ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Domingo M. Braile
Roberto Catani
Ênio Buffolo
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Maluf, M. A.
Right arrow Articles by Buffolo, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Maluf, M. A.
Right arrow Articles by Buffolo, E.

Ann Thorac Surg 2000;70:1911-1917
© 2000 The Society of Thoracic Surgeons


Original article: cardiovascular

Reconstruction of the pulmonary valve and outflow tract with bicuspid prosthesis in tetralogy of Fallot

Miguel A. Maluf, MD, PhDa, Domingo M. Braile, MD, PhDa, Célia Silva, MDa, Roberto Catani, MDa, Antônio C. Carvalho, MD, PhDa, Ênio Buffolo, MD, PhDa

a Division of Cardiovascular Surgery, Universidade Federal, São Paulo, Brazil

Accepted for publication April 17, 2000.

Address reprint requests to Dr Maluf, Al. dos Anapurús, 1580 # 73, Moema, São Paulo SP CEP 04087-005, Brazil
e-mail: miguel{at}bes-way.com.br


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Right ventricular outflow tract and pulmonary valve implant in patients with tetralogy of Fallot may be required to avoid late postoperative right ventricular impairment. The use of porcine bicuspid prosthesis might be a technical alternative, although comprehensive studies on the long-term use of these prostheses are not available.

Methods. Sixty-three patients (aged 5 months to 34 years; mean, 6 years) with tetralogy of Fallot and pulmonary hypoplasia underwent surgical repair and enlargement of the right ventricular outflow using preserved porcine pulmonary bicuspid prostheses. Fifty-two patients (82.5%) were followed and underwent clinical evaluation and serial Doppler echocardiography. The first 15 patients (29.4%), with ages ranging from 5 to 16 years (mean, 8.2 years) and postoperative follow-up of 48 to 87 months (mean, 65.1 months) underwent hemodynamic and cineangiographic evaluations.

Results. There were 11 deaths (17.4%) in the early postoperative period. Of the 52 surviving patients (82.5%), 51 (80.9%) were followed for 1 to 87 months (mean, 42.0 months). Four patients (7.6%) had additional treatment. Of the 15 patients (29.1%) undergoing hemodynamic evaluation, 9 (60%), had mild valvular pulmonary insufficiency and 6 (40%) had moderate insufficiency. Only the right ventricle-to-pulmonary artery pressure gradients and the right ventricular ejection fraction showed statistically significant differences between groups. Right ventricular dimension, although increased in all patients, did not show statistically significant differences.

Conclusions. Right ventricular outflow tract and pulmonary valve repair in patients with tetralogy of Fallot using a bicuspid porcine pulmonary prosthesis is a simple, reliable procedure with good results in postoperative medium term follow-up.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
The results of biventricular surgical repair of tetralogy of Fallot, a surgical technique started more than four decades ago [1], are closely related to the adequacy of the right ventricular outflow tract (RVOT) and pulmonary valve (PV) reconstruction [2].

The use of prostheses with no valves induced the development of valvular pulmonary insufficiency (VPI), which for many years was considered a benign residual lesion, indicating other causes for ventricular dysfunction [38]. More recently, the clinical relevance of VPI after enlargement of hypoplastic pulmonary trunk and ring was confirmed once the medium- and long-term results of the operation are better known. Studies are needed to establish the need to repair the PV using valved prostheses, thereby minimizing or preventing VPI, which is considered the cause for RV dysfunction [914]. Therefore, RV diastolic function should be carefully monitored with long-term follow-up in patients undergoing correction of tetralogy of Fallot with transannular enlargement.

Doppler echocardiography has shown the presence of diastolic flow in the pulmonary artery, synchronized with atrial systole and the respiratory cycle. The RV diastolic flow in the postoperative recovery period determines the diastolic compliance decrease and may be detected by a continuous laminar flow in the pulmonary artery [15]. It is known that the VPI is one of the most important factors that causes RV dilation because of volume increase and ejection fraction decrease after surgical correction [8, 16, 17].

This study reports on the preparation, implantation, and hemodynamic evaluation of a preserved porcine bicuspid pulmonary prosthesis used in RVOT and PV repair in patients with tetralogy of Fallot.

