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At least 271 records · Page 15Linked to original sources
PubMed1999

Autonomic modification of the atrioventricular node during atrial fibrillation: role in the slowing of ventricular rate.

BACKGROUND: Postganglionic vagal stimulation (PGVS) by short bursts of subthreshold current evokes release of acetylcholine from myocardial nerve terminals. PGVS applied to the atrioventricular node (AVN) slows nodal conduction. However, little is known about the ability of PGVS to control ventricular rate (VR) during atrial fibrillation (AF). METHODS AND RESULTS: To quantify the effects and establish the mechanism of PGVS on the AVN, AF was simulated by random high right atrial pacing in 11 atrial-AVN rabbit heart preparations. Microelectrode recordings of cellular action potentials (APs) were obtained from different AVN regions. Five intensities and 5 modes of PGVS delivery were evaluated. PGVS resulted in cellular hyperpolarization, along with depressed and highly heterogeneous intranodal conduction. Compact nodal AP exhibited decremental amplitude and dV/dt and multiple-hump components, and at high PGVS intensities, a high degree of concealed conduction resulted in a dramatic slowing of the VR. Progressive increase of PGVS intensity and/or rate of delivery showed a significant logarithmic correlation with a decrease in VR (P<0.001). Strong PGVS reduced the mean VR from 234 to 92 bpm (P<0.001). The PGVS effects on the cellular responses and VR during AF were fully reproduced in a model of direct acetylcholine injection into the compact AVN via micropipette. CONCLUSIONS: These studies confirmed that PGVS applied during AF could produce substantial VR slowing because of acetylcholine-induced depression of conduction in the AVN.

Animals↗
PubMed2002

Mortality analysis in patients with atrial fibrillation and implantable permanent pacemaker after ablation of the atrioventricular node.

OBJECT: Atrial fibrillation is associated with excess mortality. This analysis was performed to determine the magnitude of the excess mortality risk. METHODS: Life table analysis of a published study of 350 patients undergoing radiofrequency ablation of the atrioventricular node and permanent pacemaker implantation for symptomatic paroxysmal or chronic atrial fibrillation. A substantial proportion of subjects had evidence of left ventricular dysfunction. RESULTS: In this cohort, compared to expected population mortality, the relative mortality ratio was 234% and the annual excess death rate was 46 deaths/1000.

Aged↗
PubMed1986

Application of the Rosenblueth hypothesis to assess cycle length effects on the refractoriness of the atrioventricular node.

In adults, the effective refractory period of the atrioventricular (AV) node is lengthened, whereas that of the atrium, His-Purkinje system or ventricular myocardium is shortened with a shorter atrial pacing cycle length. However, in children, the effective refractory period of the AV node at shorter cycle lengths is also shortened. Based on Rosenblueth's 1-step delay hypothesis, an index of refractoriness within the AV node is defined as the longest coupling interval at the level of step delay within the AV node of an impulse that cannot be conducted to the His bundle. The slopes relating cycle length and refractoriness of the AV node are determined by both the conventional and revised methods in 9 pediatric patients with heart disease. The slope is positive for all patients using the revised method. The difference in values between the 2 methods in older children is striking because the slope is converted from a negative to a positive value. It is concluded that the AV node has the same positive slope relating cycle length and refractoriness as other cardiac tissues.

Adolescent↗
PubMed1991

[Findings in the atrioventricular node and the bundle of His in sudden and unexpected death in childhood. Histochemical study].

In 21 sudden and unexpected deaths of infants and three young children who died unexpectedly with known pathological conditions the authors examined by histochemical methods the atrioventricular node and bundle of His. The activity of "glycogen dependent" phosphorylase and the PAS reaction was in the majority week or negative. The probable cause of this finding is hypoxia, although other influences cannot be ruled out (inflammation, hypotrophy, autolysis). The activities of other enzymes (oxido-reductases ATPase, acetylcholine sterase, non-specific 1-naphtyl acetate esterase and acid phosphatase) were similar as in the normal conduction system.

