scholarly journals B-PO05-050 OUTCOMES OF HIS BUNDLE VS LEFT BUNDLE BRANCH PACING FOLLOWING AV NODE ABLATION

Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S391-S392
Author(s):  
Arshneel Singh Kochar ◽  
Eoin Donnellan ◽  
Lola Di Vincenzo ◽  
Oussama M. Wazni ◽  
Christine Tanaka-Esposito ◽  
...  
Keyword(s):  
Av Node ◽  
His Bundle

Adrenergic potentiation on spontaneous activity of canine paranodal fibers

1984 ◽  
Vol 247 (3) ◽  
pp. H415-H421
Author(s):  
W. W. Tse
Keyword(s):  
Spontaneous Activity ◽  
Tricuspid Valve ◽  
Action Potentials ◽  
Smooth Transition ◽  
Convex Side ◽  
Av Node ◽  
Junctional Tachycardia ◽  
His Bundle ◽  
Spontaneous Rate

The present study, using in vitro preparations, was designed to determine the anatomic, histological, and automatic properties of canine paranodal fibers. This tissue, together with the atrioventricular (AV) node and His bundle, constituted the three major tissues in the AV junction. The fascicles of the paranodal fibers ran parallel and adjacent to the base of the septal cusp of the tricuspid valve. The distal end of the paranodal fibers joined the lower half of the compact AV node on its convex side. Paranodal fibers when isolated were able to initiate spontaneous activity. Action potentials of many of these fibers showed primary pacemaker characteristics, i.e., a prominent phase 4 depolarization and smooth transition from phases 4 to 0. In 14 preparations, epinephrine (2.0 micrograms injected into the tissue bath) potentiated spontaneous rates to 144 +/- 6.0 beats/min from 61 +/- 5.0, an increase of 136%. Also, under the influence of epinephrine, paranodal fibers consistently generated a spontaneous rate higher than that of the AV node or His bundle, whether they were functionally connected or separated. These findings provide a basis for explaining the junctional tachycardia that occurs under adrenergic influence and demonstrate the presence of three major automatic tissues: the paranodal fibers, AV node, and His bundle in the canine AV junction.

Modulation of AV nodal and Hisian conduction by changes in extracellular space

1999 ◽  
Vol 276 (3) ◽  
pp. H953-H960
Author(s):  
Keith G. Lurie ◽  
Atsushi Sugiyama ◽  
Scott McKnite ◽  
Paul Coffeen ◽  
Keitaro Hashimoto ◽  
...  
Keyword(s):  
Extracellular Space ◽  
Left Ventricular ◽  
Conduction Time ◽  
Av Node ◽  
Total Blood ◽  
His Bundle ◽  
Induced Changes ◽  
Total Blood Flow ◽  
Dose Dependent Increase ◽  
Dose Dependent

Previous studies have demonstrated that the extracellular space (ECS) component of the atrioventricular (AV) node and His bundle region is larger than the ECS in adjacent contractile myocardium. The potential physiological significance of this observation was examined in a canine blood-perfused AV nodal preparation. Mannitol, an ECS osmotic expander, was infused directly into either the AV node or His bundle region. This resulted in a significant dose-dependent increase in the AV nodal or His-ventricular conduction time and in the AV nodal effective refractory period. Mannitol infusion eventually resulted in Wenckebach block ( n = 6), which reversed with mannitol washout. The ratio of AV nodal to left ventricular ECS in tissue frozen immediately on the development of heart block ( n = 8) was significantly higher in the region of block (4.53 ± 0.61) compared with that in control preparations (2.23 ± 0.35, n = 6, P < 0.01) and donor dog hearts (2.45 ± 0.18, n = 11, P < 0.01) not exposed to mannitol. With lower mannitol rates (10% of total blood flow), AV nodal conduction times increased by 5–10% and the AV node became supersensitive to adenosine, acetylcholine, and carbachol, but not to norepinephrine. We conclude that mannitol-induced changes in AV node and His bundle ECS markedly alter conduction system electrophysiology and the sensitivity of conductive tissues to purinergic and cholinergic agonists.

