Atrial Arrhythmias in Adults After Repair of Tetralogy of Fallot
Correlations With Clinical, Exercise, and Echocardiographic Findings
Background The long-term success of intracardiac repair of tetralogy of Fallot is hampered by the occurrence of arrhythmias. Numerous studies have stressed the potential role of ventricular arrhythmias. However, the importance of other arrhythmias in the morbidity of these patients appears to be underestimated. Furthermore, most follow-up studies have been limited to children or adolescents, whereas many patients have reached adulthood after earlier repair of tetralogy of Fallot. The aim of the present study was to determine the incidence of atrial fibrillation, atrial flutter, and other supraventricular arrhythmias in adult patients after intracardiac repair for tetralogy of Fallot and their correlation with surgical and clinical findings.
Methods and Results The study group consisted of 53 consecutive patients referred to the Thoraxcenter adult congenital heart disease clinic. They underwent repair at a mean age of 9.1 years (range, 0.7 to 55 years). The median age at the time of study was 23.2 years (range, 15 to 57 years; mean age, 26.6 years), and the mean duration of follow-up of 17.5 years (range, 1.4 to 32 years) after surgery. Records were reviewed extensively for evidence of arrhythmias. The follow-up study included routine 12-lead ECG, 24-hour continuous ambulatory monitoring, and echocardiography, and 46 patients underwent exercise testing. Sinus node dysfunction was recorded in 19 patients (36%), of whom 4 required a permanent pacemaker. Atrial fibrillation or flutter was found in 12 patients, and other supraventricular tachycardias were found in 6. The former were more frequently of older age at follow-up. Antiarrhythmic therapy and cardioversion were typically directed at control of atrial (and not ventricular) tachyarrhythmias. Ten patients (19%) showed nonsustained ventricular tachycardia; they were older at initial surgery and older at follow-up and had more intracardiac repairs and longer cardiopulmonary bypass times.
Conclusions Despite an emphasis on ventricular ectopy in past series, the main sources of morbidity in adult patients after surgical correction of tetralogy of Fallot emanated from atrial arrhythmias, which were present in one third of the patients.
The long-term success of primary intracardiac repair for tetralogy of Fallot is hampered by the occurrence of arrhythmias and late sudden death due to arrhythmias.1 2 3 4 Numerous studies have stressed the potential role of ventricular arrhythmias in these events.2 4 5 6 7 8 9 10 11 12 13 14 15 16 17 However, atrial arrhythmias are rarely mentioned, and their role in the morbidity of these patients appears to be underestimated. Only recently has attention been paid to atrial flutter3 18 as a culprit arrhythmia. Furthermore, most follow-up studies have been limited to children or adolescents, whereas many patients have reached adulthood after earlier repair of tetralogy of Fallot.
In the present report, we present a study of 53 adult patients with repaired tetralogy of Fallot who were seen at the Thoraxcenter Clinic for Adult Congenital Heart Disease to assess the clinical significance of both atrial and ventricular arrhythmias and to establish their relation to surgical and other clinical findings.
Fifty-three patients were studied who had surgically repaired tetralogy of Fallot and presented consecutively at the Clinic for Adult Congenital Heart Disease of the Thoraxcenter between July 1990 and April 1993. The evaluation of the patients included a detailed history and clinical examination; review of hospital and clinical records for evidence of arrhythmias on 24-hour ambulatory ECG (Holter) monitoring, monitor strips, and routine ECG; and exercise testing and echocardiography.
Patients were assessed clinically for functional status according to the New York Heart Association classification. Medication and symptoms were systematically recorded with an emphasis on episodes of palpitations, dizziness, syncope, and cerebral embolism. Special attention was given to signs of right-side heart failure, pulmonary and tricuspid regurgitation, residual pulmonary stenosis, and residual shunts during physical examination.
All available hospital and clinic records were reviewed for evidence of arrhythmias. The presence of an arrhythmia on any one recording (monitor strip, routine ECG, or Holter recording) was sufficient to code a patient for that rhythm disturbance, excluding arrhythmias related to cardiac catheterization or the perioperative period.