Atrioventricular Node↗
PubMed2005

Cystic tumor of the atrioventricular node of the heart appears to be the heart equivalent of the solid cell nests (ultimobranchial rests) of the thyroid.

We studied a series of 10 solid cell nests (SCNs) of the thyroid and a case of cystic tumor of the atrioventricular node (CTAVN) of the heart and reviewed the literature. The CTAVN and SCNs appeared as cystic and/or solid (squamoid) structures mainly composed of polygonal or oval cells (main cells) admixed with occasional clear cells (neuroendocrine and C cells). Main cells were immunoreactive for simple and stratified epithelial-type cytokeratins, epithelial membrane antigen, carcinoembryonic antigen, carbohydrate antigen 19.9, p63, bcl-2, and galectin-3. Neuroendocrine (and C) cells were positive for simple-type cytokeratins, carcinoembryonic antigen, calcitonin, chromogranin, synaptophysin, and thyroid transcription factor-1. Our data support the hypothesis that the CTAVN of the heart and the SCNs of the thyroid are identical structures that represent the same lesional process. The assumption that CTAVN is a ultimobranchial heterotopia fits with the known role of cardiac neural crest cells in cardiovascular development.

Adult↗
PubMed1985

Interaction between atrial excitation waves and conduction in the atrioventricular node. II. Differences in the conduction of basic rhythms with different phasic correlation between the posterior and anterior inputs.

During in vitro experiments on the right atrium of rabbit heart microelectrodes were used to record simultaneously action potentials from different cells in the atrioventricular node (AVN) under stationary basic rhythms, imposed separately or jointly at the posterior and anterior inputs. A comparison was made of the pattern of conduction in the three different phase correlations between the input excitatory waves. Causal relation is found between the changes in the phase correlation and the conduction pattern with unchanged duration of the basic cycle. The formation of more than one excitatory front in AVN has no priority connection with the anterior input. Although stimulation at the posterior input is connected with more homogeneous conduction, even then the formation and interaction of two excitatory fronts is possible; on the other hand, during independent stimulation of the anterior input the formation of a second excitatory wave is possible, which, upon entering the node posteriorly, may have a dominating influence on conduction. A special case is the differentiation of an excitatory front which enters AVN only through one of the inputs. For example, upon anterior stimulation it is possible to induce one direct excitatory front to the N-zone and a second one which first activates the posterior AN-zone and then turns antegradely. The interaction of these two fronts creates different patterns concerning the characteristics of the action potentials and the organization of conduction, being related to the complex spatial inhomogeneous structure of excitable elements in different refractory phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

XVIII. Persistent fetal dispersion of the atrioventricular node and His bundle within the central fibrous body.

In the hearts of two victims of sudden unexpected death (one age 20 years and the other 11 years) there was abnormally delayed persistence of the pattern of fetal dispersion of the A-V (atrioventricular) node and His bundle within the central fibrous body. This pattern is characterized by a splayed or excessively fragmented histological appearance of these structures viewed in cross-section. Some of the fronds of A-V nodal tissue formed loops connecting one portion of the node to another. Other fragments of nodal tissue appeared isolated within the central fibrous body, occasionally connecting directly to the crest of the interventricular septum. A number of the A-V nodal fragments were undergoing resorptive degeneration. Directly adjacent to the A-V node of the 11-year-old subject there was an island of cartilage within the central fibrous body. Since these anatomically separated fragments of A-V nodal tissue were so numerous and varied widely in size and thickness, in length, in histological organization, and in their apparent state of preservation probably extant during life, it is suggested that they form potential routes for abnormal conduction or impulse formation within the A-V junctional region and that some of these electrophysiological disturbances might be quickly lethal.

Adult↗
PubMed1986

Fatal heart block due to mesothelioma of the atrioventricular node.

A fit young man of 23 was symptom free until the time of his death despite a narrow complex complete heart block, with resting heart rates down to 35 beats/min, that was first diagnosed when he was 10. The clinical diagnosis remained congenital heart block. Necropsy showed extensive infiltration of the atrioventricular node and proximal bundle by mesothelioma tissue. Pacing had not been advised because of his excellent exercise tolerance.

