Radiofrequency Ablation of Intra-Atrial Reentrant Tachycardia After Surgical Palliation of Congenital Heart Disease
Background Intra-atrial reentrant tachycardia (IART), also called atrial flutter, is a common and potentially lethal complication of surgical correction of congenital heart disease. Medical management of IART is often problematic, which prompts an investigation of the utility of radiofrequency (RF) ablation for management of these arrhythmias.
Methods and Results Ten consecutive patients referred for treatment of recurrent IART after surgery for congenital heart disease were studied. Median age was 18.4 years, and median duration of arrhythmia was 6.4 years; a median of three antiarrhythmic drugs had been tried. Surgical procedures used were Fontan (6), Mustard/Senning (2), and biventricular repair (2). Intracardiac electrophysiological study demonstrated 30 distinct IART circuits, defined by activation sequence and cycle length. Mean IART cycle length was 323±114 ms. Cycle length was significantly longer in IART circuits that were successfully ablated compared with those that were not (381 versus 248 ms, P<.001). RF ablation was attempted in 22 of these circuits. Ablation sites were targeted to presumed exit points from zones of slow conduction by electrophysiological criteria. Sites chosen in this manner clustered in four distinct areas of the right atrium. Of 22 IART circuit ablations attempted, 17 (77%) resulted in acute termination of the tachycardia. In 8 of 10 patients in whom at least one IART circuit was successfully ablated, 4 are free of clinical tachycardia and 3 are improved over short-term follow-up. No complications were encountered.
Conclusions Multiple IART circuits may be present in patients after surgery for congenital heart defects. Activation sequences observed were diverse and different from those observed in atrial flutter in patients with normal anatomy. Interruption of IART circuits by RF ablation is feasible using mapping techniques aimed at identifying an exit point from a zone of slow conduction. Short-term follow-up suggests that RF ablation may be a useful adjunct in management of IART in these difficult patients.
Intra-atrial reentrant tachycardia (IART) is a common and potentially life-threatening complication of repair or palliation of congenital heart disease. This arrhythmia is prevalent in patients who have undergone surgical procedures involving significant alteration of the atrium, such as the Mustard and Senning operations and the Fontan procedure, and its incidence increases over time.1 2 3 4 Although IART has usually been referred to in clinical studies as “atrial flutter,” differences in atrial activation sequence and cycle length suggest that these arrhythmias are distinct from classic type I atrial flutter.
Atrioventricular reciprocating tachycardias are now managed with high success and low complication rates by use of transcatheter radiofrequency (RF) ablative techniques to eliminate their anatomic substrates.5 6 7 Successful ablation of type I atrial flutter,8 IART,9 and ectopic atrial tachycardia10 11 has been reported in patients with normal intracardiac anatomy. Five cases of successful termination of IART in patients with postoperative congenital heart disease have been reported.12 13 In prior reports of RF ablation of atrial flutter and IART, interruption of reentry has been achieved by modification of a zone of slow conduction critical for the perpetuation of the circuit,8 9 14 with ablation sites identified by activation sequence mapping and pacing entrainment criteria. In this report, initial clinical experience in the application of these techniques in postoperative patients with congenital heart disease and associated refractory IART is presented.
All patients (n=10) referred to Children’s Hospital for management of recurrent IART between April 1993 and January 1994 were included. Ablation was attempted in patients who had had multiple sustained and symptomatic episodes of atrial tachyarrhythmia and had failed therapy on at least one medication. All patients had undergone one or more prior cardiac surgeries for congenital heart disease. Informed consent was obtained under a protocol approved by the Clinical Investigations Committee of Children’s Hospital.
Definition of IART
Clinical criteria for the diagnosis of IART included episodic rapid atrial rhythm, characterized by abnormal P-wave morphology, constant cycle length, sudden onset and termination of the tachyarrhythmia, and episodic Mobitz type I atrioventricular block without interruption of the primary tachyarrhythmia.15 Additional electrophysiological criteria determined by esophageal and/or intracardiac study as necessary for confirmation of the diagnosis included the ability to reproducibly initiate and terminate the tachyarrhythmia by use of programmed atrial stimulation, the demonstration of a nonsinus mechanism by atrial activation sequence, and the elimination of accessory atrioventricular pathways or atrioventricular node reentry as diagnostic possibilities.
