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Inert characteristic and functional refractory period of the atrioventricular node in rabbit heart preparation.

The effect of heart rate on the functional refractory period (FRP) of the atrioventricular node (AVN) is studied. A conclusion is reached that FRP, being a complex characteristic of AVN, should not be directly related to conduction time, but it can serve as a measure of the maximum moment acceleration which AVN is capable of transmitting to the lower-lying structures. It is proposed to use the coefficient of relative acceleration for quantitative estimation of the inert (dynamic) properties of the node at different heart rates. It is concluded that for a longer basic cycle length (BCL) AVN is characterized by greater reserve possibilities for transformation of accelerations of the input rhythm.

Animals↗

Pathological aspects of radiofrequency catheter ablation of the canine atrioventricular node and bundle of His. With special reference to chronic incomplete atrioventricular block.

Radiofrequency catheter ablation of the atrioventricular (AV) node or bundle of His was performed in 12 adult mongrel dogs. The aim was to create chronic incomplete AV block (first- and second-degree AV block) and to examine the histopathology of the ablated lesions. However, the late electrophysiological results (2-4 weeks follow-up) were various: normal in 2 dogs, mild PR prolongation (less than 50%) in 2 dogs, first-degree AV block (PR prolongation greater than or equal to 50%) in 2 dogs, second-degree AV block in 2 dogs, complete AV block in 4 dogs. The maximally ablated area (%) of the atrioventricular conduction system in serial histologic sections from dogs with these conditions was 69%, 75%, 89.5%, 95% and 99.5%, respectively. The number of intact conduction cells at the maximally ablated site varied from 6 to 30 in the four cases of incomplete AV block. The mean ablated volume (%) of either the AV node or penetrating His bundle correlated roughly with the degree of AV block. The ablated lesions were well demarcated and almost replaced by dense fibrous tissue at 4 weeks. Interruption (3 dogs) or thinning (1 dog) of the endocardial elastic lamellae was detected, in association with endocardial thickening (mean 913 microns). Endocardial thrombi were found in 3 dogs (2 fresh, 1 organized). We conclude that radiofrequency catheter ablation does not cause severe complicated lesions. Several possible conditions for creating chronic incomplete AV block are discussed.

Animals↗

Characterization of junctional rhythm after atrioventricular node ablation.

BACKGROUND: Catheter ablation of the atrioventricular (AV) node with radiofrequency current (RFC) is associated with the short-term onset of a junctional escape rhythm (JER) in nearly all patients. However, the origin of the JER and short-term thermal effects of RFC on this junctional pacemaker activity are ill defined. METHODS AND RESULTS: Short-term and noninvasive long-term follow-up studies were performed to examine the electrophysiological characteristics of the underlying JER in 45 patients who had undergone AV nodal ablation with RFC. Baseline characteristics and responses to overdrive ventricular pacing and intravenous atropine followed by an incremental isoproterenol infusion were determined. Short- and long-term responses were compared. HV intervals before and after ablation were 49 +/- 9 and 48 +/- 9 milliseconds, respectively (P = NS). Follow-up was 11 +/- 8.3 months. JER cycle length was 1526 +/- 298 milliseconds in the short-term setting and was present in 44 patients (98%) in the long-term setting, measuring 1426 +/- 223 milliseconds (P < .005). Junctional recovery times increased exponentially as overdrive pacing rates increased-there was no difference between short-term and long-term responses. Drug responses within each study were all significant when compared with baseline. However, there was no significant difference between short- and long-term responses, except at the highest dose of isoproterenol. Intravenous atropine (1 mg) caused an 8.6 +/- 9.3% decrease in JER cycle length in the short-term setting compared with a 7.6 +/- 7.3% decrease in the long-term setting. The decreases in JER cycle length with isoproterenol infusion (short-term versus long-term) were 10.1 +/- 9.6% versus 9.6 +/- 7.4% with 1 microgram/min, 15.8 +/- 11.7% versus 17.4 +/- 8.5% with 2 micrograms/min, 17.9 +/- 11.2% versus 21.4 +/- 9.1% with 3 micrograms/min (all P = NS), and 20.6 +/- 12.1% versus 24.8 +/- 9.1% with 4 micrograms/min (P < .01). CONCLUSIONS: Radiofrequency ablation of the AV node is associated with development of a JER that is stable in the long-term setting. The lack of change in HV interval after ablation locates the junctional pacemaker proximal to the central fibrous body. The pattern of drug responses suggests an origin within the proximal His bundle at its junction with the AV node rather than the AV node itself. The overall similarity between short- and long-term characteristics of junctional pacemaker activity mitigates against any reversible thermal effects of RFC on this pacemaker focus.

