Termination of Atrioventricular Nodal Reentrant Tachycardia by Premature Stimulation From Ablating Catheter
A Reliable Guide to Identify Site for Slow-Pathway Ablation
Background Slow-pathway ablation is currently used more frequently to control atrioventricular nodal reentrant tachycardia (AVNRT). However, in patients with the common type of AVNRT, successful ablation of the slow pathway can be difficult and time-consuming. We tested a simple method to predict a site for slow-pathway ablation in patients with AVNRT of the common variety.
Methods and Results Twenty patients with symptomatic common AVNRT (13 women and 7 men; mean age, 41±21 years) were included in the study. Once the AVNRT had a stable cycle length (±10 ms) for at least 20 cycles, single extrastimuli were delivered from the ablating catheter tip beginning with 20 ms less than the tachycardia cycle length and decrementing by 10 ms until tachycardia terminated or loss of capture occurred at the pacing site. The pacing protocol was performed systematically in a stepwise fashion at four adjacent sites starting from the posterior/inferior interatrial septum near the tricuspid annulus and moving progressively more anteriorly. The pacing protocol was then repeated in the same sequence, followed by delivery of radiofrequency current at each site to determine its effect at sites where AVNRT could not be terminated with a pacing protocol. AVNRT could be terminated in the anterograde direction from at least one site in 19 patients. Tachycardia could be terminated at two or more adjacent sites in 5 patients. The longest atrial coupling interval at the site of tachycardia termination was 67±27 ms (range, 30 to 130 ms) less than the AVNRT cycle length. Resetting of subsequent His bundle depolarization (H2), producing an H-H2 interval prolongation of 26±24 ms (range, 10 to 80 ms), occurred in 17 patients before termination of the tachycardia. In 18 of the 19 patients, the slow pathway was successfully ablated at the site at which AVNRT was terminated at the longest atrial coupling interval.
Conclusions Termination of tachycardia in the anterograde direction at the longest atrial coupling interval by extrastimuli delivered from the ablating catheter can be helpful for identification of an optimal site for slow-pathway ablation in patients with the common variety of AVNRT.
Atrioventricular nodal reentrant tachycardia (AVNRT) is one of the most common paroxysmal forms of supraventricular tachycardia.1 2 3 Intracardiac electrogram recordings and programmed electrical stimulation have helped a great deal in improving our understanding of this arrhythmia. The evolution of this knowledge has led to the development of rational therapy, including transcatheter ablation using radiofrequency energy for control of AVNRT.4 5 6 7 8 9 10 11 12
To modify the AV node, slow-pathway ablation is currently performed more frequently as the initial approach.9 10 11 12 Identification of a specific ablation site is possible when retrograde conduction via the slow pathway can be demonstrated or slow-pathway potential is recorded.9 10 11 12 In patients with common AVNRT, however, retrograde slow-pathway conduction is seldom demonstrable, and recording of slow-pathway potential may be time-consuming. A stepwise approach seems more practical and therefore is frequently used, but it often necessitates several blind lesions; hence the need for a better method.10
In this study, we examined the role of slow intranodal pathway penetration of programmed atrial extrastimuli to guide the optimal site for slow-pathway ablation. The purpose of this report is to present our findings and suggest a potential therapeutic role of this relatively simple approach.
Twenty patients with AVNRT of the common variety (slow-fast) were included in the study. The mean age (±SD) of these patients was 41±21 years (range, 18 to 81 years); 7 were men and 13 were women. All patients had a history of recurrent palpitations ranging in duration from 6 months to 50 years. One patient also had a history of recurrent syncope. One patient had coronary artery disease. None of these patients had coexistent AV accessory pathways. The inclusion criteria for patients with AVNRT in this study were (1) induction of sustained AVNRT of the common variety by programmed electrical stimulation and (2) a stable cycle length of tachycardia varying by no more than 10 ms over 20 consecutive beats. Patients who also had AVNRT of the uncommon variety in which the slow pathway could be mapped in the retrograde direction were excluded from the study.
