Radiofrequency Catheter Ablation of Right Ventricular Tachycardia Late After Repair of Congenital Heart Defects
Background Ventricular arrhythmias after repair of congenital heart defects are a common finding and possibly contribute to sudden death in these patients. Optimal antiarrhythmic management has not yet been defined.
Methods and Results The study population consisted of 16 patients in whom ventricular arrhythmias occurred 11 to 42 years after complete surgical repair of congenital heart defects. Fifteen patients had a history of symptomatic sustained or nonsustained ventricular tachycardia, and 1 had frequent nonsustained ventricular tachycardia. The diagnostic mapping procedure to identify the origin of the arrhythmia included pace mapping during sinus rhythm, activation mapping, and pacing interventions during ventricular tachycardia. Catheter ablation was carried out by means of radiofrequency energy in the temperature-controlled mode. The follow-up period was 6 to 33 months (mean, 16 months). A right ventricular origin of the tachycardia in the surgically corrected area could be determined in all patients. Catheter ablation was carried out without complications. Immediate noninducibility was achieved in 15 of the 16 patients. One patient in whom the tachycardia was again inducible at repeat stimulation 1 week later was successfully treated with amiodarone. Eleven patients were taken off antiarrhythmic drugs. During follow-up, none of them had a recurrence of the tachycardia that had been ablated.
Conclusions In patients with symptomatic or frequent ventricular tachycardia late after complete surgical repair of congenital heart defects, catheter ablation by means of radiofrequency energy is feasible and safe and thus might be taken into consideration for these patients. Short-term follow-up results are promising.
Ventricular arrhythmias late after repair of congenital heart disease are a common finding, predominantly in those with tetralogy of Fallot.1 2 3 4 It is suggested that these arrhythmias contribute to sudden death in this population. The incidence of late sudden death is a point of some contention but ranges from 1% to 5% during a follow-up period of 7 to 20 years after surgery.1 5 6 7 Patients with surgical correction of ventricular septal defect or pulmonary stenosis also have a higher-than-normal risk of serious ventricular arrhythmias and sudden death.8 9 Up to now, the ideal form of antiarrhythmic therapy for these patients has not been established. No data are available concerning the risks and benefits of long-term medical antiarrhythmic management. Three case reports showed the feasibility of catheter ablation by means of either DC or radiofrequency energy in patients with surgical correction of tetralogy of Fallot.10 11
The purpose of this study was to evaluate the clinical efficacy of radiofrequency catheter ablation in patients with sustained or frequent nonsustained monomorphic ventricular tachycardia occurring late after surgical repair of congenital heart defects.
The study population consisted of 16 patients, 10 men and 6 women. The mean age was 34±13 years (range, 15 to 50 years). Nine patients had undergone surgical repair of tetralogy, 4 had surgical correction of ventricular septal defect, 2 an operation for severe congenital pulmonary stenosis, and 1 for transposition of the great vessels and associated ventricular septal defect a mean of 28 years (11 to 42 years) before the onset of the arrhythmia (Table 1).⇓
Fifteen patients had a history of symptomatic sustained or nonsustained ventricular tachycardia that could be documented electrocardiographically in all of them. Six patients had a history of syncope. Palpitations were reported by 9 patients. Four of these also complained of dizziness, possibly due to some degree of hypotension caused by the arrhythmia. The remaining patient (patient 10) was asymptomatic. On average, the patients had previously received three antiarrhythmic drugs, including metoprolol 100 mg/d, sotalol 360 mg/d, mexiletine 600 mg/d, and propafenone 750 mg/d; 8 patients were on long-term amiodarone medication (>3 months).
All electrophysiological studies were carried out in the fasting, unsedated state. The patients had been informed in detail about the stimulation, mapping, and ablation procedures and had given their written consent. All antiarrhythmic drugs had been withdrawn for at least 4 days except for those patients who had been on long-term amiodarone medication.
Programmed ventricular stimulation
Programmed stimulation was carried out in the right ventricular apex and, if the tachycardia was not inducible, in the right ventricular outflow tract. The stimulation protocol included the application of up to three extrastimuli during sinus rhythm and paced cycle lengths of 600, 500, 428, and 375 ms with a current strength twice the diastolic threshold. The pacing stimuli were 1.0 ms in duration. The end point of testing was the reproduction of the clinically documented ventricular tachycardia (Fig 1⇓). Differences in heart rate of up to 20 bpm between spontaneous and induced ventricular tachycardia were accepted if configuration, axis, and R-wave progression were identical. Isoproterenol was not used in any of the patients.
