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Ann Thorac Surg 2001;71:911-917
© 2001 The Society of Thoracic Surgeons
a Department of Cardio-thoracic Surgery, University Hospital, Rotterdam, The Netherlands
b Department of Cardiology, University Hospital, Rotterdam, The Netherlands
c Department of Pediatric Cardiology, University Hospital, Rotterdam, The Netherlands
d Department of Public Health, Erasmus University, Rotterdam, The Netherlands
Accepted for publication September 22, 2000.
Address reprint requests to Dr Takkenberg, Department of Cardio-thoracic Surgery, Thorax Center, Bd 162, University Hospital Rotterdam, PO Box 55, 3000 WB Rotterdam, The Netherlands
e-mail: takkenberg{at}thch.azr.nl
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Abstract |
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Methods. Between August 1986 and March 1999, 316 allografts (246 pulmonary, 70 aortic) were implanted in 297 patients for reconstruction of the right ventricular outflow tract. Main diagnostic groups were aortic valve pathology (n = 112, 35%), tetralogy of Fallot (n = 71, 22%), and pulmonary atresia with ventricular septal defect (n = 46, 14%). Kaplan-Meier analyses were done for survival, valve-related reoperation, and valve-related events. In addition, Cox regression analysis was used for evaluation of potential risk factors.
Results. Mean age at operation was 18 years (range, 7 days to 61 years). Mean follow-up was 4 years (range, 2 days to 12 years). Twelve patients (4%) died within 30 days after operation. Patient survival was 90% (95% confidence interval [CI], 86% to 94%) at 5 years and 88% (95% CI, 83% to 94%) at 8 years. Twenty-four reoperations were required for allograft dysfunction in 23 patients; 21 allografts were replaced. Freedom from valve-related reoperation was 91% (95% CI, 86% to 95) at 5 years and 87% (95% CI, 81% to 93%) at 8 years. Twenty-nine valve-related events were reported (2 deaths, 24 reoperations, 2 balloon dilatations, and 1 endocarditis). Freedom from valve-related events was 90% (95% CI, 85% to 94%) at 5 years after implantation, and 84% (95% CI, 77% to 91%) at 8 years. Risk factors for accelerated allograft failure were extra-anatomic position of the allograft (p = 0.03; hazard ratio, 9.7) and the use of an aortic allograft (p = 0.02; hazard ratio, 2.4).
Conclusions. Right ventricular outflow tract reconstruction with an allograft conduit has good medium-term results, although progression of allograft degeneration is noted. Aortic allografts should preferably not be used for reconstruction of the right ventricular outflow tract.
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Introduction |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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Long-term results of RVOT reconstruction with allografts have been scarcely reported thus far. Stark and colleagues [5] described 84%, 58%, and 31% freedom from conduit replacement at 5, 10, and 15 years, respectively. Niwaya and associates [6] reported 90% freedom from allograft failure after 5 years and 82% after 8 years. In other series extra-anatomic position of the allograft and the use of aortic allografts were noted as risk factors for accelerated allograft failure [3, 6–9]. We describe our experience with allograft conduits for reconstruction of the RVOT to contribute to improved knowledge on outcome after allograft implantation.
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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Patient characteristics
Our series represents a heterogeneous group in which the common denominator was the need for a right-sided allograft conduit. Patients were classified according to their primary diagnosis (Table 1). Main diagnostic groups were aortic valve disease (35%), tetralogy of Fallot (22%), and pulmonary atresia with ventricular septal defect (15%). A first allograft was implanted in 296 patients, a second in 17, a third in 2, and a fourth in 1. Prior cardiac operation was performed in 200 patients (63%), of which 95 had previous RVOT reconstruction; their actual pathologic disorder is shown in Table 2.
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Allograft properties
The Rotterdam Heart Valve Bank provided most of the allografts (n = 242), which were allocated by Bio Implant Services, Leiden, The Netherlands. Preparation and storage methods have been described earlier [10]. The National Heart Hospital, London, England, provided 16 fresh and 4 cryopreserved allograft conduits. The remaining allografts were shipped from the Hospital Clinic I, Barcelona, Spain (n = 28), the Karolinska Homograft bank, Stockholm, Sweden (n = 6), the Deutsches Herzzentrum, Berlin, Germany (n = 19), and Herzzentrum Nord Rhein Westphalen, Bad Oeynhausen, Germany (n = 1). Patient’s body surface area was used as a guideline to determine the allograft diameter. No attempt was made to achieve ABO blood type or HLA type matching.
