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Eur J Cardiothorac Surg 2007;32:462-468. doi:10.1016/j.ejcts.2007.06.009
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

The impact of pulmonary valve replacement after tetralogy of Fallot repair: a matched comparison

Aungkana Gengsakula, Louise Harrisb, Timothy J. Bradleya, Gary D. Webbb, William G. Williamsc, Samuel C. Siub, Naeem Merchantb, Brian W. McCrindlea,*

a The Division of Cardiology, Department of Pediatrics, University of Toronto, The Hospital for Sick Children, Toronto, Ontario, Canada
b The Division of Cardiology, Department of Medicine, University of Toronto, Toronto Congenital Cardiac Center for Adults, Toronto General Hospital, Toronto, Ontario, Canada
c The Division of Cardiovascular Surgery, Department of Surgery, University of Toronto, The Hospital for Sick Children, Toronto, Ontario, Canada

Received 21 February 2007; received in revised form 22 May 2007; accepted 11 June 2007.

* Corresponding author. Address: The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8. Tel.: +1 416 813 7610; fax: +1 416 813 7547. (Email: brian.mccrindle{at}sickkids.ca).


   Abstract
Top
 Abstract
1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 References
 
Objective: While there are no controlled studies, pulmonary valve replacement (PVR) after late tetralogy of Fallot repair is performed for patients with symptoms, arrhythmia or ventricular dysfunction. We sought to determine the impact of PVR on clinical outcomes. Methods: In a matched cohort study, 82 patients with PVR after tetralogy of Fallot repair without a history of ventricular arrhythmia were matched and compared with similarly followed non-PVR control subjects. A propensity-score adjusted analysis using repeated measures regression techniques was performed. Results: For the PVR subjects, the mean age was 28 years with a mean duration follow-up of 9 years. Before PVR, these subjects were significantly more likely than matched non-PVR subjects to have had non-ventricular arrhythmias, symptoms, lower functional class, longer QRS duration, lower right ventricular ejection fraction and higher right ventricular pressure, and reduced exercise duration but not aerobic capacity. During follow-up, sudden death occurred in four non-PVR subjects compared with no PVR subjects, with three episodes of ventricular tachycardia in the PVR subjects versus none in the non-PVR subjects (p = 0.49). Symptoms and functional class improved in the PVR subjects with no change in the non-PVR subjects (p < 0.001). The change in QRS duration was not significantly different between PVR and non-PVR subjects (p = 0.48). Oxygen consumption at peak exercise did not significantly change in either group. For PVR subjects, there was a significant qualitative reduction in pulmonary (p < 0.001) and tricuspid valve regurgitation (p = 0.009) and right ventricular size (p < 0.001) and dysfunction (p < 0.001) noted on echocardiography. Conclusions: Symptoms and functional status are improved after late PVR, with a reduction in pulmonary and tricuspid valve regurgitation and right ventricular size and dysfunction. While a significant impact on arrhythmia was not detected, there were no sudden deaths in the PVR subjects.

Key Words: Tetralogy of Fallot • Pulmonary valve • Arrhythmia • Sudden death • Health status


   1. Introduction
Top
 Abstract
 1. Introduction
2. Patients and methods
 3. Results
 4. Discussion
 References
 
Excellent management and surgical correction are responsible for the substantial and growing population of adults with tetralogy of Fallot (TOF). However, late sudden cardiac death has been reported to occur at a rate of 1.5 events/1000 patient-years [1]. Murphy et al. [2] and Silka et al. [1] reported a 6% prevalence of late sudden cardiac death among patients with up to 30 years of follow-up. Important ventricular and atrial arrhythmias are also prevalent, occurring in up to 35% of patients [3–5]; Harrison et al. [4] and Gatzoulis et al. [6] reported risk factors for ventricular arrhythmia and sudden death, including repair at an older age, previous transannular patch repair, severe pulmonary regurgitation, right ventricular (RV) dilatation and dysfunction, RV outflow tract aneurysm, left ventricular (LV) systolic dysfunction, QRS duration ≥180 ms and increased QRS duration rate of change during follow-up [3]. A recent study showed that pulmonary regurgitation was the predominant lesion associated with ventricular tachycardia and sudden death [6]. Pulmonary regurgitation after repair is related to abnormalities of the right ventricular (RV) outflow tract and disruption of the pulmonary valve, and results in chronic RV volume overload [7].

Pulmonary valve replacement (PVR) has been advocated to reduce RV volume overload, and thereby improve RV performance and decrease the risk of sudden death and ventricular failure, but the indications and optimal timing have yet to be established [8–12]. Controlled studies of outcomes after PVR have not been performed. We sought to determine whether PVR improves functional status and decreases the incidence of sustained arrhythmia and sudden death when compared to equivalent matched non-PVR subjects and adjusted for propensity for PVR.


