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Ann Thorac Surg 1999;67:1746-1753
© 1999 The Society of Thoracic Surgeons

Original Articles

The modified Fontan procedure: morphometry and surgical implications

Maria G. Kiaffas, MDa,b, Richard Van Praagh, MDa,b, Chrysoula Hanioti, MDa,b, Douglas W. Green, MDa,b

a Departments of Pathology and Cardiology, Children’s Hospital, Boston, Massachusetts, USA
b Departments of Pathology and Pediatrics, Harvard Medical School, Boston, Massachusetts, USA

Accepted for publication December 16, 1998.

Address reprint requests to Dr Van Praagh, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115
e-mail: gaskill{at}a1.tch.harvard.edu


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. The modified Fontan procedure for patients with only one well-formed ventricle is now widely regarded as palliative, not curative.

Methods. To improve the surgical management and postoperative follow-up of such patients, a morphometric study of 33 postmortem cases was done.

Results. The three main causes of death were congestive heart failure (82%), arrhythmias (12%), and central nervous system dysfunction (6%). The cross-sectional area of the Fontan anastomosis (FA) relative to the systemic venous area (SVA) and relative to the body surface area (BSA) revealed that the Fontan pathway was often obstructive. The mean FA/SVA index was 73% less than normal: 0.54 ± 0.22, range 0.13 to 0.98. The mean FA/BSA index was 70% less than normal: 143.52 ± 50.01 mm2/M2, range 55.09 to 261.67 mm2/M2.

Conclusions. The main surgical challenge is to minimize or eliminate prepulmonary stenosis. Although significant postoperative obstruction was often not evident hemodynamically because of small or absent gradients, the presence of important obstruction of the Fontan pathway was clearly revealed by morphometry.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Since the early 1970s, when Fontan and associates [1, 2] and Kreutzer and associates [3, 4] independently reported successful atriopulmonary anastomosis for the treatment of tricuspid atresia, advances in case selection, operative technique, and postoperative management of patients with only one well-formed ventricle have resulted in greatly improved early survival, now 92.5% at the Children’s Hospital in Boston [5].

Nonetheless, it is also widely appreciated that there is a continuing late risk for patients with a Fontan circulation and that the reasons for this continuing late risk remain incompletely understood [5, 6]. Hence, it has been suggested that although the Fontan procedure is an excellent palliative operation, it is not a curative one [6].

In an effort to improve the surgical management and the postoperative follow-up of patients with only one well-formed ventricle, a study was undertaken of all patients at our institution who have undergone autopsy examination after the modified Fontan procedure. Particular attention was focused on three questions: 1) What were the causes of early death (<= 30 days postoperatively) and late death (> 30 days postoperatively) after the modified Fontan operation? 2) Does morphometry clarify the causes of death? 3) What are the surgical and follow-up implications of these findings?


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
From 1974 to 1996 inclusive, 52 patients undergoing autopsy examination had been treated with a modified Fontan operation. The prevalence of Fontan patients in our congenital cardiac pathology database was 52/3,221 cases (1.6%). This report is based on 33 of these cases, 19 being excluded for the following reasons: 13 had terminal take-down of the Fontan procedure; 3 were excessively artifacted; and 3 heart specimens could not be found.

There was a strong male preponderance, males/females = 27/6 (4.5/1). The ages at death were: median 4.2 years; mean 6.2 ± 5.4 years; and range 0.5 to 22.6 years. The time period of this study was from 1974 to 1996, a consecutive 23-year period. All available clinical, laboratory, and surgical data were examined and correlated with the pathologic anatomic findings.

Special emphasis was placed on morphometric examination of the heart specimens with a modified Fontan procedure. Age-matched normal heart specimens (n = 66) were measured as a control series. The cross-sectional area of the total systemic venous return was measured (mm2) and was compared with the cross-sectional area of the total Fontan anastomosis (mm2). Cross-sectional areas were calculated using the equations for the area of a circle (A = {pi} r2, r being the radius) or an ellipse (A = {pi} ab/4, a being the major axis and b the minor axis).

