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PubMed1991

Cellular electrophysiology of neonatal and adult rabbit atrioventricular node.

Adult and neonatal rabbit atrioventricular node (AVN) preparations were studied using transmembrane and surface electrogram recordings. Action potentials were categorized into four types, atrionodal (AN), nodal (N), "high" nodo-His (NH) (HNH), and "low" NH (LNH), according to their action potential characteristics and their location within the A-H interval. The electrophysiological parameters of the lower three regions were identical between the two age groups. Action potentials from the neonatal AN region were lower in amplitude and maximum diastolic potential than they were in the adult. The N cell action potential parameters did not differ between the two age groups, however, there did appear to be qualitative differences. AVN conduction times (A-H intervals) were the same in both age groups, as were the antegrade and retrograde refractory periods, and the Wenckebach intervals. Pacemaker activity was significantly greater in the neonates than in the adults and, in 11 of 13 neonatal preparations, originated in the AN region or higher. In 13 of 14 adult preparations, pacemaker activity resided within the AVN.

Action Potentials↗

PubMed2006

Sustained slow pathway conduction: superior to dual atrioventricular node physiology in young patients with atrioventricular nodal reentry tachycardia?

BACKGROUND: Young patients with atrioventricular nodal reentry tachycardia (AVNRT) frequently do not display discrete dual AV node physiology (DAVNP) as classically defined. The purpose of the study was to investigate the prevalence of sustained slow pathway conduction (SSPC; PR > RR during atrial pacing) in young patients with AVNRT and compare it to dual atrioventricular node physiology. METHODS: The presence of SSPC and DAVNP was prospectively assessed before and after radiofrequency catheter ablation in 61 young patients (age 4-23 years) with typical AVNRT. RESULTS: Prior to ablation, 32 (52%) displayed DAVNP, while 46 (75%) displayed SSPC; 7 patients (11%) had neither marker. Patients with DAVNP were older than those without (15 +/- 3 vs 13 +/- 4, P = 0.027) and the prevalence increased with age (38% <13 years, 50% 13-15, 70% >15, P = 0.041), while SSPC showed no age predilection. Patients under 13 years displayed SSPC more commonly than DAVNP (81% vs 38%, P = 0.004). DAVNP persisted after ablation in 10/32 (31%) patients, compared to 6/46 (13%) with persistent SSPC after ablation. The ability to use loss of the marker (present before, absent after ablation) as a surrogate for successful ablation was greater for SSPC than for DAVNP (66% vs 36%, P = 0.001). CONCLUSION: SSPC is more common than DAVNP in young patients with AVNRT. SSPC is eliminated more frequently than DAVNP after acutely successful ablation, and appears to be a better indicator of the substrate for AVNRT. Elimination of SSPC may serve as a useful surrogate endpoint for slow pathway ablation.

Adolescent↗

PubMed1994

Electrophysiologic and histologic effects of dissection of the connections between the atrium and posterior part of the atrioventricular node.

OBJECTIVES: This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node. BACKGROUND: Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node. METHODS: Atrioventricular node function and electrical excitation of Koch's triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy. RESULTS: The compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exists from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs. CONCLUSIONS: This procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.

Animals↗

PubMedDate not supplied

New criteria for the diagnosis and treatment of atrioventricular node reentrant tachycardia.

The authors describe a new elecrocardiographic criterion to diagnose atrioventricular node reentrant tachycardia, review the electrocardiographic and electrophysiological diagnosis of this tachyarrhythmia and analyse the results of catheter ablation of fast versus slow pathway, selecting the fast pathway whenever the induction of atrioventricular node reentrant tachycardia is performed only after pharmacological maneuvers. The high specificity for atrioventricular node reentrant tachycardia of the criterion characterized by the absence of ST-segment depression found in left precordial leads from V4 to V6 suggests the need to include it in electrocardiographic algorithms for the differential diagnosis of tachycardias with a narrow QRS complex. The high primary and final success rates of catheter ablation obtained after a therapy stratification based on induction criteria, emphasize the use of the fast pathway ablation as a first option in selected cases and for the treatment of recurrences.

