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PubMed1980

Heterotopic epithelial replacement (so-called "mesothelioma") of the atrioventricular node, congenital heart block, and sudden death.

Heterotopic epithelial replacement (so-called "mesothelioma") of the atrioventricular node is a rare cause of congenital heart block and sudden death; only about 50 cases have been reported in the literature in predominantly female patients ranging in age from infancy to 86 years. The lesion is virtually impossible to diagnose clinically and can be recognized at postmortem only by histologic examination of the atrioventricular conduction tissue. A unique case is reported since the patient, a young, asymptomatic woman, was chosen by chance as the subject of an electrophysiologic study of bradycardia 6 years before her sudden death. The morphologic (light- and electron-microscopic) findings of the atrioventricular node studied at autopsy were supportive of heterotopic epithelial origin of the lesion. The disputed histogenesis is briefly discussed.

Adolescent↗

PubMed2001

Atrioventricular node reentry tachycardia in pediatric patients.

Atrioventricular node reentry tachycardia (AVNRT) is a significant cause of paroxysmal supraventricular tachycardia (SVT) in the pediatric population. Symptoms can include palpitations, chest pain, fatigue, light-headedness and syncope. AVNRT is a reentry tachycardia that is comprised of dual conduction pathways through the AV node. On electrocardiogram, AVNRT usually manifests as a regular tachycardia with a narrow QRS complex and P waves that are either absent or distort the terminal portion of the QRS complex. Electrophysiology study will reveal dual AV node pathways: a fast pathway with a short AH interval and a long effective refractory period (ERP); and a slow pathway with a longer AH interval and a shorter ERP. During tachycardia, electrophysiologic signals will reveal conduction up the midline. Introduction of premature ventricular contractions and measurement of the HA interval during SVT can help distinguish AVNRT from a SVT utilizing an accessory pathway. Radiofrequency catheter ablation (RFA) has been used increasingly in children as treatment for AVNRT. The initial approach to RFA of AVNRT was modification of AV fast pathway conduction by lesions placed near the anterosuperior aspect of the triangle of Koch, known as the anterior approach method. However, this technique was associated with a significant risk of complete AV block. Now, the posterior approach slow pathway modification is used more commonly, which positions the ablation catheter along the tricuspid annulus immediately anterior to the coronary sinus ostium. This has been associated with a lower risk of complete AV block. Using this technique, RFA should be considered the method of choice for curative therapy of AVNRT in pediatric patients.

Journal Article↗

PubMed1988

Selective hypervagotonia isolated to the atrioventricular node.

Thirteen patients with recurrent unexplained syncope or presyncope underwent electrophysiological evaluation. A prolonged effective refractory period and functional refractory period of the atrioventricular node as well as slow paced rate to atrioventricular block were the only abnormalities found. Ventricular tachycardia could not be induced. All electrophysiological abnormalities reverted to normal following atropine administration. These patients have selective hypervagotonia isolated to the atrioventricular node. Three of thirteen patients required permanent pacing, and one required propantheline to control recurrent symptoms. Selective hypervagotonia may be a distinct clinical entity that can cause symptoms and require therapy.

Adult↗

PubMed1981

So-called mesothelioma of the atrioventricular node.

A so-called mesothelioma of the atrioventricular node causing sudden, unexpected death is reported. The tumor is composed of tubular-glandular spaces and surrounded by connective tissue containing reticulin and elastic fibres. The tubular-glandular spaces are lined by a single, cuboidal or multilayered squamoid epithelium. The tumor epithelium contained epithelial mucin and carcinoembryonic antigen (CEA). At the ultrastructural level the epithelium showed tight junctions, desmosomes and a few epithelial cells had preserved blunt microvilli at the luminal cell surface. Many tumor cells contained a large number of cytoplasmic tonofilaments. Our results support the opinion, that the conducting tissue tumor is a lesion arisen from sequestered endodermal elements from the primitive forgut during cardiac organogenesis.

Adult↗

PubMed1982

Congenital polycystic tumor of the atrioventricular node: possible familial occurrence and critical review of reported cases with special emphasis on histogenesis.

