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Indian Heart Journal 2017The prevalence of ventriculo-atrial (VA) conduction varies from 20% to 90%, depending on the population studied (Militianu et al., 1997; Inoue et al., 1985; Kazmierczak...
BACKGROUND
The prevalence of ventriculo-atrial (VA) conduction varies from 20% to 90%, depending on the population studied (Militianu et al., 1997; Inoue et al., 1985; Kazmierczak et al., 1993; Ciemniewski et al., 1990; Hayes and Furman, 1983; Westveer et al., 1984). This wide range is mostly based on studies done in patients with implanted devices or impaired atrioventricular conduction. However, the prevalence of VA conduction in structurally normal heart has not been well documented till date.
OBJECTIVE
To study the prevalence and identify predictors of retrograde conduction via the His-Purkinje system and AV node in structurally normal hearts.
METHODS
We included 54 consecutive adults without structural heart disease who underwent electrophysiological (EP) study for various tachycardias. The basic parameters including PR, AH and HV intervals, atrioventricular Wenckebach point (AVWP) and anterograde effective refractory period (ERP) of atrioventricular node (AVNERP), were measured after ablation. The VA conduction was assessed basally and if absent, after isoprenaline. The VA Wenckebach point (VAWP) and retrograde ERP(VAERP) were recorded in patients showing VA conduction.
RESULTS
The mean age was 37.1±12.6years. Twenty five (46%) of the patients were men. VA conduction was present in 30 (55%) patients at baseline. Of the remaining 24 patients, 18 (34%) showed VA conduction after isoprenaline. Only 6 (11%) patients failed to reveal VA conduction even after adequate response to isoprenaline. Amongst all clinical and EP variables analysed, only the HV interval was shorter (p<0.01) in patients with VA conduction.
CONCLUSION
In structurally normal hearts, VA conduction was present at baseline in 55% of patients. Isoprenaline unmasked VA conduction in an additional 34% of the subjects. The HV interval was longer in patients without VA conduction.
Topics: Adolescent; Adult; Aged; Arrhythmias, Cardiac; Atrioventricular Node; Electrocardiography; Female; Heart Atria; Heart Conduction System; Humans; India; Male; Middle Aged; Young Adult
PubMed: 28648420
DOI: 10.1016/j.ihj.2016.12.008 -
Anesthesiology Apr 1995Propofol has been implicated as causing intraoperative bradyarrhythmias. Furthermore, the effects of propofol on the electrophysiologic properties of the sinoatrial (SA)... (Clinical Trial)
Clinical Trial Comparative Study
Propofol has no direct effect on sinoatrial node function or on normal atrioventricular and accessory pathway conduction in Wolff-Parkinson-White syndrome during alfentanil/midazolam anesthesia.
BACKGROUND
Propofol has been implicated as causing intraoperative bradyarrhythmias. Furthermore, the effects of propofol on the electrophysiologic properties of the sinoatrial (SA) node and on normal atrioventricular (AV) and accessory pathways in patients with Wolff-Parkinson-White syndrome are unknown. Therefore, this study examined the effects of propofol on the cardiac electrophysiologic properties in humans to determine whether propofol promotes bradyarrhythmias and its suitability as an anesthetic agent in patients undergoing ablative procedures.
METHODS
Twelve patients with Wolff-Parkinson-White syndrome undergoing radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (50 micrograms/kg), midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (2 micrograms.kg-1.min-1) and midazolam (1-2 mg, every 15 min, as needed). A electrophysiologic study was performed consisting of measurement of the effective refractory period of the right atrium, AV node, and accessory pathway and the shortest cycle length of the AV node and accessory pathway during antegrade stimulation plus the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway during retrograde stimulation. Determinants of SA node function including sinus node recovery time, corrected sinus node recovery time, and SA conduction time; intraatrial conduction time and atrial-His interval also were measured. Reciprocating tachycardia was induced by rapid right atrial or ventricular pacing, and the cycle length and atrial-His, His-ventricular, and ventriculoatrial intervals were measured. Alfentanil/midazolam was then discontinued. Propofol was administered (bolus 2 mg/kg + 120 micrograms.kg-1.min-1), and the electrophysiologic measurements were repeated.
RESULTS
Propofol caused a statistically significant but clinically unimportant prolongation of the right atrial refractory period. The effective refractory periods of the AV node, right ventricle, and accessory pathway, as well as the shortest cycle length, were not affected. Parameters of SA node function and intraatrial conduction also were not affected. Sustained reciprocating tachycardia was inducible in 8 of 12 patients, and propofol had no effect on its electrophysiologic properties. All accessory pathways were successfully identified and ablated.
