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Ann Thorac Surg 2003;75:399-411
© 2003 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, Rochester, MN, USA
b Division of Cardiovascular Diseases, Rochester, MN, USA
c Division of Pediatric Cardiology Rochester, Rochester, MN, USA
d Division of Biostatistics, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA
Accepted for publication September 27, 2002.
* Address reprint requests to Dr Dearani, Mayo Clinic, 200 First St, SW, Rochester, MN 55905, USA
e-mail: jdearani{at}mayo.edu
Presented at the Thirty-eighth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 28–30, 2002.
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Abstract |
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 Top Abstract IntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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METHODS: Between April 1964 and January 2001, 1270 patients underwent operation with conduit placement from the PV to PA. The present study evaluates late outcome of 1095 patients (612 males, 483 females) having an operation before July 1992. Mean age was 9.6 ± 8.2 years old. Diagnoses included pulmonary atresia/tetralogy of Fallot (459), transposition of the great arteries (TGA) (232), truncus arteriosus (193), double outlet right ventricle (DORV) (121), corrected TGA (49), septated univentricular heart (36), and other (5). A porcine-valved Dacron conduit was used in 730, homograft in 239, and non-valved conduit in 126.
RESULTS: Early mortality decreased from 23.5% prior to 1980 to 3.7% for the most recent decade. Mean follow-up was 10.9 years (maximum, 29 years). Actuarial survival for early survivors at 10 and 20 years was 77.0% ± 1.5% and 59.5% ± 2.6%. On univariate analysis, clinical and hemodynamic factors associated with late mortality were male gender, older age at operation, higher post-repair PV/systemic ventricle (SV) pressure ratio, higher distal PA pressure, and longer bypass time (p 
0.01 for all). On multivariate analysis, independent risk factors for late mortality were male gender, older age at operation, diagnosis of TGA, corrected TGA, truncus, or univentricular heart, and PV/SV pressure ratio 
0.72 (p 0.03 for all). Freedom from reoperation for conduit failure at 10 and 20 years was 55.5% ± 2.0% and 31.9% ± 2.7%. On multivariate analysis, independent risk factors for conduit failure were homograft conduit, diagnosis of TGA, younger age at operation, and smaller conduit size (p 0.007 for all). Reoperation for one conduit replacement was performed in 306 patients, two conduit replacements in 55 patients, three in 6 patients, and four in 3 patients. Overall early mortality for conduit replacement in this series was 4.9%; it was 1.7% for patients operated on from 1989 through 1992. At follow-up, 84% of survivors were in NYHA class I or II.
CONCLUSIONS: Operations that include conduit placement and replacement can be performed with low early mortality. Younger age at operation was associated with improved late survival. The diagnosis of TGA was associated with increased risk for conduit failure, and the durability of the homograft, in this series, was inferior to the porcine-valved Dacron conduit. Quality of life was excellent for most patients despite the need for reoperation.
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Throughout this article the term "pulmonary ventricle" will be used, rather than "right ventricle," because some patients had situs inversus totalis in which the ventricles were reversed with regard to right-left relationship, and others had corrected transposition in which the pulmonary ventricle was the morphologically left ventricle.
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Of the 1095 patients, 612 were male (55.9%) and 483 were female (44.1%). Age at the time of primary operation with conduit placement ranged from 1 day to 54 years old (mean 9.6 ± 8.2 years; median 8 years old) (Table 1).
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There were a total of 446 reoperations for conduit failure in 370 patients. Reoperation for one conduit replacement was performed in 306 patients, two conduit replacements in 55 patients, three in 6 patients, and four in 3 patients. Indications for conduit replacement in patients with a valved conduit included symptomatic patients with a peak systolic gradient of greater than 40–50 mm Hg, or reoperation for another reason in addition to a senescent bioprosthesis. Indications for conduit replacement in asymptomatic patients were pulmonary ventricular pressure approaching systemic pressure, the appearance or progression of arrhythmias, the appearance or progression of pulmonary ventricular size and dysfunction, the progression of pulmonary atrioventricular (tricuspid) valve regurgitation, and deterioration in exercise test performance. For patients with nonvalved conduits without obstruction, the indications for conduit replacement for symptomatic and asymptomatic patients were the same, except for exclusion of the PV pressure and the PV-PA gradient criteria.
The surgical technique for conduit placement at the primary operation has been described and illustrated previously [3, 4].
