Letters to the Editor

1998 ◽  
Vol 275 (5) ◽  
pp. H1905-H1909 ◽  
Author(s):  
Igor R. Efimov
Keyword(s):  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Letters To The Editor ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The following is an abstract of the article discussed in the subsequent letter:  Choi, Bum-Rak, and Guy Salama. Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells. Am. J. Physiol. 274 ( Heart Circ. Physiol. 43): H829–H845, 1998.—The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks Iand III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II)represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells

1998 ◽  
Vol 274 (3) ◽  
pp. H829-H845 ◽  
Author(s):  
Bum-Rak Choi ◽  
Guy Salama
Keyword(s):  
Action Potentials ◽  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks I and III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II) represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Images of Action Potential Propagation in Heart

Physiology ◽  
2000 ◽  
Vol 15 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Guy Salama ◽  
Bum-Rak Choi
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Imaging Techniques ◽  
Three Dimensional ◽  
Fiber Structure ◽  
Intercellular Coupling ◽  
Av Node ◽  
Action Potential Propagation ◽  
Voltage Sensitive Dyes

Activation and repolarization across mammalian hearts follow complex three-dimensional pathways that are governed by fiber structure, intercellular coupling, and action potentials (APs) with spatially heterogeneous properties. Voltage-sensitive dyes and imaging techniques offer new insights on how spatiotemporal heterogeneities of APs govern propagation, repolarization, and AV node conduction and help us visualize arrhythmias with previously unattainable details.

Effect of epinephrine on automaticity of the canine atrioventricular node

1975 ◽  
Vol 229 (1) ◽  
pp. 34-37 ◽  
Author(s):  
WW Tse
Keyword(s):  
Action Potentials ◽  
Present Experiment ◽  
Atrioventricular Node ◽  
Smooth Transition ◽  
Av Node ◽  
Single Fibers ◽  
His Bundle ◽  
Transmembrane Potentials ◽  
Spontaneous Rate ◽  
Microelectrode Techniques

Effects of epinephrine on the automaticity of canine AV nodal fibers were studied on spontaneously beating AV node-His bundle preparations. Transmembrane potentials of single fibers of the AV node or His bundle were recorded with microelectrode techniques. Action potentials of most AV nodal fibers were characterized by steep phase-4 depolarization and smooth transition from phases 4 to 0. Epinephrine (0.1-0.2 mug/ml) increased the spontaneous rate of the AV nodal fibers. The slope of phase 4 depolarization was increased and the threshold shifted to a more negative level. These changes probably accounted for the increase in the automaticity of the node. Also, in the presence of epinephrine, the pacemaker of the preparation was consistently located at the AV node had a higher degree of automaticity than the His bundle. The findings of the present experiment, therefore, further support the view that the AV node is automatic.

Abstract MP083: Autonomic Imbalance at the Level of Atrioventricular Node, but Not at the Level of Sinus Node, is Associated With Sudden Cardiac Death: The Atherosclerosis Risk in Community Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Srini V Mukundan ◽  
Muammar M Kabir ◽  
Jason Thomas ◽  
Golriz Sedaghat ◽  
Jonathan W Waks ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Cox Regression ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Av Node ◽  
Atherosclerosis Risk In Communities ◽  
Autonomic Imbalance ◽  
Summary Effect ◽  
Atherosclerosis Risk

Introduction: Autonomic imbalance, quantified by decreased heart rate variability (HRV), is associated with increased cardiovascular mortality. It is unknown if autonomic influences on sinus and atrioventricular (AV) nodes are equally important for the risk of sudden cardiac death (SCD). Hypothesis: Autonomic influences on sinus and AV node are equally strongly associated with increased SCD, non-sudden cardiac death (non-SCD), and non-cardiac death. Methods: Baseline visit 10-second ECGs (n=14,250) of the Atherosclerosis Risk in Communities (ARIC) cohort were analyzed. Normalized variance of P-onset to P-onset intervals (PPVN) and QRS-onset to QRS-onset intervals (QQVN) was calculated to assess autonomic influence on sinus and AV node respectively. Normalized variance of Rpeak - Rpeak intervals was determined as HRV measure. Values were log-transformed to normalize distribution. SCD served as primary outcome. Secondary outcomes were non-SCD and non-cardiac death. Three Cox regression models were constructed for dichotomized at 20 th percentile predictor variables. Results: Over median follow-up of 24.4 years, there were 497 SCDs (incidence 1.66 [95%CI 1.52-1.82], 742 non-SCDs (incidence 2.48 [95%CI 2.31-2.67], and 3,753 non-cardiac deaths (incidence 12.6 [95%CI 12.1-13.0]) per 1,000 person-years. In paired analysis, LogPPVN was significantly larger than LogQQVN (-7.28±1.06 vs. -7.72±1.24; P<0.0001). There was no difference between LogQQVN and Log RRVN (-7.72±1.24 vs -7.72±1.23; P=0.364). After full adjustment, LogRRVN and LogQQVN were significantly associated with non-SCD and SCD. Association with non-SCD was stronger. LogPPVN was independently associated with non-SCD but not SCD. No value was associated with non-cardiac death. Conclusion: Autonomic imbalance at the AV node, with likely summary effect at the bundle of His, is associated with SCD and non-SCD. Autonomic imbalance at the SA node is associated with non-SCD only. Autonomic input to SA and AV node should be further studied.