The total cross-sectional systemic venous area (SVA) equalled (Fig 1) the sum of the cross-sectional superior vena caval area (SVCA) plus the cross-sectional inferior vena caval area (IVCA) plus (when applicable) the cross-sectional area of the left superior vena cava (LSVCA) plus (when applicable) the cross-sectional area of hepatic veins connecting with the atria—as occurred in the heterotaxy syndromes with asplenia and polysplenia.



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  		Fig 1. The ratio of the Fontan area (FA) relative to the systemic venous area (SVA), ie, the FA/SVA index, varied with the operation performed and the presence or absence of a left superior vena cava (LSVC). (A) With an atriopulmonary anastomosis, FA/SVA index = c/a + b. (B) With a lateral tunnel cavopulmonary anastomosis, FA/SVA index = d + b ± c/a + b ± c. a, cross-sectional area of the inferior vena cava (IVC); b, cross-sectional area of the right superior vena cava (RSVC); c, cross-sectional area of FA in A; c, cross-sectional area of LSVC in B; d, cross-sectional area of lower RSVC anastomosed to inferior surface of right pulmonary artery (RPA); LPA, left pulmonary artery; LT, lateral tunnel; MPA, main pulmonary artery; RA, morphologically right atrium; ±, with or without.

 
The total cross-sectional area of the Fontan anastomosis, ie, the Fontan area (FA), varied depending on the procedure performed. With direct atriopulmonary anastomosis, the cross-sectional area was the total FA (Fig 1A). When the SVC (right, left, or both) was or were anastomosed to the pulmonary artery branch or branches, the SVC area(s) was (were) included in the FA (Fig 1B). The FA/SVA ratio was then calculated (Fig 1).

In the normal age-matched control heart specimens, the following measurements were made: the SVCA, the IVCA, the cross-sectional tricuspid valve area (TVA), and the pulmonary valve area (PVA). The following normal ratios were then calculated: TVA/SVCA + IVCA (ie, TVA/SVA); and the PVA/SVCA + IVCA (ie, PVA/SVA). The FA/SVA ratios were then compared with the normal TVA/SVA ratios. These areas were also indexed to the patient’s body surface area (BSA): FA/BSA compared with TVA/BSA. Statistical analysis was performed using Student’s t test with separate variances. A value of p < 0.05 was regarded as statistically significant. Data concerning late Fontan fatalities were reported, in part, in a prior pilot study based on 14 postmortem cases [7].


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
In the interest of brevity, the findings are presented in tables and figures. The types of congenital heart disease for which a modified Fontan procedure was performed are summarized in Tables 1 and 2. The modifications of the modified Fontan operation that were utilized are presented in Table 3. The surgical procedures and cardiac catheterization interventions that were performed before the Fontan procedure are summarized in Table 4.


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  		Table 1. The Hypoplastic, Atretic, or Absent RV Sinus Group (n = 16)

 

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  		Table 2. The Hypoplastic LV Sinus Group (n = 17)

 

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  		Table 3. Modifications of the Fontan Procedure (n = 33)

 

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  		Table 4. Surgical Procedures and Catheterization Interventions Before Fontan Procedure

 
Morphometric findings concerning normal control hearts (n = 66) are summarized in Tables 5, 7, and 8. The Fontan morphometry (n = 33) is presented in Tables 6, 7, and 8, and Figure 2.


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  		Table 5. Normal Morphometry (n = 66)

 

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  		Table 6. Fontan Morphometry

 

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  		Table 7. Morphometry Indexed to Body Surface Area

 

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  		Table 8. Ventricular Wall Thickness

 


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  		Fig 2. (A) Comparison of normal tricuspid valve area (TVA) with systemic venous area (SVA), ie, normal TVA/SVA indices shown with white circles, and Fontan area (FA) to SVA, ie, FA/SVA indices shown with black circles. There is almost no overlap between the normal and the much smaller Fontan indices. (B) Comparison of normal TVA to body surface area (BSA), ie, normal TVA/BSA indices (white circles) and FA/BSA indices (black circles). There is no overlap between the normal and the much smaller Fontan indices.

 
Histologic evidence of significant pulmonary vascular obstructive disease was found in only 1 of 33 Fontan patients (3%), a 4.25-year-old patient with grade 4 Heath-Edwards changes. Grade 1 changes were found in 2 other patients (6%), age 3.4 years and 14.75 years, but these findings were regarded as not clinically significant.

