Neurohumoral and Hemodynamic Mechanisms of Diuresis During Atrioventricular Nodal Reentrant Tachycardia

Thirty-two consecutive patients with paroxysmal supraventricular tachycardias, with previously defined mechanisms of the tachycardias, were interviewed by noninvestigators about whether they experienced symptoms of diuresis during or at the termination of the tachycardias, to test the hypothesis that patients with AV nodal reentrant tachycardia would have a feeling of diuresis, polyuria, or both during or at the termination of the tachycardia. Twelve of the 13 patients with AV nodal reentrant tachycardia (92%), two of the 15 patients with AV reentrant tachycardia (13%), and one of the 4 patients with atrial flutter associated with 2:1 AV conduction (25%) felt diuresis during or at the termination of the tachycardias (AV nodal reentrant tachycardia vs other forms of tachycardia; P < 0.001). In 14 of the 32 patients, the right atrial pressure and plasma atrial natriuretic peptide (ANP) concentration were measured during both the tachycardias and sinus rhythm. The mean right atrial pressure during AV nodal reentrant tachycardia was significantly elevated compared to that during other forms of tachycardia (P < 0.01). The plasma ANP concentration during AV nodal reentrant tachycardia was also elevated significantly compared to that during other forms of tachycardias (P < O.OO1). There were no significant differences in the cycle lengths of the tachycardias, age, left atrial dimensions, or the left ventricular ejection fraction between the AV nodal reentrant tachycardia and the other forms of tachycardia. We concluded that the feeling of diuresis during or at the termination of tachycardia was a more common symptom in patients with AV nodal reentrant tachycardia. The higher secretion of plasma ANP from the right atrium might be involved in the mechanism of this symptom.     

Evidence that AV nodal re-entrant tachycardia does not require participation of the entire AV node

Electrophysiologic studies in a case of AV nodal re-entrant tachycardia showed that a programmed atrial premature depolarization induced during the tachycardia did not change the tachycardia cycle but caused a delay in the following atrial echo. Analysis of such a phenomenon suggests that the atrial premature depolarization was conducted to the upper part of the AV node but not to the site of the re-entry. Therefore, AV nodal re-entry can persist without the participation of the upper part of the AV node. This case illustrates that the upper common pathway connecting the dual AV nodal pathways cranially is most likely located within the AV node and consists of AV nodal tissue.     

Cycle Length Alternation During Supraventricular Tachycardia: Occurrence and Mechanism in a Canine Model of AV Reentrant Tachycardia

Cycle length alternation (CLA) is commonly observed during supraventricular tachycardia (SVT) onset and termination. The present study was designed to gain insights into the mechanism and potential clinical relevance of CLA by comparing computer simulations of tachycardia to directly observed behavior in a canine model of AV reentrant tachycardia (AVRT). The computer model was based on the hypothesis that CLA is secondary to feedback between AV nodal output during SVT and subsequent AV nodal input, and used the measured anterograde AV nodal recovery curve (AV vs A1A2) to predict sequential AV and RR intervals during SVT. Orthodromic AVRT was created experimentally in 11 open-chested, autonomically-blocked (atropine plus nadolol) dogs using a sensing and pacing circuit that mimicked a retrograde-conducting accessory pathway. Steady-state cycle length and AV interval during experimental AVRT closely paralleled predictions made by the computer model. CLA appeared consistently at the onset of experimental AVRT at programmed VA intervals less than or equal to 100 msec (corresponding to VA less than or equal to 150 msec as measured clinically) in all dogs. The amplitude and duration of CLA increased as the VA interval decreased, and closely paralleled predictions based on the computer model. Abrupt accelerations in atrial pacing to the same rate as AVRT did not result in alternation of cycle length. In conclusion, alternation of cycle length results from feedback between AV nodal output and subsequent AV nodal input at the onset of reentrant supraventricular tachycardia, and does not require changes in autonomic tone or dual AV nodal pathways. CLA occurrence, amplitude, and duration are predictable based on AV node recovery properties, and depend on retrograde conduction properties of the reentrant circuit. The presence of CLA suggests that the AV node is an integral component of the SVT reentry circuit, and may be useful clinically to identify the mechanism of supraventricular tachycardias.     

