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The Anatomical Record Sep 2000There have been suggestions made recently that our understanding of the atrioventricular junctions of the heart is less than adequate, with claims for several new... (Review)
Review
There have been suggestions made recently that our understanding of the atrioventricular junctions of the heart is less than adequate, with claims for several new findings concerning the arrangement of the ordinary working myocardium and the specialised pathways for atrioventricular conduction. In reality, these claims are grossly exaggerated. The structure and architecture of the pathways for conduction between the atrial and ventricular myocardium are exactly as described by Tawara nearly 100 years ago. The recent claims stem from a failure to assess histological findings in the light of criterions established by Monckeberg and Aschoff following a similar controversy in 1910. The atrioventricular junctions are the areas where the atrial myocardium inserts into, and is separated from, the base of the ventricular mass, apart from at the site of penetration of the specialised axis for atrioventricular conduction. There are two such junctions in the normal heart, surrounding the orifices of the mitral and tricuspid valves. The true septal area between the junctions is of very limited extent, being formed by the membranous septum. Posterior and inferior to this septal area, the atrial myocardium overlies the crest of the ventricular septum, with the atrial component being demarcated by the landmarks of the triangle of Koch. The adjacent structures, and in particular the so-called inferior pyramidal space, were accurately described by McAlpine (Heart and Coronary Arteries, 1975). Thus, again there is no need for revision of our understanding. The key to unravelling much of the alleged controversy is the recognition that, as indicated by Tawara, the atrioventricular node becomes the atrioventricular bundle at the point where the overall axis for conduction penetrates into the central fibrous body. There are also marked differences in arrangement, also described by Tawara, between the disposition of the conduction axis in man as compared to the dog.
Topics: Atrioventricular Node; Heart Septum; Humans
PubMed: 10967539
DOI: 10.1002/1097-0185(20000901)260:1<81::AID-AR90>3.0.CO;2-3 -
Journal of the American College of... Sep 1996This study sought to investigate electrophysiologic characteristics and possible anatomic sites of multiple anterograde slow atrioventricular (AV) node pathways and to...
OBJECTIVES
This study sought to investigate electrophysiologic characteristics and possible anatomic sites of multiple anterograde slow atrioventricular (AV) node pathways and to compare these findings with those in dual anterograde AV node pathways.
BACKGROUND
Although multiple anterograde AV node pathways have been demonstrated by the presence of multiple discontinuities in the AV node conduction curve, the role of these pathways in the initiation and maintenance of AV node reentrant tachycardia (AVNRT) is still unclear, and possible anatomic sites of these pathways have not been reported.
METHODS
This study included 500 consecutive patients with AVNRT who underwent electrophysiologic study and radiofrequency ablation. Twenty-six patients (5.2%) with triple or more anterograde AV node pathways were designated as Group I (16 female, 10 male, mean age 48 +/- 14 years), and the other 474 patients (including 451 with and 23 without dual anterograde AV node pathways) were designated as Group II (257 female, 217 male; mean age 52 +/- 16 years).
RESULTS
Of the 21 patients with triple anterograde AV node pathways, AVNRT was initiated through the first slow pathway only in 3, through the second slow pathway only in 8 and through the two slow pathways in 9. Of the five patients with quadruple anterograde AV node pathways, AVNRT was initiated through all three anterograde slow pathways in three and through the two slower pathways (the second and third slow pathways) in two. After radiofrequency catheter ablation, no patient had inducible AVNRT. Eleven patients (42.3%) in Group I had multiple anterograde slow pathways eliminated simultaneously at a single ablation site. Eight patients (30.7%) had these slow pathways eliminated at different ablation sites; the slow pathways with a longer conduction time were ablated more posteriorly in the Koch's triangle than those with a shorter conduction time. The remaining seven patients (27%) had a residual slow pathway after delivery of radiofrequency energy at a single or different ablation sites. The patients in Group I had a longer tachycardia cycle length, poorer retrograde conduction properties and a higher incidence of multiple types of AVNRT than those in Group II.
CONCLUSIONS
Multiple anterograde AV node pathways are not rare in patients with AVNRT. However, not all of the anterograde slow pathways were involved in the initiation and maintenance of tachycardia. Radiofrequency catheter ablation was safe and effective in eliminating critical slow pathways to cure AVNRT.
