Author + information
- Received December 22, 2003
- Revision received April 28, 2004
- Accepted May 18, 2004
- Published online September 1, 2004.
- Janneke A.E. Kammeraad, MD⁎,
- Carolien H.M. van Deurzen, MD⁎,
- Narayanswami Sreeram, MD⁎,
- Margreet Th.E. Bink-Boelkens, MD†,
- Jaap Ottenkamp, MD‡,
- Willem A. Helbing, MD§,
- Jan Lam, MD∥,
- Martha A. Sobotka-Plojhar, MD¶,
- Otto Daniels, MD# and
- Seshadri Balaji, MD**,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Seshadri Balaji, Department of Pediatric Cardiology, Oregon Health and Science University, 707 SW Gaines Road, Mailcode CDRC-P, Portland, Oregon 97239
Objectives The goal of this research was to identify predictors for sudden death (SD) in patients with transposition of the great arteries (TGA) who have undergone atrial inflow repair.
Background Sudden death is the most common cause of late death after atrial inflow repair of TGA. Little is known about the predictors of SD.
Methods This was a retrospective, multicenter, case-controlled study. We identified 47 patients after Mustard's or Senning's operation who experienced an SD event (34 SD, 13 near-miss SD). Each patient was matched with two controls with the same operation, but without an SD event. Information on numerous variables before the event was obtained and compared with controls at the same time frame.
Results Presence of symptoms of arrhythmia or heart failure at most recent follow-up and history of documented arrhythmia (atrial flutter [AFL]/atrial fibrillation [AF]) were found to increase the risk of SD. Electrocardiogram (ECG), chest X-ray, and Holter ECG findings were not predictive of SD. Neither medication nor pacing was found to be protective. Most SD events (81%) occurred during exercise. Ventricular tachycardia/ventricular fibrillation were the recorded rhythm during SD in 21 of 47 patients.
Conclusions Presence of symptoms and documented AFL/AF are the best predictors of SD in TGA patients. Patients with these findings should be further evaluated for risk of SD.
Before the 1980s, most patients with transposition of the great arteries (TGA) were treated by atrial inflow correction using the Mustard's or Senning's operation. Many children who underwent these operations are now adults. While their survival rate has been good (1–7), arrhythmia, right ventricular (RV) dysfunction, and late death are well-recognized complications (1–9). One cause of late death is sudden death (SD) with an incidence of 2% to 15% (1–10). It was the most common cause of late death in some studies (1,2,8). Little is known about risk factors for SD in this group.
In an attempt to establish predictive factors for SD, we undertook a multicenter, retrospective, case-controlled study.
All patients who had undergone a Mustard or Senning operation from the participating institutions, and had suffered either SD or near-miss SD were included. Sudden death was defined as acute unexpected cardiovascular collapse resulting in death or from which the patient never regained consciousness (11). Near-miss SD was defined as acute cardiovascular collapse with successful cardiopulmonary resuscitation or documented appropriate implantable cardioverter-defibrillator (ICD) discharge. We excluded patients in severe heart failure who were considered terminal and whose death was expected.
With these criteria we identified 47 SD cases (34 SD and 13 near-miss SD). This group of patients will henceforth be referred to as SD group. For each of the SD patients, we matched two control patients. Matching criteria were type of operation, operation date within three years from corresponding SD case, and age at operation as close as possible to that of the corresponding SD case. Controls were obtained from the same center (and surgeon) as the corresponding SD case. According to these criteria, we were able to identify 93 suitable control patients (we were able to find only one control for one of the SD cases). All medical records were reviewed, and data from the last full assessment within five years of the event were used for analyses. For controls, data collected pertained to that which had been collected around the time of the event in the corresponding SD case.
All available electrocardiograms (ECG), chest X-rays, Holter 24-h ECGs, echocardiogram reports, exercise test reports, cardiac catheterization, and electrophysiology study reports were reviewed. Data collection was completed in September 2002. The study was approved by the institutional review boards of the participating centers.
