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


     

 Click here to read this article as a CME activity

Ann Thorac Surg 2009;87:548-553. doi:10.1016/j.athoracsur.2008.10.024
© 2009 The Society of Thoracic Surgeons
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 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):
Cheul Lee
Chang-Ha Lee
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 Kim, S.-J.
Right arrow Articles by Lee, C.-H.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Kim, S.-J.
Right arrow Articles by Lee, C.-H.
Related Collections
Right arrow Congenital - cyanotic
Right arrowRelated Article

Original Articles: Pediatric Cardiac

Inclusion of Hepatic Venous Drainage in Patients with Pulmonary Arteriovenous Fistulas

Soo-Jin Kim, MDa, Eun-Jung Bae, MDc,*, Jae-Young Lee, MDa, Hong-Gook Lim, MDb, Cheul Lee, MDb, Chang-Ha Lee, MDb

a Department of Pediatric Cardiology, Sejong General Hospital, Bucheon, Korea
b Department of Cardiac Surgery, Sejong General Hospital, Bucheon, Korea
c Department of Pediatrics, Seoul National University College of Medicine, Seoul National University Children's Hospital, Seoul, Korea

Accepted for publication October 14, 2008.

* Address correspondence to Dr Bae, Department of Pediatrics, Seoul National University College of Medicine, Seoul National University Children's Hospital, 28 Yeongeon-dong, Jongno-Gu, Seoul, 110-744, Korea (Email: eunjbaek{at}snu.ac.kr).


Pediatric cardiac surgery: The Annals of Thoracic Surgery CME Program is located online at http://cme.ctsnetjournals.org. To take the CME activity related to this article, you must have either an STS member or an individual non-member subscription to the journal.

 

   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: It is well known that hepatic vein (HV) inclusion can ameliorate cyanosis in patients with pulmonary arteriovenous fistulas (PAVFs) during the sequence of Fontan type repair. Previously, we reported that most patients with bidirectional cavopulmonary shunt (BCPS) have clinical or subclinical evidence of a right to left shunt through PAVFs.

Methods: We studied 33 patients who already had clinical and subclinical PAVFs after BCPS. All patients have taken Fontan completion with HV inclusion. The state of PAVFs was reevaluated by pulmonary angiogram, contrast echocardiography, and lung scintigraphy 7.7 ± 2.4 years after HV inclusion.

Results: After Fontan completion, the mean oxygen saturation increased from 80.2 ± 7.4% to 91.5 ± 9.8% in the entire cohort. Moreover, the amount of right-to-left shunting through the PAVFs, measured by lung scintigraphy, was decreased from a mean of 23.8 ± 15.1 to 13.0 ± 8.2%. The degree of severity, for most patients, was decreased as demonstrated by contrast echocardiography. However, 5 patients (16.7%) showed persistent PAVFs, even after the HV inclusion. They all had left isomerism with azygous continuation of the IVC and the conduit was positioned on the contralateral side to the SVC with azygous drainage.

Conclusions: Most PAVFs regressed after Fontan completion. Left isomerism with azygous continuation of the IVC had risk for persistent PAVFs when the HV conduit was positioned at the contralateral side to the SVC receiving the azygous drainage. Therefore, appropriate design avoiding unilateral streaming of HV flow should be considered for HV inclusion surgery.

The bidirectional cavopulmonary shunt (BCPS) has been increasingly implemented as a preparatory procedure for a Fontan operation. The BCPS provides an excellent first or second stage palliation in patients with a functional single ventricle and has resulted in more favorable post-Fontan outcome with lower surgical mortality rates compared with that of the nonstaged approach [1–3]. The development of pulmonary arteriovenous fistulas (PAVFs) was first noticed during the follow-up of patients who had undergone a Glenn shunt [4, 5]. Although physiologically similar to the classic Glenn operation, current methods of the BCPS have been shown to cause bilateral rather than ipsilateral PAVFs under certain conditions, but at a lower incidence. The lower incidence of the BCPS may be partly related, being that the BCPS is usually performed as one part of a staged approach, which was followed relatively quickly by final completion of the Fontan operation. The hepatic vein (HV) inclusion to pulmonary circulation has been reported to improve cyanosis in patients with PAVFs. We reported previously that most patients with the BCPS showed subclinical evidence of right to left intrapulmonary shunting [6]. However, the consequences of this pulmonary vascular abnormality after a BCPS have not determined clearly.

