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Ann Thorac Surg 2000;69:S97-S105
© 2000 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, The Montréal Children’s Hospital, Montréal, Québec, Canada
Address reprint requests to Dr Tchervenkov, Division of Cardiovascular Surgery, The Montréal Children’s Hospital, 2300 Tupper St, Rm C-828, Montréal, PQ, Canada H3H 1P3
Presented at the International Nomenclature and Database Conferences for Pediatric Cardiac Surgery, 1998–1999.
Abstract
Pulmonary atresia (PA) and ventricular septal defect (VSD) is a complex and extremely heterogeneous cardiopulmonary malformation that has not been accurately defined, as evidenced by the synonymous use of the term with tetralogy of Fallot with PA. The anatomy and morphology of the pulmonary circulation to a large extent determines the surgical approach and overall outcome, with the intracardiac anatomy playing a secondary role. Based on the characterization of the pulmonary circulation a new classification of PA-VSD is proposed. In type A, there are only native pulmonary arteries (NPA). In type B, pulmonary blood flow is provided by both NPA and by major aortopulmonary collateral arteries [MAPCA(s)]. In type C, there are only MAPCA(s) and no NPA. This new classification is proposed for the purpose of establishing a unified reporting system. The subject was debated and reviewed by members of the STS-Congenital Heart Surgery Database Committee and representatives from the European Association for Cardiothoracic Surgery. All efforts were made to include all relevant nomenclature categories using synonyms where appropriate. A comprehensive database set is presented which is based on a hierarchical scheme. Data are entered at various levels of complexity and detail which can be determined by the clinician. These data can lay the foundation for comprehensive risk stratification analyses. A minimum database set is also presented which will allow for data sharing and would lend itself to basic interpretation of trends. Outcome tables relating diagnoses, procedures, and various risk factors are presented.
I. Background
Pulmonary atresia (PA) and ventricular septal defect (VSD) is a complex, and extremely heterogeneous cardiac malformation, that has not been accurately defined to date. Most of the focus has been on the extreme variability of the pulmonary circulation, while the precise definition and description of the intracardiac malformation has been largely deficient. The questions that need to be answered are: What is PA-VSD? Is PA-VSD synonymous with tetralogy of Fallot (TOF) with PA as has been implied by reputable scholars of congenital heart disease [1]? Do major aortopulmonary collateral arteries [MAPCA(s)] occur only in the presence of PA-VSD?
Historical perspectives on nomenclature of PA-VSD
In the absence of MAPCA(s) patients with PA were probably simply categorized with the specific cardiac malformation it accompanied. However, the history of nomenclature for PA-VSD with MAPCA(s) is fascinating. This malformation was initially considered a truncus arteriosus type IV in the classification by Collett and Edwards [2]. In the same year, 1949, Manhoff and Howe used the term absence of the pulmonary artery for the condition where the pulmonary blood supply was entirely derived from systemic arteries [3]. These authors used the argument that a single great artery can hardly be considered a common trunk of the aorta and the pulmonary artery when the pulmonary arteries do not exist. In 1965, Van Praagh and Van Praagh [4] proposed their classification of truncus arteriosus demonstrating convincingly that the type IV truncus in the Collett and Edwards classification is not a truncus arteriosus, but rather a solitary aorta with absence of the pulmonary artery as proposed by Manhoff and Howe [3]. Based on embryological considerations, the term absent sixth aortic arch was used by Stuckey and associates [5]. In 1970, Sommerville used the term type D PA with a VSD [6]. The term pseudotruncus was used by Bharati and associates in 1975, to describe patients with PA-VSD [7]. The term pseudotruncus was subsequently felt to be inappropriate by Van Praagh and associates because of its vagueness and that it did not represent an entity [8]. It has since fallen out of favor.
The term MAPCA(s) was first used by Macartney, Deverall and Scott to differentiate them from the bronchial arteries [9]. The authors thought that this distinction was important for the following reasons. There was doubt as to whether the MAPCA(s) had the same embryological origins as bronchial arteries. The much larger MAPCA(s) did not resemble the more numerous and much finer systemic bronchial collaterals. Finally, MAPCA(s) did not usually travel in close relation to the bronchi as bronchial arteries.