Catheter Ablation↗

PubMed1985

Mesothelioma of the atrioventricular node.

A patient with Mobitz type 2 heart block caused by a mesothelioma of the atrioventricular node died of a subarachnoid haemorrhage at the age of 33 two years after implantation of a permanent pacemaker. Mesothelioma of the atrioventricular node is rare, and reported cases have all been diagnosed post mortem. Mesothelioma of the atrioventricular node should be considered in the differential diagnosis of heart block in children or young adults. This is the first case to be reported in Japan.

Adult↗

PubMed2000

Arterial vascularisation of the atrioventricular node.

The aim of this study was to define the anatomic characteristics of the principal arterial source of the atrioventricular node, known as the artery of the atrioventricular node. Forty hearts were studied by various anatomic and radiologic methods: dissection, injection-dissection, injection-corrosion and injection-radiography, but only 23 results were interpretable. The right coronary artery represented the commonest arterial source of the atrioventricular node (21/23 hearts) but numerous variations in the origin and topography of the nodal artery were found.

Aged↗

PubMed1987

[Mesothelioma of the atrioventricular node and sudden death].

An incomplete atrioventricular block of grade III was detected by electrocardiography in a 3.5-year-old boy one week before his sudden death. On autopsy, cardiomegaly involving a 47% increase in heart weight and a moderate adaptational endocardial fibroelastosis were noted, as was a nodular tumor sized 6 X 3 X 1.5 mm at the atrioventricular node. The tumor was concluded to be a microcystic mesothelioma that had been destructive to the node and had begun infiltrating the cardiac muscle.

Atrioventricular Node↗

PubMed2006

Connexins in the sinoatrial and atrioventricular nodes.

The sinoatrial node (SAN) and the atrioventricular node (AVN) are specialized tissues in the heart: the SAN is specialized for pacemaking (it is the pacemaker of the heart), whereas the AVN is specialized for slow conduction of the action potential (to introduce a delay between atrial and ventricular activation during the cardiac cycle). These functions have special requirements regarding electrical coupling and, therefore, expression of connexin isoforms. Electrical coupling in the center of the SAN should be weak to protect it from the inhibitory electrotonic influence of the more hyperpolarized non-pacemaking atrial muscle surrounding the SAN. However, for the SAN to be able to drive the atrial muscle, electrical coupling should be strong in the periphery of the SAN. Consistent with this, in the center of the SAN there is no expression of Cx43 (the principal connexin of the working myocardium) and little expression of Cx40, but there is expression of Cx45 and Cx30.2, whereas in the periphery of the SAN Cx43 as well Cx45 is expressed. In the AVN, there is a similar pattern of expression of connexins as in the center of the SAN and this is likely to be in large part responsible for the slow conduction of the action potential.

Action Potentials↗

PubMed1999

Variation of P-QRS relation during atrioventricular node reentry tachycardia.

OBJECTIVES: The main objective of this study was to characterize the phenomenon of variation in the P-QRS relation during atrioventricular node reentry tachycardia. BACKGROUND: Variation of P-QRS relation during tachycardia has been observed occasionally in atrioventricular node reentry tachycardia. However, the incidence, the characteristics and the mechanisms of this phenomenon have not been investigated previously. METHODS: Retrospective analysis was performed in 311 consecutive patients with slow-fast form and 108 patients with atypical or multiple form of atrioventricular node reentry tachycardia to examine whether variation of P-QRS relation with changes in AH, HA and AH/HA (A = atria; H = His bundle) ratio occurred during tachycardia. RESULTS: A total of 28 patients, 8 with slow-fast and 20 with atypical or multiple tachycardias, were found to manifest this phenomenon. There were 6 males and 22 females, with an average age of 38+/-16 years. In 10 patients, this phenomenon occurred transiently following electrical induction of the tachycardia. In 15 patients, changes in AH, HA and AH/HA ratio were associated with the occurrence of Wenckebach or 2:1 block proximal to the His bundle (H) recording site without interruption of the tachycardia. In nine patients, three with nonsustained tachycardia and six after administration of adenosine triphosphate, this phenomenon was observed at the termination of the tachycardia. This phenomenon was usually accompanied by a mild lengthening of the tachycardia cycle length. CONCLUSIONS: Variation of P-QRS relation with or without block may occur during atrioventricular node reentry tachycardia, especially in atypical or multiple-form tachycardias. It was postulated that decremental conduction in the distal common pathway, which exists between the distal link of the reentry circuit and the H, is primarily responsible for this phenomenon.

