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Ann Thorac Surg 2001;71:482-488
© 2001 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center, and The Children’s Hospital, Denver, Colorado, USA
Address reprint requests to Dr Clarke, The Children’s Hospital, Cardiothoracic Surgery, B200, 1056 19th Ave, Denver, CO 80218
e-mail: clarke.david{at}tchden.org
Presented at the The Forty-sixth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, Puerto Rico, November 4–6, 1999.
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Abstract |
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Methods. From February 1985 through March 1999, 223 children (age 5 days to 16.9 years) underwent primary RVOT reconstruction with an aortic or pulmonary homograft. Of these, 35 patients underwent homograft explant at the implanting hospital with insertion of a second homograft from 2 months to 13.3 years after the first implantation. The primary operation and reoperation patient groups were compared with regard to incidence of early death, late death, homograft-related intervention without explant, and homograft explant.
Results. Actuarial survival and event-free curves for initial and replacement homografts were not significantly different. Univariable analysis was performed for the following risk factors: weight (p < 0.0001), age (p < 0.003), homograft diameter (p < 0.0001), homograft type (p < 0.01), surgery date (not significant [NS]), gender (NS), Blood Group match (NS), and type of distal anastomosis (NS). Multivariable analysis of significant univariable risks revealed small homograft diameter to be a significant risk factor (p < 0.001) for replacement.
Conclusions. The RVOT homografts eventually require replacement. Patient and homograft survival for replacement homografts is similar to primary homografts. Reoperative homograft RVOT reconstruction is possible, with reasonably low morbidity and mortality.
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Introduction |
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Cryopreserved homografts became the conduit of choice for right ventricular outflow tract (RVOT) reconstruction in the middle 1980s. Cryopreservation solved the storage and availability problems that plagued the early use of homografts. Indeed, cryopreserved aortic and pulmonary homografts have been shown to have superior event-free survival in the RV to PA position when compared with porcine valve conduits [3]. Homograft benefits include excellent hemodynamics, resistance to infection, lack of need for anticoagulation, ease of handling, option of using pulmonary artery branches, and decreased thromboembolic events.
Despite the ongoing controversy concerning the viability of homografts, it is generally accepted that they do not grow [4]. The lack of growth of the homograft combined with its structural degeneration presents a problem for young recipients. Many homografts are placed in neonates and infants, with the knowledge that reoperation will be required. The results of RV to PA homograft replacement in pediatric patients are largely unknown.
We present our 14-year experience with repair of the RVOT using aortic or pulmonary valve homografts in children. Specifically, we examine our results with reoperative replacement of RV to PA homograft conduits in the pediatric population.
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Material and methods |
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Homografts
The implanted homografts were sterile, cryopreserved aortic and pulmonary valve conduits processed by CryoLife, Inc (Kennesaw, GA). Unicuspid homografts and nonvalve homografts were excluded from this study. Homografts were thawed per protocol as developed by CryoLife, Inc. The internal diameter of the primary homografts ranged from 9 mm to 26 mm (mean diameter 19 mm). Size range of the replacement homografts was 15 mm to 27 mm (mean diameter 22 mm) internal diameter. At the time of both primary and reoperative procedures ABO blood type matching was attempted, but was not always possible because of limited homograft availability.
Surgical technique
The surgical technique for both primary and reoperative procedures has been described previously [5]. Use of pulmonary homografts was favored over aortic unless pulmonary hypertension was present or a longer conduit was needed to complete the distal anastomosis. The appropriate homograft size was determined by standardized CryoLife, Inc. charts, based on gender and body surface area. The larger end of the normal size range was favored in an attempt to use the largest homograft technically possible. All patients were placed on cardiopulmonary bypass with or without deep hypothermic circulatory arrest. During homograft replacement procedures, all calcified tissue was removed. Distal anastomoses were performed using a running 5-0 or 6-0 Prolene suture (Ethicon, Somerville, NJ). One of three variations of the distal anastomosis were performed: (1) to the main PA; (2)separately to right and left pulmonary arteries; or (3) as a flap extension onto the left or right PA (Table 2). Proximal anastomoses from the homograft to the RV were sewn with 5-0 polytetrafluoroethylene suture. A gusset of pericardium or polytetrafluoroethylene was used to patch remaining anterior defects in the RVOT. Proximal anastomoses were performed with the cross-clamp off. No circumferential extensions were incorporated into the distal homograft to PA connection.