The main causes of death in these 33 Fontan patients are presented in Table 9. Congestive heart failure was by far the leading cause of death in the series as a whole (27 of 33 patients, 82%; Table 9). The main causes of early death from congestive heart failure are given in Table 10, while the findings associated with late death from congestive heart failure are summarized in Table 11.


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  		Table 9. Main Causes of Death in Fontan Patients (n = 33)

 

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  		Table 10. Death From Congestive Heart Failure (n = 27)

 

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  		Table 11. Death From Congestive Heart Failure (continued) (n = 27)

 
Arrhythmias were the second most common cause of death in this series, occurring in 4 of these 33 Fontan patients (12%; Table 9). Early and late arrhythmic deaths are summarized in Table 12.


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  		Table 12. Death From Arrhythmia (n = 4; 12%)

 
Central nervous system dysfunction was the immediate cause of death in 2 patients: probable air embolism in 1, and hemorrhage in the distribution of the right middle cerebral artery in the other. Central nervous system dysfunction was thought to be related to preventable surgical technical problems; hence, this cause of death will not be considered further.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Why was congestive heart failure by far the leading cause of early and late death in these 33 Fontan patients (82%; Tables 9–11)? We think that the morphometric data (Tables 5–8) help to answer this question. In the normal heart, the cross-sectional area of the tricuspid valve (TVA) typically is almost twice the summed cross-sectional areas of the superior and inferior vena cava, the systemic venous area: in 66 normal hearts, the mean TVA/SVA ratio was 1.98 ± 0.68, ranging from 0.73 to 5 (Table 5).

However, the fundamental assumption of the Fontan procedure [1–4] is that it is acceptable for a normal-sized pulmonary artery to serve as the outlet for the right atrium. The normal cross-sectional pulmonary valve area (PVA) relative to the SVA, ie, the normal PVA/SVA ratio, averaged only 0.77 ± 0.27, ranging from 0.31 to 2.07 (Table 5). Thus, the normal PVA/SVA ratio averaged 61% less than the normal TVA/SVA ratio: 1.98 to 0.77 = -61.11% (Table 5).

Direct comparison of the normal PVA relative to the normal TVA showed that the normal PVA/TVA ratio averaged 0.42 ± 0.22, ranging from 0.19 to 0.60 (Table 5). In other words, the cross-sectional area of the normal pulmonary valve is, on average, only about 40% of the cross-sectional area of the normal tricuspid valve. Hence, our hypothesis is that the basic concept of the Fontan procedure may be obstructive to systemic venous return to the lungs (Fig 3).



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  		Fig 3. Obstructive Fontan procedure in a 13.25-year-old boy. (A) Anastomosis between the lower superior vena cava (SVC) and the undersurface of the right pulmonary artery (RPA); cross-sectional area 55 mm2. (B) Anastomosis of the upper SVC with the superior surface of the RPA; cross-sectional area 77 mm2. The inferior vena cava at its junction with the right atrium (RA), not shown; cross-sectional area 902 mm2. The FA/SVA ratio = 132/979 (0.1348, or 13.48%). The area of the lower SVC-RPA anastomosis in A is 93.9% less than that of the IVC. The area of the left-sided tricuspid valve is 396 mm2. The summed cavopulmonary anastomoses shown in A and B = 132 mm2, 67% less than the area of the left-sided tricuspid valve (the only functioning atrioventricular valve). (C) Same patient also had restrictively small bulboventricular foramen (BVF), indicated by 1-mm probe. BVF measures 8 x 6 mm; cross-sectional area 37.7 mm2, resulting in subaortic stenosis (treated with Damus-Kaye-Stansel procedure) and marked left ventricular hypertrophy (13 mm in thickness). Diagnosis: single left ventricle (LV) with infundibular outlet chamber, transposition of the great arteries {S, L, L}, double-inlet LV, right-sided mitral valve patched closed, atrial septum closed. FW, free wall; PV, pulmonary valve; RL, right lung; TV(L), tricuspid valve, left-sided; VS, ventricular septum.

 
The fact that the normal TVA is so much larger than the normal PVA may explain, at least in part, why the right atrial free wall (normally about 1 mm in thickness) is so much thinner than the right ventricular free wall (normally 3 to 4 mm in thickness). The normal TVA/PVA ratio averaged 2.68 ± 0.73, ranging from 1.65 to 5.2 (Table 5).

