Atrial Ectopy Originating from the Posteroinferior Atrium During Radiofrequency Catheter Ablation of Atrioventricular Nodal Reentrant Tachycardia

Atrial ectopy sometimes appears during RF ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, its origin, characteristics, and significance are still unclear. To examine these issues, we analyzed 67 consecutive patients with AVNRT (60 with slow-fast AVNRT and 7 with fast-slow AVNRT), which was successfully eliminated by RF ablation to the sites with a slow potential in 63 patients and with the earliest activations of retrograde slow pathway conduction in 4 patients. During successful RF ablation, junctional ectopy with the activation sequence showing H-A-V at the His-bundle region appeared in 52 patients (group A) and atrial ectopy with negative P waves in the inferior leads preceding the QRS and the activation sequence showing A-H-V at the His-bundle region appeared in 15 patients (group B). Atrial ectopy was associated with (10 patients) or without junctional ectopy (5 patients). Before RF ablation, retrograde slow pathway conduction induced during ventricular burst and/or extrastimulus pacing was more frequently demonstrated in group B than in group A (9/15 [60%] vs 1/52 [2%], P < 0.001). Successful ablation site in group A was distributed between the His-bundle region and coronary sinus ostium, while that in group B was confined mostly to the site anterior to the coronary sinus ostium. In group B, atrial ectopy also appeared in 21% of the unsuccessful RF ablations. In conclusion, atrial ectopy is relatively common during slow pathway ablation and observed in 8% of RF applications overall and 22% of RF applications that successfully eliminated inducible AVNRT. Atrial ectopy appears to be closely related to successful slow pathway ablation among patients with manifest retrograde slow pathway function.     

Inducible atrioventricular nodal reentrant echo behind organic 2:1 infra-hisian block during sinus rhythm

A 77-year-old male patient with an intermittent 2:1 infra-Hisian block during sinus rhythm was presented with dizziness and near-syncope. During electrophysiological (EP) study, dual atrioventricular (AV) nodal pathways and retrograde fast pathway were easily induced by atrial and ventricular programmed stimulation, respectively. A typical slow-fast AV nodal reentrant echo beat also could be demonstrated by single atrial extrastimulation. Atrioventricular nodal reentrant tachycardia (AVNRT) can occasionally exhibit 2:1 AV block. Conversely, AV nodal reentry property had been rarely reported behind 2:1 infra-Hisian block. The EP presentation from this case may support the notion that tissues below the His are not part of the reentrant circuit of AVNRT.     

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.     

Double Atrial and Double Ventricular Responses During Slow-Fast Fast-Slow Atrioventricular Nodal Reentrant Tachycardia

A case was described with fast-slow form of atrioventricular nodal reentrant tachycardia as related with simultaneous fast and slow pathway conduction both antegrade and retrograde. Fast-slow form of tachycardia was induced by premature right atrial stimulation or incremental right ventricular pacing when the last paced beat conducted to the atria via both fast and slow pathways of the atrioventricular node causing double atrial response. Fast-slow form of tachycardia was spontaneously shifted to slow-fast form when the atrial echo, possibly through the retrograde intermediate pathway, was conducted antegradely over the fast and slow pathways simultaneously, producing double ventricular response.     

Specificity of Retrograde Conduction in Screening for Atrioventricular Nodal Reentrant Tachycardia

Baseline AV conduction properties (antegrade and retrograde) are often used to assess the presence of dual AV nodal physiology or concealed AV accessory pathways. Although retrograde conduction (RET) is assumed to be a prerequisite for AV nodal reentrant tachycardia (AVNRT), its prevalence during baseline measurements has not been evaluated. We reviewed all cases of AVNRT referred for radiofrequency ablation to determine the prevalence of RET at baseline evaluation and after isoproterenol infusion. Results: Seventy-three patients with AVNRT underwent full electrophysiological evaluation. Sixty-six patients had manifest RET and inducible AVNRT during baseline atrial and ventricular stimulation. Seven patients initially demonstrated complete RET block despite antegrade evidence of dual AV nodal physiology. In 3 of these 7 patients AVNRT was inducible at baseline despite the absence of RET. In the other four patients isoproterenol infusion was required for induction of AVNRT, however only 3 of these 4 patients developed RET. One of these remaining patients had persistent VA block after isoproterenol. Conclusions: The induction of AVNRT in the absence of RET suggests that this is not an obligatory feature of this arrhythmia. Therefore, baseline AV conduction properties are unreliable in assessing the presence of AVNRT and isoproterenol infusions should be used routinely to expose RET and reentrant tachycardia.     