An adequate surgery database had been maintained in only five of the eight participating centers in our study. In those five centers, a total of 582 Mustard's or Senning's operations were performed with a mean SD incidence of 6%. The incidence of SD was different for each of these five centers, ranging between 3% and 11%. Of the 47 SD cases in our study population, 5 had undergone Senning's operation and 42 Mustard's operation.
Transposition of the great arteries was called simple if the ventricular septum was intact or when a small, hemodynamically insignificant ventricular septal defect was present. Complex TGA was defined as the presence of a ventricular septal defect requiring closure or another lesion, such as ventricular outflow tract obstruction requiring surgical intervention. Closed patent ductus arteriosus, aberrant vessels, and repaired coarctation of the aorta did not constitute “complex.”
Heart size measured on X-ray was divided into normal (cardiothoracic [CT] ratio ≤50%) and enlarged (CT ratio >50%). The RV size was subjectively assessed as normal or enlarged from the echocardiography reports from each institution. Likewise, RV function was assessed as satisfactory, moderately impaired, or severely impaired. Exercise tolerance during exercise tests was quantified as normal (100%), slightly decreased (80% to 100%), decreased (60% to 80%), or poor (<60%), given as the percentage of the normal value expected for age, body weight, and gender. Sinus node disease (SND) was defined as absence of sinus rhythm with presence of atrial or junctional escape rhythm as dominant rhythm. Sparse sinus beats occurring within a dominant escape rhythm were also considered SND. Patients with paroxysmal episodes of atrial flutter(AFL)/fibrillation (AF), whose underlying rhythm was sinus, were not considered to have lost sinus rhythm. Frequent supraventricular or ventricular extra systoles were noted as arrhythmia if >100 extra beats per h.
Descriptive statistics are reported as frequency, median, or mean value and range or standard deviations as appropriate. Data were analyzed using SPSS software for Windows (SPSS Inc., Chicago, Illinois).
Risk factors for SD event were identified by univariate conditional logistic regression analyses. Results are reported as odds ratios with 95% confidence intervals for significant predictors. Because many risk factors were tested within the same data set, we considered a p value of <0.005 as statistically significant.
Baseline characteristics, preoperative palliation, early postoperative arrhythmia, and reoperations are shown in Table 1.
Thirty-four events (81%) occurred during exercise, 5 (12%) patients died during sleep, and 3 (7%) patients had a preexisting sustained AFL/AF going on during the 1 to 2 days before the event. For 5 of the 34 patients who died, no information was available regarding the circumstances of their death.
Mean age at event was 12.3 years (median, 9.7 years; range, 0.3 to 32.0 years) and average interval postsurgery 10.6 years (median, 7.9 years; range, 0.3 to 28.8 years). A total of 30 of 47 events (64%) occurred <12 years after surgery. No clustering in either age or follow-up time was found.
Autopsy reports were available for 14 patients (41%). They showed bronchopneumonia (n = 2), fibrosis around the conduction system (n = 2), detached pacemaker lead (n = 1), pulmonary vein stenosis (n = 1), pulmonary vein stenosis with pulmonary hypertension (n = 1), one pulmonary vein from left lung (n = 1), fresh thrombus in the coronary artery and irreversible pulmonary hypertension (n = 1), fresh thrombus in coronary artery (n = 1), and left ventricular outflow tract obstruction (n = 1). No abnormalities were found in three patients.
For eight SD cases, rhythm documentation was available at time of event and showed ventricular tachycardia (VT) or ventricular fibrillation (VF). Of the 13 patients with a near-miss SD, 10 had documented VT or VF at the time of the event; the other 3 patients had loss of consciousness without pulsations felt by onlookers, and, in all, cardiopulmonary resuscitation was successful, without need for defibrillation.
A total of 7 of 13 patients with near-miss SD received either an ICD (n = 4) or a pacemaker (n = 3). Of the three patients receiving pacemakers, one had SND and two had poor escape rhythm after medication to suppress arrhythmia.
Four patients, who suffered a near-miss SD, died at follow-up. Two died from neurologic damage within 24 h and 2 months, respectively, despite regaining heart rhythm. One other patient died of VF while awaiting heart transplantation 14 months after the initial event. The fourth patient died six years after the initial event from an unknown cause.