Since the ideal extracardiac conduit has yet to be developed and repeated operations remain inevitable, our operation of choice for malfunctioning PV-PA conduits has evolved into an autologous tissue reconstruction in which a pericardial roof is placed over the fibrous bed of the explanted conduit [5, 6]. The technique of reoperation is described below.
Transesophageal echocardiography is used routinely. Repeat sternotomy is done with special care because the conduit and valve ring or calcified homograft often can be adherent to the sternum or can be eroded into it. Central cannulation is preferred whenever possible, but femoral artery and vein cannulation may be required to establish cardiopulmonary bypass before or during resternotomy. After resternotomy, sufficient dissection is performed to allow central cannulation. The conduit is identified but not dissected free. When feasible, direct pressure measurements in the cardiac chambers, conduit, and distal pulmonary arteries are obtained. We prefer aortic and right atrial cannulation with mild to moderate hypothermia without aortic occlusion in the absence of atrial or ventricular septal defects. Bicaval cannulation is performed when additional intracardiac repair is required. Aortic occlusion is used for additional procedures that would require cardioplegic arrest (e.g., repair of atrial septal defect, VSD, aortic valve replacement, etc.).
After cardiopulmonary bypass is established, a longitudinal incision is made over the anterior aspect of the obstructed conduit. The conduit is dissected free from the external fibrous peel and excised (Fig 1A). The sides and the floor of the conduit bed are preserved. Calcified homografts are managed by an endarterectomy technique that leaves the adventitia of the homograft and adjacent fibrous tissue as the floor of the new reconstruction. The right and left pulmonary arteries are measured with probes and distal suture-line stenoses are relieved. The pulmonary ventricular outflow tract is examined and any fibromuscular outlet obstruction is resected. Concomitant intracardiac procedures are then performed.
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Glutaraldehyde-preserved bovine pericardium is utilized for construction of the roof of the new conduit. The distal suture line and the shape of the patch are altered as necessary to provide relief of any proximal right or left pulmonary artery stenoses. The suture line is restricted to the fibrous peel at the edge of the conduit bed to avoid injury to adjacent, obscured coronary arteries. Insertion of a bioprosthetic valve is routine. We prefer to use the largest possible stented porcine heterograft prosthesis (usually 29 or 31 mm in the adult). The valve is generally positioned to minimize compression by the sternum; in patients with TGA, truncus, and corrected TGA, this is usually close to the distal anastomosis (Fig 1B). In some patients, such as those with pulmonary atresia and tetralogy of Fallot, the prosthesis can often be placed at the native valvar level or just proximal to the level of the pulmonary annulus in the pulmonary ventricular outflow tract (Fig 1C). The valve is usually secured with mattress sutures that are buttressed with felt pledgets posteriorly and laterally in the conduit bed. Anteriorly, the sewing ring is attached to the pericardial roof with continuous monofilament suture. The reconstruction is completed by sewing the proximal pericardial patch to the pulmonary ventricular outflow tract.
After rewarming and discontinuation of cardiopulmonary bypass, pressures are routinely measured in the pulmonary ventricle and distal pulmonary artery. Assessment by intraoperative transesophageal echocardiography is performed. Occasionally, resection of overlying sternal bone and costal cartilage is required to prevent compression of the reconstruction at the time of sternal closure.
The follow-up status of patients was determined by review of the patient records, and by written questionnaires to the patient or families and, when needed, to the local physicians. Telephone interviews were conducted with patients who did not respond to the written questionnaire. Data requested included functional status, the occurrence of cardiovascular events, and any reoperation or hospitalization. If the patient had died, the death certificate and/or medical records of the hospital and physician were reviewed.
Early mortality was defined as death occurring within 30 days of operation or at any time during the operative hospitalization. The probability of survival was estimated by the Kaplan-Meier method. Survival curves of the patients were compared with the expected curves of persons of the same age and sex, as derived from vital statistics for the West North Central region of the United States. The statistical significance of observed versus expected survival and freedom from reoperation were assessed with a one-sample log-rank test. The associations of continuous variables with survival and freedom from reoperation, and the associations of combinations of variables with survival and freedom from reoperation were evaluated with Cox proportional hazards models. Variables found to be significant (p < 0.05) or that approached significance (p < 0.15) according to univariate analysis were then evaluated multivariately with Cox models.