GUEST EDITORS’ NOTE: The term pseudotruncus is discussed in the Truncus Arteriosus article by Marshall L. Jacobs in this supplement as follows:
Pseudotruncus has often been used as a synonym for Collett and Edwards type IV truncus. As discussed above, pseudotruncus is not really a form of truncus arteriosus and is best defined as a form of pulmonary atresia with ventricular septal defect with MAPCA(s) (major aortopulmonary collaterals).
Current terminology
Five reputable textbooks were surveyed for patients with PA-VSD. In one they were discussed in the chapter of "Tetralogy of Fallot" [10]. The second textbook had a chapter entitled "Surgical management of pulmonary atresia with ventricular septal defect" [11]. In the third, the title of the chapter was "Pulmonary atresia and ventricular septal defect," and in it the authors state that PA-VSD is frequently considered pathologically to represent the most severe end of the spectrum of TOF [12]. The fourth textbook had a chapter entitled "Tetralogy of Fallot and pulmonary atresia and ventricular septal defect" [1], beautifully demonstrating the dilemma in definition and terminology. Finally, in Kirklin and Barratt-Boyes’s textbook of cardiac surgery, while the chapter has the title "Ventricular septal defect and pulmonary stenosis or atresia", the section on PA carries the heading of "Tetralogy of Fallot with pulmonary atresia" [13]. These authors correctly point out in the last section of that chapter, only a paragraph long "Combined valvar and infundibular pulmonary stenosis or atresia and ventricular septal defect," which includes only 1 patient with PA, that not all patients with PA-VSD are morphologically TOF [13]. This probably offers the first clue to the subtle but real difference between TOF with PA and PA-VSD.
Most recent surgical papers have consistently used the term PA-VSD, particularly the ones dealing with surgical treatment in the presence of MAPCA(s), and in most of these the intracardiac anatomy remained undefined, except to say that there is a VSD [14–20]. In a recent paper, we were reluctant to use the term PA-VSD in the title because of its lack of specificity, and because one of our patients had severe pulmonary stenosis [21]. Instead our title was: "One-stage midline unifocalization and complete repair in infancy versus multiple-stage unifocalization followed by repair for complex heart disease with major aortopulmonary collaterals" and we defined in each patient the precise intracardiac malformation, such as TOF with PA, double outlet right ventricle (DORV), PA or transposition of the great arteries (TGA) with complete atrioventricular septal defect (CAVSD) [21].
Definitions
Atresia is the absence or closure of a natural passage of the body according to Webster’s dictionary. Pulmonary atresia (PA) has been defined, in the context of TOF as the lack of luminal continuity between the right ventricle (RV) and the pulmonary trunk [13]. However, PA may occur also with corrected TGA [8], and in that case there is lack of luminal continuity between the left ventricle (LV) and the pulmonary trunk. Therefore the broad definition we are proposing is the following:
PA is the lack of luminal continuity and absence of blood flow from a ventricle or a rudimentary chamber and the pulmonary artery. In its severe form, there is either partial or complete absence of the native pulmonary arteries.
PA may occur in biventricular hearts with intact ventricular septum (IVS) or with a VSD, as well as in hearts with a univentricular atrioventricular connection. The fact that PA may occur with virtually any form of congenital heart disease is supported by the classic studies of Van Praagh and associates [8] as well as Bharati and associates [7].
A ventricular septal defect is defined as an opening or hole in the interventricular septum [22, 23].
Therefore from these two definitions we can define PA-VSD.
Pulmonary atresia-ventricular septal defect is defined as a group of congenital cardiac malformations in whom there is lack of luminal continuity and absence of blood flow from either ventricle and the pulmonary artery, in a biventricular heart that has an opening or a hole in the interventricular septum. In its severe form there is either partial or complete absence of the native pulmonary arteries.
Since PA-VSD has been frequently used interchangeably with TOF, PA it would be useful to define the latter.
Tetralogy of Fallot with Pulmonary atresia is a congenital cardiac malformation, characterized by the extreme underdevelopment of the right ventricular infundibulum with marked anterior and leftward displacement of the infundibular septum often fused with the anterior wall of the right ventricle resulting in complete obstruction of blood flow into the pulmonary artery and associated with a large outlet, subaortic ventricular septal defect [13].