Evidence that AV Nodal Re-Entrant Tachycardia Does Not Require Participation of the Entire AV Node

Electrophysiologic studies in a case of A V nodal re-entrant tachyca rdia showed thai a programmed alrial premature depolarization induced during the tachycardia did not change the tachycardia cycle but caused a delay in the following atrial echo. Analysis of such a phenomenon suggests that the atrial premature depolarization was conducted to the upper part of the AV node but not to the site of the re-entry. Therefore, AV nodal re-entry can persist without the participation of the upper part of the AV node. This case illustrates that the upper common pathway connecting the dual AV nodal pathways cranially is most likely located within the AV node and consists of A V nodal tissue.     

Atypical AV nodal reentry with bystander accessory pathway: an unusual mechanism of preexcited tachycardia

We present an unusual mechanism of preexcited tachycardia--atypical AV nodal reentry with bystander AP. It can be differentiated from other preexcited tachycardias by its variable degree of preexcitation (either spontaneous or in response to atrial pacing), higher degree of preexcitation with pacing near the origin of the AP than during tachycardia, inability to preexcite the tachycardia by either late atrial or ventricular premature beats, the presence of nonpreexcited atypical AV nodal reentry tachycardia following successful AP ablation, and by exclusion of atrial tachycardia.     

Simultaneous AV Nodal Reentrant and Ventricular Tachycardias

Simultaneous AV nodal reentrant and ventricular tachycardias were observed during the course of an electrophysiological study in a 51-year-old patient who suffered from recurrent attacks of sustained ventricular tachycardia. Occurrence of simultaneous tachycardias was facilitated by the fact that both tachycardias had a similar cycle length. Ventricular tachycardia was most probably initiated by AV nodal tachycardia previously induced by atrial extrastimulation following the administration of atropine.     

A Wide QRS Complex Tachycardia with Different Initiation Patterns: What is the Mechanism?

A 47-year-old man with palpitations underwent electrophysiologic testing (EPS). Burst atrial pacing while infusing isoproterenol induced non-reproducible wide QRS tachycardias with an unusual pattern of an H-A-V activation with the same tachycardia cycle length and two different initiation patterns. The tachycardia had the earliest atrial activation at the His bundle region. No dual atrioventricular (AV) nodal physiology was demonstrated by programmed atrial stimulation. Though a definite diagnosis of AV nodal reentrant tachycardia was not obtained, slow pathway ablation was performed in order to avoid inadvertent AV block as a complication. Thereafter, no tachycardias were induced by repeat burst atrial pacing.     

Reentrant Junctional Tachycardias

AKHTAR, M.: Reentrant Junctional Tachycardias. Most of the tachycardia arising in the atrioventricular (AV) junction are reentrant in nature. The two most common variety are AV nodal reentry and AV reentry utilizing an accessory pathway of the Kent bundle type. Typically these tachycardias have narrow QRS complex and are regular but an associated right or left bundle branch block could result in a wide QRS complex. Other mechanisms for wide QRS in AV junctional tachycardia include: (a) antidromic reentry; (b) preexcited tachycardia using two accessory pathways; (c) AV nodal reentry with incidental accessory pathway participation; and (d) atriofascicular (nodoventricular) Mahaim participation. A variety of surface ECG and intracardiac electrophysiological methods are used to delineate the precise mechanisms which is essential for successful nonpharmacological therapy in these patients.     