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Results |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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The mean follow-up for the 867 early survivors was 10.9 years with a maximum of 29 years. There were 246 known late deaths ranging from 34 days to 24 years (mean, 6.4 ± 5.6 years) after the initial operation. The causes of late death are illustrated in Table 8. Overall survival, excluding early mortality, was 85.2% ± 1.2%, 77.0% ± 1.5%, 69.4% ± 1.8%, and 59.5% ± 2.6% at 5, 10, 15, and 20 years, respectively (Fig 2). Univariate analyses of discrete and continuous variables are depicted in Tables 9 and 10, respectively. Multivariate analysis of factors affecting late mortality is illustrated in Table 11. Male gender, older age at operation, a diagnosis other than pulmonary atresia/tetralogy of Fallot or DORV, and patients with a PV/SV pressure ratio of 0.72 or greater were at higher risk for late mortality. The PV/SV pressure ratio was the only significant risk factor of the continuous variables with univariate analysis of late mortality that was entered into the multivariate model. This measurement was available in the majority of patients, and it takes into account the other continuous variables found to be significant with univariate analysis.
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Overall survivorship free of reoperation for conduit failure for the initial PV-PA conduit implanted is illustrated in Figure 5. Survivorship free of reoperation for conduit failure was 84.1% ± 1.4%, 55.5% ± 2.0%, 39.6% ± 2.2%, and 31.9% ± 2.7% at 5, 10, 15, and 20 years, respectively.
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0.007 for all). Survivorship free of reoperation for conduit failure for the initial PV-PA conduit, stratified according to the diagnostic categories, is illustrated in Figure 6.
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Comment |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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The primary late problem related to extracardiac conduit operations is the need for conduit replacement because of patient somatic growth or progressive deterioration and calcification of the conduit. Our early experience and that of others with irradiated homografts was disappointing because of calcification and degeneration resulting in both stenosis and regurgitation, often within the first year following implantation [7, 8].
The Hancock glutaraldehyde-preserved porcine-valved Dacron conduit, which became available in 1972, had the advantage of ready availability in many sizes and it was longer and more versatile, especially for dealing with concomitant pulmonary artery abnormalities. The porcine valve within the Dacron tube became calcified, but usually over a longer period of time compared with irradiated homografts. In addition to valvar degeneration, the Hancock conduit developed obstructive intimal fibrocalcific peels in the graft portion of the conduit [25, 26], a phenomenon not seen with homografts. In explanted Hancock conduits, significant obstruction occurred at the valvar level in approximately one-third, within the graft (intimal peel) in one-third, and in both the valve and graft in one-third [25]. In our experience, more recently available Dacron conduits with porcine or pericardial valves (e.g., Tascon, Carpentier-Edwards, and Ionescu-Shiley conduits) have not revealed any long-term advantages compared with the Hancock conduit.
The introduction of cryopreserved homografts in the 1980s led to a resurgence of interest in using homografts for procedures that required an extracardiac conduit. Intermediate-term follow-up of our series of cryopreserved aortic (n = 230) and pulmonary (n = 118) homografts demonstrated a freedom from reoperation for aortic homograft failure of 70% at 5 years, which was not significantly different from the freedom from reoperation of 72% at 5 years for the irradiated homograft series [10]. Pulmonary homografts appear to be more durable than aortic homografts, especially with respect to calcification and when used in young children and in the absence of pulmonary hypertension [10, 15, 17].
In the current study, there was little difference in durability between irradiated and cryopreserved homografts 8 years after operation, and both were inferior to the Hancock conduit (Fig 7). This observation appears to be in contrast to the reports of Clark and Bishop [24] and others [15] that cryopreserved homografts are superior to other types of conduits. These differences are likely due to multiple factors. The majority of homografts used in our series were aortic, whereas the majority in Clarke and Bishop’s series were pulmonary [24]. We have also noted that cryopreserved aortic homografts calcify more quickly and fail from stenosis more rapidly than pulmonary homografts [10]. However, pulmonary homografts fail more rapidly from regurgitation, especially when pulmonary artery pressures are elevated, and in addition, there is a small but distinct incidence of anastomotic dehiscence [10]. The technique of conduit implantation differed between our study and theirs. Nearly all patients in our series had the conduit placed in an extra-anatomic position (i.e., nonorthotopic), whereas 50% of the conduits in their series had the conduit placed in a partial or complete orthotopic position (i.e., as in the Ross procedure). Because most of our patients had the conduit placed in an extra-anatomic position, the proximal anastomosis of the homograft required a hood to facilitate its connection to the ventriculotomy. In the early part of our series, the hood was constructed with either Dacron or pericardium. Subsequent experience has demonstrated that Dacron hoods also contribute to late obstruction. Currently, when a homografts is utilized, the hood is constructed with autologous or bovine pericardium. Finally, in our series, there were multiple diagnoses that required a PV-PA conduit. When conduit durability was analyzed with regard to diagnosis, the best results were obtained in the tetralogy of Fallot/pulmonary atresia group, and the worst results were noted for other diagnostic groups, especially for the TGA group. In contrast, the majority of patients in Clarke and Bishop’s series had the diagnosis of tetralogy of Fallot. All of these factors may explain the better durability of the cryopreserved homograft conduit noted in their series.
