Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1999;100:II-151-II-156

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mainwaring, R. D.
Right arrow Articles by Moore, J. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mainwaring, R. D.
Right arrow Articles by Moore, J. W.
Related Collections
Right arrow Pulmonary circulation and disease
Right arrow Other Treatment
Right arrow Pediatric and congenital heart disease, including cardiovascular surgery

(Circulation. 1999;100:II-151.)
© 1999 American Heart Association, Inc.


Surgery for Congenital Heart Disease

Effect of Accessory Pulmonary Blood Flow on Survival After the Bidirectional Glenn Procedure

Richard D. Mainwaring, MD; John J. Lamberti, MD; Karen Uzark, PhD; Robert L. Spicer, MD; Mark W. Cocalis, MD; John W. Moore, MD

From the Cardiac Institute, Children’s Hospital–San Diego, San Diego, Calif.

Correspondence to Richard D. Mainwaring, MD, Alfred I. duPont Hospital for Children, Nemours Cardiac Center, 1600 Rockland Rd, Wilmington, DE 19803. E-mail rmainwar{at}nemours.org


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Background—The bidirectional Glenn procedure (BDG) is used in the staged surgical management of patients with a functional single ventricle. Controversy exists regarding whether accessory pulmonary blood flow (APBF) should be left at the time of BDG to augment systemic saturation or be eliminated to reduce volume load of the ventricle. The present study was a retrospective review of patients undergoing BDG that was conducted to assess the influence of APBF on survival rates.

Methods and Results—From 1986 through 1998, 149 patients have undergone BDG at our institution. Ninety-three patients had elimination of all sources of APBF, whereas 56 patients had either a shunt or a patent right ventricular outflow tract intentionally left in place to augment the pulmonary blood flow provided by the BDG. The operative mortality rate was 2.2% without APBF and 5.4% with APBF. The late mortality rate was 4.4% without APBF and 15.1% with APBF. Actuarial analysis demonstrates a divergence of the Kaplan-Meier curves in favor of patients in whom APBF was eliminated (P<0.02). One hundred seven patients have subsequently undergone completion of their Fontan operation, so the actuarial analysis includes the operative risk of this second operation.

Conclusions—The results suggest that the elimination of APBF at the time of BDG may confer a long-term advantage for patients with a functional single ventricle.


Key Words: blood flow • Fontan procedure • mortality • morbidity


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
The bidirectional Glenn procedure (BDG) is used as the first of 2 operations to achieve separation of the systemic and pulmonary circulations in patients with a functional single ventricle.1 This 2-staged approach to Fontan completion has resulted in a significant reduction in mortality rates during the past decade.2 3 4 The original premise for this approach was based on the elimination of ventricular volume work at an early age and the stepwise accommodation of ventricular geometry to the reduction in volume load.5 6 Other factors that have favorably influenced outcome include the earlier elimination of systemic–pulmonary artery shunts7 and the influence of interventional cardiology techniques.8 Improved results have made BDG an integral part of the management of single-ventricle patients.9

A number of controversies remain regarding the BDG, including the timing of the procedure and the interval to Fontan completion. In addition, there exists a controversy regarding the use or elimination of accessory pulmonary blood flow (APBF). Advocates for the provision of APBF cite more "physiological" levels of oxygen saturation, inhibition of arteriovenous malformations, and the potential to decrease the development of pulmonary arterial collateral vessel development.10 It has also been proposed that APBF may stimulate pulmonary artery growth, resulting in patients being better candidates for the Fontan procedure.11 Conversely, advocates for the elimination of APBF emphasize the importance of eliminating volume loads to allow the remodeling of the ventricle that occurs after this procedure. The elimination of APBF results in a degree of hypoxemia that is usually well tolerated in infancy and permits adequate growth of the pulmonary arteries to allow completion of the Fontan procedure. However, as a consequence of these divergent opinions and observations, there remain a variety of algorithms that have evolved regarding the management of single-ventricle patients and the use of APBF at the time of BDG.

