Successful Radiofrequency Energy Ablation of Automatic Junctional Tachycardia Preserving Normal Atrioventricular Nodal Conduction

Successful Radiofrequency Energy Ablation of Automatic Junctional Tachycardia Preserving Normal Atrioventricular Nodal Conduction FREDERICK A. EHLERT, JEFFREY J. GOLDBKRGER, BARBARA J. DEAL, D. WOODROW BENSON, and ALAN H. KADISH From the Divisions of Cardiology, Departments of Pediatrics and of Medicine, Northwestern University Medical School, Children's Memorial Hospital, and Northwestern Memorial Hospital, Chicago, Illinois

EHLERT, F.A., ET AL.: Successful Radiofrequency Energy Ablation of Automatic Junctional Tachycardia Preserving Normal Atrioventricular Nodal Conduction. Automatic junctional tachycardia is frequently refractory to medical management and difficult to treat with nonpharmacoJogical methods. A 12-yearoJd female with symptomatic, refractory automatic junctional tachycardia is reported. Earliest atriai activation during supraventricuJar tachycardia was in the posterior portion of the intraatrial septum. The patient underwent electrophysioIogicaJ study and successful radiofrequency current ahiation of the ectopic automatic focus within the atrioventricuiar junction. Normal atrioventricular junctionai conduction was maintained, and at 7-month foJlow-up the patient has been free of tachycardia. (PACE, VoJ. 16, January, Part I 1993]

radiofrequency ablation, automatic junctionai tachycardia, atrioventricuiar conduction

Introduction Junctional ectopic tachycardia has been described in infancy,^ where it is frequently refractory to medical therapy and is associated with a high mortality. Automatic junctional tachycardia has also been described in older children and adults,^ where pharmacological therapy also has a low rate of efficacy and attempts at nonpharmacological treatment have yielded higher success rates. Therapy has included direct current catheter ablation of the atrioventricular (AV) junction,^-^ which frequently has serious potential complications especially in children, and radiofrequency current ablation"* of the AV junction. Both of these procedures usually result in the need for permanent cardiac pacing. The purpose of this report is

Address for reprints: Alan H. Kadish. M.D.. Wesley Pavilion Room 582, Northwestern Memorial Hospital. 250 East Superior Street, Chicago. Illinois 60611. Fax: (312) 908-6003. Received March 25,1992; revision May 13,1992; accepted May 30,1992.

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to describe the treatment of a patient with automatic junctional tachycardia using radiofrequency energy catheter ablation of the automatic focus within the AV junction while preserving normal AV conduction.

Case Report Clinical History The patient is a 12-year-old female who presented at age 11 years with the complaint of dizziness and headache while engaged in physical activity. During a symptomatic tachycardia episode she was noted to have an irregular pulse at rates of 120-160 beats/min and was referred to a local emergency room. On physical examination at 12 years of age, she weighed 33,6 kg. She was in no distress; her heart rate was 120 beats/min and irregularly irregular, blood pressure was 102/56 mmHg, respirations 18/min. The cardiac exam revealed normal first and second heart sounds without murmurs or gallops. The physical exam was otherwise unremarkable. The electrocardiogram

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avR

V2

avL

avF

Figure 1. Electrocardiogram on initial presentation, showing aufomafjc functional tachycardia, with atrioventricular dissociation and capture beats. Asterisks indicate P waves of sinus origin dissociated from tachycardia beats. showed nonsustained bursts of irregular tachycardia with a normal QRS configuration at rates to 150 beats/min (Fig. 1). The QRS axis was 90° in the frontal plane and the QRS duration was 85 msec, AV dissociation and occasional beats of sinus origin resulting in identical QRS morphology were noted. The QRS axis, duration and morphology of capture beats were identical to the tachycardia beats. The chest X ray was normal. The tachycardia did not respond to vagal maneuvers, and the patient was treated with 2,5 mg of intravenous verapamil, which resulted in a return to sinus rhythm. The patient underwent transesophageal and transvenous electrophysiological testing. During these studies, the only observed arrhythmia was a tachycardia (cycle length = 430 msec) with a normal QRS configuration and the following characteristics: (1) all QRS complexes ofthe tachycardia were of normal duration (80 msec] and preceded by a normal His deflection (HV interval = 50 msec), (2) occasional atrial fusion complexes