Two quadripolar catheters (6F, Bard) were inserted percutaneously through the right and left femoral veins and advanced to the right ventricular apex and the His bundle region. A quadripolar catheter with a deflectable 4-mm tip electrode (Mansfield Webster Polaris 7F, Osypka Cerablate 7F, Boston Scientific 7F) was introduced into the right femoral vein and advanced to the right ventricle.
Biplane fluoroscopy was used to identify catheter position by right and left anterior oblique projections, including the posterior anterior view. Bipolar endocardial electrograms were recorded from the right ventricular apex, the His bundle, and the right ventricle and registered with a seven-channel ink-jet recorder (Siemens Elema) at filter settings of 50 to 500 Hz. The mapping procedure to detect an adequate site for ablation included pace mapping during sinus rhythm, endocardial activation mapping, and pacing interventions during ventricular tachycardia. The mapping technique has recently been described.12 Ten to 15 right ventricular sites were mapped in each patient. Mapping was carried out with the ablation catheter. Pace mapping during sinus rhythm was performed with the cycle length of the clinical and inducible tachycardia. The exit site of the tachycardia was assumed if paced QRS complexes showed identical QRS complexes with respect to axis, bundle-branch morphology, and R-wave progression compared with the clinical and inducible ventricular tachycardia (Fig 2⇓). When an adequate site was localized, ventricular tachycardia was induced by programmed right ventricular stimulation. An adequate site for ablation was assumed if the endocardial activation sequence preceded the QRS complex of the surface ECG and/or mid-diastolic potentials as an indication of an area of slow conduction could be registered. Furthermore, at this site we tried to entrain the tachycardia with trains of stimuli at cycle lengths of 50 to 100 ms below the rate of the tachycardia. If the tachycardia could be entrained without altering the QRS configuration (“entrainment with concealed fusion”) with a prolonged stimulus-to-QRS interval, it was assumed that stimulation was performed in an area of slow conduction and identified a target site for catheter ablation (Fig 3⇓).
In patients with nonsustained ventricular tachycardia, entrainment was attempted in the same way. If the tachycardia was stopped by this intervention, it was induced again and single stimuli were used. If the tachycardia could be reset by a single stimulus without changes in morphology, this was defined as entrainment with concealed fusion as well.
Catheter ablation was performed in patients with inducible sustained and nonsustained ventricular tachycardia if at least one mapping criterion besides an exact pace map during sinus rhythm could be found.
The position of the tip of the ablation catheter was verified by biplane fluoroscopy. Radiofrequency current (unipolar output mode, continuous unmodulated waveform, 500 kHz) was generated with a conventional generator (Osypka 200 S). Radiofrequency catheter ablation was performed in the temperature-controlled mode (60°C to 70°C, 10 to 30 seconds). The duration of each application was regulated according to temperature, impedance, and energy delivery.
If the clinical tachycardia was no longer inducible after the ablation procedure, the patients were observed in the electrophysiology laboratory for 15 to 30 minutes. Thereafter, programmed stimulation was repeated. If the tachycardia was again inducible, the ablation procedure was continued, or it was terminated if the session exceeded 6 hours or if the patient was unwilling to proceed.
After catheter ablation, the patients were monitored continuously in the coronary care unit. The plasma concentrations of creatine kinase and its MB fraction were measured directly after the ablation procedure and in 2-hour intervals during the first 12 hours. Careful two-dimensional echocardiography was carried out during the first 6 hours after the ablation procedure and was repeated the following day. Repeat programmed stimulation and ambulatory monitoring were performed 5 to 7 days later.
All patients were followed up in our outpatient clinic at 3-month intervals during the first year and thereafter at 6-month intervals. During the visits, ECGs, treadmill test, and 24-hour ambulatory monitoring were carried out. Repeat electrophysiological study was performed only after discontinuation of amiodarone treatment or in case of clinical symptoms or ventricular tachycardia documented during ambulatory monitoring.
Clinical Presentation and Electrophysiological Findings
Tetralogy of Fallot
Nine patients had undergone surgical correction of tetralogy, including ventriculotomy, pulmonary valvulotomy, and patch repair of ventricular septal defect between the ages of 3 and 5 years (mean, 4 years). Six of these patients had a history of syncope, and palpitations were reported in 3. Sustained ventricular tachycardia had been documented in 7 patients and frequent nonsustained ventricular tachycardia (15 and 22 episodes/24 h with 10 to 25 ventricular premature beats [VPBs]) in the remaining 2. The mean rate of the tachycardia was 171 bpm.