We previously reported our experience with the BDG and the influence of APBF.12 This report, in which we evaluated 92 patients through mid-1994, reported that the incidence of effusions and the likelihood of prolonged hospital stay were higher when APBF was used. Actuarial analysis did not reveal a statistical difference in survival rates for the 2 groups; however, there was a trend toward improved survival rates in the patients without APBF. The purpose of this update was to evaluate the effect of APBF on survival rates after BDG in a larger cohort of patients and with a longer duration of follow-up.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
This study is a retrospective review of our experience with BDG in patients with a functional single ventricle. The medical records were reviewed, and 2 groups were formulated based on the presence or absence of APBF, which is defined as either a systemic–pulmonary artery shunt or a patent right ventricular outflow tract. Aortopulmonary collaterals are not included in this definition of APBF.

From 1986 through August 1998, 149 patients underwent BDG at Children’s Hospital–San Diego as part of the staged surgical management leading to Fontan completion. Excluded from this analysis were 4 patients (2 with and 2 without APBF) in whom surgery failed to achieve pulmonary blood flow to both lungs secondary to technical considerations. (Details for these 4 patients are given in our previous report.12 ) In addition, there were 8 patients who underwent BDG as part of a one and one-half ventricle approach. This cohort was also excluded from this study because they were not patients with a functional single ventricle in whom Fontan completion was contemplated.

Figure 1Down shows the number of BDGs performed annually and delineates those with and without APBF. Fifty-six of the 149 patients had inclusion of APBF. The median age of these patients at time of surgery was 10 months (range, 2.5 to 195 months), and the median weight was 7.1 kg (range, 3.9 to 37 kg). The median year of surgery was 1991. Ninety-three patients had no APBF at the time of BDG; the median age for these patients was 8 months (range, 2.2 to 46 months), and the median weight was 6.1 kg (range, 3.9 to 15.8 kg). The median year of surgery for patients without APBF was 1994. The diagnoses and ventricular morphology for the 2 groups are listed in Table 1Down.



View larger version (15K):
[in this window]
[in a new window]
 
Figure 1. BDG procedures performed at the Children’s Hospital–San Diego from February 1986 through August 1998. Filled column represents number of patients who underwent BDG with APBF. Hatched column represents number of patients who underwent BDG as sole source of pulmonary blood flow.


View this table:
[in this window]
[in a new window]
 
Table 1. Diagnoses and Ventricular Morphology of Patients Undergoing BDG

Pleural effusions were defined as the need for chest tube drainage for >7 days. Prolonged hospitalization was defined as a length of stay of >14 days.

Results of this study are reported as either the mean±SEM value or the median and range values. Statistical comparison of the 2 groups was performed with the use of 2-tailed log-rank analysis. Kaplan-Meier survival curves were constructed using the product-limit method. A comparison of the Kaplan-Meier curves was performed using Fisher’s exact test. A P value of <0.05 was considered significant.


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
There were 5 operative deaths, for an overall early mortality rate of 3.3%. Three of these early deaths occurred in patients with APBF (5.4%), and 2 occurred in patients without APBF (2.2%). One hundred forty-four patients underwent successful BDG; this total included 53 with APBF and 91 without APBF. The incidence of pleural effusions was 16% with APBF and 2% without APBF. The length of hospital stay for the 2 groups is shown in Figure 2Down; the median length of stay was 8 days for both groups. Prolonged hospital stay occurred in 13 patients (24%) with APBF and 7 patients (8%) without APBF (P<0.05); the causes for prolonged hospital stay are listed in Table 2Down.



View larger version (29K):
[in this window]
[in a new window]
 
Figure 2. Length of hospital stay for patients undergoing BDG with and without APBF. Filled column represents number of patients who underwent BDG with APBF. Hatched column represents number of patients who underwent BDG as sole source of pulmonary blood flow.


View this table:
[in this window]
[in a new window]
 
Table 2. Causes for Prolonged Hospital Stay After BDG

Of the 144 patients who underwent successful BDG, 142 have been followed for an average duration of 70±12 months (Figure 3Down). There were 2 patients who were lost to follow-up (1 in 1990 and 1 in 1992); both were from the APBF group. These 2 patients have been dropped from the actuarial curve at the point of last contact.



View larger version (15K):
[in this window]
[in a new window]
 
Figure 3. Flow chart of 149 study patients.

There were 12 late deaths: 8 patients (15.1%) with APBF and 4 patients (4.4%) without APBF. Seven of these deaths occurred in the interim between BDG and the Fontan procedure. The remaining 5 deaths either occurred perioperatively at the time of Fontan completion or were late deaths after the Fontan procedure. The causes of early and late deaths are summarized in Table 3Down.