Data regarding symptoms just before the event were available for 45 SD patients and 92 controls. Presence of symptoms of arrhythmia (palpitations and syncope) and heart failure (recurrent upper respiratory tract infections, decreased exercise tolerance, tiredness, and shortness of breath) were significant risk factors for SD (Table 2).
Standard 12-lead ECG
Electrocardiograms were available for 44 SD cases and 84 controls. Twenty-six SD patients (59%) showed sinus rhythm on ECG, as did 54 controls (64%) (Table 3)(p = NS). Mean QRS duration, QT and QTc intervals, and heart rate are listed in Table 3and showed no difference between the two groups (Table 2). A QRS duration of >100 ms was noted in 12 of 39 SD cases (31%) and 15 of 78 control patients (19%) (ventricular paced patients were excluded from this analysis). This was not statistically significant (Table 2). QT dispersion times were not significantly different between the two groups either (Table 2).
Holter 24-h ambulatory ECG monitoring
Holter 24-h ECG was available in 26 SD cases and 40 controls. The dominant heart rhythm on Holter is shown in Table 3. Presence of nonsinus rhythm at baseline just failed to reach statistical significance as a risk factor for SD (Table 2). The mean of the mean, minimum and maximum heart rates on 24-h Holter recording was similar for the two groups (Table 2).
A total of 42% (11 of 26) of SD cases and 23% (9 of 40) controls showed episodes of arrhythmia on Holter. This difference was not statistically significant (Table 2). Three (12%) of SD patients and one control (3%) had AF. Three SD cases (12%) had frequent supraventricular extrasystoles. One SD patient had frequent ventricular extrasystoles. Ventricular tachycardia was present in two SD cases. One SD case and four controls showed episodes of sinus arrest. One SD case and four controls showed episodes of junctional escape at rest or at night.
Arrhythmia during follow-up
Of 47 SD cases, 34 (72%) had a documented arrhythmia before their event, in contrast with only 47 of 93 controls (51%). Presence of arrhythmia was a significant risk factor for SD (Table 2). Atrial flutter or atrial fibrillation was the chief tachyarrhythmia. Presence of SND barely approached significance (Table 2).
In 15 SD cases (30%) and 9 controls (10%), more than 1 arrhythmia was diagnosed. A total of 28 SD cases suffered SND, and, of these, 14 (50%) also had AFL/AF. One SD patient with SND had frequent ventricular extrasystoles. Of the 41 controls with SND, 9 (22%) also had documented AFL/AF. The mean interval between surgery and first arrhythmia was 4.0 years (range, 0 to 22.3 years) for SD cases and 3.7 years (range, 0 to 15.6 years) for controls. The mean interval between the first episode of arrhythmia and SD event was 7.2 years (range, 0.5 to 27.4 years). No association was found between the occurrence of SD and the time of onset of arrhythmia.
A total of 8 SD cases (17%) and 15 controls (16.1%) had a pacemaker, which was implanted at average follow-up after surgery of 12.1 years (range, 0.1 to 26.1 years) for SD cases and 8.6 years (range, 0 to 24.3 years) for controls. Although controls tended to get a pacemaker implanted earlier, statistical analysis could not be performed due to small numbers.
A total of 7 of 8 SD cases received a pacemaker for SND, as did 14 of 15 controls. The others (1 SD and 1 control) had complete atrioventricular block. Pacemaker implantation turned out to have no protective value against SD (Table 2).
At the time of event, 20 SD patients (43%) and 17 controls (18%) were using cardiac medication. Of 20 SD patients, 18 were on digoxin (4 also on verapamil and 1 also on beta-blocker), and 2 were on beta-blocker. Of the 17 controls, 9 were on digoxin (2 of whom were also on beta-blocker), 3 on verapamil, 2 on sotalol, and 1 on amiodarone. Two (2%) were using an angiotensin-converting enzyme inhibitor. The use of cardiac medication appeared to increase the risk for an SD event (Table 2).
