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Ann Thorac Surg 2003;76:542-554
© 2003 The Society of Thoracic Surgeons
a Divisions of Cardiology and Cardiovascular-Thoracic Surgery, Children’s Memorial Hospital, and the Departments of Pediatrics and Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois USA
* Address reprint requests to Dr Mavroudis, Division of Cardiovascular-Thoracic Surgery M/C #22, Children’s Memorial Hospital, 2300 Children’s Plaza, Chicago, IL 60614, USA.
e-mail: cmavroudis{at}childrensmemorial.org
Presented at the Thirty-eighth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 28–30, 2002.
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Abstract |
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METHODS: Between July 1992 and January 2002, 29 patients had operations for refractory atrial (n = 24) or ventricular (n = 5) arrhythmias. Mechanisms of arrhythmia included atrial reentry (n = 11), atrial fibrillation (n = 5), automatic atrial (n = 3), accessory connections (n = 6), atrioventricular nodal reentry (n = 2), and ventricular tachycardia (n = 5). Median age at operation was 12.3 years (range, 6 days to 45 years). Two patients had structurally normal hearts; the remaining 27 patients underwent concomitant repair of structural heart disease, including atrioventricular valve replacement or repair (n = 8), anatomy-specific repair of Ebstein’s anomaly (n = 4), tetralogy of Fallot repair or revision (n = 4), atrial septal defect closure (n = 3), ventricular septal defect repair (n = 2), Mustard takedown with arterial switch (n = 2), initial Fontan (n = 2), right ventricle-to-pulmonary artery conduit revision (n = 2), Norwood procedure (n = 1), 1 ventricular repair for Uhl’s anomaly (n = 1), Mustard baffle revision (n = 1), pulmonary valve replacement with aneurysm resection (n = 1), and aortic valve replacement with complex repair (n = 1).
RESULTS: No patient developed heart block, and the surgical mortality rate was 7%. One patient died after Mustard takedown and arterial switch operation, and 1 neonate died after repair of severe Ebstein’s anomaly. There was one late death after arterial switch conversion at another institution. Recurrent clinical supraventricular tachycardia was present in 2 patients (2 of 27, 7.4%) and 2 patients had new-onset tachycardias with different underlying mechanisms of arrhythmia at late follow-up (median follow-up 47 months).
CONCLUSIONS: Successful surgical therapy of arrhythmias can be performed safely at the time of repair of complex congenital heart disease or in patients with failed catheter ablation procedures. Early consideration for single-stage therapy of arrhythmia and structural heart disease is indicated.
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsCommentDiscussionReferences |
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We previously reported our experience with Fontan conversion and arrhythmia operations to treat patients with established Fontan operations and atrial reentry tachycardia or atrial fibrillation [10–13]. In these studies isthmus ablation and later the modified right atrial maze procedure were developed to treat the various anatomic single-ventricle substrates. In addition to these redo Fontan patients with arrhythmias, we have also accumulated experience treating predominantly young patients with arrhythmias, many with associated complex congenital heart disease. The purpose of this study is to review our experience with arrhythmia operations since the advent of catheter ablation, excluding patients who underwent Fontan conversion.
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsCommentDiscussionReferences |
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Mechanisms of arrhythmia included atrial reentry (n = 11); atrial fibrillation (n = 5); automatic atrial (n = 3), manifest (Wolff-Parkinson-White) (n = 4), or concealed (n = 2) accessory connections; atrioventricular nodal reentry (n = 2); and ventricular tachycardia (n = 5). Three patients had two mechanisms of arrhythmia. One patient with atrioventricular nodal reentry and 1 patient with concealed accessory connections had associated atrial reentry tachycardias. One patient with atrial fibrillation had concealed accessory connections. All patients had recurrent arrhythmias with symptoms, including congestive heart failure (n = 11), syncope (n = 4) or presyncope (n = 2), and palpitations (n = 12). Patients had received prior antiarrhythmic drug therapy, with a mean of 2.3 medications per patient. Seven patients had undergone 11 prior ablation procedures. Preoperative intracardiac electrophysiology studies to determine tachycardia mechanism and anatomic foci were performed in 21 patients, excluding 2 neonates with automatic atrial tachycardia, 2 neonates with Ebstein’s anomaly, and 4 patients with atrial fibrillation. Epicardial mapping was performed in 23 patients (except 5 patients with atrial fibrillation, and 1 patient with ventricular tachycardia) using a hand-held roving probe (18 patients) or a multiple-array epicardial sock (5 patients).
