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Benjamin J Scherlag

Publications and source records attributed to Benjamin J Scherlag.

At least 19 recordsLinked to original sources
PubMed2007

Gradients of atrial refractoriness and inducibility of atrial fibrillation due to stimulation of ganglionated plexi.

INTRODUCTION: The mechanism(s) whereby atrial ectopy induces atrial fibrillation (AF) is still poorly understood. METHODS AND RESULTS: In 12 dogs, we determined the refractory period (RP) along the right atrium (RA) and right superior pulmonary vein (RSPV), and AF inducibility with and without concurrent stimulation of the anterior right ganglionated plexi (ARGP) at the base of the RSPV. Multielectrode catheters were attached to the RSPV and RA with the distal electrodes close to ARGP. The RP and window of vulnerability (WOV), i.e., the longest S1-S2 minus the shortest S1-S2 at which AF was induced, were measured before and during incremental levels of ARGP stimulation. Mapping of the onset of AF was performed using the EnSite mapping system (St. Jude Medical, St. Paul, MN, USA) positioned in the RA. A single premature depolarization (PD) from the RSPV that did not induce AF without ARGP stimulation could do so with ARGP stimulation. The onset of AF consistently arose at the myocardium subtending the ARGP. With GP stimulation, the average WOV at the RSPV-atrial junction was significantly wider than at the RA appendage (65 +/- 27 vs. 8 +/- 17 msec, P < 0.05) or further along the RSPV sleeve (48 +/- 39 vs. 10 +/- 20 msec, P < 0.05). Even without GP stimulation, high intensity (10-20 mA) premature stimuli delivered at the RA appendage induced AF, originating from atrial tissue subtending the ARGP, presumably due to axonal conduction that activated the ARGP. CONCLUSION: GP stimulation, subthreshold for atrial excitation, converts isolated PDs into AF-inducing PDs, suggesting that autonomic tone may play a critical role in the initiation of paroxysmal AF.

Animals↗
PubMed2006

Interactive atrial neural network: Determining the connections between ganglionated plexi.

BACKGROUND: The electrophysiologic functions of the intrinsic cardiac autonomic nervous system (ANS) are not well understood. OBJECTIVES: The purpose of this study was to investigate the functional interactions between ganglionated plexi within the intrinsic cardiac ANS. METHODS: The hearts of 21 dogs were exposed via right and/or left thoracotomy to expose the (1) anterior right ganglionated plexi near the caudal end of the sinoatrial node, (2) inferior right ganglionated plexi at the junction of inferior vena cava and atria, and (3) superior left ganglionated plexi near the junction of left superior pulmonary vein and left pulmonary artery. Ganglionated plexi were stimulated at 0.6 to 8.0 V (square waves, 20 Hz, 0.1-ms duration). Sinus rate, AH interval during atrial pacing, and ventricular rate during atrial fibrillation were compared before and after ganglionated plexi stimulation and after their ablation. RESULTS: Anterior right ganglionated plexi stimulation induced significant AH prolongation and slowing of ventricular rate and sinus rate. When inferior right ganglionated plexi was ablated, slowing of sinus rate by anterior right ganglionated plexi stimulation was unaltered, but inhibition of AV conduction was eliminated. Superior left ganglionated plexi stimulation induced similar effects on sinus and AV nodal function, and sinus rate slowing was markedly attenuated by anterior right ganglionated plexi ablation. Ablation of both anterior right ganglionated plexi and inferior right ganglionated plexi eliminated AV conduction inhibition but not sinus rate slowing by superior left ganglionated plexi stimulation. CONCLUSION: This study provides functional evidence for the interconnections between ganglionated plexi to modulate sinus and AV nodal function, supporting clinical evidence that interconnections within the intrinsic cardiac ANS are critical elements in identifying the targets for atrial fibrillation ablation.

Animals↗
PubMed2006

The effects of caffeine on the inducibility of atrial fibrillation.