   2. Patients and methods
Top
 Abstract
 1. Introduction
 2. Patients and methods
3. Results
 4. Discussion
 References
 
A retrospective matched cohort study was undertaken at two institutions by a medical record review of patients who had undergone primary complete repair of TOF and anatomic variants. The institutional research ethics board of both participating institutions approved the study.

2.1 Patient population
2.1.1 PVR subjects
Repaired TOF patients who underwent PVR between January 1, 1974 and December 31, 2003 (30 years) were included. Patients with a history of ventricular arrhythmias, such as episodes of ventricular tachycardia, or placement of an automatic implantable defibrillator before PVR were excluded from the study. Patients with cardiac anatomy including ventricular septal defect with pulmonary valve stenosis or atresia, double chambered right ventricle, multiple aorticopulmonary collateral arteries, non-confluent pulmonary artery branches or other complex congenital heart diseases and anatomy precluding biventricular repair were excluded. Patients were also excluded if the PVR occurred at the time of initial repair. Patients with double outlet right ventricle with pulmonary stenosis were included.

2.1.2 Non-PVR subjects
Repaired TOF patients who did not have PVR were matched with PVR patients by their date of birth, cardiac diagnosis (TOF vs double outlet right ventricle) and age when complete repair was undertaken. A possible matching non-PVR subject was selected if they had a similar or greater duration of follow-up after the date of the PVR for its matched PVR subject.

2.2 Measurements
Chart review was undertaken for documented evidence of episodes of (1) sustained ventricular tachycardia (VT), defined as VT persisting for more than 30 s or requiring termination because of hemodynamic collapse; (2) sudden cardiac death, defined as a sudden and unexpected cardiac arrest leading ultimately to death even if delayed by artificial methods; and (3) death of non-cardiac cause. Serial clinic visit data, electrocardiograms (ECG), echocardiograms, cardiopulmonary testing and magnetic resonance imaging (MRI) data were recorded for assessment of cardiac status including symptoms, QRS duration, severity of RV dysfunction and dilatation, degree of pulmonary and tricuspid regurgitation, cardiac function and exercise capacity.

2.3 Data analysis
Data are described as frequencies, medians with ranges and means with standard deviations as appropriate. Comparisons between the matched pairs of PVR and non-PVR subjects were made using mixed linear regression analysis for repeated measures for continuous variables, and general estimating equations for dichotomous and ordinal category variables. In order to adjust for differences regarding important confounding baseline characteristics between PVR and non-PVR subjects, a propensity score was derived for all study subjects. The propensity score was derived by entering key baseline variables (missing values were informatively imputed) into a multiple logistic regression and outputting the probability that each individual subject was a case given their individual baseline characteristics. This probability, or the propensity of a study subject to be a PVR subject versus a non-PVR subject, was then used as an adjustment variable in the comparisons of outcomes for matched pairs of PVR and non-PVR subjects in the mixed linear and general estimating equation regression analyses. Baseline measurement was taken to be the value closest in time immediately preceding the PVR for the PVR subjects, and closest in age to the matched PVR subject at the time before PVR for the non-PVR subjects. The variables that were used in the derivation of the propensity score included gender, underlying diagnosis of double outlet right ventricle with pulmonary stenosis, age at repair, repair at another institution, repair with a conduit, repair with a transannular patch, QRS duration on ECG, estimated RV pressure from echocardiography, results of cardiopulmonary exercise, and cardiac medication use. The propensity score together with the time interval of the measurements from the PVR date were included as additional adjusting factors in the repeated measures analysis, along with the interaction term of the group and whether the measurement was made before or after PVR taken, to indicate if a significant difference existed in the change over time between matched PVR and non-PVR subjects. All analyses were performed using SAS statistical software Version 8.2. The authors had full access to the data and take responsibility for its integrity. All authors have read and agree to the manuscript as written.


   3. Results
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
4. Discussion
 References
 
3.1 Characteristics of PVR subjects
Of the 82 PVR subjects, the PVR was performed at a Toronto institution for all but one subject, at a mean age of 28 ± 13 years and a mean time of 19 ± 10 years after complete repair. Reasons for performing PVR included the presence of symptoms in 87%, important pulmonary regurgitation in 89%, RV dilation in 78% and important tricuspid regurgitation in 40%. Concomitant procedures performed at the time of PVR included pulmonary arterioplasty in 48%, RV outflow tract obstruction repair in 30%, RV outflow tract aneurysm repair in 29%, tricuspid valve repair in 23%, closure of residual atrial septal defect in 17%, closure of residual ventricular septal defect in 10%, RV conduit replacement in 5% and aortic valve repair in 2%. In addition, three patients had right atrial Maze procedures and two had intraoperative atrial ablations at the time of their PVR.