The purpose of this study was to determine the effect of redirecting the HV effluent to the pulmonary circulation in the patients who already had PAVFs.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Thirty-three patients with evidence of intrapulmonary shunting after a BCPS were enrolled in this study. Eleven patients had clinical PAVFs and 22 had subclinical PAVFs. Twenty patients were female and 13 were male. The systemic venous anatomy was notable for a bilateral superior vena cava (SVC) in 12 patients, a contralateral SVC to inferior vena cava (IVC) in 5, and IVC interruption with azygous continuation in 15 patients. Surgical procedures prior to the BCPS had been performed in 17 patients, primarily to augment (n = 9) or limit (n = 8) pulmonary blood flow, or to augment the ascending aorta and aortic arch (n = 2).

Eighteen patients underwent a BCPS at a median age of 8.5 months (range, 3 to 28). Fifteen patients underwent the Kawashima operation (BCPS in patients with IVC interruption) at a median age of 20 months (range, 7 to 124) and 14 patients had left isomerism (polysplenia syndrome). Twelve patients who had bilateral SVC underwent a bilateral BCPS. Eight patients had pulsatile pulmonary blood flow. The median systemic arterial oxygen saturation (SaO 2) at the time of PAVFs diagnosis was 80.2% (range, 60% to 90%). Eleven patients (33.3%) had clinical PAVFs and 21 (66.7%) had subclinical PAVFs before the Fontan operation. Among the 11 patients with the clinical PAVFs, 7 patients (63.6%) had an interrupted IVC and 9 patients (81.8%) had the heterotaxy syndrome. The Sejong General Hospital Institutional Review Board reviewed and approved this study and individual consent was waived.

Diagnosis of the PAVFs
Contrast echocardiography, lung scincitigraphy, and pulmonary angiography were performed for the diagnosis of PAVFs before and after HV inclusion. To exclude venovenous collaterals and to evaluate the status of PAVFs on each side of the lung separately, we did SVC venography and contrast echocardiography at each branch pulmonary artery.

According to our previous study [6], clinical PAVFs were considered by the following: (1) a systemic arterial desaturation of 80% or less on room air, without any evidence of parenchymal lung disease; and (2) one or more positive findings on one or more of the three diagnostic modalities (an extrapulmonary shunt fraction greater than 11% on technetium-99-labeled macroaggregated albumin (99mTcMAA) lung scintigraphy, a positive contrast echocardiogram, or positive pulmonary angiographic results). In addition, we defined the subclinical PAVFs as systemic arterial saturation more than 80% and one or more signs of intrapulmonary shunting on one or more of the three modalities used for the diagnosis of PAVFs as described previously.

After HV inclusion, we considered the PAVFs completely resolved when the Sa was greater than 90% on room air and when there was no evidence of intrapulmonary shunting by the diagnostic modalities used for diagnosing the PAVFs.

Statistical Analysis
The SPSS statistical program for Windows version 14 (SPSS, Chicago, IL) was used to perform the data analysis. Data are expressed as mean, median, and range and a p value less than 0.05 was considered statistically significant. Risk factors were evaluated by multivariate analysis for the development of PAVFs and included the following: the age at the BCPS (more or less than 12 months), the interval from the BCPS to HV inclusion (more and less than 2 years), the presence of pulsatile blood flow during the BCPS stage, heterotaxy, left isomerism, IVC interruption, follow-up duration, weight at surgery, gender, previous cardiac operations, concomitant cardiac operation, and presence of a bilateral or contralateral SVC. The analysis was performed with the Cox proportional hazards regression model.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
Before the HV inclusion procedure, the median SaO 2 was 81% (range, 60 to 90), the median mean pulmonary arterial pressure was 12 mm Hg (range, 8 to 20), the pulmonary vascular resistance was 1.2 WU (range, 0.3 to 2.4 WU) and the ventricular end-diastolic pressure was 9 mm Hg (range, 5 to 20). In the clinical PAVFs group, the median SaO 2was 72% (range, 60% to 87%), the median mean pulmonary arterial pressure was 12 mm Hg (range, 9 to 20 mm Hg), the pulmonary vascular resistance was 0.7 WU (range, 0.3 to 2 WU), the ventricular end-diastolic pressure was 9 mm Hg (range, 6 to 20 mm Hg), and the hemoglobin level was 15.2 g/dL (range, 13.5 to 19.6 g/dL).