This prosthesis was originally an experimental model [18] and was approved for clinical use [19] by the Medical Ethical Committee of the São Paulo Federal University.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
From June 1991 to September 1998, 63 patients with tetralogy of Fallot and pulmonary hypoplasia consecutively underwent RVOT reconstruction with bicuspid porcine pulmonary prostheses. Thirty-six patients (57.1%) were men and 27 patients (42.9%) were women. Age ranged from 5 months to 34 years (mean, 6.0 years). Eleven patients (17.4%) had had prior Blalock-Taussig operation; 6 patients (9.5%) had pulmonary valve atresia and 2 patients (3.1%) had an absent pulmonary valve (Table 1). Fifty-two patients (82.5%) were followed-up for 1 to 87 months (mean, 42.0 months), in the postoperative medium-term follow-up. Only one patient (1.9%) was lost to follow-up after the first postoperative year. Two patients (3.8%) underwent residual ventricular septal defect closure and 2 patients (3.8%) needed treatment to correct a pulmonary branch stenosis. Forty-eight patients (94.1%) were in New York Heart Association functional class I and 3 patients (5.9%) were in class II.


View this table:
[in this window]
[in a new window]
 
Table 1. Patient Characteristics and Data in Hemodynamic Study

 
Prostheses construction
The preparation of the biological material had several phases for the manufacture of the prosthesis. The valve and pulmonary trunk were isolated from the pig’s heart, followed by cleaning, tanning, tissue conservation, according to rules established by the Laboratório Biomédica (S.J. do Rio Preto, Brasil).

The bicuspid prosthesis was manufactured using two segments of the pulmonary artery: (1) the trunk, ring, and pulmonary valve, and (2) only the pulmonary trunk (supravalvar area). The diameter of the pulmonary ring was measured using Hegar’s dilator and the grafts were classified according to the size in millimeters. One longitudinal incision was made in the concave part, removing a slice of the wall with one of the pulmonary valve cusps. A proportional wall segment was removed from the nonvalved portion (Fig 1).



View larger version (139K):
[in this window]
[in a new window]
 
Fig 1. Prosthesis construction. Two segments of the pulmonary valve are used. In one segment (a), a longitudinal incision is made in the graft’s concave part and a slice of the wall is removed with one of the cusps. In the other segment (b), the supravalvar portion was used.

 
Finally, the two structures were ligated by their proximal tips and were superimposed in a 3- to 5-mm extension, with continuous anchored polypropylene 5-0 suture. The suture was started at the graft’s concave face, followed by the insertion of the fibromuscular ring cusp. A similar suture was performed in the convex side (Fig 2).



View larger version (112K):
[in this window]
[in a new window]
 
Fig 2. Finished prosthesis. Concave aspect of the bicuspid prosthesis.

 
Surgical technique
The operation was carried out with extracorporeal circulation, moderate hypothermia (28°C), aortic clamping, and myocardial protection with intermittent infusion of cold blood cardioplegia solution at the aorta root according to routine procedure [19]. The patients underwent intracardiac correction through the right atrium for ventricular septal defect closure and through the right ventricular infundibulum for infundibular pulmonary stenosis resection.

All of the patients had hypoplasia of the pulmonary ring, and therefore, the RVOT repair was carried out by opening the pulmonary ring in the anterior valvular junction and one or two native cusps were maintained, followed by implant of a porcine pulmonary bicuspid prosthesis (Fig 3). In patients with pulmonary atresia or an absent pulmonary valve, a new cuspid was constructed using tissue from the pulmonary artery posterior wall, providing support to the bicuspid. The size of the graft was chosen according to the patient’s weight [20]: an 8-mm graft was used if the patient weighed less than 10 kg, and a 10- to 20-mm graft, for more than 10 kg.



View larger version (118K):
[in this window]
[in a new window]
 
Fig 3. Intraoperative photograph showing the right ventricle outflow tract reconstruction with bicuspid prosthesis.

 
Postoperative follow-up
Fifty-two patients (82.5%) were followed-up for a period of 1 to 87 months (mean, 42.0 months), with no mortality. The postoperative follow-up included a clinical evaluation, serial Doppler echocardiographic study, and hemodynamic study in patients with postoperative follow-up of more than 48 months. Exercise tests were carried out to evaluate the functional ability in patients with no residual defects (ventricular septal defect or pulmonary stenosis).