By contrast, in these 33 modified Fontan hearts, the cross-sectional area of the Fontan anastomosis or anastomoses relative to the summed caval cross-sectional areas, ie, the FA/SVA index, averaged only 0.54 ± 0.22, ranging from 0.13 to 0.98 (Table 6). Consequently, the FA/SVA index averaged 73% less than the normal TVA/SVA ratio: 1.98 to 0.54 = -72.73% (Table 6). Not only were the means of the FA/SVA index and the normal TVA/SVA ratio significantly different (p < 0.0001), even the ranges of these two ratios showed almost no overlap (Fig 2; Tables 5, 6).

Morphometry indexed to body surface area (Table 7; Fig 2B) yielded results that were not significantly different from those indexed to systemic venous area (Tables 5, 6; Fig 2A). For example, the normal mean tricuspid valve area indexed to body surface area (BSA) (471.25 mm2/M2; Table 7) compared with the mean Fontan area indexed to BSA (143.52 mm2/M2; Table 7) equalled -69.54%. In other words, the mean Fontan area indexed to BSA was approximately 70% less than the normal tricuspid valve area indexed to BSA—very similar to the reduction of the Fontan area compared with the normal tricuspid valve area when both were indexed to the systemic venous area: 73% (p = NS).

In Fontan hearts, the mean systemic venous area indexed (312.79 mm2/M2; Table 7) was significantly larger than the normal systemic venous area indexed (260.16 mm2/M2; Table 7), the Fontan systemic venous area indexed being 20.23% greater than normal (p = 0.0031). This enlargement of the systemic venous area in the Fontan patients is considered to suggest obstruction of the Fontan pathway, myocardial dysfunction, or both.

Whether the FA/SVA index (Fig 2A) or the FA/BSA index (Fig 2B) will prove to be the more sensitive indicator of obstruction of the Fontan pathway remains to be determined.

In the group of Fontan patients that died early from congestive heart failure (Table 10), morphometry showed in these 6 patients that the FA/SVA ratio averaged only 0.36 ± 0.08, ranging from 0.28 to 0.51. Hence, the FA/SVA ratio in this subgroup was 82% less than normal (1.98 to 0.36 =-81.82%). The morphometric findings of the present study (Tables 5, 6) strongly suggest that the Fontan procedure may well be obstructive [8] far more often than has been appreciated hitherto.

What is the significantly obstructive FA/SVA index or FA/BSA index?
The answer to this very important question is unknown at the present time. We think that it will have to be answered prospectively, both clinically and hemodynamically, bearing in mind such important variables as cardiac output/min/M2.

What is the average FA/SVA index or FA/BSA index in our living Fontan patients?
Again, this information is unknown at present. We hope that it will be possible to measure these new indices (Tables 6, 7) accurately in vivo by means of two- or three-dimensional echocardiography or by magnetic resonance imaging. The potential diagnostic and surgical importance of these indices is that they may help to detect, localize, and quantitate the severity of prepulmonary stenosis in the Fontan pathway, facilitating precise noninvasive follow-up.

Regarding the currently favored lateral tunnel type of modified Fontan procedure [9], it is noteworthy that the normal cross-sectional SVCA is often much smaller than the normal cross-sectional IVCA: the SVCA/IVCA ratio averaged 0.31 ± 0.15, ranging from 0.06 to 0.81 (Table 5). These morphometric data suggest that in the lateral tunnel Fontan, the SVC orifice can be significantly obstructive to the return of the inferior vena caval blood flow to the lungs.

Obstruction at the superior vena caval orifice (Fig 3A) appears to explain, at least in part, why fenestration of the Fontan baffle [10] can be hemodynamically and clinically advantageous as part of the lateral tunnel modified Fontan operation [5]. Fenestration appears to decompress the obstructed intra-atrial portion of the Fontan pathway, thereby lessening the clinical picture of congestive heart failure with pleural effusions, ascites, and protein-losing enteropathy.