scholarly journals MyoR Modulates Cardiac Conduction by Repressing Gata4

2014 ◽  
Vol 35 (4) ◽  
pp. 649-661 ◽  
Author(s):  
John P. Harris ◽  
Minoti Bhakta ◽  
Svetlana Bezprozvannaya ◽  
Lin Wang ◽  
Christina Lubczyk ◽  
...  
Keyword(s):  
Transcriptional Repression ◽  
Atrioventricular Node ◽  
Electrical Activation ◽  
Cardiac Conduction ◽  
Specific Gene ◽  
Dependent Manner ◽  
Regulatory Circuit ◽  
Genetic Deletion ◽  
Repression Domain ◽  
Av Delay

The cardiac conduction system coordinates electrical activation through a series of interconnected structures, including the atrioventricular node (AVN), the central connection point that delays impulse propagation to optimize cardiac performance. Although recent studies have uncovered important molecular details of AVN formation, relatively little is known about the transcriptional mechanisms that regulate AV delay, the primary function of the mature AVN. We identify here MyoR as a novel transcription factor expressed in Cx30.2+cells of the AVN. We show that MyoR specifically inhibits a Cx30.2 enhancer required for AVN-specific gene expression. Furthermore, we demonstrate that MyoR interacts directly with Gata4 to mediate transcriptional repression. Our studies reveal that MyoR contains two nonequivalent repression domains. While the MyoR C-terminal repression domain inhibits transcription in a context-dependent manner, the N-terminal repression domain can function in a heterologous context to convert the Hand2 activator into a repressor. In addition, we show that genetic deletion of MyoR in mice increases Cx30.2 expression by 50% and prolongs AV delay by 13%. Taken together, we conclude that MyoR modulates a Gata4-dependent regulatory circuit that establishes proper AV delay, and these findings may have wider implications for the variability of cardiac rhythm observed in the general population.

Anatomy and physiology of the atrioventricular node

ESC CardioMed ◽  
2018 ◽  
pp. 1957-1958
Author(s):  
M. J. Pekka Raatikainen
Keyword(s):  
Atrioventricular Node ◽  
Cardiac Conduction ◽  
Ventricular Rate ◽  
Pacemaker Activity ◽  
Av Block ◽  
Anatomy And Physiology ◽  
Specialized Tissue ◽  
Crucial Part ◽  
Decremental Conduction ◽  
Sinoatrial Node Dysfunction

The atrioventricular node (AVN) and the surrounding area is a crucial part of the cardiac conduction system. It consists of specialized tissue located at the base of the atrial septum within the triangle of Koch. The inherent physiological function of the AVN is to delay cardiac impulse propagation between the atria and the ventricles, and to function as a backup pacemaker in the setting of sinoatrial node dysfunction or advanced atrioventricular (AV) block. AV nodal conduction and pacemaker activity are under strict control by the autonomic nervous system. Due to the unique property of decremental conduction, the AVN protects the heart from an excessive ventricular rate during rapid atrial arrhythmias. On the other hand, the AVN is also an important source of brady- and tachyarrhythmias, and a target for various pharmacological and non-pharmacological arrhythmia therapies.

P508Biventricular pacing versus His bundle pacing after atrioventricular node ablation in heart failure patients with permanent atrial fibrillation and narrow QRS

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
D Zizek ◽  
B Antolic ◽  
D Zavrl-Dzananovic ◽  
L Klemen ◽  
M Jan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Rate Control ◽  
Atrioventricular Node ◽  
Short Term ◽  
Av Node ◽  
Permanent Atrial Fibrillation ◽  
Narrow Qrs ◽  
Qrs Duration ◽  
Lv Ejection Fraction