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were noted between atrial depolarizations of sinus and junctional origins as well as between ectopic atrial and junctional origins, (3) the tachycardia could not be reproducibly initiated or terminated with programmed stimulation, (4) 1:1 ventriculoatrial conduction with a VA interval of 45 msec, (5) after the administration of adenosine, the tachycardia terminated with an atrial depolarization, and (6) after isoproterenol infusion at 0.02 meg/ kg per minute, the tachycardia became incessant. When the infusion was increased to 0.05 mcg/kg per minute, sinus tachycardia (cycle length = 380 msec) developed and suppressed the supraventricular tachycardia. After the isoproterenol infusion was discontinued, the supraventricular tachycardia reappeared as tbe sinus rate decreased. Over the ensuing 8 months the patient failed multiple medical regimens including verapamil (7 mg/kg per day), flecainide (3 mg/kg per day), flecainide and atenolol (3 mg/kg per day), and atenolol and digoxin. The patient was referred

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to our institution for further diagnosis and treatment. The mechanism of supraventricular tachycardia could not be determined with certainty from the available data although it was most consistent with an automatic junctional tachycardia or AV junctional reentry. Thus, the patient was referred for invasive electrophysiological testing to establish a diagnosis and for possible radiofrequency ablation to "cure" the medically refractory supraventricular tachycardia. Procedure Using a right femoral transvenous approach and fluoroscopic guidance, 6-Fr quadripolar catheters were placed in the high right atrium and the right ventricular apex, and a 6-Fr steerable quadripolar catheter with a 3-inm tip and a 5-mm intraelectrode distance (Boston Scientific Corp., Watertown, MA, USA) was placed across the tricuspid valve to record a His-bundle electrogram. A 12-pole catheter was placed in the coronary sinus via a right internal jugular approach. Baseline

electrophysiological parameters, obtained in the drug-free state, are presented in Table 1. Nonsustained bursts of tachycardia (cycle length: 380-440 msec) were present throughout the procedure. During the tachycardia, all QRS complexes were preceeded by a His-bundle electrogram with an HV interval of 45 msec. The tachycardia could not be terminated or initiated with atrial or ventricular programmed stimulation and was not induced witb isoproterenol infusion at 0.02 mcg/kg per minute. Initiation of the tachycardia during the procedure was spontaneous and not preceded hy a long AH interval (Fig, 2): atrial fusion is noted on the fourth beat. During atrial programmed stimulation there was no evidence of dual AV nodal pathways; AV junctional echoes were not produced with up to three premature atrial extrastimuli. Termination of the tachycardia during the procedure was spontaneous (Fig. 3): termination with an atrial depolarization is noted on the third beat. Mapping of the region of AV junction was performed with tbe steerable catheter; retrograde atrial acti-

Table I. Electroptiysiological Parameters Upon Presentation, At the Time of Radiofrequency Ablation and 2 Days After Radiofrequency Ablation

Eiectrophysiology Study at Ablation Rhythm

CL PR QRS QT AH HV AV BCL Atrial ERP (@ PCL 400) AVN ERP (@ PCL 400) VA BCL Ventricular ERP ((« PCL 400) VA ERP ( ^ PCL 400)

Junctional/Sinus 600 msec 120 msec 100 msec (RBBB) 330 msec 70 msec 45 msec 280 msec 220 msec < 270 msec 320 msec 240 msec < 240 msec

Eiectrophysiology Study 2 Days Postablation Sinus 910 msec 110 msec 85 msec 410 msec 60 msec 35 msec 300 msec 260 msec < 360 msec 350 msec 210 msec < 280 msec

AH = AH interval; AV = atrioventricular; AVN = atrioventricular node; BCL = block cycle length; CL = cycle length; ERP = effective refractory period; HV = HV interval; msec = milliseconds; PCL = pacing cycle length; PR = PR interval; RBBB = right bundle branch block; QRS = QRS interval; QT = QT interval; VA = ventriculoatrial.

