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Ann Thorac Surg 2003;76:1901-1905
© 2003 The Society of Thoracic Surgeons

Original article: cardiovascular

Risk factors for sudden death after repair of tetralogy of Fallot

Georg D. A. Nollert, MDa*, Sabine H. Däbritz, MDa, Michael Schmoeckel, MDa, Calin Vicol, MDa, Bruno Reichart, MDa

a Clinic of Cardiac Surgery, Klinikum Großhadern, University of Munich, Munich, Germany

Accepted for publication June 6, 2003.

* Address reprint requests to Dr Nollert, Clinic of Cardiac Surgery, Klinikum Großhadern, Marchioninistr 15, 81366 Munich, Germany
e-mail: gnollert{at}hch.med.uni-muenchen.de


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Sudden cardiac death remains the most common cause of death after repair of tetralogy of Fallot. It has been suggested that sudden cardiac death is related to right ventricular hypertrophy or dilation. However, it is uncertain whether the preoperative patient status or operative techniques predispose for sudden cardiac death.

METHODS: From 1958 to 1977, 658 patients underwent repair of tetralogy of Fallot at our institution at a median age of 12.2 ± 8.6 years. One third had at least one previous palliative operation 4.6 ± 2.5 years earlier. A total of 490 patients survived the first postoperative year and were analyzed for sudden cardiac death. During a follow-up period of 25.3 ± 5.8 years (range, 1.0 to 35.5 years), 42 patients died, and 15 (36%) of those deaths were as a result of sudden cardiac death.

RESULTS: Actuarial 10-year, 20-year, and 30-year survival rates were 97%, 94%, and 89%. Freedom from sudden cardiac death was 99%, 98%, and 95% after 10, 20, and 30 years. The risk of sudden cardiac death increased after 10 years from 0.06%/y to 0.20%/y. Univariate predictors (p < 0.1) of sudden cardiac death were use of an outflow tract patch (p = 0.068), male sex (p = 0.048), no previous palliation (p = 0.013), and higher preoperative New York Heart Association status (p = 0.014). Multivariate analysis confirmed these risk factors except use of an outflow tract patch.

CONCLUSIONS: The most important risk factors for sudden cardiac death were higher preoperative New York Heart Association class and no previous palliation. Thus, early surgical intervention is recommended. The risk of sudden cardiac death increases with time, suggesting that long-term follow-up by specialized cardiologists or pediatricians should be intensified. However, all patients who died suddenly had at least two risk factors at the time of surgery.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Sudden cardiac death caused by ventricular tachycardia and fibrillation remains the most common cause of death after repair of tetralogy of Fallot (TOF) [1]. It has been suggested that sudden cardiac death is related to postoperative right ventricular hypertrophy or dilation [2, 3] mainly as a result of pulmonary valve stenosis or regurgitation [4, 5]. Furthermore, several electrocardiographic markers, especially prolongation of the QRS complex, have been proposed as indicators of sustained ventricular tachycardia and sudden death during follow-up [2]. However, it is uncertain whether risk factors related to the preoperative patient status or operative techniques predispose for sudden cardiac death.

This study analyzes our historic (1958 to 1977), long-term experience in the correction of patients with TOF and pulmonary stenosis for preoperative and intraoperative risk factors of sudden cardiac death [6]. The patient population is very homogeneous as almost all patients were operated on by one surgeon, using the same technique without major changes in the operative management.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 Acknowledgments
 References
 
Patients
Details of our patient population has been described earlier [1, 7]. In short, from 1958 to 1977, 739 patients with the diagnosis of TOF with pulmonary stenosis underwent complete surgical repair at the Clinic of Surgery at Munich University. We attempted to contact all patients who survived the immediate postoperative period. In 16 cases, we were unable to locate them (follow-up 98% complete), but information from the German Resident Registry (Einwohnermeldeamt) indicated that they were alive at least 12 years postoperatively. All foreigners (n = 52) as well as those known to have moved outside Germany (n = 13) were excluded from follow-up. To analyze the factors that influence sudden death during long-term survival we excluded the steep, nonlinear, first phase of the survival curve. The curve becomes linear after 1 year. Therefore, all patients who died in the operative period within 30 days (n = 139; 19%) and the first year (n = 29; 4%) were separated from further analyses. Mortality during the first postoperative year was mainly attributable to heart failure and rhythm disturbances caused by insufficient intraoperative cardioprotective measures [1].