View this table:
[in this window]
[in a new window]
 
Table 3. Causes of Early and Late Deaths After BDG

Actuarial analysis was performed for patients undergoing BDG with and without APBF. Figure 4Down demonstrates the actuarial survival curves when the operative mortality rate of the procedure is included. A comparison of these 2 curves demonstrates a survival advantage in the patients in whom APBF was eliminated (P<0.02). Figure 5Down demonstrates the actuarial survival curves when operative mortality is excluded, again demonstrating improved survival without APBF (P<0.04).



View larger version (15K):
[in this window]
[in a new window]
 
Figure 4. Actuarial analysis of patients undergoing BDG with and without APBF. This analysis includes operative mortality rate at time of BDG.



View larger version (14K):
[in this window]
[in a new window]
 
Figure 5. Actuarial analysis of patients undergoing BDG with and without APBF when operative mortality rate is excluded.

One hundred thirty-five patients in this series (149 minus 5 operative deaths, 7 interim deaths, and 2 lost to follow-up) were potentially eligible for Fontan completion. Of these patients, 25 (9 with and 16 without APBF) have had BDG relatively recently (average follow-up, 6±1 month) and, therefore, have not had their Fontan evaluation. Three patients (2 with and 1 without APBF) in this series were deemed unsuitable candidates for Fontan completion due to elevated pulmonary vascular resistance; these 3 patients remain alive in a palliated state. One hundred seven patients have undergone completion of their Fontan procedure; this includes 36 patients with APBF (77% of surviving cohort) and 71 patients without APBF (81% of survivors in this cohort). There were 3 early deaths after the Fontan procedure, which were attributed to low cardiac output in 2 patients and a cerebrovascular accident in 1. There also were 2 late deaths after the Fontan procedure; both were related to progressive hypoxemia and pulmonary dysfunction. The probability of undergoing BDG and ultimately achieving Fontan success was 74% with APBF and 92% without APBF (P<0.01) (Figure 6Down).



View larger version (15K):
[in this window]
[in a new window]
 
Figure 6. Probability of achieving Fontan survival based on presence or absence of APBF at time of BDG.


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
The purpose of this report was to evaluate the effect of APBF on survival after BDG. One hundred forty-nine BDGs were performed at our institution from 1986 to 1998. The early mortality rate was 5.4% with APBF and 2.2% without APBF, and the late mortality rate was 15.1% with and 4.4% without APBF. These data suggest that the elimination of APBF may confer a survival advantage in patients undergoing BDG.

The reasons for the divergence of the survival curves in this series remain uncertain. The BDG results in an immediate decrease in both preload and afterload, as well as favorable alterations in ventricular geometry. It has been hypothesized that these changes may have long-term beneficial effects on the preservation of myocardial performance.13 14 The inclusion of APBF will increase the volume work of the ventricle, thereby mollifying the beneficial effects seen in the absence of APBF. The inclusion of APBF may also have an adverse effect on pulmonary vasculature, because it represents a high-pressure source of pulmonary blood flow that may lead to alterations in pulmonary vascular resistance.7 The elimination of APBF may result in an improvement in both myocardial performance and pulmonary vascular resistance, which may confer advantages not only at the time of Fontan but also in the long term. In our series, the incorporation of APBF resulted in a combined early and late mortality rate that was significantly greater than that seen in patients without APBF. Some of the late deaths were cardiac related (eg, Fontan mortality), whereas others were clearly not related to cardiac issues (eg, tracheal complication). The disparity between the actuarial curves continues to widen during the first 2 years, suggesting that APBF may have adverse effects that manifest well after the perioperative time period.

The incidence of pleural effusions requiring chest tube drainage for >7 days was 8-fold higher in patients with APBF than in those without APBF, an observation that we and others have previously reported.12 15 Similar observations relating the incidence of effusions to the presence of significant aortopulmonary artery collateral vessels have been made in patients undergoing the Fontan procedure.16 The cause of effusions after BDG and Fontan procedures remains uncertain, but the incidence clearly increases in the presence of left-to-right shunts. In theory, APBF or aortopulmonary collaterals provide competitive flow to the lungs and may increase pressures in the systemic venous pathways. Also, these additional sources of pulmonary blood flow represent a "steal" from the systemic circulation and thus may contribute to the incidence of low cardiac output and the endocrinologic changes that have been associated with pleural effusions.17 Because the presence of effusions is a principal determinant of length of stay for this operation, it is not surprising that patients with APBF had longer lengths of stay in the hospital.