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Statistical methods
Events used for analysis of homograft survival were hospital death, late valve-related death, homograft explant, and homograft-related surgical or balloon intervention without replacement. Actuarial survival and event-free curves were generated using the Kaplan-Meier method [6] and were compared using the log-rank test. Confidence limits (CL) of 95% were used to report survival. Univariable and multivariable analysis of risk factors for homograft survival was performed using Cox’s proportional hazards methods [7]. Regression coefficients and risk ratios were also reported. Statistical significance was defined as a p value of less than or equal to 0.05.
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Results |
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Of the 35 patients who underwent replacement of their RV to PA homograft at the UCHSC or TCH, 3 children (9%) died early postoperatively. Original surgical diagnoses were truncus arteriosus in 2 patients and pulmonary atresia with ventricular septal defect in 1 patient. Two patients died of myocardial failure, and one death was due to hemorrhage from the distal homograft suture line. Actuarial survival curves for patients who underwent primary versus reoperative homograft placement are shown in Figure 1.
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Homograft survival
Actuarial event-free curves for primary and replacement homografts are illustrated in Figure 2. For patients receiving initial homografts who survived beyond the first month, the longest surviving homograft was 14 years. A total of 22 patients (11%) suffered late death at 1 month to 10.8 years (mean 11.3 months) after surgery. Eight children (4%) underwent a total of nine surgical or catheter homograft revisions from 3 days to 11.8 years (mean: 1.8 years) postoperatively. Homograft replacement occurred 2 months to 13.7 years (mean: 5.9 years) postoperatively in 38 patients (20%). Freedom from early death, surgical or catheter intervention without homograft replacement, valve-related late death, or homograft explant at 5, 10, and 14 years postoperatively was 71%, 58%, and 25%, respectively.
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Risk factors for homograft replacement
Risk factors for homograft replacement were sought in the 192 patients surviving 1 month after their initial surgery. Factors examined using univariable analysis were patient weight and age at operation, homograft internal diameter, homograft type, surgery date, gender, ABO match, and type of distal anastomosis. Statistically significant risk factors were weight, age (Fig 3), homograft diameter (Fig 4), and homograft type (Fig 5). Surgery date, patient gender, ABO match, and distal anastomosis were not risk factors for homograft replacement (Table 3). When weight, age, homograft diameter, and homograft type were considered in a multivariable analysis, the only significant risk factor for replacement was homograft diameter (Table 3).
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Comment |
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Early mortality was 14% in patients who underwent initial placement of an RV to PA homograft. Early postoperative survival has improved over time. There were 20/101 (20%) early deaths in patients operated on from 1985 through 1989, 7/74 (9%) early deaths from 1990 through 1994, and 4/48 (8%) early deaths in patients operated on from 1995 through 1999. A large percentage (74%) of all early deaths were from cardiac failure; there were no early deaths directly due to homograft failure. This early mortality might reflect the patients’ underlying disease processes. However, as homograft insertion often requires a ventriculotomy that may contribute to postoperative cardiac dysfunction and failure, a causal relationship between death and homograft insertion cannot be excluded.
Cardiac failure was also the main cause of early mortality in the reoperative homograft recipients (6%), although there were only three early deaths. In the reoperative homograft group, there was one death due to hemorrhage from the distal homograft suture line during the postoperative period. There were no deaths due to hemorrhage from operating on a previously entered chest. The low mortality in this reoperative homograft group coincides with other reports that RV to PA homograft replacement is relatively safe [8–10].
For patients who survived beyond the initial operative period, the actuarial survival remains relatively stable (Fig 1). This was observed in patients who underwent primary as well as reoperative homograft implantation. Although the reoperative homograft group exhibits better survival than the primary homograft group, the two curves are not significantly different. Because most of the difference appears to be a result of early mortality, further data will need to be collected. A natural bias might have been introduced in the early mortality of the two groups if higher risk patients died after their initial surgery and never entered the reoperative homograft group.
Complications occurred in 53% of the primary procedures and might be reflective of the underlying complex pathology. The percentage of patients in the reoperative homograft group that had complications was lower than the primary procedure group at 26%. This was despite the fact that these patients underwent reoperative sternotomies. The higher incidence of hemidiaphragm paralysis in the reoperative group, however, could be attributed to difficulties visualizing the phrenic nerve because of scarring and adhesions from the initial surgery.