Usefulness of Intravenous Propofol Anesthesia for Radiofrequency Catheter Ablation in Patients with Tachyarrhythmias: Infeasibility for Pediatric Patients with Ectopic Atrial Tachycardia

General anesthesia is sometimes required during radiofrequency catheter ablation (RFCA) of various tachyarrhythmias because of an anticipated prolonged procedure and the need to ensure stability during critical ablation. In this study, we examine the feasibility of using propofol anesthesia for RFCA procedure. There were 150 patients (78 male, 72 female; mean age 30 years, range 4-96 years) in the study. Electrophysiologic study was performed before and during propofol infusion in the initial 20 patients and was performed only during propofol infusion in the remaining 130 patients. In the initial 20 patients, propofol infusion increased the sinus rate and facilitated AV nodal conduction. The accessory pathway effective refractory period, as well as the sinus node recovery time, atrial effective refractory period, and ventricular effective refractory period were not significantly changed. There were 152 tachyarrhythmias in 150 patients (24 atrial flutter, 31 AV nodal reentrant tachycardia, 68 AV reciprocating tachycardia, 12 ventricular tachycardia, and 17 atrial tachycardia). Most (148/152) tachycardias remained inducible after anesthesia and RFCA was performed uneventfully. However, in four of the seven pediatric patients with ectopic atrial tachycardia, the tachycardia terminated after propofol infusion and could not be induced by isoproterenol infusion. Consequently, RFCA could not be performed. Intravenous propofol anesthesia is feasible during RFCA for most tachyarrhythmias except for ectopic atrial tachycardia in children.     

Termination of pacemaker endless loop tachycardia by an atrial extrasystole

This article documents the termination of a pacemaker endless loop tachycardia by a critically timed atrial extrasystole. Although predictable electrophysiologically, this mode of termination has not been previously reported. The observation is conceptually important because it provides the final link in establishing the similarity of endless loop tachycardia and spontaneous reentrant AV nodal or junctional tachycardias in terms of initiation and termination by single atrial or ventricular extrasystoles.     

Extended Protocol for Demonstration of Dual AV Nodal Physiology

The incidence of dual atrioventricular (AV) nodal physiology was evaluated in 22 patients (14 males, 8 females, age 52 ± 18 years) undergoing electrophysiology studies for evaluation of ventricular tachycardia/honsustained ventricular tachycardia (n = 11), supraventricular tachycardia (n = 5), and syncope (n = 6). Patients with AV node reentrant tachycardia were excluded. Thirteen patients had riormal left ventricular function and nine patients (seven with coronary artery disease, two with dilated cardiomyopathy) had depressed left ventricular function. Single atrial extrastimuli (A2) were introduced after eight-beat drives at paced cycle lengths of 550 msec and 400 or 450 msec beginning at coupling intervals of 650 and 500 or 550 msec, respectively. The coupling interval was decreased at 10-msec intervals until AV node or atrial refractoriness. A second atrial extrastimulus (A3) was then added. A2 was fixed at 50 msec greater than the atrial or AV nodal refractory period. A3 was coupled to A2 at 650 and 500 or 550 msec and decremented as with single extrastimulation. Dual AV nodal physiology was defined by a 50-msec increase in A2H2 or A3H3 with a 10-msec decrement in the coupling interval or a discontinuous H1H2 versus A1A2 or H2H3 versus A2A3 curve. Using a single extrastimulus, 1 of 22 patients demonstrated dual AV nodal physiology. Using double extrastimuli, an additional four patients with dual AV nodal physiology were identified. The occurrence of dual AV nodal physiology determined using double extrastimuli is increased compared to using only a single extrastimulus (P = 0.03). In conclusion, dual AV nodal physiology can be demonstrated with greater frequency using an extended rather than a standard protocol.     

The Response of Regular Re-entrant Supraventricular Tachycardia to Right Heart Stimulation

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.     