Intracardiac Electrophysiological Technique
Antiarrhythmic medications were discontinued for at least five half-lives in all patients; however, 4 patients had received amiodarone less than 1 month before intracardiac study. After cannulation of the femoral artery and vein(s), patients were administered 100 IU/kg heparin (maximum, 5000 IU), with repeat doses used to maintain activated clotting time >150% of control. After hemodynamic and angiographic study, three electrophysiology catheters (Webster Laboratories) were positioned in the right atrium: a 7F deflectable catheter (2-5-2–mm electrode spacing, 4-mm tip electrode) used as a mapping and ablation catheter and two 6F or 7F deflectable decapolar electrode catheters (2-5-2-5-2-5-2-5-2–mm electrode spacing) used as reference mapping catheters. Because of the variable and complex atrial anatomy of these patients, straight anteroposterior and lateral views were used both for angiography and subsequent intracardiac mapping. In general, the decapolar catheters were initially positioned so that they mapped bands of the anterior and posterior atrial surfaces in a craniocaudal orientation (Fig 1⇓). In two patients, an esophageal electrode was used to facilitate atrial pacing. Programmed stimulation was performed at twice diastolic threshold using a 2.0-ms pulse width. Up to 12 intracardiac signals were recorded and filtered between 40 and 400 Hz for display on a 16-channel system, along with four surface ECG leads (Arrhythmia Research Technologies).
Standard atrial extrastimulus testing (up to S3 and burst pacing) was used to induce and terminate IART. In five studies, administration of isoproterenol (0.005 to 0.02 μg · kg−1 · min−1) was needed to achieve sustained IART. Activation sequence maps were constructed with the three electrode catheters to determine the overall morphology of the reentrant circuit. The initial positions of the decapolar catheters were altered as needed to define the atrial activation sequence.
Possible zones of slow conduction were identified by the presence of low-amplitude, fractionated electrograms of long duration occurring in atrial electrical diastole, defined as the period occurring between surface P waves, and an observation of relatively large shifts in electrogram timing associated with small movements of the mapping catheter. Atrial stimulation with fixed-rate pacing was performed using the roving quadripolar catheter to determine entrainment characteristics of the IART. Concealed entrainment was considered to have occurred when the tachycardia was accelerated to the pacing cycle length without alteration of the atrial activation sequence and with continuation of the tachycardia at its prepacing cycle length on the first postpacing beat.16 When possible, entrainment was determined at several anatomic sites to assist in anatomic mapping of the zone of slow conduction, and attempts were made to demonstrate a shift from transient to concealed entrainment when the pacing catheter was moved across the presumed zone of slow conduction. However, if the IART was terminated by entrainment pacing and/or if sustained IART had been difficult to induce by programmed stimulation, entrainment studies were limited. Target areas for application of RF energy were identified by the following criteria: (1) local atrial activation preceding the onset of the surface P wave by ≥30 ms, as well as all other sharp electrograms in the activation sequence of atrial electrical systole, and (2) anatomic site adjacent to a slow zone of conduction. Electrophysiological criteria are presented in Fig 2⇓.
RF energy was generated at 500 kHz with a voltage-controlled RF generator (Radionics RFG-3C, Radionics, Inc) and was delivered in a unipolar fashion between the distal 4-mm tip of the mapping/ablation catheter and an adhesive ground patch electrode on the chest wall. During each application of RF energy, power (in watts) and duration were set by the operator, and voltage, current, and impedance were continuously monitored. RF energy was applied in a power range from 5 to 40 W, with the lower end of that range necessary in several patients because of impedance rises noted when application commenced at 20 W. If the tachycardia was not affected after 15 to 20 seconds of RF application, it was terminated, and endocardial mapping resumed. If the IART terminated, became irregular, or changed in rate, the application was continued for 40 to 60 seconds and the power increased to 35 to 40 W or until an impedance rise occurred. After a successful lesion, attempts were made to reinduce the ablated IART by programmed atrial stimulation with and without infusion of isoproterenol. Additional lesions were placed at the anatomic site of a successful ablation to reduce the likelihood of possible recurrence. If additional discrete circuits of IART were identified either before or after a successful ablation, endocardial mapping and ablation procedures were repeated. After completion of the study, patients were monitored continuously for 18 to 24 hours, and a chest radiograph and 12-lead ECG were performed. In cases in which all inducible IART had apparently been eliminated, patients were discharged with no antiarrhythmic medications specifically targeted at the IART. Outpatient follow-up visits were performed 1, 3, and 6 months after the procedure and included a 12-lead ECG and Holter monitoring.