Topics: Adult; Aged; Atrioventricular Node; Cardiac Pacing, Artificial; Catheter Ablation; Electrophysiology; Female; Humans; Male; Middle Aged; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 8772763
DOI: 10.1016/0735-1097(96)00217-3 -
Biophysical Journal Oct 2009Mathematical models are a repository of knowledge as well as research and teaching tools. Although action potential models have been developed for most regions of the...
Mathematical models are a repository of knowledge as well as research and teaching tools. Although action potential models have been developed for most regions of the heart, there is no model for the atrioventricular node (AVN). We have developed action potential models for single atrio-nodal, nodal, and nodal-His cells. The models have the same action potential shapes and refractoriness as observed in experiments. Using these models, together with models for the sinoatrial node (SAN) and atrial muscle, we have developed a one-dimensional (1D) multicellular model including the SAN and AVN. The multicellular model has slow and fast pathways into the AVN and using it we have analyzed the rich behavior of the AVN. Under normal conditions, action potentials were initiated in the SAN center and then propagated through the atrium and AVN. The relationship between the AVN conduction time and the timing of a premature stimulus (conduction curve) is consistent with experimental data. After premature stimulation, atrioventricular nodal reentry could occur. After slow pathway ablation or block of the L-type Ca(2+) current, atrioventricular nodal reentry was abolished. During atrial fibrillation, the AVN limited the number of action potentials transmitted to the ventricle. In the absence of SAN pacemaking, the inferior nodal extension acted as the pacemaker. In conclusion, we have developed what we believe is the first detailed mathematical model of the AVN and it shows the typical physiological and pathophysiological characteristics of the tissue. The model can be used as a tool to analyze the complex structure and behavior of the AVN.
Topics: Action Potentials; Animals; Atrial Fibrillation; Atrioventricular Node; Biological Clocks; Bundle of His; Calcium Channels, L-Type; Membrane Potentials; Models, Cardiovascular; Neural Conduction; Neural Pathways; Neurons; Rabbits; Time Factors
PubMed: 19843444
DOI: 10.1016/j.bpj.2009.06.056 -
Pacing and Clinical Electrophysiology :... Jun 2010The atrioventricular node (AVN) has mystified generations of investigators over the last century and continues today to be at the epicenter of debates among anatomists,... (Review)
Review
The atrioventricular node (AVN) has mystified generations of investigators over the last century and continues today to be at the epicenter of debates among anatomists, experimentalists, and electrophysiologists. Over the years, discrepancies have remained in regard to correlating components of AVN structure to function, as evidenced by studies from microelectrodes, optical mapping, and the electrophysiology laboratory. Historically, the AVN has been defined by classical histological methods; however, with recent advances in molecular biology techniques, a more precise characterization of structure is becoming attainable. Distinct molecular compartments are becoming apparent based on connexin staining and genotyping, providing new insight into previously characterized functional aspects of the AVN and its surrounding structures. Advances in optical mapping have provided a unique opportunity for correlating structure and function--unmasking properties of the native AVN pacemaker and providing further insight into basic mechanisms involved in AV conduction. Additionally, procurement of explanted human hearts have provided a unique opportunity to further characterize the human AVN structurally and functionally with both molecular biology techniques and optical mapping. With the elucidation of basic elements of both structure and function via molecular investigation and optical mapping, new opportunities are becoming apparent in utilizing the unique properties of the AVN for pursuing novel clinical applications relevant to clinical electrophysiology.
Topics: Animals; Atrioventricular Node; Humans; Voltage-Sensitive Dye Imaging
PubMed: 20180918
DOI: 10.1111/j.1540-8159.2010.02699.x -
Journal of the American College of... Dec 1998This study sought to examine the frequency of persistent fetal dispersion of the atrioventricular (AV) node and fragmentation of the atrioventricular bundle (His) bundle...
OBJECTIVES
This study sought to examine the frequency of persistent fetal dispersion of the atrioventricular (AV) node and fragmentation of the atrioventricular bundle (His) bundle in the cardiac conduction system of sudden cardiac death cases and control subjects to establish their importance as the cause of death.
BACKGROUND
These are two of the most frequent lesions reported in published reports in the cardiac conduction system in unexplained sudden deaths.
METHODS
We have studied the conduction system of 347 hearts: 249 hearts from sudden cardiac death cases and 98 control hearts. The sudden cardiac death cases were divided, according to the pathology found, in three groups: group I: ischemic heart disease, 137 cases; group II: nonischemic heart disease, 48 cases, and group III: unexplained sudden cardiac deaths, 64 cases. The control group (group IV) consisted of patients with unnatural deaths and extracardiac natural deaths.