Hemodynamic study
Hemodynamic and cineangiographic evaluation were carried out in the first 15 patients (29.4%), after 48 to 87 postoperative months (mean, 65.1 months). The patients age ranged from 5 to 16 years (mean, 8.2 years) (Table 1).

Right ventriculography in right anterior oblique position and left anterior oblique position and pulmonary arteriography in anterior posterior projection were carried out in all of the patients. The dimensions were established in systole and diastole. The measurements were obtained by visualization of the heart images (including the prosthesis to the insertion of valves) and superposed in a graded film with identical magnification that was compared to the catheter’s diameter.

In some patients it was difficult to establish the position of the pulmonary ring because of the presence of the RVOT prosthesis. The degree of VPI was evaluated by the quantitative method after injection of a contrast solution into the pulmonary artery and the VPI was classified as mild when regurgitation was less than 50% (group 1) and moderate when it was more than 50% (group 2) (Figs 4 and 5).



View larger version (157K):
[in this window]
[in a new window]
 
Fig 4. Postoperative pulmonary artery cineangiogram in anteroposterior projection shows mild pulmonary regurgitation.

 


View larger version (113K):
[in this window]
[in a new window]
 
Fig 5. Postoperative pulmonary artery cineangiogram in anteroposterior projection shows moderate pulmonary regurgitation.

 
Statistical analysis
The Student’s t test was used for statistical analysis and a p value less than 0.05 was considered statistically significant. The surviving patients’ curve was prepared according to Kaplan-Meier method, comparing two or more functions by the log-rank test.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
There were 11 deaths (17.4%) in the early postoperative follow-up, not one related to RVOT reconstruction and included all death for any cause occurring within 30 days of operation (stroke, respiratory failure, multiorgan failure, and severe infection).

No late postoperative mortality was recorded. Of the 52 surviving patients (82.5%), 51 (80.9%) were clinically followed-up for 1 to 87 months (mean, 42.0 months) and one patient (1.9%) was lost to follow-up in the first postoperative year. The survival estimate, excluding early mortality, was 100% in a maximum of 7 years (Fig 6).



View larger version (17K):
[in this window]
[in a new window]
 
Fig 6. Kaplan-Meier survival curve for 52 patients with tetralogy of Fallot who underwent right ventricle outflow tract reconstruction with preserved porcine pulmonary bicuspid prostheses.

 
Hemodynamic data
Of the 15 patients (29.4%) undergoing hemodynamic and cineangiographic evaluations, no residual blood flow from left to right (2 patients had been operated for residual ventricular septal defect closure) or significant gradient between the RV and the pulmonary artery (1 patient undergoing right pulmonary artery enlargement and the other for stent placement in the right and left pulmonary arteries) were observed.

The patients were divided into two groups: group 1 (9 patients; 60%), VPI was less than 50%; group 2 (6 patients; 40%), VPI was more than 50% (Table 2).


View this table:
[in this window]
[in a new window]
 
Table 2. Postoperative Data Comparing Patients in Each Group

 
Mean RV systolic pressure was mildly increased in both groups: 34.8 ± 5.4 mm Hg (range, 30 to 45 mm Hg) in group 1 and 38.1 ± 8.9 mm Hg (range, 30 to 53 mm Hg) in group 2, and there was no statistical difference between the two groups (p = 0.389) (Fig 7). Mean pulmonary artery systolic pressure was mildly increased in both groups: 28.4 ± 6.9 mm Hg (range, 12 to 36 mm Hg) in group 1 and 24.6 ± 9.9 mm Hg (range, 11 to 38 mm Hg) in group 2, and no statistically significant difference was observed (p = 0.401). Mean pulmonary artery diastolic pressure was 5.6 ± 4.1 mm Hg (range, 1 to 14 mm Hg) in group 1 and 6.0 ± 3.6 mm Hg (range, 2 to 11 mm Hg) in group 2, and there was no statistically significant difference between the two groups (p = 0.877) (Fig 8). Mean right ventricular to pulmonary artery systolic gradient was 6.6 ± 4.4 mm Hg (range, 0 to 8 mm Hg) in group 1 and 13.5 ± 4.9 mm Hg (range, 8 to 13 mm Hg) in group 2, and a statistically significant difference was observed (p = 0.015) (Fig 9).