Chest X-rays were available for 42 SD patients and 77 controls. In 31 SD cases (64%) and 40 (52%) controls, the heart size was enlarged (p = NS) (Table 2).
Echocardiography data are listed in Table 4.Right ventricular size was similar for SD cases and controls. Sudden death cases, however, tended to have a more impaired RV function and slightly more tricuspid regurgitation than controls. The incidence of baffle obstruction, as identified by echocardiography, was similar for the two groups. The paucity of available echocardiograms prevented us from performing reliable statistical analysis.
Data on cardiac catheterization were available in 16 SD cases and 27 controls. Mild systemic baffle obstruction was found in 4 SD cases (25%) and 5 controls (19%). A baffle leak was found in 3 SD patients (19%) and 4 (15%) controls. Mild pulmonary venous obstruction was found in 1 SD and 2 controls. One SD patient had both systemic and pulmonary venous obstruction. Left ventricular outflow tract obstruction was found in 1 SD and 5 control patients. One SD patient had abnormal pulmonary venous drainage to the superior vena cava and another had a calcified conduit from the left ventricle to the pulmonary artery. One control patient had a patent ductus arteriosus detected.
Two of the SD cases and two of the controls with mild systemic venous baffle obstruction and one control patient with pulmonary venous obstruction subsequently underwent baffle repair. Two of four control patients with a baffle leak underwent repair. Two of the SD patients with an obstruction were also found to have a baffle leak.
Only 12 electrophysiology studies (2 SD cases, 10 controls) were performed. Both SD case patients showed SND. Control patients showed SND alone (n = 3), atrioventricular node dysfunction (n = 1), SND plus atrioventricular node dysfunction (n = 3), and inducible VT (n = 1). Two controls had a normal electrophysiology study. No statistical analysis was performed on the catheterization and electrophysiology data, due to small numbers.
Exercise tests were available in 13 SD cases and 38 controls. In the SD group, exercise capacity was normal in 2 (15%), slightly decreased in 5 (39%), decreased in 2 (15%), and poor in 4 (31%). In the control group, exercise capacity was normal in 8 (21%), slightly decreased in 19 (50%), decreased in 9 (24%), and poor in 2 (5%).
Arrhythmias were induced during exercise in five (38%) SD cases and nine (24%) controls, including AF degenerating into VF in one SD patient. The others had junctional rhythm (two SD cases and seven controls) or ventricular ectopy (two SD cases and two controls) either during exercise or during the recovery phase. Statistical analyses could not be performed on exercise test data due to small numbers.
In a large cohort of adult survivors with congenital heart disease, Oechslin et al. (12) found SD was the most common cause of late death. In patients operated by Mustard's or Senning's operation for TGA, studies have shown an incidence of SD varying from 2% to 15% (1–9), and some have reported SD to be the most important cause of late death (1,2,8). A population based study by Silka et al. (11) reported 7 SD among 172 TGA patients, giving an incidence of 4.9 per 1,000 patient-years.
Our study found presence of symptoms and presence of documented AFL/AF to be associated with risk of SD. Interestingly, both arrhythmic and heart failure symptoms were associated with SD. Use of cardiac medications was also a risk factor. It is not possible to say whether this indicates that patients on medications were a sicker group or whether this represents a negative side effect of the drugs themselves.
Few of the SD in our study had undergone Senning's operation. Although paucity of numbers precluded direct comparison, this finding probably reflects the superior outcome for the Senning operation when compared with the Mustard operation, as reported by several authors (4,5,10).
As early as 1972, El-Said et al. (13) remarked on the frequent occurrence of arrhythmias after the Mustard operation. Both bradyarrhythmias (primarily sinus node dysfunction) and tachyarrhythmia (primarily AFL/AF) are common after the Mustard/Senning approach for TGA (14–16). Modifications of surgical technique have not reduced the risk (3,5,16–18). Bradyarrhythmias do, however, appear to be less important than tachyarrhythmias with respect to mortality (1,3,8,9). We, like others, found no association between SND and risk for SD (5,8,18).