CONCLUSIONS
Propofol has no clinically significant effect on the electrophysiologic expression of the accessory pathway and the refractoriness of the normal AV conduction system. In addition, propofol has no direct effect on SA node activity or intraatrial conduction; therefore, it does not directly induce bradyarrhythmias. It is thus a suitable agent for use in patients undergoing ablative procedures who require either a neuroleptic or general anesthetic.
Topics: Adolescent; Adult; Alfentanil; Anesthesia; Atrioventricular Node; Catheter Ablation; Electrophysiology; Female; Heart Conduction System; Heart Rate; Humans; Male; Midazolam; Propofol; Sinoatrial Node; Wolff-Parkinson-White Syndrome
PubMed: 7717560
DOI: 10.1097/00000542-199504000-00011 -
Journal of the American College of... May 1992Flecainide is effective against certain supraventricular arrhythmias (atrial fibrillation and atrioventricular [AV] node reentrant tachycardia), but its mechanisms of...
UNLABELLED
Flecainide is effective against certain supraventricular arrhythmias (atrial fibrillation and atrioventricular [AV] node reentrant tachycardia), but its mechanisms of action are unknown. Previous in vitro work suggests that flecainide attenuates rate-dependent action potential duration shortening, producing tachycardia-dependent prolongation of the refractory period. This study was designed to assess whether similar changes occur in vivo and whether the effects of flecainide on AV node conduction depend on heart rate and on direction of propagation (anterograde vs. retrograde). The effects of flecainide at three clinically relevant concentrations were assessed in open chest, morphine-chloralose-anesthetized dogs. Flecainide increased atrial refractory period in a concentration- and rate-related fashion (e.g., dose 3 increased the atrial effective refractory period by 9 +/- 4% at a cycle length of 1,000 ms but by 36 +/- 5% and 55 +/- 10% at a basic cycle length of 400 and 300 ms, respectively; p less than 0.001 for each). Flecainide attenuated the action potential duration accommodation (measured by monophasic action potentials) to heart rate, causing tachycardia-dependent action potential duration prolongation and accounting for most of the rate-dependent atrial effective refractory period changes. Flecainide increased Wenckebach cycle length, but the concentration-response curve was much steeper in the retrograde (slope 41 +/- 7 ms/mumol.liter-1) than in the anterograde direction (17 +/- 4 ms/mumol.liter-1; p less than 0.01), indicating more potent effects on retrograde conduction. The depressant action of the drug on the AV node was also rate dependent, with an effect on the AH interval at a basic cycle length of 400 ms that averaged 1.8, 1.5 and 2 times that at a basic cycle length of 1,000 ms for doses 1 (p less than 0.05), 2 (p less than 0.01) and 3 (p less than 0.001), respectively.
CONCLUSIONS
1) Flecainide suppresses atrial action potential duration accommodation to heart rate changes in vivo, leading to rate-dependent atrial effective refractory period prolongation, which may be important in suppressing atrial fibrillation. 2) The drug has frequency- and direction-dependent effects on AV node conduction, which may lead to selective antiarrhythmic actions during AV node reentry.
Topics: Action Potentials; Analysis of Variance; Animals; Atrial Function; Atrioventricular Node; Cardiac Catheterization; Chloralose; Depression, Chemical; Dogs; Dose-Response Relationship, Drug; Female; Flecainide; Heart Atria; Heart Rate; Least-Squares Analysis; Male; Morphine; Time Factors
PubMed: 1564235
DOI: 10.1016/0735-1097(92)90342-k -
Circulation Research Jul 2020The heartbeat is organized by the cardiac conduction system (CCS), a specialized network of cardiomyocytes. Patterning of the CCS into atrial node versus ventricular...
RATIONALE
The heartbeat is organized by the cardiac conduction system (CCS), a specialized network of cardiomyocytes. Patterning of the CCS into atrial node versus ventricular conduction system (VCS) components with distinct physiology is essential for the normal heartbeat. Distinct node versus VCS physiology has been recognized for more than a century, but the molecular basis of this regional patterning is not well understood.
OBJECTIVE
To study the genetic and genomic mechanisms underlying node versus VCS distinction and investigate rhythm consequences of failed VCS patterning.