View larger version (35K):
[in this window]
[in a new window]
 
Fig 7. Mean ventricular systolic pressure (RVSP) obtained at cardiac catheterization was mildly increased in both groups, but there was no statistical difference between the two groups. (PR = pulmonary regurgitation.)

 


View larger version (41K):
[in this window]
[in a new window]
 
Fig 8. Mean pulmonary artery systolic pressure (PASP) obtained at cardiac catheterization was mildly increased in both groups, but no statistically significant difference was observed. (PR = pulmonary regurgitation.)

 


View larger version (36K):
[in this window]
[in a new window]
 
Fig 9. Mean right ventricle–pulmonary artery systolic gradient (RV-PA) obtained at cardiac catheterization. A statistically significant difference was observed. (PR = pulmonary regurgitation.)

 
Mean RV end-diastolic volume was increased in both groups, when compared to normal volume values: 236.0 ± 85.7 mL (range, 98.6 to 348.3 mL) in group 1 and 275.2 ± 72.2 mL (range, 82.8 to 396 mL) in group 2, and no statistically significant difference was observed (p = 0.170) (Fig 10A).



View larger version (39K):
[in this window]
[in a new window]
 
Fig 10. (A) Mean right ventricular end-diastolic volume (RVEDV) obtained at cardiac catheterization was increased in both groups, but no statistically significant difference was observed. (B) Mean right ventricular en- systolic volume (RVESV) obtained at cardiac catheterization was increased in both groups, but no statistically significant difference was observed. (C) Mean right ventricular stroke volume (RVSV) obtained at cardiac catheterization was increased in both groups, but no statistically significant difference was observed. (PR = pulmonary regurgitation.)

 
Mean RV end systolic volume was increased in both groups, when compared to normal volume values: 118.0 ± 51.8 mL (range, 48 to 200 mL) in group 1 and 137.4 ± 87.0 mL (range, 49.8 to 299 mL) in group 2, and no statistically significant difference was observed (p = 0.597) (Fig 10B).

Mean RV stroke volume was increased in both groups when compared to normal volume values: 111.8 ± 45.2 mL (range, 48.9 to 198.7 mL) in group 1 and 137.3 ± 88.2 mL (range, 49.8 to 200 mL) in group 2, and there was no statistically significant difference (p = 0,087) (Fig 10C).

Mean RV ejection fraction was 50.1% ± 8.3% (range, 35.7% to 61.4%), in group 1 and 61.9% ± 6.1% (range, 53% to 69.2%) in group 2, and there was statistically significant difference between the two groups (p = 0.01).


    Comment
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
The patients undergoing tetralogy of Fallot repair have an excellent prognosis and good late survival in about 90% of the patients, 10 years after the operation. In 95% of the patients, social reintegration is possible, 92% they show good physical ability during exercise and 79.3% practice sports [21].

The hemodynamic evaluation of these patients shows decreased right to left ventricular pressure ratio in the postoperative follow-up, and it is either maintained or might be increased. The persistence of residual lesions such as ventricular septal defect or pulmonary stenosis might impair the long-term result and significantly change the patient’s prognosis [20].

It is difficult to establish the number of patients who had surgical correction of tetralogy of Fallot and required a redo operation. In general, it depends on the anatomic lesion of each patient and the kind of surgical approach used, as well as the type of surgical reconstruction used [2224].

Our group has been investigating VPI after RVOT reconstruction for more than 10 years; the use of prostheses lacking a valve or monocuspid prostheses have not shown satisfactory results. In 1991 we started using a preserved porcine pulmonary bicuspid prosthesis in the reconstruction of RVOT and PV in patients with tetralogy of Fallot aiming at decreasing residual VPI [19]. This procedure was also used for the reconstruction of pulmonary ventricular outflow tract in another group of patients: transposition of the great arteries with pulmonary stenosis, truncus arteriosus, and pulmonary atresia with intact interventricular septum (pulmonary artery with interventricular septum).

Of the 52 surviving patients (82.5%), 51 (80.9%) had clinical follow-up, with a course of mild to moderate VPI, no calcification, dysfunction, or infection in the 1 to 87 months (mean, 42.0 months) after operation.