All 33 patients with intrapulmonary right-to-left shunting underwent a Fontan completion using an extracardiac conduit between February 1997 and June 2004. The HV inclusion procedures were done at a median age of 41 months (range, 22 to 143). A time interval between a BCPS and a HV inclusion procedure was 23 months (range, 11to 133). An expanded polytetrafluoroethylene tube conduit (Gore-tax stretch vascular graft; W. L. Gore & Assoc, Flagstaff, AZ) was used. The median diameter of the conduit was 18 mm (range, 16 to 22 mm), the indexed mean diameter of the conduit was 30.9 ± 7.2 mm/m2, and the indexed mean area of the conduit was 449.5 ± 104.0 mm2/m2 for the BCPS patients. The median diameter of the conduit was 17 mm (range, 14 to 22 mm), the indexed mean diameter of the conduit was 22.2 ± 4.1 mm/m2, and the indexed mean area of the conduit was 306.4 ± 78.9 mm2/m2 for the Kawashima patients. We chose a smaller-sized graft for previous Kawashima procedures (p = 0.000 for the diameter and p = 0.000 for the area of the conduit). Most of the patients who had clinical PAVFs (8 of 11) did not require fenestration. Concomitant surgical procedures are shown in Table 1.


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

  		Table 1 Additional Procedures Done With the Fontan Operation (18 Patients, 23 Procedures)
 
The median duration of hospitalization after the HV inclusion was 19 days (range, 10 to 74 days). The postoperative central venous pressure was 15 mm Hg (range, 11 to 18) and the median duration of the intensive care unit stay was 4.5 days (range, 1 to 24 days). The median SaO 2 in room air at the time of patient discharge was 89.6% (range, 61% to 100%). There was one hospital death. The patient died immediately after HV inclusion, with severe cyanosis, low cardiac output secondary to poor ventricular function, and ultimately multiorgan failure. Two late deaths were not directly related to the PAVFs. One was due to a protein-losing enteropathy after 25 months and the other was a sudden death four years after the Fontan operation. All surviving patients (n = 30) had close follow-up at a median duration of 7.7 years (range, 3.1 to 10.2 years). All patients underwent contrast echocardiography, pulmonary angiogram, and lung scintigraphy.

After the HV inclusion procedure, the mean SaO 2 increased from 80.2 ± 7.4% (range, 60% to 90%) to 91.5 ± 9.8% (range, 54% to 98%) in all patients (p = 0.000) and from 73.9 ± 9.4% (range, 60% to 87%) to 91.1 ± 13.2%(range, 54% to 98%) in the clinical PAVFs group (p = 0.031) (Fig 1). The hypoxemia had gradually improved until median 4 months (range, 1 to 13 months) after discharge. Moreover, the amount of right-to-left shunting through the PAVFs, detected by lung scintigraphy, was decreased from a mean of 23.8 ± 15.1% (range, 7% to 63%) to 13.0 ± 8.2% (range, 4% to 33%) in all patients (p = 0.001) (Fig 2). The severity score on contrast echocardiography in the whole cohort was improved as shown in Figure 3.


Figure 1
View larger version (27K):
[in this window]
[in a new window]

  		Fig 1. Change of oxygen saturation after the hepatic vein inclusion in patients who had pulmonary arteriovenous fistula. Line graph depicting systemic arterial saturation (SaO2) at the time PAVFs were diagnosed, at the time of hospital discharge after HV inclusion, and at most recent follow-up. Solid symbols (bullet) and lines represent patients with clinical PAVFs and open symbols ({circ}) with dashed lines represent patients with subclinical PAVFs before Fontan procedure. (HV = hepatic vein; PAVF = pulmonary arteriovenous fistula.)

 

Figure 2
View larger version (24K):
[in this window]
[in a new window]

  		Fig 2. Change in the lung perfusion scan after hepatic vein inclusion in patients who had pulmonary arteriovenous fistula (PAVF).

 

Figure 3
View larger version (17K):
[in this window]
[in a new window]

  		Fig 3. Change in the contrast echocardiogram after hepatic vein inclusion in patients who had pulmonary arteriovenous fistula. (A) Clinical PAVFs. (B) Subclinical PAVFs. (PAVM = pulmonary arteriovenous malformation; PAVFs = pulmonary arteriovenous fistulas.)

