Fast-Slow Type of Atrioventricular Nodal Reentrant Tachycardia: Horizontal Dissociation of the AV Node During Tachycardia

Two patients with recurrent supraventricular tachycardia are presented. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. In patient 1 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response. In patient 2 the ventriculoatrial conduction was not observed. In both patients, the unchanged atrial cycle length during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia the first AH interval was shorter than the subsequent HA interval. In patient 2 verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (280 mg/day) suppressed the tachycardia in patient 1. These findings suggest that the mechanism of tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has tendency to show incessant form.     

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.     

Automatic Tachycardia Recognition

A microcomputer algorithm for tachycardia identification, suitable for use in un implanted antitachycardia pacemaker, is described. The system employs an atrial and ventricular electrogram, detects a sustained fast rate in either chamber, and awakens the main program to perform detailed analysis of the tachycardia and its immediately preceding beats. The algorithm distinguishes atrial, ventricular, and AV nodal and re-entrant tachycardia from high rates due to sinus tachycardia. For testing of the program, we used a data base of twenty-two tape-recorded and documented arrhythmias provoked during electrophysiologic studies in which atrial and ventricular bipolar electrodes were in place; twenty-one of twenty-two wave successfully detected. These included atrial fibrillation, atrial flutter, atrial tachycardia, AV nodal re-entrant tachycardia, AV re-entrant tachycardia using an accessory pathway, and ventricular tachycardia with and without ventriculo-atrial conduction.     

Sinus Node Modification Using Radiofrequency Current in a Patient with Persistent Inappropriate Sinus Tachycardia

Radiofrequency catheter modification of the sinus node for persistent inappropriate sinus tachycardia has not been previously reported. This article describes a patient in whom radiofrequency current was used to ablate an incessant automatic tachycardia focus mapped to the region of the sinus node, where a discrete multicomponent electrogram demonstrating earliest atrial activation was recorded. A transient junctional rhythm developed immediately after ablation, with rapid subsequent emergence of a stable rhythm having normal sinus nodal characteristics.     

Sinus Node Reentrant Tachycardia

This review article discusses the electrophysiological basis of sinus node reentry, clinical features of sinus node reentry, and the management of this uncommon tachycardia with drugs and ablative therapy. It also proposes the use of the term "sinoatrial reentrant tachycardia" for this form of tachycardia.     

Coincident Idiopathic Left Ventricular Tachycardia and Atrioventricular Nodal Reentrant Tachycardia: Control by Radiofrequency Catheter Ablation of the Slow Atrioventricular Nodal Pathway

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.     

Incessant Atrio‐Ventricular Node Reentrant Tachycardia Induced by Unapparent Dual Atrio‐Ventricular Node Conduction

We present the case of a patient with incessant slow‐fast atrio‐ventricular (AV) node reentrant tachycardia induced by dual AV node conduction with aborted conduction to the ventricles. The unapparent conduction over the slow pathway was suspected here because of spontaneous nodal echoes without QRS complexes occurring during sinus rhythm, manifested as isolated premature atrial beats and which repetitively induced the tachycardia.     

AV Node Reentry Tachycardia in Infants

The purpose of this study was to determine the frequency of atrioventricular (AV) node reentry tachycardia in infants undergoing transesophageal electrophysiological study for paroxysmal tachycardia. The records of all 52 infants < 1-year-old with structurally normal hearts who underwent transesophageal study for paroxysmal tachycardia over a 3-year period were reviewed. Those with a diagnosis of AV node reentry tachycardia underwent complete data review, and follow-up of > 12 months was obtained. Six of 52 infants had a diagnosis of the common type of AV node reentry tachycardia. Tachycardia was diagnosed at a mean age of 2.1 months (range 1 day to 10 months), and 3 of 6 underwent transesophageal study within the first month. Although no patient had structural heart disease, three patients had significant noncardiac disease. Follow-up of 15–38 months (mean 24 ± 7.8) revealed recurrences in 2 of 6 patients. The mean tachycardia cycle length was 240 ms (range 200–310 ms), and the transesophageal ventriculoatrial intervals ranged from < 30 to 55 ms. All patients had an inducible reentrant tachycardia with a ventriculoatrial interval that remained constant even when tachycardia cycle length increased following verapamil or adenosine administration, or decreased following isoproterenol infusion. Five of 6 had evidence for discontinuous AV node conduction curves. In our patients the substrate for AV node reentry tachycardia was present early in life, and AV node reentry tachycardia can be a clinical problem even in the newborn period.     