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HRA

Figure 2. Surface electrocardiogram and intracardiac eieclrograms showing initiation of j'unc-

tional tachycardia. The first three beats are sinus rhythm. The high righf atrial component of the fourth beat is of sinus origin/oilowed by pseudo-shortening of the AH interval due to fusion with the first beat of the tachycardia. The following beats are the junctionaJ tachycardia. Although a discrete atria] eJectrogram is not easily identified in the His-bundle electrogram during the tachycardia, comparison to tracings in sinus rhythm shows a negative deflection of the atrial electrogram farrow) representing retrograde atriai activation. Each major time gradation equals 100 msec. A ^ atrial electrogram, CS = coronary sinus electrogram, H ^ His electrogram, HBE = His-bundle electrogram, HRA = high right atrium, V ^ ventricular electrogram.

vation was earliest along the inferior intraatrial septum. Atrial activation times are presented in Figure 4. A diagnosis of automatic junctional tachycardia was made based on: [1] a normal QRS tachycardia with a normal HV interval, (2) VA dissociation during the tachycardia as documented on the 12lead electrocardiogram [although a 1:1 VA relationship was present at the electrophysiological study), (3) a retrograde atrial activation sequence that was midline, (4) inability to initiate or termi-

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nate the tachycardia with atrial or ventricular programmed stimulation, (5) absence of dual AV nodal pathways, (6) initiation of the tachycardia during sinus rhythni without AH interval prolongation, and (7) the absence of an accessory AV connection. The retrograde atrial activation was earliest along the inferior septum, suggesting that the caudal region of the AV junction may have been responsible for the tachycardia. Thus, it was elected to proceed with supraventricular tachycardia ablation by directing radiofrequency lesions

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JV-A> . Figure 3. Surface electrocardiogram and intracardiac electrograms showing termination of junctional tacbycardia. The third and fourth beats show ihe tachycardia slowing. The fifth beat represents atrial fusion between beats of sinus and junctional origin. The arrow denotes the negative atrial electrogram noted in the His-bundJe recording during tachycardia frepresenting retrograde atria] activation) as compared to the atrial electrogram in sinus rhythm. Each major time gradation equals 100 msec. Abbreviations as per Figure 2.

at the tricuspid annulus near the site of earliest retrograde atrial activation, Radiofrequency energy, supplied as a continuous sine-wave at 550 kHz (Model 3B, Radionics Inc., Burlington, MA, USA), was delivered at the site of earliest atrial activation. Surrounding the region of earliest atrial activation, 14 radiofrequency lesions were delivered in the inferior third ofthe intraatrial septum (at least 2 cm from regions where the His-bundle electrogram was recorded) and along the inferoposterior aspect of the tricuspid annulus. With administration of the 14th lesion, delivered 1 cm helow the coronary sinus os, the junctional tachycardia ahruptly terminated. Intracardiac electrograms at the site of the successful lesion are presented in Figure 5. The AV ratio

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at this site was 1:2; atrial activation at this site preceded the onset of retrograde P wave on the surface electrocardiogram by 25 msec, activation of the high right atrium by 50 msec and activation of the proximal coronary sinus catheter by 10 msec. Lesions were applied with a mean current of 380 mA and a mean voltage of 42 V; the total time of radiofrequency energy administration was 14.0 minutes. FoUow-Up

Electrophysiological testing 2 days after the modification procedure revealed normal sinus rhythm at a cycle length of 910 msec. After sedation, the sinus cycle length fell to 1,050 msec and

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a junctional escape rhythm was noted. Electrophysiological parameters are presented in Table I. Infusion of isoproterenol at a rate of 0.02 mg/kg per minute produced a decrease in the sinus cycle length to 430 msec. Holter monitor recording 2 days after the procedure showed predominantly sinus rhythm with periods of sinus bradycardia and junctional escape rhythm noted. No episodes of junctional tachycardia were noted on monitoring. In the 7 months since discharge, the patient has not had recurrence of symptoms; repeat Holter monitoring has been unremarkable.