More than one third of the patient population had at least one previous operation (n = 181; 36.9%; Table 1). The mean age at the time of palliation was 6.0 ± 7.5 years, and the time interval to definitive correction was 4.6 ± 2.5 years. Table 1 shows a survey of patient characteristics including concomitant cardiac malformations and previous palliative operations.


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  		Table 1. Preoperative Data

 
Operative methods
The intracardiac correction was performed through a horizontal right ventricular incision. However, if the decision was made to use an outflow tract patch, a longitudinal incision was made. Outflow tract patches were either used in the subvalvular (preserving pulmonary valve competence; n = 32; 7%) or transvalvular (including splitting of the valvular ring; n = 68; 14%) position. All other patients had primary ventriculotomy closure. A concomitant patent foramen ovale was left open whereas all other accompanying defects were corrected (including atrial septal defect type II). The postrepair ratio of systolic right-to-left ventricular pressure was reduced to 0.5 or lower in 60% of the cases; another 27% showed a moderately elevated ratio of 0.5 to 0.7. In 13% of the patients the ratio remained high (>0.7). During the intracardiac maneuver, the aorta remained clamped for 24 ± 10 minutes; the average bypass-time was 52 ± 16 minutes. A cardioplegic solution was not used in any of the cases. Detailed information on the operative techniques used are described in previous papers [6, 8].

Follow-up and statistical methods
Follow-up consisted of a written questionnaire. Telephone interviews were used, if the patient did not answer repeated letters. If a patient had died during long-term follow-up (n = 49), the closest living relative and the patient's physician were contacted to evaluate the cause of death. If the cause of death remained uncertain, we tried to get this information from the official death certificate. In four cases we were unable to achieve certainty of the cause of death. Although all or some of these fatalities may be caused by sudden cardiac death, we did not consider them to be sudden death and excluded these cases from the presented analysis. However, labeling these cases as sudden death would not change the risk analysis; in fact the presented p values would become only more significant.

The probability of long-term survival was estimated by the Kaplan-Meier method. Differences between groups were calculated by the log-rank test. The association of factors to long-term survival was first tested in an univariate model. Every univariate variable reaching or approaching significance (p < 0.1) was then tested in a Cox multivariate model and removed stepwise if no significant influence was proved. Statistical analyses were facilitated with the help of SPSS (SPSS Inc, Chicago, IL) statistical software.


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 Acknowledgments
 References
 
Overall survival and freedom from sudden cardiac death
The mean duration of follow-up was 25.3 years (median, 25.4 years; range, 1.06 to 35.5 years). Actuarial 10-year, 20-year, 30-year, and 36-year survival in the 490 patients who survived the first postoperative year was 97%, 94%, 89%, and 85%, respectively. Freedom from sudden cardiac death was 99%, 98%, and 95% after 10, 20, and 30 years, respectively. The risk of sudden cardiac death increased 10 years postoperatively from 0.06%/y to 0.20%/y (Fig 1). During long-term follow-up 42 patients died. Most fatalities were related to the heart (n = 31; 74%), with sudden cardiac death (n = 15; 36%) as the single most common cause. Table 2 describes the causes of late death in detail.



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  		Fig 1. Freedom from sudden cardiac death (%) during long-term follow-up after correction of tetralogy of Fallot. All patients who died within the first year after correction were excluded for calculation of freedom from sudden cardiac death. The curve shows two different phases, which are distinct. The early, low-risk phase lasts 10 years; thereafter the risk increases. Mortality risk (r) per year as a linearized number is calculated for each phase. Note the break in the y-axis. (OP = operation; p.o. = postoperative.)