Data are presented as either mean±SD or median and range, as appropriate. Comparison among data sets was performed with Student’s t test for unpaired data and ANOVA. Statistical significance was determined as P<.05.
Ten consecutive patients (median age, 18.4 years; range, 12.0 to 43.5 years) were catheterized 12 times between April 1993 and January 1994. Six patients with variants of single-ventricle anatomy had had a Fontan procedure involving the creation of a direct anastomosis between the pulmonary arteries and either the right atrial appendage or the roof of the right atrium. Two patients with transposition of the great arteries had had an atrial baffling procedure (1 Senning, 1 Mustard) to redirect caval blood flow to the subpulmonary left ventricle and pulmonary venous blood flow to the subaortic right ventricle. Two patients had had a repair of a ventricular septal defect with right ventricular outflow tract obstruction. Each patient had undergone from 1 to 5 cardiac surgical procedures (median, 2.5). All had had at least one right atriotomy, and 9 of 10 patients had at least one other discontinuity of the right atrial surface (creation of a Fontan anastomosis via the atrial appendage, conduit, or direct atriopulmonary connection, atrial septostomy, and/or cannulation of the right atrial appendage for cardiopulmonary bypass). Patients undergoing Mustard and Senning procedures also had creation of extensive atrial suture lines. Anatomy and surgical history of the patients are presented in Table 1⇓.
The median age at which the major cardiac surgical procedure was performed was 4.8 years (range, 0.9 to 26.6 years); the median age at onset of tachycardia was 11.8 years (range, 4.6 to 27.8 years); and the median age at electrophysiological study was 18.4 years (range, 12.0 to 43.5 years). Patients had received a median of three antiarrhythmic medications (range, 1 to 7), and permanent atrial antitachycardia pacing had been attempted in 3 of 10 patients.
Mapping and Ablation
Thirty discrete IART circuits, from 1 to 5 in each patient, were identified by cycle length and activation sequence mapping. Of the 30 circuits, 22 (73%) were mapped and ablation was attempted; in 8 circuits in which no ablation was attempted, 6 terminated spontaneously or with atrial pacing and could not subsequently be reinduced, and 2 were deferred because of procedure duration. Of the 22 circuits in which ablation was attempted, all were sustained and demonstrated stable P-wave morphology and electrogram sequence. Of these 22 circuits, 17 (77%) were successfully terminated by application of RF energy. In 8 of 10 patients, at least one IART circuit was terminated by application of RF energy. The anatomic locations of the 22 mapped exit points at which ablation was attempted are presented in Fig 3⇓. With two exceptions, these anatomic sites were grouped into four areas: (1) at or near the site of the Fontan anastomosis (ostium of the right atrial appendage or atriopulmonary anastomosis), with activation sequence suggesting a circuit proceeding around the anastomosis (2 patients); (2) at the lateral junction of the right atrium and the superior vena cava (6 patients); (3) at the lateral junction of the right atrium and the inferior vena cava (2 patients); or (4) near the triangle of Koch (8 patients).
Data for the individual IART circuits encountered are presented in Table 2⇓. Mean cycle length was 323±114 ms, with a range from 181 to 610 ms. The mean cycle length of the 20 IART circuits observed in the 6 Fontan patients was longer than that observed in the 10 IART circuits from the non-Fontan group (369±113 versus 232±34 ms, P<.001). Mean cycle length of the 17 IART circuits successfully interrupted by ablation was 381±112 ms, compared with 275±47 ms for the 5 circuits in which ablation attempts were unsuccessful and 231±66 ms for the 8 circuits in which no ablation was attempted (P=.002 by ANOVA). Cycle lengths observed at each catheterization were not correlated with any hemodynamic or angiographic measurement.