INTRODUCTION: There is widespread belief that caffeine consumption is linked to atrial arrhythmias; however, there is a relative lack of systematic evidence to support the assertion. The purpose of this study was to investigate whether caffeine, in doses equivalent to daily use in the general population, alter the propensity for atrial fibrillation (AF) in an experimental model comparing normal and simulated predisposition to AF. METHODS AND MATERIAL: Caffeine (caffeine Na benzoate, 50:50 mixture) was administered intravenously at 1, 3, and 5 mg/kg doses in dogs producing serum levels of 2 to 4, 5 to 7, and 8 to 10 microg/mL. To simulate focal AF, premature stimulation from the right superior pulmonary vein was delivered at 2x, 4x, and 10x threshold at a rate of 180/min (S(1)-S(2) = 330 milliseconds) without and then with low-level stimulation of ganglionated plexi (GP) at the entrance of the right superior pulmonary vein. The window of vulnerability (WOV), a measure of the propensity for AF inducibility, was determined by the longest coupling interval of the premature beat (S(1)-S(2)) minus the shortest S(1)-S(2), which induced AF. The cumulative WOV is the sum of the individually determined WOV. RESULTS: At each serum level of caffeine, the cumulative WOV was lower without rather than with GP stimulation compared with control. The cumulative WOV for both the stimulated, that is, predisposed to AF, and nonstimulated, that is, normal groups, exhibited a significantly lower average as compared with that exhibited by the control group (P <or= .003-.02). CONCLUSION: These findings suggest that the presence of caffeine may result in an unexpected reduction in the propensity for AF in healthy individuals and in those with a predisposition for AF (enhanced AF inducibility caused by the stimulation of the GP).

Animals↗
PubMed2006

The neural basis of atrial fibrillation.

This review addresses recent basic and clinical studies which suggest that targeting autonomic nerves and ganglia on the heart can result in suppression of atrial fibrillation (AF) with less damage to myocardium than the presently employed procedure which involves extensive pulmonary vein (PV) isolation from the rest of the left atrium. CLINICAL STUDIES: Clinical electrophysiologists in 1998 discovered that the majority of patients with paroxysmal form of AF, resistant to drugs and cardioversion, had focal, ectopic firing arising from the myocardial sleeves covering the PVs. They developed a strategy which called for inducing radiofrequency lesions which would supposedly isolate the PVs from the atria thereby curing this form of AF. To date this strategy has had limited success (70-85%). A new approach relies on targeting the ganglionated plexi (GP) at the entrances of the PVs. Several clinical reports provide evidence that this new approach can increase the success rate for radiofrequency ablation of paroxysmal AF (91-99%). BASIC STUDIES: Experimental investigations in animal studies, both in vivo and in vitro, have accumulated evidence for a mechanistic basis for the ablation of GP to terminate paroxysmal AF. Specifically, release of the neurotransmitter, acetylcholine, from these GP causes shortening of atrial and PV sleeve refractoriness. In addition, the concomitant release of adrenergic neurotransmitters mobilizes excess calcium intracellularly leading to early afterdepolarizations and triggered firing particularly in PV cells. We conclude that hyperactivity of these local cardiac GP play a critical role in initiating the paroxysmal form of AF resistant to drugs and cardioversion. Targeting the GP for ablation can substantially increase the success rate for terminating AF in these patients.

Action Potentials↗
PubMed2006

Sodium-calcium exchange initiated by the Ca2+ transient: an arrhythmia trigger within pulmonary veins.