Anterior

Discussion Figure 4. Map of atrial activation during junctional tachycardia. Activation times fin msec) are relative

to the onset of the P wave on the surface electrocardiogram. Asterisk denotes the site of the successful radiofrequency lesion. CS - coronary sinus. His His bundle, MV = mitral valve, TV - tricuspid valve.

This report describes successful long-term elimination of automatic junctional tachycardia with preservation of AV junctional conduction. This patient had an unusual junctional tachycardia in that activation mapping revealed that earliest retrograde atrial activation was present in the inferior portion of the intraatrial septum. Prior studies have suggested that the AV junction may

jriiiiiiiii

Figure 5. Surface electrocardiogram and intracardiac electrograms during tachycardia at the successful site of radiofrequency ablation. The atrial electrogram at this site preceded the onset of retrograde P wave on the surface electrocardiogram by 25 msec, activation of the high right atrium by 50 msec, and activation of the proximal coronary sinus catheter by 10 msec as demonstrated by the vertical line. The arrow indicates the negative deflection of (he retrograde P wave on the surface electrocardiogram. Abbreviations as per Figure 2; Map = mapping catheter.

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anatomically extend close to the coronary and the findings of the present study suggest that any region of the AV junction may be responsible for automatic junctional tachycardia. Precise mapping of the intraatrial septum may allow identification of the region responsible for automatic junctional tachycardia and may allow ablation of the tachycardia focus with preservation of AV conduction.

tion^ and suggest that the automatic focus responsible for the junctional tachycardia does not necessarily involve the entire AV junction. If the automatic focus is located at some distance from the His-bundle electrogram, ablation may be successfully performed with a low risk of developing complete heart block.

Prior Studies

Diagnoses other than automatic junctional tachycardia were carefully considered. Atrial tachycardia and atrioventricuiar reentrant tachycardia were excluded because of the AV dissociation noted on the initial 12-lead electrocardiogram, although 1:1 VA relationship was present at the electrophysiological study. Ventricular tachycardia with normal QRS duration has been described in children," however the QRS complex of this tachycardia was identical to that in sinus rhythm and the HV interval was identical to that in sinus rhythm. Thus, a ventricular origin of the tachycardia seems unlikely. AV junctional reentry is always present in the differential diagnosis of automatic junctional tachycardia. The short VA interval observed during the tachycardia would suggest a diagnosis of typical AV junctional reentrant tachycardia. In typical AV junctional reentrant tachycardia, retrograde conduction is via the anterior or fast AV nodal pathway. However, in this patient's tachycardia, earliest retrograde atrial activation occurred near the coronary sinus os. If AV junctional reentrant tachycardia was present, this sequence of atrial activation would imply that retrograde conduction was via the posterior or slow AV nodal pathway,^ and therefore, would not represent typical AV junctional reentrant tachycardia. Prior studies have shown that the VA time in atypical AV junctional reentrant tachycardia is > 60 msec.'^ In the present study, the VA time during tachycardia is 0 msec and is therefore not consistent with atypical AV junctional reentrant tachycardia. In addition. AV junctional reentry was highly unlikely because of the absence of dual AV nodal pathways, the inability to initiate or terminate the tachycardia with programmed stimulation, initiation without AH interval prolongation and the significant degree of cycle length variation noted (380-440 msec]. Although it is theoretically

In patients with automatic junctional tachycardia refractory to medical management, attempts at nonpharmacological therapy have been made with varying success. Gillette et al.' and Villain et al.^ have reported using direct current energy at low doses [1.5-3 J/kg) to ahlate the AV junction in patients with junction ectopic tachycardia. However, experience with direct current shock in children remains limited and smaller size hearts in children potentially make the risk of barotraumatic complications greater.^ In addition, a majority of patients treated in this manner required permanent pacemaker implantation. Villain et al.^ also reported the use of surgical ablation of the AV junction in patients with automatic junctional tachycardia. Surgical therapy required permanent pacemaker placement in all patients and had an associated 50% mortality. VanHare et al.'' reported using radiofrequency energy to ablate the AV junction in a 10-month-old patient with junctional ectopic tachycardia. This report differs from previous reports in that mapping in the region of the AV node was undertaken, the site of earliest atrial activation was identified and radiofrequency energy was selectively delivered in that region. While experience with radiofrequency catheter ablation in children is also limited, extensive experience in adults®'^ has shown low complication rates and preliminary pediatric experience^" confirms the apparent safety of the procedure. Interestingly, in the treatment of junctional ectopic tachycardia, previous reports of AV junctional ablation using radiofrequency* and direct current ablations' showed evidence of some degree of preserved AV conduction. These results and the present report reinforce the complex anatomy of the AV junc-