3.2 Baseline characteristics in comparison with non-PVR subjects
A total of 82 PVR subjects were identified and individually matched to 82 non-PVR subjects. While there were significant differences between matched subjects regarding the variables used to match, the magnitude of the differences was small. A comparison of demographic and patient characteristics is given in Table 1 . PVR subjects differed significantly from their matched non-PVR subjects for older age at repair, having been less likely to have had repair in a Toronto institution and greater use of transannular patching at repair.


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  		Table 1 Demographic and surgical characteristics
 
3.3 Time-related events
From the date of PVR, three of the PVR subjects had an episode of sustained VT (two monomorphic, one polymorphic), but there were no sudden cardiac deaths. During the same time period, there were four sudden cardiac deaths and one patient had sustained VT (monomorphic) in the non-PVR subjects after the date of the PVR for their matched PVR subject. None of the four non-PVR subjects who had sudden cardiac death had a documented episode of VT at any time prior to their death. Kaplan–Meier estimates of time-related freedom from either sudden cardiac death or sustained VT are shown in Fig. 1 . There were no significant differences regarding the time-related risk of events between PVR and non-PVR subjects (p = 0.49), even after adjusting for propensity score (p = 0.30).


Figure 1
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  		Fig. 1. Kaplan–Meier estimates of time-related freedom from either sudden cardiac death or sustained ventricular tachycardia.

 
There were two deaths of non-sudden cardiac etiology among the PVR subjects; one from fulminant endocarditis with multi-organ failure, and one from cellulitis resulting in serum sickness and respiratory failure. In the non-PVR subjects, one death occurred secondary to heart failure associated with severe tricuspid regurgitation.

3.4 Symptoms and functional status
Symptoms and functional status at baseline and latest follow-up are shown in Table 2 . Median follow-up interval after PVR date did not differ significantly between PVR subjects (5.9 years; range, 0.1–24.9) and matched non-PVR subjects (6.1 years; range, 0.1–25.1; p = 0.6). At baseline, PVR subjects were significantly more likely to have symptoms, particularly fatigue (p < 0.001), dyspnea (p < 0.001), palpitations (p < 0.001), chest pain (p = 0.04) and ankle swelling (p = 0.04). They were also significantly more likely to have job limitations (p < 0.001) and lower NYHA functional class (p < 0.001). After PVR at latest follow-up, there were no significant differences in the frequency of symptoms or limitations between matched PVR and non-PVR subjects, with no significant change over the follow-up interval in the non-PVR subjects. There was significant improvement after PVR for the PVR subjects for all symptoms and limitations except chest pain and ankle swelling, with a marked improvement in NYHA functional class (p < 0.001). Differences in the change from before to after PVR date between the matched PVR and non-PVR subjects were significant for symptoms, limitations and NYHA functional class except for syncope, ankle swelling and chest pain. The differences remained significant after adjusting for the follow-up interval after PVR and propensity score.


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  		Table 2 Symptoms and functional status
 
3.5 Arrhythmias and electrocardiographic changes
Non-ventricular tachyarrhythmias (atrial flutter, atrial fibrillation) appeared to be more common in the PVR subjects than the non-PVR subjects, both before the date of the PVR (17% vs 0%) and during follow-up after PVR (15% vs 6%). Permanent pacemaker implantation was performed before the date of the PVR in 7% of the PVR subjects and 4% of the non-PVR subjects, and during follow-up after the PVR date in 6% of the PVR subjects and 1% of the non-PVR subjects. Only one non-PVR subject had placement of an automatic implantable cardiodefibrillator, occurring after the PVR date of its matched PVR subject.

QRS duration changes are shown in Table 3 . At baseline and at latest follow-up, QRS duration was significantly greater in the PVR subjects than in the non-PVR subjects, with a significant increase during the follow-up interval only noted in the PVR subjects. The change in QRS duration for the matched pairs was not significantly different for PVR subjects versus matched non-PVR subjects (p = 0.48), even when adjusted for propensity score and time from PVR date (p = 0.60). Likewise, there were no significant differences in the changes in mean QRS axis, ventricular rate or PR interval.