In 1964, Lillehei and colleagues [2] suggested the use of a cuspid prosthesis for RVOT reconstruction. Marchand [12] used a bicuspid aortic homograft and Egushi and Asano [13] used a bicuspid pulmonary prosthesis with the same end result.

For the reconstruction of RVOT one or two native cuspids should be preserved and adjusted to the prosthesis cuspids to produce a tri- or tetracuspid valve, decreasing VPI. Eight patients (12.6%) with atresia or absent pulmonary valve had their pulmonary valve reconstructed using a plicature of the posterior wall of the PA (shelf), after that a bicuspid prosthesis was implanted, and did not require the interposition of a tubular prosthesis or an implant of a prosthesis with three leaflets.

Different degrees of pulmonary stenosis or VPI are unavoidable after tetralogy of Fallot repair. The long-term RV performance in the presence of residual VPI is controversial. Lange and colleagues [25] showed that RV end-diastolic volume increases and RV ejection fraction decreases as a consequence of RV impairment, secondary to residual VPI or ventricular septal defect. Bove and associates [8] have also reported RV function worsening in the presence of VPI. In the study by Sunakawa and colleagues [26], the patients with VPI grade 3 or greater showed worsening of ventricular function with a significant RV end-diastolic volume increase and RV ejection fraction decrease.

Conflicting data are reported by other researchers [9, 11, 12, 2022], who concluded that VPI seems to be well tolerated in the absence of residual pulmonary stenosis.

Several factors contribute to these controversies: (1) Although the cineangiographic techniques used allow a semiquantitative evaluation of VPI, the method is considered acceptable to evaluate the effects of the different degrees of VPI, after RV volume evaluation. (2) The clinical evaluation of the patients based on their symptomatology provide limited information on the long-term VPI effects. (3) Other factors, in addition to VPI, might affect RV function after tetralogy of Fallot repair. The cumulative effect of these factors might intensify the deleterious effect of VPI, resulting in the early RV dysfunction.

The hemodynamic and cineangiographic evaluations of the patients undergoing bicuspid prosthesis implant followed up for 48 to 87 postoperative months (mean, 65.1 months) found significant gradients of right ventricle to pulmonary artery ratio between the groups (group 1: 6.6 ± 4.4 mm Hg; group 2: 13.5 ± 4.9 mm Hg, p = 0.015) and RV systolic pressure showed a mild increase (group 1, 34.8 ± 5.4 mm Hg; group 2, 38.1 ± 8.9 mm Hg, p = 0.389). According to these data it might be concluded that the use of bicuspid prostheses provided adequate RVOT reconstruction.

The reconstruction of the pulmonary valve is a complex surgical procedure and depends on several factors: (1) the anatomic conditions of the pulmonary valve, which might be atresic, stenotic, or there are cases where the pulmonary valve is absent; and (2) the type of valved prosthesis used, such as monocuspid or bicuspid, the last for variable postoperative periods. Our concern with the possible long-term VPI effects is related to RV dysfunction. This has lead us to adopt a relatively conservative approach, and use bicuspid prostheses in the past 8 years.

The use of valved grafts for RVOT repair to avoid VPI has been adopted by several groups using different materials [2, 11, 13, 2730]. In 1967, Marchand [12] introduced monocuspid homografts with excellent results. This type of RVOT repair was very well accepted and routinely adopted by several services; however, the presence of diastolic murmur and the early postoperative finding of different degrees of pulmonary insufficiency was interpreted as an inadequate aligning of the graft leaflet with the pulmonary valve native leaflets in the early postoperative follow-up. Therefore, when the enlargement of the pulmonary ring is strictly necessary, the use of an open tile-shaped prosthesis allows the ring to grow at the expense of its posterior wall. On the other hand, with a valved prosthesis adjusted for the right closure at the time of the operation, the growth of the pulmonary ring might make the prosthesis less continent. On the other hand, the growth of the native valve might also be expected, although it cannot be clinically proved.

The clinical follow-up of 51 patients for 1 to 87 months allowed the conclusion that there was no worsening VPI in serial Doppler echocardiography and showed the mobility of the prosthesis cuspids in several patients. The possibility of shortening and cuspid adherence to the wall, or loss of cuspid coaptation from the growth of the pulmonary ring posterior wall certainly cannot be excluded as the cause for VPI worsening in longer postoperative periods than the one studied.