Ventricular septal defect
Four patients had undergone surgical repair of a muscular (n=3) or a membranous (n=1) ventricular septal defect between the ages of 5 and 18 years (mean, 11 years). Three of them had a history of palpitations and presyncope. The remaining patient had no clinical symptoms of arrhythmia, but ECG recordings revealed frequent monomorphic nonsustained ventricular tachycardia with up to 28 beats with a rate of 170 bpm. The other 3 patients also had recurrent nonsustained ventricular tachycardia with up to 48 consecutive VPBs recorded during long-term ECG with a mean rate of 143 bpm. Another patient (patient 14) had had surgery at the age of 3 years to correct transposition of the great vessels with prosthetic outflow tract reconstruction of the pulmonary artery and patch closure of a muscular ventricular septal defect. She suffered from frequent palpitations and two episodes of presyncope and had sustained ventricular tachycardia with a rate of 160 bpm documented electrocardiographically.
Two patients had undergone repair of severe congenital infundibulary pulmonary stenosis at the ages of 16 and 17 years, respectively. Both had palpitations due to nonsustained ventricular tachycardia (24 and 30 episodes/24 h with up to 36 consecutive VPBs). The rate of the tachycardia was 130 bpm in both patients.
The mean cycle length of the tachycardia in all patients was 377±74 ms (f=158±31 bpm), and the mean duration of the arrhythmia was 2 years. Patients with tetralogy more often had sustained ventricular tachycardia and a more rapid heart rate than those with other congenital heart defects (Table 1). A left bundle-branch block morphology was present in all patients, with right axis in 8 patients, superior axis in 3, and normal axis in 5. In all patients, the rate of the tachycardia was >20% faster than the preceding sinus rhythm; thus, an accelerated ventricular rhythm could be excluded.
Two-dimensional echocardiography and right and left ventricular catheterization were performed in all patients. Residual defects could be ruled out. A residual shunt defect was excluded by oximetry. None had evidence of pulmonary hypertension. Right ventricular pressure and right ventricular ejection fraction at rest were in the normal range. Furthermore, patients >35 years old underwent coronary angiography. Coronary artery disease could be excluded in all of them.
Programmed Ventricular Stimulation
Programmed ventricular stimulation at the right ventricular apex (n=11) or outflow tract (n=5) induced monomorphic sustained ventricular tachycardia in 11 patients and nonsustained ventricular tachycardia with 16 to 38 consecutive beats in 5. The number of extrastimuli required for induction of the arrhythmia was one in 2 patients, two in 13 patients, and three in the remaining patient. All induced tachycardias were identical with the clinically documented arrhythmia with respect to axis, bundle-branch block morphology, R-wave progression in the precordial leads, and rate.
A right ventricular origin of the tachycardia could be determined in all patients. The arrhythmogenic area could be localized in the surgically corrected area. In patients with repair of tetralogy, it was localized predominantly in the area of the scar of the infundibulectomy (n=7), and in 2 patients who underwent ventriculotomy, it was found to be in the area of the closure of the ventricular septal defect (Fig 4⇓). In patients with patch closure of ventricular septal defect, the origin of the tachycardia could be identified in the right ventricular septum in 3 and in the right ventricular outflow tract in the patient with a membranous defect. In the patient with transposition and associated ventricular septal defect, the arrhythmogenic area was localized in the right ventricular septum. The target sites for ablation in the 2 patients with pulmonary stenosis were the basal right ventricular septum and the right ventricular outflow tract.
At these sites, a good pace map during sinus rhythm could be found in 15 of the 16 patients (94%); in one patient (patient 15), there were slight differences in the R-wave progression in the precordial leads. After induction of ventricular tachycardia by programmed stimulation, an area of slow conduction, defined as mid-diastolic low-amplitude endocardial potential, could be found in 3 patients (19%). The mean endocardial activation time of the endocardial electrogram preceding the QRS complex of the surface ECG at the ablation site was −69±16 ms. In 9 of the 11 patients with inducible sustained ventricular tachycardia (82%), stimulation during ventricular tachycardia led to an entrainment of the tachycardia without changes in axis and morphology. In addition, a prolonged stimulus-to-QRS interval (10 to 120 ms) was found in these patients. Entrainment or resetting was also possible in 3 of the 5 patients with inducible nonsustained ventricular tachycardia in whom the arrhythmia lasted for 15 to 18 seconds (Table 2⇓).
Catheter ablation was carried out without any complications during the procedure or thereafter. Creatine kinase levels during the first 12 hours did not exceed 150 U/L; the maximum level of the MB fraction was 17 U/L. Two-dimensional echocardiography directly after catheter ablation and 1 day later did not reveal pericardial effusion or tamponade in any of the patients. A total of 17 ablation sessions were performed in the 16 patients. The duration of one session ranged from 45 minutes to 4 hours (mean, 150 minutes). The mean x-ray exposure was 36±16 minutes. Radiofrequency energy was applied 3 to 11 times (mean, 7 times) at a mean temperature of 67±13°C for a mean of 26±5 seconds.