Fast pathway ablation in a patient with PR prolongation

The classical form of typical atrioventricular node reentrant tachycardia (AVNRT) is a “slow-fast” pathways tachycardia, and the usual therapy is an ablation of the slow pathway since it carries a low risk of atrioventricular (AV) block. In patients with long PR interval and/or living on the anterograde slow pathway, an alternative technique is required. We report a case of a 42-year-old lady with idiopathic restrictive cardiomyopathy, persistent atrial fibrillation status post pulmonary vein isolation, and premature ventricular complex ablation with a systolic dysfunction, who presented with incessant slow narrow complex tachycardia of 110 bpm that appeared to be an AVNRT. Her baseline EKG revealed a first-degree AV block with a PR of 320 ms. EP study showed no evidence of anterograde fast pathway conduction. Given this fact, the decision was to attempt an ablation of the retrograde fast pathway. The fast pathway was mapped during tachycardia to its usual location into the anteroseptal region, then radiofrequency ablation in this location terminated tachycardia. After ablation, she continued to have her usual anterograde conduction through slow pathway and the tachycardia became uninducible. In special populations with prolonged PR interval or poor anterograde fast pathway conduction, fast pathway ablation is the required ablation for typical AVNRT.     

Fulguration for AV Nodal Tachycardia: Results in 42 Patients with a Mean Follow-Up of 23 Months

HAISAGUERRE, M., ET AL.: Fulguration for AV Nodal Tachycardia: Results in 42 Patients with a Mean Follow-Up of 23 Months. This report describes a catheter ablation technique to treat atrioventricular nodal reentrant tachycardia while preserving anterograde conduction, and its application in 42 patients with drug-refractory repetitive episodes of tachycardia. One of these patients had common and reverse forms of tachycardia. Using atrial activation in the His-bundle lead as a reference, the optimal ablation site was selected by positioning an electrode catheter to obtain a synchronous or earlier atrial activation than the reference during tachycardia. At this site, His-bundle deflection was completely absent, or was present at a low amplitude (< 0.1 mV). In the majority of patients, these criteria were found in the immediate vicinity of the site of proximal His-bundle recording (adjacent to the reference catheter). Shocks of 160 or 240 joules (J) were delivered at this site (mean ± SD = 518 ± 392 J/session) with a resulting preferential abolition of impairment of fast retrograde conduction. Anterograde conduction, though modified, was preserved in all patients, except for four (10%) patients who remained in complete heart block. Thirty patients (70%) remained free of arrhythmia without medication or pacemaker for a mean follow-up period of 23 ± 13 (2–63) months. Six other patients (15%) were controlled with a previously ineffective medication.     

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.     

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.     

Pacemaker-like syndrome complicating slow pathway ablation for AV nodal reentrant tachycardia

This case report describes pacemaker-like syndrome after successful slow pathway ablation for atrioventricular (AV) nodal reentrant tachycardia due to recurrence of single AV nodal echo beats during sinus rhythm. The resultant AV dyssynchrony was responsible for the symptom complex. Following ablation of retrograde ventriculoatrial conduction, the AV nodal echo beats were eliminated and the pacemaker-like syndrome resolved.     

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.     