OBJECTIVES: The hypothesis that an increased or prolonged Ca2+ transient during an abbreviated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by enhanced forward sodium-calcium (Na-Ca) exchange was examined. BACKGROUND: Because pulmonary veins have the shortest action potential of any cardiac tissue, we examined this hypothesis in canine pulmonary vein sleeves during interventions further shortening the action potential and increasing the calcium transient. METHODS: Extracellular bipolar electrode, intracellular microelectrode, and isometric force (a surrogate marker for the Ca2+ transient) recordings were obtained from superfused canine pulmonary veins. RESULTS: An elevation and prolongation of the terminal phase of repolarization (EADs) were observed during interventions increasing contractile force; isoproterenol or norepinephrine (3.2 x 10(-11) to 3.2 x 10(-7)M), hypothermia, and pacing (post-extrasystolic potentiation, post-pacing pause). The EAD formation was prevented by ryanodine (10 microM) or reversed by transiently increasing [Ca2+](o) from 1.35 to 5 mM (inhibition of forward Na-Ca exchange). Pacing-induced EADs were enhanced by re-introduction of normal Tyrode solution (Na+ = 130 mM) after substitution of 30 mM NaCl with 30 mM LiCl (stimulation of forward Na-Ca exchange). With norepinephrine or isoproterenol (3.2 x 10(-8)M) + acetylcholine (10(-7)M) (to enhance the Ca2+ transient and further shorten the abbreviated action potential, respectively), tachycardia-pause initiated arrhythmia (1,132 +/- 153 beats/min) lasting >1 s was observed. Rapid firing was prevented by either suppression of the Ca2+ transient (ryanodine) or transiently increasing [Ca2+](o). CONCLUSIONS: The data show EAD formation in superfused canine pulmonary veins, enhanced by an increased Ca2+ transient and increased Na-Ca exchange current. With subsequent shortening of the action potential with acetylcholine, tachycardia-pause triggers rapid firing within the PV sleeve.

Action Potentials↗
PubMed2006

Experimental model for paroxysmal atrial fibrillation arising at the pulmonary vein-atrial junctions.

BACKGROUND: The mechanism(s) by which pulmonary veins (PVs) become ectopically active and subsequently initiate and sustain atrial fibrillation (AF) remains poorly understood. OBJECTIVES: The purpose of this study was to produce an acute canine model of paroxysmal AF arising from the PVs. METHODS: In 11 dogs, a thoracotomy was performed and a 26-gauge needle with a polyethylene tube attached was inserted into a fat pad containing autonomic ganglia at the base of the PV. The 11 dogs were divided into two groups: acetylcholine (ACh) 1-10 mM (group I, n = 5) or carbachol (CARB) 1-10 mM (group II, n = 6) injected (0.5 mL) into the fat pad. RESULTS: Within 2 to 5 minutes after injection of parasympathomimetics into the fat pad, a sequence of heart rate slowing, spontaneous premature depolarizations, and spontaneous AF was observed in four of 11 dogs. In seven dogs, single premature extrastimuli easily induced AF. AF was sustained for an average of 10 minutes (ACh) and 38 minutes (CARB), with the shortest AF cycle length seen at the PV-atrial junction adjacent to the fat pad (AF cycle length 75 +/- 41 ms for ACh and 37 +/- 12 ms for CARB). CONCLUSION: Acute autonomic remodeling produced by injection of parasympathomimetics into the fat pad resulted in spontaneous or easily induced sustained AF with short AF cycle length; the most rapid firing rate was observed in the PV and atria adjacent to the injected fat pad. These findings resemble paroxysmal AF in patients, suggesting that hyperactive autonomic ganglia may be a critical element in patients exhibiting focal AF arising from the PV.

Acetylcholine↗
PubMed2006

The intrinsic cardiac nervous system and atrial fibrillation.

PURPOSE OF REVIEW: Radiofrequency ablation techniques to cure cardiac arrhythmias have focused on destroying myocardial tissue involved in abnormal excitation or conduction. This review will address recent basic and clinical studies which suggest that targeting autonomic nerves and ganglia on the large vessels and the heart, within the pericardium, can result in cardiac arrhythmia suppression with little, if any, damage to healthy myocardium. RECENT FINDINGS: Basic reports have shown that electrical stimulation of autonomic nerves on the heart itself can facilitate the induction of atrial fibrillation. The initial investigations found that the lowest threshold for inducing atrial fibrillation was at the entrances of the pulmonary veins. Moreover, beta-blockade blunted this response whereas atropine abolished atrial fibrillation inducibility. Subsequent studies found that ganglionated plexi clustered at the pulmonary vein entrances (within fat pads) could be stimulated without atrial excitation. Now, premature beats induced in the pulmonary veins could be converted to atrial fibrillation with a significantly greater propensity than without ganglionated plexi stimulation. Furthermore, ablation of these ganglionated plexi abolished atrial fibrillation inducibility. Clinical studies have been forthcoming clearly implicating these intrinsic cardiac ganglia in clinical atrial fibrillation. SUMMARY: Previous ablation procedures have focused on destroying myocardial sites that participated in the initiation and perpetuation of various tachyarrhythmias. New basic and clinical findings may allow targeting autonomic elements at a few specific sites on the heart that are directly related to arrhythmia formation, thereby reducing extensive damage to healthy myocardium.