 

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  		Table 2. Causes of Death During Long-Term Survival

 
Analysis of risk factors
Many preoperative and postoperative factors were tested for whether they influenced freedom from sudden cardiac death. Univariate correlates (p < 0.1) of sudden cardiac death were use of an pulmonary outflow patch (p = 0.068; Fig 2), male sex (p = 0.048; Fig 3), no previous palliation (p = 0.013; Fig 4), and higher preoperative New York Heart Association (NYHA) status (p = 0.014; Fig 5). The influence of an outflow tract patch was independent from the position (transannular or subvalvular) of the patch (p = 0.56). Patients who died suddenly had either two (n = 2), three (n = 9), or four (n = 4) of these risk factors. In multivariate analysis, only male sex (p = 0.055), no previous palliation (p = 0.041), and higher preoperative NYHA status (p = 0.008) correlated (p < 0.1) with sudden cardiac death. Higher preoperative NYHA status was associated with increased hematocrit values (p = 0.007) and erythrocyte counts (p = 0.001). Table 3 shows the results of univariate and multivariate analyses of freedom from sudden cardiac death.



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  		Fig 2. Freedom from sudden cardiac death (%) according to a right ventricular outflow tract patch. In the majority of patients no outflow tract patch was necessary. If the ring of the pulmonary valve was severely hypoplastic, a patch through the annulus (n = 69) was used to widen the outflow tract. In some patch patients, a patch up to, but not through, the annulus (n = 32) seemed sufficient to relieve obstruction. (OP = operation.)

 


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  		Fig 3. Freedom from sudden cardiac death (%) according to sex. The risk for male patients to die suddenly during 30 years' long-term follow-up was more than 3 times higher than for females (6.7% versus 2%). (OP = operation.)

 


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  		Fig 4. Freedom from sudden cardiac death (%) according to previous palliative operations. Long-term survivors with a previous palliative operation showed a reduced risk of sudden cardiac death. The single patient with a previous palliation who died sudden was a female patient with a Blalock-Taussig shunt and preoperative New York Heart Association class III. She needed a transannular patch during corrective surgery. (OP = operation.)

 


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  		Fig 5. Freedom from sudden cardiac death (%) according to preoperative New York Heart Association (NYHA) status. No patient with preoperative NYHA class I or II died suddenly during 30 years' long-term follow-up, whereas the risk in patients with NYHA class IV was 14%. (OP = operation.)

 

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  		Table 3. Risk Factors for Sudden Cardiac Death

 

   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
Acknowledgments
 References
 
The excellent long-term survival after correction of TOF even in the very early years of cardiac surgery is well recognized [1, 5, 9, 10]. However, sudden cardiac death remains the most common cause of death during long-term follow-up and is the most important reason that life expectancy remains lower than in the normal population [1]. It has been speculated that the incidence of sudden cardiac death might decrease if patients survive into adulthood [5, 10]. Our results indicate the opposite. The risk of sudden cardiac death increased threefold 10 years after surgery and remained stable up to 30 years.

Impact of an outflow tract patch on freedom from sudden cardiac death
In our series use of an outflow tract patch tended to increase the risk of sudden cardiac death (p = 0.068). Differences between subannular and transvalvular patches were insignificant. The influence of an outflow tract patch on long-term survival has been controversial [1, 5, 9]. In a recent large multicenter study Gatzoulis and associates [4] demonstrated that outflow tract patching increases the incidence of ventricular tachycardia and sudden cardiac death significantly. The patch leads to pulmonary regurgitation, right ventricular enlargement, and increase in QRS duration, independent of subvalvular or transannular implantation [11]. Pulmonary valve replacement in patients with pulmonary valve regurgitation and dilation of the right ventricle demonstrated a decrease in ventricular arrhythmias [12].