 
Among the patients with clinical PAVFs, 9 patients improved and 1 patient (10%) had persistent PAVFs (Fig 4A). Among the patients with subclinical PAVFs, 16 patients improved and four patients (20%) showed persistent clinical or subclinical PAVF (Fig 4B). All 5 patients who showed persistent PAVFs even after HV inclusion procedure had left isomerism with an interrupted IVC and had the conduit position on the contralateral side to the SVC with azygous drainage (Fig 5; Table 2). The PAVFs persisted even after Fontan completion and were unilateral in the ipsilateral side of azygous drainage.


Figure 4
View larger version (20K):
[in this window]
[in a new window]

  		Fig 4. Follow-up of pulmonary arteriovenous fistulae after hepatic vein inclusion. (A) Clinical PAVFs. (B) Subclinical PAVFs. (PAVFs = pulmonary arteriovenous fistulas.)

 

Figure 5
View larger version (20K):
[in this window]
[in a new window]

  		Fig 5. The anatomy of the systemic veins and the Fontan conduit in 5 patients with persistent pulmonary arteriovenous fistula (PAVF). Dots indicate PAVFs. (PAVFs = pulmonary arteriovenous fistulas.)

 

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

  		Table 2 Anatomy and Outcome of Pulmonary Arteriovenous Fistulae in Patients With Left Isomerism
 
Among them, 4 patients who had severe hypoxia underwent a Fontan revision with rerouting of the hepatic venous flow to the azygous vein to reverse the progression of the severe PAVFs in 10.3 years (range, 7.8 to 12.3 years) after an initial BCPS, and 5.5 years (range, 2.4 to 11.3 years) after Fontan completion. The redirection procedure is as follows. After the extracardiac conduit was divided and its superior end was oversewn, a Gore-Tex tube graft was interposed between conduit stump and the azygous vein. One underwent coil embolization for one markedly dilated the pulmonary arteriovenous malformation, which appeared to be an irreversible form of PAVF, before the hepatic vein-azygous vein rerouting procedure, and two patients underwent balloon angioplasty for central pulmonary artery stenosis to increase hepatic flow to the lung with the PAVFs. However, even these procedures, their SaO 2 did not show significant improvement (73% to 79%; pre- and post-Fontan revision, respectively) and it suggests that the status of their PAVFs already was irreversible.

The univariate analysis demonstrated the interrupted IVC (p = 0.000), heterotaxy syndrome (p = 0.004), left isomerism (p = 0.000), and presence of bilateral or contralateral SVC to HV (p = 0.005) as predictors of persistent PAVFs even after HV inclusion. The multivariate analysis demonstrated interrupted IVC (p = 0.000) as a predictor of persistent PAVFs even after HV inclusion.


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
The association of PAVFs with anomalous systemic venous drainage, in patients with congenital cardiopulmonary disease, was described in 1965 [7]. It is well-documented in patients with interrupted IVC. Several factors have been postulated as the cause for this deleterious communication. Recent reports support the concept that the presence of left isomerism or an interrupted IVC, and exclusion of the hepatic venous blood from the pulmonary circulation, are two major risk factors [8].

It was not until 1994, when Srivastava and colleagues [9] conclusively demonstrated that PAVFs were due to the absence of a "hepatic factor" or a "mesenteric factor" 10], and that an unidentified element in the hepatic venous drainage inhibited the recruitment and dilatation of preexisting pulmonary arteriovenous connections. Duncan and Desai [11] further elaborated the mechanisms for the etiology of PAVFs and demonstrated that they were likely due to greatly increased numbers of abnormal and dilated channels, and suggested an angiogenic process as well as recruitment of preexisting channels that dilated when there was an absence of hepatic venous return to the pulmonary circulation. Alternatively, these authors hypothesized that the liver may be responsible for the degradation of a vasodilating substance that is not removed after a BCPS.

Clinically important PAVFs may develop in up to 52.4% of patients after the Kawashima operation; it can cause clinically severe arterial oxygen desaturation and heart failure [12]. In addition, we noted clinically important PAVFs in up to 50% of patients after the Kawashima operation in a previous study [6] and recommended early detection of PAVFs using contrast echocardiography or lung scintigraphy in patients with left isomerism and an interrupted IVC who had a Kawashima procedure. We also demonstrated [6] that subclinical PAVFs were significantly prevalent in patients with a BCPS. We ultimately performed Fontan completion within 1 to 2 years of the Kawashima operation in all patients with left isomerism and azygous continuation of the IVC.

