Asian Cardiovasc Thorac Ann 2001;9:187-191
© 2001 Asia Publishing EXchange Pte Ltd
Ventricular Outflow Tract Reconstruction With Polystan Valved Conduit
Kim Yong Jin, MD,
Choi Yong Soo, MD,
Lee Jeong Ryul, MD,
Rho Joon Ryang, MD
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Department of Thoracic and Cardiovascular Surgery Seoul National University Hospital Seoul, Korea
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For reprint information contact: Kim Yong Jin, MD Tel: 82 2 760 2340 Fax: 82 2 764 3664 email: kyj{at}plaza.snu.ac.kr Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, 28 Yongon-dong Chongno-gu, Seoul 110-744, Korea.
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Abstract
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Experience with Polystan valved conduits in children with congenital heart disease was reviewed. From May 1997 to October 2000, 52 Polystan valved conduits were used for reconstruction of the pulmonary ventricular outflow tract in 50 patients. The median age was 24 months (range, 7 days to 19 years), body weight was 11 kg (range, 2.8 to 52 kg), and conduit size at operation was 19 mm (range, 12 to 24 mm). Early mortality was 12% (6/50). Late mortality was 6% (3/50). The median follow-up of survivors was 25 months (range, 2 to 43 months). Three patients underwent conduit replacement; 2 received larger conduits in a second-stage operation for ventricular septal defect closure. There was no death at reoperation. Polystan valved conduits can be used for reconstruction of the pulmonary ventricular outflow tract in congenital heart disease, with no significant conduit-related problems.
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INTRODUCTION
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Extracardiac valved conduits have been used to reconstruct pulmonary ventricular outflow tracts in congenital heart disease. Xenografts and allografts are currently used, but allografts are considered the better conduit.1 However, allografts have limited availability, especially in young children. In addition, young patients have been noted to develop accelerated allograft stenosis relative to older age groups.2 Therefore, xenografts are commonly used in many centers. Carpentier-Edwards porcine conduits and cryopreserved allografts were mainly used in our hospital in the past. Recently, we have used Polystan conduits (Polystan, Vaerløse, Denmark) to correct congenital malformations. This report describes the early and intermediate results of Polystan conduits in the recon-struction of pulmonary ventricle-to-pulmonary artery continuity. The term "pulmonary ventricle" is used rather than "right ventricle" because some patients had corrected transposition or situs inversus.
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PATIENTS AND METHODS
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From May 1997 to October 2000, 52 Polystan conduits were used for reconstruction of the pulmonary ventricular outflow tract in 50 patients. The median age at operation was 24 months (range, 7 days to 19 years), and median body weight was 11 kg (range, 2.8 to 52 kg). Diagnoses are listed in Table 1
. Eight patients (16%) had undergone no previous operation, 69 procedures had been performed in 42 patients, including 22 conduit interpositions in 19 patients (Table 2
). The types of conduits previously inserted are listed in Table 3
. For reconstruction of the pulmonary ventricular tract, allografts were selected when available, especially for children with complex defects.
All procedures were performed using standard techniques such as hypothermic cardiopulmonary bypass, bicaval venous cannulation, and aortic cannulation with periods of low flow or hypothermic circulatory arrest. In cases of additional intracardiac repairs such as atrial or ventricular septal defect closure, infundibular muscle resection, or distal pulmonary artery reconstruction, the aorta was crossclamped and cold cardioplegic solution was infused into the aortic root. Polystan conduits were used in the reconstruction of pulmonary ventricular outflow tracts. Proximal anastomosis was supplemented in some patients with a hood of bovine pericardium or Gore-Tex vascular patch to make the conduit curvature smooth. There were no technical problems encountered in placing Polystan conduits. Only 8 patients underwent Polystan conduit placement without any concomitant procedures. Concomitant procedures performed in 42 patients are listed in Table 4
.
Early mortality was defined as death occurring within 30 days of the operation. The follow-up status of the patients was determined by retrospective review of hospital records or by telephone interviews. One patient was lost to follow-up. Statistical analyses were performed using SPSS version 8.0 software (SPSS, Inc., Chicago, IL, USA). Median and range were calculated for descriptive variables. Actuarial data were analyzed using Kaplan-Meier formulae. Differences between groups were evaluated by a log-rank test.
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RESULTS
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The diameter of the conduits ranged from 12 mm to 24 mm; the median diameter was 19 mm. Conduits expanded proximally with bovine pericardium or a Gore-Tex vascular patch caused no problems in the operative field and they were not considered to have caused any hemodynamic problems. The mean ages at operation in relation to conduit size are depicted in Figure 1
. There were 6 early hospital deaths (12%). The causes of early mortality are listed in Table 5
. Sudden cardiac failure manifested at 8 days postoperatively in patient no. 2; thrombosis was found in his conduit. One patient with rhesus-negative AB blood type died from hemorrhage. Three more patients died of pneumonia during follow-up (Table 6
). The median follow-up of survivors was 25 months (range, 2 to 43 months).
Using Kaplan-Meier survival analysis, the actuarial survival rates including early deaths were 83.8%, 81.6%, and 81.6% at 6, 12, and 43 months, respectively (Figure 2
). Survival in those who had a small-sized conduit was significantly lower at 43 months (Figure 3
). There was a statistically significant difference in survival between patients with 12- to 16-mm conduits and those with 18- to 20-mm conduits (p = 0.0168) or 22- to 24-mm conduits (p = 0.0286). Age at operation, sex, body weight, and diagnosis had no statistically significant effect on patient survival. Significant postoperative complications were encountered in 16 patients: low cardiac output syndrome in 6, arrhythmia in 2, delayed sternal closure in 2, reexploration for bleeding in 2, mediastinitis in 2, prolonged ventilator support (more than 10 days) in 2, chylothorax in 2, bacterial endocarditis in 1, and seizure in 1.