Follow-up
After implantation of the allograft, patients were seen at regular intervals by their cardiologists, with the exception of 17 patients who migrated to other countries or were living abroad. All follow-up data were collected retrospectively from hospital records. Follow-up was 95% complete. Allograft functional status was evaluated by physical examination, electrocardiography, echocardiography, and, if necessary, cardiac catheterization. The day of implantation was considered the starting point of patient survival. End points in patient survival were death or last follow-up date. Patients lost to follow-up were censored at last date of follow-up (n = 17; mean follow-up [±SD], 3.2 years ± 3.0; range, 1 week to 8 years). Starting point of allograft survival also was the day of implantation. End points were allograft dysfunction as defined by Edmunds and coworkers [11] or last follow-up date.
Data analysis
Patient data were entered into a computerized relational database (Microsoft Access 97). All statistical analyses were performed using SPSS 8.0 for Windows (Chicago, IL). Cumulative survival estimates were made at 5 and 8 years using the Kaplan-Meier method [12]. The log-rank test was used for univariate assessment of the effect of potential risk factors on patient survival, freedom from valve-related reoperation, and freedom from valve-related events. To investigate independent risk factors for mortality and morbidity caused by allograft failure, the Cox proportional hazard model was used. Risk factors were selected with a backward stepwise method (criteria for elimination: p > 0.20). Young age at implantation (< 4 years of age versus 
4 years of age) and small allograft diameter (< 23 mm versus 23 mm) were defined according to their distribution in the patient population (Fig 1A, B). After evaluation of the frequency distribution of donor age, young donor age was arbitrarily set at less than 30 years of age (Fig 1C). With regard to implantation position, all autograft procedures were labeled as anatomic, and any other allograft implantation for reconstruction of the RVOT was labeled as extra-anatomic. Young age at time of implantation (< 4 years), small allograft diameter (< 23 mm), extra-anatomic position of the allograft, ABO incompatibility between donor and recipient, young donor age (< 30 years), and an aortic allograft were considered to be potential risk factors for allograft dysfunction [4, 6–9]. Association between potential risk factors was studied calculating Pearson’s correlation coefficient (two-tailed testing).
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Results |
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Donor characteristics
The donor group consisted of 191 male and 117 female donors (male-female ratio, 6:1) with a mean age of 33 ± 18 years (median, 38; range, 0 to 64 years). The characteristics of 8 donors could not be traced. Mean allograft diameter was 22 ± 5 mm (median, 24; range, 10 to 31 mm). Of the 316 allografts, 300 were cryopreserved, and 16 were fresh.
Follow-up
Follow-up ranged from 2 days to 12 years with a mean follow-up time of 4 ± 3 years (median, 3 years). Total number of patient-years was 1,209.
Survival
Twelve patients (4%) died within 30 days of operation. Causes of early death were heart failure (n = 4), bleeding (n = 4), hypoxic encephalopathy (n = 1), respiratory insufficiency (n = 1), pulmonary thromboembolism (n = 1), and arrhythmia (n = 1). All deaths were non–valve-related. No allografts showed signs of degeneration at pathologic examination. Fifteen patients died later than 30 days after implantation. Two of these deaths were valve-related. In 1 patient calcification of the allograft valved conduit caused stenosis resulting in acute right heart failure. Endocarditis destroyed the allograft in another patient, resulting in right ventricular failure. Causes of non–valve related late death were heart failure (n = 6), respiratory insufficiency (n = 2), sepsis (n = 2), myocardial infarction (n = 1), arrhythmia (n = 1), and hypoxic encephalopathy (n = 1). In the 13 non–valve-related late deaths, severe pulmonary regurgitation because of structural valve failure was present at the last echocardiographic examination before death in 3 patients (2 died of right heart failure, 1 of arrhythmia) and moderate in 1, and mild pulmonary regurgitation was also present in 1 other patient. Furthermore, 1 patient with mild pulmonary stenosis and mild pulmonary regurgitation was noted. In the other 7 patients no pulmonary regurgitation or stenosis was present. Patient survival at 1 month was 96% (95% confidence interval [CI], 94% to 98%) and 93% (95% CI, 90% to 96%) at 1 year. Five- and 8-year survival were respectively 90% (95% CI, 86% to 94%) and 88% (95% CI, 83% to 94%; Fig 2). Univariate analysis revealed that younger donor age was the only risk factor for death (p = 0.04; hazard ratio [HR], 2.3; 95% CI, 1.0 to 5.0).