Immediate noninducibility of either sustained or nonsustained ventricular tachycardia was achieved in 15 of the 16 patients (94%) after the procedure. Repeat ventricular stimulation 5 to 7 days later revealed noninducibility in 14 patients (88%). Entrainment of the tachycardia had not been possible in the 2 nonresponders.
A 36-year-old woman with a history of repair of tetralogy of Fallot and recurrent syncope who was still inducible after the ablation procedure (patient 2) underwent implantation of an automatic cardioverter-defibrillator system with an antitachycardia pacing mode and experienced two episodes of ventricular tachycardia during the first year after the attempt at ablation. Another 35-year-old man with repair of tetralogy of Fallot (patient 1) in whom the clinical tachycardia was again inducible at repeat stimulation 1 week after catheter ablation and who was unwilling to undergo a second attempt at ablation was successfully treated with amiodarone.
Follow-up data were assessed in all 14 patients in whom sustained ventricular tachycardia could not be induced at repeat stimulation. The mean follow-up time was 16±9 months (6 to 33 months). No recurrences of the arrhythmia that had been ablated occurred during that time. Eleven patients were discharged without antiarrhythmic medication. Three of these had been on long-term amiodarone treatment. These patients underwent repeat stimulation 6 weeks after withdrawal of the drug and remained noninducible. In another patient in whom amiodarone medication was discontinued (patient 3), programmed ventricular stimulation 6 weeks later induced a new type of ventricular tachycardia with different axis, morphology, and cycle length without clinical manifestation. However, amiodarone was administered again, and the patient was noninducible at repeat programmed stimulation. In 3 patients who were unwilling to undergo a repeat electrophysiological test, amiodarone medication was continued (200 mg/d, 5 d/wk). One of these patients (patient 12) changed his mind 4 months later, the drug was withdrawn, and he was noninducible at repeat stimulation 6 weeks later. In the patient with transposition of the great vessels (patient 14), repeat stimulation 1 week after catheter ablation induced nonsustained ventricular tachycardia with 8 consecutive echo beats of different morphology from the ablated one. It was judged to be a nonclinical arrhythmia, and the patient was taken off antiarrhythmic drugs. Three months later, she suffered from palpitations again. The tachycardia formerly judged “nonclinical” was documented in a 12-lead ECG and was reproducible in sustained form by means of programmed stimulation. The arrhythmogenic area could be localized in the right ventricular outflow tract in the area of the anastomosis of the conduit between the pulmonary artery and the right ventricle. However, no good wall contact could be achieved in this area; thus, repeat catheter ablation could not be carried out. Sotalol was administered, and the patient was noninducible under this regimen and was free of arrhythmia thereafter (Table 2⇑).
Catheter ablation has become an established therapeutic tool in the treatment of supraventricular and atrioventricular tachycardia. In patients with ventricular tachycardia, the indication for catheter ablation is still under debate. In patients with idiopathic ventricular tachycardia and bundle-branch reentrant ventricular tachycardia, excellent results have been achieved.13 14 15 16 17 18 Even in patients with coronary artery disease and one morphology of recurrent sustained ventricular tachycardia, catheter ablation is feasible and shows acceptable results.12 19
To date, no data are available about the incidence and the ideal treatment of ventricular tachycardia late after surgical repair of congenital heart disease. There is agreement that ventricular tachycardia contributes to sudden death in these patients. One of the predisposing factors for the development of late ventricular arrhythmias in patients with tetralogy of Fallot is older age at repair. Our results show that during long-term follow-up, even patients with early surgical correction at the age of 3 to 5 years may develop symptomatic ventricular arrhythmias. In patients with unsuccessful medical antiarrhythmic management, alternative therapeutic regimens have to be applied. In some patients with surgical repair of tetralogy of Fallot, antitachycardia surgery has been applied.20 One case report by Oda et al10 and another two patients reported by Burton and Leon11 demonstrated the feasibility of catheter ablation in patients with right ventricular outflow tract tachycardia late after repair of tetralogy of Fallot without recurrence of the arrhythmia during short-term follow-up. The present study confirms these results and shows promising follow-up results during the first year, comparable to those in patients with idiopathic ventricular tachycardia.