RESULTS
Persistent fetal dispersion of the AV node was observed in 70 cases (20.17%) of all groups with a frequency (40.81%) statistically higher in the control group. Fragmentation of the His bundle was observed in 95 cases (31.77%), and the frequency was statistically higher in the control group, too (47.67%).
CONCLUSIONS
Persistent fetal dispersion of the AV node and fragmentation of the His bundle can be a normal variation present during many years in life and must not be considered the anatomic substrate for arrhythmias and sudden death without electrocardiographic abnormalities.
Topics: Adult; Aged; Atrioventricular Node; Bundle of His; Death, Sudden, Cardiac; Female; Humans; Male; Middle Aged
PubMed: 9857868
DOI: 10.1016/s0735-1097(98)00458-6 -
Heart Rhythm May 2018Aging is associated with an increased incidence of atrioventricular nodal (AVN) dysfunction.
Structural and functional remodeling of the atrioventricular node with aging in rats: The role of hyperpolarization-activated cyclic nucleotide-gated and ryanodine 2 channels.
BACKGROUND
Aging is associated with an increased incidence of atrioventricular nodal (AVN) dysfunction.
OBJECTIVE
The aim of this study was to investigate the structural and functional remodeling in the atrioventricular junction (AVJ) with aging.
METHODS
Electrophysiology, histology, and immunohistochemistry experiments on male Wistar Hannover rats aged 3 months (n = 24) and 2 years (n = 15) were performed. Atrio-His (AH) interval, Wenkebach cycle length (WBCL), and AVN effective refractory period (AVNERP) were measured. Cesium (2 mM) was used to block hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, while ryanodine (2 μM) was used to block ryanodine 2 (RyR2) channels. Protein expression from different regions of the AVJ was studied using immunofluorescence. The expression of connexins (connexin 43 and connexin 40), ion channels (Hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4), voltage sensitive sodium channel (Na1.5), and L-Type calcium channel (Ca1.3)), and calcium handling proteins (RyR2 and sarco/endoplasmic reticulum calcium ATPaset type 2a (SERCA2a)) were measured. Morphological characteristics were studied with histology.
RESULTS
Without drugs to block HCN and RyR2 channels, there was prolongation of the AH interval, WBCL, and AVNERP (P < .05) with aging. In young rats only, cesium prolonged the AH interval, WBCL, and AVNERP (P < .01). Ryanodine prolonged the AH interval and WBCL (P < .01) in both young and old rats. Immunofluorescence revealed that with aging, connexin 43, HCN4, Na1.5, and RyR2 downregulate in the regions of the AVJ and connexin 40, SERCA2a, and Ca1.3 upregulate (P < .05). Aging results in cellular hypertrophy, loosely packed cells, a decrease in the number of nuclei, and an increase in collagen content.
CONCLUSION
Heterogeneous ion channel expression changes were observed in the AVJ with aging. For the first time, we have shown that HCN and RyR2 play an important role in AVN dysfunction with aging.
Topics: Aging; Animals; Atrioventricular Node; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; Immunohistochemistry; Male; Models, Animal; Patch-Clamp Techniques; Rats; Rats, Wistar; Ryanodine; Ryanodine Receptor Calcium Release Channel
PubMed: 29288034
DOI: 10.1016/j.hrthm.2017.12.027 -
Circulation Nov 2007The atrioventricular (AV) node is essential for the sequential excitation and optimized contraction of the adult multichambered heart; however, relatively little is...
BACKGROUND
The atrioventricular (AV) node is essential for the sequential excitation and optimized contraction of the adult multichambered heart; however, relatively little is known about its formation from the embryonic AV canal. A recent study demonstrated that signaling by Alk3, the type 1a receptor for bone morphogenetic proteins, in the myocardium of the AV canal was required for the development of both the AV valves and annulus fibrosus. To test the hypothesis that bone morphogenetic protein signaling also plays a role in AV node formation, we investigated conduction system function and AV node morphology in adult mice with conditional deletion of Alk3 in the AV canal.
METHODS AND RESULTS
High-resolution optical mapping with correlative histological analysis of 28 mutant hearts revealed 4 basic phenotypic classes based on electrical activation patterns and volume-conducted ECGs. The frequency of AV node conduction and morphological abnormalities increased from no detectable anomalies (class I) to severe defects (class IV), which included the presence of bypass tracts, abnormal ventricular activation patterns, fibrosis of the AV node, and twin AV nodes.