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Twenty-four reoperations were performed for allograft dysfunction in 23 patients. Allograft dysfunction was related to structural valve failure in 21 patients, characterized by stenosis in 19 patients and regurgitation in the remaining 2. Eighteen of the explanted allografts showed calcification. One allograft, replaced for structural valve failure, was not calcified. A false aneurysm in one sinus was responsible for the regurgitation in this patient. Conduit failure was nonstructural in 5 patients. On two occasions a prosthetic extension of the conduit caused stenosis near the proximal anastomosis of the allograft. A pericardial patch and a surgical membrane obstructed the allograft in 2 other patients, and 1 patient suffered from supravalvular stenosis near the distal anastomosis. In 21 operations the allograft was replaced, in 2 patients extension material causing allograft stenosis was removed, and in 1 patient a pulmonary allograft patch was used for enlargement of the RVOT. Freedom from reoperation was 91% (95% CI, 86% to 95%) after 5 years and 87% (95% CI, 81% to 93%) after 8 years. Log-rank testing revealed younger age at operation (< 4 years; p = 0.02; HR, 2.6; 95% CI, 1.1 to 5.7), smaller allograft diameter (< 23 mm; p = 0.01; HR, 3.5; 95% CI, 1.4 to 9.1), extra-anatomic position of the allograft (p = 0.02; HR, 10.1; 95% CI, 1.4 to 74.7), young donor age (< 30 years; p = 0.01; HR, 3.5; 95% CI, 1.3 to 9.5), and aortic allograft (p = 0.008; HR, 4.2; 95% CI, 1.8 to 9.6) as potential risk factors for valve-related reoperation. After multivariate testing, extra-anatomic position (p = 0.06; HR, 7.2; 95% CI, 0.94 to 54.9) and the use of an aortic allograft (p = 0.006; HR, 3.3; 95% CI, 1.4 to 7.8) turned out to be the most important risk factors for reoperation.
Besides the 24 valve-related reoperations, 5 more valve-related events were noted. The 2 valve-related deaths are described above. Two patients required balloon dilatation for allograft stenosis. The remaining valve-related event occurred in a patient who suffered from endocarditis 5 months after successful reoperation for a stenotic left pulmonary artery and recurrent ventricular septal defect. This endocarditis was successfully treated medically. Valve thrombosis, embolism, and bleeding events were not observed during follow-up.
Ninety percent (95% CI, 85% to 94%) of the patients were free from any valve-related event 5 years after implantation. After 8 years this percentage was reduced to 84% (95% CI, 77% to 91%). Event-free survival (81%; 95% CI, 76 to 87%, at 5 years and 76%; 95% CI, 69% to 83%, at 8 years after operation) is displayed in Figure 2. Univariate analysis showed that young age at operation (< 4 years; p = 0.02; HR, 2.4; 95% CI, 1.2 to 5.1), younger donor age (< 30 years; p = 0.01; HR, 3.3; 95% CI, 1.3 to 8.4), extra-anatomic position of the allograft (p = 0.01; HR, 11.8; 95% CI, 1.6 to 87.4), small diameter (< 23 mm; p = 0.004; HR, 3.6; 95% CI, 1.5 to 8.5), and an aortic allograft (p = 0.005; HR, 2.9; 95% CI, 1.4 to 6.1) were potential risk factors for the occurrence of valve-related events after implantation of the allograft. All potential risk factors for the occurrence of valve-related events were positively correlated (Pearson’s R 0.32; p < 0.01). In particular patient age at operation was highly correlated with type of allograft used, donor age, and allograft diameter (Pearson’s R 0.50; p < 0.01). Extra-anatomic position (p = 0.03; HR, 9.7; 95% CI, 1.3 to 72.6) and aortic allograft (p = 0.02; HR, 2.4; 95% CI, 1.1 to 5.1) were the most important independent risk factors found (Table 3).
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The early mortality was 2 (2.6%), and late mortality concerned another 10 patients. Eleven reoperations had to be performed. Thirteen valve-related events were noted (1 death, 12 reoperations). Eight-year survival in this group was 84% (95% CI, 75% to 92%). Freedom from reoperation at 8 years was 75% (95% CI, 60% to 90%). Freedom from valve-related events was 73% (95% CI, 58% to 88%) at 8 years. Univariate analysis did not reveal any risk factors for death, but the use of an aortic allograft tended to be associated with valve-related reoperation (p = 0.08; HR, 6.5; 95% CI, 0.8 to 50.8) and valve-related events (p = 0.09; HR, 3.7; 95% CI, 0.8 to 16.6).