Fifty-three patients had multiple routine 12-lead ECGs, and 52 patients underwent 24-hour continuous ambulatory ECG (Holter) monitoring with a mean of 1.4 tracings (range, 1 to 4 tracings) per patient. One pacemaker-dependent patient in sinus rhythm with complete heart block declined Holter monitoring. Modified chest leads V3 and V5 were recorded with Oxford MR 14 recorders. The tapes were analyzed by trained technicians using Cardiodata prodigy or an Oxford medilog MP-14 analyzer. Representative tracings were reviewed by one of authors with special attention paid to P-wave morphology. The diagnosis of ventricular tachycardia (three or more consecutive ventricular premature beats) was made carefully to avoid misinterpretation of supraventricular as ventricular tachycardia in view of the high prevalence of complete right bundle-branch block. Sinus bradycardia was diagnosed as a sinus rate of <50 beats per minute during waking hours. Any combination of at least two of sinus bradycardia, abrupt sinus pauses (>1 second in the absence of respiratory variation), and escape beats was coded as sinus node dysfunction. Supraventricular tachycardia consisted of an abrupt salvo of three or more consecutive atrial premature beats at a rate of >100 beats per minute. Atrial fibrillation, atrial flutter, and ectopic atrial rhythm were diagnosed using conventional criteria.
Ventricular arrhythmias were categorized in four groups by using modified Lown criteria19 : (1) no ventricular arrhythmias or premature ventricular beats of <30 per hour, (2) multiform premature ventricular complexes or couplets of <30 per hour, (3) >30 premature ventricular beats per hour, or (4) ventricular tachycardia (defined as three or more consecutive ventricular beats with a mean rate of >100 beats per minute). Invasive electrophysiological studies were not performed.
Two-dimensional echocardiography with color Doppler and velocity profiles and M-mode recordings were performed in all patients with a Toshiba SSH 140 A with 3.75- and 2.5-MHz transducers or a Vingmed CFM 750 with a 3.25-MHz transducer. Images were obtained from conventional precordial, subcostal, and suprasternal views. Two-dimensional guided M-mode measurements were made of the left atrial (normal, <45 mm) and left ventricular (normal, <60 mm) end-diastolic dimensions. Right atrial enlargement was identified on four-chamber views if the right atrium was larger than the left. Left ventricular function was assessed qualitatively as normal or abnormal (eg, hypokinesis, akinesis) on two-dimensional images. Color Doppler was used to localize residual shunts (accepted only if confirmed by velocity measurements) and to quantify valvular regurgitation. Regurgitation was determined from multiple views. Tricuspid insufficiency was graded as severe if the insufficiency jet reached the posterior wall of the right atrium. Pulmonic insufficiency was judged as severe if back flow extended from the bifurcation of the pulmonary arteries with a long broad jet beyond the pulmonic valve far into the right ventricular outflow tract. The maximum velocity of regurgitation was determined by continuous-wave Doppler interrogation to assess the maximum instantaneous systolic right ventricular and diastolic pulmonary artery pressure gradient using the modified Bernoulli equation.
Symptom-limited exercise on a bicycle ergometer was performed in 46 patients. Exercise tests were not performed in 7 patients. One patient was hemiparetic and 6 others declined, of whom 1 was pacemaker dependent. Work load was increased stepwise by 20 W/min, and the test was terminated when the subject approached exhaustion or a sustained arrhythmia occurred. Performance was compared with standardized data based on age, sex, and height.20 Rhythm was monitored continuously throughout the test and recovery period. The tracings were reviewed by the authors.
Continuous variables presented as mean±SD or median (range) were analyzed using two-tailed Student’s t test. Univariate analysis for categorical variables was performed using the χ2 test or Fisher’s exact test. Differences were considered significant if the null hypothesis could be rejected at the .05 probability level.
The study group of 53 patients underwent complete repair of tetralogy of Fallot at a mean age of 9.1±9.0 years (range, 0.7 to 55 years). The median age at the time of study was 23.3 years (range, 15 to 57 years; mean, 26.6 years). Mean duration of follow-up was 17.5 years (range, 1.4 to 32 years). Twenty-eight patients (53%) were women.