Effect of disopyramide and disobutamide on conduction in perfused rabbit hearts

1981 ◽  
Vol 59 (11) ◽  
pp. 1192-1195
Author(s):  
Peter E. Dresel ◽  
Keith D. Cameron
Keyword(s):  
Antiarrhythmic Agent ◽  
Conduction System ◽  
Atrioventricular Conduction ◽  
Cardiac Conduction ◽  
Conduction Time ◽  
Related Effect ◽  
Av Node ◽  
His Bundle ◽  
Time Changes ◽  
His Bundle Recording

The effects of disopyramide (DP) and a new antiarrhythmic agent, disobutamide (DB) on cardiac conduction were studied using His bundle recording from modified rabbit Langendorff preparations electrically driven at 3 and 4 Hz. Both disopyramide (4–16 μg/mL) and disobutamide (1–30 μg/ml) slowed conduction throughout the atrioventricular conduction system, i.e., SA, AH, and HV intervals were increased in a dose-related manner. Conversion of the conduction time changes to percent changes indicates that disobutamide has a relatively equal effect on each part of the system whereas disopyramide exhibited significantly less effect on AV nodal conduction. Slowing of conduction in the AV node by DP was clearly related to rate. Changes in SA and HV intervals were rate related to a lesser degree. No such rate-related effect was evident with disobutamide. Block of atrial conduction occurred in two out of six hearts when the rate was increased at 8 μg/mL of DP and in three additional hearts at 16 μg/mL. This was interpreted to indicate a change in atrial excitability such that 2 × threshold currents no longer excited the tissues. This was not observed at any concentration of DB.

scholarly journals P1500 Reptilian heart in a man

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
E O Ozpelit ◽  
E E O Ozcan ◽  
M E O Ozpelit ◽  
N O Ozgul
Keyword(s):  
Human Evolution ◽  
Peak Velocity ◽  
Pulmonary Regurgitation ◽  
Maximum Velocity ◽  
Heart Model ◽  
Av Node ◽  
His Bundle ◽  
Diastolic Velocity ◽  
Qrs Duration ◽  
The One

Abstract 40 year old man admitted to hospital due to tachycardia episode. His normal ECG was consistent with RBBB with a QRS duration of 200msec. He had undergone a VSD operation when he was 6. He had a 3/6 systolic murmor . On TTE, there was a VSD patch and a residual tiny VSD with a L-R shunt. The maximum systolic gradient of VSD shunt was measured as 92mmHg .There was also moderate tricuspid regurgitation (TR) with a peak velocity of 5.1m/sec and estimated sPAP of 103mmHg. Considering the measured sPAP and the VSD shunt gradients, his systolic blood pressure (SBP)should approximately be equal to sum of those two ( 103+ 92 = 195mmHg). However his BP was 140/90mmHg.When we examined his heart for a possible explanation for this inconsistency, we noticed a systolic aliasing inside the RV with a maximum velocity of 3.1m/sec and systolic gradient of 38mmHg. However the chamber with lower pressure (P) was the one to which the VSD shunt was directed, and this chamber was in direct continuity with pulmonary artery. So to confirm the P in this chamber we also used pulmonary regurgitation flow and measured a peak diastolic velocity of 3.8m/sec, meaning a mean PAP of 60mmHg .Cardiac catheterization also confirmed a sPAP of 116mmHg and mPAP of 65mmHg. The systolic aortic P was 145mmHg and systolic LV P was 152mmHg. So the unexpectedly high gradient of VSD shunt was still a mystery for us. While searching the literature to explain this , we noticed that the patients’ heart was resembling the reptilian heart model. The reptilian heart has two atria and one ventricle with 3 segments seperated via muscular ridges. In our patients’ heart ,the small chamber with high P in the RV was the cavum venosum, the larger chamber of RV with VSD was the cavum pulmonale, and the left ventricle was the cavum arteriosum. (Fig) The reptilian hearts typically have noncompacted myocardium which was actually the case in our patient. The reptilian hearts also have unique conduction system with no AV node and His bundle, and slow depolarization of ventricle from left to right. When we performed EPS, we found that the patient had no AV node and His bundle. Bringing together all these findings, we conclude that the patient has a reptilian heart with all anatomical, electrical and physiological features. And the answer to the mystery of inconsistent P recordings was hidden in ECG. The RBBB with very long QRS duration causes a delay between contraction of ventricles resulting in a dynamic P gradient between ventricles. We demonstrated this dinamic bidirectional shunt on CW recording when we obtained a more optimal recording of the shunt flow.This case demonstrates us one more evidence of human evolution; arising from single cell and developing to fish, to reptiles and to mammals. The evolution takes place again and again during neonatal life. If there is an embryological arrest, as occured in our patient, we can easily see the clues of this amazing human evolution. Abstract P1500 Figure