Although not statistically significant, our actuarial event-free curves for primary and reoperative homografts demonstrated improved survival in the replacement homograft group (Fig 2). This result is different from Stark and colleagues [11], who reported a lower survival for reoperative versus primary homografts. They attributed this lower survival in reoperative homografts to technical factors caused by adhesions and calcification. Perhaps other factors such as immunologic effects could explain lower survival in replacement homografts. One could hypothesize that placement of a second homograft into a patient previously sensitized by a prior homograft could promote failure contributed by immune mechanisms [12–15]; however, this would not explain the differences between the findings of Stark and colleagues and our own reoperative homograft results. Our policy for RV to PA homograft replacement is to remove all calcified tissue and take down all adhesions necessary to accomplish this task. In addition, we usually replace the initial homograft with a larger homograft because of the growth of the child. This might postpone explantation, as smaller homograft diameter was shown in this study to be a risk factor for homograft replacement.
The actuarial event–free survival of primary homografts in the current study appear lower than survival reported by others [11, 16, 17]. Our results, however, include early mortality as an end point in addition to surgical or balloon intervention, valve-related death, and homograft replacement. Inclusion of early mortality in actuarial curves studying the survival of homografts is controversial. Including early death in our event-free curves shifted both the primary and reoperative graphs downward.
Statistically significant univariable risk factors for homograft replacement were low weight, young age, small homograft diameter, and homograft type (aortic). Multivariable analysis of weight, age, diameter, and homograft type demonstrated homograft diameter to be the only risk factor. It seems intuitive that younger patients weigh less and require homografts of smaller diameter, which could lead to outgrowth and eventual replacement [15]. This was especially true for homografts less than or equal to 15 mm [8, 9, 18]. None of the above risk factors were found to be significant by Stark and colleagues [11]; however, their study excluded patients who died in the first 90 days after surgery. These excluded patients might have represented a group of younger age, lower weight children who received smaller diameter homografts, which might have biased the risk factor results of that study.
When risk of replacement was compared between aortic and pulmonary homografts, the aortic homograft was determined to be a risk factor. Differences between aortic and pulmonary homograft failure rates was not found to be statistically significant by Leblanc and colleagues [9] or Yankah and associates [18]. Although there was not a statistical difference in the results reported by Yankah and associates, there was a trend toward earlier replacement of the aortic homografts when compared to pulmonary homografts. The results reported here might be biased against aortic homografts because they were often chosen for use in patients with pulmonary hypertension. In addition, the determination of homograft type as a risk factor might be secondary to the fact that aortic homografts were implanted into significantly younger patients than were pulmonary homografts and therefore significantly smaller aortic homografts were implanted. For primary procedures, mean age (p = 0.0004) and implanted homograft size (p = 0.0003) for aortic versus pulmonary homograft recipients were significantly different by the Wilcoxon rank sum test. Aortic homograft recipients ranged from 5 days to 14.3 years of age (mean age 1.5 years), and pulmonary homograft recipients ranged from 6 days to 16.9 years of age (mean age 3.1 years). Similarly, mean internal diameter of primary aortic homografts was 17 mm (range 10 to 26 mm) and for pulmonary homografts was 19 mm (range 9 to 26 mm).
Glutaraldehyde-preserved porcine valved conduits continue to be used to reconstruct right ventricular outflow in pediatric patients [19, 20]. Porcine valved conduits are a justifiable option in younger patients, who often experience early immunologic reactions to both porcine and homograft valve conduits that result in valve explantation. Early and late homograft failure is much less common in older pediatric recipients and homograft valve conduits are preferred over glutaraldehyde-preserved porcine valves, which are reputed to have a more finite survival [3].
In summary, homografts used in pediatric RVOT reconstruction will usually require explantation, especially homografts of 15 mm or less. Replacement homograft survival is better than (but not statistically significantly different from) primary homograft survival. Reoperative homograft RVOT reconstruction demonstrates good midterm event-free survival and can be accomplished with reasonably low morbidity and mortality.