Aged↗

[Ventricular fibrillation after radiofrequency ablation of the atrioventricular node].

The authors report the case of a 77 year old patient who underwent radiofrequency ablation of the atrioventricular node for chronic. Invalidating atrial fibrillation, refractory to pharmacological therapy. A single chamber ventricular pacemaker was implanted one week before interruption of AV conduction. Eleven applications (7 on the right and 4 on the left side of the interventricular septum) were required for successful ablation. Four hours later, the patient developed episodes of non-sustained polymorphic ventricular tachycardia and torsades de pointe. These arrhythmias were initiated by long cycle-short cycle sequences and preceded by changes of ventricular repolarisation (prolongation of the spontaneous and paced QTc and JTc intervals). Eight days after ablation, the patient had an episode of ventricular fibrillation reduced by external DC shock. This arrhythmia was also preceded by changes in ventricular repolarisation. This case demonstrates the potential proarrhythmogenic effect of radiofrequency ablation of the AV node with changes in ventricular repolarisation which induces malignant ventricular arrhythmias. The authors suggest an appropriate preventive attitude. The progression in two distinct phases (immediate and late) imposes prolonged arrhythmia monitoring.

Aged↗

The early development of the atrioventricular node and bundle of His in the embryonic chick heart. An electrophysiological and morphological study.

The development of the atrioventricular node and bundle of His of embryonic chick hearts was studied by electrophysiological and morphological techniques. The dorsal wall of the AV canal and the interatrial septum were explored to determine if they contribute to the formation of the AV node and bundle of His. The resting membrane and action potentials of the interatrial septum cells were systematically analyzed and found to undergo progressive differentiation with development. The earliest identification of the AV node and upper bundle of His group of cells was achieved at 5 1/2-6 days of development by the electrical recording of their corresponding characteristic action potentials, from a circumscribed area located in the lowest and dorsal segment of the interatrial septum. The morphological and anatomical characterization of the cells was made following electrical recording and labelling with charcoal particles. The earlier AV node and bundle of His responses had similar characteristics to those of the adult heart. It is concluded that the AV node and upper bundle of His cells derive from the low interatrial septum. The possibility that AV canal cells contribute to this event was discarded. The functional relationship of the Av node and bundle of His with other cardiac tissues during the early development of the heart is discussed.

Animals↗

Congenital polycystic tumor of the atrioventricular node (endodermal heterotopia, mesothelioma): a histogenetic appraisal with evidence for its endodermal origin.

The small, variously designated, primary atrioventricular node tumor has been considered to be of endothelial, endodermal, or mesothelial origin. To identify its derivation, we studied seven tumors using silver staining and immunocytochemical labeling with a variety of antibodies. Cytoplasmic argyrophil granules but not argentaffin granules were found in isolated cells among the more numerous tubule-lining cells in four tumors. Serotonin and calcitonin were demonstrable in seven and six tumors, respectively, in a similar distribution to that of the argyrophil cells. A positive reaction of different distribution from that of the argyrophil cells was noted in a varying number of tubule-lining cells for carcinoembryonic antigen, epithelial membrane antigen, and blood group antigen in seven, four, and seven tumors, respectively. No activity was noted in the tumor cells for factor VIII-related antigen or a number of peptides. An endodermal rather than mesothelial or epithelial origin for the tumor is substantiated by the presence of neuroendocrine cells in the midst of the more numerous carcinoembryonic-antigen-positive lining cells of the tumor tubules.