The Fontan anastomosis or anastomoses (Fig 1) often were not the only site or sites of obstruction in the Fontan pathway. The pulmonary artery branches frequently were also sites of obstruction (Table 6). To quantitate the degree of pulmonary artery branch obstruction, the narrowest cross-sectional area of the right pulmonary artery (RPA) and the narrowest cross-sectional area of the left pulmonary artery (LPA) were summed in 14 Fontan heart specimens with unartifacted pulmonary artery branches, this RPA area plus LPA area being termed the total pulmonary area (TPA; Table 6).

The pulmonary artery branches usually were not as obstructive as the Fontan anastomosis. The TPA/SVA ratio averaged 0.79 ± 0.67, ranging from 0.24 to 2.6, while the FA/SVA ratio averaged 0.54 ± 0.22, ranging from 0.13 to 0.98 (Table 6). Although the pulmonary artery branches usually were less obstructive than the Fontan anastomosis, the lower end of the range (0.24) indicated that the TPA/SVA ratio occasionally was much smaller than the average FA/SVA ratio (0.54) (Table 6). Direct comparison of the TPA with the FA confirmed that, on average, the TPA was larger than the FA: the TPA/FA ratio averaged 1.37 ± 1.1, ranging from 0.41 to 4.79 (Table 6).

Because this type of clinically and surgically relevant morphometry (Tables 5–7) has not been reported previously, to our knowledge, many other measurements by other investigators need to be done, particularly in vivo, using echocardiography (including Doppler) and magnetic resonance imaging.

Arrhythmias
In addition to systemic venous obstruction, another important disadvantage associated with the present design of the lateral tunnel Fontan is that it is arrhythmogenic [11–14]. The lateral tunnel baffle often is sutured to the crista terminalis, just lateral to the entry of the SVC. The crista terminalis corresponds internally to the sulcus terminalis externally, where the sinoatrial node is located. Hence, deep sutures into the crista terminalis can traumatize the SA node and can lead to thrombosis of the SA nodal artery, resulting in sick sinus syndrome. In turn, sick sinus syndrome is associated with sudden arrhythmic death, as occurred after the Mustard procedure—an atrial switch procedure for transposition of the great arteries. The SVC part of the Mustard baffle and the SVC part of the lateral tunnel Fontan baffle are both sutured in similar ways beneath the orifice of the SVC.

Systemic ventricular hypertrophy
Systemic ventricular hypertrophy and enlargement were often marked in the Fontan hearts compared with normal controls (Table 8; Fig 3C). The normal free wall thickness of the left ventricle (LV) averaged 6.6 mm. In the Fontan hearts, when the LV was the systemic ventricle, the LV free wall thickness averaged 10.1 mm, 53% greater than normal. When the right ventricle (RV) was the systemic ventricle, the RV free wall averaged 10.2 mm in thickness, 54% greater than the average thickness of the normal systemic LV. After the modified Fontan procedure, systemic ventricular hypertrophy is disadvantageous for ventricular diastolic function [15], and systemic ventricular hypertrophy is also an independent risk factor for sudden arrhythmic death [16].

Surgical implications
Since the two main causes of death after the modified Fontan procedure were congestive heart failure (82%) and arrhythmias (12%) (Table 9), the guiding principles in the surgical management of such patients should be: 1) to eliminate or minimize all forms of prepulmonary stenosis that obstruct systemic venous return to the lungs; and 2) to eliminate or minimize all causes of arrhythmias—both atrial and ventricular.

How best to achieve these goals is the challenge. Promising new approaches include the following: 1) A large incision of the right atrial appendage (RAA) anterior to the SVC, with direct anastomosis of the RAA to the PA [17], avoids stenosis both at the RA-SVC orifice (Table 5) and at the RAA-PA anastomosis, and also avoids damage to the SA node by not placing sutures into the crista terminalis. A vital dye (such as tricarbocyanine dye II and Evans blue) may be instilled into the aortic root along with the cardioplegia solution, making the sinoatrial nodal artery more readily visible, thereby making it possible to avoid inadvertent surgical injury of this artery. (This suggestion of visualizing the sinoatrial nodal artery by means of cardioplegia solution was made to us by Dr Guillermo Kreutzer of Buenos Aires, the independent co-inventor of the Fontan-Kreutzer procedure.) 2) An extracardiac and extrapericardial cavopulmonary anastomosis [18, 19] or conduit between the IVC and the RPA can be constructed that is both large enough to be nonobstructive and that is also not arrhythmogenic.