scholarly journals Functional mathematical model of dual pathway AV nodal conduction

2011 ◽  
Vol 300 (4) ◽  
pp. H1393-H1401 ◽  
Author(s):  
A. M. Climent ◽  
M. S. Guillem ◽  
Y. Zhang ◽  
J. Millet ◽  
T. N. Mazgalev
Keyword(s):  
Atrial Fibrillation ◽  
Mathematical Model ◽  
Refractory Period ◽  
Effective Refractory Period ◽  
Atrial Pacing ◽  
Wave Fronts ◽  
Av Node ◽  
Inferior Margin ◽  
His Bundle ◽  
Av Conduction

Dual atrioventricular (AV) nodal pathway physiology is described as two different wave fronts that propagate from the atria to the His bundle: one with a longer effective refractory period [fast pathway (FP)] and a second with a shorter effective refractory period [slow pathway (SP)]. By using His electrogram alternance, we have developed a mathematical model of AV conduction that incorporates dual AV nodal pathway physiology. Experiments were performed on five rabbit atrial-AV nodal preparations to develop and test the presented model. His electrogram alternances from the inferior margin of the His bundle were used to identify fast and slow wave front propagations. The ability to predict AV conduction time and the interaction between FP and SP wave fronts have been analyzed during regular and irregular atrial rhythms (e.g., atrial fibrillation). In addition, the role of dual AV nodal pathway wave fronts in the generation of Wenckebach periodicities has been illustrated. Finally, AV node ablative modifications have been evaluated. The model accurately reproduced interactions between FP and SP during regular and irregular atrial pacing protocols. In all experiments, specificity and sensitivity higher than 85% were obtained in the prediction of the pathway responsible for conduction. It has been shown that, during atrial fibrillation, the SP ablation significantly increased the mean HH interval (204 ± 39 vs. 274 ± 50 ms, P < 0.05), whereas FP ablation did not produce significant slowing of ventricular rate. The presented mathematical model can help in understanding some of the intriguing AV node mechanisms and should be considered as a step forward in the studies of AV nodal conduction.

Differential effect of verapamil isomers on sinus node and AV junctional region

1983 ◽  
Vol 244 (1) ◽  
pp. H80-H88
Author(s):  
H. O. Gloor ◽  
F. Urthaler
Keyword(s):  
Sinus Rhythm ◽  
Sinus Node ◽  
Conduction Time ◽  
Av Node ◽  
Junctional Rhythm ◽  
His Bundle ◽  
Sinus Node Artery ◽  
Rate Dependent ◽  
Av Conduction ◽  
Differential Responsiveness

The l- and d-isomers of verapamil were selectively perfused into the sinus node artery and atrioventricular (AV) node artery of 48 dogs. Injection of l-verapamil into the sinus node artery during sinus rhythm and into the AV node artery during AV junctional rhythm depresses both sinus rhythm and AV junctional rhythm significantly more than does the d-isomer. l-Verapamil is three to four times more powerful than d-verapamil. Injection of the isomers into the AV node artery during sinus rhythm rapidly impairs AV conduction. Increments in conduction time are measured exclusively at the level of the A-H interval of the His bundle electrogram, and l-verapamil is six times more powerful than d-verapamil. Neither d- nor l-verapamil in concentrations that exert a profound negative chronotropic effect or cause AV block, has any significant effect on transatrial or His bundle conduction. Thus these concentrations of d-verapamil have little or no significant effect on the fast sodium channel, but both verapamil isomers affect the slow channel. The main difference in action between l- and d-verapamil appears to be only quantitative in nature. The sinus node is significantly more sensitive to the negative chronotropic action of verapamil than is the AV junctional pacemaker, and this differential responsiveness appears to be related to the different intrinsic rates of the two pacemakers. During sinus rhythm (either in the presence or absence of atropine) sinus node automaticity is less affected than AV conduction when verapamil is given parenterally. We propose that this greater negative dromotropic effect of verapamil is also in part due to a rate-dependent process, since during sinus rhythm AV junctional cells have to be depolarized at frequencies significantly higher than their intrinsic rates.