Oxygen saturation levels are typically in the 80% range for most infants undergoing BDG without APBF. However, saturation levels may be considerably <80% in patients <4 months old or in children >4 or 5 years old. It remains unclear why pediatric patients at either end of the age spectrum have marked differences in their physiology compared with those in the middle of the spectrum. These observations suggest that APBF may be both beneficial and necessary at the age extremes. From an institutional standpoint, we have performed most of our BDGs when the children were 6 to 12 months old. We then proceeded with Fontan completion {approx}1 year later. By establishing this programmatic approach, we have largely avoided the extreme hypoxemia that may be seen in very young infants or in older children.

Advocates for the inclusion of APBF suggest that the increase in pulmonary blood flow will result in higher levels of oxygenation and thus obviate excessive hypoxemia.18 Any benefit of improved oxygenation must offset the increase in ventricular volume work attendant to this approach. An inherent difficulty of including APBF is the regulation of flow through that additional source, because excessive pulmonary blood flow may have all of the adverse effects noted above. Because the eventual goal in these patients is to separate their systemic and pulmonary circulations, it seems that success in achieving this would be a logical end point. The present series provides midterm follow-up of the BDG and suggests that survival is appreciably higher in patients in whom APBF is eliminated.

Pulmonary artery growth patterns have been a theoretical concern in terms of the interim between the BDG and completion of the Fontan procedure.19 20 It is not surprising that pulmonary artery growth is diminished after BDG, because the pulmonary-to-systemic flow ratio is appreciably <1.21 Pulmonary artery growth patterns are improved when APBF is included,11 and this has been presented as a plausible argument for APBF. Some reports have correlated pulmonary artery size with successful Fontan outcome,22 whereas others have found it not to be predictive of operative survival.23 24 If pulmonary artery size were universally accepted as an indicator of survival, then inclusion of APBF would be a way to achieve this end. In our experience, 97% of the patients who were evaluated for completion of their Fontan procedure subsequently underwent this operation with a <3% operative mortality rate. None of our patients have been turned down for Fontan completion due to pulmonary artery size criteria; therefore, our experience suggests that pulmonary artery growth is satisfactory for Fontan completion regardless of whether APBF is used.

The development of pulmonary arteriovenous malformations (AVMs) has been another theoretical concern after BDG. Pulmonary AVMs have been seen after a classic Glenn shunt and after the Kawashima operation. Both of these procedures exclude hepatic venous circulation to the lungs on the first pass, suggesting a "hepatic factor" in the cause of pulmonary AVMs.25 Advocates for APBF have suggested that the accessory source will allow sufficient hepatic venous blood to pass through the lungs to prevent pulmonary AVM formation.11 However, we have seen the development of pulmonary AVMs only in the setting of heterotaxy with interrupted vena cava and azygous continuation (eg, polysplenia or left isomerism). There were 4 patients in our series with this anatomy, 2 of whom subsequently developed pulmonary AVMs. One of these 2 patients had APBF, indicating that a source of APBF may not protect from AVM formation. More importantly, none of our BDG patients with situs solitus have developed pulmonary AVMs detectable either clinically or with echocardiography and pulmonary angiography, which were routinely performed before Fontan completion. It is conceivable that the presence of small AVMs could have been overlooked in this evaluation, but none have surfaced during follow-up of the Fontan patients. Thus, we believe that pulmonary AVM formation is not an indication for inclusion of APBF.