Animals↗
PubMed2006

Experimental model simulating right ventricular outflow tract tachycardia: a novel technique to initiate RVOT-VT.

BACKGROUND: The mechanism(s) whereby a discrete area of myocardium in the RVOT becomes arrhythmogenic remains unknown. METHODS: In 13 dogs, a circular catheter was placed in the proximal pulmonary artery (PA) to contact the endovascular circumference of the PA. A 50-msec train of high-frequency stimulation (HFS, 200 Hz), coupled to atrial pacing, was applied at each bipolar pair of the circular catheter. The coupling interval was adjusted so that the 50-msec train occurred during the ventricular refractory period, that is, the QRS complex, in order to prevent stimulation of the myocardial sleeve within the proximal PA. RESULTS: In all dogs, HFS induced ventricular premature depolarizations and VTs with a left bundle branch block (LBBB) morphology and inferior axis (average 6.8 +/- 1.6 V). Earliest activation was consistently recorded from the proximal PA. Esmolol, a short-acting beta-blocker (1 mg/kg), was administered intravenously in 11 dogs. The inducible ventricular ectopy was abolished in 10 dogs (>12 V, P < 0.05) and the response to HFS was blunted in one dog (10-11 V). After 30 minutes, the response to HFS returned to pre-esmolol levels. CONCLUSIONS: Stimulation of the sympathetic input to the proximal PA induces ventricular ectopy and VTs exhibiting a left bundle branch block morphology and inferior axis, closely simulating clinical RVOT-VT. Beta-blockade either abolishes or blunts this response, corroborating the sympathetic etiology in this model and in some clinical cases of RVOT tachycardias.

Animals↗
PubMed2005

Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation.

OBJECTIVES: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF). BACKGROUND: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown. METHODS: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness. RESULTS: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p </=0.05. The fewest number of APDs from the RSPV required to induce AF during AG stimulation was as follows: control (no stimulation) 7 +/- 4, 2.4 V; 3 +/- 1, p </=0.05. In seven dogs, lidocaine (2%, 0.4 cc), a neuronal blocker, was injected into the fat pad, resulting in the loss of AF inducibility in six of seven dogs at the same AG stimulation levels. Three of seven dogs showed AF inducibility only with AG stimulation >/=9.3 V. CONCLUSIONS: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF.

Animals↗
PubMed2005

Delineation of AV conduction pathways by selective surgical transection: effects on antegrade and retrograde transmission.

INTRODUCTION: The role for transitional cells as determinants of AH and HA conduction was examined in the superfused rabbit AV junction. METHODS: Bipolar electrodes and microelectrodes were used to record antegrade A-H and retrograde H-A activation, before and after transection of the transitional cell input to the compact AV node. RESULTS: During pacing from the high right atrium, inferior to the coronary sinus os, beneath the fossa ovalis, or on the anterior limbus, AV Wenckebach block (WB) was mediated by identical transitional cells grouped in close apposition to the compact AV node. Paced WB cycle lengths were shorter from the high right atrium (196+/-12 msec) and inferior to the coronary sinus os (195+/-8 msec) versus the fossa ovalis (217+/-9 msec) or anterior limbus (206+/-11 msec). With His bundle pacing, retrograde HA WB (211+/-17 msec) was observed within the N cell region within the compact AV node. After transection of posterior and superior transitional cell input to the compact AV node, the antegrade AH WB cycle length was prolonged (245+/-18 msec), with an increased WB incidence within the NH region (compact AV node)(5% to 41%; p=0.014). The incidence of retrograde HA WB determined within the NH region was increased (30% to 88%), with a decrease in the stimulus-fast pathway conduction time (98+/-7 to 49+/-6 msec; p<0.01). CONCLUSIONS: The data demonstrate (1) a common transitional cell population determining AH WB, independent of atrial stimulation site, and (2) a plasticity of transitional cell-compact AV node connections, with rapid AH and HA conduction favored by removal of posterior/superior AV nodal input.