METHODS AND RESULTS
Using mouse genetics, we found that the balance between T-box transcriptional activator, , and T-box transcriptional repressor, , determined the molecular and functional output of VCS myocytes. Adult VCS-specific removal of or overexpression of re-patterned the fast VCS into slow, nodal-like cells based on molecular and functional criteria. In these cases, gene expression profiling showed diminished expression of genes required for VCS-specific fast conduction but maintenance of expression of genes required for nodal slow conduction physiology. Action potentials of -deficient VCS myocytes adopted nodal-specific characteristics, including increased action potential duration and cellular automaticity. Removal of in vivo precipitated inappropriate depolarizations in the atrioventricular (His)-bundle associated with lethal ventricular arrhythmias. TBX5 bound and directly activated -regulatory elements at fast conduction channel genes required for fast physiological characteristics of the VCS action potential, defining the identity of the adult VCS.
CONCLUSIONS
The CCS is patterned entirely as a slow, nodal ground state, with a T-box dependent, physiologically dominant, fast conduction network driven specifically in the VCS. Disruption of the fast VCS gene regulatory network allowed nodal physiology to emerge, providing a plausible molecular mechanism for some lethal ventricular arrhythmias.
Topics: Action Potentials; Animals; Arrhythmias, Cardiac; Atrioventricular Node; Body Patterning; Female; Gene Expression Regulation, Developmental; HEK293 Cells; Heart Rate; Heart Ventricles; Humans; Male; Mice, Knockout; T-Box Domain Proteins; Time Factors; Transcription, Genetic
PubMed: 32290757
DOI: 10.1161/CIRCRESAHA.118.314460 -
Journal of the American College of... Mar 1994This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) 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.
Topics: Animals; Atrioventricular Node; Cardiac Pacing, Artificial; Dogs; Female; Heart Atria; Heart Conduction System; Male; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 8113554
DOI: 10.1016/0735-1097(94)90756-0 -
The Annals of Thoracic Surgery May 2009
Topics: Atrioventricular Node; Endocardial Cushion Defects; Heart Defects, Congenital; Heart Septal Defects, Ventricular; Heart Valve Diseases; Heart Ventricles; Humans; Tricuspid Valve
PubMed: 19379893
DOI: 10.1016/j.athoracsur.2009.03.006 -
Journal of the American Heart... Dec 2013The cardiac conduction system consists of the sinus node, nodal extensions, atrioventricular (AV) node, penetrating bundle, bundle branches, and Purkinje fibers....
BACKGROUND
The cardiac conduction system consists of the sinus node, nodal extensions, atrioventricular (AV) node, penetrating bundle, bundle branches, and Purkinje fibers. Node-like AV ring tissue also exists at the AV junctions, and the right and left rings unite at the retroaortic node. The study aims were to (1) construct a 3-dimensional anatomical model of the AV rings and retroaortic node, (2) map electrical activation in the right ring and study its action potential characteristics, and (3) examine gene expression in the right ring and retroaortic node.
METHODS AND RESULTS
Three-dimensional reconstruction (based on magnetic resonance imaging, histology, and immunohistochemistry) showed the extent and organization of the specialized tissues (eg, how the AV rings form the right and left nodal extensions into the AV node). Multiextracellular electrode array and microelectrode mapping of isolated right ring preparations revealed robust spontaneous activity with characteristic diastolic depolarization. Using laser microdissection gene expression measured at the mRNA level (using quantitative PCR) and protein level (using immunohistochemistry and Western blotting) showed that the right ring and retroaortic node, like the sinus node and AV node but, unlike ventricular muscle, had statistically significant higher expression of key transcription factors (including Tbx3, Msx2, and Id2) and ion channels (including HCN4, Cav3.1, Cav3.2, Kv1.5, SK1, Kir3.1, and Kir3.4) and lower expression of other key ion channels (Nav1.5 and Kir2.1).
CONCLUSIONS
The AV rings and retroaortic node possess gene expression profiles similar to that of the AV node. Ion channel expression and electrophysiological recordings show the AV rings could act as ectopic pacemakers and a source of atrial tachycardia.
Topics: Action Potentials; Animals; Atrioventricular Node; Bundle of His; Heart Conduction System; Models, Anatomic; Proteome; Purkinje Fibers; Rats; Sinoatrial Node; Transcriptome
PubMed: 24356527
DOI: 10.1161/JAHA.113.000246 -
Journal of Cellular and Molecular... Jun 2015The presence of distinct electrophysiological pathways within the atrioventricular node (AVN) is a prerequisite for atrioventricular nodal reentrant tachycardia to...