We can see that based on the above definitions, TOF, PA is a specific type of PA-VSD where the intracardiac malformation is more accurately defined. The presence or absence of MAPCA(s) does not change these definitions. Therefore TOF, PA, MAPCA(s) is a specific type of PA-VSD, MAPCA(s) where the intracardiac malformation is more accurately defined.
GUEST EDITORS’ NOTE: The term TOF with PA is discussed in the Tetralogy of Fallot article by Marshall L. Jacobs in this supplement as follows:
The proper location in the nomenclature system for lesions classified as TOF with PA or any subtypes of TOF with PA was debated extensively at the First International Nomenclature Conference for Pediatric Cardiac Surgery, Chicago, Illinois, September 19–20, 1998. Some feel strongly that these lesions should be grouped with TOF and others feel strongly that these lesions should begrouped with PA-VSD. These lesions may be entered into the hierarchical database either under TOF with PA or PA-VSD. Thus, any given center or surgeon may decide to group these lesions under either TOF with PA or PA-VSD.Regardless of where in the database the lesion is entered, for our purposes of analysis, it was agreed that lesions coded as TOF with PA or any subtypes of TOF with PA will not be analyzed with TOF but instead will be analyzed with PA-VSD.
This definition was also debated extensively at the Third International Nomenclature Conference for Pediatric Cardiac Surgery, New Orleans, Louisiana, April 23, 1999. At the Third International Nomenclature Conference for Pediatric Cardiac Surgery, the decision was made that TOF with PA would not be considered a subtype of TOF on the short diagnosis list (see section IV. Diagnosis and Procedure Short Lists of this manuscript); TOF with PA would thus not be a choice on the short diagnosis list. TOF with PA would instead be coded under PA-VSD on the short diagnosis list. Although TOF with PA can be accessed via the TOF hierarchy in the hierarchical nomenclature system, it will not be analyzed with TOF but instead will be analyzed with PA-VSD.
This article will discuss the simplest forms of TOF with PA, ie, that form characterized by confluent pulmonary arteries with a ductus arteriosus as the sole source of pulmonary blood flow and that form characterized by the left pulmonary artery (LPA) arising from a ductus (not really PA if the right pulmonary artery (RPA) still connects to the RV). These lesions will be discussed further in the article covering PA-VSD. TOF with multiple aortopulmonary collaterals (also known as PA-VSD, MAPCA(s)s or pseudotruncus) is also discussed in the article covering PA-VSD.
Morphology of PA-VSD
Pulmonary circulation
The type of intracardiac malformation is not predictive of the pulmonary circulation, whose precise definition is therefore independent of the former [24]. The pulmonary circulation in PA-VSD is characterized by extreme heterogeneity and variability in terms of origin of blood flow, the presence or absence of the NPA, the presence or absence of MAPCA(s), and the distal distribution of the pulmonary blood flow in terms of pulmonary parenchymal segments supplied with frequent arborization abnormalities [21]. The NPA may be severely hypoplastic, either confluent or nonconfluent, or may be completely absent. They may derive their blood flow from either the ductus arteriosus, communicating MAPCA(s) or both. MAPCA(s) are large and distinct arteries, highly variable in number, that usually arise from the descending thoracic aorta, but uncommonly may originate from the aortic arch or the subclavian, carotid or even the coronary arteries.
Rabinovitch and associates have categorized systemic pulmonary collateral arteries into three types, based on their site of origin as well as the way they connect to the pulmonary circulation [25]. These are direct aortopulmonary collaterals, indirect aortopulmonary collaterals, and true bronchial arteries. Only the first two should be considered MAPCA(s).
The etiology and pathogenesis of the pulmonary circulation was studied by Kutsche and Van Mierop, who concluded that in PA-VSD the pulmonary ostium becomes atretic much earlier in development, shortly after the truncoconal partitioning but before closure of the ventricular septum [26]. On the other hand, in PA-IVS, PA occurs much later after cardiac septation has been completed. This explains why in PA-IVS blood flow is provided by the ductus arteriosus into well developed, main, and confluent branch pulmonary arteries and there are no MAPCA(s), whereas in PA-VSD the pulmonary circulation is so heterogeneous and highly variable with the high incidence of MAPCA(s).