In conclusion, the surgical correction of the tetralogy of Fallot must be carefully performed, avoiding residual lesions. In the presence of pulmonary ring hypoplasia RVOT and PV repair is strictly necessary to avoid long-term RV dysfunction. The preserved porcine pulmonary bicuspid prosthesis, which is routinely used in our service, is a reliable prosthesis with satisfactory results in the postoperative medium-term follow-up.


    Acknowledgments
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
We thank the following persons for their contributions and logistical support: Werther B. Carvalho, PhD, and PICU group; Jose L. Andrade, PhD, and Cardiology group; and Solange O. Dourado and the Research and Publication Division of Laboratório Biomédica for revision of this text.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Lillehei C.W., Cohen M., Warden H.E., Warco R.L. Complete anatomical correction of the tetralogy of Fallot defects. Report of successful surgical case. Arch Surg 1956;73:526-531.
  2. Lillehei C.W., Levy M., Adams P., Anderson R.L. Corrective surgery for tetralogy of Fallot. Long term follow-up by postoperative recatheterization in 69 cases and certain surgical considerations. J Thorac Cardiovasc Surg 1964;48:556-576.
  3. Sunderland C.O., Matarazzo R.G., Lees M.H., et al. Total correction of tetralogy of Fallot in infancy. Postoperative hemodynamic evaluation. Circulation 1973;48:398-442.[Abstract/Free Full Text]
  4. Muraoka R., Yokota M., Matsuda K., Tabata R., Hikasa Y. Long-term hemodynamic evaluation of primary total correction of tetralogy of Fallot during the first two years of life. Arch Jpn Chir 1973;42:315-319.
  5. Radley-Swith R., Yacoub M. Late results of total correction of Fallot’s tetralogy in the first year of life. Circulation 1975;51:228-232.
  6. Castañeda A.R., Freed M.D., Williams R.G., Norwood W.T. Repair of tetralogy of Fallot in infancy. Early and late results. J Thorac Cardiovasc Surg 1977;74:372-375.[Medline]
  7. Calder A.L., Barratt-Boyes B.G., Brandt P.W., Neutze J.M. Postoperative evaluation of patients with tetralogy of Fallot repaired in infancy. J Thorac Cardiovasc Surg 1979;77:704-720.[Abstract]
  8. Bove E.L., Byrum C.J., Thomas F.D., Kavey R.E.W., Sondheimer H.M. The influence of pulmonary insufficiency on ventricular function following repair of tetralogy of Fallot. J Thorac Cardiovasc Surg 1983;85:691-696.[Abstract]
  9. Edwards J.E., Carey L.S., Neufeld H.N., Lester R.G. Congenital heart disease, volume 2. Philadelphia: WB Saunders, 1965.
  10. Barratt-Boyes B.G., Lowe J.B., Cole D.S., Kelly D.T. Homograph valve replacement for aortic valve. Thorax 1965;20:495-501.
  11. Ross D.N., Somerville J. Correction of pulmonary atresia with a homograph aortic valve. Lancet 1966;2:1446-1447.[Medline]
  12. Marchand P. The use of a cusp-bearing homograph patch, the outflow tract and pulmonary artery in Fallot’s tetralogy and pulmonary valvular stenosis. Thorax 1967;22:497-509.[Abstract/Free Full Text]
  13. Eguchi S., Asano K. Homograph of pulmonary artery on ascending aorta with valve as a right ventricular outflow. J Thorac Cardiovasc Surg 1968;56:413-420.[Medline]
  14. Asano K., Eguchi S. A new method of right ventricular outflow reconstruction in corrective surgery for tetralogy of Fallot. J Thorac Cardiovasc 1970;59:512-517.[Medline]
  15. Gatzoulis M.A., Clark A.L., Cullen S., Newman C.G.H., Redington A.N. Right ventricular diastolic function 15 to 35 years after repair of tetralogy of Fallot. Circulation 1995;91:1775-1781.[Abstract/Free Full Text]
  16. Oku H., Shirotani H., Sunakawa A., Yokoyama T. Postoperative long-term results in total correction of tetralogy of Fallot: hemodynamics and cardiac function. Ann Thorac Surg 1986;41:413-418.[Abstract]
