Asian Cardiovasc Thorac Ann 2008;16:189-193
© 2008 Asia Publishing EXchange Ltd
Bicuspidized Pulmonary Homograft for Truncus Arteriosus Repair
Vichai Benjacholamas, MD,
Jule Namchaisiri, MD,
Apichai Khongphatthanayothin, MD1,
Pornthep Lertsapcharoen, MD1
Cardiothoracic Unit, Department of Surgery
1 Cardiac Unit, Department of Pediatrics, King Chulalongkorn Memorial Hospital, Chulalongkorn University, Bangkok, Thailand
For reprint information contact: Vichai Benjacholamas, MD, Tel: 66 2 256 4944, Fax: 66 2 256 4974, Email: vichaicu{at}hotmail.com, Department of Surgery, King Chulalongkorn Memorial Hospital, Chulalongkorn University, Rama IV Road, Pratumwan, Bangkok 10330, Thailand.
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ABSTRACT
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Primary repair is preferable to palliation in infants with truncus arteriosus. At our institute, an appropriately small homograft valved conduit is not available for every patient; a bicuspidized pulmonary valve homograft is an alternative. Between December 1996 and August 2005, 24 patients aged 28 days to 21 months with truncus arteriosus underwent primary repair with a homograft valved conduit; bicuspidized homografts were used in 15 of them. In the 18 (75%) patients who survived to hospital discharge, 5-year survival was 94% (75% for tricuspid homografts and 100% for bicuspidized homografts, which was not significantly different). Freedom from reoperation or balloon angioplasty in all 18 survivors was 89% at 5 years. Freedom from reoperation in tricuspid and bicuspidized homograft groups at 5 years was 67% and 100%, respectively; the difference was not statistically significant. Bicuspidized homografts worked as well as tricuspid conduits in the intermediate term. The remodeled homografts showed excellent hemodynamic characteristics and appear to be a reasonable alternative when an appropriate size of valved homograft is unavailable.
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INTRODUCTION
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Truncus arteriosus communis (TAC) is an uncommon complex congenital cardiac malformation that represents 2%–4% of all congenital heart defects.1–3 The features of TAC include a single great artery arising from the base of the heart, which supplies the systemic, coronary, and pulmonary blood flow, and a large ventricular septal defect. The 2 main classification systems used to describe the anatomy of TAC are those of Collet and Edwards and Van Praagh and Van Praagh.4 Without surgical treatment, < 25% of children born with TAC are expected to survive beyond the 1st year of life.3 The first successful surgical correction of TAC was performed in 1967 by McGoon and colleagues5 who closed the ventricular septal defect and established right ventricular-pulmonary artery continuity using an aortic valved homograft. Since then, early repair to avoid progressive pulmonary vascular obstructive disease has been encouraged. Reconstruction of the right ventricular outflow tract (RVOT) with a homograft valved conduit in the neonatal or infancy period is now the optimal treatment for TAC.6–8 Because of a lack of appropriately sized homografts, Michler and colleagues9 introduced the use of a surgically downsized homograft in small neonates in 1994. In our country, cryopreserved homograft valved conduits are supplied by the Thai Red Cross Society; however, the supply of small homografts is limited, and they are not available for every patient. As we believed that the hemodynamic profile would be similar in tricuspid and bicuspid valved conduits, we tailored tricuspid homografts into bicuspid valved conduits. Because a pulmonary homograft appears to be more durable than an aortic homograft, we used pulmonary valved homografts for all except 1 bicuspidized conduit.10 We report the surgical technique and midterm results.
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PATIENTS AND METHODS
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Between December 1996 and August 2005, 24 patients (10 boys and 14 girls) underwent total primary repair of TAC at King Chulalongkorn Memorial Hospital. The mean age at operation was 6.88 ± 4.90 months (range, 28 days to 21 months) and the mean weight was 4.78 ± 1.43 kg (range, 2.5–6.8 kg). All patients were in cardiac failure and 4 of them needed ventilatory support at the time of surgery. Two patients had severe malnutrition in addition to heart failure, and one had tracheal stenosis from prolonged intubation at the time of surgical repair. The associated cardiac lesions are listed in Table 1
. Details of the truncal valve morphology are given in Table 2. Most patients had 3 truncal valve leaflets. Moderate truncal valve regurgitation was demonstrated in only 1 patient who had 4 truncal valve leaflets. According to the classification of Collet and Edwards, 17 patients had type I TAC, 6 had type II, and 1 had type II + IV.
The operation was performed through a median sternotomy, using bicaval cannulation with full-flow cardiopulmonary bypass in 23 patients, and with a period of circulatory arrest in one who had associated interrupted aortic arch. The pulmonary arteries were occluded at the onset of bypass, and cold crystalloid cardioplegia was delivered through the truncal vessel after cross clamping the aorta. The mean cross clamp time was 74.6 ± 20.5 min (range 47–120 min). The mean cardiopulmonary bypass time was 177.2 ± 29.8 min (range 128–258 min). In type I TAC, the pulmonary arteries were excised from the truncal vessel, and the defect was closed directly in all except 1 patient in whom a homograft patch was used. In type II TAC, the truncal vessel was transected, the pulmonary bifurcation was mobilized to the left side of the aorta, and the aorta was reconstructed by direct end-to-end anastomosis. The intramural coronary artery was corrected in 2 of the 3 cases. The ventricular septal defect was closed through a right ventriculotomy with a Dacron patch, using interrupted mattress sutures in all patients. Right ventricle-pulmonary artery continuity was established with the various homografts listed in Table 3. The mean diameter of all homograft conduits was 15.5 ± 1.7 mm (range, 12–18 mm). The mean diameter of tricuspid valved conduits was 15.7 ± 2.19 mm (range, 12–18 mm). Bicuspidized valved conduits were prepared on the operating table. A tricuspid conduit of 20–26 mm in diameter was selected according to the patient’s weight. A longitudinal incision was made on the oversized conduit. One cusp of the homograft was resected, and the rest was wrapped around a dilator of appropriate size and oversewn (Figure 1). The mean diameter of the conduit after size reduction was 15.5 ± 1.41 mm (range, 13–18 mm). Usually, the diameter of the bicuspidized homograft was closed to the patient’s tricuspid valve diameter.