Up to now, it has not been clear whether the surgical procedure for correction of the defect itself is responsible for the development of ventricular arrhythmia, since ventricular arrhythmias also occur in patients who have not had surgery.21 In these patients, however, they are suspected to be the consequence of chronic right ventricular hypertension and hypertrophy, which was not present in any of our patients. In 1980, Horowitz et al22 reported results of endocardial mapping in four patients with tetralogy of Fallot. The reentrant circuits of the tachycardia could be localized in the right ventricular outflow tract and thus might be caused by the previous operation. Other mapping studies also localized the arrhythmogenic substrate in the right ventricular outflow tract even if no scar was visible.23 24 Our mapping results demonstrate that the origin of the arrhythmia could be localized in the surgically corrected area in all patients.
The value of programmed stimulation and the inducibility of sustained ventricular tachycardia is also a matter of discussion. Deal et al25 reported on nine patients after repair of tetralogy of Fallot, four with clinical ventricular tachycardia and five with frequent VPBs and ventricular pairs. All of those with clinical ventricular tachycardia had inducible sustained or nonsustained ventricular tachycardia, as did three of the remaining patients. In our study group, which included nine patients with tetralogy of Fallot, all had inducible monomorphic ventricular tachycardia. Horowitz et al22 reported similar results. Deal et al25 pointed out that the response to invasive serial drug testing was unlikely in the presence of elevated right ventricular systolic pressure.
All patients had received several antiarrhythmic drugs, including amiodarone, which were unable to suppress the arrhythmia. However, it must be taken into consideration that drug therapy in our study group had been performed empirically, and the patients investigated had been referred because of insufficiently treated nonsustained or sustained ventricular tachycardia. The results show that catheter ablation by means of radiofrequency energy can reliably and safely eliminate the arrhythmia. Furthermore, antiarrhythmic drug medication could be discontinued in the majority of these patients. This might be of special interest for these young patients, since long-term antiarrhythmic treatment may cause considerable problems due to side effects. However, it must be taken into account that both catheter ablation and discontinuation of amiodarone treatment thereafter may unmask a second morphology of ventricular tachycardia (see patients 3 and 14). Downar et al24 also reported five ventricular tachycardias in four patients.
Interpretation of the results of endocardial mapping and its predictive value with respect to the success of catheter ablation is limited because once a good pace map during ventricular tachycardia or early endocardial activation was obtained and at least one other finding considered to be of diagnostic significance was present, catheter ablation was attempted. As described in the patient with surgical correction of transposition of the great vessels, mapping appears to be rather difficult because of the anatomic situation in special cases. Our findings suggest that in patients with ventricular tachycardia late after surgical correction of congenital heart defects, a good pace map during sinus rhythm may point to the arrhythmogenic area. Early endocardial activation is not predictive of success. This finding corresponds to the results of Coggins et al14 in patients with idiopathic ventricular tachycardia of right ventricular origin and with those of Burton and Leon11 in two patients with tetralogy of Fallot. It might perhaps be extrapolated to ventricular tachycardias of right ventricular origin, especially those originating from the right ventricular outflow tract. A good pace map during ventricular tachycardia and entrainment with identical QRS complexes and a prolonged stimulus-to-QRS interval or continuous resetting of the tachycardia more precisely indicates an adequate site for ablation. This is in agreement with our previously published results in patients with coronary artery disease12 and agrees with previous results of other authors.26 27 28 In our study population, entrainment of the tachycardia was found in 12 of the 14 responders but not in the two nonresponders. Horowitz et al22 and Kugler et al23 found continuous electrical activity in the right ventricular outflow tract. However, mid-diastolic potentials, considered to be a sign of slow conduction and therefore a critical part of the reentrant circuit, could be found in only a minority of our patients (n=3) and could not be related to success or failure of the procedure. Nevertheless, the ability to induce the tachycardia by programmed ventricular stimulation suggests reentry as the mechanism of ventricular tachycardia in these patients. Furthermore, the fact that the arrhythmogenic area determined by the mapping procedure was localized in the surgically corrected area indicates possible reentrant ventricular tachycardia.
In patients with hemodynamically stable ventricular tachycardia late after surgical repair of congenital heart defects originating in the right ventricle, catheter ablation by means of radiofrequency energy is feasible and safe. Thus, in our opinion it might be taken into consideration for these generally young patients to avoid long-term antiarrhythmic therapy. The results obtained in patients with ventricular tachycardia late after repair of congenital heart disease without residual defects are comparable to those in patients with idiopathic ventricular tachycardia. However, longer follow-up periods are required to confirm these promising results.
- Received December 13, 1995.
- Revision received July 29, 1996.
- Accepted July 31, 1996.
- Copyright © 1996 by American Heart Association
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