Atrial mapping data in 14 of the 17 successfully ablated circuits identified local electrical activity at the exit point of the zone of slow conduction preceding the onset of the surface P wave by 40 to 159 ms (mean, 89±32 ms). The precise onset of P wave activity could not be determined in the other 3 cases. In 16 of 17 cases, a zone of slow conduction was identified anatomically adjacent to the successful electrogram. In all 8 circuits in which entrainment pacing was performed before attempted ablation, concealed entrainment was demonstrated. From 1 to 23 applications of RF energy were required to interrupt the IART circuits (median, 4), with the duration of the successful application ranging from 0.8 to 36 seconds until success (median, 14.2 seconds). From 0 to 12 (median, 1.5) additional lesions were placed at or near the anatomic site of successful tachycardia terminations. Such additional RF applications were generally deemed appropriate to enlarge the RF lesion if the IART circuit had required either many RF applications or very prolonged application of RF energy before tachycardia interruption. Maximum power of the successful application ranged from 20 to 43 W (median, 35 W). Impedance rises were encountered even at power settings of 15 to 20 W, particularly in Fontan patients. Consequently, RF applications were often begun at power settings of 5 to 7.5 W and increased to the range of 20 to 40 W or until an impedance rise. Most commonly, successful ablation was signalled by abrupt termination of the IART (Fig 4A⇓). However, in 3 cases, prolongation of the IART cycle length was noted before the termination of the arrhythmia, and in one case, an irregular rhythm possessing the same activation sequence as the tachycardia was observed, suggesting a variable exit block from the zone of slow conduction (Fig 4B⇓).
Two ablation sessions were required for patients 1 and 2. Patient 1 had a recurrence of tachycardia within 72 hours of his first ablation procedure, and a second procedure, during which an additional 2 IART circuits were mapped and 1 was successfully ablated, was performed 9 days later. After the patient’s second ablation procedure, he had a symptom-free interval of 2 months before a clinical recurrence. He is currently experiencing occasional nonsustained episodes of IART on amiodarone, which had previously been an ineffective antiarrhythmic agent. Patient 2 had a symptom-free interval of 6 months after his first ablation, with no inducible IART observed during a programmed atrial stimulation study performed 2 months after the ablation. At his second ablation, performed 7 months after the first, 3 IART circuits were mapped and 1 was successfully ablated. Within 48 hours of the second procedure, the patient had a recurrence of IART. An atrial antitachycardia pacemaker was implanted, and sotalol therapy was reinstituted; this patient continues to have problematic IART. In neither of these cases was there evidence, by cycle length or site targeted for ablation, of recurrence of an IART circuit previously thought to be ablated, but the possibility of recurrence of such circuits in a modified form cannot be excluded.
Ablation failed despite prolonged efforts in patients 4 and 10. In patient 4, 2 IART circuits were observed. A right atrial angiogram revealed a very large right atrium, and difficulty was encountered in obtaining accurate catheter placement in the atrium, despite the use of curved guiding sheaths. After extensive attempts to map the IART circuits, entrainment pacing maneuvers resulted in the initiation of sustained atrioventricular node and sinoatrial reentrant tachycardias, and attempts to ablate the initial IART were abandoned. In patient 10, who had undergone a Senning procedure for transposition of the great vessels, a single IART was identified, with an apparent zone of slow conduction in the isthmus between the ostium of the inferior vena cava and the tricuspid annulus. A suture line associated with the Senning repair lies between these two structures. Unipolar applications of RF energy made on both sides of the suture line and a bipolar application from the pulmonary venous to the systemic venous sides of the repair were unsuccessful.
No complications specific to ablation were encountered. In patients with previously implanted pacemakers, no damage was incurred to either lead or generator. Patient 3 had significant blood loss from his femoral venous cannulation site approximately 6 hours after the procedure, which required transfusion with 1 unit of packed red blood cells. AP fluoroscopy times ranged from 36.2 to 96.5 minutes, with a median of 52.6 minutes.