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Differential Diagnoses of the Arrhythmia

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possible that the tachycardia initiation shown in Figure 2 represents a 2-for-l response to the third sinus b e a t / ^ this is extremely unlikely because multiple spontaneous initiations showed variable coupling to sinus beats and because " s l o w " pathway c o n d u c t i o n was not otherwise seen. T h u s , this tachycardia represents an automatic junctional tachycardia. This article represents a single case report. In other patients, mapping may reveal that the earliest atrial activation occurs in the His-bundle electrogram. In these cases it may not be possible to separate the source of the automatic tachycardia from t h e His-bundle electrogram; thus, radiofre-

quency ablation could result in complete heart block. Summary The present study reports the use of radiofrequency energy to ablate an ectopic automatic focus within the AV junction while preserving AV conduction. The tachycardia was eliminated without the loss of AV conduction; tachycardia has not recurred at 7-month follow-up. Radiofrequency current catheter ablation may represent a safe and effective treatment for automatic junctional tachycardia, and may provide the best method to maintain AV conduction.

References 1. Gillette P, Garson A, Porter C, et al. Junctional ectopic tachycardia: A new proposed treatment by transcatheter His ablation. Am Heart J 1983; 106: 619-623. 2. Ruder M. Davis J, Eldar M, et al. Clinical and electrophysiologic characterization of automatic junctional tachycardia in adults. Circulation 1986; 73: 930-937. 3. Villain E, Vetter V, Garcia ], et al. Evolving concepts in the management of congenital junctional ectopic tachycardia. Circulation 1990; 81: 1544-1549. 4. VanHare G, Velvis H, Langberg J. Successful transcatheter ahiation of congenital junctional ectopic tachycardia in a ten-month-old infant using radiofrequency energy. PACE 1990; 13:730-735. 5. Sung RJ, Styperek JL, Myerhurg RJ, et al, Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed stimulation in man. Amer J Cardiol 1978; 42:404-415. 6. Sherf L, James T, Woods W. Function of the atrioventricular node considered on the hasis of observed histologic and fine structure. J Am Coll Cardiol 1985; 5:770-80. 7. Moak J, Friedman R, Carson A Jr. Electrical ahiation of atrial muscle. I. Early and late anatomic observations in canine atria. Am Heart J1987; 113: 1397-1404,

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8. Lee MA, Morady F, Kadish A, et al. Catheter modification of the atrioventricular junction with radiofrequency energy for control of atrioventricular nodal reentry tachycardia. Circulation 1991; 83: 827-835. 9. Jackman WM, Wang X, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White Syndrome) by radiofrequency current. N Engl J Med 1991: 324: 1605-1611. 10. VanHare G, Lesh M, Scheinman M, et al. Percutaneous radiofrequency catheter ablation for supraventricular arrhythmias in children. J Am Coll Cardiol 1991; 17:1613-1620. 11. Vetter VL, Josephson ME, Horowitz LN. Idiopathic recurrent sustained ventricular tachycardia in children and adolescents. Amer J Cardiol 1981; 47; 315-22. 12. Benditt D, Pritchett E, Smith W, et al. Ventriculoatriat intervals: Diagnostic use in paroxysmal supraventricular tachycardia. Ann Intern Med 1976; 91; 161-166. 13. Kim SS, Lai R, Ruffy R. Paroxysmal nonreentrant supraventricular tachycardia due to simultaneous fast and slow pathway conduction in dual atrioventricular node pathways, J Am Coll Cardiol 1987; 10:456-61.

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