One limitation of this study relates to the retrospective and nonrandomized design. This study format may always be subject to criticism insofar as there is the potential for a selection process or learning curve that could bias the results. The inclusion of APBF was our preferred surgical approach from 1986 to 1990, whereas from 1991 to 1998, we have usually, but not always, eliminated APBF. Since 1991, the use of APBF has related to referral source (eg, cardiologist preference) rather than to patient diagnosis or physiology. The 2 groups were similar with regard to age and weight at surgery, duration of follow-up, and percentage of patients who have completed their Fontan procedure. The groups were dissimilar in the year of surgery, because the group with APBF tended to be earlier in the series. There also was some dissimilarity with regard to diagnoses, because most of our experience with hypoplastic left heart accrued in the 1990s. As a consequence, the group without APBF had a disproportionate number of patients with hypoplastic left heart syndrome and a higher percentage of patients with right ventricular morphology. This dissimilarity potentially may have favored the group with APBF, because hypoplastic left heart syndrome and right ventricular morphology have been considered risk factors in some studies. All of the procedures (149 BDG and 107 Fontan) were performed by the 2 surgeons (R.D.M. and J.J.L.); we believe that the disparity between the actuarial curves is indicative of the effect of APBF on survival and not a function of the study design. The only way to prove this point would be to embark on a prospective, multi-institutional trial. This type of study not only could evaluate the influence of APBF on survival but also could assess some of the factors that may ultimately contribute to survivability, such as the effect of APBF on ventricular cavity size, pressure, and wall thickness and the influence of APBF on native aortopulmonary collateral vessel development.

In summary, the results of this study demonstrate a significant survival advantage when APBF is eliminated at the time of BDG. In addition, the probability of continuing to a successful Fontan procedure completion was higher in the patients without APBF. We postulate that this survival advantage may be based on improvement in pulmonary resistance and ventricular function. It is our belief that the elimination of APBF at the time of BDG will improve the long-term outlook after Fontan procedure completion.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Hopkins RA, Armstrong BE, Serwer GA, Peterson RJ, Oldham HN. Physiological rationale for a bidirectional cavopulmonary shunt. J Thorac Cardiovasc Surg. 1985;90:391–398.[Abstract]

2. Mayer JE Jr, Bridges ND, Lock JE, Hanley FL, Jonas RA, Castaneda AR. Factors associated with marked reduction in mortality for Fontan operations in patients with single ventricle. J Thorac Cardiovasc Surg. 1992;103:444–452.[Abstract]

3. Castaneda AR. From Glenn to Fontan: a continuing evolution. Circulation. 1992;86(suppl II):II-80–II-84.

4. Lamberti JJ, Mainwaring RD, Spicer RL, Uzark KC, Moore JW. Factors influencing perioperative morbidity during palliation of the univentricular heart. Ann Thorac Surg. 1995;60:S550–S553.

5. Jacobs ML, Rychik J, Rome JJ, Apostolopoulou S, Pizarro C, Murphy JD, Norwood WI Jr. Early reduction of the volume work of the single ventricle: the hemi-Fontan operation. Ann Thorac Surg. 1996;62:456–462.[Abstract/Free Full Text]

6. Seliem MA, Baffa JM, Vetter JM, Chen SL, Chin AJ, Norwood WI Jr. Changes in right ventricular geometry and heart rate early after hemi-Fontan procedure. Ann Thorac Surg. 1993;55:1508–1512.[Abstract]

7. Mietus-Snyder M, Lang P, Mayer JE, Jones RA, Castaneda AR, Lock JE. Childhood systemic-pulmonary shunts: subsequent suitability for Fontan operation. Circulation. 1987;76(suppl III):III-39–III-44.

8. Moore JW, Spicer RL, Perry JC, Mathewson JW, Kirkpatrick SE, George L, Uzark K, Mainwaring RD, Lamberti JJ. Percutaneous use of stents to correct pulmonary artery stenosis in young children after cavopulmonary anastomosis. Am Heart J. 1995;130:1245–1249.[Medline] [Order article via Infotrieve]

9. Mainwaring RD, Lamberti JJ, Uzark K. The bidirectional Glenn: palliation of the univentricular heart. In: Karp RB, Laks H, Wechsler AS, eds. Advances in Cardiac Surgery. St Louis, Mo: Mosby–Year Book Inc; 1994:115–140.

10. Allgood NL, Alejos J, Drinkwater DC, Laks H, Williams RG. Effectiveness of the bidirectional Glenn shunt procedure for volume unloading in the single ventricle patient. Am J Cardiol. 1994;74:834–836.[Medline] [Order article via Infotrieve]

11. Uemura H, Yagihara T, Kawashima Y, Okada K, Kamiya T, Anderson RH. Use of the bidirectional Glenn procedure in the presence of forward flow from the ventricles to the pulmonary arteries. Circulation. 1995;92(suppl II):II-228–II-232.