In addition, patients aged younger than 1 year at the time of operation were studied (n = 39). The main diagnostic groups were common arterial trunk (n = 21, 54%) and pulmonary atresia with ventricular septal defect (n = 4, 10%). Mean allograft diameter was 15 ± 2.4 mm; range, 10 to 19 mm) and mean donor age was 8 ± 7 years; range, 0 to 33 years). The early mortality was 2 (5.1%), and late mortality concerned another 6 patients. Eight reoperations had to be performed. Nine valve-related events were noted (1 death, 8 reoperations). Eight-year survival in this group was 75% (95% CI, 61% to 89%). Freedom from reoperation at 8 years was 67% (95% CI, 46% to 88%). Freedom from valve-related events was 65% (95% CI, 44% to 86%) at 8 years. Univariate analysis did not reveal any risk factors for death, valve-related reoperation, or valve-related events.
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Comment |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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Risk factors for allograft failure
Known independent risk factors for allograft failure are the use of aortic allografts and extra-anatomic position of the allograft [4, 6–9]. These factors were confirmed by multivariate analysis in our study. In the RVOT, the pulmonary allograft is preferred above the aortic allograft because apparently the aortic allograft in pulmonary position is more prone to degeneration. Albert and associates [7] found a freedom from valve replacement and valve-related death in patients with an aortic allograft of 76% after 5 years compared with a 94% freedom from valve replacement or valve-related death in patients with a pulmonary allograft. Bando and colleagues [8] reported 70% freedom from allograft failure in aortic allografts to 94% in pulmonary allografts after 5 years. A lower content of elastic tissue and a lower amount of total calcium in the wall of the pulmonary allograft in comparison to the aortic allograft are argued to play a role in this difference [14].
Multivariate analysis revealed that allografts implanted in extra-anatomic position were more likely to fail than an allograft used in a pulmonary autograft procedure, where the allograft is implanted in anatomic position in an anatomically normal heart. Extra-anatomic position has been recognized as a risk factor for allograft dysfunction by other authors as well [4, 6, 9].
Age at operation is said to be another important determinant of allograft survival [3, 6, 9, 13]. This is, however, not supported by the multivariate risk factor analysis in our present study. Allografts implanted at younger age tend to be more prone to degeneration than those implanted in older patients. More complex disease process and usage of allografts with small diameter from younger donors in this group are possible explanations for the difference in allograft failure between patients operated on at younger (< 4 years) and older ages. The strong correlation that was found between patient age at operation and the other potential risk factors in the multivariate model supports this hypothesis. The subanalysis of young patient age at operation also illustrates the relationship between the following risk factors: young patient age at operation, young donor age, and small allograft diameter. Patients operated on at a young age in general receive an allograft with a small diameter. The heart will outgrow the allograft after a few years, resulting in the need for reoperation. To prevent this some authors advise using an allograft with a relatively larger diameter [15]. However, implanting too large an allograft entails a risk for compression or kinking of the allograft.
A final explanation for limited allograft survival, especially in younger patients, may be accelerated immune-mediated deterioration of the allograft. Recently both Vogt and coworkers [16] and Rajani and associates [17] found histologic evidence for immune-related structural damage of pulmonary allografts. Inasmuch as allograft implantation is performed without blood type ABO antigens or HLA matching, a specific immunologic response of the valve recipient directed against donor antigens could be expected. In an in vitro study, Hoekstra and colleagues [18] have demonstrated that HLA class II (DR) discrepancy of human valve tissue could activate immune-competent cells. The same group found an increase of antidonor HLA antibodies and destructive cytotoxic T lymphocytes in the peripheral blood of allograft recipients. Additionally, animal studies have clearly outlined the ability of this specific immune response to damage the freshly implanted allograft [19]. However, the clinical relevance of such donor-specific immune activation still remains uncertain. In the present study, blood type ABO antigen mismatch was not a significant risk factor for allograft failure, which is in accordance with the results from other studies [5, 6]. Nevertheless, a recent retrospective study suggests that the formation of circulating antidonor HLA antibodies is associated with a decrease of the long-term "homovital" aortic valve allograft performance [20]. Unfortunately, in our series the HLA typing of pulmonary allograft recipients was not available; therefore the results of HLA (mis)match could not be analyzed during this study.
Conclusions
In summary RVOT reconstruction with allografts still is confirmed as a good surgical solution, although progressive allograft failure is noted and careful monitoring of patients is warranted. Further research should reveal a possible general pattern of allograft degeneration, the clinical importance of immunologic findings, and the best timing for reoperation. The use of aortic allografts is associated with graft dysfunction and should only be used in case of a shortage of pulmonary allografts. Our study failed to reveal young donor age and smaller allograft diameter as independent risk factors for accelerated allograft degeneration in younger patients. Nevertheless we advise the use of relatively large allografts in younger patients to postpone reoperation as long as possible.
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Acknowledgments |
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