Surgical arrhythmia techniques
Atrial reentry tachycardia and automatic atrial foci were treated with a combination of resection, isolation, and cryoablation of affected atrial tissue. Cryoablation was performed using 3-, 5-, and 15-mm circular probes (Frigitronics, CooperSurgical, Inc, Shelton, CT) at -60°C for 90 seconds. Atrial fibrillation was treated using the Cox-maze III procedure [9]. Atrioventricular nodal reentry tachycardia was addressed using cryoablation modification of the slow pathway of the atrioventricular node in the region of the coronary sinus. Accessory connections were divided using both epicardial and endocardial resection techniques. Sites of ventricular tachycardia underwent endocardial resection and cryoablation in 4 patients with epicardial resection and cryoablation in 1 patient.
Surgical repair of congenital heart disease was performed in concert with the arrhythmia operation using standard techniques. Postoperative electrophysiology studies were performed before hospital discharge on all surviving patients except those with atrial fibrillation or automatic atrial tachycardia. Pacing protocols for patients with atrial tachycardia included atrial incremental pacing and single, double, and triple atrial extrastimulation. Ventricular stimulation in patients with ventricular tachycardia consisted of single, double, and triple extrastimulation at two paced cycle lengths from both the right ventricular apex and outflow tract. All patients underwent study in the baseline state and after infusion of isoproterenol at 0.1 µg/kg per minute. Patients with atrial fibrillation received amiodarone therapy for 3 months postoperatively.
Arrhythmia recurrence was assessed by review of symptoms, continuous 24-hour electrocardiographic monitoring before discharge and at a minimum of yearly thereafter, and interrogation of pacemakers or implanted defibrillators at routine visits.
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Results |
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Median postoperative hospital stay was 9 days (range, 5 to 83 days). Surgical complications (7 of 29, 24%) included perioperative supraventricular tachycardia (SVT) (4 of 29, 14%), congestive heart failure (n = 1), prolonged ventilator dependence (n = 1), and prolonged chest tube drainage (n = 1). No patient developed heart block.
Operative findings
The details of surgical repairs and operative findings are summarized in Tables 1–6.
Gross anatomic findings associated with the tachycardia focus were noted intraoperatively in 10 of 29 patients (34%). All three patients with automatic atrial
tachycardia had identifiable areas of discrete dysplastic tissue at the site of earliest atrial activation, at the base of the right atrial appendage. All 5 patients with ventricular tachycardia had scar tissue. Endocardial fibroelastosis was noted in the three patients with tetralogy of Fallot. In the patient with a ventricular septal defect, a discrete white fibrous plaque was seen at the site of the jet lesion from the ventricular septal defect. In the
patient with a normal heart, a discrete white fibrous plaque was noted on the epicardial surface of the left ventricular outflow tract. In this patient, a fat pad was resected from a
focal area between the first and second diagonal branches of the left anterior descending coronary artery. On microscopic examination, a dense concentration of hypertrophied nerve fibers was present. One neonate with tetralogy of Fallot and atrial reentry
tachycardia had greyish, dysplastic tissue resected from the right atrial wall involving the mid-crista terminalis. One patient with atrial fibrillation had a jet lesion of the internal base of the superior vena cava directly opposite the flow of the coronary fistula.
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Late postoperative tachycardia
Median duration of follow-up was 47 months. Among the 21 patients in the atrial arrhythmia group who survived, in addition to the patient with persistent perioperative recurrence of accessory connection-mediated tachycardia, documented recurrence of the clinical SVT occurred in 2 additional patients (2 of 21, 9.5%) (Table 7). In a patient who underwent cryoablation of atrial reentry tachycardia, the recurrence occurred 1 month postoperatively and was responsive to treatment with sotalol; there has been no recurrence of the SVT, and the patient is not taking anti-arrhythmic medications. In another patient with a normal heart who underwent cryoablation of atrial reentry tachycardia after not responding to 10 anti-arrhythmic medications and two ablation procedures, the tachycardia recurred 5 years postoperatively during pregnancy. She underwent ablation of the atrioventricular node with pacemaker implantation at another institution.
