Effect of Dual Atrioventricular Node Pathways on Atrioventricular Reentrant Tachycardia
Background Dual atrioventricular (AV) node pathway physiology is frequently observed in patients with AV accessory pathways.
Methods and Results To examine the implications of this, we identified 36 patients (19 men and 17 women; mean±SD age, 30±13 years) with both phenomena. The 36 patients had 48 accessory pathways. Twenty-seven patients had bidirectional and 9 had unidirectional accessory pathways. Of the 34 patients with inducible atrioventricular reentry, 17 used the slow and 11 used the fast anterograde AV node pathway exclusively during AV reentrant tachycardia, whereas 6 patients used both the fast and the slow AV node pathways. AV node reentrant tachycardia was inducible in addition to AV reentry in 7 patients. Both the cycle length and AH intervals were significantly longer during slow pathway–dependent (cycle length, 411±58 milliseconds [ms]; AH, 229±42 ms) than during fast pathway–dependent (cycle length, 322±40 ms; AH, 121±25 ms; P<.05) reentrant tachycardias. Two patients had only AV node reentrant tachycardia inducible despite the presence of the accessory pathway. Four patients with technically difficult accessory pathways were managed by AV node modification with slow pathway (3) or fast pathway (1) ablation. Three of them remained free of symptoms 7, 14, and 25 months after the procedure whereas 1 patient had recurrence of arrhythmia.
Conclusions AV reentrance with dual AV node pathways frequently depends exclusively on either the slow or the fast AV node pathway for clinical tachycardia. This may provide additional options for ablation in technically difficult cases when the accessory pathway is not otherwise problematic.
Dual atrioventricular (AV) node pathway physiology is known to occur in 8% to 40%1 2 3 4 of patients with accessory AV pathways, leading to a variety of possible reentrant circuits.5 6 7 8 9 10 11 To examine the implications for radiofrequency ablation, we evaluated the contribution of the fast and slow AV node pathways and accessory pathways in a consecutive series of patients assessed for arrhythmia associated with the Wolff-Parkinson-White syndrome.
We reviewed the records of 382 consecutive patients with accessory AV pathways who were referred for electrophysiological testing between January 1, 1990, and August 31, 1993, because of documented paroxysmal supraventricular tachycardia or palpitations. We identified 43 patients (12%) who also had dual antegrade AV node pathway physiology or AV node reentrance. In 7 patients, no tachycardia was inducible during electrophysiological testing; these patients were excluded from further study. The remaining 36 patients (19 men and 17 women; mean±SD age, 30±13 years) were the subjects of the present study.
The study protocol has been described.12 13 Briefly, standard electrode catheters were positioned in the coronary sinus, the right ventricular apex, the high right atrium, and at the His bundle region. Programmed stimulation was performed at twice diastolic threshold with 2-millisecond (ms) square-wave pulses. Atrial and ventricular extrastimulus testing at two cycle lengths (600 and 400 ms) was performed until atrial and ventricular refractoriness was reached. Atrial and ventricular incremental pacing was performed until AV and ventriculoatrial block occurred, respectively. If reentrant tachycardia was not inducible with these techniques, burst pacing and double atrial or ventricular extrastimuli were tried as well as isoproterenol and atropine administration. After radiofrequency ablation, the above protocol was repeated 30 minutes after the last energy application, with extrastimulus testing usually performed at at least one cycle length (600 ms).
The criteria used for the diagnosis of AV reentry and AV node reentry have been described.13 Dual AV node pathways required at least a 50-ms increment in the AH interval for a 10-ms decrement in coupling interval during atrial extrastimulus testing. AV node reentrance manifested as either AV node echo cycles or AV node reentrant tachycardia. When antegrade conduction over the accessory pathway masked antegrade conduction over the fast AV node pathway, the diagnosis of dual AV node pathways was based on the test performed after successful accessory pathway ablation.
Participation of the slow or fast AV node pathway as the antegrade limb of AV reentrant tachycardia was determined by comparison of the AH interval during tachycardia with that observed during slow AV node pathway conduction with atrial extrastimuli, incremental pacing, or AV node reentry. Tachycardia induced by atrial extrastimuli after the discontinuity (“jump”) in the AH interval was considered to use the slow AV node pathway for antegrade conduction.