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  		Table 3 Electrocardiography
 
3.6 Exercise testing
Changes in ventilation and exercise variables are shown in Table 4 . While the available data are limited, there were no significant differences between PVR subjects and matched non-PVR subjects for any of the variables, with the only significant difference after PVR being higher percent predicted VO2 at peak exercise in the control subjects. For all variables, both groups showed important limitations in both ventilation and exercise capacity. There were few noteworthy changes within each group, and changes did not significantly differ between groups for any variable, even after adjustment for propensity score and time from PVR.


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  		Table 4 Cardiopulmonary exercise testing
 
3.7 Echocardiography and MRI
Changes in echocardiographic variables are shown in Table 5 . Follow-up time from PVR date was similar between PVR subjects (n = 78, median 5.6 years) and matched non-PVR subjects (n = 73, median 5.9 years; p = 0.85). At baseline and at latest follow-up, estimated RV systolic pressure was significantly greater in the PVR subjects than in the non-PVR subjects, with a trend towards a decrease during the follow-up interval only noted in the PVR subjects. The change in RV systolic pressure for the matched pairs was not significantly different for PVR subjects versus matched non-PVR subjects (p = 0.26), even when adjusted for propensity score and time from PVR date (p = 0.22). For LV fractional shortening, there were no significant differences at baseline or follow-up, or changes from baseline between groups (p = 0.71), even after adjusting for propensity score and time from PVR date (p = 0.72). There were significantly greater changes (improvement) in PVR versus matched non-PVR subjects, both unadjusted and adjusted, for qualitative grades of RV dysfunction (p = 0.001; p = 0.001), RV dilation (p < 0.001; p < 0.001), pulmonary regurgitation (p < 0.001; p < 0.001) and tricuspid regurgitation (p = 0.008; p = 0.009).


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  		Table 5 Echocardiography and magnetic resonance imaging
 
Changes in MRI variables are shown in Table 5. The number of both PVR and non-PVR subjects who had MRI was small, particularly for complete measurements both before and after PVR for matched pairs.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
References
 
4.1 The potential impact of PVR
Late sustained VT, while uncommon, has been identified as a major risk factor for sudden cardiac death after repair of TOF [4–6,9,13–15]. Pulmonary regurgitation and RV outflow tract obstruction are the predominant hemodynamic lesions encountered [7,8,16]. Previous studies initially suggested VT was associated with RV hypertension and secondary to residual pulmonary valve stenosis [8,12]. However, Gatzoulis et al. noted that isolated RV outflow tract obstruction was not a predisposing factor for late VT, but that ventricular arrhythmia was associated with the severity of pulmonary regurgitation and resulting RV dilation [6,17]. This raises the possibility that PVR, by improving or stabilizing the hemodynamic milieu, might decrease the risk of sudden death from ventricular arrhythmia, but optimal timing for PVR has yet to be established [8,9,12,18–20]. Nonetheless, given that an important proportion of PVR patients in our series had resection of RV outflow tract aneurysms or repair of residual or recurrent RV outflow obstruction, we cannot exclude the possibility that these concomitant procedures may have contributed to the low incidence of ventricular arrhythmia and sudden death. It is possible that these procedures may remove important foci of arrhythmia. However, a recent review of patients undergoing re-operations did not show a significant impact of VT ablation on subsequent arrhythmia-free survival [20].

4.2 PVR and sudden cardiac death
The cohort of patients with late PVR reported in this study had excellent long-term survival, and there were no sudden cardiac deaths over nearly 9 years of follow-up or 28 years since initial repair. Matched for a similar duration of follow-up, the control group exhibited a prevalence of sudden cardiac death of 5%, comparable to other reports [1,2]. In a recent large multi-center retrospective study with a mean of 21 years of follow-up, Gatzoulis et al. observed a 2% prevalence of sudden death for patients repaired at a mean age of 8 years [6]. While the majority of sudden deaths are attributable to arrhythmia, Silka et al. also identified circulatory causes, such as embolic events and acute ventricular failure, as contributing to sudden death after TOF repair [1]. Furthermore, not all arrhythmia-related deaths were secondary to ventricular arrhythmias in their study, and heart block was also reported.

4.3 Arrhythmias
None of our patients after PVR died suddenly. Previous studies in TOF patients with VT from our center suggested PVR with intra-operative ablation may reduce recurrent late arrhythmia in patients after TOF repair [12,20,21]. In the present study, we specifically studied patients without pre-existing VT, to determine whether PVR, by stabilizing or possibly reversing the hemodynamic changes, might prevent VT. We noted no significant differences in the prevalence of VT and sudden cardiac death during follow-up between the groups, although the prevalence was low. There is a supposition that if PVR were performed while the patient was still low risk or asymptomatic, this strategy might possibly prevent or decrease the risk of VT. In addition, we found that the prevalence of non-ventricular arrhythmias in PVR patients was greater than in the low risk non-PVR group, both before and after PVR. A previous study has shown that the development of atrial arrhythmias was associated with re-operation, older age at repair and important pulmonary regurgitation [5].