The presence of distinct electrophysiological pathways within the atrioventricular node (AVN) is a prerequisite for atrioventricular nodal reentrant tachycardia to occur. In this study, the different cell contributions that may account for the anatomical and functional heterogeneity of the AVN were investigated. To study the temporal development of the AVN, the expression pattern of ISL1, expressed in cardiac progenitor cells, was studied in sequential stages performing co-staining with myocardial markers (TNNI2 and NKX2-5) and HCN4 (cardiac conduction system marker). An ISL1+/TNNI2+/HCN4+ continuity between the myocardium of the sinus venosus and atrioventricular canal was identified in the region of the putative AVN, which showed a pacemaker-like phenotype based on single cell patch-clamp experiments. Furthermore, qPCR analysis showed that even during early development, different cell populations can be identified in the region of the putative AVN. Fate mapping was performed by in ovo vital dye microinjection. Embryos were harvested and analysed 24 and 48 hrs post-injection. These experiments showed incorporation of sinus venosus myocardium in the posterior region of the atrioventricular canal. The myocardium of the sinus venosus contributes to the atrioventricular canal. It is postulated that the myocardium of the sinus venosus contributes to nodal extensions or transitional cells of the AVN since these cells are located in the posterior region of the AVN. This finding may help to understand the origin of atrioventricular nodal reentrant tachycardia.
Topics: Animals; Atrioventricular Node; Avian Proteins; Chick Embryo; Gene Expression Regulation, Developmental; Heart; Homeodomain Proteins; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; Imaging, Three-Dimensional; Immunohistochemistry; In Situ Hybridization; LIM-Homeodomain Proteins; Membrane Potentials; Microscopy, Fluorescence; Myocardium; Myocytes, Cardiac; Patch-Clamp Techniques; Reverse Transcriptase Polymerase Chain Reaction; Troponin I
PubMed: 25752780
DOI: 10.1111/jcmm.12525 -
Journal of the American College of... Apr 1987The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway)... (Comparative Study)
Comparative Study
The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.
Topics: Adult; Atrioventricular Node; Cardiac Pacing, Artificial; Electrocardiography; Female; Heart Atria; Heart Conduction System; Heart Ventricles; Humans; Male; Middle Aged; Tachycardia, Atrioventricular Nodal Reentry; Tachycardia, Supraventricular
PubMed: 3558978
DOI: 10.1016/s0735-1097(87)80231-0 -
International Journal of Cardiology Apr 2021Catheter ablation of the specialized atrioventricular junction (AVJ) with a right-side approach is an effective therapy for refractory atrial fibrillation with fast...
BACKGROUND
Catheter ablation of the specialized atrioventricular junction (AVJ) with a right-side approach is an effective therapy for refractory atrial fibrillation with fast ventricular rate. Our aim is to assess the efficacy of the procedure in a single center experience and investigate the histologic findings of AVJ after catheter ablation.
METHODS
A) Analysis of AVJ ablation efficacy in a consecutive series of patients with refractory atrial fibrillation; B) Histopathologic study of the conduction system by serial section technique and clinical-electrophysiologic correlation in four patients who underwent AVJ ablation.
RESULTS
A) Right-sided AVJ ablation was successful in all 87 consecutive patients (mean procedural time 19.2±17.9 min). Energy applications ranged from 1 to 27 (mean 5.8±5.1) with eight patients (9%) requiring > 15 applications. B) Fibrotic disruption of atrioventricular (AV) node and/or His bundle interruption was found in three cases with previous AVJ ablation. In the case requiring a left side approach, the compact AV node and common His bundle appeared undamaged whereas extensive fibrosis of the summit of the ventricular septum, branching His bundle and proximal bundle branches was found. Noteworthy, a continuity between the septal and anterior tricuspid valve leaflets was present.
CONCLUSION
Our data confirm that the ideal site for ablation of the specialized AVJ is the AV node. In selected cases with unsuccessful AV node ablation, a shift towards the His bundle is needed. A continuity between the septal and anterior leaflets of the tricuspid valve may protect the His bundle as to require multiple shocks and prolong the procedure.
Topics: Atrial Fibrillation; Atrioventricular Node; Bundle of His; Catheter Ablation; Heart Conduction System; Humans
PubMed: 33412181
DOI: 10.1016/j.ijcard.2020.12.075