Abstract Background Atrioventricular (AV) node ablation with biventricular (BiV) pacemaker implantation is a feasible rate control strategy for symptomatic permanent atrial fibrillation (AF) with rapid ventricular response and tachycardia-induced heart failure (HF). However, certain controversy exists since BiV pacing delivers non-physiological ventricular resynchronization and does not return left ventricular (LV) activation times to those seen in individuals with intrinsically narrow QRS. Permanent His bundle pacing (HBP) is a physiological alternative to conventional and BiV pacing. By capturing the native conduction system, depolarization of the ventricles through the His-Purkinje system induces normal synchronous ventricular activation. Purpose The aim of the study was to compare short-term outcomes between BiV pacing and HBP after AV node ablation in HF patients with symptomatic permanent AF and narrow QRS. Methods A total of 25 consecutive HF patients with permanent AF and narrow QRS (≤110 ms) who underwent AV node ablation in conjunction with BiV pacing or HBP in our centre were enrolled. Post-implant QRS duration, echocardiographic data, and New York Heart Association (NYHA) functional class were assessed in short-term follow-up. Results Among 25 HF patients (aged 68 ± 7 years, 52% female, QRS 96 ± 9 ms, LVEF 37 ± 7%, NYHA II-IV), 13 received BiV pacing and 12 HBP. Implant and ablation procedures were acutely successful in both groups. In BiV group 1 patient had a LV lead dislodgement and 1 patient in the HBP group had an acute HB lead threshold increase after AV node ablation. In HBP group post-implant QRS duration was shorter compared to BiV (103 ± 15 ms vs. 177 ± 13 ms, p &lt; 0.001). At a median follow-up of 6 months, patients treated with HBP had greater increase in LV ejection fraction compared to BiV (44 ± 10 vs. 37 ± 6, p = 0.045). A trend toward greater reduction of LV volumes (EDV 119 ± 54 ml vs. 153 ± 33 ml, p = 0.07; ESV 75 ± 34 ml vs. 97 ± 26 ml, p = 0.09) and improvement of NYHA class (2.1 ± 0.7 vs. 2.7 ± 0.8, p = 0.08) was also observed in HBP group compared to BiV group. Conclusion In rate control refractory HF patients with permanent AF and narrow QRS atrioventricular node ablation in conjunction with HBP demonstrated superior electrical resynchronization and greater increase in LV ejection fraction compared to BiV pacing. Larger prospective studies are warranted to address clinical outcomes between both pace and ablate strategies.

Effects of hypoxia on atrioventricular node of adult and neonatal rabbit hearts

1989 ◽  
Vol 256 (5) ◽  
pp. H1337-H1343 ◽  
Author(s):  
M. L. Young ◽  
R. C. Tan ◽  
B. M. Ramza ◽  
R. W. Joyner
Keyword(s):  
Cycle Length ◽  
Atrioventricular Node ◽  
The Other ◽  
Adult Rabbit ◽  
Atrial Pacing ◽  
Isolated Perfused Heart ◽  
Heart Model ◽  
Perfused Heart ◽  
Av Node ◽  
The Difference

We used an isolated perfused heart model to assess the effects of graded hypoxia (95, 45, 20, 10, or 0% O2, exposure for 5 min) on the adult and neonatal (0-3 days) rabbit atrioventricular (AV) node. The AV nodal function was assessed by measuring the A-H interval at a constant atrial pacing cycle length, the longest pacing cycle length resulting in Wenckebach periodicity [Wenckebach cycle length (WCL)] and the AV nodal effective refractory period (AVNERP). The A-H intervals remained stable in neonatal hearts until O2 saturation was decreased to 10%. On the other hand, the A-H intervals began to increase in adult rabbit hearts at 20% O2. In 95% O2, the AV nodal WCL was longer in adult hearts than in the neonatal hearts (165 +/- 8 ms vs. 142 +/- 7 ms). The effect of hypoxia on the AV nodal WCL was significantly greater in adult hearts than in neonatal hearts when the O2 saturation was decreased to 20% (a 54% increase in adults vs. a 14% increase in neonates, P = 0.02). The difference was greater at lower levels of O2. In 95% O2 at comparable basis driving cycle length (240 ms), the A-H intervals were equal in neonatal and adult hearts (43 +/- 3 vs. 43 +/- 7 ms), but the AVNERP of the neonates was significantly longer than that of the adults (133 +/- 21 vs. 97 +/- 19 ms, P = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Chronic atrial fibrillation in patients with paroxysmal atrial fibrillation, atrioventricular node ablation and pacemakers

EP Europace ◽  
1999 ◽  
Vol 1 (1) ◽  
pp. 30-34 ◽  
Author(s):  
J. M. McComb ◽  
G. M. Gribbin
Keyword(s):  
Atrial Fibrillation ◽  
Multivariate Analysis ◽  
Pacemaker Implantation ◽  
Atrioventricular Node ◽  
Chronic Atrial Fibrillation ◽  
Atrial Arrhythmias ◽  
Av Node ◽  
Surface Ecg ◽  
History Of ◽  
Atrial Rhythm

Abstract Aims This study examined the factors associated with the development of chronic (or permanent) atrial fibrillation (AF) in patients who had undergone atrioventricular (AV) node ablation with permanent pacing because of paroxysmal AF. Methods A retrospective review of case notes of all 65 consecutive patients identified as having had paroxysmal atrial arrhythmias, AV node ablation and permanent pacemaker implantation was performed. Atrial rhythm was established from all pacing records and from the surface ECG. Treatment with anti-arrhythmic drugs and with warfarin was recorded. A multivariate analysis was undertaken, using atrial rhythm on final ECG and chronic AF as outcome measures. Results During a mean follow-up of 30 months, 42% of patients with paroxysmal AF had developed chronic AF. Multivariate analysis showed that increasing age, history of electrical cardioversion and VVI pacing all contributed to the development of chronic AF. 25/62 patients were taking warfarin, and four had had strokes (2·5%/year). Conclusions The majority of patients with paroxysmal atrial arrhythmias treated with AV node ablation and pacing develop chronic AF eventually. Stroke remains a risk, particularly in those who develop chronic AF.

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