There was no late recurrence of ventricular tachycardia among the 5 patients with ventricular arrhythmia. Neither tetralogy of Fallot patient with implanted defibrillators for ventricular tachycardia has received appropriate discharges for ventricular arrhythmias, although atrial reentry tachycardia developed in 1 patient 4 years postoperatively at age 39 years.
One patient with atrial reentry tachycardia had palpitations terminating spontaneously and is receiving beta-blocker medication. The patient with persistent perioperative tachycardia from an accessory connection continues to have recurrent SVT requiring medication. Another patient with Wolff-Parkinson-White syndrome and Ebstein’s anomaly underwent successful surgical ablation of the accessory connection, but atrial reentry tachycardia developed 3 years postoperatively at age 16.8 years. A repeat ablation procedure was unsuccessful, and he is receiving medication. Overall, 3 patients with SVT require anti-arrhythmic medications during late follow-up (3 of 26, 11.5%).
Late follow-up
Two patients (2 of 26, 7.7%) underwent pacemaker implantation for late development of sinus bradycardia. One patient with transposition of the great arteries died 11 months postoperatively after an arterial switch operation at another institution. One patient with Uhl’s anomaly underwent an extracardiac total cavopulmonary connection 3 years after a 1 ventricular repair.
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Comment |
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TopAbstractIntroductionPatients and methodsResultsCommentDiscussionReferences |
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We have categorized our experience based on arrhythmia mechanism because each type of arrhythmia has different electrophysiologic substrates, is approached with a different ablative strategy, and carries the possibility of multiple associated arrhythmias. The various ablative procedures that were used in this series evolved over the course of the study pursuant to the types of arrhythmias, the anatomic substrates, and increased experience derived from catheter ablation studies.
Arrhythmia mechanism
Surgical arrhythmia therapy had the highest success in patients with SVT. In our group of 24 patients with atrial reentry, automatic atrial, atrioventricular nodal reentry tachycardia, and atrial fibrillation, surgical treatment of the clinical tachycardia was successful in 92%. The clinical tachycardia recurred in 2 patients (8%), one after an arrhythmia-free interval of several years. Success in these patients is likely related to the ability to excise notably abnormal tissue and create deep lines of block with the assurance of complete lesion continuity between anatomic obstacles, such as the venae cavae or pulmonary veins. Surgical therapy of accessory connections in association with complex ventricular anatomy was less successful, failing in 1 patient with dextrocardia, heterotaxy syndrome, and complete atrioventricular canal defect. Previously published reports of accessory connection operations in young patients with structural heart disease have focused on patients with atrial or ventricular septal defects or Ebstein’s anomaly [2, 25–29]. In the complex heart it is possible to have abnormal accessory connection locations, such as between the aortic and mitral valves. Concern over the location of the atrioventricular node may also be a limiting factor. Similar to a previous report [29], surgical therapy of multiple accessory connections in patients with Ebstein’s anomaly allows definitive endocardial resection of the right posterior and lateral atrial wall where most connections are found. When present in combination with significant tricuspid regurgitation or atrial septal defects, the surgical approach may be preferable to several lengthy catheter ablation procedures. Definitive therapy for atrial fibrillation with associated complex congenital heart disease is available surgically with outstanding results, as we have demonstrated in patients with single ventricle repairs. The low rate of recurrence in this small series of patients with atrial fibrillation is comparable to that reported in adult patients [30, 31] and demonstrates better outcome compared with the right atrial maze procedure reported by Theodoro and colleagues [32].
Surgical treatment of ventricular tachycardia was less successful in our experience. In the 2 patients without prior cardiac operation, discrete abnormal anatomic findings relating to the ventricular tachycardia were identified, allowing successful resection of the dysplastic tissue. In contrast, treatment of ventricular tachycardia occurring late after repair of congenital heart disease was successful in only 1 of 3 patients, as measured by inducibility of ventricular tachycardia at electrophysiologic study postoperatively in the other 2 patients. One of these patients had multiple tachycardia morphologies that were not mapped. We speculate that failure may be related to a deep endocardial focus of tachycardia, possible origin on the left ventricular septal surface, or inadequate mapping. These results are comparable to those reported by others [33, 34], where ventricular tachycardia persisted postoperatively in 30% to 50% of patients with tetralogy of Fallot [35]. Based on these results, patients with postoperative tetralogy of Fallot are more likely candidates for implantable defibrillators if tachycardia remains inducible.