Atrial flutter/atrial fibrillation has been identified as a predictor of sudden cardiac death by others. Flinn et al. (3) reported 9 SD among 372 survivors and showed a weak association between AFL/AF and SD. Sarkar et al. (4) reported that documented AFL/AF resulted in a 21-fold increase in the risk of late SD. In contrast, Gelatt et al. (1) could not find a relationship between the incidence of AFL/AF and SD. Janousek et al. (19) studied 359 patients after Mustard/Senning operation. Fifteen patients (4.2%) died suddenly. By multivariate analysis, they found severe tricuspid regurgitation and/or RV dysfunction and medically uncontrolled supraventricular tachycardia to be the risk factors for SD. Our findings are somewhat similar to those of Janousek et al. (19). It is difficult to determine whether arrhythmia is the cause or the effect of ventricular dysfunction. To date, there is no study (including ours) that has been able to determine which of these factors is primary.
Because the presence of AFL/AF could function as surrogate marker for these structural problems (20), hemodynamic assessment is indicated in patients presenting with arrhythmia.
We found neither drug therapy (albeit mostly digoxin only) nor pacemaker to reduce the risk of SD. Whether newer modalities like catheter ablation of AFL/AF can alter the impact of AFL/AF on SD remains to be seen (21–24). However, because AFL/AF may be secondary to ventricular dysfunction, it is also possible that even curing the arrhythmia may not impact the risk of SD.
Presence of symptoms (of arrhythmia or heart failure) was a significant risk factor for SD. Previous studies have not reported this association. Indeed, Gewillig et al. (8) found that neither functional status nor symptoms had prognostic value for late death. In our series, only 33% of the SD cases were symptom-free before their event, compared with 71% of the controls. Arrhythmic symptoms such as palpitations, dizziness, and syncope were the most predictive for SD by a factor of 21.6 (95% confidence interval of 2.80 to 166.8). Heart failure symptoms resulted in a 4.4-fold increase in the risk for an SD event. We also noted a significant association between the presence of documented arrhythmia (a separate risk factor for SD) and arrhythmic symptoms (Pearson chi-square = 10.0; p = 0.002).
Right ventricular failure has been shown to be a risk factor for late death in Mustard and Senning patients (1,6,8). Janousek and colleagues (19) demonstrated a relationship between RV failure and SD in this patient group. Whether RV failure causes, or is caused by, AFL/AF is unclear. Millane et al. (25) have shown that perfusion and wall motion abnormalities are common in the systemic RV late (10 to 20 years) after Mustard's operation and postulated this to be the cause of systemic RV dysfunction. Poor ventricular function causes RV enlargement and progressive tricuspid regurgitation, resulting in atrial volume and pressure overload. This atrial overload may contribute to the development of arrhythmias (1,20). In this context, Gatzoulis et al. (20) showed the occurrence of AFL/AF often after RV failure, identifying AFL/AF as surrogate marker for RV failure.
We were unable to show an association between RV function and SD because few patients had undergone adequate echocardiography or catheterization.
The QRS dispersion and duration are reported as markers of inhomogeneity of ventricular depolarization and as predictors of dangerous arrhythmias and SD in patients with tetralogy of Fallot (26,27). In Mustard patients, QT dispersion was identified as predictor of clinical arrhythmia (20). We were unable to measure QRS dispersions. However, we did not find any differences with respect to QRS, QT, QTc intervals, and QT dispersion times between SD cases and controls.
Mode of death
Of the seven SDs in the study by Silka et al. (11), five died during active physical exertion. In our study, of the 47 SD events, 34 (81%) occurred during physical exercise. From a hemodynamic perspective, the atrial inflow repair of TGA suffers from two main drawbacks. First, the systemic RV seems intrinsically suboptimal compared with the LV (28). Second, the absence of an adequate capacitance chamber (namely the atrium), which has been replaced by a baffle, inherently imposes limits to ventricular filling (29). During exercise, these patients may not be able to augment cardiac output in the face of rising demand due to the above-mentioned two factors. Given these limitations, it is possible that occurrence of an arrhythmia during exercise will cause further deterioration leading to death. In addition, this inability to increase cardiac output may be amplified by coexisting baffle obstruction, pulmonary vein stenosis, or ventricular disease. This finding argues for the use of stringent exercise restrictions in high-risk patients.