Adenosine Triphosphate↗

PubMedDate not supplied

Effects of perhexiline maleate on the refractory periods of isolated atrial muscle and atrioventricular node of the rabbit.

The electrophysiologic effects of perhexiline maleate were studied with glass microelectrodes in three types of isolated rabbit heart preparations: (a) sinoatrial node preparation; (b) left atrial free-wall preparation; and (c) atrioventricular node preparation. The spontaneous firing rate of the sinoatrial node was decreased by 10-15% at a concentration of 10(-5) g/ml. The sinus node recovery time after atrial overdrive was prolonged by about 50%. The effective refractory period of the left atrial free wall showed concentration-dependent prolongation at concentrations above 10(-7) g/ml. Although this period was shortened after washing with perhexiline-free Tyrode solution, it did not return to the control lever. The effective refractory period of the right atrium was prolonged by 15% at a concentration of 10(-5) g/ml, but the functional refractory period did not change. The conduction time, effective refractory period, and functional refractory period of the atrioventricular node were significantly increased. Previous reports had claimed that perhexiline had pharmacologic effects on Purkinje fibers and ventricular myocardium at lower concentrations than on the atrium, but we found significant actions on the atrium and the atrioventricular node in therapeutic concentrations.

Animals↗

PubMed1981

Sudden death from occlusive disease of the atrioventricular node artery.

Non-atherosclerotic focal occlusive disease of the atrioventricular node artery was the only significant pathological lesion found at autopsy in 2 individuals aged 40 and 17 yr who died suddenly and unexpectedly. The cases were observed amongst 115 autopsies categorized as sudden cardiac death and performed during an 18 mth period. Occlusive disease of the atrioventricular node artery is a poorly documented entity of unknown aetiology and pathogenesis. We believe it is a more frequent pathological finding in sudden cardiac death than has been previously recognized and that it deserves more attention than it currently receives.

Adolescent↗

PubMedDate not supplied

Primary cardiac lymphoma with infiltration of the atrioventricular node: remission with reversal of the atrioventricular block induced by chemotherapy.

We describe a rare case of primary cardiac lymphoma associated with complete atrioventricular block, with recovery following systemic chemotherapy. A 61 year-old woman was admitted because of a massive pericardial effusion and complete atrioventricular block. Echocardiography disclosed several polypoid masses in the right atrium. A diagnosis of primary cardiac lymphoma was made. After three cycles of chemotherapy, the patient achieved a complete remission, the ECG showed first-degree atrioventricular block, and echocardiography revealed disappearance of the right atrial masses. This is the first report of a patient recovering from primary cardiac lymphoma and complete atrioventricular block following systemic chemotherapy. We conclude that aggressive treatment of this malignancy can improve cardiac function and the patient's prognosis.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1986

Influence of current strength on excitability and conduction of human atrium and atrioventricular node.

The influence of current strength on excitability and conduction of atrium and atrioventricular node was assessed in 25 patients using different current strengths (2, 3, 4, 5, 7, 10, 15 mA) and introducing extrastimuli (parasinusal zone) after the eighth paced complex of a basic drive (100 beats X min-1). Bipolar stimulation with the distal pole as cathode was performed so that effective and functional refractoriness of atrium and atrioventricular node, and the maximum value of atrial latency (interval between the extrastimulus and the beginning of atrial activity), intra-atrial conduction time, and AH interval could be determined at each current strength. In some patients atrioventricular nodal effective refractoriness could or could not be determined at each current strength, whereas in others the determination was possible only at the highest or the lowest current strengths. Moreover, the increase in current strength induced a progressive parallel reduction in both atrial effective and functional refractoriness; induced a progressive lengthening of intra-atrial conduction time (this was seen only in patients with a history of atrial arrhythmias); allowed the maximum possible lengthening of AH interval; and did not visibly influence atrioventricular nodal refractoriness and atrial latency. By altering atrial refractoriness and intra-atrial conduction time current strength affects the prematurity of the atrial impulse and the time at which it reaches the atrioventricular node. These findings should be taken into account when diagnostic and therapeutic electrophysiological procedures are performed.

