablation of atrioventricular nodal reentrant tachycardia.

A recent anatomic study has revived interest in the inferior extensions of the compact atrioventricular node in humans. The rightward extension is on the right atrial aspect, close to the septal attachment of the tricuspid valve leaflet and, hence, closely related to the anticipated slow pathway considered to play a role in atrioventricular nodal reentrant tachycardia (AVNRT). This report documents a patient, 65 years of age, with dilated cardiomyopathy and AVNRT. The tachycardia was successfully terminated using selective radiofrequency (RF) ablation, delivered at a site where a slow potential was recorded and validated by atrial pacing, located between the tricuspid valve and the os of the coronary sinus (CS), close to its superior rim. In subsequent years the patient developed progressive heart failure and eventually died. Histopathologic examination revealed extensive scar tissue at the site of the burn, extending onto the crest of the underlying ventricular septum. Serial sections revealed the compact AV node superiorly and an inferior extension surfacing from the scar which could be traced inferiorly beyond the os of the CS. This is the first documentation of RF ablation interrupting an inferior extension of the compact AV node in a patient successfully ablated for AVNRT. The observation suggests that the slow pathway in this patient found its anatomic substrate in the inferior extension of the compact AV node.

Aged↗

Characterization of beta 1- and beta 2-adrenoceptor subtypes in the rat atrioventricular node by quantitative autoradiography.

We characterized beta-adrenoceptor subtypes in the atrioventricular node of the rat heart by quantitative autoradiography. Consecutive 16-microns-thick sections from single rat hearts containing the atrioventricular node were incubated with increasing concentrations of [125I]iodocyanopindolol. After exposure to [3H]Ultrofilm, optical densities corresponding to the atrioventricular node were determined by computerized densitometry after comparison with [125I]standards. The computer program LIGAND was used for analysis of receptor subtypes. Delineation of beta-adrenoceptor subtypes was achieved by incubating consecutive tissue sections with 50 pM [125I]iodocyanopindolol in the presence of increasing concentrations of the beta 1-selective antagonist atenolol or the beta 2-selective antagonist ICI 118,551. The atrioventricular node contains a higher concentration of beta-adrenoceptors than the adjacent interventricular septum. We estimated that the proportions of beta 1- and beta 2-adrenoceptors in the atrioventricular node were about 56% and 44% of the total binding capacity respectively.

Animals↗

Double loop figure-of-8 reentry as the mechanism of multiple atrioventricular node reentry tachycardias.

Seven patients with multiple atrioventricular node reentry tachycardia were analyzed to unravel the mechanism of these tachycardias. Six of the seven patients showed anterograde dual atrioventricular node pathways and one showed anterograde conduction through the fast pathway. Three types of retrograde pathways were noted among these seven patients: (1) the fast pathway with the earliest atrial activation at the His bundle area; (2) the intermediate pathway with the earliest atrial activation at the ostium of the coronary sinus; and (3) the slow pathway with the earliest atrial activation at the ostium of the coronary sinus. All seven patients used the intermediate pathway for retrograde conduction. However, one patient showed evidence of retrograde slow pathway conduction with demonstrable retrograde dual pathways, and another showed evidence of retrograde fast pathway conduction with a shift of atrial activation sequence when conduction switched to the intermediate pathway. Four different types of reentry circuits using either the fast or the slow pathway as the anterograde limb and one of the three retrograde pathways as the retrograde limb were demonstrated in these seven patients, resulting in two types of tachycardias in four patients and three types of tachycardias in three patients. A change in tachycardia type could be induced with atrial or ventricular stimulation. A radiofrequency current delivered to the inferior aspect of Koch's triangle along the tricuspid anulus in five patients resulted in selective ablation or modification of the intermediate pathway or the slow pathway, with preservation of anterograde atrioventricular conduction and abolition of tachycardias. The findings suggest that a double loop figure-of-8 reentry circuit including a fast pathway, a slow pathway, and an intermediate pathway is responsible for multiple atrioventricular node reentry tachycardias.