CONCLUSIONS
The present findings demonstrate that bone morphogenetic protein signaling is required in the myocardium of the AV canal for proper AV junction development, including the AV node.
Topics: Animals; Atrioventricular Node; Body Surface Potential Mapping; Bone Morphogenetic Protein Receptors, Type I; Genotype; Heart Block; Heart Conduction System; Mice; Mice, Mutant Strains; Myocardium
PubMed: 17998461
DOI: 10.1161/CIRCULATIONAHA.107.696583 -
Progress in Biophysics and Molecular... 2008To characterize the effects of inhibition of Ryanodine receptor (RyR), TTX-sensitive neuronal Na+ current (iNa), "rapidly activating" delayed rectifier K+ current (iKr)... (Review)
Review
AIMS
To characterize the effects of inhibition of Ryanodine receptor (RyR), TTX-sensitive neuronal Na+ current (iNa), "rapidly activating" delayed rectifier K+ current (iKr) and ultrarapid delayed rectifier potassium current (IKur) on the pacemaker activity of the sinoatrial node (SAN) and the atrioventricular node (AVN) in the mouse.
METHODS
The structure of mouse AVN was studied by histology and immunolabelling of Cx43 and hyperpolarization-activated, cyclic nucleotide-binding channels (HCN). The effects of Ryanodine, TTX, E-4031 and 4-AP on pacemaker activities recorded from mouse intact SAN and AVN preparations have been investigated.
RESULTS
Immuno-histological characterization delineated the structure of the AVN showing the similar molecular phenotype of the SAN. The effects of these inhibitors on the cycle length (CL) of the spontaneous pacemaker activity of the SAN and the AVN were characterized. Inhibition of RyR by 0.2 and 2 microM Ryanodine prolonged CL by 42+/-12.3% and 64+/-18.1% in SAN preparations by 163+/-72.3% and 241+/-91.2% in AVN preparations. Inhibition of TTX-sensitive iNa by 100 nM TTX prolonged CL by 22+/-6.0% in SAN preparations and 53+/-13.6% in the AVN preparations. Block of iKr by E-4031 prolonged CL by 68+/-12.5% in SAN preparations and 28+/-3.4% in AVN preparations. Inhibition of iKur by 50 microM 4-AP prolonged CL by 20+/-3.4% in SAN preparations and 18+/-3.0% in AVN preparations.
CONCLUSION
Mouse SAN and AVN showed distinct different response to the inhibition of RyR, TTX-sensitive INa, IKr and iKur, which reflects the variation in contribution of these currents to the pacemaker function of the cardiac nodes in the mouse. Our data provide valuable information for developing virtual tissue models of mouse SAN and AVN.
Topics: 4-Aminopyridine; Animals; Anti-Arrhythmia Agents; Atrioventricular Node; Mice; Piperidines; Potassium Channel Blockers; Pyridines; Ryanodine; Sinoatrial Node; Tetrodotoxin
PubMed: 17850852
DOI: 10.1016/j.pbiomolbio.2007.07.003 -
American Heart Journal May 1996During radiofrequency catheter ablation of slow atrioventricular node pathway conduction in patients with atrioventricular node reentrant tachycardia, an... (Review)
Review
Localization of the origin of the atrioventricular junctional rhythm induced during selective ablation of slow-pathway conduction in patients with atrioventricular node reentrant tachycardia.