Atrioventricular Node↗

Dynamic behavior of the atrioventricular node: a functional model of interaction between recovery, facilitation, and fatigue.

The wide variety of delays that the atrioventricular node can generate in response to an increased rate are explained by dynamic interactions between the three intrinsic properties of recovery, facilitation, and fatigue. The functional model presented suggests that any deviation of nodal conduction time from its minimum basal value represents, at any given time, the net sum of the effects produced by these properties. When a constant fast atrial rate is suddenly initiated, the node first "sees" a shortening in recovery time and responds by an increase in conduction time. This increase further shortens the recovery time of the ensuing beat, which is accordingly further delayed, and so on until a steady state is reached or a block occurs. However, these events do not occur alone. The second beat at the fast rate is conducted with a shorter conduction time than expected from the recovery time alone, and is therefore facilitated. These facilitatory effects develop within one short cycle and dissipate within one long cycle. They affect increasingly the conduction time of beats occurring with shorter cycle lengths. While steady-state effects of recovery and facilitation occur within seconds, nodal conduction time continues to increase slowly over several minutes when a rapid rate is maintained. This effect is attributed to fatigue, which develops and dissipates with a slow, symmetric time course. The dynamics of these properties can now be directly studied with selective stimulation protocols, and have many implications for the understanding of nodal behavior in the context of supraventricular tachyarrhythmias.

Animals↗

Histological evidence for cell proliferation activity in cystic tumor (endodermal heterotopia) of the atrioventricular node.

Cystic tumor (endodermal heterotopia) of the atrioventricular (AV) node in a 95-year-old female is described. Electrocardiograms showed complete AV blockage with a narrow QRS morphology resulting from the long-standing first degree of AV blockage since age 61. A cardiac pacemaker was implanted at age 83. The patient died of pneumonia at age 95. Autopsy demonstrated a normal heart weight (320 g), normal coronary artery and normal myocardium. Histological examination of the conduction system revealed a marked fibrotic sinoatrial (SA) node and a cystic lesion in the lower right atrium, including the approaches to the AV node. The bundle of His and its branches were completely intact. Cellular nests and cystically dilated tubules were scattered within a loose tissue stroma, which measured 18 x 12 x 5 mm. There were several mitotic figures among the tubules, as well as nuclear fragments similar to apoptotic bodies and exfoliation of the tumor cells. Immunohistochemical studies demonstrated a positive reaction for epithelial membrane antigen, carcinoembryonic antigen, CA19-9, cytokeratin and secretory component in the tubular cells, and a negative reaction for thrombomodulin. Endocrine cells among the tubules were positive only for calcitonin and serotonin. Ultrastructurally, sparse microvilli and desmosome-like structures between the tumor cells were observed. These findings support that this lesion originates from the endoderm. Moreover, it is likely that progression in the degree of AV block may be explained by the cell proliferation activity of the tumor.

Aged↗

[Electrophysiological heterogeneity of rabbit atrioventricular node cells: possible relationship to fast and slow pathways].

Catheter ablation has been applied for the therapy of atrioventricular nodal re-entrant tachycardia for several years. Although this procedure is quite successful, the cellular electrophysiological mechanisms underlying fast and slow conductions remain unknown. Therefore, the characteristics of the action potential waveform of rabbit atrioventricular node (AVN) cells obtained from different regions within Koch's triangle were studied using nystatin-permeabilized patch methods, and 64 AVN cells were used for this study. Based on gross morphology, AVN cells were classified into three groups: ovoid cells, rod shaped cells, and cells with an intermediate shape. Results obtained by measuring the maximum velocity dV/dt of action potentials fell into four subgroups: Group I (dV/dt < 5 V/sec, n = 23), Group II (dV/dt > 5 but < 10 V/sec, n = 20), Group III (dV/dt > 10 but < 20 V/sec, n = 13), and Group IV (dV/dt > 20 V/sec, n = 8). Ovoid cells had the smallest dV/dt, whereas the rod shaped cells had the highest dV/dt. The maximum diastolic potential was more negative in Groups III and IV than in Groups I and II. A notch in the phase II of the action potential was observed in 23% of Group III cells and 56% of those in Group IV, but was not present in Groups I and II. These findings provide further evidence that AVN cells are heterogeneous both in morphology and electrophysiological characteristics. Provided that values of dV/dt can be related to conduction velocity, our findings suggest that cells in Groups III and IV may contribute to fast conduction pathways whereas those in Groups I and II are responsible for slow conduction pathways.