Relation between the AH interval and the ablation site in patients with atrioventricular nodal reentrant tachycardia

The determinants of slow pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT) are still unknown, and great differences in the AH interval during slow pathway conduction are observed between patients. In 35 patients with typical AVNRT who underwent successful slow pathway ablation (defined as complete elimination of dual pathway physiology), the A2H2 interval at the "jump" during programmed atrial stimulation and the AH interval during AVNRT (as a reflection of slow pathway conduction time) and the fluoroscopic distance between the successful ablation site and the His-bundle recording site and between the coronary sinus ostium (CSO) and the His-bundle recording site were determined. The mean (+/- SEM) AH interval during slow pathway conduction was 323 +/- 12 ms with programmed stimulation and 310 +/- 10 ms during AVNRT. The mean number of energy applications was 8 +/- 1 (range 1-21). The mean distances between (1) the successful ablation site and the His bundle recording site and (2) between the CSO and the His-bundle recording site were 24 +/- 1 and 28 +/- 1 mm in the RAO and 23 +/- 1 and 28 +/- 1 mm in the LAO projections, respectively. The AH interval during slow pathway conduction correlated significantly with the distance between the successful ablation site and the His-bundle (P < 0.001) but not with the distance between CSO and His-bundle recording site. There is a significant correlation between the AH interval during slow pathway conduction and the distance of the successful ablation site from the His bundle. This relationship (1) suggests that, in addition to functional factors, anatomic factors influence slow pathway conduction and (2) may be helpful in determining the initial energy application site during slow pathway ablation.     

A Direct Midseptal Approach to Slow Atrioventricular Nodal Pathway Ablation

Objectives: The purpose of this study was to describe a midseptal approach to selective slow pathway ablation for the treatment of AV nodal reentrant tachycardia (AVNRT). In addition, predictors of success and recurrence were evaluated. Methods: Selective ablation of the slow AV nodal pathway utilizing radiofrequency (RF) energy and a midseptal approach was attempted in 60 consecutive patients with inducible AVNRT. Results: Successful slow pathway ablation or modification was achieved in 59 of 60 patients (98%) during a single procedure. One patient developed inadvertent complete AV block (1.6%). A mean of 2,7 ±1.4 RF applications were required with mean total procedure, ablation, and fluoroscopic times of 191± 6.3, 22.8 ± 2.3, and 28.2 ±1.8 minutes, respectively. The PR and AH intervals, as well as the antegrade and retrograde AV node block cycle length, were unchanged. However, the fast pathway effective refractory period was significantly shortened following ablation (354± 13 msec vs 298 ± 12 msec; P= 0.008). The A/V ratio at successful ablation sites were no different than those at unsuccessful sites (0.22 ± 0.04 vs 0.23± 0.03). Junctional tachycardia was observed during all successful and 60 of 122 (49%) unsuccessful RF applications (P < 0.0001). A residual AV nodal reentrant echo was present in 15 of 59 (25%) patients, During a mean follow-up of 20.1± 0.6 months (11.5–28 months) there were four recurrences (5%), 4 of 15 (27%) in patients with and none of 44 patients without residual slow pathway conduction (P = 0.002). Conclusions: A direct midseptal approach to selective ablation of the slow pathway is a safe, efficacious, and efficient technique. Junctional tachycardia during RF energy application was a highly sensitive but not specific predictor of success and residual slow pathway conduction was associated with a high rate of recurrence.     

Diagnostic Approach to Narrow Complex Tachycardia with VA Block

Narrow complex tachycardia with VA block is rare. The differential diagnosis usually consists of (1) junctional tachycardia (JT) with retrograde block: (2) AV nodal reentrant tachycardia (AVNRT) with proximal common pathway block; and finally (3) nodofascicular tachycardia using the His-Purkinje system for antegrade conduction and a nodofascicular pathway for retrograde conduction. Analysis of tachycardia onset and termination, the effect of bundle branch block on tachycardia cycle length, and the response to atrial and ventricular premature depolarization must be carefully done. Making the correct diagnosis is crucial as the success rate in eliminating the tachycardia will depend on tachycardia mechanism.     

Catheter Ablation for Recurrent Tachyarrhythmias. Clinical Experience with Two Different Techniques of Ablation in 21 Patients