Neonatal operations
Five patients were infants with associated complex heart disease, including severe Ebstein’s anomaly with accessory connections (2 patients), hypoplastic left heart syndrome with incessant automatic atrial tachycardia, tetralogy of Fallot with recurrent atrial reentry tachycardia, and ventricular septal defect with automatic atrial tachycardia. The mean age at surgical repair was 25 days. The complexity of both the congenital heart disease and hemodynamically unstable tachycardia made these small patients poor candidates for a catheter approach. Cardiopulmonary bypass allowed adequate mapping of tachycardia while maintaining stable blood pressure, with successful elimination of the clinical tachycardia. One patient with Ebstein’s anomaly and pulmonary atresia died of low cardiac output on the first postoperative day. In this complex substrate of patients, we believe the combined surgical and arrhythmia approach provided optimal therapy and eliminated the need for long-term anti-arrhythmic medications.
Of note, late atrial reentry tachycardia developed in 2 patients postoperatively who had Ebstein’s anomaly with Wolff-Parkinson-White syndrome and tetralogy of Fallot with ventricular tachycardia. Both of these lesions are associated with an incidence of late atrial tachycardia greater than 25% [32, 35, 36]; neither patient had atrial reentry tachycardia operation. We believe that these results support the concept of a prophylactic right atrial maze procedure in older patients who have operations for congenital heart disease, including tetralogy of Fallot, atrioventricular valve operation, and atrial septal defects. A prospective, multicenter investigation of prophylactic arrhythmia operations in this patient population would be welcome, as only such a study would accrue sufficient numbers of patients to draw conclusions about its efficacy.
This series demonstrates that surgical arrhythmia therapy can be performed for patients in whom the catheter ablation approach fails and can be successfully incorporated into repair of complex congenital heart disease in all age groups. Variations in atrial and ventricular anatomy that may limit the catheter approach can be directly addressed surgically, assuring lesion depth and continuity of anatomic lines of block. Patients who require surgical intervention for hemodynamic abnormalities can be spared a lengthy catheter ablation procedure by careful preoperative arrhythmia mapping and definitive surgical arrhythmia therapy, with results comparable or superior to results achieved in the catheterization laboratory. Patient size or anatomic complexity should not be limiting factors in the combined surgical arrhythmia approach. Furthermore, because older patients undergoing surgical revision of prior surgical repairs of congenital heart disease are at increased risk for the later development of atrial arrhythmias [35–40], we believe that incorporation of arrhythmia therapy into any planned surgical revision in older patients should be considered.
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Discussion |
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TopAbstractIntroductionPatients and methodsResultsCommentDiscussionReferences |
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In the late 1970s and early 1980s, the importance of the electrophysiologists in this sequence of visits for a child with congenital heart disease began to grow as more and more patients in their late follow-up developed problems in the area of arrhythmias. From the information presented by both this paper and the previous one, one can see that that circle may be turning back again to have those patients revisit their surgeon.
It is well recognized that atrial arrhythmias occur after the Fontan operation and the Mustard procedures for transposition of the great arteries. Those have been well characterized now. Much of this work is actually attributable to the work of Dr Jim Cox, who is given a lot of credit, for obvious reasons, for his development of the maze procedure, but in fact his research laboratory concentrated a great deal of effort on arrhythmias with pediatric diagnoses as well.
This is the largest single-center experience that I am aware of for arrhythmia surgery in children and young adults outside of the arrhythmia surgery that is being done now after Fontan procedures. The authors are certainly to be complimented on their outstanding work in this area, both clinically and in this presentation that we have heard this morning. Many of these are quite complex operations. The group at Children’s Memorial Hospital in Chicago is obviously leading the way in this endeavor.
Arrhythmia surgery is quite different conceptually from most congenital heart operations. For the most part, you cannot really see what you are doing and the impact that you are having, but you have to have some level of faith in the preoperative or intraoperative testing that is done. My questions to the authors really relate to this aspect of it and the success that one might see afterwards.
First of all, why not study all of these patients in the electrophysiology laboratory? Would that provide a little bit better mapping prior to undertaking repair than what was presented today? Obviously one should strive for 100% success. That might be achieved with better planning preoperatively.