Before the catheter ablation and after informed consent was obtained, each patient underwent a complete electrophysiological evaluation in a postabsorptive state. All antiarrhythmic medications were discontinued for at least five half-lives before the study. Patients were anesthetized with intravenous diprivan. Three quadripolar electrode catheters were introduced percutaneously via femoral veins and positioned under fluoroscopic guidance in the high right atrium, the His bundle region, and the right ventricular apex. A fourth 6F decapolar electrode catheter was inserted via a jugular vein and positioned in the coronary sinus. Surface ECG leads (I, II, and V1), intracardiac electrograms, and time lines were displayed simultaneously on a multichannel oscilloscope (PPG Midas system, Biomedical) and printed on a thermal recorder. Programmed electrical stimulation was performed with a programmable digital stimulator (Bloom Associates). The stimulation protocol consisted of atrial and ventricular incremental pacing and extrastimulation. The induction of AVNRT was attempted repeatedly to determine the most reliable and reproducible method of tachycardia initiation. The stimulation protocol was repeated after isoproterenol was infused and titrated in patients in whom AVNRT could not be induced at baseline. In patients requiring isoproterenol administration, all electrophysiological parameters (before and after ablation) were measured during isoproterenol infusion at the same infusion dose. Intravenous heparin was administered as an initial dose of 3000 U and subsequent boluses of 1000 U/h during the procedure. Each patient underwent a follow-up study 1 day and 6 to 8 weeks after the ablative procedure.
Pacing was initiated from the radiofrequency catheter tip at twice diastolic threshold. Before initiation of the AVNRT, catheter contact and pacing threshold were determined by pacing from the catheter tip during sinus rhythm. After tachycardia initiation, single extrastimuli were delivered with increasing prematurity, beginning with a coupling interval 20 ms less than the tachycardia cycle length. The coupling interval was then decreased by 10-ms decrements until one of two outcomes occurred: tachycardia was terminated, or there was a loss of capture at the pacing site due to atrial refractoriness.
The pacing protocol used in this study followed a stepwise approach used in our laboratory for ablation of the slow pathway.10 As shown in Fig 1⇓ (right anterior oblique [30°] radiographic view), the region extending from the most posterior portion of tricuspid annulus adjacent to the coronary sinus ostium to the His bundle recording site was divided into posterior (P), medial (M), and anterior (A) sites. In each case, the following steps were taken to position the ablation catheter. (1) The catheter was positioned at the His bundle region to record the most distal His bundle potential. (2) While the deflectable tip was fully bent, the catheter was slowly withdrawn along the tricuspid septal annulus down to the most posterior/inferior aspect of the interatrial septum adjacent to the coronary sinus ostium (site P). This site was considered optimal for testing if the bipolar recording obtained from the distal electrode showed an A/V electrogram ratio of 0.1 to 0.5. After initiation of tachycardia, the pacing protocol was performed systematically in a stepwise fashion starting from the posterior/inferior interatrial septum near the tricuspid annulus. Sites more anterior to the M region (ie, sites A1 and A2) were not tested. These posterior and medial sites were chosen because of our cumulative experience showing successful outcome of slow-pathway ablation at these sites without significant risk of AV nodal block.10 12 To assess whether radiofrequency pulses delivered at the sites at which pacing failed to terminate the tachycardia were able to eliminate the tachycardia, the ablating catheter was repositioned at the posterior/inferior aspect of the interatrial septum. The pacing protocol was repeated in the same order as above (ie, P1, P2, M1, and M2, in that order), and irrespective of whether or not single extrastimuli delivered from the ablating catheter tip terminated the tachycardia, this was followed by delivery of radiofrequency current. Programmed stimulation was performed after each delivery of radiofrequency current to assess inducibility of AVNRT. If tachycardia was induced, the catheter tip was advanced more anteriorly to the next adjacent site in a stepwise fashion. The pacing protocol was repeated before delivery of each radiofrequency current.
Radiofrequency current was delivered between the distal electrode of the ablating catheter and an external adhesive patch electrode (Scotchplate 1149C, 3M Co) placed on the chest. The radiofrequency ablation unit was a Radionics RFG-3C lesion generator. The ablation catheter was a 7F deflectable quadripolar catheter with a 4-mm bulbous-tip electrode (Webster). In each site, one pulse of radiofrequency energy (30 to 35 W for 20 to 50 seconds) was delivered before the catheter was placed in a new site.
Programmed stimulation was repeated at 30 minutes and 1 day after a successful ablation. Complete electrophysiological studies were performed 6 to 8 weeks after the procedure in patients with successful results. Isoproterenol infusion was routinely used when baseline study could not initiate AVNRT. All patients underwent two-dimensional echocardiography/Doppler studies 1 day after the procedure to look for any complications.