Adult↗

[Electrophysiological effects of different dosage of adenosine triphosphate on normal sinoatrial and atrioventricular node].

In order to study the electrophysiological basis of smaller dosage that would terminate PSVT effectively and decrease side effects remarkably, we have observed the electrophysiological effects of ATP in different dosage (5mg, 10mg, 15mg) on the sino-atrial node (SAN) and atrioventricular node (AVN). Cardiac electrophysiological investigations were carried out in 62 patients with history of PSVT by using the method of trans-esophagus ECG and body surface ECG continuously and simultaneously, during the normal sinus rhythm and PSVT. The results showed that when the effect of 10mg ATP on SAN was not clinically significant yet, it did strikingly block the AVN conduction enough to terminate the PSVT with no severe arrhythmias. 37 cases of 62 patients were provoked PSVT during control electrophysiological study, the PSVTs of 33 cases out of these 37 patients (89.7%) were terminated by using 10mg ATP. There was no serious bradyarrhythmias after PSVT termination. We suggest that 10mg ATP is a reliable dose for PSVT termination.

Adenosine Triphosphate↗

Electrophysiologic effects of berberine on isolated sinoatrial and atrioventricular nodes of rabbit.

Berberine (Ber) 0.1-30 mumol/L decreased the APA, Vmax, maximal depolarization potentials (MDP) and rate of spontaneous impulse initiation in sinoatrial node (SAN) and atrioventricular node (AVN) cells with prolongation of APD50, APD95 and ERP in a dose-dependent manner. The depression of SAN function was shown by increasing sinus cycle length (SCL), sinus recovery time (SRT) as well as corrected sinus recovery time (CSRT). In atria (crista terminalis, CT) higher concentrations of Ber were needed to prolong APD50, APD95, and ERP as compared with SAN and AVN. The effects of Ber on SAN were not antagonized or reversed by atropine (1 mumol/L), alpha 2-receptor agonist BHT-920 (10 mumol/L) or alpha 1-receptor agonist phenylephrine (10 mumol/L), but those effects of Ber on SCL, APA and Vmax could be reversed by norepinephrine (0.1 mumol/L). In calcium free Tyrode's solution, the inhibitory effects of Ber still revealed on SAN but on atria only prolongations of APD50 and APD95 were observed.

Action Potentials↗

Freeze-fracture studies of the sinoatrial and atrioventricular nodes of the caprine heart, with special reference to the nexus.

The caprine sinoatrial node (SAN) and atrioventricular node (AVN) were studied by freeze-fracture techniques, and their nexus or gap junction structure were compared with that of ordinary atrial and ventricular muscle cells. The general features of the nexus in both the SAN and AVN were essentially identical. Approximately two-thirds of the nexuses observed in the nodal cells consisted of typical macular arrangements of nexal particles, and the remaining third, of atypical configurations of either circular arrangements or linear arrays of particles in continuity with the macular nexuses. Such atypical nexuses were never observed in the ordinary adult myocardial cells. Quantitative analysis revealed that all of the nexuses in the nodal cells measured, were less than 0.1 micron 2, whereas the majority of the nexuses in ordinary myocardial cells (64% in the atrium and 76% in the ventricle) were larger than 0.1 micron 2. No significant differences in diameter and center-to-center distance of nexal particle were found between the nodal cells and ordinary myocardial cells.

Animals↗

Autonomic modulation of sinus and atrioventricular nodes in premature low-birth-weight infants.