Before the definitive surgical correction, 27 patients received an aortopulmonary shunt (Blalock-Taussig in 16, Waterson in 10, and Potts in 1). During the total correction, 47 of the 53 patients had caval cannulation, right atriotomy was performed in 36, and infundibulectomy was done in 51. Pericardial patches for enlargement of the right ventricular outflow tract (transannular) were used in 43 patients, and Dacron patches for closure of the ventricular septal defect were used in all. Five patients received a pulmonary valve bioprosthesis (allograft). A patent foramen ovale was closed in 13. Mean cardiopulmonary bypass time for the first repair was 134±45 minutes. Seventeen patients (30%) required two or more intracardiac operations: 10 closures of a residual ventricular septal defect, 10 implantations of a pulmonary valve bioprosthesis (allograft), and one tricuspid valve replacement.
Clinical Evaluation and Follow-up
At follow-up, 31 of 53 patients (58%) were in New York Heart Association functional class I, 19 (36%) were in class II, and 3 (6%) were in class III (Table 1⇓). Palpitations were felt by 17 patients (32%), and 10 patients (19%) had syncope or near-syncope. Cerebral embolism (not including perioperative events) occurred in 4 patients (7%). On physical examination, a diastolic murmur of pulmonary insufficiency was present in 49 of the 53 patients (92%). None of the 53 patients had edema, and only 4 had elevation of jugular venous pressure.
Eight patients were judged cyanotic, but cyanosis was never severe, and no patient had clubbing. In 4 patients, measured arterial saturations were 96%, 94%, 89%, and 88%. The 2 hypoxemic patients (and 1 without hypoxemia) had residual ventricular septal defects and elevated right ventricular diastolic pressures. The other 5 patients showed no echocardiographic evidence of shunting.
Diuretic use in 9 patients (17%) probably accounted for the low incidence of elevated venous pressure and the absence of edema. Digoxin was administered to 10 patients (19%), and antiarrhythmic agents (propafenone, sotalol, amiodarone) were given to 13 (24%) (9 patients with atrial fibrillation or flutter and 4 with ventricular tachycardia). Three patients received long-term anticoagulation (warfarin).
Cardioversion was used in 6 patients: four times for sustained symptomatic supraventricular tachycardia, once for atrial fibrillation, and once for atrial flutter. It was never required for ventricular arrhythmias.
Two patients died during the study period. The first patient had syncopal episodes and ventricular tachycardias on ambulatory monitoring. Because of severe pulmonary regurgitation and peripheral pulmonary stenosis with high right ventricular pressure (72/7 mm Hg), a pulmonary homograft was implanted together with patch enlargement of the right pulmonary artery. This patient died suddenly at home, 2 weeks after this second operation. The second patient had severe pulmonary regurgitation and a high right ventricular pressure (103/7 mm Hg) after her first repair, but she was considered inoperable because of left pulmonary atresia after a left-side Blalock-Taussig shunt. She was taking amiodarone and procaineamide for frequent attacks of atrial flutter and supraventricular tachycardia and died suddenly. Both patients had demonstrated premature ventricular complexes on their routine ECG.
Six of the 27 women delivered 10 live infants without complications.
Monitor strips during hospitalization showed atrial fibrillation or flutter in 7 patients. Routine 12-lead ECG showed chronic atrial fibrillation or flutter in 3 patients, and 2 patients were in ectopic rhythm. Six patients were pacemaker dependent (2 because of surgically induced complete heart block and 4 because of sinus node dysfunction). Six patients showed premature ventricular complexes on their routine ECG. On Holter monitoring, 6 patients (11%) showed atrial fibrillation or flutter, and 47 (89%) showed ventricular arrhythmias. Exercise testing demonstrated ventricular ectopy in 22 patients (48%), of which four were episodes of nonsustained ventricular tachycardia.
On a review of monitor strips, routine ECGs, and Holter recordings, some degree of sinus node dysfunction was recorded in 19 patients (36%). In 4, it was severe enough to require a permanent pacemaker. Atrial tachyarrhythmia was present in 18 patients (34%), consisting of sustained supraventricular tachycardia in 6 (11%), of whom 4 required DC cardioversion, and atrial fibrillation or flutter was present in 12 patients (23%). Ventricular arrhythmias were found in 47 (89%). No ventricular arrhythmias or <30 premature ventricular complexes per hour were found in 6 patients (11%); 17 patients (32%) demonstrated multiform ventricular extrasystoles or couplets; 20 patients (38%) had >30 premature ventricular complexes per hour; and 10 patients (19%) had ventricular tachycardia.