scholarly journals Can atrioventricular node ablation be safely performed in patients with permanent His bundle pacing? Data from a multicentric registry

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Chaumont ◽  
N Auquier ◽  
A Mirolo ◽  
E Popescu ◽  
A Milhem ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Rate Control ◽  
Atrioventricular Node ◽  
Atrial Arrhythmia ◽  
Av Node ◽  
His Bundle ◽  
His Bundle Pacing ◽  
Ventricular Lead ◽  
Qrs Duration

Abstract Introduction Ventricular rate control is essential in the management of atrial fibrillation. Atrioventricular node ablation (AVNA) and ventricular pacing can be an effective option when pharmacological rate control is insufficient. However, right ventricular pacing (RVP) induces ventricular desynchronization in patients with normal QRS and increases the risk of heart failure on long term. His bundle pacing (HBP) is a physiological alternative to RVP. Observational studies have demonstrated the feasibility of HBP but there is still very limited data about the feasibility of AVNA after HBP. Purpose To evaluate feasibility and safety of HBP followed by AVNA in patients with non-controlled atrial arrhythmia. Methods We included in three hospitals between september 2017 and december 2019 all patients who underwent AVNA for non-controlled atrial arrhythmia after permanent His bundle pacing. No back-up right ventricular lead was implanted. AVNA procedures were performed with 8 mm-tip ablation catheter. Acute HBP threshold increase during AVNA was defined as a threshold elevation &gt;1V. His bundle capture (HBC) thresholds were recorded at 3 months follow-up. Results AVNA after HBP lead implantation was performed in 45 patients. HBP and AVNA were performed simultaneously during the same procedure in 10. AVNA was successful in 32 of 45 patients (71%). Modulation of the AV node conduction was obtained in 7 patients (16%). The mean procedure duration was 42±24min, and mean fluoroscopy duration was 6.4±8min. A mean number of 7.7±9.9 RF applications (347±483 sec) were delivered to obtain complete / incomplete AV block. Acute HBC threshold increase occurred in 8 patients (18%) with return to baseline value at day 1 in 5 patients. There was no lead dislodgment during the AVNA procedures. Mean HBC threshold at implant was 1.26±[email protected] and slightly increased at 3 months follow-up (1.34±[email protected]). AV node re-conduction was observed in 5 patients (16% of the successful procedures) with a second successful ablation procedure in 4 patients. No ventricular lead revision was required during the follow-up period. The baseline native QRS duration was 102±21 ms and the paced QRS duration was 107±18 ms. Conclusion AVNA combined with HBP for non-controlled atrial arrhythmia is feasible and does not compromise HBC but seems technically difficult with significant AV nodal re-conduction rate. The presence of a back-up right ventricular lead could have changed our results and therefore would require further evaluation. Unipolar HBP after AV node ablation Funding Acknowledgement Type of funding source: None

Morphology and electrophysiology of the mammalian atrioventricular node

1988 ◽  
Vol 68 (2) ◽  
pp. 608-647 ◽  
Author(s):  
F. L. Meijler ◽  
M. J. Janse
Keyword(s):  
Mammalian Species ◽  
Conduction Block ◽  
Atrioventricular Node ◽  
Conduction Delay ◽  
Conduction Time ◽  
Av Node ◽  
Crista Terminalis ◽  
His Bundle ◽  
Transitional Cells ◽  
Av Bundle

The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)

Sign in / Sign up

Export Citation Format

Share Document