There were 126 patients in this study who received a nonvalved conduit (Table 5). Almost all were a Dacron tube graft (n = 111). It is difficult to draw definitive conclusions in this subset of patients because of the careful patient selection that was made for those who received a nonvalved conduit. These conduits were utilized selectively at the time of complete repair in the absence of pulmonary hypertension, hypoplastic pulmonary arteries, or significant pulmonary ventricular dysfunction; analysis of some of these patients has been published previously [27]. Some of the nonvalved conduits were utilized for staged palliation in patients with pulmonary atresia and VSD. Overall, freedom from reoperation for conduit failure was no different for nonvalved conduits than for valved conduits in this series. It is our current practice to place a pulmonary valve in PV-PA conduits to avoid the long-term deleterious sequelae of pulmonary regurgitation on the pulmonary ventricle.
Over the last three decades, we have used many different types of conduits in an attempt to reduce the incidence of late conduit failure. Because of continued disappointment with the durability of all of these conduits, when replacement of a failed conduit was necessary, we began to construct autologous tissue conduits, with or without a valve [5, 6], in order to avoid a prosthetic conduit completely. The woven Dacron conduit provides the best conduit peel and is the one that is easiest to reconstruct. However, this technique may be used after explantation of other types of conduits, including homografts. In the latter case, the posterior wall of the homograft can be retained and calcification in the lateral edges endarterectomized as needed to allow suture placement. We continue to prefer this autologous tissue reconstruction technique, which has given encouraging results in a median follow-up of 7.5 years [6]. Although it is not always technically feasible to reconstruct a new conduit using the external peel of the explanted conduit, we have been able to perform this reconstruction in more than 100 patients with various cardiac anomalies from May 1983 to July 2001. A detailed analysis of this group of patients will be reported separately, but preliminary results demonstrate a far better freedom from reoperation compared with studies of patients conventional conduits [3]. We attribute the durability of this type of conduit to the large size of the pulmonary bioprosthesis that can be placed and the lack of intimal peel formation.
There is general agreement that most congenital cardiac anomalies should be repaired during the neonatal period or within the first year of life. Although this is appropriate for some anomalies that would require a conduit (e.g., truncus), other more complex anomalies (e.g., TGA-PS-VSD) requiring a conduit may be better managed with initial palliation with a shunt and subsequent correction after the first 2 to 3 years of life. Indeed, the ideal age for complete repair of an anomaly like TGA-PS-VSD is still controversial. Disadvantages of early repair include difficulty in both satisfactory intracardiac baffle construction and in dealing with tricuspid valve anomalies [4]. Additionally, conduit deterioration is more rapid in younger children. However, palliation as provided by a Blalock-Taussig shunt does moderately increase ventricular volume load and does not completely correct arterial desaturation, factors that can, if present long-term, have deleterious effects on myocardial function. Consideration of all of these factors is essential when planning corrective or palliative operations, especially when an extracardiac conduit is required.
Our approach to an infant who is undergoing a corrective operation with a conduit is to use a homograft (preferably pulmonary if pulmonary hypertension is not present) to establish PV-PA continuity. The handling characteristics of the homograft are favorable and facilitate reconstruction in an infant or small child. The use of the Hancock conduit in the infant has been problematic because of the rigid ring at the valve level; this is more likely to cause coronary artery compression with sternal closure. In general, we choose the conduit size based on a table of patient age and height [9], and are careful not to oversize the conduit in infants. Although the durability of the homograft has been disappointing in our experience, we still feel it is the conduit of choice for initial cardiac repair in the infant and small child. The valved bovine jugular venous conduit is new and is currently being evaluated [28]. It is also soft, pliable, and available in many sizes. If late results are satisfactory, the favorable handling characteristics of this conduit should make it a good alternative to the homograft.
