scholarly journals The Anatomy, Development, and Evolution of the Atrioventricular Conduction Axis

2018 ◽  
Vol 5 (3) ◽  
pp. 44 ◽  
Author(s):  
Robert Anderson ◽  
Shumpei Mori ◽  
Diane Spicer ◽  
Damian Sanchez-Quintana ◽  
Bjarke Jensen
Keyword(s):  
Atrioventricular Node ◽  
Atrioventricular Conduction ◽  
Significant Part ◽  
Current Understanding ◽  
Ventricular Activation ◽  
Mechanisms Of Development ◽  
Development And Evolution

It is now well over 100 years since Sunao Tawara clarified the location of the axis of the specialised myocardium responsible for producing coordinated ventricular activation. Prior to that stellar publication, controversies had raged as to how many bundles crossed the place of the atrioventricular insulation as found in mammalian hearts, as well as the very existence of the bundle initially described by Wilhelm His Junior. It is, perhaps surprising that controversies continue, despite the multiple investigations that have taken place since the publication of Tawara’s monograph. For example, we are still unsure as to the precise substrates for the so-called slow and fast pathways into the atrioventricular node. Much has been done, nonetheless, to characterise the molecular make-up of the specialised pathways, and to clarify their mechanisms of development. Of this work itself, a significant part has emanated from the laboratory coordinated for a quarter of a century by Antoon FM Moorman. In this review, which joins the others in recognising the value of his contributions and collaborations, we review our current understanding of the anatomy, development, and evolution of the atrioventricular conduction axis.

Effect of adenosine on atrioventricular conduction in children and young patients with supraventricular tachycardia

1996 ◽  
Vol 6 (4) ◽  
pp. 308-314
Author(s):  
Parvin C. Dorostkar ◽  
Macdonald Dick ◽  
Gerald A. Serwer ◽  
Sarah LeRoy ◽  
Brian Armstrong
Keyword(s):  
Supraventricular Tachycardia ◽  
Accessory Pathway ◽  
Young Patients ◽  
Atrioventricular Node ◽  
Atrioventricular Conduction ◽  
Ventricular Pacing ◽  
Accessory Pathways ◽  
Before And After ◽  
Ventricular Activation ◽  
Retrograde Conduction

AbstractAdenosine, when given as an intravenous bolus, has been shown to produce atrioventricular nodal block in humans. To examine the effect of adenosine on conduction across both accessory pathways and the atrioventricular node in children, we reviewed our experience with adenosine administered during both atrial and ventricular pacing in 42 patients with atrioventricular resting tachycardia and in eight patients with atrioventricular nodal reentry tachycardia. Adenosine was administered as a mean bolus of 195 μg/kg/dose during both atrial and ventricular pacing, examining antegrade and retrograde conduction before and after radiofrequency ablation. In those patients with persistent or intermittent pre-excitation, anomalous ventricular activation was either unchanged (n=8) or increased (n=11). Retrograde conduction (either through the accessory pathway alone in three, or across both the accessory pathway and the atrioventricular node in 19) persisted in 92% of the 24 patients studied. Adenosine produced either first or third degree antegrade heart block in all patients studied without pre-excitation (those with either dual atrioventricular nodal pathways or concealed accessory pathways). Adenosine produced retrograde block in all of the eight patients with dual atrioventricular nodal pathways. In contrast, retrograde conduction persisted in 82% (14/17) of patients with concealed accessory pathways (p=0.001). When used to examine retrograde conduction, adenosine was a sensitive (82%) and highly specific (producing retrograde atrioventricular block in all patients with dual atrioventricular nodal pathways) predictor of tachycardia supported by a concealed accessory pathway. Adenosine yielded a sensitivity and specificity of 96% and a positive predictive value of 99.5% for the success of ablation of accessory pathways. These data indicate that the pattern of adenosine-induced changes in either antegrade or retrograde atrioventricular conduction, or conduction in both directions, in young patients with supraventricular tachycardia is related to the mechanism of the tachycardia. Adenosine, therefore, is a useful adjunct in the electrophysiologic evaluation of supraventricular tachycardia in children.

