Author + information
- Received February 19, 1996
- Revision received May 2, 1996
- Accepted May 13, 1996
- Published online October 1, 1996.
- FRANK BOGUN1,
- BRADLEY KNIGHT,
- RAUL WEISS,
- MARWAN BAHU,
- RAJIVA GOYAL,
- MARK HARVEY,
- EMILE DAOUD,
- K.CHING MAN,
- S.ADAM STRICKBERGER and
- FRED MORADY*
- ↵*Address for correspondence: Dr. Fred Morady, University of Michigan Medical Center, 1500 East Medical Center Drive, B1F245, Ann Arbor, Michigan 48109-0022.
Objectives. The purpose of this study was to assess the clinical efficacy of radiofrequency ablation of the slow pathway in patients with documented but noninducible paroxysmal supraventricular tachycardia (PSVT) who have evidence of dual atrioventricular (AV) node pathways.
Background. Patients with a documented history of PSVT at times do not have inducible PSVT in the electrophysiology laboratory. Because dual AV node pathways serve as the substrate for AV node reentrant tachycardia (AVNRT), ablation of the slow pathway potentially may be useful in these patients.
Methods. The subjects in this prospective study were seven consecutive patients who underwent an electrophysiologic procedure because of documented PSVT and were found to have dual AV node physiology or inducible single AV node echo beats, but no inducible PSVT despite the administration of isoproterenol and atropine. Their mean (±SD) age was 33 ± 13 years, and they had been symptomatic for 12 ± 12 years. The frequency of the episodes of PSVT ranged from ≥1/day to 1/month. The rate of the documented episodes ranged from 170 to 260 beats/min, and discrete P waves were not apparent. Slow pathway ablation was performed with 9 ± 4 applications of radiofrequency energy using a combined anatomic and electrogram mapping approach.
Results. All evidence of dual AV node pathways was eliminated in six patients, and dual AV node physiology remained present in one patient. During a mean follow-up period of 15 ± 10 months (range 8 to 27), no patient had a recurrence of symptomatic tachycardia (success rate 95% confidence interval 65% to 100%).
Conclusions. Slow pathway ablation may be clinically useful in patients with documented but noninducible PSVT who have evidence of dual AV node pathways.
Patients who have had documented episodes of paroxysmal supraventricular tachycardia (PSVT) at times do not have inducible tachycardia in the electrophysiology laboratory [1, 2]. The presence of dual atrioventricular (AV) node pathways, which serve as the substrate for AV node reentrant tachycardia (AVNRT), suggests a possible predilection for this type of tachycardia. Furthermore, AVNRT may not always be reproducibly inducible. Accordingly, an American College of Cardiology/American Heart Association (ACC/AHA) task force report on guidelines for clinical electrophysiologic and catheter ablation procedures concluded that evidence of dual AV node pathways in patients with a history of PSVT tachycardia who do not have inducible tachycardia in the electrophysiology laboratory may be an indication for slow pathway ablation . However, evidence of dual AV node pathways may be present in individuals who have never had PSVT [4, 5], and no previous studies have demonstrated or assessed the value of slow pathway ablation in patients with documented but noninducible PSVT. Therefore, the purpose of this prospective study was to assess the clinical efficacy of slow pathway ablation in patients with documented episodes of PSVT who do not have inducible tachycardia but who have evidence of dual AV node pathways.
Characteristics of subjects. The study subjects included seven consecutive patients who met the following criteria: recurrent episodes of PSVT documented by an electrocardiographic (ECG) recording; the absence of inducible PSVT both in the baseline state and after the administration of isoproterenol and atropine; the absence of any evidence of an accessory pathway; the presence of a slow AV node pathway, as manifested by either dual AV node physiology or AV node echo beats. During the time that these seven patients were recruited for this study, 324 other patients with a history of PSVT underwent an electrophysiologic procedure and were found to have inducible AVNRT.
The clinical characteristics of the seven patients in this study are described in Table 1. There were five women and two men with a mean (±SD) age of 33 ± 12 years. They had been symptomatic from PSVT for 12 ± 12 years. The incidence of episodes of PSVT ranged from at least once per day to once per month, with the duration of episodes ranging from 5 min to 4 h. Three patients had a history of syncope in association with an episode of PSVT. Based on a physical examination, a 12-lead ECG, and an echocardiogram, none of the patients had any evidence of structural heart disease.