The follow-up time was not significantly different between the patients with and those without arrhythmias (Table 1⇑). Compared with patients without arrhythmias, patients with atrial fibrillation or flutter (P=.04) or ventricular tachycardia (P=.017) were older. Age at total repair was higher for patients with ventricular tachycardia (P=.013). There was no association with a previous shunt operation. Longer cardiopulmonary bypass time (P=.0016) and multiple repairs (P=.02) appeared to be associated with ventricular tachycardia.
In most categories of atrial or ventricular arrhythmias, New York Heart Association class I predominated. As expected, palpitations and near-syncope were noted in the patients with atrial fibrillation or flutter and in patients with ventricular tachycardia. The occurrence of cerebral embolism was unrelated to the presence of arrhythmia. All six episodes of cardioversion were required for atrial tachycardia; there was no need for cardioversion to terminate ventricular arrhythmias as sustained ventricular tachycardia was never documented.
Echocardiographic results are shown in Table 2⇓. There was almost uniform presence of right atrial enlargement (52 of 53; 98%). There were 4 patients with left atrial enlargement, and 3 of these showed atrial fibrillation or flutter as well as ventricular tachycardia. Three patients had a left ventricular abnormality (enlargement or contraction abnormality), and 2 of the 3 had atrial fibrillation or flutter (P=.05). One patient with a segmental contraction abnormality had a transection of a coronary artery branch at the time of initial repair due to an abnormal course of the coronary artery across the right ventricular outflow tract. Small echocardiographically detectable ventricular septal defects were seen in 25 patients and were significantly associated with atrial fibrillation or flutter (P=.03). Of the 4 patients with left atrial enlargement but without left ventricular abnormality or residual aortopulmonary shunt, all had ventricular septal defects. No correlation could be found between severe tricuspid or pulmonic insufficiency and atrial or ventricular rhythm disturbances. The mean tricuspid insufficiency jet velocity was 2.8 m/s, corresponding to a tricuspid pressure gradient of 31 mm Hg. There was no correlation of the right ventricular pressure with any arrhythmia.
Peak performance was 29% to 112% of the predicted normal value (mean, 77%). Patients with tricuspid or pulmonic insufficiency reached peak levels of exercise that were similar to those of the other patients. Exercise capacity was significantly lower in the group with atrial fibrillation or flutter (65%; P=.03).
During exercise, 48% of the patients showed ventricular ectopy, of whom 4 demonstrated unsustained ventricular tachycardia. No test was terminated because of sustained arrhythmia. No patients were found to have previously unsuspected ventricular arrhythmias.
Despite an emphasis in past series on the importance of ventricular ectopy2 4 5 6 7 8 9 10 11 12 13 14 15 16 17 and its high prevalence in the present study (89% of the patients), most complaints emanated from patients with atrial arrhythmias.
Incidence of Arrhythmias
The incidence of arrhythmias in adults with surgically repaired tetralogy of Fallot was higher than previously reported (Table 3⇓). Atrial arrhythmias were found in 34% and ventricular arrhythmias were found in 89%, exceeding frequencies found in previous series that exclusively used ambulatory monitoring.2 4 5 6 7 8 9 10 11 12 13 14 The presence of supraventricular tachycardia in 11% of our patients parallels the experiences of Miyamura et al10 (19%) and Waien et al17 (14% to 24%) but is substantially higher than in most other series that used ambulatory monitoring.15 16 17 Atrial flutter and fibrillation in particular are remarkable by their absence in other tetralogy of Fallot follow-up studies. In five studies,8 21 22 23 24 only 13 cases of atrial fibrillation or flutter were reported in 1140 patients. On the other hand, in a collaborative study of 380 patients with atrial flutter (age, 1 to 25 years), only 30 (8%) had tetralogy of Fallot (28 repaired, 2 with shunts only); the denominator (ie, the total number of patients with tetralogy of Fallot from whom these 30 were drawn) was not given.18
With respect to supraventricular tachycardia, surface ECGs do not permit separation of atrioventricular nodal reentry from accessory pathways or ectopic atrial foci. However, the clinical importance of this rapid supraventricular rhythm is manifested by the need to cardiovert 4 of 6 of these patients. Similarly, without invasive testing it is not possible to distinguish atrial flutter from atrial reentry around surgical scars. Nevertheless, the need for management of this tachyarrhythmia is equally urgent.