Electric Stimulation↗

PubMed1990

Anticholinergic action of quinidine sulfate in the rabbit atrioventricular node.

Anticholinergic action of quinidine sulfate was electrophysiologically studied by recording spontaneous action potentials and membrane current of the rabbit atrioventricular node. In the presence of 0.1 mumol/l carbachol, the spontaneous activity of the atrioventricular nodal preparations was markedly inhibited, whereas subsequent addition of 1, 5 and 20 mumol/l quinidine restored automaticity in a concentration-dependent manner. In some preparations, quinidine at concentrations of 5 mumol/l and higher slowed the spontaneous activity by its direct membrane action even in the presence of carbachol. The dose-response curve for acetylcholine action on the spontaneous firing frequency showed that one molecule of acetylcholine bound to one muscarinic receptor of the atrioventricular node cell (Hill coefficient = 1.2). A parallel shift of this curve towards higher acetylcholine concentrations was observed at 0.03, 0.1 and 0.3 mumol/l but not at 1 and 3 mumol/l quinidine, suggesting a noncompetitive antagonism of quinidine against acetylcholine. Voltage clamp experiments revealed that 5 mumol/l quinidine reduced the slow inward current, hyperpolarization-activated inward current, and delayed rectifying K+ current, through its membrane actions. Quinidine at this concentration almost completely suppressed the acetylcholine-activated K+ current, which showed a relaxation phenomenon. Hence, the direct blockage of the acetylcholine-activated K+ current by quinidine was considered responsible for the anticholinergic action of this drug. We conclude that quinidine is a non-specific ionic channel blocker that inhibits all the membrane currents in the atrioventricular node including the acetylcholine-activated K+ current.

Action Potentials↗

PubMed1990

Reappraisals of atrioventricular node reentrant tachycardia: lessons learned from surgical treatment.

The exact site of reentrant circuit involved in the atrioventricular node reentrant tachycardia was questioned. Seven patients (6 females and 1 male), aged 21 to 64 years (mean = 40 +/- 17 years), with refractory nodal reentry, underwent surgical treatment. The associated cardiac diseases included rheumatic valvar disease in two and an atrial septal defect. Electrophysiologic studies before surgery showed dual nodal pathways in 4 patients. Right atrial endocardial mapping was performed and the earliest retrograde atrial activation during tachycardia was mapped to the apex of the triangle of Koch in 6 patients and near the orifice of coronary sinus in one. Perinodal dissection was performed according to the location of earliest retrograde atrial activity. Care was taken to preserve as much of the atrioventricular node and its arterial supply as was possible. Immediately after surgery, conduction in an antegrade direction recovered and the tachycardia could no longer be reproduced. There was no surgical mortality or morbidity. At 10 to 26 months of follow-up, all patients remain free of tachycardia without antiarrhythmic drugs. Four patients underwent repeated electrophysiologic studies at 2 weeks to 6 months after surgery. Dual nodal pathways were no longer demonstrated. It is concluded that the perinodal atrial tissue plays a part in the atrioventricular nodal reentry, and that surgical dissection is a simple and effective treatment for patients with refractory atrioventricular node reentrant tachycardia.

Adult↗

PubMed2001

Long-term survival after ablation of the atrioventricular node and implantation of a permanent pacemaker in patients with atrial fibrillation.