Analysis of Variance↗
PubMed2005

Experimental model of inappropriate sinus tachycardia: initiation and ablation.

OBJECTIVE: The purpose of the present study was to develop an experimental model of inappropriate sinus tachycardia (IST) by injecting a catecholamine into a fat pad containing autonomic ganglia (AG) innervating the sinus node (SN). METHODS: Initial protocols in 3 groups of pentobarbital anesthetized dogs consisted of (1) slowing the heart rate (HR) by electrical stimulation of AG in the fat pad; (2) the effect of intravenous injection of epinephrine (0.1-0.3 mg) on the HR and systolic blood pressure (BP); (3) the response of SN rate to intravenously injected isoproterenol (1 microgm/kg). These studies established a reference for the response to epinephrine injection (mean dose 0.2 +/- 0.9 mg, n = 14) into the fat pad at the base of the right superior pulmonary vein (RSPV). ECG leads, right atrial and His bundle electrograms, BP and core body temperature were continuously monitored. RESULTS: Epinephrine, injected into the fat pad, caused a significant increase in heart rate (HR, average: 211 +/- 11/min, p < 0.05 compared to control) but little change in systolic BP, 149 +/- 10 mmHg, p = NS (Group I, N = 8). The tachycardia lasted >30 minutes. Ice mapping and P wave morphology showed the tachycardia origin in the SN in 6/8 and in the crista terminalis (CT) in 2. Injection of 0.4 cc of formaldehyde into the FP restored HR (159 +/- 16) toward baseline (154 +/- 18). In Group II (N = 6), the same regimen induced a significant increase in both HR and systolic BP (194 +/- 17/min and 230 +/- 24 mmHg, respectively) compared to control values (143 +/- 23/min, 162 +/- 24 mmHg) which lasted for > 30 minutes. Ice mapping and P wave morphology showed that the pacemaker was in the SN (1), overlying the CT (2), or atrioventricular junction (2). Formaldehyde (0.4 cc) injected into the FP restored both HR and systolic BP toward baseline values (148 +/- 29/min and 152 +/- 24 mmHg, p = NS) and prevented, slowing of the HR by electrical stimulation of the AG; moreover, the same dose of epinephrine injected intravenously increased HR and SBP but only for 2-5 minutes; Isoproterenol (1 microg/kg) injected intravenously induced essentially the same increase in sinus rate after AG ablation as in the control state (194 +/- 15/min vs 193 +/- 23/min, p = NS). CONCLUSION: Experimental IST is mainly localized in the SN or CT. Ablation of the AG terminates IST without impairing the SN response to an adrenergic challenge.

Animals↗
PubMed2005

Electrical stimulation to identify neural elements on the heart: their role in atrial fibrillation.

EXPERIMENTAL STUDIES: Anesthetized dogs were subjected to a right then left thoracotomy. Two modes of electrical stimulation were used to activate ganglionated plexi (GP) on the epicardium of the atria: (1) Near the base of each pulmonary vein (PV), trains of high frequency stimuli (HFS) were coupled to each atrial paced beat so as to fall within the refractory period to achieve nerve stimulation without atrial excitation; and (2) Continuous HFS was applied via plaque electrodes sutured to epicardial fat pads (containing a GP) near the right superior (RS) and left superior (LS) PVs. The chest was then closed. An ablation catheter, inserted percutaneously, was positioned fluoroscopically in the right atrium across from the epicardial plaque electrode near the RSPV. Transeptal puncture was used to place an ablation catheter at the LSPV-left atrial junction. HFS applied to each of the epicardial fat pads induced atrial fibrillation (AF) and also caused high grade AV block due to a strong parasympathetic effect on the AV node. Radiofrequency ablation from the right and left atrial endocardium abolished the vagal response to HFS delivered to the plaque electrodes on the fat pads close to the RSPV and LSPV, respectively. CLINICAL STUDIES: Sixty (60) patients with paroxysmal or persistent AF underwent PV antrum isolation (27 patients) or PV antrum isolation plus left atrial GP ablation (33 patients). Endocardial HFS at the border of the PV antra near the 4 GPs produced AF and high grade AV block (vagal response) during AF. RFA at these sites abolished the vagal response. Testing in a small number of patients with very short follow-up suggests that adding GP ablation to PV antrum isolation may increase ablation success (absence of AF recurrence) from 70% to 91%. CONCLUSIONS: These basic and clinical studies suggest that localized cardiac autonomic ganglia (GPs) may play a critical role in the initiation and maintenance of AF.