The higher frequency of arrhythmias in the present study may be explained by the methods we used and by patient selection. We carefully sifted through all available material in search of rhythm disturbances as they appeared on monitor strips, routine ECG tracings, and Holter records. The accumulation of multiple Holter tracings in response to complaints increased the chances for detection of arrhythmias in the present study. Furthermore, because we included only adults, the study preferentially selected patients who were older at surgery or who had a longer follow-up interval after surgery and therefore were more likely to represent an earlier era of surgical repair.23 Only three other studies using ambulatory monitoring have been limited to adults.15 16 17 Finally, other studies traced patients who had previously undergone surgery at a single institution,22 who were selected from among volunteers,13 15 17 or who were chosen to participate.2
In contrast, the present study covers all repaired patients who presented at the sole geographic center for adult patients with congenital heart disease in the Rotterdam area. Referral may have been triggered by having reached the upper age for pediatric care, by unfamiliarity of the adult cardiologist or family physician with such patients, or by new symptoms. These indications for referral may account for a higher frequency of arrhythmias. The problems our patients present should not be seen as aberrations from the usual—perhaps more benign—outlook for all patients with successfully repaired tetralogy of Fallot. We stress that they are more likely to be representative of the postrepair tetralogy population referred to well-equipped adult cardiovascular centers.
The pathological significance of supraventricular tachycardia is hard to interpret. Brief salvos of supraventricular tachycardia have been found on ambulatory monitoring in as many as 22% of healthy individuals.26 Nevertheless, patients with residual cardiac abnormalities may not tolerate sustained tachycardia, and four of six episodes of cardioversion were required for this arrhythmia. Evidence that transient sinus node dysfunction was noteworthy is provided by the need for pacemakers in 4 such patients and persistent ectopic atrial rhythm in 2 other patients.
Atrial flutter and fibrillation have not been found on routine ambulatory monitoring of healthy persons.25 26 27 28 On the contrary, they are a marker of poor hemodynamics.22 Atrial flutter and junctional rhythm have been reported in 18% and 46%, respectively, during follow-up of patients with repaired ostium secundum atrial septal defect.29 After atrial baffle repair of transposition of the great arteries, atrial fibrillation and flutter occur frequently (25%) and continue to increase with duration of follow-up.30 Atriotomy and atrial sutures may play a role in the development of atrial arrhythmias in these patients and may also be of significance in tetralogy patients.
In the present study, the age at follow-up was significantly higher in the patients with atrial fibrillation or flutter. In addition to age, the presence of left-side pathology in several of our patients appeared to be related to arrhythmias. Three of 4 patients with left atrial enlargement by echocardiography had atrial arrhythmias. None had left ventricular abnormalities or mitral insufficiency. However, all had small residual ventricular septal defects that, in combination with their older age at the time of surgery, may have had some importance. A voluminous shunt (4.3:1) was found only once in a patient demonstrating atrial flutter or fibrillation who had no left-side chamber abnormalities. On the other hand, we found a significant correlation between left ventricular abnormalities and the incidence of atrial arrhythmias, although this, to our knowledge, was never described in postoperative tetralogy of Fallot patients. The near-universal presence of right-side chamber enlargement prevented any correlation with arrhythmias. Neither pulmonic insufficiency nor tricuspid insufficiency was more frequent among patients with rhythm disturbances.
Much of the morbidity in our patients was due to atrial arrhythmias: 66% of patients with fibrillation or flutter complained of palpitations, and 50% noted dizziness or near-syncope. Antiarrhythmic therapy and cardioversion were typically directed at control of symptomatic atrial—not ventricular—arrhythmias. The relative importance of atrial tachyarrhythmias is also indicated by the fact that even though approximately half of the 10 patients with ventricular tachycardia complained of palpitation or near-syncope, all except 2 symptomatic patients also had atrial flutter or fibrillation. Conversely, among the 10 symptomatic patients with atrial tachyarrhythmias, ventricular tachycardia was present in only 2. Furthermore, patients with atrial arrhythmias demonstrated reduced exercise capacity.