Cardiac surgery for arrhythmias

Cardiac arrhythmia surgery was initiated in 1968 with the first successful division of an accessory AV connection for the Wolff-Parkinson-White Syndrome. Subsequent surgical procedures included the left atrial isolation procedure and the right atrial isolation procedure for automatic atrial tachycardias, discrete cryosurgery of the AV node for AV nodal reentry tachycardia, the atrial transection procedure, corridor procedure and Maze procedure for atrial fibrillation, the right ventricular disconnection procedure for arrhythmogenic right ventricular tachycardia, the encircling endocardial ventriculotomy, subendocardial resection procedure, endocardial cryoablation, the Jatene procedure, and the Dor procedure for ischemic ventricular tachycardia. Because of monumental strides in the treatment of most refractory arrhythmias by endocardial catheter techniques during the past decade, the only remaining viable surgical procedures for cardiac arrhythmias are the Maze procedure for atrial fibrillation and the Dor procedure for ischemic ventricular tachycardia. Nevertheless, the 25-30 years of intense activity in the field of cardiac arrhythmia surgery provided the essential foundation for the development of these catheter techniques and represent one of the most exciting and productive eras in the history of medicine. In one short professional career, we have witnessed the birth of arrhythmia surgery, its adolescence as an "esoteric" specialty, its prime as an enlightening yet exhausting period, and finally its waning years as a source of knowledge and wisdom on which better methods of treatment have been founded. One could hardly ask for a more rewarding experience.     

Right Atrial-ventricular Dissociation and Entrainment while Pacing from High Right Atrium and Coronary Sinus during Circus Movement Tachycardias

Thirteen patients with circus movement tachycardias (CMT) were studied. Twelve had left-sided, and one, right-sided, accessory pathways. Entrainment was possible during overdrive high right atrial stimulation in 13/13 patients, and during coronary sinus pacing in 10/12 patients. The minimal pacing rates required for this to occur were 10 to 31 beats/min faster than those of the tachycardias. Short episodes of right atrial-ventricular dissociation occurred while pacing from the high right atrium (6/13 patients), but not from the coronary sinus (0/13 patients). It is possible to explain this phenomenon by postulating the existence of two distinct atrioventricular (AV) nodal inputs (one for right-sided and the other for left-sided impulses); it could also have been an expression of the close distance existing between the AV node and the coronary sinus. Entrainment, by defining a range of pacing rates followed by resumption of the tachycardia upon the cessation of stimulation, indicated that faster rates were needed for the CMT to be interrupted. However, regardless of the pacing rate and pacing site, tachycardia termination occurred when an anterograde impulse was blocked at the AV node. The information obtained from this study suggests that some patients with drug-resistant CMT may benefit from pacing modes capable of terminating the arrhythmia "through entrainment" at the slowest atrial rate at which this is possible.     

Computer Model of the Atrioventricular Node Predicts Reentrant Arrhythmias

Introduction: Following atrial premature beats, the AV node may exhibit sustained reentrant tachyarrhyth-mias, isolated echo beats, or discontinuities in the recovery curve (the plot of conduction time versus atrial cycle length). A computer model was used to examine the hypothesis that spatial variation of AV nodal passive electrical resistance may account for these phenomena. Methods and Results: A computer model of a rectangular lattice of elecirotonically linked elements whose ionic kinetics simulated nodal ionic flux was developed. the model showed that there exists a resistance value that minimizes the effective refractory period, because high resistance prevents depolarization of distal elements, while low resistance allows leakage of depolarizing current by electrotonic transmission, preventing activation of proximal elements. High resistances stabilized reentry by slowing conduction. Simulations incorporating equal resistance values between elements predicted increased AV nodal conduction times with increasing prematurity of atrial impulses. A model with a gradual change in resistance between fibers produced discontinuities and tachycardia, but not both simultaneously. Uniform anisotropy produced preferential transverse block, leading to echo beats and “fast-slow” tachycardia, but not recovery curve discontinuities. Nonuniform anisotropy could produce reentry, but tachycardia often occurred without discontinuities. Dividing the lattice into two electrotonically linked parallel pathways with different resistance values (“dual pathway model”) predicted recovery curve discontinuities, echo beats, and tachycardia. At critical atrial cycle lengths, only the (high resistance) slow pathway conducted antegradely, while the fast pathway conducted retrogradely, to generate the typical “slow-fast” tachycardia. Responses of the dual pathway model to ablation were consistent with clinical data, including the previous observation of a decrease in fast pathway effective refractory period after slow pathway ablation. Conclusion: Differences in passive electrical resistance of electrotonically linked dual pathways within the AV node may account for functional longitudinal dissociation, reentrant arrhythmias, and responses to catheter ablation therapy.     