Animals↗
PubMed2005

Triggered firing in pulmonary veins initiated by in vitro autonomic nerve stimulation.

BACKGROUND: Rapid firing within pulmonary vein sleeves frequently initiates atrial fibrillation. The role of the autonomic nervous system in facilitating spontaneous firing is unknown. OBJECTIVES: The purpose of this study was to determine if autonomic nerve stimulation within canine atrium and pulmonary vein sleeves initiates arrhythmia formation. METHODS: Extracellular bipolar and intracellular microelectrode recordings were obtained from isolated superfused canine pulmonary veins (N = 28) and right atrium (N = 5) during local autonomic nerve stimulation. RESULTS: Autonomic nerve stimulation decreased pulmonary vein sleeve action potential duration (APD90 = 160 +/- 17 to 92 +/- 24 ms; P < .01) and initiated rapid (782 +/- 158 bpm) firing from early afterdepolarizations in 22 of 28 pulmonary vein preparations. The initial spontaneous beat had a coupling interval of 97 +/- 26 ms. Failure to induce arrhythmia was associated with a failure to shorten APD90 (151 +/- 18 to 142 +/- 8 ms; P = .39). Muscarinic receptor blockade (atropine: 3.2 x 10(-8) M) prevented APD90 shortening in 8 of 8 preparations and suppressed firing in 6 of 8 preparations, whereas beta1-adrenergic receptor blockade (atenolol: 3.2 x 10(-8) M) suppressed firing in 8 of 8 preparations. Suppression of the Ca transient with ryanodine (10(-5) M) completely suppressed firing in 6 of 6 preparations. Inhibition of forward Na/Ca exchange by a transient increase in [Ca+2]o completely suppressed firing in 4 of 6 preparations. The same stimulus trains produce atropine-suppressed APD90 shortening in superfused right atrial free wall but fail to produce triggered arrhythmia. CONCLUSIONS: The data demonstrate triggered firing within canine pulmonary veins with combined parasympathetic and sympathetic nerve stimulation. Both an enhanced Ca transient and increased Na/Ca exchange may be required for arrhythmia formation.

Animals↗
PubMed2004

Variability of AV nodal potentials recorded, in vivo: direct demonstration of dual AV nodal physiology.

OBJECTIVES OF STUDY: We developed a method to record extracellular A-V nodal potentials in the beating dog heart, in vivo. METHODS: In eleven Na-pentobarbital anesthetized, open-chest dogs, an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted through a purse-string suture in the coronary sinus (CS) distal to the ostium and positioned electrographically so that the tip electrode recorded a His bundle (Hb) potential. RESULTS: Stable recordings of A-V nodal potentials (amplitude, 178 +/- 94 microV; duration 78 +/- 26 msec) were consistently made during sinus rhythm from the second and/or third bipolar pairs of electrodes. Programmed atrial stimulation and vagal stimulation resulted in loss of amplitude and increased duration of the A-V nodal potentials associated with A-H prolongation. In another series of experiments, crushing the sinus node in 6 dogs resulted in AV nodal rhythms with AV nodal potentials of varying amplitudes (132 to 840 microV) and durations (range 25 to 71 msec) as the earliest activation which preceded the Hb, atrial and ventricular deflections. One dog, showing dual AV nodal physiology as documented from the AV nodal function curve, had two distinctly different AV nodal potentials. The low-level, longer duration potentials were associated with longer (slow pathway) A-H intervals; whereas the shorter higher amplitude potentials (fast pathway) showed shorter A-H intervals, each occurring at a critical paced cycle length. CONCLUSION: We conclude that consistent extracellular AV nodal electrograms can be recorded in vivo although the configuration of these potentials varies depending on heart rate, autonomic stimulation and different arrhythmic conditions such as AV nodal escape rhythms and dual AV nodal physiology.