Adolescent↗
PubMed1989

Complete heart block in the 18p--syndrome. Congenital calcification of the atrioventricular node.

Complete heart block exists when the atria and ventricles beat completely independently of each other. It is heterogeneous with respect to pathogenesis. Occasionally, complete heart block may be symptomatic in infancy. Rarely, it is associated with genetic syndromes. Cardiac abnormalities are unusual in the 18p-syndrome. We describe a female stillborn infant who had 18p-syndrome with hydrops fetalis and complete heart block secondary to atrioventricular node calcification.

Abnormalities, Multiple↗
PubMed2003

Change in the retrograde atrial activation sequence following radiofrequency modification of the atrioventricular node: implications for the electrophysiologic circuit of a variant of atrioventricular nodal reentrant tachycardia.

INTRODUCTION: Despite the great success in treating AV nodal reentrant tachycardia (AVNRT) with radiofrequency modification of the AV node, the dimensions of the electrophysiologic circuit of this arrhythmia remain unclear, and simple models fail to explain all tachycardia-related phenomena. METHODS AND RESULTS: We describe three unusual cases of supraventricular tachycardia (SVT). In all three cases, retrograde atrial activation during ventricular pacing or during SVT manifested local left atrial electrograms recorded from the coronary sinus preceding the septal atrial electrograms (eccentric activation), with earliest atrial activity at the lateral or posterolateral mitral annulus. Electrophysiologic maneuvers and observations were consistent with AVNRT as the mechanism in each case. In all cases, radiofrequency modification of the AV node eliminated inducible SVT and abolished dual pathway AV nodal physiology. The retrograde atrial activation sequence during ventricular pacing changed after ablation in each case, with septal atrial electrograms preceding left atrial electrograms recorded from the coronary sinus (concentric activation). CONCLUSION: The observations in these cases cannot be explained by the traditional model of slow, fast, and intermediate AV nodal pathways. A model incorporating a circuit close to the AV node with left atrial and coronary sinus connections is proposed.

Atrial Function↗
PubMed1996

Characteristics of the delayed rectifier K current compared in myocytes isolated from the atrioventricular node and ventricle of the rabbit heart.

The delayed rectifier potassium current (IK) is known to be important in action potential repolarisation and may contribute to the diastolic pacemaker depolarisation in pacemaker cells from the heart. In this study, using whole-cell patch clamp, we investigated the characteristics of IK in morphologically normal cells from the atrioventricular node (AVN) and ventricle of the rabbit heart. Cells were held at -40 mV and 5 microM external nifedipine was used to block L-type calcium current (ICa,L). Significant IK was observed with pulses to potentials more positive than -30 mV. The steady-state activation curve in both cell types showed maximal activation at between + 10 and + 20 mV. Half-maximal activation of IK occurred at -4.9 and -4.1 mV with slope factors of 8.3 and 12.4 mV in ventricular and AVN cells, respectively. Using pulses of increasing duration, significant IK tails after repolarisation from + 40 mV were observed with pulses of 20 ms and increased with pulses up to 100-120 ms in both cell types. Pulses of longer duration did not activate further IK and this suggested that only the rapid component of IK, called IKr, was present in either cell type. Moreover, IK tails after pulses to all potentials were blocked completely by E-4031, a selective blocker of IKr. The reversal potential of IK varied with the concentration of external K. Superfusion of AVN cells with medium containing 4, 15 and 40 mM [K+]o resulted in reversal potentials of -81, -56 and -32 mV, respectively, which are close to values predicted if the IK channel were highly selective for K. The time constants for deactivation of IK in ventricle and AVN on return to -40 mV after a 500-ms activating pulse to + 60 mV were 480 ms and 230 ms, respectively. The faster deactivation of IK in AVN cells was a distinguishing feature and suggests that there may be differences in the IKr channel protein between ventricular and AVN cells.

Action Potentials↗