Definition of Terms
All intervals were measured from the onset of local electrograms. At least two H-H intervals were measured before and after the pacing stimulus. All tachycardia cycles are labeled Ae and H for atrial and corresponding His deflection. The atrial and His deflections in response to the extrastimulus (S2) are designated A2 and H2, respectively. The criteria used to verify AVNRT (common variety) have been discussed in detail before and were used for the purpose of this study as well.10 The H-to-H2 interval change was considered to have occurred if H-H2 minus H-H was at least 10 ms different. The relation between Ae-A2 (prematurity) and corresponding H-H2 throughout the coupling zone was also measured at each pacing site.
Sustained AVNRT of the common variety (cycle length, 325±42 ms) was induced in all patients (Table⇓) either during baseline study (15 patients) or after isoproterenol infusion (5 patients). Dual-pathway physiology was demonstrated in 16 patients during the electrophysiology study.
Termination of AVNRT by Premature Extrastimuli
In 19 patients, AVNRT terminated in the anterograde direction by premature extrastimuli delivered from the tip of the ablating catheter (Figs 2 through 4⇓⇓⇓). In 14 patients, AVNRT was terminated at only one of the four sites tested by the atrial extrastimuli. In 5 patients (patients 1 through 5), tachycardia was terminated at two adjacent sites. In 1 patient (patient 12), the tachycardia was terminated at three adjacent sites. AVNRT cycle length, the longest atrial coupling interval (Ae-A2) at which the tachycardia was terminated by the atrial extrastimuli, and the sites are given in the Table⇑. The longest atrial coupling intervals (Ae-A2) that resulted in tachycardia termination measured 67±27 ms (range, 30 to 130 ms) less than the tachycardia cycle length. In the 5 patients (patients 1 through 5) in whom termination was noted from two adjacent sites, the longest atrial coupling interval causing tachycardia termination from the two sites differed by 62±19 ms (range, 40 to 60 ms). In the only patient (patient 12) in whom the tachycardia was terminated from three sites, the longest atrial coupling intervals from the three sites were 270, 240, and 210 ms, respectively. In the remaining patient (patient 8) with AVNRT cycle length of 250 ms, the tachycardia was not terminated by the extrastimuli at any of the four sites.
AVNRT could not be induced in 18 patients after delivery of radiofrequency current at the site at which termination of AVNRT was accomplished at the longest atrial coupling interval. Only 2 of these patients had single AV nodal reentrant echo beat inducible after ablation despite isoproterenol infusion; hence, no further lesions were given. The mean power of the pulse that abolished the tachycardia was 32±8 W for 35±10 seconds. The total number of pulses given was 3±1 (range, 1 to 5). The mean procedure time was 131±35 minutes (range, 81 to 209 minutes). In 4 of the 5 patients with termination of tachycardia at two adjacent sites, radiofrequency current delivered at the sites of termination with shorter atrial coupling intervals (which were posterior to the sites of termination with longer coupling intervals) did not abolish the tachycardia. In 1 patient, tachycardia was not inducible after ablation at the site of termination with a shorter coupling interval, 40 ms shorter and posterior to the site of termination with the longest coupling interval; hence, the effect of radiofrequency current at the site of termination with the longer coupling interval could not be evaluated. In the remaining patient whose tachycardia was not terminated, a stepwise approach was used and the slow pathway was ablated after four radiofrequency pulses. Thus, overall, at 18 sites at which pacing terminated the tachycardia, a single radiofrequency pulse was successful in eliminating the tachycardia. On the contrary, at 26 other sites at which radiofrequency pulses were given in this study and pacing either did not terminate the tachycardia or the tachycardia was terminated at shorter coupling intervals as well, the radiofrequency pulses were ineffective in eliminating the tachycardia. The shortest cycle length of 1:1 AV conduction prolonged from 293±30 to 367±48 ms (P<.001) after slow-pathway ablation. AV nodal effective refractory period also prolonged, from 245±30 to 298±53 (P<.01) ms. The AH interval and shortest cycle length of 1:1 ventriculoatrial (VA) conduction remained unchanged.