Congenital polycystic tumor of the atrioventricular node is a rare tumor of disputed histogenesis. It constant location in the atrioventricular node separates it from other cardiac cysts and tumors of indisputable endodermal origin. New studies of the embryogenesis of conduction tissues provide a reasonable explanation for the site of the lesion. Morphologic and histochemical features of the tumor fail to conclusively favor either a mesothelial or an endodermal genesis. A recently studied case provides some new morphologic observations (complex desmosomes, granule-containing epithelial cells) and suggests the possibility of of familial occurrence.

Aged↗

PubMed1991

Identification of the rate-dependent functional refractory period of the atrioventricular node in simulated atrial fibrillation.

We continuously observed successive pairs of R-R intervals during atrial fibrillation and hypothesized that the shortest R-R interval for a given preceding R-R interval in a pair represents the functional refractory period of the atrioventricular node at that preceding interval. To test this hypothesis we simulated atrial fibrillation in 28 isolated cross-perfused canine hearts and obtained an R-R interval scatterplot by plotting the R-R intervals as a function of the immediately preceding R-R interval. This scatterplot enabled us to detect a series of the shortest R-R intervals for a wide range of preceding R-R intervals, and this allowed us to estimate the rate-dependent functional refractory period of the atrioventricular node in simulated atrial fibrillation. The estimated functional refractory periods correlated well with those measured by the conventional method (r = 0.93). We conclude that the proposed method makes it possible to estimate the rate-dependent functional refractory periods of the atrioventricular node in atrial fibrillation.

Animals↗

PubMed1992

Accessory atrioventricular node and bundle: a cause of antidromic reentry tachycardia.

Two patients are described with antidromic reentry tachycardia successfully treated by interruption of an anterior septal accessory atrioventricular node and bundle. This anomalous connection resembles an atrioventricular conduction sling seen in complex congenital heart malformations. It has atrioventricular node-like properties, is located in the anterior septal area, will only conduct antegrade, and has an insulated connection to the right bundle branch. Rather than nodoventricular, nodofascicular, atriofascicular, or Mahaim, a more appropriate label for the connection is accessory atrioventricular node and bundle.

Adult↗

PubMed1984

An ultrastructural study of the effects of right cervical sympathectomy on the sinuatrial and atrioventricular nodes in the heart of the monkey (Macaca fascicularis).

This study describes the ultrastructural changes in the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis) after right cervical sympathectomy. Obvious changes in the nodal cells were seen one day after operation. Numerous glycogen particles grouped together to form electron-dense patches containing vacuoles in the cytoplasm. At three days after operation, intracellular organelles exhibited fragmentation and dissolution. By five and seven days after operation, the affected cells were vacuolated and some were swollen and appeared to have degenerated. Simultaneously, there was massive infiltration of macrophages were present nodal tissues. Axon profiles and terminals showing various degrees of degeneration were present in the vicinity of the nodal cells throughout the period of study. It is concluded that right cervical sympathectomy resulted in a rapid degeneration in some of the cells in the sinuatrial and atrioventricular nodes.

Animals↗

PubMed1991

Comparison of pre- and postoperative conduction patterns in patients surgically cured of atrioventricular node reentrant tachycardia.

Patients with atrioventricular (AV) node reentrant tachycardia characteristically have short and constant retrograde His-atrium conduction times (H2A2 intervals) during the introduction of ventricular extrastimuli. It has therefore been suggested that the tachycardia circuit involves retrograde conduction up an accessory pathway located in perinodal tissue. If the mechanism of surgical cure of AV node reentrant tachycardia is interruption of this accessory pathway, postoperative changes in retrograde conduction would be expected. Thirteen patients with drug-refractory AV node reentrant tachycardia underwent surgery. Preoperatively, H2A2 intervals were short and constant. During AV node reentrant tachycardia, earliest atrial activation was seen near the His bundle and was 0 to 25 ms before ventricular activation in all patients except one. Surgery consisted of dissection of right atrial septal and anterior inputs to the AV node and central fibrous body. Postoperatively, the H2A2 interval remained short and constant compared with preoperative values although it was slightly prolonged (74 +/- 18 versus 61 +/- 21 ms, p less than 0.005). Twelve of the 13 patients are free of tachycardia after 28 +/- 13 months and no patient has had evidence of AV node block. Thus, surgical cure of AV node reentrant tachycardia is highly successful; however, there is no reason to postulate an accessory pathway or use of perinodal tissue as part of the tachycardia circuit and the mechanism of surgical success remains obscure.