New Approach for Atrioventricular Conduction Modulation by Ablation at a Distance From the Atrioventricular Node

2021 ◽  
Author(s):  
José Luis Ibáñez Criado ◽  
Alicia Ibáñez Criado ◽  
Teresa Barrio-López ◽  
Thomas Brouzet ◽  
Eduardo Castellanos ◽  
...  
Keyword(s):  
Atrioventricular Node ◽  
Atrioventricular Conduction ◽  
New Approach

Anomalous Atrioventricular Excitation (Wolff-Parkinson-White Syndrome)

PEDIATRICS ◽  
1959 ◽  
Vol 23 (5) ◽  
pp. 902-902
Keyword(s):  
Atrioventricular Node ◽  
Atrial Arrhythmias ◽  
White Syndrome ◽  
Pr Interval ◽  
Ventricular Activation ◽  
Excitation Pattern ◽  
Retrograde Conduction ◽  
Wolff Parkinson White Syndrome

Vectorcardiographic and electrocardiographic data in 4 patients with the Wolff-Parkinson-White syndrome are presented. These studies support the concept that the mechanism responsible for the pre-excitation pattern is a functioning accessory neuromuscular bridge that by-passes the atrioventricular node. Early delivery of the impulse from the sino-auricular node to the lower chambers initiates premature ventricular activation with consequent shortening of the PR interval and lengthening of the QRS interval. Retrograde conduction through the accessory tract may be observed, and is a possible explanation of the atrial arrhythmias that occur in this syndrome.

The spatial distribution and relative abundance of gap-junctional connexin40 and connexin43 correlate to functional properties of components of the cardiac atrioventricular conduction system

1993 ◽  
Vol 105 (4) ◽  
pp. 985-991 ◽  
Author(s):  
R.G. Gourdie ◽  
N.J. Severs ◽  
C.R. Green ◽  
S. Rothery ◽  
P. Germroth ◽  
...  
Keyword(s):  
Spatial Distribution ◽  
Relative Abundance ◽  
Atrioventricular Node ◽  
Conduction System ◽  
Atrioventricular Conduction ◽  
Purkinje Fibre ◽  
Purkinje Fibres ◽  
Atrioventricular Bundle ◽  
Junctional Protein ◽  
Gap Junctional

Electrical coupling between heart muscle cells is mediated by specialised regions of sarcolemmal interaction termed gap junctions. In previous work, we have demonstrated that connexin42, a recently identified gap-junctional protein, is present in the specialised conduction tissues of the avian heart. In the present study, the spatial distribution of the mammalian homologue of this protein, connexin40, was examined using immunofluorescence, confocal scanning laser microscopy and quantitative digital image analysis in order to determine whether a parallel distribution occurs in rat. Connexin40 was detected by immunofluorescence in all main components of the atrioventricular conduction system including the atrioventricular node, atrioventricular bundle, and Purkinje fibres. Quantitation revealed that levels of connexin40 immunofluorescence increased along the axis of atrioventricular conduction, rising over 10-fold between atrioventricular node and atrioventricular bundle and a further 10-fold between atrioventricular bundle and Purkinje fibres. Connexin40 and connexin43, the principal gap-junctional protein of the mammalian heart, were co-localised within atrioventricular nodal tissues and Purkinje fibres. By applying a novel photobleach/double-labelling protocol, it was demonstrated that connexin40 and connexin43 are co-localised in precisely the same Purkinje fibre myocytes. A model, integrating data on the spatial distribution and relative abundance of connexin40 and connexin43 in the heart, proposes how myocyte-type-specific patterns of connexin isform expression account for the electrical continuity of cardiac atrioventricular conduction.

Re-evaluation of the structure of the atrioventricular node and its connections with the atrium

EP Europace ◽  
2020 ◽  
Vol 22 (5) ◽  
pp. 821-830 ◽  
Author(s):  
Robert H Anderson ◽  
Damian Sanchez-Quintana ◽  
Shumpei Mori ◽  
Jose Angel Cabrera ◽  
Eduardo Back Sternick
Keyword(s):  
Atrioventricular Node ◽  
Atrial Septum ◽  
Atrioventricular Conduction ◽  
Marked Variation ◽  
Compelling Evidence ◽  
Serial Sections ◽  
Atrial Myocardium ◽  
Cavotricuspid Isthmus ◽  
Fibrous Body ◽  
Bundle Of His