Of 10 patients in whom RF ablation of IART was attempted, 4 (patients 3, 5, 8, and 9) are off antiarrhythmic therapy directed toward their IART and are currently asymptomatic except for occasional nonsustained palpitations. One patient who remains off antiarrhythmic therapy (patient 6) had a single undocumented, self-terminated episode of tachycardia lasting 2 hours. Three patients have had recurrence of sustained atrial flutter necessitating resumption of medical therapy. Two of these 3 patients (patients 1 and 7) are clinically improved on previously ineffective regimens. In the third (patient 2), tachycardia remains clinically problematic despite atrial antitachycardia pacing and sotalol therapy. The 2 patients in whom no IART circuit could be successfully interrupted (patients 4 and 10) remain on antiarrhythmic therapy. An atrial antitachycardia pacemaker was also implanted in patient 10. For the 8 patients in whom at least one IART circuit was successfully ablated, follow-up currently ranges from 1.3 to 10.8 months (median, 4.0 months). All patients remained on digoxin for hemodynamic indications. Procedure results and follow-up are summarized in Fig 5⇓.
Although IART is rare in patients with structurally normal hearts, it is seen frequently in postoperative patients with a spectrum of congenital lesions. A steadily increasing prevalence of atrial tachyarrhythmias has been reported in survivors of extensive atrial surgery, such as atrial baffle procedures for transposition of the great arteries and the Fontan procedure for variants of univentricular heart, with rates approaching or exceeding 50% at 10 years.1 2 3 4 IART is a cause of significant postoperative morbidity in this group and may be a lethal event in some patients.3 17 18 Electrophysiological studies in animals and humans have established the reentrant nature of these tachycardias and the importance of anatomic and functional obstacles to atrial conduction in the initiation and maintenance of these arrhythmias.19 20 21 Although the specific factors predisposing these patients to IART have not been identified, possibilities include (1) atrial scarring caused by multiple atriotomies, long suture lines, and pericardial inflammation; (2) the presence of abnormal atrial wall stress in disordered hemodynamic states; (3) abnormal atrial anatomy associated with the congenital lesion itself; and (4) changes in atrial refractoriness associated with sinus node dysfunction and concomitant bradycardia.
Management of IART may be problematic in these patients. The underlying congenital lesions and the surgical procedures that create the substrate for the development of this arrhythmia are often associated with a marginal hemodynamic status, which may limit options for arrhythmia management. Antiarrhythmic drugs may aggravate sinus node dysfunction and/or cause deterioration of ventricular function. Although atrial antitachycardia pacing may be useful in selected patients,13 effective use of this modality requires placement of a pacing lead that can accurately sense atrial electrograms both in sinus rhythm and tachycardia, a requirement that may be difficult to meet in many postoperative patients with congenital heart disease. This report demonstrates the feasibility of using RF ablation in the management of IART associated with congenital heart disease. At least one IART circuit was successfully ablated in 8 of 10 patients, and 7 were clinically improved over short-term follow-up. Thus, RF ablation may represent an additional therapeutic option for selected patients in this expanding group.
Accurate localization of a vulnerable area of atrial myocardium for ablation of these tachycardia circuits is more complicated than localization of accessory pathways. Several mapping criteria were used in early reports on the ablation of type I atrial flutter, ectopic atrial tachycardia, and IART in normal hearts.8 9 10 11 12 In this study, activation sequence mapping, identification of a zone of slow conduction by electrogram morphology and timing, and entrainment pacing were all used to map sites vulnerable to ablation in IART, resulting in successful interruption of 77% of the circuits mapped.
The number and duration of RF lesions required to achieve termination of IART was higher than those for accessory pathway ablation in our laboratory. This finding is consistent with other reports of ablation of classic atrial flutter, in which the application of continuous linear RF lesions across a vulnerable isthmus of atrial tissue has been shown to be effective.22 The effective region in these studies was between the tricuspid annulus and either the inferior vena cava or the coronary sinus. Activation mapping and entrainment pacing techniques have characterized this area electrophysiologically as a zone of slow conduction during classic atrial flutter.22 23 However, when a corridor of tissue is the target for ablation, it remains unclear whether its most vulnerable point will be determined by the anatomy of the corridor or its electrophysiological properties. This problem is compounded in the mapping and ablation of sites in IART associated with congenital heart disease, because one or both of the anatomic obstacles that define the critical isthmus of atrial tissue to be ablated are likely to be at unknown locations within the atrium. In the absence of true sequential atrial activation sequence mapping with an electrode density sufficient to define clearly the areas of functional block, it is difficult to rationally propose the length and orientation of a linear ablative lesion that will effectively interrupt the reentrant circuit. It is possible that this uncertainty, combined with the primary use of point lesions in this study, may account for the relatively long duration of effective lesions before termination of tachycardia, given the relation between RF lesion size and duration.24 In some cases, gradual lesion growth might also explain the observations of slowing of tachycardia before complete termination.