Action Potentials↗
PubMed2004

Fast pathway-His bundle connections in the rabbit heart.

OBJECTIVES: The incidence and the physiologic roles for direct fast pathway-His bundle connections were examined in 102 rabbit hearts. METHODS: Extracellular bipolar and intracellular microelectrode recordings were made from the superfused rabbit AV junction. RESULTS: In 13 of 27 preparations demonstrating anterior extensions of the fast pathway, the retrograde HA ERP and 2:1 block cycle length were shortened (128 +/- 12 and 145 +/- 5 msec, respectively) versus the remaining 89 preparations (178 +/- 15 and 185 +/- 10 msec, respectively, p < 0.01). The former values were similar to the ERP and 2:1 block cycle length of fast pathway transitional cells (128 +/- 23 and 141 +/- 4 msec, respectively), suggestive of a direct fast pathway-His bundle connection. A deflection recorded between the A and H potentials of the His bundle electrogram could be dissociated from both atrial and His bundle activation. Intracellular microelectrode recordings and light microscopy confirmed the deflection to be an accessory pathway consisting of an anterior extension of fast pathway transitional cells connecting the atrium and His bundle. Transection along the AV groove anterior to the compact AV node ( N = 5) increased the retrograde ERP and Wenckebach block cycle length by severing the AH connection, or transection of the penetrating bundle ( N = 4) produced antegrade AH block without altering rapid retrograde conduction. CONCLUSIONS: Fast pathway-His bundle connections were present in 13 of 102 rabbit hearts, providing an anatomic and physiologic basis for rapid retrograde VA conduction and a possible retrograde pathway for sustained AV nodal reentrant tachycardia.

Afferent Pathways↗
PubMed2003

Slow:fast and slow:slow AV nodal reentry in the rabbit resulting from longitudinal dissociation within the posterior AV nodal input.

OBJECTIVE: The anatomic and electrophysiologic bases for multiple forms of sustained AV nodal tachycardia were determined in the rabbit. METHODS: Intracellular microelectrode recordings were used to identify antegrade and retrograde conduction limbs of sustained tachycardias observed in 23 of 152 superfused rabbit AV junctions. RESULTS: Slow:slow tachycardias (196 +/- 12 msec cycle length) with nearly equal AH and HA intervals (99 +/- 12; 97 +/- 11 msec, respectively) and early atrial activation near the coronary sinus os were observed in 14 preparations and slow:fast tachycardias (189 +/- 11 msec cycle length) with an AH > HA interval (141 +/- 12; 48 +/- 10 msec, respectively) and early atrial activation along the anterior limbus of the fossa ovalis were observed in 11 preparations. Both tachycardias were associated with longitudinal dissociation and localized reentry within the triangle of Koch. Slow:fast and slow:slow tachycardias exhibited counterclockwise and clockwise reentry circuits, respectively. Both circuits were present in two preparations. Slow:fast AV nodal reentrant tachycardias could be reset with stimuli introduced near the coronary sinus os and the anterior AV nodal input. Slow:slow tachycardias could be reset only by stimuli introduced near the coronary sinus os. The fraction of the tachycardia cycle length contained within the compact AV node was greater for slow:fast (0.35 +/- 0.07) than slow:slow reentry (0.15 +/- 0.05, p = 0.026), suggesting a longer lower common pathway for slow:fast tachycardia. CONCLUSIONS: Longitudinal dissociation within the posterior AV nodal input incorporating the AV node can provide the reentrant substrate for two different clinical forms of sustained AV nodal tachycardias.

Animals↗