4.4 Serial ECG findings and hemodynamic changes
The QRS duration for the PVR patients in our study was longer than for the non-PVR subjects, and remained so after PVR. QRS duration continued to be prolonged after PVR during the follow-up period, although it was shorter immediately after PVR. However, there were no significant differences in QRS prolongation during the follow-up interval in high-risk patients after PVR compared with non-PVR patients.

Pulmonary and tricuspid regurgitation improved after PVR in comparison to the non-PVR subjects, with a concomitant reduction in RV dimension both by echocardiographic and MRI criteria. RV volumes/dimensions, albeit smaller for the non-PVR subjects, continued to increase over the corresponding duration of follow-up. RV function appeared improved by echocardiography after PVR, but there was no significant improvement in ejection fraction by MRI. This suggests that while PVR can reduce RV size, the impact on RV function might have been limited by pre-existing scarring and fibrosis, and improvements may have a variable time course. It is possible that we operated too late in these patients and that earlier PVR performed before substantial RV dysfunction occurs might protect RV function and decrease the risk of VT. This is supported by a previous study that showed that PVR should be undertaken before the RV end-diastolic volume reaches 170 ml/m2 [22].

4.5 Functional status
This study showed PVR was associated with subjective improvement in symptoms, functional capacity and status. This was not associated with significant improvements in exercise capacity, with no significant improvement in oxygen consumption at peak exercise noted at cardiopulmonary exercise testing. The lack of improvement in objective exercise performance may reflect the presence of persistent RV dysfunction noted after PVR. The matched non-PVR subjects had fewer symptoms with no progression during follow-up. Previous studies have shown an improvement in NYHA class and exercise tolerance after PVR [11,21,23–25]. This suggests that PVR should be considered earlier and the onset of symptoms may be a late and suboptimal indicator for PVR.

4.6 Study limitations
This was a retrospective study of a patient cohort from two tertiary centers. Referral bias could influence the observed prevalence of events; however, the Hospital for Sick Children and the Toronto Congenital Cardiac Center for Adults serve as the regional referral centers for congenital heart disease in Ontario. The study is a non-randomized comparison based on observational data. We matched the PVR patients and the non-PVR subjects in order to minimize potential bias, and further adjusted for propensity for PVR (baseline differences between cases and their matched control subject). There were changes in medical technology during the study period resulting in the use of different investigations over the duration of the study. For example, only more recently has MRI been used routinely at our institution. For the majority of the patients, the presence of symptoms was a commonly used indication for PVR, and this reporting could not be objectively verified. The prevalence of VT in our study was noted to be low, and we did not have sufficient statistical power to determine an impact of PVR on this outcome.

4.7 Conclusion and clinical application
PVR improved symptoms, functional status and decreased pulmonary regurgitation, tricuspid regurgitation and RV size. RV function remained impaired after PVR. While there were no sudden cardiac deaths in the PVR patients, we were unable to demonstrate a significant impact on the prevalence of subsequent VT or sudden death. The outcome for patients after TOF repair and subsequent PVR are encouraging, but better criteria are needed to guide patient selection for PVR before pathophysiological changes become irreversible. Ongoing research incorporating multiple modalities is needed to define timing for PVR that optimally prevents morbidities and allows for complete recovery of functional abnormalities.


   Acknowledgments
 
We would like to acknowledge the contributions of James Wengle, Kim Haberer, Patrick Glasgow, and Anna Bilanovic in assisting in data collection, entry and analysis, and Rommel Tuason in assisting in the identification of patients and data from the Toronto Adult Congenital Cardiac Clinic's databases and records.


   Footnotes
 
\#9734; The study was funded by a grant-in-aid from the Heart and Stroke Foundation of Ontario (NA4109 and NA4876). Dr McCrindle acknowledges support from the CIBC World Markets Children's Miracle Foundation.


   References
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 References
 

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 Eur. J. Cardiothorac. Surg.Home page
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Late risk of outcomes for adults with repaired tetralogy of Fallot from an inception cohort spanning four decades
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 Circ Cardiovasc ImagingHome page
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Functional Analysis of the Components of the Right Ventricle in the Setting of Tetralogy of Fallot
Circ Cardiovasc Imaging, September 1, 2008; 1(2): 141 - 147.
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P. Lurz, L. Coats, S. Khambadkone, J. Nordmeyer, Y. Boudjemline, S. Schievano, V. Muthurangu, T. Y. Lee, G. Parenzan, G. Derrick, et al.
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