Surgical redirection of the hepatic venous blood flow to the pulmonary arterial circulation causes PAVFs to regress [13, 14]. The Fontan procedure reliably leads to regression of the PAVFs that occur after a BCPS [9]. Shah and colleagues [14] and Duncan and Desai [11] corroborated these findings and showed that PAVFs would regress within 7 months after Fontan completion. By contrast, several reports demonstrated the development of PAVFs after the Fontan procedure [10, 15]. In these cases, it was closely associated with the uneven perfusion of the hepatic venous drainage and the excluded HV blood flow from the pulmonary circulation similar to TCPS.

In our study, the hypoxia improved within 2 months to 2 years after cavopulmonary incorporation of the hepatic vein and not only clinical PAVFs but also subclinical PAVFs resolved in the majority of patients after the HV inclusion. The time course of improved SaO 2 after the HV inclusion was inconsistent with the explanation that hypoxia improved simply because the hepatic right-to-left shunting was eliminated; the early postoperative SaO 2 was very low in most patients, improving by the time of hospital discharge to some extent, and only gradually increasing to above 90% over the next month to year. Elimination of the hepatic right-to-left shunting alone should have improved the hypoxemia immediately after the redirection of the HV flow, whereas resolution of the PAVFs might be expected to occur gradually. Fenestration of the HV pathway may prevent sufficient HV flow from reaching the pulmonary circulation, and should be limited to patients with specific indications. Fortunately, in our study most of the patients with PAVFs did not require fenestration because the PAVF itself may have lowered the pulmonary resistance, and may function as a fenestration after the Fontan completion during the early postoperative period.

However, 5 patients had severe hypoxemia due to the PAVFs even after the HV inclusion procedure in our study. They all had left isomerism with azygous continuation of the IVC and had the HV conduit on the contralateral side to the SVC receiving azygous drainage. This anatomic configuration caused streaming of the flow in the HV-PA pathway such that the HV blood flowed exclusively or primarily to one lung, in which the PAVFs had resolved, while the PAVFs persisted in the contralateral lung. Even the presence of bilateral SVCs could not prevent streaming of the hepatic venous blood to one lung in 3 patients with bilateral SVCs in our study. Even if bilateral SVCs are present, the SVC receiving the azygous return carries at least 50% of the upper body venous return and essentially all of the lower body and nonsplanchnic abdominal venous return. If this SVC was contralateral or had only small offset to the HV conduit, there was no mechanical impetus for the HV effluent to flow to the lung on that side [16].

As investigators have shown using in vitro and computational simulations, offset between the IVC-PA and SVC-PA connections can produce complete or near-complete streaming of the HV effluent to the ipsilateral lung [17]. It is therefore essential to design the hepatic venous channel in relation to the anastomosis between the SVC and pulmonary artery. However, sometimes it is not easy to achieve balanced perfusion of the hepatic venous blood to the lungs bilaterally in patients with left isomerism with an interrupted IVC. The reason is that the position of the conduit may be inevitably in the contralateral side of azygous continuation, if the main mass of ventricle is in the same side of the azygous continuation. In this anatomy, a more medially connected initial BCPS would facilitate more balanced perfusion after Fontan completion.

The presence of the conduit position on the side contralateral to the SVC with azygous drainage, or the side with a solitary SVC without interrupted IVC, was not associated with resolution of hypoxemia after the HV inclusion. The options for redirection of the hepatic venous drainage include rerouting of the hepatic veins to the azygous vein as an attractive option [18]. In addition, when the resolution of the PAVF does not occur, even after the HV inclusion, the large PAVFs may be embolized at catheterization or surgical resection may be required.