Respiratory vagal activity is expressed by heart rate variability (HRV) at approximately 1 month of age in premature low-birth-weight infants (PLBWI). However, the autonomic inputs into the sinus node (SAN) and atrioventricular node (AVN) in PLBWI are unclear. We evaluated the variability in PP and PR intervals at day zero (day 0) and 1 month (1 month) after birth in 16 PLBWI (gestation 32.3 +/- 1.3 weeks, birth weight 1.578 +/- 257 g). The polygraph was recorded during sleep on day 0 and at 1 month. PP and PR intervals and the number of respiratory cycles were measured, and frequency analysis was performed by auto-correlation fast Fourier transforms. Power spectral density (PSD: ms(2)) was calculated for the low frequency domain (LF: 0.036 approximately 0.146 Hz), high frequency domain (HF: 0.146 approximately 0.390 Hz), total frequency (TF: 0.036 approximately 2.000 Hz), and respiratory sinus arrhythmia (RSA: frequency bandwidth of 0.3 Hz with peak respiratory frequency as median), and the PSD ratio in the PP and PR intervals (LF/HF, RSA/TF) were compared. Compared with day 0, a decrease in the LF/HF ratio and an increase in the RSA/TF ratio in PP intervals were observed at 1 month, consistent with expression of respiratory vagal activity. For PR intervals, on the other hand, the LF/HF ratio increased, indicative of accentuated sympathetic activity. However, the respiratory vagal input was weak, and the RSA/TF ratio remained unchanged. These observations suggest that, in PLBWI at 1 month, AVN conduction was not predominatly influenced by respiratory-related vagal activity, but was controlled by autonomic regulation, independent of the SAN.

Atrioventricular Node↗

Comparative aspects of the dual role of the human atrioventricular node.

As well as transmitting the impulse from the atria to the ventricles the atrioventricular node has two other important functions namely: synchronisation of atrial and ventricular contractions by a varying delay; and protection of the ventricles from rapid atrial arrhythmias. The relative importance of these two functions appears to differ in large and small mammalian hearts. In small mammals synchronisation of atrial and ventricular contractions is the major function of the atrioventricular node, whereas protection from rapid atrial arrhythmias may be its most important function in large mammals. Atrioventricular conduction time in sinus rhythm is ten times longer in the whale (500 ms) than in the rat (50 ms). A whale heart, however, is about 100 000 times heavier than a rat heart. During atrial fibrillation the ventricular rate in a dog heart is only three times faster than in a horse, whereas a horse heart may be 40 times as heavy as that of a dog. Hence there is a considerable discrepancy between the size of the mammalian heart and the functions of its atrioventricular node. Analysis of several anatomical and functional aspects of atrioventricular conduction systems in mammals of all sizes showed that the importance of the delaying role of the atrioventricular conduction system diminishes as the size of the mammal increases, whereas the protective role of the atrioventricular node probably increases. The function of the human atrioventricular node seems to be intermediate between that of of the small and large mammals.

Animals↗

Cryosurgical modification of the atrioventricular node for treatment of atrioventricular junctional reentrant tachycardia.

Surgical correction of atrioventricular nodal reentrant tachycardia with preservation of atrioventricular nodal conduction in a 28-year-old woman is reported. At surgery, electrophysiologic mapping techniques were used during tachycardia to reveal and enable ablation of the appropriate site of atrial activation. Postoperative electrophysiologic studies indicated successful atrioventricular nodal modification.

Journal Article↗

Radiofrequency catheter ablation of accessory pathways and modification of atrioventricular node in children and adolescents.

Catheter ablation of an accessory pathway and atrioventricular node modification using 550 kHz radiofrequency was attempted in 23 children and adolescents between five and 19 years of age (mean = 15.7 years). Fifteen children had accessory-pathway-mediated tachycardia and eight had atrioventricular node reentrant tachycardia. Accessory pathways were present in ten children. Two patients had associated congenital heart disease. Symptoms included disabling palpitations and episodes of syncope. Ablation was attempted from the right and left sides of the heart. Single-catheter technique was used in seven patients. Eleven of the 15 patients with accessory pathways were treated completely. Two patients had recurrences, and one of them died after the arrhythmia surgery. There were two failures. Two patients with incomplete interruption of the accessory pathways were followed up clinically. There were three cases with temporary systemic embolization and one with severe pain related to radiofrequency energy application. Atrioventricular node modification was done by fast-pathway ablation in six, and by slow-pathway ablation in two patients. Two patients with fast-pathway ablation had recurrences of clinical arrhythmia, and one of them underwent a successful second session. There were no complications associated with the procedure in this group of patients. Radiofrequency catheter application was initially successful in 21 (84%) out of 25 procedures, and ultimately curative in 16 (69%) out of 23 patients. There were some serious complications which resolved in the immediate post-procedure period. Radiofrequency catheter ablation appears to be a safe and successful method for the management of supraventricular tachycardia secondary to accessory pathways or atrioventricular node reentrant tachycardia in children and adolescents.