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Discussion |
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I also appreciated having a chance to review this manuscript before this talk because you have so much information, and I think it will be very valuable to our group of congenital heart surgeons to have an opportunity to look at these data when they finally do (and as I am sure they will) come out in print in the Annals.
I wanted to share very briefly with you a similar experience that we have had at Duke. These are our data compiled by Dr Joe Forbess, in reviewing 186 patients in essentially the same time frame as your patient group who received RV to PA homografts. For all of those patients, the size of the homograft was variable up until about the age of 10 years, and at about 10 years of age the homografts start to plateau in terms of size.
When we looked at the outcome for homografts (and, like you, we also looked at homograft survival rather than patient survival so that each homograft became its own entity) it was clear that homografts in patients older than 10 years fared much better long-term than homografts in patients under 1 year of age. These data are compiled for patients far older than the 36 months of age who constituted your older age group.
We also found, quite interestingly, that when we compared the outcome for aortic versus pulmonary homografts in the RV to PA position, there was fairly similar long-term homograft survival, with need for replacement eventually in both of those categories.
Finally, we looked at about 60 patients who had Ross procedures and it is interesting that the pulmonary homograft in the patients receiving Ross procedures, even though this group includes several patients less than 10 years of age and in fact down to just a few weeks of age, fare much better in these patients than they do in all of the other patients included in the group of congenital anomalies.
I think that our experience, which is similar in size to yours, corroborates some of the information that you had that homograft survival is indeed related to age or weight of the patient or to size of the homograft. Interestingly, we found that there was not really an advantage to pulmonary versus aortic homografts in the RV to PA position for children. As they are going to have to be replaced anyhow, we usually will use whatever seems to be the best fit for the patient. We are intrigued about the outcome for the Ross procedure patients, and I wonder if you can, using the experience that you have generated at Denver children’s, could just answer a few questions for us.
First, are you currently selecting pulmonary versus aortic homografts, since you showed a slide that suggested pulmonary homografts work better? Second, how would you explain, based on your experience, the outcome for homografts in patients receiving Ross procedures, as even in young patients these homografts seem to do quite well? Third, do you see any alternatives coming along in the future for these patients in lieu of cryopreserved homografts? And finally, you just mentioned that you did most of these operations on non-crossclamped patients. I suspect that either these patients had their hearts fibrillating or empty beating at the time. If the hearts were kept empty and beating, did you do that even for patients who had residual cardiac defects?
Once again, I think this was an excellent series and it is a great honor for us to hear it presented here at the Southern Thoracic. Thank you.
DR BIELEFELD: Thank you, Dr Ungerleider. One of the reasons that our series of aortic homografts did worse than our series of pulmonary homografts was because we did show a bias when choosing an aortic versus pulmonary homograft. If we suspected that there was going to be a higher pulmonary blood pressure in the patient, we favored the use of an aortic homograft. We are still collecting data to determine whether pulmonary hypertension is a risk factor for homograft failure.
In regard to our experience with the Ross procedure, we have approximately 25 pediatric patients over a broad range of ages. Homograft survival has been excellent in children who had Ross procedures. We did not examine original diagnosis or type of procedure as a risk factor for homograft survival.
As far as alternatives, we are excited about work being done in conjunction with CryoLife, Inc on decellularized porcine grafts. We hope that the decellularization process will reduce any immune response that might cause degeneration.
Finally, with regard to your question about our technique of placing RV to PA homografts without crossclamping the aorta, this technique was used in most study patients. However, if residual defects were present, the aorta would be crossclamped and the heart arrested with cardioplegia.
Thank you again.
DR CHRISTOPHER J. KNOTT-CRAIG (Oklahoma City, OK): I enjoyed your paper very much and congratulate you. In the light of your findings that patients younger than 6 months have a less advantageous outcome after homograft replacement, have you altered your management of certain patients in whom placement of a homograft can be delayed beyond that age, eg, patients with tetralogy and pulmonary atresia?
DR BIELEFELD: Was your question, Have we considered using alternatives?
DR KNOTT-CRAIG: Do you now manage those patients by placing a shunt first, correcting them by placing a homograft at a later age, hoping that the homograft would not need to be replaced so soon?
DR BIELEFELD: Yes, We actually tend, at our institution, to shunt our younger tetralogy of Fallot patients and then later on, usually around 6 months, take them back to place a homograft.
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