Whatever technique is used, it is important that the lungs be perfused with hepatic venous blood so as to avoid the development of pulmonary arteriovenous malformations [20, 21].

Other considerations of surgical importance include: 1) relatively well developed and nonobstructive pulmonary artery branches [22]; 2) absence of pulmonary vascular obstructive disease; 3) absence of atrioventricular valvar regurgitation or stenosis [18]; and 4) minimal systemic ventricular hypertrophy (Table 8) [23] because of the association of hypertrophy with diastolic dysfunction [15] and arrhythmias [16].

To detect significant postoperative obstruction, which may well not be evident hemodynamically because of small or absent gradients, Fontan patients should also be assessed morphometrically using these new indices of the Fontan area/systemic venous area (FA/SVA), or the Fontan area/body surface area (FA/BSA) (Figs 1, 2; Tables 6, 7).


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Fontan F., Mounico F.B., Baudet E., Simineau S., Gordo J., Goufrant P. "Correction" de l’atrésie tricuspidienne. Rapport de deux cas "corrigés" par l’utilisation d’une technique chirurgicale nouvelle. Ann Chir Thorac Cardiovasc 1971;10:39-47.[Medline]
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  4. Kreutzer G., Galíndez E., Bono H., de Palma C., Laura J.P. An operation for the correction of tricuspid atresia. J Thorac Cardiovasc Surg 1973;66:613-621.[Medline]
  5. Gentles T.L., Mayer J.E., Gauvreau K., et al. Fontan operation in five hundred consecutive patients: factors influencing early and late outcome. J Thorac Cardiovasc Surg 1997;114:376-391.[Abstract/Free Full Text]
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  9. De Leval M.R., Kilner P., Gewillig M., Bull C. Total cavopulmonary connection: a logical alternative to atriopulmonary connection for complex Fontan operations—experimental studies and early clinical experience. J Thorac Cardiovasc Surg 1988;96:682-695.[Abstract]
  10. Bridges N.D., Lock J.E., Castaneda A.R. Baffle fenestration with subsequent transcatheter closure: modification of the Fontan operation for patients at increased risk. Circulation 1990;82:1681-1689.[Abstract/Free Full Text]
  11. Fishberger S.B., Wernovsky G., Gentles T.L., et al. Factors that influence the development of atrial flutter after the Fontan. J Thorac Cardiovasc Surg 1997;113:80-86.[Abstract/Free Full Text]
  12. Gandhi S.K., Bromberg B.I., Schuessler R.B., et al. Characterization and surgical ablation of atrial flutter after the classic Fontan repair. Ann Thorac Surg 1996;61:1666-1679.[Abstract/Free Full Text]
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  14. Durongpisitkul K., Porter C.J., Cetta F., et al. Frequency of atrial tachyarrhythmia after modified Fontan operation: a comparison between total cavopulmonary connection and atriopulmonary connection. Pediatrics 1996;98(suppl):528 (abstract).
  15. Grossman W., Bain D.S. Cardiac catheterization, angiography and intervention, 4th ed. Philadelphia: Lea and Febiger, 1990:333.
  16. Myerburg R.J., Castellanos A. Cardiac arrest and sudden cardiac death. In: Braunwald E., ed. Heart disease: a textbook of cardiovascular medicine, 4th ed. Philadelphia: WB Saunders Co, 1992:756-789.
  17. Aoki M, Imai Y, Takanashi Y, et al. Long-term results of atrial appendage-to-pulmonary artery direct anastomosis for Fontan-type procedures. The Second World Congress of Pediatric Cardiology and Cardiac Surgery, Honolulu, Hawaii, May 11–15, 1997;Abstracts:65.
  18. Yagihara T., Yamada O., Kawashima Y. Long term follow-up of the right heart bypass operation. Rev Argent Cardiol 1996;64:399-403.
  19. Van Son J.A.M., Falk V., Mohr F.W. Intracardiac or extracardiac conduit modification of the Fontan procedure in hearts with univentricular atrioventricular connection and left superior caval vein draining to coronary sinus. Cardiol Young 1997;7:215-219.
  20. Srivastava D., Preminger T., Lock J.E., 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]
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