Action Potentials↗

Radiofrequency versus pharmacologic modification of the atrioventricular node.

Although transcatheter radiofrequency modification of the atrioventricular (AV) node has been proposed as curative treatment in AV nodal reentry tachycardias, its role for the control of the ventricular rate in atrial tachyarrhythmias remains unclear. The aim of this study was to analyze the acute effect of radiofrequency current on AV nodal conduction and refractoriness, and to compare it with the effects of two antiarrhythmic drugs such as amiodarone (class III) and flecainide (class I). Twenty-one dogs were studied: (1) radiofrequency group (5 W for less than 45 seconds; 2 to 12 discharges; seven dogs); (2) amiodarone group (5 mg/kg intravenously; seven dogs); and (3) flecainide group (2 mg/kg intravenously; seven dogs). The following parameters were measured under basal conditions and after each procedure: AH interval, AV nodal functional refractory period, Wenckebach cycle length, minimum R-R interval during atrial fibrillation, and fitting of AV nodal function curve to a hyperbolic equation using its linear transformation. The AV nodal effective refractory period could not be calculated in any dog in the basal study because it was shorter than the atrial functional refractory period.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗

Mitral regurgitation after atrioventricular node catheter ablation for atrial fibrillation and heart failure: acute hemodynamic features.

BACKGROUND: Radiofrequency catheter ablation of the atrioventricular node and pacemaker insertion have been associated with occasional development of mitral regurgitation (MR). Ventricular pacing might result in MR if (1) left ventricular (LV) compliance is decreased and/or (2) mitral valve leaflet apposition is disturbed. We studied acute hemodynamic changes resulting from initiation of ventricular pacing in patients undergoing ablation. METHODS AND RESULTS: Thirteen patients (10 men and 3 women) with a mean age of 73.4 +/- 8. 6 years, with chronic atrial fibrillation and congestive heart failure, had permanent ventricular pacemaker insertion with lead placement at the right ventricular (RV) apex. The following hemodynamic recordings were obtained before ablation (during atrial fibrillation) and then immediately after ablation (during RV pacing): heart rate, mean arterial pressure, LV end-diastolic pressure (LVEDP), mean pulmonary capillary wedge pressure, V-wave amplitude, and cardiac index. Presence of MR was assessed by V-wave amplitude and the results of LV angiography. In patients who had MR, recordings were also obtained during temporary ventricular pacing from the RV outflow tract (RVOT). As a group there were no significant changes in any hemodynamic measurement. Before ablation, mild MR by LV angiogram was present in 5 patients, but none had large V-wave amplitude. After ablation, mild MR was present by LV angiogram in 6 patients, and in 3 of these patients large V-wave amplitude developed (mean amplitude 42.7 +/- 2.2 mm Hg; assigned to group 1). This was associated with a rise in LVEDP in 1 patient (consistent with reduced LV compliance), but LVEDP was unchanged in the other 2 patients (suggesting abnormal mitral valve leaflet apposition). All patients in group 1 exhibited a fall in V-wave amplitude when the pacing site was moved to the RVOT. CONCLUSIONS: Both reduced LV compliance and disturbed mitral valve leaflet apposition contribute to MR after ablation. MR is reduced by pacing from the RVOT.

Aged↗

Pharmacological classification of adenosine receptors in the sinoatrial and atrioventricular nodes of the guinea-pig.