Castañeda and associates have divided patients with TOF with PA into 4 groups with respect to the anatomy of the pulmonary circulation [10]. In groups I and II, the pulmonary circulation is through the ductus arteriosus into the native, confluent pulmonary arteries, with the main pulmonary artery being present in group I and absent in group II. Neither group has MAPCA(s). In group III, the NPA are very hypoplastic and do not supply all the bronchopulmonary segments. There are MAPCA(s) supplying a variable degree of pulmonary parenchyma. The NPA receive their blood flow either through a ductus arteriosus or from communicating MAPCA(s). Finally, in group IV there are no NPA, with the entire pulmonary blood supply provided by MAPCA(s).
Intracardiac anatomy
The intracardiac anatomy is independent of the pulmonary circulation [24]. In the vast majority of the cases of PA-VSD the intracardiac anatomy is that of TOF. A rudimentary infundibulum may be identified upon careful inspection, partially or completely fused with the anterior wall of the RV. This is usually the case in the presence of a main pulmonary artery (MPA).
The presence of a MPA can also serve as a guide for the intracardiac diagnosis according to which ventricle it is attached, whether it has a lumen or is a fibrous cord. If the MPA or fibrous chord originates from RV and the aorta also arises entirely or predominantly from the RV, the diagnosis is then DORV with PA. If on the other hand the MPA or fibrous cord originates from the LV along with the aorta, we have double outlet left ventricle (DOLV) with PA, or if the aorta arises from the RV we have TGA with PA.
In many of the patients with PA-VSD however, there is no MPA or a fibrous cord that originates from the heart. In these cases the precise intracardiac diagnosis can not be made with certainty. For example, if the aorta arises entirely from the RV, it will be impossible to establish if there is DORV with PA or TGA with PA. Therefore, in these situations the malformation is simply called by its general name, PA-VSD.
Proposal for a new nomenclature for PA-VSD
The new nomenclature for PA-VSD must be anatomically and morphologically accurate, and must include all forms of congenital heart disease that fulfill the previously described definitions. Both the pulmonary circulation and the intracardiac malformation must be described independently, because both components carry surgical implications. However, in the overwhelming majority of the cases, the precise anatomy of the pulmonary circulation carries a far greater impact on the surgical options.
Pulmonary circulation
We propose to divide the patients with PA-VSD into 3 types, according to the anatomy and morphology of the pulmonary circulation. This new classification is inspired by the similarity of the surgical options for each type, and is based on the presence or absence of NPA and the presence or absence of MAPCA(s).
PA-VSD type A
NPA are present. Pulmonary blood flow is supplied by the patent ductus arteriosus. There are no MAPCA(s). Surgical options: primary intracardiac repair is possible. Alternatively, an initial systemic-to-pulmonary shunt may be performed with intracardiac repair delayed to a later date. Pulmonary unifocalization is not required. However, creation of a pulmonary confluence between the RPA and LPA may be necessary if they are discontinuous.
PA-VSD type B
Both NPA and MAPCA(s) are present. Surgical options: single-stage midline bilateral pulmonary unifocalization with concomitant or delayed intracardiac repair may be possible. Alternatively a multistage surgical approach may consist of preliminary operations to develop the NPA, sequential unilateral pulmonary unifocalizations to centralize pulmonary blood flow, and finally followed by intracardiac repair, if the criteria for repairability are fulfilled.
PA-VSD type C
There are no NPA. The pulmonary circulation is supplied by MAPCA(s) only. Surgical options: single-stage midline bilateral pulmonary unifocalization with concomitant or delayed intracardiac repair may be possible. Alternatively, a multistage surgical approach may consist of preliminary operations to centralize pulmonary blood flow, such as sequential unilateral pulmonary unifocalizations, followed by intracardiac repair if the criteria for repairability are fulfilled.
MAPCA(s) without PA-VSD
Rarely, MAPCA(s) may occur in patients that do not have PA-VSD, but have severe pulmonary stenosis [21]. We have seen two such patients at The Montreal Children’s Hospital in the last 13 years. Since the surgical approach in these patients will have significant similarities to the one for PA-VSD with MAPCA(s), they should be considered in the database on PA-VSD. This decision is also supported by the fact that there is no other diagnostic heading they can be grouped under, and therefore, these patients will otherwise be lost for analysis.
The pulmonary circulation in patients with MAPCA(s) without PA-VSD resembles the one found in PA-VSD type B or type C. Since these patients have MAPCA(s), there can not be type A.
The intracardiac anatomy in patients that have MAPCA(s) without PA should be specifically defined in each case.
Intracardiac anatomy
The second level of definition is for the intracardiac anatomy. This level of definition will define intracardiac anatomy, the atrio-ventricular (AV) connection, and the ventriculo-arterial (VA) connection.
PA-VSD, AV concordance
PA-VSD, AV discordance
For more details on PA-VSD, AV discordance, refer to the article by Wilkinson and colleagues on Atrioventricular Discordance in this Supplement.
II. PA-VSD comprehensive hierarchical nomenclature system
PA-VSD hierarchy level 1
PA-VSD hierarchy level 2
PA-VSD hierarchy level 3
PA-VSD hierarchy level 4
Modifiers for PA-VSD
Segment (source: NPA, MAPCA(s), both, or neither)
III. Surgical treatment options for PA-VSD
The surgical treatment of PA-VSD has been largely determined by the morphology of the pulmonary circulation. In the patients with confluent NPA and no MAPCA(s) (PA-VSD, type A) initial palliative systemic-to-pulmonary shunt in the neonatal period is necessary to provide reliable pulmonary blood flow. This is usually followed at a later date by intracardiac repair, usually with the use of a conduit to establish right ventricular to pulmonary artery continuity. In recent years some groups, including ours, have increasingly favored a primary neonatal intracardiac repair [27, 28]. If MPA is present, such repair can usually be performed by opening the atretic segment and performing a reconstruction with a transannular patch, avoiding a conduit, not unlike a standard tetralogy repair. Even in the presence of discontinuity between the RPA and LPA, establishment of a pulmonary artery confluence by direct anastomosis may allow complete repair in the neonatal period [29] (personal experience, C.I.T.).
In the presence of MAPCA(s) the surgical treatment of PA-VSD (types B and C) has been a lot more complex and challenging. Traditionally these patients were considered unrepairable, and were only operated on if severely symptomatic, performing a systemic-to-pulmonary shunt for severe cyanosis or banding of MAPCA(s) for severe congestive heart failure. Since the 1980s several groups have advocated a more aggressive surgical approach consisting of staged pulmonary unifocalization procedures which if successful, are followed by intracardiac repair [14–19]. This multistage approach has resulted in complete repair in 12% to 60% of the patients in 6 large published series [14–19]. Despite success in approximately half of the patients, this surgical approach has been questioned by some [14]. Recently, a single-stage midline unifocalization and repair was introduced by Reddy, Liddicoat and Hanley [20] and adopted by a few groups [20, 21, 30]. In the only comparison of the two philosophically different approaches, Tchervenkov and associates [21] have suggested the superiority of the single-stage approach. Their review however, was retrospective with the obvious limitations pertaining thereto. A prospective randomized study, although highly desirable and necessary, is probably unlikely at the present time due to the heavy bias that exists within each surgical group. The only hope that exists is probably the prospective collection of data with the proper stratification of the patients. It is unclear in most of the surgical series how many of the patients with PA-VSD, MAPCA(s) had NPA that may have had an impact on successful surgical repair. This is why we feel that the proposed classification of the patients with PA-VSD into types A, B, and C will allow for a more relevant comparison of cases according to the complexity of the pulmonary circulation.
PA-VSD treatment hierarchy level 1
PA-VSD treatment hierarchy level 2
PA-VSD treatment hierarchy level 2 comments
Palliation, systemic-to-pulmonary artery shunt
The various modifications of the systemic-to-pulmonary artery shunt procedures are described in detail in the "Single Ventricle" article of this supplement by Jacobs and colleagues and are not represented in detail in this article. Obviously, the hierarchical description of these procedures described in detail in the "Single Ventricle" article may be applied to certain forms of PA-VSD.
Transplantation, heart (can be entered in the database scheme for cardiomyopathy)
Cardiac transplantation can be coded separately in the database under the cardiomyopathy section as described in the cardiomyopathy article of this supplement.
Transplantation, heart + lung(s)
Heart + lung transplantation can be coded separately in the database under the cardiomyopathy section and the end-stage lung disease section as described in the cardiomyopathy and end-stage lung disease articles of this supplement.
Transplantation, lung(s)
Lung transplantation can be coded separately in the database under the end-stage lung disease section as described in the end-stage lung disease article of this supplement.
Transplantation, lung(s) + intracardiac repair
Lung transplantation can be coded separately in the database under the end-stage lung disease section as described in the end-stage lung disease article of this supplement. This coding would be combined with the coding from the specific section for the cardiac repair.
Important PA-VSD treatment modifiers
Additional comments regarding therapeutics
In addition to the above basic treatment options for PA-VSD, several other therapeutic issues must be addressed and coded in other areas of the database. First, a separate part of the database must allow for coding of incisions for this and all other diagnoses (median sternotomy, submammary incision, right thoracotomy, left thoracotomy, minimally invasive incisions, including partial sternotomy, parasternal incision, mini-thoracot- omy, etc). Second, a separate part of the database must allow for coding of cardiac incisions for this and all other diagnoses (aortotomy, pulmonary arteriotomy, right atriotomy, right ventriculotomy, left ventriculotomy, etc). Third, a separate module of the database must permit coding of patch materials (Dacron, Gore-Tex, bovine pericardium, autologous pericardium, glutaraldehyde fixated autologous pericardium, etc), conduit type, conduit materials, conduit size, and use of other biological or prosthetic materials.
Procedures directed at associated lesions (thymectomy, closure of patent foramen ovale, closure of atrial septal defect, etc) can be coded as additional or secondary procedures under the primary PA-VSD procedure.
Finally, details regarding management of cardiopulmonary bypass, myocardial protection, and associated issues will be recorded in another related and linked module of the database.
IV. Diagnosis and procedure short lists
V. Potential diagnostic related risk factors
Due to the extreme heterogeneity of the anatomic and morphologic features of patients with PA-VSD, potential diagnostic risk factors in addition to the presence or absence of MAPCA(s) and the neopulmonary artery size index have not been clearly identified. This is a general list of potential risk factors:
A. Preoperative
B. Intraoperative
C. postoperative
Database should include a list of postoperative variables common to all open cardiac surgical procedures.
VI. Outcome studies
References
This article has been cited by other articles:
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  K. Ozden, B. Mutlu, G. Kahveci, F. Bayrak, L. Saltik, S. Guran, and Y. Basaran Pulmonary atresia and ventricular septal defect with MAPCAs associated with right sided endocarditis and paradoxical embolic event Eur J Echocardiogr, August 1, 2007; 8(4): 292 - 295. [Abstract] [Full Text] [PDF]
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 K. J. Roche, R. Rivera, M. Argilla, N. R. Fefferman, L. P. Pinkney, H. Rusinek, and N. B. Genieser Assessment of Vasculature Using Combined MRI and MR Angiography Am. J. Roentgenol., April 1, 2004; 182(4): 861 - 866. [Abstract] [Full Text] [PDF]
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 |
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 S. K. Prasad, N. Soukias, T. Hornung, M. Khan, D. J. Pennell, M. A. Gatzoulis, and R. H. Mohiaddin Role of Magnetic Resonance Angiography in the Diagnosis of Major Aortopulmonary Collateral Arteries and Partial Anomalous Pulmonary Venous Drainage Circulation, January 20, 2004; 109(2): 207 - 214. [Abstract] [Full Text] [PDF]
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 M. Griselli, S. P. McGuirk, D. S. Winlaw, O. Stumper, J. V. de Giovanni, P. Miller, R. Dhillon, J. G. Wright, D. J. Barron, and W. J. Brawn The influence of pulmonary artery morphology on the results of operations for major aortopulmonary collateral arteries and complex congenital heart defects J. Thorac. Cardiovasc. Surg., January 1, 2004; 127(1): 251 - 258. [Abstract] [Full Text] [PDF]
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 M. Barbero-Marcial Classification of pulmonary atresia with ventricular septal defect Ann. Thorac. Surg., July 1, 2001; 72(1): 316 - 316. [Full Text] [PDF]
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C. I. Tchervenkov Classification of pulmonary atresia with ventricular septal defect: Reply Ann. Thorac. Surg., July 1, 2001; 72(1): 316 - 317. [Full Text] [PDF]
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