Within the 5 years before the electrophysiologic procedure, five patients had required 13 ± 23 (range 1 to 60) emergency room visits because of persistent episodes of PSVT. In three of these patients, the tachycardia was terminated by either adenosine or verapamil administered intravenously. In the other two patients, the tachycardia terminated spontaneously before the administration of medication. In these five patients, the PSVT was recorded on a 12-lead ECG or rhythm strip (Fig. 1). In the other two patients, at least one episode of PSVT was documented with a Holter monitor or a continuous loop recorder (Fig. 2). The rate of the documented episodes of PSVT ranged from 170 to 260 beats/min, and discrete P waves were not apparent. A mean of 3 ± 3 antiarrhythmic medications had been prescribed before referral. Before referral, three patients already had undergone one electrophysiologic test, which had demonstrated no inducible PSVT.
Electrophysiologic testing and catheter ablation. Electrophysiologic tests were performed in the postabsorptive state after written informed consent was obtained and after antiarrhythmic drug therapy had been discontinued for at least 5 half-lives. Three 7F quadripolar electrode catheters were inserted in a femoral vein and positioned in the high right atrium, the His bundle position, and the right ventricle. Leads V1, I, II and III and the intracardiac electrograms were recorded on a Mingograph-7 recorder (Siemens, Solna, Sweden). Pacing was performed with a programmable stimulator (Bloom Associates).
Atrial and ventricular overdrive pacing and programmed stimulation were performed to determine the conduction and refractoriness properties of the AV node, to rule out the presence of an accessory pathway and to induce supraventricular tachycardia. Attempts to induce supraventricular tachycardia by atrial and ventricular overdrive pacing and programmed stimulation were repeated during a 2- to 8-μg/min infusion of isoproterenol titrated to result in a sinus rate of 120 to 130 beats/min, and again after the intravenous administration of 0.8 to 1.5 mg of atropine. In accordance with the selection criteria for this study, none of the patients had inducible PSVT or evidence of an accessory pathway, but all patients had evidence of dual AV node pathways. This evidence consisted of either dual AV node physiology, defined as an increment of 50 ms or more in the A2H2 interval in association with a 10-ms decrement in the A1A2 interval [6, 7], or the presence of AV node echo beats. Atrioventricular node echo beats were defined as reproducible echo beats during programmed atrial stimulation which were coincident with the QRS complex, which had a concentric pattern of atrial activation and which occurred with prolongation of the A2H2 interval to ≥200 ms (Fig. 3).
Radiofrequency catheter ablation of the slow pathway was performed with a catheter that had a 4-mm distal electrode and a deflectable tip (Mansfield EP or EP Technologies) using a combined anatomic and electrogram mapping approach . Radiofrequency energy was delivered at 500 kHz as a continuous sine wave at power settings of 5 to 50 W (EP Technologies). The end point of the ablation procedure was the elimination of slow pathway function, manifested as elimination of either dual AV node physiology or prolonged A2H2 intervals associated with AV node echo beats, both before and during the infusion of isoproterenol.
Follow-up. The patients were seen in an outpatient clinic 3 months after the ablation procedure. The follow-up period ranged from 8 to 27 months, at which point all patients were interviewed by telephone regarding recurrence of tachycardia-related symptoms.
Statistical analysis. Continuous variables are expressed as the mean value ± SD and were compared using a t test for paired variables. The McNemar test was used to compare the incidence of dual AV node pathways before and after slow pathway ablation.
Using the Student t test, the AV block cycle length, the AV node effective refractory period and the ventriculoatrial block cycle length among the seven study subjects were compared with the corresponding values in a concurrent group of 34 consecutive patients who underwent an electrophysiologic procedure for PSVT and who were found to have inducible AVNRT in the baseline state.
Atrioventricular node properties. The mean AV block cycle length, the AV node effective refractory period and the ventriculoatrial block cycle length in the seven patients in this study are shown in Table 2. These values did not differ significantly from the corresponding values in 34 other patients who did have inducible AVNRT (Table 2).
Before ablation, each of the seven patients had dual AV node physiology or single AV node echo beats, or both, either in the baseline state or during isoproterenol infusion (Table 3).
Slow pathway ablation. A mean of 9 ± 4 applications of radiofrequency energy (mean duration 49 ± 13 s) were delivered at a mean power of 36 ± 7 W. The mean fluoroscopy time was 20 ± 7 min. No complications occurred during the procedure. The electrophysiologic measurements before and after slow pathway ablation are displayed in Table 3. All evidence of dual AV node pathways was eliminated in six patients. The maximal A2H2 interval in these patients decreased from 313 ± 43 to 200 ± 39 ms (p = 0.06). One patient had persistent slow pathway function manifested as dual AV node physiology without AV node echo beats.
Follow-up. None of the patients has been treated with any antiarrhythmic medications or has had symptomatic tachycardia during a mean follow-up period of 15 ± 10 months (range 8 to 27, success rate 95% confidence interval 65% to 100%).