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Figure 1. (A) A longitudinal incision was made on the oversized conduit; (B) One cusp of the homograft was resected; (C) The bicuspid homograft wrapped around a dilator of appropriate size and oversewn.
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Kaplan-Meier analysis was used to determine survival rates and freedom from reoperation. Comparisons of survival and reoperation rates between tricuspid and bicuspidized homografts were performed by the log-rank test. A p value of less than 0.05 was considered significant.
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RESULTS
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Overall, the hospital mortality was 25% (6/24). It was 33.3% (3/9) in the tricuspid homograft group, and 20% (3/15) in the bicuspidized group. The causes of death are listed in Table 4. In patients who survived the operation, the function of the homograft was evaluated by echocardiography prior to hospital discharge. There was no pulmonary valve stenosis or regurgitation in any patient.
The median follow-up period was 39 months (range, 4–108 months). No patient was lost to follow-up. The function of the homograft was assessed in all survivors by echocardiography every 4 months. The majority (15/18, 83.33%) had trivial or mild pulmonary valve stenosis or regurgitation. Only 3 patients showed calcification of the homograft with significant pulmonary valve stenosis and/or regurgitation (Table 5). There was 1 late death 1 year after the initial repair. This patient had 4 truncal valve leaflets with a moderate degree of regurgitation, and did not undergo truncal valve repair at the initial operation. The homograft used in this patient was a tricuspid aortic valve. The cause of death was ventricular failure secondary to truncal valve regurgitation. For patients who survived the operation, the overall 5-year survival was 94%; it was 75% for those with a tricuspid homograft, and 100% for those with a bicuspidized homograft ( p > 0.05; Figure 2). Six patients have survived for more than 5 years; all have a pulmonary homograft (2 tricuspid and 4 bicuspid). During follow-up, 2/18 (11%) hospital survivors required reoperation. One had a calcified tricuspid pulmonary homograft (16-mm in diameter) with severe pulmonary valve regurgitation. Her conduit was changed at 66 months after the first operation. The explanted homograft was heavily calcified and very rigid. The other patient underwent reoperation after 28 months because of a false aneurysm, 29 x 33 mm, in the RVOT area. The tricuspid aortic homograft (17 mm in diameter) in this patient was still functioning well. The explanted homograft had some calcification but no significant restriction of the valve. The diameters of both explanted homografts had not changed since implantation. The freedom from reoperation or balloon angioplasty in all 18 survivors was 89% at 5 years (Figure 3). The freedom from reoperation in tricuspid and bicuspidized homograft groups at 5 years was 67% and 100%, respectively ( p > 0.05; Figure 4).
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Figure 2. Probability of long-term survival after initial survival of complete truncus arteriosus repair.
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Figure 3. Freedom from conduit-related reoperation in all patients who survived the initial complete truncus arteriosus repair.
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DISCUSSION
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Right ventricular outflow tract reconstruction with a homograft valved conduit is the most widely reported technique for total repair of TAC.6–8 Lack of availability of small homografts is a significant problem in many institutions, including ours. Many alternative techniques have been used to reconstruct the RVOT, such as a Dacron valved conduit, fresh autologous pericardial valved conduit, porcine aortic root bioprosthesis, bovine valved venous xenograft, and the bicuspidized homograft valved conduit.9,11,12 We prefer the bicuspidized homograft valved conduit. The freedom from reoperation or balloon angioplasty of 89% at 5 years compares well with previous reports that varied from moderately good (43%–51%) to excellent (89%–90%).10,13–17 Because of its better durability, most of the conduits used in our patients were pulmonary homografts (especially in the bicuspidized group), which may partly explain our excellent results. The diameter of the homograft conduit used was close to the diameter of the patient’s tricuspid valve, and most were > 15 mm. Because somatic outgrowth usually occurs in conduits < 15 mm, this may be another reason for the high freedom from reoperation in our series.17
In our patients, mortality, hemodynamic burden, conduit failure, and freedom from reoperation were not significantly different between those with tricuspid or bicuspidized homografts. Evaluation of proximal coronary artery anatomy is essential in repair of TAC, and anomalies must be regarded as risk factors for operative death. An intramural left coronary artery was recognized in 3/24 patients. It was not corrected in the first patient who subsequently died from myocardial ischemia, whereas the 2 subsequent patients underwent correction and survived to discharge.
Primary repair in infancy is still the treatment of choice for TAC. The surgically downsized bicuspidized homograft valved conduit demonstrated an excellent hemodynamic profile in the intermediate term follow-up. Its function was as good as that of the native tricuspid homograft. It serves as a good alternative when an appropriate size of homograft valved conduit is not available.
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REFERENCES
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ABSTRACT
INTRODUCTION