Postoperative echocardiographic evaluation was scheduled in survivors. The pressure gradient across the Polystan valved conduit, pulmonary insufficiency, insufficiency of the atrioventricular valve of the pulmonary ventricle, and ventricular function were checked. Four patients had mild pulmonary stenosis and one had a transvalvular velocity of 4 msec1 on echocardiographic evaluation. Pulmonary regurgitation was found in 8 patients (16%); it was mild in 5 cases and moderate in 3. Mild tricuspid regurgitation was also found in those who had pulmonary stenosis or regurgitation; 3 patients had combined pulmonary stenosis and regurgitation. Catheterization data were obtained in 5 patients who showed moderate to severe stenosis of the peripheral pulmonary arteries or stenosis and insufficiency of the valved conduits on echocardiography. Three of them had moderate to severe pressure gradients between the main and peripheral pulmonary arteries, and these patients were potential candidates for reoperation. One with a pressure gradient of 25 mm Hg and 2 others with no gradient required reoperation during follow-up (Table 7
). Two required repair of ventricular septal defects that were not closed at the first operation, and the Polystan valved conduits were replaced with larger sizes. The third patient manifested postoperative mediastinitis and bacterial endocarditis; the conduit was replaced with an allograft. There was no death or significant complication in these 3 patients.
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DISCUSSION
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The use of extracardiac valved conduits has allowed correction of complex congenital heart lesions, but the ideal prosthesis is not yet available. The optimal characteristics of an extracardiac conduit are easy implantation, lack of degeneration or development of obstruction, growth ability, no insufficiency, and no need for anticoagulants.3 Cryopreserved allografts have been considered the conduit of choice and good short-term results have been reported.1,4,5 However, allografts are inferior to commercial xenografts in terms of availability and variety of sizes. The long-term results with allografts were comparable to those of xenografts in some reports.6,7 The disadvantages of xenografts are operative bleeding, coronary compression by the valve ring, and inadequacy in neonates with thin and friable pulmonary arteries.8 Inevitable long-term failure of xenografts is implicated with neointimal peel overgrowth, valve degeneration, calcification, and obstruction.7
The Polystan valved conduit is a jersey-type woven polyester tubular vascular prosthesis supplied with a tricuspid valve in the middle position. The tube is lined with porcine pericardium that has a thickness of 0.1 to 0.15 mm. The mesothelial side of the pericardium is on the luminal side of the tube. The 3 cusps are also made from porcine pericardium. The prosthesis is totally covered on the inner surface by pericardium. Conduits are available in 7 sizes with internal diameters of 12 to 24 mm in 2-mm increments. The Polystan valved conduit has some presumptive advantages over other xenografts: low bleeding risk, possible resistance to neointimal overgrowth owing to the pericardial lining of the inner surface, and no compression of the coronary arteries because there is no valve ring or stent. The possibility of reducing operative bleeding by coating a knitted Dacron valved conduit with collagen, or prevention of neointimal hyperplasia by using woven Teflon conduits, has not yet been proven.9
The early mortality of 12% in this study was considered acceptable considering the complex lesions and associated procedures in this group of patients. Only one death was due to conduit thrombosis, and another patient died of operative bleeding. Most of the mortality occurred in patients with a small valve size; valve size was found to have a significant effect on patient survival. Razzouk and colleagues10 compared 4 types of valved implants over 25 years; predictors of patient survival were found to be diagnosis and valve size. We believe that a small valve size per se does not cause perioperative problems so much as the complexity of heart lesions, preoperative ventricular function, and the need for concomitant procedures. Our previous experience indicated that size mismatch is an important factor in small children because too large a conduit at the initial operation can evoke coronary compression, bleeding, sternal erosion, and distortion of the pulmonary arteries.11 Sano and colleagues11 suggested using a conduit 5 to 8 mm larger in diameter than the size of the main pulmonary artery (normalized to the patient's weight and body surface area).
There were no deaths among those who underwent replacement of the Polystan conduit. Low mortality rates for conduit replacement have been reported, and the need for reoperation has a minimal effect on longevity and late clinical status.9,11,12 Longer follow-up is required to determine freedom from reoperation in this group of patients. Reoperation may be required for conduit problems, especially in a significant number of small children. Somatic overgrowth sometimes makes conduit replacement inevitable. The decision to reoperate is influenced by symptoms, transconduit gradient, and dysfunction of the pulmonary ventricle. Conduits are considered to be obstructed when the gradient is more than 50 mm Hg.1,10 The earliest indication of conduit failure is development of tricuspid insufficiency.1,11 A number of studies showed that symptoms may be absent despite moderate obstruction.1315 Conduit replacement should be performed if significant pulmonary ventricular dysfunction develops.
The long-term durability of extracardiac valved conduits is not yet ideal. Creation of viable pulmonary artery autografts has been tried through tissue engineering by endothelialization with autologous cells.16 However, xenografts including the Polystan valved conduit will continue to play a role in pulmonary ventricular outflow tract reconstruction until an ideal conduit is available.
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