After the first 2 to 3 years of life, we now prefer to use the porcine-valved conduit for PV-PA reconstruction based on results from the current study. Despite the eventual development of conduit obstruction (valvar and intimal peel), this conduit was consistently more durable than the homograft (irradiated or cryopreserved) in this series, even after adjusting for age at operation and size of the conduit.
It cannot be ignored that most of the late deaths in this series were cardiac-related. The majority of these were either sudden and presumed to be due to arrhythmia, or from congestive heart failure (Table 8). We believe that it is reasonable to assume that many of these deaths may have been conduit-related, as autopsy reports available on some patients often demonstrated hypertrophied or dilated right ventricles with significantly obstructed conduits. Our indications for conduit replacement have evolved over the last three decades. The challenge has been when to advise reoperation in the asymptomatic patient. We believe that strong consideration be given to conduit replacement in asymptomatic patients when the pulmonary ventricular pressure is approaching systemic pressure. Conduit replacement is clearly indicated when there is the appearance or progression of arrhythmias (atrial or ventricular), progression of pulmonary ventricular dysfunction, progression of tricuspid regurgitation, or deterioration of exercise performance. The importance of continued follow-up for all patients on a regular basis cannot be overemphasized so that the timing of reoperation is optimized.
The cause of death in the large number of patients who died from heart failure is likely multifactorial. Some may be due to conduit dysfunction and delayed conduit replacement. Others may be due to the many patients that were at an older age at the time of initial repair. Older age was identified as a risk factor for late mortality in this study. Palliated patients with systemic-PA shunts were likely exposed to increased volume loading of the systemic ventricle. This may have contributed to the development of ventricular dysfunction and predisposed them to later development of congestive heart failure even after complete repair was performed. In the current era, complete repair of anomalies requiring an extracardiac conduit are performed either during infancy (e.g., truncus, complex tetralogy of Fallot) or within the first few years of life (usually prior to 5 years old) for more complex anomalies (e.g., TGA-VSD-PS). We anticipate that the number of late deaths due to arrhythmia and heart failure will be reduced if these factors are recognized and considered when planning the primary corrective operation and reoperation for conduit failure.
The search continues for the ideal extracardiac conduit. Despite the limitations of conduits, they have allowed the vast majority of patients to survive repair of complex congenital cardiac defects. Although the need for reoperation is inevitable, the risk of reoperation is low and the majority of patients enjoy good quality of life.
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Discussion |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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It is, however, perplexing to me that the homografts implanted in this series performed so poorly relative to the porcine valved conduits. The reasons for this are not entirely clear. At the University of Colorado, we have experienced a similar evolution in the management of these patients, but analysis of our results of these operations performed over the same time period produced quite different results.
Actuarial valved conduit survival curves representing our experience illustrate that porcine conduits performed significantly worse than cryopreserved homografts. Only 10% of the porcine compared to 50% of the homografts remained free of reoperation for replacement at 15 years. How can we account for this striking difference in results?
There are some contrasting features of the two series that could account for this discrepancy. In our series, the majority of the porcine conduits placed were Carpentier-Edwards, not Hancock, and the homografts were all cryopreserved, and 90% were pulmonary not aortic tissue. Although I am not aware of any studies which have demonstrated a difference in performance of different porcine conduits, pulmonary homografts have previously been shown to fare better in this anatomic position.
Another possible explanation may relate to anatomy and implantation techniques. TGA, truncus, and pulmonary atresia require that proximal connection be made to the surface of the ventricle. Some have used a tubular extension for this connection. I would like to ask whether this was used in this series.
Tetralogy variants allow a partial anatomic placement, as you can see in the middle panel, and with a Ross procedure, illustrated in the far right-hand panel, a normal anatomic positioning is achieved nearly 100% of the time. In your series it appeared that approximately 80% of patients required the extreme extra-anatomic placement that is illustrated here on the far right, and in our series, however, this accounted for only about 50% of the population. Could you please comment on these or other explanations for the contrasting results that we have seen?
Finally, could you comment on the surprising durability of the stented porcine valve used in your reoperations for conduit failure? It is truly remarkable that none of these have required reoperation over the last 20 years.
Once again, congratulations for an excellent study and presentation, and I would like to thank the Society for the privilege of discussing it.
DR JOHN W. BROWN (Indianapolis, IN): This is a very nice study, Dr. Dearani and your colleagues are to be commended. Your conduit replacement of choice is a strut-mounted tissue valve roofed over by pericardium, but you didn’t tell us how many of these re-dos you have done. I would be interested in your follow-up on this group of patients. We have also used this technique in older patients and found it satisfactory, but our follow-up is only 2 or 3 years.