Adult↗

PubMed1991

Indications for modification of coexisting dual atrioventricular node pathways in patients undergoing surgical ablation of accessory atrioventricular connections.

Concomitant susceptibility to atrioventricular (AV) node reentrant tachycardia has been demonstrated in certain patients having reentrant tachycardia utilizing accessory AV connections. For those patients undergoing accessory connection ablation, AV node surgical modification may be warranted during the same operative procedure. To assess indications for a combined operative procedure, this study evaluated potential predictors of subsequent spontaneous AV node reentrant tachycardia in patients undergoing ablation of accessory AV connections. Among 62 consecutive patients undergoing surgical ablation of an accessory AV connection, 13 (21%) manifested dual AV node pathways. The latter were identified preoperatively in five patients (four with concealed and one with bidirectional accessory connections) and postoperatively in seven (all seven with bidirectional accessory connections). In one patient with a bidirectional accessory connection, dual AV node pathways could not be demonstrated preoperatively, but AV node reentrant tachycardia was induced. Operative ablation of an accessory connection was successful in all patients. However, postoperatively, 2 of the 13 patients had inducible AV node reentrant tachycardia, 5 had AV node "echo" beats and 6 had no inducible arrhythmia. During 26 +/- 7 months of follow-up study, the two patients with inducible AV node reentrant tachycardia postoperatively had symptomatic AV node reentrant tachycardia. In addition, the one patient with inducible AV node reentrant tachycardia preoperatively had recurrence of this tachycardia 4 months after attempted surgical modification of the AV node. Consequently, although dual AV node pathways appear to be common in patients undergoing surgical ablation of an accessory AV connection (21%), only a small group (3 of 13) of these patients are at risk for subsequent clinical AV node reentrant tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1989

Specific 125I-endothelin-1 binding sites in the atrioventricular node of the porcine heart.

The quantitative receptor autoradiographic method we used revealed that specific 125I-endothelin-1 binding sites are highly concentrated in the atrioventricular node of the porcine heart. 125I-Endothelin-1 binding to the atrioventricular node, interatrial and interventricular septa was displaced by unlabeled endothelin-1 with Kd values of 53 pM, 2.03 nM and 3.48 nM, respectively. Knowledge of the existence of specific 125I-endothelin-1 binding sites in the porcine heart helps with understanding the physiology of endothelin, a possible endogenous Ca2+ channel agonist.

Animals↗

PubMed1985

'So-called mesothelioma' of the atrioventricular node--immunohistochemical study.

So-called mesothelioma of the atrioventricular node is a rare lesion and a cause of sudden, unexpected death. A case of congenital complete heart block accompanied by polyclonal immunoblastosis is presented. The histological features of our case are fundamentally similar to that of the cases previously reported. Immunohistochemical findings indicated that the tumor may have originated from aberrant epithelial or mesothelial tissue.

Adult↗

PubMed1985

Congenital polycystic tumor of the atrioventricular node. Autopsy study with immunohistochemical findings suggesting endodermal derivation.

Atrioventricular node congenital polycystic tumor, a lesion that causes heart block and sudden unexpected death, has been postulated to arise from the lymphatics, foregut endoderm, cardiac mesoderm, and mesothelium since its initial description in 1911. No theory concerning the histogenesis of this tumor has been completely satisfactory, either from an embryologic or a clinical standpoint. Biologic studies including cell culture systems from the lesions as well as optimal ultrastructural examination have been compromised due to postmortem autolysis. We studied four examples of this entity by standard histochemical stains for mucopolysaccharides, and by modified immunohistochemical labeling for carcinoembryonic antigen, factor VIII, and keratin. Results suggest an origin from foregut endoderm. The lesion has not been reported to be outside the region of the atrioventricular junction, but was demonstrated in the thymus gland in one of our cases.

Adult↗

PubMed1993

Immunohistochemical delineation of the conduction system. II: The atrioventricular node and Purkinje fibers.