In conclusion, most patients who had PAVFs improved after inclusion of the hepatic venous flow to the pulmonary circulation. However, some patients may have hypoxemia due to persistent PAVFs if they had streaming of the hepatic venous flow into the unilateral pulmonary artery even after the HV inclusion. These cases had left isomerism with azygous continuation of the IVC, and had the conduit position at the contralateral side to the SVC receiving the azygous drainage. Furthermore it is essential to design a BCPS and hepatic venous channel to achieve the best offset from the initial stage of palliation. Although there are limited experiences on the direct anastomosis of the hepatic veins to the azygous vein, the primary Kawashima operation may be combined with a direct anastomosis of the hepatic veins to the azygous vein as a complete Fontan operation, especially for the high risk patients for persistent PAVFs after conventional Fontan procedure.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Castaneda AR. From Glenn to Fontan. A continuing evolution. Circulation 1992;86:80-84.
  2. Jonas RA. Indications and timing for the bidirectional Glenn shunt versus the fenestrated Fontan circulation J Thorac Cardiovasc Surg 1994;108:522-524.[Free Full Text]
  3. Lamberti JJ, Spicer RL, Waldman JD, et al. The bidirectional cavopulmonary shunt J Thorac Cardiovasc Surg 1990;100:22-29.[Abstract]
  4. Mathur M, Glenn WW. Long-term evaluation of cava-pulmonary artery anastomosis Surgery 1973;74:899-916.[Medline]
  5. McFaul RC, Tajik AJ, Mair DD, Danielson GK, Seward JB. Development of pulmonary arteriovenous shunt after superior vena cava-right pulmonary artery (Glenn) anastomosis. Report of four cases. Circulation 1977;55:212-216.[Abstract/Free Full Text]
  6. Kim SJ, Bae EJ, Cho DJ, et al. Development of pulmonary arteriovenous fistulas after bidirectional cavopulmonary shunt Ann Thorac Surg 2000;70:1918-1922.[Abstract/Free Full Text]
  7. Anabtawi IN, Ellison RG, Ellison LT. Pulmonary arteriovenous aneyrysms and fistulas. Anatomical variations, embryology, and classification. Ann Thorac Surg 1965;1:277-285.
  8. Kawashima Y. Cavopulmonary shunt and pulmonary arteriovenous malformations Ann Thorac Surg 1997;63:930-932.[Free Full Text]
  9. Srivastava D, Preminger T, Lock JE, et al. Hepatic venous blood and the development of pulmonary arteriovenous malformations in congenital heart disease Circulation 1995;92:1217-1222.[Abstract/Free Full Text]
  10. Uemura H, Yagihara T, Hattori R, Kawahira Y, Tsukano S, Watanabe K. Redirection of hepatic venous drainage after total cavopulmonary shunt in left isomerism Ann Thorac Surg 1999;68:1731-1735.[Abstract/Free Full Text]
  11. Duncan BW, Desai S. Pulmonary arteriovenous malformations after cavopulmonary anastomosis Ann Thorac Surg 2003;76:1759-1766.[Abstract/Free Full Text]
  12. Kim SJ, Kim WH, Lim HG, Lee CH, Lee JY. Improving results of the Fontan procedure in patients with heterotaxy syndrome Ann Thorac Surg 2006;82:1245-1251.[Abstract/Free Full Text]
  13. Knight WB, Mee RB. A cure for pulmonary arteriovenous fistulas? Ann Thorac Surg 1995;59:999-1001.[Abstract/Free Full Text]
  14. Shah MJ, Rychik J, Fogel MA, Murphy JD, Jacobs ML. Pulmonary AV malformations after superior cavopulmonary connection: resolution after inclusion of hepatic veins in the pulmonary circulation Ann Thorac Surg 1997;63:960-963.[Abstract/Free Full Text]
  15. Moore JW, Kirby WC, Madden WA, Gaither NS. Development of pulmonary arteriovenous malformations after modified Fontan operations J Thorac Cardiovasc Surg 1989;98:1045-1050.[Abstract]
  16. McElhinney DB, Kreutzer J, Lang P, Mayer Jr JE, del Nido PJ, Lock JE. Incorporation of the hepatic veins into the cavopulmonary circulation in patients with heterotaxy and pulmonary arteriovenous malformations after a Kawashima procedure Ann Thorac Surg 2005;80:1597-1603.[Abstract/Free Full Text]
  17. Walker PG, Howe TT, Davies RL, Fisher J, Watterson KG. Distribution of hepatic venous blood in the total cavo-pulmonary connection: an in vitro study Eur J Cardiothorac Surg 2000;17:658-665.[Abstract/Free Full Text]
  18. Baskett RJ, Ross DB, Warren AE, Sharratt GP, Murphy DA. Hepatic veinto the azygous vein anastomosis for the pulmonary arteriovenous fistulae Ann Thorac Surg 1999;68:232-233.[Abstract/Free Full Text]

Related Article

Invited Commentary
James S. Tweddell
Ann. Thorac. Surg. 2009 87: 553-554. [Extract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
J. S. Tweddell
Invited commentary.
Ann. Thorac. Surg., February 1, 2009; 87(2): 553 - 554.
[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 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):
Cheul Lee
Chang-Ha Lee
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 Kim, S.-J.
Right arrow Articles by Lee, C.-H.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Kim, S.-J.
Right arrow Articles by Lee, C.-H.
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