The second question relates to their level of aggressiveness in ablating the patients in the electrophysiology lab. At least in our center, our electrophysiologists are quite aggressive about attempting to ablate patients with all sorts of atrial arrhythmias, regardless of the type, and will endeavor to do so before undertaking operations, whether it is in conjunction with repair of a congenital cardiac lesion or apart from that.
And finally, after the procedure has been performed, I could not quite gather from the presentation or the manuscript whether there was actually intraoperative testing performed in an effort to reinduce the arrhythmia to assess the success of the procedure.
I have one further question relating to patients with tetralogy of Fallot and ventricular tachycardia. I wonder if you could expand a little bit on that group. We are seeing more and more patients late in the follow-up of repair of tetralogy of Fallot that present with ventricular arrhythmias. The decision about who to treat aggressively with either a defibrillator or with an attempt at ablation of their focus in the operating room is not quite clear to me, and I wonder if the authors could expand a little bit on that subject.
DR DEAL: Thank you, Dr Huddleston, for your comments. In terms of why not study all patients in the electrophysiology laboratory preoperatively, it is our policy to study all patients with a re-entrant rhythm who are of an age to accept study. The patients in our series who did not undergo preoperative study were the atrial fibrillation patients in whom we cannot map atrial fibrillation, as well as the automatic atrial tachycardia patients. Only one of these patients was studied. The other two were neonates, who were operated on in the first week of life and did not require catheterization, so we did not map them preoperatively. But your point is well taken, and I think the crux of success is based on very thorough preoperative electrophysiologic mapping. As you know, some patients may not be inducible in the operating room.
To answer the second question—why not ablate all patients?—it is our policy to assess the hemodynamics of a patient, and certainly patients with structurally normal hearts would not go to the operating room without two or three prior ablation procedures. And then based on the findings at the ablation, we make an assessment as to whether improved techniques or a different laboratory would have a better outcome with the catheter technique before moving to the operating room.
In patients with concomitant structural heart disease, if they require surgical intervention and we can localize the arrhythmia and we know that it is something that can be handled in between 6 and 15 minutes in the operating room, we make a decision not to proceed with a potentially lengthy ablation procedure under anesthesia in the catheterization laboratory. However, if the patient has good hemodynamics, we will attempt one or two settings of radiofrequency ablation to attempt to eliminate the arrhythmia.
During the procedure we do intraoperative electrophysiologic mapping, and we do not repeat the intraoperative mapping postoperatively except in ventricular tachycardia patients, because they are generally quite sick patients with very complex surgical repairs. We base our strategy on the intraoperative and preoperative electrophysiologic mapping and attempt to correlate that with anatomic findings. At the end of this potentially long day in the operating room, it is our decision not to reoperate at that time should atrial tachycardia be inducible. We will not be able to assess whether inducible supraventricular tachycardia is due to poor ventricular function, the inotropic effects of medications, or true failure of the arrhythmia operation.
And finally, with regard to the tetralogy patients with ventricular tachycardia, how do you decide who to ablate? Again, in our patients, if you have sustained ventricular tachycardia that is symptomatic (so this is not nonsustained ventricular tachycardia), all patients undergo extensive preoperative electrophysiologic mapping to the extent that they are hemodynamically stable, and we usually attempt an ablation preoperatively. However, some patients do not tolerate the ventricular tachycardia hemodynamically because of their significant pulmonic stenosis or regurgitation, and it is a decision to attempt to ablate in the operating room.
I think our limited success in patients with ventricular tachycardia or tetralogy of Fallot (1 of 3 patients was not inducible, 2 of 3 were inducible and received defibrillators but have not had late ventricular tachycardia) is very comparable to the results reported by Harrison and Williams in Canada, where between 30% and 50% of patients remained inducible after ventricular tachycardia surgery. We speculate that the focus of ventricular tachycardia may be either deep endocardially on the left ventricular septal surface, or there may be multiple morphologies or, finally, that our mapping may be inaccurate. But I think it is a difficult group of patients, and we believe in implanting the defibrillator if they remain inducible.
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References |
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TopAbstractIntroductionPatients and methodsResultsCommentDiscussionReferences |
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This article has been cited by other articles:
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 H. Laks, D. Marelli, M. Plunkett, and J. Myers Adult Congenital Heart Disease Card. Surg. Adult, January 1, 2008; 3(2008): 1431 - 1464. [Full Text]
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