The correlation between patients with ventricular tachycardia and older age at first repair was described by others2 7 8 9 21 but is not universally supported.13 14 The age at follow-up was significantly greater for patients with ventricular tachycardia, whereas the follow-up intervals were similar. Thus, age at first repair and age at follow-up probably should not be considered independent variables. Longer cardiopulmonary bypass time and multiple repairs emerged as significant and have been reported previously.3 14 23 Damage to the myocardium may have already occurred when older patients were operated on, or the anatomy in these patients may have been more complex. Prior aortopulmonary shunt procedures were not more frequent among patients with ventricular arrhythmias (as noted previously7 14 ) despite reports of such association.22
Of the 10 patients with ventricular tachycardia, 60% had palpitations, and 50% had near-syncope. However, when patients with concomitant atrial arrhythmias were removed, the frequency of these same symptoms no longer reached significance. Sustained ventricular tachycardia was never documented, and cardioversion was therefore never required for termination of ventricular arrhythmias.
Although we anticipated a linkage between ventricular ectopy and severe pulmonary regurgitation with secondary marked dilatation of the right side of the heart, no such correlation could be confirmed. This confirms the recent report of Joffe et al.31 Reberger et al32 measured right ventricular volumes by nuclear magnetic resonance velocity mapping in patients after surgical correction of tetralogy of Fallot and found a virtually normal range of right ventricular ejection fractions in the majority of their patients with pulmonary regurgitation. However, in the present study, no direct measure of right ventricular function was made, so that, on the basis of the echocardiographic Doppler studies of the amount of pulmonary regurgitation alone, we could not differentiate between patients with and those without myocardial decompensation.
All 3 patients with a left ventricular abnormality had ventricular arrhythmias; 2 of the 3 had ventricular tachycardia, but these numbers were too small to achieve statistical significance.
In contrast to previous reports suggesting the advantage of exercise over resting ECGs to assess clinical risk from arrhythmias,1 7 this approach yielded no clinically useful new information when compared with Holter testing.
Despite the availability of ambulatory monitoring, the two deaths that occurred during this 3-year period were signaled by the presence of premature ventricular complexes on routine ECG. This finding was limited to only 4 other patients and, when complicated by right ventricular hypertension, should be taken seriously.
Adults with repaired tetralogy of Fallot presenting at centers caring for such patients may differ from those in published series: patients are older and are more likely to have complaints and to have had multiple operations, valvular prostheses, pacemakers, pregnancies, and cardiac medication.
Although it might be assumed that pressure or volume overload of the right atrium and right ventricle would cause dilatation and predispose to arrhythmias, no such relation was demonstrated. Instead, an interesting but not fully understood association with left-side abnormalities and residual ventricular septal defect was found.
Despite an emphasis in past series on the importance of ventricular ectopy and its high prevalence in the present series, the main sources of morbidity in these adult patients emanated from atrial arrhythmias: atrial fibrillation, atrial flutter, supraventricular tachycardia, and sinus node dysfunction. These were present at one time or another in one third of our patients. Antiarrhythmic therapy and cardioversion were typically directed at control of symptomatic or sustained atrial tachyarrhythmias. Pacemakers were needed twice as often for sinus bradycardia as for heart block.
These observations should be useful to physicians who assume the late care of adults with repaired tetralogy. They broaden the focus of attention from ventricular ectopy and atrioventricular block to include atrial and sinoatrial dysrhythmias, paralleling the delayed emergence of these rhythm disturbances in patients with previous Mustard, Fontan, and atrial septal defect repairs.
We gratefully acknowledge the support of the Netherlands Heart Foundation and the vital assistance of Dr John Hess and Dr Folkert Meiboom.
- Received September 8, 1994.
- Revision received December 20, 1994.
- Accepted December 27, 1994.
- Copyright © 1995 by American Heart Association
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