Abstract 5286: Human AV Junctional Pacemaker Shift Due to Cholinergic and Adrenergic Stimulations: Optical Imaging with a Novel Long Wavelength Voltage-Sensitive Dye

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Vadim V Fedorov ◽  
Christina M Ambrosi ◽  
William J Hucker ◽  
Alexey V Glukhov ◽  
Kelley V Foyil ◽  
...  
Keyword(s):  
Animal Models ◽  
Heart Association ◽  
Av Node ◽  
Voltage Sensitive Dye ◽  
Long Wavelength ◽  
His Bundle ◽  
Temporary Pacemaker ◽  
Pacemaker Shift ◽  
Exit Block ◽  
Reentrant Arrhythmias

It is well known that under different physiological and pathologic conditions, the atrioventricular junction (AVJ) may become the pacemaker of the heart. However, unlike the well-characterized AVJ pacemaker in animal models, autonomic control of the human AVJ pacemaker has not been studied. Explanted human hearts with different types of cardiomyopathy (n=7) were obtained at the time of cardiac transplantation and perfused with cardioplegic solution. The AVJ was cannulated, isolated from the rest of the heart, immobilized with the excitation-contraction uncoupler blebbistatin (10 μmol/L) and optically mapped using the infrared voltage sensitive dye di-ANBDQBS. Imaging was conducted with 100x100 CMOS camera from endocardial field of view ranging 24x24 to 36x36mm 2 , which allowed to simultaneously map right side of intratrial and intraventricular septa, coronary sinus (CS) and His bundle regions. In control, we found AVJ rhythm of 31+/−15 bpm (2409+/−1264 ms) in all human preparations which originated in compact AV node (N-region, n=4) and/or region between AV node and His bundle (NH-region, n=3). Isoproternol (Iso, 1 μM) induced AVJ rhythm acceleration up to 68+/−12 bpm (913+/−192 ms), temporary pacemaker shift to CS region (n=2) and improved conduction in both slow and fast pathways, which induced reentrant arrhythmias in 3/5 preparations. Acetylcholine (ACh, 1–3 μM) slowed rhythm to 21+/−6 bpm (3130+/−1146 ms) and conduction in both pathways up to complete block, and induced temporary pacemaker shift to CS region in 3/4 preparations. Moreover, we found bifocal activation in 3/4 preparation when two main pacemakers (CS and compact AV node) worked asynchronously with different frequencies, accompanied by the exit block from AV node. We showed by high-resolution optical mapping for the first time that unlike in animal models (rabbit and rat) in isolated coronary perfused human AVJ leading pacemaker localized mostly in the N- or NH-regions. Beta-adrenergic (Iso) and cholinergic (ACh) stimulations of AVJ can significantly accelerate or slow rhythm and conduction, as well as induced pacemaker shift to CS, and result in reentrant arrhythmias. This research has received full or partial funding support from the American Heart Association, AHA Midwest Affiliate (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, South Dakota & Wisconsin).

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 Reversal of left bundle branch block–induced cardiomyopathy by His bundle pacing

2019 ◽  
Vol 48 (2) ◽  
pp. 030006051988418
Author(s):  
Fei Liu ◽  
Lijun Zeng ◽  
Xiaomeng Yin ◽  
Lianjun Gao ◽  
Yunlong Xia ◽  
...  
Keyword(s):  
Left Bundle Branch Block ◽  
Heart Function ◽  
Nonischemic Cardiomyopathy ◽  
Bundle Branch Block ◽  
His Bundle ◽  
His Bundle Pacing ◽  
Temporary Pacemaker ◽  
Nonischemic Dilated Cardiomyopathy ◽  
The Right

A 61-year-old woman was referred to our institution for evaluation of severe nonischemic dilated cardiomyopathy and left bundle branch block (LBBB). After permanent His bundle pacing, the LBBB was immediately corrected; however, the right bundle branch was injured during the procedure. Subsequent recovery of the right bundle branch block and normalization of heart function were observed during follow-up. This case indicates that LBBB might result in the development of nonischemic cardiomyopathy and emphasizes the necessity of a temporary pacemaker during His bundle pacing for patients with LBBB.

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.

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