Atrial Tachycardia as a Proarrhythmic Effect of Radiofrequency Catheter Ablation for Atrioventricular Nodal Reentrant Tachycardia

Radiofrequency catheter ablation is now the first line treatment for atrioventricular nodal reentrant tachycardia. The success rate is high with a low incidence of complications. However, a possible proarrhythmic effect of radiofrequency energy has been rarely reported and no study has demonstrated a direct correlation between the anatomic site of the radiofrequency application and the origin of a new post‐ablation arrhythmia. We present a case of a focal atrial tachycardia that occurred after slow pathway radiofrequency catheter ablation for atrial nodal reentrant tachycardia and originating close to the previous ablation site. This tachycardia was successfully treated with a second ablation session. (PACE 2011; 34:e33–e37)     

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.     

Physiology of "Atypical" Atrioventricular Junctional Reentrant Tachycardia Occurring Following Radiofrequency Catheter Modification of the Atrioventricular Node

The physiology of atypical atrioventricular junctional reentrant tachycardia (AVJRT) occurring following catheter modification of the AV node is poorly defined. Six patients undergoing radiofrequency current catheter modification of the AV node had inducible atypical AVJRT before or after AV nodal modification. Typical AVJRT was differentiated from atypical AVJRT by a ventriculoatrial (VA) time < 60 msec in the His-bundle electrogram recording. Five of six patients had typical AVJRT and two had atypical AVJRT prior to AV nodal modification. Following anterior approach AV nodal modification, previously undetected atypical AVJRT was induced in four patients. Earliest retrograde atrial activation in the posterior septum was documented in all patients with atypical AVJRT prior to modification and in three of four patients with atypical AVJRT following modification. The AH intervals during tachycardia were 320 +/- 52 msec in typical AVJRT, 88 +/- 33 msec in the premodification atypical AVJRTs, and 172 +/- 12 msec in the postmodification atypical AVJRTs (P = 0.0001). The AH/HA ratios were 4.1 +/- 0.9 in typical AVJRT, 0.5 +/- 0.2 in the premodification atypical AVJRTs, and 0.9 +/- 0.2 in the postmodification atypical AVJRTs (P = 0.0001). Two patients with postmodification atypical AVJRT underwent further posterior approach AV node modification that resulted in VA block. One patient with postmodification atypical AVJRT had further anterior approach AV nodal modification that resulted in heart block. The retrograde limb of the atypical AVJRT seen following anterior approach AV nodal modification is a posterior, slow pathway.     

Sustained "Slow-Fasf" and "Fast-Slow" AV Nodal Re-entrant Tachycardia in a Patient with Recurrent Supraventricular Tachycardia

A case is presented of a 21-year-old woman with recurrent paroxysmal supraventricular tachycardia. Eleclrophysioiogic study demonstrated the presence of both antegrade and retrograde dual AV nodal conduction pathways and both conventional slow-fast and atypical fast-slow forms of the AV nodal re-entrant tachycardia could be induced. Both tachycardias were successfully suppressed with a combination of digoxin and verapamil.     

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.     

Narrow Complex Tachycardia with VA Block: Diagnostic and Therapeutic Implications

To review our experience with cases of narrow complex tachycardia with VA block, highlighting the difficulties in the differential diagnosis, and the therapeutic implications. Prior reports of patients with narrow complex tachycardia with VA block consist of isolated case reports. The differential diagnosis of this disorder includes: automatic junctional tachycardia, AV nodal reentry with final upper common pathway block, concealed nodofascicular (ventricular) pathway, and intra-Hissian reentry. Between June 1994 and January 1996, six patients with narrow complex tachycardia with episodes of ventriculoatrial block were referred for evaluation. All six patients underwent attempted radiofrequency ablation of the putative arrhythmic site. Three of six patients had evidence suggestive of a nodofascicular tract. Intermittent antegrade conduction over a left-sided nodofascicular tract was present in two patients and the diagnosis of a concealed nodofascicular was made in the third patient after ruling out other tachycardia mechanisms. Two patients had automatic junctional tachycardia, and one patient had atroventricular nodal reentry with proximal common pathway block. Attempted ablation in the posterior and mid-septum was unsuccessful in patients with nodofascicular tachycardia. In contrast, those with atrioventricular nodal reentry and automatic junctional tachycardia readily responded to ablation. The presence of a nodofascicular tachycardia should be suspected if: (1) intermittent antegrade preexcitation is recorded, (2) the tachycardia can be initiated with a single atrial premature producing two ventricular complexes, and (3) a single ventricular extrastimulus initiates SVT without a retrograde His deflection. The presence of a nodofascicular pathway is common in patients with narrow complex tachycardia and VA block. Unlike AV nodal reentry and automatic junctional tachycardia, the response to ablation is poor.     