In 8 patients, multiple discrete IART circuits were observed. These were distinguished by cycle length and atrial activation, suggesting that multiple anatomic circuits may mediate IART in these patients. In several patients, these findings were concordant with clinical observation of tachycardias with multiple cycle lengths and P-wave morphologies. Prior electrophysiological studies of IART have also documented the occurrence of multiple circuits.9 15 However, it was not necessary to eliminate all of the observed IART circuits to effect the short-term improvement of arrhythmia control observed in this group. In 3 patients currently free of symptoms off antiarrhythmic medications (patients 3, 5, and 8), five nonreproducible tachycardias were induced but not ablated. Four of these tachycardias were nonsustained and not mapped; in one, an ablation was attempted but failed. It is possible that these circuits observed were not clinically significant, either because they were normally unstable and nonsustained or because they were purely an artifact of programmed stimulation. Alternatively, some of the morphologically distinct IARTs that were not ablated may have been reliant at some point in their circuit on an area that was ablated in the process of terminating an apparently different IART; ie, a single critical point might affect multiple IART pathways.
This question may be partially addressed by examination of the anatomic distribution of mapped exit points. They were grouped into four distinct areas distributed along the presumed course of the crista terminalis: the superior and inferior lateral right atrial walls, the surgically created Fontan anastomosis, and the isthmus of atrial tissue bridging the inferior vena cava and the tricuspid valve. Circuits related to the lateral right atrial wall might plausibly be mediated by the creation of complete or functional block in tissue related to a right atriotomy scar. A similar type of reentrant loop has been demonstrated in human IART.20 Similarly, reentrant circuits related to a Fontan anastomosis have at their center a large area of atrial discontinuity. Circuits mapped to the area posterior to the triangle of Koch are unlikely to have undergone surgical manipulation, but the zone of slow conduction is in the same location as that seen in typical atrial flutter in adults without congenital heart disease.
The apparent relation of many of these circuits to the site of prior atriotomy suggests that atrial myocardium surrounding the incision may be critical in the maintenance of IART, similar to the role of the peri-infarction zone in reentrant ventricular tachycardia observed after myocardial infarction.25 It is possible that slow anisotropic conduction across the crista terminalis further predisposes lesions in these areas to serve as substrates for IART.26 If this is true, a significant fraction of the IARTs observed in this study might have been avoided by prophylactic modification of the right atriotomy at the time of surgery. Extension of the atriotomy to either the inferior vena cava or the tricuspid annulus would presumably have the effect of interrupting a critical isthmus of atrial tissue.
Introduction of electrophysiology catheters bearing a high density of electrodes may facilitate rapid and comprehensive mapping of reentrant tachycardia circuits in vivo in the future. Successful ablations of IART in this study confirm the presence of critical areas for reentrant circuit interruption and tend to support the criteria used, which included systematic mapping of the IART circuit and localization of presumed zones of slow conduction and sites of earliest atrial activation. The substrate for these arrhythmias includes abnormal atrial muscle chronically exposed to altered hemodynamics and surgical interventions. Thus, it may be expected that some patients will develop new and clinically significant IART after “successful” ablation procedures. Nevertheless, management of IART in these patients is often sufficiently difficult to justify the development of this technique as a palliative adjunct to current therapy, as well as a curative therapy in those cases in which an IART circuit can be clearly mapped and a well-defined area of atrial tissue ablated. Additional experience and longer follow-up of these patients may indicate the potential of this technique to assist in the management of IART after congenital heart surgery.
Dr Saul is supported in part by National Institutes of Health NHLBI Clinical Investigator Award No. K08-HL-02380-03 and a grant from the Whitaker Foundation. Dr Weindling is supported by National Institutes of Health Training Grant No. 7301.
Reprint requests to John K. Triedman, MD, Department of Cardiology, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115.
Presented in part at the 43rd Scientific Sessions of the American College of Cardiology, Atlanta, Ga, March 16, 1994.
- Received August 15, 1994.
- Accepted September 23, 1994.
- Copyright © 1995 by American Heart Association
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