Radiofrequency ablation immediately followed the diagnostic study. For accessory pathway ablation,14 radiofrequency current was applied between the 4-mm tip electrode of the ablation catheter and a backplate. Ablation was not temperature controlled. The duration of ablation attempts ranged between 10 and 45 seconds. If loss of preexcitation was not observed during the first 10 seconds of energy delivery, current was discontinued. AV node modification was performed using an anatomic approach.15 The operative ablation of accessory pathways16 and operative AV node modification17 have been described.
Mean AH intervals and tachycardia cycle lengths were compared using Student’s t test. Two distinct AH intervals and tachycardia cycle lengths due to a switch between fast and slow AV node pathways within an episode of tachycardia were considered as two distinct tachycardias for statistical purposes.
The 36 patients had a total of 48 accessory pathways. There was a preponderance of left lateral and posteroseptal14 pathways as is usually found in patients with Wolff-Parkinson-White syndrome. The accessory pathway was unidirectional in 9, conducting retrogradely only in 8, and conducting anterogradely only in 1. Typical discontinuous curves relating AH interval to prematurity of an atrial extrastimulus (dual pathways) were observed in 26 of 36 patients (72%). AV node reentry was observed in 26 patients with single echo cycles observed in 17 and sustained AV node reentrant tachycardia in 9 patients. Ten patients had dual AV node pathways without AV node reentrance.
Dual pathway physiology or AV node reentrance was observed before ablation in 24 patients. This diagnosis was made by presence of dual AV node pathways (n=8), alternation of AH intervals during AV reentry (n=6), induction of sustained AV node reentrant tachycardia (n=7), or observation of single AV node reentrant cycles (n=3). The diagnosis was made only after ablation of the accessory pathway in 12 patients. This was manifest as single AV node echo cycles (n=8), dual pathways (n=2), or sustained AV node reentrant tachycardia (n=2).
The most common arrhythmia was AV reentry without coexistent AV node reentry (27 patients [75%]; Table⇓). Two (6%) patients had only AV node reentry, whereas 7 (19%) had both AV reentry and AV node reentry. Of the 34 patients with AV reentry, 17 used the slow and 11 used the fast anterograde AV node pathway exclusively, whereas 6 used both the slow and the fast AV node pathways alternately (Figs 1⇓ and 2⇓).
Use of the fast or slow anterograde AV node pathway influenced the cycle length of AV reentrant tachycardia, and, as expected, this was related to the AH interval (Figs 3⇓ and 4⇓). The cycle length of tachycardia in patients using the fast AV node pathway anterogradely was shorter than that in patients using the slow pathway (mean±SD, 322±40 versus 411±58 ms, respectively; P<.001). The AH interval was shorter in AV reentry using the fast pathway than that using the slow pathway (121±25 versus 229±42, P<.001).
The coexistence of dual AV node pathways and AV node reentrance with AV tachycardia resulted in spontaneous termination of tachycardia in some patients. This occurred as a result of the occurrence of a long–short cycle with block in the AV node or accessory pathway of the subsequent cycle. Alternatively, the occurrence of AV node reentrant atrial echo cycles sometimes terminated AV reentry (Fig 5⇓).
Accessory pathway bystander participation in AV node reentrant tachycardia was potentially possible in 6 patients where the anterograde refractory period of the accessory pathway permitted accessory pathway conduction at the cycle length of tachycardia. However, this was not observed in any of the study patients, suggesting that this phenomenon is usually limited by concealed retrograde conduction into the accessory pathway.
Most patients underwent accessory pathway ablation by either catheter14 or surgery.16 One patient had a failed accessory pathway ablation. Three patients had both radiofrequency accessory pathway ablation and slow AV node pathway ablation. Three patients had only slow AV node pathway radiofrequency ablation. The latter patients had AV reentry dependent on slow AV node pathway conduction and the accessory pathway was not considered to be otherwise problematic. None of these patients had inducible arrhythmia at conclusion of the procedure despite intact accessory pathway conduction. One patient had multiple tachycardias including AV node reentry and both antidromic and orthodromic reentry related to two accessory pathways. Fast AV node pathway ablation done inadvertently during an attempt at slow pathway ablation was performed and resulted in noninducibility of tachycardia despite intact accessory pathway conduction in both directions.