Between 1984 and 1988, 21 patients underwent catheter ablation for drug refractory arrhythmias. Nine patients presented atrial flutter, atrial fibrillation or atrial tachycardia, nine had supraventricular tachycardia (one AV nodal reentrant tachycardia, one reciprocating tachycardia due to concealed accessory pathway and seven XMPW syndrome). Three had ventricular tachycardia. Fourteen patients were treated with direct current shock ablation (DC) and seven patients with radiofrequency ablation (RF). Eight patients underwent ablation of the His bundle. In six patients permanent AV block could be induced and in two first-degree AV block. All became asymptomatic (two with additional antiarrhythmic drug therapy). In four patients with WPW syndrome DC ablation of the accessory pathway was attempted. In one patient a permanent block in the accessory pathway and in another an intermittent block were obtained. In the two remaining patients with accessory pathways the ablation failed to interrupt the retrograde conduction in one the retrograde conduction was modified: however, in the other no change could be demonstrated. Two patients underwent ventricular foci ablation, with one partial success (arrhythmia controlled with associated drug therapy) and one failure. Three patients had RF His bundle ablation (two for atrial flutter and one for atrial fibrillation). One complete atrioventricular block, one first degree AV block and one first degree AV block associated with right bundle branch block were induced. Recurrence of tachyarrhythmias was prevented only in the patient with complete atrioventricular block. RF ablation of accessory pathway was performed in three patients. It resulted in anterograde block in the accessory pathway in the first patient; a slight modification of the retrograde refractory period in the second and no change was noted in the last one. The first of these three patients could then be controlled with drug therapy. The other two patients underwent surgical dissection of the pathway. One patient underwent an unsuccessful attempt of ventricular focus ablation with RF energy. Complications were more common with DC than with RF ablation but serious ventricular arrhythmias were also observed during RF ablation. Thus, DC ablation was completely successful in eight of 14 patients (57%), partially successful with the addition of drug therapy in three patients (21%) and failed in 22%. HF ablation was successful in only one patient (14.5%) and partially successful in another one (14.5%). This relatively low success rate is due in part to the design of the device and the electrodes used in this study. With technical improvements of RF ablation it seems reasonable to expect that this method will play a significant role in the management of drug refractory arrhythmias, since RF ablation, when compared to DC ablation, has the major advantage not to require general anesthesia during the procedure.     

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.     

Radiofrequency catheter ablation therapy of swallowing-induced atrioventricular nodal reentrant tachycardia: report of two cases

We describe two patients who presented with a history of recurrent palpitations on swallowing of solid food. The event-recorder and Holter monitoring documented episodic supraventricular tachycardia (SVT) initiated by atrial premature contractions (APCs). During electrophysiological study (EPS), swallowing of solid food consistently induced APCs and their activation sequence, morphology of P wave were suggestive of their right atrial origin in them. Drug challenge did not affect the APC onset during the swallowing. During EPS, slow-fast variety of atrioventricular nodal reentrant tachycardia (AVNRT) was induced and successful radiofrequency (RF) catheter ablation of slow pathway resulted in total relief of their symptoms.     

Double Ventricular Responses to a Single Atrial Depolarization in a Patient with Dual AV Nodal Pathways

Electrophysiological study was performed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). Double ventricular responses through dual AV nodal pathways were observed by atrial extrastimulus technique followed by initiation of AVNRT. The difference in conduction time between the slow and fast AV nodal pathways was longer than 320 msec. A ventricular extrastimulus delivered during sinus rhythm, which was not followed by ventriculoatrial conduction, also induced AVNRT. These findings indicated the presence of an antegrade critical delay and retrograde block in the slow AV nodal pathway, criteria necessary for the occurrence of a double ventricular response.     

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.     

Transvenous Ablation with High Frequency Energy for Atrioventricular Junctional (AV Nodal) Reentrant Tachycardia

We performed transcatheter AV junction ablation with high frequency energy in four patients with AV nodal reentrant tachycardia where extensive trials of several antiarrhythmic drugs failed to prevent further recurrences of tachycardia. Initially high frequency catheter ablation induced complete AV block in all patients. A recuperation of AV 1:1 conduction followed some time later, persisting in follow-up. No complications have been encountered in either the acute phase or the follow-up (from 6 to 8 months; mean +/- SD: 8.7 +/- 2.5 months). The electrophysiological study was carried out 6 weeks following ablation, and all patients showed AV 1:1 conduction. No dual nodal pathway was encountered and no tachycardia could be triggered. With refinement of the method, the potential application of high frequency energy to interrupt intranodal or perinodal connections responsible for reentrant supraventricular tachycardia or to retard AV nodal conduction appears promising.