Sinus Node Reentrant Tachycardia in a Neonate

A neonate presented with paroxysmal atrial tachycardia. Transesophageal electrophysiological study demonstrated sinus node reentrant tachycardia, which was induced and terminated with programmed electrical stimulation. The tachycardia would also terminate in the atrium with adenosine. Empiric digoxin treatment successfully suppressed the tachycardia which then recurred with discontinuation of the digoxin at 6 weeks. The child was retreated with digoxin with no further recurrences for 18 months. Transesophageal electrophysiological study at 20 months showed prolonged sinus node recovery times and no inducible arrhythmias. The child has remained free of arrhythmias at 4 years.     

Radiofrequency Catheter Ablation of Sinus Node Reentrant Tachycardia

Sinus node reentrant tachycardia is a relatively uncommon (5%-5%) form of recurrent paroxysmal supraventricular tachycardia (SVT). We describe a case of symptomatic sinus node reentrant tachycardia in a 67-year-old male with ischemic heart disease, congestive heart failure, and depressed ventricular function. Adenosine administered during an electrophysiology study caused prolongation of the tachycardia cycle length due to atrial cycle length prolongation (without atrio-His prolongation) prior to tachycardia termination. Right atrial mapping revealed the earliest site of atrial activation in the high lateral right atrium just below the superior vena cava. Low energy (10 and 20 W) radiofrequency lesions were applied ai this site with termination of the tachycardia within 3 seconds of radiofrequency energy delivery. Tachycardia could not be reinduced after delivery of the radiofrequency lesions. The sinus node function immediately and 6 weeks after radiofrequency catheter ablation remained normal and the patient was without clinical recurrence of SVT. Mapping of sinus node reentrant tachycardia and elimination of the reentrant circuit with radiofrequency catheter ablation is possible without causing sinus node dysfunction. Adenosine causes prolongation of the atrial cycle length followed by termination of sinus node reentrant tachycardia.     

Atrial Tachycardia Mimicking Atrioventricular Nodal Reentry Tachycardia

Background

The term supraventricular tachycardia (SVT) is used to describe tachydysrhythmias that require atrial or atrioventricular nodal tissue for their initiation and maintenance. SVT can be used to describe atrioventricular nodal reentry tachycardia, atrioventricular reentry tachycardia, and atrial tachycardia (AT). AT is the least common of these SVT subtypes, accounting for only 10% of cases. Although the suggested initial management of each SVT subtype is different, they all can present with similar symptoms and electrocardiographic findings.

Objective

Discuss the pathophysiology, diagnosis, and treatment of AT as compared with other types of SVT.

Case Report

We report a 56-year-old woman with symptoms and electrocardiographic findings consistent with SVT. Although standard treatment with intravenous adenosine failed to convert the SVT, it revealed AT as the cause of the tachydysrhythmia. The AT was successfully terminated with beta-blockade and the patient eventually underwent successful radioablation of three separate AT foci.

Conclusions

AT frequently mimics other more common forms of SVT. AT might be recognized only when standard treatment of SVT has failed. Identification of AT in this setting is crucial to allow for more definitive therapy.     

Atrioventricular Dissociation During Paroxysmal Junctional Tachycardia

We describe the rare occurrence of atrioventriculor dissociation in three patients during paroxysmal functional tachycardia. The mechanism of tachycardia was atrioventricular nodal reentry in two patients. The third patient had reentrant tachycardia that utilized the A V node for at least part of the reentrant circuit. This patient also had a nodoventricular pathway that may have participated in the reentrant circuit. In two patients, ventricular tachycardia was diagnosed prior to electrophysiologic assessment and medication to prevent tachycardia was not successful. After electrophysiological studies, treatment directed at suppressing AV nodel reentry prevented recurrent tachycardia. These case studies demonstrate the importance of detailed electrophysiological assessment of tachycardia in patients whose arrhythmia does not respond to empirical antiarrhythmic therapy. (PACE, Vol. 4, November-December, 1981)     

Inappropriate Sinus Tachycardia Following Radiofrequency Ablation of AV Nodal Tachycardia: Incidence and Clinical Significance

The incidence and consequences of inappropriate sinus tachycardia following modification of the AV nodal area with radiofrequency energy were prospectively studied in a consecutive series of 118 patients. Twelve (10%) patients developed this complication, which persisted less than 1 week in all but three patients. Inappropriate sinus tachycardia was only observed after fast pathway ablation. Only four patients required temporary treatment with a beta blocker.     

Profound Hypotension Due to Slow Atrioventricular Nodal Pathway Conduction during Atrial Tachycardia

Paroxysmal supraventricular tachycardia (SVT) may have a variety of hemodynamic effects depending on rate, patient volume status, and presence of structural heart disease or left bundle branch block. We report a case of a patient with atrial tachycardia and dual atrioventricular (AV) nodal physiology who developed profound hypotension during transition from fast to slow AV nodal pathway conduction, despite similar tachycardia cycle length. This case illustrates the potential importance of AV timing in determining the hemodynamic effect of SVT.