It is unclear whether exercise testing can be used as a risk-stratifying test for SD. Although it is of interest that one of our SD patients had VF induced by exercise, abnormal exercise tests were common in both SD and control patients. Meijboom et al. (30) showed that exercise capacity correlates well with the patients own health self-assessment. This further supports the importance of symptoms in this patient group.
Arrhythmia during SD
Silka et al. (11) reported that each of the seven SDs in their study was due to an arrhythmia. They documented polymorphic VT or VF as the terminal rhythm in four patients (11). We found 10 of 13 patients with near-miss SD (n = 13) had documented VT or VF as did 8 SD patients for whom rhythm documentation at time of event was available. Thus, polymorphic VT/VF seems to be the final rhythm in most cases of SD. Routine follow-up ECGs or 24-h Holter recordings showed few rhythm disturbances and were consequently of little help in identifying patients at risk. Scagliotti et al. (31) postulated that inducible polymorphic VT at electrophysiology study may be a marker for SD and advocated the use of electrophysiology studies as risk-stratifying tests in these patients. No study to date has explored this hypothesis.
Based on our findings, we would recommend undertaking electrophysiologic study for inducible VT/VF in patients presenting with symptoms, and those with documented AFL/AF. Where VT/VF is inducible using moderately aggressive pacing protocols, an ICD should be considered.
This study has limitations inherent to any retrospective study, limiting data collection to variables available from clinical records. Decisions on cardiac testing were based solely on clinical grounds and were not standardized for the different patients. The participation of eight different centers with different approaches to management and follow-up made it difficult to obtain uniform data. If an SD case patient developed an arrhythmia after the last clinical visit and before the event, this would have been missed and could potentially lead to underestimation of the importance of an arrhythmia.
We chose to perform this study in a case-matched control setting. Such a design is open to criticism when data on pertinent variables are not available. In our study, this limitation results in certain pieces of data being available in only small subsets of patients with consequent inability to perform statistical comparisons. We have not described data on operation technique. Several studies have shown that the type of operation, the year of birth, and era of operation influence late outcome in Mustard and Senning patients (9,10). To exclude the influence of these factors, we matched SD cases and controls for these variables and have, in addition, used controls operated and followed-up in the same center and surgeon as the corresponding SD case.
Presence of symptoms of arrhythmia or heart failure and presence of documented AFL/AF are the best predictors of SD in patients who have survived a Mustard or Senning operation. It is not possible to say whether AFL/AF directly contributes to SD or is merely a marker for it. Most of the SD occurred during exercise, and when rhythm documentation was available during the SD event, it showed VT/VF. Further studies with larger patient cohorts may help us decide whether any specific tests, such as an echocardiogram, cardiac catheterization, and, particularly, exercise testing or electrophysiology testing can improve the accuracy of identifying patients at risk for SD.
The authors thank C. Uiterwaal, MD, for his advice and help in the organization of the statistic database and M. Schipper and W. Buysscher, affiliated with the Center of Biostatistics, University of Utrecht, Utrecht, the Netherlands, for statistical analyses.
Supported by a grant from the Association of European Pediatric Cardiology. Dr. Kammeraad was supported by a grant from the VSB Foundation, the Netherlands, and a Trajectum grant from the University of Utrecht, the Netherlands. The current address for Dr. Kammeraad is the Department of Pediatrics, Deventer Hospital, Deventer, the Netherlands. The current address for Dr. Sreeram is the Department of Pediatric Cardiology, University Hospital Cologne, Cologne, Germany.
- Abbreviations and acronyms
- atrial fibrillation
- atrial flutter
- implantable cardioverter-defibrillator
- right ventricle/ventricular
- sudden death
- sinus node disease
- transposition of the great arteries
- ventricular fibrillation
- ventricular tachycardia
- Received December 22, 2003.
- Revision received April 28, 2004.
- Accepted May 18, 2004.
- American College of Cardiology Foundation
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