  17. Graham T.P., Cordell D., Atwood G.F. Right ventricular volume characteristics before and after palliative and reoperative operation in tetralogy of Fallot. Circulation 1976;54:417-423.[Abstract/Free Full Text]
  18. Maluf MA. Reconstituição da valva pulmonar e via de saída do ventrículo direito com prótese bivalvular ou prótese tubular valvada de artéria pulmonar suína. UNIFESP: São Paulo, 1991:10–90.
  19. Maluf M.A., Verde J.L., Catani R., et al. Reconstituição da valva pulmonar e via de saída do ventrículo direito, com prótese bivalvular ou prótese tubular valvada de tronco pulmonar de porco. Estudo experimental e aplicação clínica. Rev Bras Cir Cardiovasc 1993;8:20-38.
  20. Pacifico A.D., Kirklin J.W., Blackstone E.H. Surgical management of pulmonary stenosis in tetralogy of Fallot. J Thorac Cardiovasc Surg 1977;74:382-395.[Abstract]
  21. Ilbani M.W., Idriss F.S., Deleon S.Y., et al. Factors that exaggerate the deleterious effects of pulmonary insufficiency on the deleterious effects of pulmonary insufficiency on the right ventricle after tetralogy repair. Surgical implications. J Thorac Cardiovasc Surg 1987;93:36-44.[Abstract]
  22. Calza G., Panizzon G., Rovida S., Aiguepelse J. Incidence of residual defects determining the clinical outcome after correction of tetralogy of Fallot: postoperative late follow-up. Ann Thorac Surg 1989;47:428-435.[Abstract]
  23. Fuster V., McGoon D.C., Kennedy M.A., Ritter D.G., Kirklin J.W. Long term evaluation (12 to 22 years) of open heart surgery for tetralogy of Fallot. Am J Cardiol 1980;46:635-642.[Medline]
  24. McGoon D.C. Long-term effects of prosthetic materials. Am J Cardiol 1982;50:621-630.[Medline]
  25. Lange P.E., Onnasch D.G.W., Bernhard A., Heintzen P.H. Left and right ventricular adaptation to right ventricular overload before and after surgical repair of tetralogy of Fallot. Am J Cardiol 1982;50:786-789.[Medline]
  26. Sunakawa A., Nakamura Y., Shinohara T., et al. Angiocardiographic evaluation of ventricular septal defect. Pre and post-operative cardiac volume characteristics. Jpn Cir J 1983;47:625-628.
  27. Trusler G.A., Iyengar S.R., Mustard W.T. Reconstruction of the pulmonary valve and outflow tract: report of 25 cases. J Thorac Cardiovasc Surg 1973;65:245-251.[Medline]
  28. Ionescu M.I., Tandon A.P., Macartney F.J. Long term sequential hemodynamic evaluation of right ventricular outflow tract reconstruction using a valve mechanism. Ann Thorac Surg 1979;27:426-434.[Abstract]
  29. Duran C.M.G., Revuelta J.M., Pomar J.L. A new composite xenograft monocusp patch for reconstruction of the right ventricular outflow tract. A preliminary report. Cardiovasc Dis 1980;7:58-62.
  30. Bailey L.L., Petry E.L., Doroshow J.G., Wareham E.E. Biologic reconstruction of right ventricular outflow tract. J Thorac Cardiovasc Surg 1981;82:779-784.[Abstract]



This article has been cited by other articles:


Home page
Ann. Thorac. Surg.Home page
J. A. Quintessenza, J. P. Jacobs, V. O. Morell, J. M. Giroud, and R. J. Boucek
Initial Experience With a Bicuspid Polytetrafluoroethylene Pulmonary Valve in 41 Children and Adults: A New Option For Right Ventricular Outflow Tract Reconstruction
Ann. Thorac. Surg., March 1, 2005; 79(3): 924 - 931.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Domingo M. Braile
Roberto Catani
Ênio Buffolo
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Maluf, M. A.
Right arrow Articles by Buffolo, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Maluf, M. A.
Right arrow Articles by Buffolo, E.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS