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 Online Discussion
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 Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhang, B.
Right arrow Articles by Li, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, B.
Right arrow Articles by Li, X.
Related Collections
Right arrow Congenital - cyanotic
Right arrowRelated Article

Ann Thorac Surg 2007;83:2176-2181
© 2007 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Unidirectional Monovalve Homologous Aortic Patch for Repair of Ventricular Septal Defect With Pulmonary Hypertension

Bo Zhang, MD, Shuming Wu, MD*, Jiali Liang, MD, Guangfu Zhang, MD, Guanhua Jiang, MD, Min Zhou, MS, Xiangling Li, MD

Department of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China

Accepted for publication February 2, 2007.

* Address correspondence to Dr Wu, Department of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China (Email: shumingwumd{at}126.com).


This article has been selected for the open discussion forum on the CTSNet Web Site: http://www.ctsnet.org/sections/newsandviews/discussions/index.html

 

   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: Severe pulmonary hypertension is a common complication of congenital cardiac defects with large left to right shunt, and the closure of a large ventricular septal defect (VSD) with elevated pulmonary vascular resistance (PVR) is associated with significant morbidity and mortality. A unidirectional monovalve homologous aortic patch was designed to close the large VSD with severe pulmonary hypertension in an effort to decrease the morbidity and mortality.

Methods: Twenty-seven patients (mean age, 15.0 ± 5.6 years) with large VSD with severe pulmonary hypertension (pulmonary vascular resistance, 15.2 ± 3.8 Wood units) were repaired with a unidirectional monovalve homologous aortic patch. According to body surface area and the preoperative arterial oxygen saturation, the monovalve homologous aortic patches were fenestrated on the aortic wall with a diameter of 4 to 8 mm.

Results: Two patients died of pulmonary hypertensive crisis and cardiac arrest postoperatively. All of the survival patients were followed up (5 months to 10 years) and the cardiopulmonary function was well improved with no late death. Obvious opening and closing of the monovalve was detected by early postoperative echocardiography in seven patients. A small amount of right to left shunt was detected in three patients three months after operation, and in two of them the shunt still existed three years after operation.

Conclusions: Closure of a large VSD in patients with severe pulmonary hypertension could be performed with low morbidity and mortality when a unidirectional monovalve homologous aortic patch was used and the long-term result was satisfactory.

A large ventricular septal defect (VSD) exposes the patient to risk of developing pulmonary artery hypertension and tends to worsen with age. The course of the disease is variable and depends on the size of the defect, the magnitude of the left-to-right shunt, and the pulmonary vascular response to increased pulmonary flow and pressure [1]. Pulmonary artery pressure is hyperkinetic in the early phase but may eventually become a fixed elevation associated with a fixed increase of pulmonary vascular resistance (PVR) [2]. The clinical symptomatic manifestations are decreased exercise tolerance, cyanosis, congestive heart failure, hemoptysis, and finally death (Eisenmenger syndrome).

In most industrialized countries closure of a large VSD is usually performed at an early age, before the onset of elevated PVR [3]. But in China, the diagnosis and surgical treatment in some patients with a large VSD is delayed because of problems in the health care system. This circumstance puts these patients at increased risk of significant morbidity and mortality when surgical closure of the VSD is performed. This report documents the experience of closure of the VSD in a group of patients with severe pulmonary hypertension using a unidirectional monovalve homologous aortic patch in an effort to reduce the risk of operation.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Twenty-seven patients with large VSD and pulmonary hypertension underwent surgical closure of their VSD with the unidirectional monovalve homologous aortic patch between May 1995 and January 2006. The study was approved by the Institutional Ethics Committee and all patients or their guardians provided informed consents. This group consisted of 16 males and 11 females. The patients ranged in age from 6 to 31 years with a mean age of 15.0 ± 5.6 years. Isolated VSD was found in 21 patients. In 2 patients, the VSD was a part of double-outlet right ventricle (DORV). Three patients were associated with patent ductus arteriosus and one was associated with aortopulmonary window (Table 1).


View this table:
[in this window]
[in a new window]

  		Table 1 Diagnosis and Concomitant Operation Performed
 
Preoperative Evaluation
Exertional dyspnea was presented in all patients and hemoptysis in five patients. Resting cyanosis was found in two patients and exertional cyanosis in 17. A systolic murmur was audible in 15 patients. Eleven patients were classified in New York Heart Association (NYHA) functional class II, 15 in class III, and one in class IV. Preoperative electrocardiogram was performed in all patients: there was right axis deviation in all patients, right ventricular hypertrophy in 24 patients, and biventricular hypertrophy in three patients. Chest roentgenogram showed dilation of the main pulmonary artery in all patients with a tumor-like enlargement in seven patients. Cardiothoracic ratio ranged from 0.44 to 0.67 (mean, 0.54 ± 0.06). All patients had preoperative echocardiography and cardiac catheterization for hemodynamic assessment. Bidirectional shunt through the intracardiac or extracardiac defect was present in all patients. The shunt ratio of pulmonary to systemic circulation ranged from 0.5 to 2.0 (mean, 1.2 ± 0.5). When catheterizations were performed, inhalation of 100% oxygen was routinely employed in all patients and pulmonary artery pressure had light decrease in 15 of these patients. Other managements to decrease PVR, including infusion of prostaglandin E1 and inhalation of nitric oxide, were not routinely employed. Total PVR ranged from 10.9 to 24.3 Wood units (mean, 15.2 ± 3.8 Wood units) and pulmonary vascular resistance index (PVRI) ranged from 8.5 to 16 U/m2 (mean, 12.4 ± 2.5 U/m2). Mean pulmonary artery pressure ranged from 65 to 98 mm Hg (mean, 81 ± 12 mm Hg), and in 16 patients it was higher than 80 mm Hg. The ratio of systolic pulmonary artery pressure to systolic systemic arterial blood pressure (SPAP/SABP) ranged from 0.8 to 1.2 (mean, 1.05 ± 0.10). Arterial oxygen saturation (SaO 2) ranged from 87% to 93% (mean, 89% ± 1%). Biopsy of the lung was performed in 15 patients.

Operation
Moderately hypothermic cardiopulmonary bypass (CPB, 28° to 32°C) with cold blood potassium cardioplegic arrest was used in all patients. There were 21 cases with perimembranous VSD, four cases with subpulmonary VSD, and two cases of DORV with subaortic VSD. All of the VSD were repaired with the unidirectional monovalve homologous aortic patch. The concomitant operation included ligation of ductus arteriosus in three cases and repair of aortopulmonary window in one case.

Homologous aortic conduit was harvested from the adults who had brain death less than six hours and preserved with liquid nitrogen. After being thawed and rinsed, the conduit was longitudinally divided between the right and left coronary leaflet. The right and left coronary leaflet were removed but the noncoronary leaflet and anterior mitral leaflet were reserved to form a large aortic patch with the monovalve (Fig 1). The patch was further tailored to the appropriate size according to the diameters of VSD and fenestrated above the nadir of the noncoronary leaflet with diameters ranging from 4 to 8 mm. The size of the fenestration was governed by the body surface area (BSA) and the preoperative SaO 2. A 4-mm fenestration was made if the patient’s BSA was less than 1 m2 and preoperative SaO 2 was higher than 91%; a 6-mm fenestration was made if the patient’s BSA was less than 1 m2 and preoperative SaO 2 was less than 91% or the patient’s BSA was larger than 1 m2 and preoperative SaO 2 higher than 91%; and an 8-mm fenestration was made if the patient’s BSA was larger than 1 m2 and preoperative SaO 2 was less than 91% (Table 2). The patch was sewn into place by using interrupted mattress sutures with a pledget (Fig 2). The noncoronary leaflet was faced to the left ventricular side with its free edge toward left ventricular outflow tract (Fig 3). Associated anomalies were corrected simultaneously. Lung biopsies were performed in 15 cases.


Figure 1
View larger version (65K):
[in this window]
[in a new window]

  		Fig 1. Illustration of double flap valve patch in profile tailored with homologous aorta. The noncoronary leaflet and anterior mitral leaflet were reserved to form a large aortic patch with monovalve. The patch was tailored to the appropriate size according to the diameters of the ventricular septal defect and fenestrated above the nadir of noncoronary leaflet with diameters ranging from 4 to 8 mm.

 

View this table:
[in this window]
[in a new window]

  		Table 2 The Standard for the Diameter of Fenestration
 

Figure 2
View larger version (84K):
[in this window]
[in a new window]

  		Fig 2. Illustration of the unidirectional monovalve homologous aortic patch in place.

 

Figure 3
View larger version (24K):
[in this window]
[in a new window]

  		Fig 3. Illustration of the double flap valve patch in profile with open valve. Lateral view of flap valve and ventricular septal defect patch. (LV = left ventricle; RV = right ventricle.)

 
Postoperative Management
A Swan-Ganz catheter (Swan-Ganz, Edwards Lifesciences, Irvine, CA) was inserted into the pulmonary artery after discontinuation of CPB. Pulmonary and systemic artery pressures were monitored continuously. The function of the unidirectional valve was examined by echocardiography. Prostaglandin E1 (Detai Corporation Ltd, Beijing, China) was routinely used to decrease pulmonary pressure. Mechanical ventilation time ranged from 16 to 51 hours (average, 28 hours). Echocardiographic assessment was performed in all patients. No aspirin and other anticoagulation were used. The follow-up was obtained through periodic consultation and echocardiographic assessment in the out-patient department.

Statistics
Variables were presented as mean ± standard deviation. Paired t tests were used to analyze the data. A significant difference was considered when the p value was less than 0.05.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
Postoperative Data
The postoperative systolic pulmonary artery pressure was 68 ± 15 mm Hg (p < 0.01 vs preoperative value). The SPAP/SABP was 0.78 ± 0.20:1 (p < 0.01 vs preoperative ratio). Fluctuations in SaO 2 were also observed when pulmonary artery pressures approached systemic pressures. Before discharge, the SaO 2 were 97% ± 2% under inhalation of oxygen. At follow-up, the SaO 2 were 95% ± 2% without inhalation of oxygen (significantly different from preoperative saturations p < 0.01) (Table 3).


View this table:
[in this window]
[in a new window]

  		Table 3 Preoperative and Postoperative Hemodynamic Status
 
The pathology of pulmonary vascular disease in 15 patients who were subjected to lung biopsy was graded by Heath-Edwards classification [4]. There were nine patients in grade II, five in grade III, and one in grade IV.

Two patients died after operation. One patient (18 years old; preoperative SPAP/SABP was 1.0; PVRI was 15 U/m2) with aortopulmonary window died of pulmonary hypertensive crisis and acute right heart failure at the seventh postoperative day. The other one (23 years old; preoperative SPAP/SABP was 1.1; PVRI was 14.3 U/m2) died at the eighteenth postoperative day because of sustained pulmonary hypertension and cardiac arrest resulting from excessive activities. The postoperative SPAP/SABP of these two patients were all above 0.95 and 1.0 (12 patients postoperative SPAP/SABP were larger than 0.9 in this group). The size of the fenestration was 6 mm (patient 1) and 8 mm (patient 2). Their lung biopsies were graded in class III and the postoperative echocardiographic assessment showed apparent valve movement and a small amount of right to left shunt. The operative mortality was 7.4%. Two patients who had pulmonary hypertensive crisis at the fifth and seventh postoperative day were cured with reintubation and mechanical ventilation for 42 to 51 hours.

Follow-Up Data
The follow-up time was 5 months to 10 years (average, 4.1 ± 1.3 years) without late death. Symptoms were relieved, cyanosis disappeared, and no hemoptysis was found in all survived patients. The heart function improved with 15 patients in NYHA functional class I, 9 patients in class II, and 1 patient in class III. In two patients, a small amount of right to left shunt still existed at three years final follow-up and their heart functions were in NYHA functional class II and III. A close relation was noted when the patients’ lung biopsy and their postoperative heart function were compared. In four patients with lung biopsy graded in class III or IV, their heart functions were in NYHA functional class II and III.

The postoperative echocardiographic assessment of the flap valve activity and right to left shunt were as follows: at the first postoperative day, no valve activity and shunt were found in three cases. Small valve activity but no right to left shunt was detected in 14 cases. Apparent valve movement and small amount of right to left shunt was detected in 10 cases. On the seventh postoperative day, apparent valve movement and a small amount of right to left shunt were detected in only three cases. In all patients, valve movement and small amount of right to left shunt could be induced by activity or cough on the seventh postoperative day. At three years final follow-up, a small amount of right to left shunt still remained in two cases (Table 4). No patch aneurysm was found in all patients.


View this table:
[in this window]
[in a new window]

  		Table 4 Postoperative Echocardiographic Assessment
 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
Pulmonary hypertension is a severe complication of large VSD. Historically, surgical closure of a large VSD with severe pulmonary hypertension was associated with high mortality rate [5–10]. Even in the present era, postoperative pulmonary hypertension remains a significant risk factor for morbidity and mortality [11, 12]. Acute congestive heart failure, pulmonary hypertensive crisis, and acute respiratory failure are the principal causes of postoperative death [13, 14]. Cardiopulmonary bypass, infusion of protamine, and other factors that could cause the release of vasoactive substances such as thromboxane A2 and catecholamine could result in pulmonary vasoconstriction and acute pulmonary hypertension [15–17]. Pulmonary hypertensive crisis can be associated with acute congestive heart failure, which is the main cause of death [18–21]. Fifteen years ago, we used nonfenestrated patch closure for children less than six years old with severe pulmonary hypertension and resistance, but the operative mortality was very high. In recent years, creation of an intracardiac shunt to prevent right ventricular failure has been used with success [22–24]. The modification allowed more patients to be extubated within 48 hours and with lower operative mortality. The double patch flap valve, made of Dacron or Gore-Tex graft and autologous pericardium, was designed to function like the fossa ovalis of the atrial septum [25] to allow some blood to flow from right to left while pulmonary artery pressure increases to prevent acute right heart failure [26]. When pulmonary artery pressure decreases, the unidirectional valve closes and blocks the left to right shunt. Finally, the pericardium adheres to the Dacron patch producing secure closure of the septal defect.

It was found that the double patch with flap valve made of Dacron or Gore-Tex graft and autologous pericardium was not level and smooth. Destruction of red blood cell and hemoglobinuria could be caused in some patients [24]. Moreover, when the pericardial flap valve was constructed, it was difficult to control the width of the pericardial valve and the distance from the free edge of the pericardial valve to the superior border of the fenestration. If the pericardial valve was too wide and too loose, and the distance from the free edge to the superior border of the fenestration was too short, a small amount of left to right shunt would exist after operation. On the contrary, the valve might press close to the patch, and thus the flap valve would not be opened easily. Because the rough surface of pericardium was easy to adhere to the Dacron patch, it would be closed up in the early stage postoperatively. We observed that the flap valves of pericardium were always closed up in 7 to 10 days after operation and lost its shunt function. In addition, some reports indicated that the flap valve of pericardium could crinkle and was unable to cover up the fenestration. Left to right shunt would be persistent while the right ventricular pressure decreased [27]. Because of the problems mentioned above, the fenestrated monovalve homologous aortic patch was chosen to close the VSD with severe pulmonary hypertension. The results demonstrated that the flap valve of fenestrated homologous aortic patch had virtues of good activity, integrity, fitting to physiology, and worked well. The follow-up echocardiography result showed that in two cases, the flap valve still worked well thee years after operation. This technique provides persistent right ventricle unloading while pulmonary pressure increases (resulting from activity, hypoxia, etc).

As to the diameter of fenestration, there is not a wide accepted standard at present. In the literature, it ranges from 3 mm to 10 mm [22, 24, 27]. The standard we adopted is that the diameter of fenestration was governed by patients’ BSA and the preoperative SaO 2 because the patients’ BSA and the preoperative SaO 2 are closely related to the actual amount of right to left shunt. We found that 4 to 8 mm fenestration was large enough to unload the right ventricle without significant SaO 2 decrease caused by a too large right to left shunt. The postoperative echocardiography showed that the flap valve worked well in the early and late stages.

According to our experience, it was important that the fenestration should be made at the bottom of the noncoronary sinus. In vitro study, the distance from the bottom to the free edge of the noncoronary valve ranged from 11 mm to 14 mm. If the fenestration was too high, the free edge of the noncoronary leaflet would be herniated from the fenestration and it was inevitable that left to right shunt would exist while the right ventricular pressure decreased postoperatively. If the length of the noncoronary leaflet was less than 12 mm, a transverse oval hole should be made or in another choice, another homologous aortic patch with a larger noncoronary leaflet should be chosen. The distance from the superior border of the fenestration to the free edge of the noncoronary leaflet should not be less than 5 mm. Thus, the noncoronary leaflet could fully cover the fenestration of the aortic wall and left to right shunt could be avoided. No left to right shunt was found in this group.

Current wisdom suggests that operation to close the septal defect should not be performed when PVRI is more than 12 U/m2, the ratio of pulmonary to system flow is less than 1.5, and oxygen saturation is less than 90%. However, recent reports show that patients with pulmonary hypertension improved their hemodynamics and exercise capability after closure of the septal defect. It implies that pulmonary vascular remodeling might take place [22–24]. Thus, the indication of surgical intervention on VSD with severe pulmonary hypertension should be changed with the use of a fenestrated unidirectional flap valve patch. We subjectively felt that the maintenance of hemodynamic condition was quite easy in most patients of this group. Postoperative echocardiography demonstrated that the valve opened easily and blood flowed from right to left when pulmonary artery pressure was higher than systemic artery pressure, which might reduce the right ventricular load. As cardiac function improved and hemodynamics became stable (1 to 12 weeks after operation), the flap valve gradually adhered to the aortic wall. In only two cases, a small amount of right to left shunt still existed at three years final follow-up, but no cyanosis was found. The patients’ heart functions were in NYHA class II and III.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Wells WJ, Lindesmith GG. Ventricular septal defectIn: Arciniegas E, editor. Pediatric cardiac surgery. Chicago, Illinois: Year Book Medical; 1985. pp. 141-153.
  2. Arciniegas E. Ventricular septal defectIn: Glen WWL, editor. Thoracic and cardiovascular surgery. East Norwalk, Connecticut: Appleton-Century-Crofts; 1983. pp. 745-756.
  3. Bando K, Turrentine MW, Sharp TG, et al. Pulmonary hypertension after operations for congenital heart disease: analysis of risk factors and management J Thorac Cardiovasc Surg 1996;112:1600-1609.[Abstract/Free Full Text]
  4. Heath D, Edwards JE. The pathology of hypertensive pulmonary vascular disease: a description of six grades of structural changes in the pulmonary artery with special reference to congenital cardiac septal defects Circulation 1958;18:533-547.[Medline]
  5. Frontera-Izquierdo P, Cabezuelo-Huerta G. Natural and modified history of isolated ventricular septal defect: a 17-year study Pediatr Cardiol 1992;13:193-197.[Medline]
  6. Kirklin JW, Barratt-Boyes BG. Cardiac surgery. New York, New York: John Wiley & Sons; 1986. pp. 599.
  7. Yamaki S, Mohri H, Haneda K, Endo M, Akimoto H. Indication for surgery based on lung biopsy in cases of ventricular septal defect and/or patent ductus arteriosus with severe pulmonary hypertension Chest 1989;96:31-39.[Medline]
  8. Friedli BG, Kidd BSL, Mustard WT, Keith JD. Ventricular septal defect with increased pulmonary vascular resistance Am J Cardiol 1974;33:403-409.[Medline]
  9. John S, Korula R, Jairaj PS, et al. Results of surgical treatment of ventricular septal defect with pulmonary hypertension Thorax 1983;38:279-283.[Abstract]
  10. Kannan BR, Sivasankarans, Tharakan JA, et al. Long-term outcome of patients operated for large ventricular septal defects with increased pulmonary vascular resistance Indian Heart J 2003;55:161-166.[Medline]
  11. Bando K, Turrentine MW, Sun K, et al. Surgical management of complete atrioventricular septal defects J Thorac Cardiovasc Surg 1995;110:1543-1554.[Abstract/Free Full Text]
  12. Carotti A, Albanese SB, Minniti G, et al. Increasing experience with integrated approach to pulmonary atresia with ventricular septal defect and major aortopulmonary collateral arteries Eur J Cardiothorac Surg 2003;23:719-726.[Abstract/Free Full Text]
  13. Harrison AM, Cox AC, Davis S, et al. Failed extubation after cardiac surgery in young children: incidence, etiology, risk factors Pediatr Crit Care Med 2002;3:148-152.[Medline]
  14. Brown KL, Ridout DA, Goldman AP, et al. Risk factors for long intensive care unit stay after cardiopulmonary bypass in children Crit Care Med 2003;31:28-33.[Medline]
  15. De Souza CA, Spyt TJ. Release of vasoactive substance during cardiopulmonary bypass Ann Thorac Surg 1992;56:397-398.
  16. Komai H, Yamamoto F, Tanaka K, et al. Increased lung injury in pulmonary hypertensive patients during open heart operations Ann Thorac Surg 1993;55:1147-1152.[Abstract]
  17. Hopkins RA, Bull C, Haworth SG, et al. Pulmonary hypertensive crises following surgery for congenital heart defects in young children Eur J Cardiothorac Surg 1991;5:628-634.[Abstract]
  18. Hallman GL, Cooley DA, Wolfe RR, et al. Surgical treatment of ventricular septal defect associated with pulmonary hypertension J Thorac Cardiovasc Surg 1964;48:588-600.[Medline]
  19. Ikawa S, Shimazaki Y, Nakano S, et al. Pulmonary vascular resistance during exercise late after repair of large ventricular septal defects J Thorac Cardiovasc Surg 1995;109:1218-1224.[Abstract/Free Full Text]
  20. Wessel DL. Current and future strategies in the treatment of childhood pulmonary hypertension Progr Pediatr Cardiol 2001;12:289-318.
  21. Schulze-Neick I, Li J, Penny DJ, Redington AN. Pulmonary vascular resistance after cardiopulmonary bypass in infants: effect on postoperative recovery J Thorac Cardiovasc Surg 2001;121:1033-1039.[Abstract/Free Full Text]
  22. Novick WM, Gurbuz AT, Watson DC, et al. Double patch closure of ventricular septal defect with increased pulmonary vascular resistance Ann Thorac Surg 1998;66:1533-1538.[Abstract/Free Full Text]
  23. Novick WM, Sandoval N, Lazorhysynets VV, et al. Flap valve double patch closure of ventricular septal defects in children with increased pulmonary vascular resistance Ann Thorac Surg 2005;79:21-28.[Abstract/Free Full Text]
  24. Zhou Q, Lai Y, Wei H, Song R, Wu Y, Zhang H. Unidirectional valve patch for repair of cardiac septal defects with pulmonary hypertension Ann Thorac Surg 1995;60:1245-1249.[Abstract/Free Full Text]
  25. Ad N, Barak J, Birk E, Diamant S, Vidne BA. A one-way, valved, atrial septal patch in the management of postoperative right heart failure: an animal study J Thorac Cardiovasc Surg 1994;108:134-139.[Abstract/Free Full Text]
  26. Robicsek F. Flap-valve closure of ventricular septal defects Ann Thorac Surg 2006;81:788.[Free Full Text]
  27. Pang XY, Li WH, Song HM, et al. Application of one way valved patch in treatment of patients with congenital heart disease with severe pulmonary hypertension Natl Med J China 2004;84:888-889.

Related Article

Invited commentary
Alan G. Magee
Ann. Thorac. Surg. 2007 83: 2181. [Extract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
S. K. Choudhary, S. Talwar, and B. Airan
A simple technique of unidirectional valved patch for closure of septal defects.
J. Thorac. Cardiovasc. Surg., November 1, 2007; 134(5): 1357 - 1358.
[Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
A. G. Magee
Invited commentary
Ann. Thorac. Surg., June 1, 2007; 83(6): 2181 - 2181.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Online Discussion
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 Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhang, B.
Right arrow Articles by Li, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, B.
Right arrow Articles by Li, X.
Related Collections
Right arrow Congenital - cyanotic
Right arrowRelated Article

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