Main findings. The results of this study demonstrate the clinical utility of slow pathway ablation in patients who have had spontaneous episodes of PSVT and who have evidence of dual AV node pathways but no inducible PSVT in the electrophysiology laboratory. Slow pathway ablation was effective in eliminating recurrences of symptomatic tachycardia, implying that these patients had been symptomatic from AVNRT, which could not be induced during the electrophysiologic procedure despite the use of isoproterenol and atropine. The incidence of noninducibility among patients with spontaneous episodes of AVNRT appears to be ∼2%.
Possible reasons for noninducibility of AVNRT. A significant proportion of patients who undergo an electrophysiologic procedure because of a history of PSVT do not have inducible tachycardia in the baseline state, but are found to have inducible AVNRT during infusion of isoproterenol or after the administration of atropine [1, 2]. This is usually attributable to sluggish anterograde slow pathway conduction and/or sluggish or absent retrograde pathway conduction, which is reversed by beta-adrenergic stimulation or vagolysis. However, the patients in this study continued to not have inducible AVNRT despite the use of isoproterenol and atropine.
The presence of excellent ventriculoatrial conduction and the occurrence of single AV node echo beats with atrial programmed stimulation during isoproterenol infusion in all seven patients in this study indicate that inadequate retrograde fast pathway function was unlikely to have been responsible for the noninducibility of tachycardia. Inadequate anterograde delay in the slow pathway is also an unlikely explanation for the noninducibility of tachycardia, in light of the occurrence of retrograde fast pathway conduction and single AV node echo beats in each patient. Anterograde block in the slow pathway after retrograde conduction through the fast pathway suggests that relatively slow anterograde slow pathway conduction or the inability of the slow pathway to adapt to a sudden increase in rate was the factor which prevented the induction of AVNRT. This would be consistent with the finding that the mean AV block cycle length tended to be longer in the patients in this study than in other patients who had inducible AVNRT. It is possible that neither isoproterenol nor atropine adequately reproduced the autonomic state which allowed for spontaneous episodes of AVNRT outside of the electrophysiology laboratory.
Other possible reasons for noninducibility. In patients who have had documented episodes of a supraventricular tachycardia with a regular rate but who do not have inducible PSVT in the electrophysiology laboratory, possible explanations other than AVNRT include automatic atrial tachycardia, intraatrial reentrant tachycardia not inducible at the time of the electrophysiologic procedure or atrial flutter with 1:1 or 2:1 conduction in which the flutter waves are not apparent and which mimics PSVT. Therefore, it should not be assumed that slow pathway ablation will be therapeutic in all patients with spontaneous but noninducible PSVT. Electrocardiographic findings often can distinguish atrial tachycardia from AVNRT, thereby identifying patients unlikely to benefit from slow pathway ablation. In the patients in this study, the ECG recordings of spontaneous episodes of tachycardia were all compatible with AVNRT. The value of the ECG in differentiating atrial tachycardia from AVNRT highlights the importance of obtaining documentation of spontaneous episodes of tachycardia before performing an electrophysiologic procedure, whenever possible, in patients who have had PSVT.
Study limitations. A limitation of this study is that the sample size consisted of only seven patients. However, these seven patients were drawn from a pool of 324 patients with PSVT who did have inducible AVNRT in the electrophysiology laboratory. Therefore, the small sample size in this study is a reflection of the low probability of noninducibility in patients with AVNRT.
Clinical implications. The results of this study provide the first validation for the recommendation by the ACC/AHA Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures that slow pathway ablation may be indicated in patients with spontaneous episodes of PSVT who have evidence of dual AV node pathways but noninducible PSVT in the electrophysiology laboratory. The committee considered the presence of dual AV node pathways in patients with spontaneous but noninducible PSVT to be a class II indication for slow pathway ablation, reflecting the uncertainty and divided opinion that has existed regarding the clinical utility of slow pathway ablation in this setting . However, because the results of the present study clearly demonstrate clinical benefit to the patient, and although confirmatory studies are necessary, it may be appropriate to consider reclassifying the presence of dual AV node pathways in patients with spontaneous but noninducible PSVT as a class I indication for slow pathway ablation.
A.1 Abbreviations and Acronyms
ACC = American College of Cardiology
AHA = American Heart Association
AV = atrioventricular
AVNRT = atrioventricular node reentrant tachycardia
ECG = electrocardiogram, electrocardiographic
PSVT = paroxysmal supraventricular tachycardia
↵1 Dr. Bogun was supported by a grant from the Deutsche Forschungsgemeinschaft, Bonn, Germany.
- Received February 19, 1996.
- Revision received May 2, 1996.
- Accepted May 13, 1996.
- THE AMERICAN COLLEGE OF CARDIOLOGY
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