Using an antibody that reacts specifically with the myocytes of the conduction system of the bovine heart, we have studied the atrioventricular node and the spatial distribution of the Purkinje fibers in the bovine heart. This study was complemented by studying the distribution of the gap junction protein connexin43 in these areas in the bovine heart and in the human heart. The large Purkinje fibers in the bovine heart are arranged in a two-dimensional network underneath the endocardium. At discrete sites, these fibers branch to the Purkinje fibers situated between the muscle bundles of the ventricular mass. These intramural Purkinje fibers are arranged in sheets that form a complex three-dimensional network of lamellas. Contacts with the ventricular myocytes are found throughout the myocardial wall, with the exception of a subepicardial layer of 2-mm thickness, ie, 10% to 15% of the wall thickness. The spatial arrangement of the Purkinje fibers correlates well with data on electrophysiology. Connexin43 was not detected in the myocytes of the atrioventricular node, whereas in the Purkinje fibers of the atrioventricular bundle and of the bundle branches, abundant expression of connexin43 was found in both humans and cows. In the bovine Purkinje fibers, a remarkable subcellular distribution of connexin43 is found: it occupies the entire plasma membrane facing other Purkinje cells but not that facing the surrounding connective tissue. The structural differences in architecture of the ventricular conduction system in humans and cows seems not to result in substantial differences in conduction velocities. However, the Purkinje fiber network in the bovine heart may explain the efficient ventricular excitation, as reflected by the relatively short QRS complex compared with that in the human heart, where intramural Purkinje fibers are not found.

Adult↗

PubMed1997

Amiodarone blocks L-type calcium current in single myocytes isolated from the rabbit atrioventricular node.

1. Single myocytes were isolated from the rabbit atrioventricular node (AVN) and whole cell patch clamped, using a Cs(+)-based internal dialysis solution. Depolarizing voltage clamps from a holding potential of -40 mV were applied to investigate the effects of the antiarrhythmic agent amiodarone on L-type calcium current (ICa,L). 2. The current-voltage (I-V) relation for ICa,L was bell shaped in normal Tyrode's solution, with a peak at +10 mV. After a 1-min exposure to 10 microM amiodarone, ICa,L at all potentials between -30 mV and +60 mV was largely and reversibly blocked (n = 4). In 13 cells, peak ICa,L was blocked by 85% after amiodarone application. 3. The time course of the blocking effect was monitored during continuous pulsing (at 0.33 Hz) from -40 mV to +10 mV to observe the time course of ICa,L blockade. This could be described by a single exponential function with a rate constant of 0.21 per second. In other cells, amiodarone was applied for 30 sec without any stimulation; and, when stimulation was resumed, the ICa,L amplitude with the first pulse was 22% of the control amplitude (n = 4), indicating that a substantial portion of the blockade of ICa,L by amiodarone was tonic in nature. 4. In addition to the effect of amiodarone on the ICa,L channel, when the beta adrenergic agonist isoprenaline (1 microM) was applied to cells that had been pretreated with amiodarone, ICa,L amplitude was increased by 44.5 +/- 10.8% (n = 4). In cells that had received no such pretreatment with amiodarone, isoprenaline increased the ICa,L amplitude by 101.5 +/- 5.9% (n = 4). Thus, isoprenaline produced a larger increase in ICa,L in the absence of amiodarone than in its presence (P < 0.001). 5. It is concluded that, in single AVN cells, amiodarone exerts a direct ICa,L blocking action. In addition, the attenuated increase in ICa,L with isoprenaline in amiodarone pretreated cells appears consistent with an antagonism of beta adrenergic stimulation of ICa,L.

Adrenergic beta-Agonists↗

PubMed1983

Effect of nifedipine and AQ-A 39 on the sinoatrial and atrioventricular nodes of the rabbit and their antiarrhythmic action on atrioventricular nodal reentrant tachycardia.