Abstract Aims The anatomic substrates for atrioventricular nodal re-entry remain enigmatic, but require knowledge of the normal arrangement of the inputs and exist from the atrioventricular node. This knowledge is crucial to understand the phenomenon of atrioventricular nodal re-entry. Methods and results We studied 20 human hearts with serial sections covering the entirety of the triangle of Koch and the cavotricuspid isthmus. We determined the location of the atrioventricular conduction axis and the connections between the specialized cardiomyocytes of the conduction axis and the adjacent working atrial myocardium. The atrioventricular node was found at the apex of the triangle of Koch, with entry of the conduction axis to the central fibrous body providing the criterion for distinction of the bundle of His. We found marked variation in the inferior extensions of the node, the shape of the node, the presence or absence of a connecting bridge within the myocardium of the cavotricuspid isthmus, the connections between the compact node and the myocardium of the atrial septum, the presence of transitional cardiomyocytes, and the ‘last’ connection between the working atrial myocardium and the conduction axis before it became the bundle of His. Conclusion The observed variations of the inferior extensions, combined with the arrangement of the ‘last’ connections between the atrial myocardium and the conduction axis prior to its insulation as the bundle of His, provide compelling evidence to support the concept for atrioventricular nodal re-entry as advanced by Katritsis and Becker.

Dynamic counterbalance between direct and indirect vagal controls of atrioventricular conduction in cats

1999 ◽  
Vol 277 (6) ◽  
pp. H2129-H2135 ◽  
Author(s):  
Shi-Liang Chen ◽  
Toru Kawada ◽  
Masashi Inagaki ◽  
Toshiaki Shishido ◽  
Hiroshi Miyano ◽  
...  
Keyword(s):  
Transfer Function ◽  
Vagal Stimulation ◽  
Normal Sinus Rhythm ◽  
Gaussian White Noise ◽  
Atrioventricular Node ◽  
Atrioventricular Conduction ◽  
Step Response ◽  
Conduction Time ◽  
Pass Filter ◽  
Low Pass Filter

The vagal system regulates the atrioventricular conduction time ( T AV) via two opposing mechanisms: a direct effect on the atrioventricular node and an indirect effect through changes in heart period ( T AA). To evaluate how dynamic vagal activation affects T AV, we stimulated the vagal nerve with frequency-modulated Gaussian white noise and estimated the transfer function from vagal stimulation to the T AV response under conditions of no pacing and constant pacing in anesthetized cats. The effect of changes in T AA on T AV was estimated by a random-pacing protocol. The transfer function from vagal stimulation to T AV has low-pass filter characteristics. Constant pacing increased the maximum step response in T AV(2.4 ± 1.2 vs. 6.3 ± 2.2 ms/Hz, P < 0.01). The time constant did not differ between the vagal effect on T AV and that on T AA (2.9 ± 1.2 vs. 2.3 ± 0.5 s). Because changes in T AA reciprocally affected T AVwithout significant delay, the direct and indirect effects were dynamically counterbalanced and exerted stable T AV transient response during vagal stimulation under normal sinus rhythm.

Differential vagal effects on antegrade vs. retrograde atrioventricular conduction

1987 ◽  
Vol 253 (5) ◽  
pp. H1059-H1068 ◽  
Author(s):  
T. Mitsuoka ◽  
T. Mazgalev ◽  
L. S. Dreifus ◽  
E. L. Michelson
Keyword(s):  
Vagal Stimulation ◽  
Atrioventricular Node ◽  
Rabbit Heart ◽  
Heart Tissue ◽  
Atrioventricular Conduction ◽  
Conduction Time ◽  
Crista Terminalis ◽  
Time Optimal ◽  
Fixed Phase ◽  
Atrioventricular Nodal Conduction

The influence of postganglionic vagal stimulation (PGVS) on antegrade and retrograde atrioventricular nodal conduction was studied in 17 isolated rabbit heart tissue preparations by pacing at the crista terminalis or His bundle, respectively. The effect of short bursts of PGVS on prolongation of atrioventricular conduction was phase dependent with respect to the cardiac cycle. This phasic dependency was more pronounced during antegrade atrioventricular conduction. Although the control retrograde atrioventricular conduction time was longer than the antegrade (P less than 0.05) at or near the time in the cycle during which vagal stimulation caused maximal prolongation of conduction time (optimal phase), PGVS-induced maximal prolongation of the antegrade atrioventricular conduction time was significantly greater than that of the retrograde (P less than 0.02). Moreover, when PGVS was introduced at a fixed phase in the cycle, but with increasing amplitude, antegrade atrioventricular conduction time was progressively prolonged, and block was observed first in the antegrade direction, whereas retrograde atrioventricular conduction continued. Microelectrode recordings during these experiments showed consistently that PGVS-induced hyperpolarization in the N region of the atrioventricular node was greater during antegrade atrioventricular conduction. This suggests that vagal effects depended not only on the intensity and phase of stimulation, but also on electronic influences which apparently are different during antegrade and retrograde conduction.

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