During radiofrequency catheter ablation of slow atrioventricular node pathway conduction in patients with atrioventricular node reentrant tachycardia, an atrioventricular junction rhythm is frequently observed. The origin and relation to ablation success of this junctional rhythm was examined in this study. By using standard intracardiac electrophysiology techniques, we studied the radiofrequency energy-induced atrioventricular junctional rhythm in 43 consecutive patients with atrioventricular node reentrant tachycardia undergoing selective ablation of slow-pathway conduction. The frequency of atrioventricular junctional activity was correlated with successful and unsuccessful attempts at ablation of slow-pathway conduction. Also, we compared the sequence of retrograde atrial activation of radiofrequency energy-induced atrioventricular junctional beats in a subgroup of 22 patients with the retrograde activation sequence observed during pacing from the right ventricular apex and the site of successful ablation of slow-pathway conduction. A total of 201 radiofrequency-energy applications was delivered in 43 patients with > or = 5 atrioventricular junctional beat(s) induced during 110 (55%) of 201 ablation attempts. Atrioventricular junctional activity was noted during 98% of successful ablations but only 43% of the unsuccessful attempts (sensitivity, 98%; specificity, 57%; negative predictive value, 99%). The mean time to appearance of atrioventricular junctional beats was 8.8 +/- 4.1 sec (mean +/- SD) after the onset of radiofrequency-energy application. In 22 (100%) of 22 patients in whom detailed atrial mapping was performed, the retrograde atrial activation sequence of the radiofrequency-induced atrioventricular junctional beats was earliest in the anterior atrial septum, identical to that seen during pacing from the right ventricular apex. Earliest retrograde atrial activation was at the posterior septum in all patients during pacing from the successful ablation site, a markedly different activation pattern compared with that seen during either radiofrequency ablation or ventricular pacing. Whereas the occurrence of atrioventricular junctional activity during radiofrequency ablation does not necessarily herald a successful ablation of slow atrioventricular node pathway conduction, its absence strongly suggests that the energy is being applied in an unsuccessful fashion. Furthermore, it appears that radiofrequency energy-induced atrioventricular junctional beats originate not from the endocardium in contact with the ablating catheter tip but instead appear to exit remotely from the anterior atrial septal region. This finding supports the existence of specialized tissues in the atrioventricular junction that preferentially transmit the effects of radiofrequency energy to an anterior exit site, possibly identical to the atrial exit site of the retrograde fast atrioventricular node conduction pathway.
Topics: Atrioventricular Node; Cardiac Pacing, Artificial; Catheter Ablation; Female; Humans; Male; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 8615313
DOI: 10.1016/s0002-8703(96)90176-3 -
Journal of the American Heart... Apr 2017Clinical benefits from His bundle pacing (HBP) in heart failure patients with preserved and reduced left ventricular ejection fraction are still inconclusive. This study...
Benefits of Permanent His Bundle Pacing Combined With Atrioventricular Node Ablation in Atrial Fibrillation Patients With Heart Failure With Both Preserved and Reduced Left Ventricular Ejection Fraction.
BACKGROUND
Clinical benefits from His bundle pacing (HBP) in heart failure patients with preserved and reduced left ventricular ejection fraction are still inconclusive. This study evaluated clinical outcomes of permanent HBP in atrial fibrillation patients with narrow QRS who underwent atrioventricular node ablation for heart failure symptoms despite rate control by medication.
METHODS AND RESULTS
The study enrolled 52 consecutive heart failure patients who underwent attempted atrioventricular node ablation and HBP for symptomatic atrial fibrillation. Echocardiographic left ventricular ejection fraction and left ventricular end-diastolic dimension, New York Heart Association classification and use of diuretics for heart failure were assessed during follow-up visits after permanent HBP. Of 52 patients, 42 patients (80.8%) received permanent HBP and atrioventricular node ablation with a median 20-month follow-up. There was no significant change between native and paced QRS duration (107.1±25.8 versus 105.3±23.9 milliseconds, =0.07). Left ventricular end-diastolic dimension decreased from the baseline (<0.001), and left ventricular ejection fraction increased from baseline (<0.001) in patients with a greater improvement in heart failure with reduced ejection fraction patients (N=20) than in heart failure with preserved ejection fraction patients (N=22). New York Heart Association classification improved from a baseline 2.9±0.6 to 1.4±0.4 after HBP in heart failure with reduced ejection fraction patients and from a baseline 2.7±0.6 to 1.4±0.5 after HBP in heart failure with preserved ejection fraction patients. After 1 year of HBP, the numbers of patients who used diuretics for heart failure decreased significantly (<0.001) when compared to the baseline diuretics use.
CONCLUSIONS
Permanent HBP post-atrioventricular node ablation significantly improved echocardiographic measurements and New York Heart Association classification and reduced diuretics use for heart failure management in atrial fibrillation patients with narrow QRS who suffered from heart failure with preserved or reduced ejection fraction.
Topics: Aged; Aged, 80 and over; Atrial Fibrillation; Atrioventricular Node; Bundle of His; Cardiac Pacing, Artificial; Catheter Ablation; Female; Heart Failure; Humans; Male; Middle Aged; Stroke Volume
PubMed: 28365568
DOI: 10.1161/JAHA.116.005309