The effects of two drugs that apparently block slow inward current--nifedipine and the new compound AQ-A 39--were studied on the isolated sinoatrial (SA) and atrioventricular (AV) nodes of the rabbit heart using intracellular microelectrodes. Nifedipine and AQ-A 39 both slowed the sinus rate associated with a decrease in the rate of diastolic depolarisation. Conduction through the AV node was consistently impaired; this effect was enhanced with increasing atrial rates or with decreasing coupling intervals of premature beats. The action potential amplitude was significantly reduced in SA nodal and upper (AN) AV nodal fibres but was not significantly affected in lower (NH) AV nodal and in atrial fibres. The maximum diastolic potential showed little or no alteration. In all fibre types studied, the action potential duration was shortened with nifedipine but was significantly prolonged with AQ-A 39. Prevention of AV nodal reentrant tachycardia by nifedipine was related to an increase in the effective refractory period of the AV node. AQ-A 39 prevented the tachycardia by both slowing of AV nodal conduction and by prolongation of action potential duration in the AV nodal and atrial compartments of the reentrant circuit associated with the appearance of different gap phenomena of the AV conduction. The maximum possible A-H interval was, however, not shortened by either drug and single atrial echo beats could still be initiated. The results suggest that nifedipine and AQ-A 39 both have a direct depressant action on the slow inward current-dependent electrical activity of the SA and AV node but have opposite effects on the repolarisation phase resulting in different antiarrhythmic mechanisms.

Action Potentials↗

PubMedDate not supplied

Comparison of rejection in the atrioventricular node and bundles with the working myocardium in transplanted hearts.

At present the monitoring of heart transplant patients for rejection is done by endomyocardial biopsy. It has been proposed that ECG assessments of conduction delay may provide a noninvasive means of detecting rejection. To determine whether rejection in the atrioventricular node and conduction bundles reflects rejection in the working myocardium, we studied 21 transplanted hearts from 21 cardiac allograft recipients. Twenty of the hearts were obtained at autopsy, and one was obtained from a patient who underwent a second transplant procedure. The atrioventricular conduction tissues, the ventricular and atrial free walls, and the interventricular and interatrial septa from these hearts were examined for histologic evidence of rejection. Of the 21 hearts, 17 showed histologic changes of acute allograft rejection. Of the 17, rejection involved the conducting system and the myocardium equally in 11. In 6 of the 17 hearts, rejection involved the working myocardium more severely than it did the conducting system. Of interest, nonrejection pathologic changes were also noted in the conducting systems of several hearts. Severe accelerated arteriosclerosis was found in the artery to the atrioventricular node in one case, and lesser degrees of accelerated arteriosclerosis in this artery were found in two additional cases. In one case, lymphoid infiltrates, consistent with posttransplant lymphoproliferative disorder, were noted in the vicinity of the atrioventricular node, and several hearts demonstrated operative trauma or ischemic changes that appeared to involve the conducting system. These results suggest that although there may be a morphologic basis for using electrophysiologic changes in the conducting system to monitor heart allograft recipients for rejection, caution should be exercised in interpreting these changes.

Adult↗

PubMed1998

Preserved autonomic modulation of the sinus and atrioventricular nodes following posteroseptal ablation for treatment of atrioventricular nodal reentrant tachycardia.

INTRODUCTION: Following radiofrequency catheter ablation of AV nodal reentrant tachycardia (AVNRT), inappropriate sinus tachycardia may occur, possibly due to damage to autonomic cardiac nerve fibers. Furthermore, inducibility of AVNRT is often critically dependent on the autonomic balance. We investigated whether successful ablation of AVNRT is associated with an alteration of autonomic input to the sinus and AV nodes. METHODS AND RESULTS: To estimate changes in the autonomic modulation of the sinus and AV nodes, power spectra of beat-to-beat PP and PR intervals were analyzed from high-quality nighttime ECG recordings of 11 patients before and after radiofrequency application. Normalized HF power (nHF) of PP and PR intervals was used as an index of efferent vagal modulation and the LF/HF ratio as an index of sympathovagal balance of the sinus node (PP) and AV node (PR). Before ablation, LF/HF(PP) was 3.2 and nHF(PP) was 0.3 in the sinus node. For the AV node, LF/HF(PR) was 1.2 and nHF(PR) was 0.5. Following ablation, LF/HF(PP) (3.5) and nHF(PP) (0.3) of the PP intervals did not change. Similarly to the sinus node, there were no changes in the autonomic modulation of the AV node, as both LF/HF(PR) (1.2) and nHF(PR) (0.5) remained unchanged. CONCLUSION: Our results indicate that autonomic control of the sinus and AV nodes is preserved following successful radiofrequency ablation of AVNRT. The effects of posteroseptal radiofrequency current application are not necessarily mediated by changes in the autonomic input to the AV node.

Adult↗