Avoidance of an outflow tract patch may lead to the acceptance of higher postoperative systolic right-to-left ventricular pressure ratios. In contrast to previous studies [13, 14], increased right-to-left ventricular pressure ratios did not influence sudden cardiac death even in case of substantially elevated ratios (>0.7). An association between high right ventricular pressures, ventricular arrhythmia, and sudden death was also not seen by Gatzoulis and colleagues [4]

Impact of sex on freedom from sudden cardiac death
Little is known on the impact of sex on survival and sudden cardiac death in TOF patients. Previous studies stated no effect on survival [15, 16], especially on sudden cardiac death. In our own study group we saw a trend toward better overall survival in women (p = 0.14) [1]; for sudden cardiac death this trend was significant. However, in most studies impact on sudden cardiac death was not evaluated [4, 5] or the low incidence of sudden death (n < 10) was likely to be insufficient to demonstrate an effect [15, 16]. In a recent study from the Mayo Clinic [17] describing long-term survival in patients with pulmonary ventricle to pulmonary artery conduits, most of them being TOF patients with pulmonary atresia, male sex was isolated as a risk factor for survival. It remains speculative why the incidence of sudden cardiac death was 3 times higher in male compared with female patients.

Impact of previous palliative surgery on freedom from sudden cardiac death
Age at surgery has been identified as an important predictor of arrhythmias and sudden cardiac death [4, 18]. In our study the occurrence of sudden cardiac death was independent of age at surgery. Most children in our series had correction of their TOF not before the age of 10, and with very few exceptions only those with previous palliations were relieved from cyanosis at younger age (mean, 6 years). Only a single patient with previous palliation, who needed an outflow tract patch during subsequent correction, died suddenly. It may be concluded that long-standing pulmonary stenosis and right ventricular hypertrophy do not predispose for sudden death but long-standing cyanosis does. This hypothesis is supported by the fact that a subset of patients of our study group, namely those with favorable anatomy who survived into adulthood, tended to have a decreased incidence of sudden cardiac death [7].

A previous Pott or Waterston shunt is commonly associated with adverse outcome [4]. Only 6 patients received a central shunt for palliation in our study group with no late sudden death; therefore our data are insufficient for analysis.

Impact of preoperative new york heart association status on freedom from sudden cardiac death
According to our multivariate analysis preoperative NYHA status is the single most important risk factor for sudden cardiac death during long-term follow-up. Preoperative NYHA status highly correlated with preoperative hematocrit values and erythrocyte count, suggesting that in preoperative TOF patients NYHA status is strongly associated with the severity of hypoxia. It may be hypothesized that severe hypoxia in hypertrophied hearts could lead to microscopic myocardial infarctions with scars, which possibly serve as the substrate for arrhythmia. However, preoperative NYHA status has not been evaluated and described as a risk factor for sudden cardiac death, and the mechanisms remain speculative.

In summary, the most important risk factors for sudden cardiac death in our historic patient group were higher preoperative NYHA class and no previous palliation. Thus early correction is recommended to protect the heart from chronic cyanosis and failure. The risk of sudden cardiac death increases with time, suggesting that long-term follow-up by specialized cardiologists or pediatricians should be intensified. However, all patients who died suddenly had at least two risk factors at the time of surgery, and low-risk groups may be identified who can be relieved from the threat of sudden death.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
References
 