12. Mainwaring RD, Lamberti JJ, Uzark K, Spicer RL. Bidirectional Glenn: is accessory pulmonary blood flow good or bad? Circulation. 1995;92(suppl II):II-294–II-297.

13. Donofrio MT, Jacobs ML, Spray TL, Rychik J. Acute changes in preload, afterload, and systolic function after superior cavopulmonary connection. Ann Thorac Surg. 1998;65:503–508.[Abstract/Free Full Text]

14. Chang AC, Hanley FL, Wernovsky G, Rosenfeld HM, Wessel DL, Jonas RA, Mayer JE, Lock JE, Castaneda AR. Early bidirectional cavopulmonary shunt in young infants–postoperative course and early results. Circulation. 1993;88(pt 2):149–158.

15. Frommelt MA, Frommelt PC, Berger S, Pelech AN, Lewis DA, Tweddell JS, Litwin SB. Does an additional source of pulmonary blood flow alter outcome after a bidirectional cavopulmonary shunt? Circulation. 1995;92(suppl II):II-240–II-244.

16. Spicer RL, Uzark K, Moore JW, Mainwaring RD, Lamberti JJ. Aortopulmonary collateral vessels and prolonged pleural effusions after modified Fontan procedures. Am Heart J. 1996;131:1164–1168.[Medline] [Order article via Infotrieve]

17. Mainwaring RD, Lamberti JJ, Carter TL, Moore JW, Nelson JC. Renin, angiotensin II, and the development of effusions following bidirectional Glenn and Fontan procedures. J Card Surg. 1995;10:111–118.[Medline] [Order article via Infotrieve]

18. Alejos JC, Williams RG, Jarmakani JM, Galindo AJ, Isabel-Jones JB, Drinkwater D, Laks H, Kaplan S. Factors influencing survival in patients undergoing the bidirectional Glenn anastomosis. Am J Cardiol. 1995;75:1048–1050.[Medline] [Order article via Infotrieve]

19. Slavik Z, Webber SA, Lamb RK, Horvath P, LeBlanc JG, Keeton BR, Monro JL, Tuma S, Tax P, Reich O, Sandor GGS, Daubeney PEF, Salmon AP. Influence of bidirectional superior cavopulmonary anastomosis on pulmonary arterial growth. Am J Cardiol. 1995;76:1085–1086.[Medline] [Order article via Infotrieve]

20. Mendelsohn AM, Bove EL, Lupinetti FM, Crowley DC, Lloyd TR, Beekman RH. Central pulmonary artery growth patterns after the bidirectional Glenn procedure. J Thorac Cardiovasc Surg. 1994;107:1284–1290.[Abstract/Free Full Text]

21. Salim MA, Case CL, Sade RM, Watson DC, Alpert BS, DiSessa TG. Pulmonary/systemic flow ratio in children after cavopulmonary anastomosis. J Am Coll Cardiol. 1995;25:735–738.[Abstract]

22. Nakata S, Yasuharu I, Yoshinori T, Kurosawa H, Tenzuka K, Nakazawa M, Ando M, Takao A. A new method for quantitative standardization of cross sectional areas of the pulmonary arteries in congenital heart diseases with decreased pulmonary blood flow. J Thorac Cardiovasc Surg. 1984;88:610–619.[Abstract]

23. Girod DA, Rice MJ, Mair DD, Julsrud PR, Puga FJ, Danielson GK. Relationship of pulmonary artery size to mortality in patients undergoing the Fontan operation. Circulation. 1985;72(suppl II):II-93–II-96.

24. Bridges ND, Farrell PE, Pigott JD, Norwood WI, Chin AJ. Pulmonary artery index: a nonpredictor of operative survival in patients undergoing modified Fontan repair. Circulation. 1989;80(suppl I):I-216–I-221.

25. Srivastava D, Preminger T, Lock JE, Mandell V, Keane JF, Mayer JE, Kozakewich H, Spevak PJ. Hepatic venous blood and the development of pulmonary arteriovenous malformations in congenital heart disease. Circulation. 1995;92:1217–1222.[Abstract/Free Full Text]





This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mainwaring, R. D.
Right arrow Articles by Moore, J. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mainwaring, R. D.
Right arrow Articles by Moore, J. W.
Related Collections
Right arrow Pulmonary circulation and disease
Right arrow Other Treatment
Right arrow Pediatric and congenital heart disease, including cardiovascular surgery