H-H2 Response to Ae-A2
While the H-H2 interval was 10 ms shorter (compared with H-H) in 2 patients before termination of the tachycardia, H-H2 interval prolongation (mean, 26±24 ms; range, 10 to 80 ms) occurred in 17 patients at the site of termination with the longest coupling interval (Table⇑). Figs 2 through 4⇑⇑⇑ show examples of various types of resetting responses in patients 9, 10, and 17. Fig 5⇓ shows H-H2 response to Ae-A2 at the four sites tested in patients 9 and 10. In these two patients, an H-H2 interval prolongation was observed at the site of successful slow-pathway ablation. At other sites, there was minimal H-H2 interval prolongation or no change, or H2 occurred earlier than expected. Of the 17 patients with H-H2 interval increase before termination of the tachycardia, no H-H2 interval change was observed in 13 patients at longer atrial coupling intervals. In four patients, H2 activation occurred earlier by 10 ms at longer coupling intervals, followed by an H-H2 interval increase at shorter coupling intervals. Fig 4⇑ is a graphic demonstration of such a response in patient 17.
None of the patients had inducible AVNRT at 1-day and 6- to 8-week follow-up electrophysiology study. During a mean follow-up of 6±3 months, no patient had clinical evidence of tachycardia. Echocardiography done 1 day after the ablation showed no evidence of any complications.
In this study, the termination of AVNRT at the longest coupling interval by premature stimulation from the ablating catheter tip identified the site for successful slow-pathway ablation. It was indeed the slow pathway that was ablated in all of these patients, because after ablation, (1) AVNRT could not be induced; (2) PR and AH intervals remained unchanged; and (3) the shortest cycle length of 1:1 AV conduction and (4) AV nodal effective refractory period were significantly prolonged in all patients.
Previous reports have suggested that the slow pathway can be successfully ablated by either identification of slow-pathway potentials or use of a stepwise approach.9 10 Alternatively, when retrograde slow-pathway conduction can be demonstrated, mapping of the earliest atrial activation can also lead to a successful outcome. This latter approach, although ideal in patients with uncommon (fast-slow) AVNRT, is seldom an option in patients with common AVNRT, because retrograde fast-pathway conduction does not permit evaluation of retrograde slow-pathway propagation even if present. However, in many patients, retrograde atrial activation via the slow pathway may not be demonstrable, even if retrograde fast-athway block was achieved. This indeed was the case in 77% of the patients who underwent retrograde fast-pathway ablation during our earlier experience.10 In the absence of demonstrable retrograde slow-pathway conduction to the atria or identifiable slow-pathway potentials, the anatomic approach remains the only practical method for slow-pathway ablation.
This study, therefore, highlights a rather simple and reliable method of identifying the site for successful slow-pathway ablation in patients with AVNRT of the common variety. At the site of termination of AVNRT with the longest coupling interval, a successful ablation of the slow pathway was achieved in 18 of the 19 patients.
Significance of Resetting by Extrastimuli
Introduction of premature stimuli during AVNRT may reset the tachycardia if the premature impulse penetrates the reentrant circuit.13 14 15 By definition, the resetting phenomenon is considered to have occurred if the H-H2 interval is different from the AVNRT cycle length. Once the A2 impulse penetrates the AVNRT and resets the tachycardia, A2 is likely to terminate the tachycardia on further shortening of the coupling intervals (Ae-A2), unless loss of atrial capture is encountered. However, the ability to reset and/or terminate tachycardia depends on the tachycardia cycle length, size of the excitable gap, and distance and conduction time from the site of stimulation to the tachycardia circuit.16 17 18 Single extrastimuli delivered from high atrial sites rarely terminate AVNRT, particularly when the tachycardia is rapid. Uniform resetting and termination of tachycardia with atrial extrastimuli and subsequent successful slow-pathway ablation suggest proximity of the ablating catheter tip to the reentrant circuit at those sites. From these posterior and midseptal sites, intranodal penetration of A2 was possible in all except 1 patient with relatively rapid tachycardia (cycle length, 250 ms).
All of the resetting responses observed in this study can be explained on the basis of excitable gap and recovery properties of the tissue encountered by A2. A progressive increase in the A2-H2 and consequently H-H2 intervals at progressively shorter Ae-A2 intervals suggests incomplete recovery of the slow pathway during propagation of A2 in the orthodromic direction. Its block in the orthodromic direction will result in tachycardia termination. In the presence of a larger excitable gap, more complete recovery of the slow pathway from prior impulse and A2 penetration farther downstream could conceivably result in A2-H2 (and H-H2) shortening, as observed in some patients. In all of the above scenarios, the A2 impulse in all likelihood also propagated in the antidromic direction to a variable degree along the slow pathway, resulting in either block or collision with oncoming reentrant impulse.