BACKGROUND: In patients with atrial fibrillation that is refractory to drug therapy, radio-frequency ablation of the atrioventricular node and implantation of a permanent pacemaker are an alternative therapeutic approach. The effect of this procedure on long-term survival is unknown. METHOD: We studied all patients who underwent ablation of the atrioventricular node and implantation of a permanent pacemaker at the Mayo Clinic between 1990 and 1998. Observed survival was compared with the survival rates in two control populations: age- and sex-matched members of the Minnesota population between 1970 and 1990 and consecutive patients with atrial fibrillation who received drug therapy in 1993. RESULTS: A total of 350 patients (mean [+/-SD] age, 68+/-11 years) were studied. During a mean of 36+/-26 months of follow-up, 78 patients died. The observed survival rate was significantly lower than the expected survival rate based on the general Minnesota population (P<0.001). Previous myocardial infarction (P<0.001), a history of congestive heart failure (P=0.02), and treatment with cardiac drugs after ablation (P=0.03) were independent predictors of death. Observed survival among patients without these three risk factors was similar to expected survival (P=0.43). None of the 26 patients with lone atrial fibrillation died during follow-up (37+/-27 months). The observed survival rate among patients who underwent ablation was similar to that among 229 controls with atrial fibrillation (mean age, 67+/-12 years) who received drug therapy (P=0.44). CONCLUSIONS: In the absence of underlying heart disease, survival among patients with atrial fibrillation after ablation of the atrioventricular node is similar to expected survival in the general population. Long-term survival is similar for patients with atrial fibrillation, whether they receive ablation or drug therapy. Control of the ventricular rate by ablation of the atrioventricular node and permanent pacing does not adversely affect long-term survival.

Adult↗

PubMed1977

Ultrastructure of the mesothelioma of the atrioventricular node.

In order to determine the histogenesis of tumors of the atrioventricular node, so-called conduction tumors, two such tumors were serially blocked for electron microscopy. Ultrastructurally these tumors were composed of nests of cells arranged in small channels and tubules set in a connective tissue stroma. The cells lining the tubules were flattened or low cuboidal and had abundant microvilli over the lumen surface. The cells were joined by specialized junctions along their lateral adjacent borders, especially at the luminal surfaces, and intercellular spaces delineated by specialized junctions were frequent. Microvilli, intercellular spaces bounded by tight junctions, and complex intercellular junctions are features of mesothelial cells, and especially of benign mesothelioma of the genital tract. These results strongly suggest that the cardiac conduction tumor is derived from mesothelial cells and is in fact a mesothelioma of the atrioventricular node.

Atrioventricular Node↗

PubMedDate not supplied

The influence of hypoxia and metabolic inhibitors on the excitation process in atrioventricular node.

In small specimens prepared from the atrioventricular node of rabbits, the influence of hypoxia and metabolic inhibitors (Na-cyanide, 2.4 dinitrophenol, 2-desoxyglucose) on the av-node action potential was studied. The action potentials in these specimens proved to be of slow response type regardless of their origin, either the N or the NH-region of the node. 1. Following superfusion with O2-poor Tyrode solution, Vmax of the atrioventricular action potential gradually declined within 90 min and attained finally a new steady state. A mean decrease of 30.2 +/- 9.4% was obtained. Frequency a automatic impulse formation went down by almost the same amount within only 20 min. On return to an oxygenated Tyrode solution, or in the continued presence of O2 deficiency after an increase of the external glucose concentration from 11 mM to 33 mM, full recovery of these effects occurred. 2. After administration of Na-cyanide (1 X 10(-3) M), a similar Vmax decrease of 29.0 +/- 7.0% appeared. It took only 20 min for full development and was accompanied by a decrease reversible within 10-20 min on return to a cyanide-free medium. Poisoning the atrioventricular cell with 2.4 dinitrophenol (1 X 10(-3) M) led to the same result. Treatment with 2-desoxyglucose (3 X 10(-2) M) evoked a more pronounced Vmax diminution of 50%. 3. The inhibitor of K conductance, 4-aminopyridine (2 X 10(-3) M) did not remove the metabolically induced changes of Vmax of the atrioventricular action potential. After poisoning of oxydative phosphorylation, this compound caused in some cases evan a further reduction of Vmax. 4. The beta-adrenergic compound isoproterenol (9.2 X 10(-6) M) restored the hypoxia or cyanide-induced suppression of both Vmax and frequency of automatic impulse formation. The particularly pronounced response of Vmax led to an increase far exceeding the initial control values obtained under normal metabolic conditions of the atrioventricular cell.

2,4-Dinitrophenol↗