Pacemaker-mediated Tachycardias: A New Modality of Treatment

Three Patients with pacemaker interactive drug resistant tachycardia underwent invasive electrophysiological studies. In the first patient, the retrograde conduction of the artificial reciprocating tachycardia was provided by two right-sided accessory pathways and the antegrade conduction by an atrial synchronous plus generator. In addition, AV nodal tachycardia occurred alternately. In the second patient with intermittent atrial flutter, the AV node and, coincidentally, an AV sequential pulse generator provided high-rate antegrade conduction to the ventricles. In the third patient with surgical complete heart block, intermittent AV-nodal tachycardia induced retrograde atrial activation while an atrial synchronous pacemaker provided the antegrade conduction. Electrode catheter exploration of the heart allowed localization and closed-chest ablation of the accessory pathways or AV node by delivering two to seven 200-Joule direct-current shocks through the appropriate electrode of the exploring catheter, Thereby, pacemaker-mediated arrhythmias could be controlled in these patients in the follow-up of 6 to 8 months.     

Rapid AV Nodal Re-entrant Tachycardias Presenting with Syncope or Pre-syncope: Use of Eiectrophysioiogicai Studies to Select Therapy

Five patients with recurrent syncope or pre-syncope due to rapid supraventricular tachycardias underwent electrophysiological study. In each patient, an AV nodal re-entrant tachycardia could be induced. By leaving a coronary sinus catheter in place, the effects of drugs on the ability to induce tachycardia could be tested on sequential days. Drug effects were highly variable, but in each patient it was possible to determine a drug which prevented induction of tachycardia. Patients treated with this drug have had no recurrent symptoms or tachycardias with a followup of 4-21 months. Although AV nodal re-entry is highly dependent on autonomic tone, electrophysiological study appears to be a useful means of selecting therapy in patients with severe, symptomatic tachycardias.     

V-A block during atrioventricular nodal reentrant tachycardia: reentry confined to the AV node

Retrograde block during atrioventricular (AV) nodal reentrant tachycardia is considered a rare phenomenon that can potentially occur in the AV node or in the atrium. A patient with slow-fast AV nodal reentrant tachycardia and transient VA block localized in the AV node is presented. Pharmacological and stimulation maneuvers identified the site of block in the AV node and not in the atrium. Thus, AV nodal reentry can be confined to the AV node.     

Multiple Anterograde and Retrograde AV Nodal Pathways: Demonstration by Multiple Discontinuities in the AV Nodal Conduction Curves and Echo Time Intervals

Programmed electrical cardiac stimulation was performed in a 40-year-old man with documented recurrent, sustained ventricular tachycardia which was refractory to standard medical therapy. Both the presence of several discontinuities in the AV nodal conduction curves during atrial and ventricular stimulation and the time intervals of the AV nodal echo phenomena suggested the presence of multiple AV nodal pathways. The results of this study are of interest in further increasing our understanding of the electrophysiologic behavior of the human AV node.     

Unmasking of Retrograde Conduction by Isoproterenol in a Concealed Accessory Pathway

A 52-year-old female with no structural heart disease presented with a right bundle branch block (RBBB)/right axis deviation tachycardia with a cycle length of 300 msec. P waves were not discernible on the surface ECG. Baseline electrophysiology study in the drug-free state revealed no evidence for anterograde or retrograde conducting accessory pathways (APs) or for dual AV node physiology. Retrograde VA block with AV dissociation was present at a ventricular paced cycle length of 600 msec (sinus cycle length of 635–700 msec). AV nodal Wenckebach occurred during decremental atrial pacing at a cycle length of 300 msec. During isoproterenol administration, a left lateral AP with retrograde only conduction became manifest with 1:1 VA conduction to 380 msec. No anterograde AP conduction was present. Orthodromic reciprocating tachycardia with a cycle length of 285–315 msec was easily induced. We conclude that total functional conduction block can exist in APs, and unmasking of total conduction block can be accomplished with isoproterenol. All patients with undiagnosed tachycardias should have full repeat stimulation studies during adrenergic stimulation if the initial baseline evaluation is nondiagnostic.