Prof Doctor Werner Klinner operated on the vast majority of these patients. His dedication to the treatment of patients with tetralogy of Fallot is rewarded by the excellent long-term outcome and quality of life.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Nollert G., Fischlein T., Bouterwek S., Bohmer C., Klinner W., Reichart B. Long-term survival in patients with repair of tetralogy of Fallot: 36-year follow-up of 490 survivors of the first year after surgical repair. J Am Coll Cardiol 1997;30:1374-1383.[Abstract]
  2. Gatzoulis M.A., Till J.A., Somerville J., Redington A.N. Mechanoelectrical interaction in tetralogy of Fallot: QRS prolongation relates to right ventricular size and predicts malignant ventricular arrhythmias and sudden death. Circulation 1995;92:231-237.[Abstract/Free Full Text]
  3. Gillette P.C., Yeoman M.A., Mullins C.E., McNamara D.G. Sudden death after repair of tetralogy of Fallot. Circulation 1977;56:566-571.[Abstract/Free Full Text]
  4. Gatzoulis M.A., Balaji S., Webber S.A., et al. Risk factors for arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot: a multicentre study. Lancet 2000;356:975-981.[Medline]
  5. Murphy J.G., Gersh B.J., Mair D.D., et al. Long-term outcome in patients undergoing surgical repair of tetralogy of Fallot. N Engl J Med 1993;329:593-599.[Abstract/Free Full Text]
  6. Klinner W., Reichart B., Pfaller M., Hatz R. Late results after correction of tetralogy of Fallot necessitating outflow tract reconstruction. Comparison with results after correction without outflow tract patch. Thorac Cardiovasc Surg 1984;32:244-247.[Medline]
  7. Nollert G., Fischlein T., Bouterwek S., et al. Long-term results of total repair of tetralogy of Fallot in adulthood: 35 years follow-up in 104 patients corrected at the age of 18 or older. Thorac Cardiovasc Surg 1977;45:178-181.
  8. Zenker R., Klinner W. Total correction of tetralogy of Fallot. Review of 315 cases with late results. Dis Chest 1967;51:311-314.
  9. Kirklin J.W., Wallace R.B., McGoon D.C., DuShane J.W. Early and late results after intracardiac repair of tetralogy of Fallot. 5-year review of 337 patients. Ann Surg 1965;162:578-589.[Medline]
  10. Lillehei C.W., Varco R.L., Cohen M., et al. The first open heart corrections of tetralogy of Fallot. A 26–31 year follow-up of 106 patients. Ann Surg 1986;204:490-502.[Medline]
  11. d'Udekem Y., Ovaert C., Grandjean F., et al. Tetralogy of Fallot: transannular and right ventricular patching equally affect late functional status. Circulation 2000;102(Suppl 3):III-116-122.
  12. Therrien J., Siu S.C., Harris L., et al. Impact of pulmonary valve replacement on arrhythmia propensity late after repair of tetralogy of Fallot. Circulation 2001;103:2489-2494.[Abstract/Free Full Text]
  13. Garson A., Jr, Randall D.C., Gillette P.C., et al. Prevention of sudden death after repair of tetralogy of Fallot: treatment of ventricular arrhythmias. J Am Coll Cardiol 1985;6:221-227.[Abstract]
  14. Katz N.M., Blackstone E.H., Kirklin J.W., Pacifico A.D., Bargeron L.M., Jr Late survival and symptoms after repair of tetralogy of Fallot. Circulation 1982;65:403-410.[Abstract/Free Full Text]
  15. Rosenthal A., Behrendt D., Sloan H., Ferguson P., Snedecor S.M., Schork A. Long-term prognosis (15 to 26 years) after repair of tetralogy of Fallot: I. Survival and symptomatic status. Ann Thorac Surg 1984;38:151-156.[Abstract]
  16. Jonsson H., Ivert T. Survival and clinical results up to 26 years after repair of tetralogy of Fallot. Scand J Thorac Cardiovasc Surg 1995;29:43-51.[Medline]
  17. Dearani J.A., Danielson G.K., Puga F.J., et al. Late follow-up of 1095 patients undergoing operation for complex congenital heart disease utilizing pulmonary ventricle to pulmonary artery conduits. Ann Thorac Surg 2003;75:399-410.[Abstract/Free Full Text]
  18. Joffe H., Georgakopoulos D., Celermajer D.S., Sullivan I.D., Deanfield J.E. Late ventricular arrhythmia is rare after early repair of tetralogy of Fallot. J Am Coll Cardiol 1994;23:1146-1150.[Abstract]



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