Adolescent↗

Effects of ajmaline on rate-dependent atrioventricular node properties. Potential role in experimental atrioventricular re-entrant tachycardia.

Ajmaline is a well-known atrioventricular (AV) node depressant agent, but its effects on functional properties of the AV node and on experimental AV re-entrant tachycardia have not been explored. The aims of the present study were (1) to determine whether ajmaline administration modifies the rate-dependent properties of the AV node and (2) to correlate these changes with the actions of ajmaline on an in vitro model of AV re-entrant tachycardia. Selective stimulation protocols and mathematical formulations were used to quantify independently AV node recovery, facilitation, and fatigue in 10 isolated rabbit AV nodes. Ajmaline decreased facilitation and fatigue and had no significant effect on AV node recovery. The most important effect of ajmaline was rate-induced prolongation of AV node effective refractory period, resulting in a greater increase in tachycardia cycle length. AV re-entrant tachycardia was sustained when AV effective refractory period divided to tachycardia cycle length was less than 1, ajmaline suppressed AV re-entrant tachycardia by increasing the slope of the AV effective refractory period divided to tachycardia cycle length versus tachycardia rate relation, causing the critical ratio of 1 to be attained at a slower rate. A mathematical model incorporating quantitative descriptors of recovery, facilitation, and fatigue accounted for changes in nodal conduction time, AV effective refractory period, tachycardia cycle length, and AV effective refractory period divided to tachycardia cycle length under all conditions. It can be concluded that (1) ajmaline increases AV conduction time, decreases AV node fatigue, and facilitation, without altering AV node recovery. (2) Ajmaline significantly prolongs AV effective refractory period in a rate-dependent manner. (3) These changes play a role in ajmaline's actions on experimental AV re-entrant tachycardia. Ajmaline's ability to terminate re-entrant supraventricular tachycardia may be due, at least in part, to its ability to amplify the rate-induced prolongation of the nodal refractory period.

Action Potentials↗

Changes in the conductivity and in the functional refractory period of the atrioventricular node during hypoxia.

The experiments were carried out on preparations from rabbit right atrium, containing the sinoatrial node, the interatrial barrier, the atrioventricular node and the His-bundle. Surface electrodes were used to record the atrial and His-electrograms. The conduction time (AH-interval) was measured and the functional refractory period of the node was determined during normoxia (95% O2, 5% CO2) and hypoxia (30% O2, 65% N2 and 5% CO2) for 45 min. Hypoxia causes a considerable delay in conduction. This delay is greater for the shorter coupling-intervals and at the higher frequencies of the imposed rhythm. The shifting of the conduction times towards the higher values during hypoxia is not parallel compared with hypoxia. In the case of hypoxia the refractory curve of the A-V node is situated higher than the curve during normoxia, owing to the greater duration of the H1H2 intervals. The functional refractory period is increased and shifted toward the longer coupling-intervals. The results obtained show that during hypoxia the functional refractory properties of the atrioventricular node are impaired, which, combined with the delayed conduction through it, creates conditions for serious disturbances in the function of the atrioventricular conduction system.

Animals↗

Reentry within the atrioventricular node: surgical cure with preservation of atrioventricular conduction.

Paroxysmal supraventricular tachycardia (PSVT) is commonly caused by reentry within the atrioventricular (AV) node. This arrhythmia was abolished by operative dissection of the AV junction in a patient with disabling tachycardia that was not controlled by drugs. The operation was intended to create complete AV block, but AV conduction persisted after surgery. An electrophysiologic study 1 year after the operation revealed that the operation changed AV conduction in both the antegrade and retrograde directions, which may explain the absence of tachycardia. The patient has been free of arrhythmias for 18 months.

Atrioventricular Node↗