All patients with initially successful accessory pathway ablation remain free of tachycardia during a mean follow-up of 21.3 months (range, 7 to 49 months). Of the 3 patients undergoing slow AV node pathway ablation, 2 are free of tachycardia after 25 and 7 months, and 1 had recurrence after 14 months. The latter patient was found to have persistent dual AV node pathways and inducible AV reentrant tachycardia and subsequently underwent both slow AV node pathway ablation and accessory pathway ablation. The patient undergoing fast AV node pathway ablation has not had recurrence of tachycardia and persists with anterograde preexcitation and anterograde slow AV node pathway conduction (14 months).
Results of the present study confirm the relatively frequent (12%) coexistence of dual AV node pathways in patients with manifest or concealed Wolff-Parkinson-White syndrome previously reported to be between 8% and 40%.1 2 3 4 The coexistence of dual AV node pathways in this context had significant effects on the manifestations of tachycardia with some practical therapeutic implications pertaining to radiofrequency ablation. Some patients with the Wolff-Parkinson-White pattern electrocardiographically only had inducible AV node reentrant tachycardia with no relation of clinical tachycardia to the manifest preexcitation. Others had both inducible AV reentry and AV node reentry. Most patients had AV reentry as the only tachycardia mechanism, with the majority requiring either the slow anterograde AV node pathway (56%) or the fast anterograde AV node pathway (30%) exclusively as the anterograde limb of the reentrant circuit. These observations highlight the importance of a detailed diagnostic study before therapeutic radiofrequency ablation18 to ensure that ablation is not directed against a clinically insignificant accessory pathway. The observations also permit alternate therapeutic options in patients with AV reentry, ie, slow or fast AV node pathway ablation in selected patients in whom accessory pathway ablation is technically difficult and anterograde accessory pathway conduction is not problematic. It may be argued that slow AV node pathway ablation is preferred in some of these individuals as a technically simpler and more expedient procedure than accessory pathway ablation. The ideal candidate for this preferred approach would have clinical AV reentry dependent on the slow AV node pathway and an accessory pathway with a long anterograde refractory period.
The observation of two populations of AH intervals during AV reentrant tachycardia in this study was related to dual AV node pathway physiology (Figs 1⇑ and 2⇑). However, alternating AH intervals may be observed in the absence of dual pathways,19 20 and this may be related to functional oscillation of the AH interval between two points on the curve relating AH interval to prematurity of atrial extrastimuli. In the present study, the presence of variable AH intervals within a given episode of tachycardia contributed to spontaneous termination of tachycardia in some patients.
The AH interval during AV reentrant tachycardia was found to be a reliable indicator for the presence of anterograde slow or fast AV node pathway conduction. The longest AH interval during tachycardia using the fast AV node pathway was 160 ms, whereas the AH interval was never less than 180 ms in patients using the slow anterograde AV node pathway. These data suggest that an AH interval during AV reentrant tachycardia of longer than 180 ms may raise the suspicion of anterograde slow pathway conduction. The observation also underscores the difficulty of attempting to distinguish AV node reentrant tachycardia from AV reentrant tachycardia by cycle length alone since patients using slow pathway conduction anterogradely may well have cycle lengths similar to patients with typical AV node reentry.
In conclusion, the frequent occurrence of dual AV node pathway conduction underscores the importance of detailed electrophysiological assessment before and after ablation of an accessory pathway. Although there is therapeutic relevance for only a small segment of the total population with the Wolff-Parkinson-White syndrome, alternative ablation strategies directed at the AV node may be considered in individuals when clinical tachycardia depends on either the slow or the fast AV node pathway and the accessory pathway is not otherwise problematic. Appropriate therapy will also be carried out in those presenting with sustained AV node reentry as the exclusive or concomitant clinical arrhythmia. The absence of clinical tachycardia during follow-up in those with only dual pathway physiology with or without single echo cycles would argue against the routine ablation of the slow pathway in these patients.
- Received September 29, 1994.
- Revision received December 1, 1994.
- Accepted December 3, 1994.
- Copyright © 1995 by American Heart Association
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