1. The effects of seven agonist and three antagonist adenosine receptor ligands were compared on the guinea-pig sinoatrial (SA) node (isolated right atrium) and atrioventricular (AV) node (perfused whole heart). Single agonist concentration-effect curves were obtained to 5'-N-ethylcarboxamidoadenosine (NECA), R(-)-N6-(2-phenylisopropyl)adenosine (R-PIA), N6-cyclohexyladenosine (CHA), 2-chloroadenosine (CADO),),S(+)-N6-(2-phenylisopropyl)adenosine (L-PIA), 2-phenylaminoadenosine (CV 1808) and N6-aminoadenosine (MeAdo). Adenosine and/or NECA curves were obtained in the absence and presence of the antagonists 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), 9-chloro-2 (2-furanyl)-5,6-dihydro-1,2,4-triazolo[1,5-c]quinazolin-5-imine (CGS15943) and N6-(endonorbornan-2-yl)-9-methyladenine (N-0861). 2. A formal comparison of the agonist and antagonist potency data was made by fitting the data to a straight line using a least squares procedure based on principal components analysis to account for the variance on both axes. The antagonist affinity estimates made on the two assays did not deviate significantly from the line of identity. 3. The agonist p[A]50 data obtained on the two assays did not deviate from the line of identity, indicating that there were no significant differences in potencies between the two assays. The p[A]50 ratio of R-PIA and S-PIA was 1.24+/-0.09 in the SA node and 1.36+/-0.11 in the AV node, indicating no difference in the stereoselectivity of the PIA isomers between the two tissues. 4. The agonist potency and antagonist affinity data obtained are consistent with previous findings showing that the AV and SA node data are pharmacologically indistinguishable and belong to the adenosine A1-receptor class. No evidence for the reported A3-receptor was found.

Adenosine↗

The artery of the atrioventricular node: an anatomic study based on 38 injection-dissections.

The origin and course of the artery of the atrioventricular node (AAVN) was studied in 45 anatomic specimens by the method of injection-dissection in 38 human hearts removed at medicolegal autopsies from black Senegalese subjects. Though sometimes double, the AAVN is classically solitary. Its coronary origin, which is always distal, occurred on the right side in the great majority of cases, at the level of the "U-turn of James", and on the left side at the level of the terminal portion of the circumflex a. At the level of Koch's triangle, its course is marked by a close relationship with the zone of attachment of the septal cusp of the right atrioventricular valve on the one hand, and with the orifice of the coronary sinus on the other. In cardiac surgery, respect for the area of Koch's triangle, the base of the interatrial septum and the region of the intersection of the cardiac sulci will reduce the risks of injury to the AAVN.

Adolescent↗

Induction of atrioventricular node reentry by simultaneous anterograde conduction over the fast and slow pathways.

Atrio-ventricular node reentry (AVNRT) is typically induced with an anterograde block over the fast pathway (FP) and conduction over the slow pathway (SP), with subsequent retrograde conduction over the FP. Rarely, a premature atrial complex (PAC) conducts simultaneously over the FP and SP to induce AVNRT. Previous publications have reported that conduction over the fast and slow pathway of the atrioventricular node can occur successively one after the other, thus leading to dual ventricular depolarization from what initially was a single atrial impulse. We report a case of an 18-year-old male patient referred for repeated bursts of ectopic activity. Evaluation of the patient's electrocardiographic recordings suggested the presence of dual ventricular activations for each atrial beat. The electrophysiological study revealed that the patient had simultaneous conduction over the fast and slow pathways of the atrioventricular node giving rise to a non-reentrant tachycardia, along with an absence of retrograde (ventriculoatrial) conduction, and a significant atrio-His bundle jump (A-H jump) through the slow pathway from the fast pathway during programmed electrical stimulation from the right atrium. Ablation of the slow pathway at the base of the Koch triangle yielded a cessation of the dual ventricular response, absence of the nonreentrant tachycardia and no A-H jump.

Adolescent↗

Ultrastructural study of the effects of 6-hydroxydopamine on the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis).