We have not wanted to put a second pulmonary homograft in any patients because of the reported concern that the second pulmonary homograft will have a shorter durability than the first one due to the patients antigenic response. What we have done in about 50 or 60 re-do homograft patients, is to split the pulmonary homograft lengthwise, add a Gore-Tex monocusp to the inside, and then roof over the new enlarged conduit with either pericardium of Gore-Tex. This technique has worked out well with follow-up now up to 8 years. This is much less expensive than a strut-mounted tissue valve and using pericardium. So I would like your comments about other techniques for conduit reoperations. Thank you very much.
DR DEARANI: I would like to thank the discussants for all of their comments and questions. Dr. Clarke has noted superior durability of the homograft over the porcine-valved conduit in his experience, which is in contrast to the results that we have presented today. I believe there may be multiple reasons why this may be the case and Dr. Clarke has already pointed out some of these differences. The most common porcine-valved conduit in our series was the Hancock conduit and the most common in his series was the Carpentier-Edwards conduit. To our knowledge, there are no data to suggest one is better than the other. In addition, 90% of the homografts in his series were cryopreserved, whereas in our series, approximately 50% were cryopreserved. However, our data show that cryopreserved homografts follow the same poor freedom-from-reoperation curve as the early irradiated homografts. In the University of Colorado series, the majority of homografts were pulmonary, whereas in our series, most were aortic homografts. It is true in our experience as well that cryopreserved aortic homografts calcify more quickly and fail from stenosis more rapidly than pulmonary homografts. However, pulmonary homografts fail more rapidly from pulmonary regurgitation, especially when pulmonary artery pressures are elevated.
We think there are multiple reasons for the good durability of the Hancock conduit noted in this series. First, the average age of the children in this series was 8 years of age. This is significantly different from the age most conduit operations are performed currently. The majority of corrective operations requiring conduits are performed in the first few months or years of life. Our current practice is to use pulmonary homografts for children who undergo their primary operation up until three or four years of age. After 3 to 4 years of age, if their primary operation is going to involve a conduit, we now would use the Hancock conduit given the favorable results noted in this study. We recognize that the good results with the Hancock conduit are also partly related to the relatively large size of the Hancock conduits utilized (mean 22 mm). It is important to note though that analysis of our data indicated that homografts were at significantly higher risk (p = 0.001) for conduit failure even after adjusting for age at operation and size of the conduit. Because of handling characteristics and anatomical space constraints, we do not favor the use of the Hancock conduit in the infant or small child within the first few years of life.
Additional differences between the University of Colorado series and our series include the anatomy and implantation technique. All of the patients in our series had the conduit placed in an "extra-anatomic" position (i.e., nonorthotopic), whereas 50% of the conduits in the University of Colorado series had the conduit placed in the partial or complete orthotopic position. Dr. Clarke has asked about the proximal connection of the conduit to the ventriculotomy. Early on, the proximal hoods were constructed with pericardium, Dacron or Hemashield. We have since learned that the Dacron and Hemashield hoods also can contribute to significant obstruction. Currently, when a hood is required we prefer autologous or bovine pericardium.
In our series, when durability of the conduit was analyzed with regard to diagnosis, the best results were obtained for the group of patients with tetralogy of Fallot and pulmonary atresia, whereas the worst results were noted in the transposition group. Many of the conduits in the University of Colorado experience had the diagnosis of tetralogy of Fallot. This may also explain the lower risk of reoperation noted in their series.
Dr. Brown asked questions about the peel technique for conduit replacement. We began using the peel technique in 1985. Our technique utilizes a large porcine bioprosthesis placed in the conduit bed, which is then roofed over with bovine pericardium. To date, we have done over 100 of these procedures and are looking at the late follow-up. To the best of our knowledge, there have been no repeat operations for bioprosthetic valve failure or pathway obstruction to date. We believe the excellent durability is due to the large size of the bioprosthesis inserted (27, 29, or 31 mm in the adult) and the lack of intimal peel formation (no prosthetic graft material). In addition, the peel technique as we have described it is also applicable to previously-placed homografts. The posterior wall of the calcified homograft is maintained intact and its lateral edges are endarterectomized to allow suture placement for the pericardial roof. While we have selectively used the Gore-Tex monocusp technique of right ventricular outflow tract reconstruction in primary operations for tetralogy of Fallot, we have not used this technique at reoperation for conduit failure given the lack of data demonstrating long-term durability of monocusp valves.
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