Limitations of the Study
The reason for the difference in successful site among various patients remains unexplained. The location of slow pathways, or atrial approaches to the slow pathways, may vary among different individuals. Furthermore, this study also cannot address the precise location or exact relation of the ablating electrodes to the slow pathway. The catheter positions were determined fluoroscopically, and the original pacing sites and the subsequent ablation sites might therefore not be exactly the same, although fluoroscopically these were in similar regions. One can also argue as to whether ablation from sites other than those chosen on the basis of resetting responses might have been equally successful. This is unlikely, however, because other radiofrequency lesions were applied along the posterior and midseptal area and were not successful in abolishing AVNRT. Lesions outside the zone selected here are seldom effective for ablation of the slow pathway. It is conceivable that in some patients, multiple atrial inputs into the slow pathway may exist, in which case ablation of single or several adjacent sites is unlikely to abolish AVNRT. Notwithstanding the above criticisms, the slow-pathway ablation approach guided by the ease of A2 penetration of the AV node as detailed here seems logical and is successful. This represents an improvement over the existing anatomic approaches to slow-pathway ablation.
Summary and Clinical Implications
This study highlights a simple and reliable approach to localizing the site for successful slow-pathway ablation by use of the response to extrastimuli from the ablating catheter tip. If the tachycardia can be terminated at a given site, tachycardia termination from other sites should be attempted. The site at which the AVNRT termination occurs with the longest atrial coupling interval is where initial radiofrequency current should be applied. This approach should minimize the number of radiofrequency pulses by identifying the site for successful slow-pathway ablation in patients with common AVNRT. A randomized study comparing this method with previously published methods such as a purely anatomic approach, mapping of slow-pathway potentials, and “inferior” or “midseptal” approach may be useful to compare the number of radiofrequency pulses, procedure time, and complications in patients undergoing slow-pathway ablation in patients with AVNRT.
- Received July 21, 1994.
- Revision received September 19, 1994.
- Accepted October 2, 1994.
- Copyright © 1995 by American Heart Association
Goldreyer BN, Damato AN. The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation. 1971;43:679-687.
Epstein LM, Scheinman MM, Langberg JJ, Chilson D, Goldberg HR, Griffin JC. Percutaneous catheter modification of the atrioventricular node: a potential cure for atrioventricular nodal reentrant tachycardia. Circulation. 1989;80:757-768.
Goy JJ, Fromer M, Schlaepfer J, Kappenberger L. Clinical efficacy of radiofrequency current in the treatment of patients with atrioventricular node reentrant tachycardia. J Am Coll Cardiol. 1990; 16:418-423.
Lee MA, Morady F, Kadish A, Schamp DJ, Chin MC, Scheinman MM, Griffin JC, Lesh MD, Pederson D, Goldberger J. Catheter modification of the atrioventricular junction with radiofrequency energy for control of atrioventricular nodal reentry tachycardia. Circulation. 1991;83:827-835.
Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, Moulton KP, Twidale N, Hazlitt H, Prior MI. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med. 1992;327:313-318.
Jazayeri MR, Hempe SL, Sra JS, Dhala AA, Blanck Z, Deshpande SS, Avitall B, Krum DP, Gilbert CJ, Akhtar M. Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia. Circulation. 1992;85:1318-1328.
Kay GN, Epstein AE, Dailey SM, Plumb VJ. Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia: evidence for involvement of perinodal myocardium within the reentrant circuit. Circulation. 1992;85:1675-1688.
Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S, Dhala A. Atrioventricular nodal reentry: clinical, electrophysiological, and therapeutic considerations. Circulation. 1993;88:282-295.
Schuger CD, Steinman RT, Lehmann MH. The excitable gap in atrioventricular nodal reentrant tachycardia: characterization with ventricular extrastimuli and pharmacologic intervention. Circulation. 1989;80:324-334.
Rosenthal ME, Miller JM, Josephson ME. Demonstration of an excitable gap in the common form of atrioventricular nodal reentrant tachycardia. J Electrophysiol. 1987;1:334-342.
Almendral JM, Stamato NJ, Rosenthal ME, Marchlinski FE, Miller JM, Josephson ME. Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap. Circulation. 1986;74:722-730.
Josephson ME. Resetting and entrainment of ventricular tachycardia associated with infarction: clinical and experimental studies. In: Josephson ME, Wellens HJJ, eds. Tachycardias: Mechanisms and Management. Mount Kisco, NY: Futura Publishing Co, Inc; 1993:505-536.