The present study examined the ultrastructural changes in the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis) after 6-hydroxydopamine (6-OHDA) at survival times of 1, 3, 5, 7 and 14 days. Changes ranged from dissolution of the cytoplasm to amorphous appearance and darkening of the nodal cells. Initially, the ultrastructural changes were quite similar in both sinuatrial (SA) and atrioventricular (AV) nodal cells but in the later stage, especially at fourteen days, affected SA nodal cells showed empty-looking appearance while affected AV nodal cells displayed a darkened appearance. The cardiac neurons also showed ultrastructural changes such as diffuse accumulation of glycogen particles, distended cisternae of the rough endoplasmic reticulum and increased lipofuscin granules. Some of the vacuolated axonal profiles containing large dense-cored vesicles were in close association with the somata of the cardiac neurons. There were also changes in the non-neuronal cells such as darkening and vacuolation of the cells capping the neurons. Macrophages and Schwann cells were activated to engulf the degenerating nodal cells and axonal profiles. The ultrastructural changes in the nodal cells and the cardiac neurons reflect a disturbance in the cell metabolism presumably brought about by the impairment of the sympathetic nervous system.

Adrenergic Agents↗

[Standard of transesophageal atrial pacing to diagnose dual atrioventricular node pathway].

In order to assess the diagnostic methods of dual atrioventricular node pathway (DAVNP), we performed transesophageal atrial pacing in 58 patients with palpitation. These patients were classified into two groups, group A comprising 40 patients without broken A-V conduction curve during pacing, compared with group B of 18 patients with broken A-V conduction curve. In our study, both atypical Wenckebach cycle and 3:2 A-V conduction during the increment atrial pacing (IAP) had no significant difference between the two groups (P greater than 0.05). The maximum increments of SR interval in Wenckebach cycle of group A and B during pacing (Wenckebach delta SRmax) were 83.59 +/- 20.92 ms and 125.00 +/- 32.52 ms respectively (P less than 0.001) and at the cut-off point of Wenckebach delta SRmax at 120 ms the specificity and positive predicative value were very high (96.88% and 90.91%), but sensitivity was not so high (71.43%). The minimum increments of RS interval (delta RSmin) in a greater change of SR interval showed a significant difference between the two groups and the specificity and positive predicative value were also high, but the sensitivity was not so high, either (78.57%). We conclude that the diagnostic value of both Wenckebach delta SRmax and delta RSmin, when the SR interval is of greater change during pacing to the DAVNP, is rather significant. As the sensitivity is very low, isolated atypical Wenckebach phenomenon is not as reliable a diagnostic criterion to the DAVNP as previously supposed.

Adult↗

Surgery for Wolff-Parkinson-White syndrome interrupts efferent vagal innervation to the left ventricle and to the atrioventricular node in the canine heart.

The hypothesis that cardiac surgery to interrupt accessory pathways also interrupts autonomic nerves to the canine ventricle and to the atrioventricular node was tested in four groups of dogs. Group 1 (n = 6) underwent dissection of the atrioventricular fat tissue and cryolesion created by application of a cryoprobe at -60 degrees C for 2 min along the lateral left atrioventricular groove, the same surgical procedure as carried out in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the left ventricular free wall. Group 2 (n = 6) underwent dissection of the atrioventricular fat pad alone and group 3 (n = 6) dissection and cryolesion along the posterior left atrioventricular groove as performed in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the posterior paraseptal area. Group 4 consisted of 11 non-operated control dogs. Four to 13 days after surgery the ventricular effective refractory period (ERP) was determined during bilateral ansae subclaviae stimulation (4 ms pulses, 2-3 Hz, and 2-3 mA), noradrenaline infusion (0.5 micrograms.kg-1.min-1), and bilateral vagal stimulation (4 ms pulses, 20 Hz, and current strength to induce asystole or complete atrioventricular block). Atrioventricular nodal conduction (AH interval) and spontaneous sinus cycle length were also determined in group 3 dogs. Ansae subclaviae stimulation and noradrenaline infusion shortened effective refractory period significantly at each left ventricular test site. The amount of effective refractory period shortening induced by ansae subclaviae stimulation did not differ among the test sites except for the posterior left ventricle in group 1 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