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Ann Thorac Surg 2005;79:29-36
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Additional Pulmonary Blood Flow Has No Adverse Effect on Outcome After Bidirectional Cavopulmonary Anastomosis

^a Clinic for Cardiovascular Surgery, University Hospital, Bern, Switzerland
^b Clinic for Pediatric Cardiac Surgery, Centre Chirurgical Marie-Lannelongue, University Paris Sud, Le Plessis-Robinson, France

Accepted for publication June 2, 2004.

^* Address reprint requests to Dr Berdat, Clinic for Cardiovascular Surgery, Swiss Cardiovascular Center Bern, Inselspital, CH-3010 Bern, Switzerland (E-mail: pascal.berdat{at}insel.ch).

	Abstract

Top Abstract Introduction Material and Methods Results Comment References

 
BACKGROUND: Controversy continues over whether additional sources of pulmonary blood flow are beneficial in combination with a bidirectional cavopulmonary anastomosis. We have therefore assessed the effects of additional pulmonary blood flow on outcome after bidirectional cavopulmonary anastomosis.

METHODS: From 1996 to 2000, 106 patients underwent bidirectional cavopulmonary anastomosis, either isolated (group 1, n = 54), or with additional pulmonary blood flow through the pulmonary artery (group 2, n = 30) or a Blalock-Taussig shunt (group 3, n = 22).

RESULTS: Superior vena cava syndrome was more frequent in group 2 and less in groups 1 and 3 (p < 0.05). Low-output syndrome was more frequent in group 2 and less in group 3 (p = 0.01). Repeated-measures analysis of variance showed higher oxygen saturations with additional pulmonary blood flow (p < 0.05) and significant changes over time (p < 0.0001). Pulmonary pressures, systemic ventricular fractional shortening, end-diastolic diameter index, end-diastolic pressure, and atrioventricular valve regurgitation remained unaffected by additional pulmonary blood flow. Pulmonary artery pressures were lower in group 2 than 3 (p < 0.05). Fractional shortening (p < 0.05) and atrioventricular valve regurgitation (p < 0.0001) changed significantly over time. Fractional shortening showed a strong trend toward different changing patterns with or without additional pulmonary blood flow (p = 0.055), and atrioventricular valve regurgitation showed different changing patterns among the groups (p < 0.005). End-diastolic diameter and pulmonary artery dimensions, which were smaller than normal, remained unchanged. In logistic regression, smaller body surface area at bidirectional cavopulmonary anastomosis, single ventricle, and bidirectional cavopulmonary anastomosis with a Blalock-Taussig shunt were associated with early death. Actuarial survival including total cavopulmonary connection did not differ among groups (p = 0.96).

CONCLUSIONS: We conclude that additional pulmonary blood flow has no adverse effect on outcome after cavopulmonary anastomosis. Additional flow through the main pulmonary artery offers different advantages and disadvantages concerning perioperative complications and pulmonary artery growth compared with additional flow through a Blalock-Taussig shunt.

	Introduction

Top Abstract Introduction Material and Methods Results Comment References

 
The bidirectional Glenn anastomosis (BDG) has become a standard intermediate step toward the Fontan circulation in the management of single-ventricle physiology [1, 2]. Advantages of this procedure include relief of the volume load on the single ventricle, avoidance of pulmonary artery distortion after pulmonary artery banding or modified Blalock-Taussig (BT) shunts, simplification of an eventual total cavopulmonary connection (TCPC), and prevention of pulmonary hypertension. Controversy still exists regarding potential pulmonary artery growth and the usefulness of leaving additional pulmonary blood flow (APBF) with the BDG [3–9]. Additional pulmonary blood flow through a stenosed pulmonary artery or a BT shunt may improve arterial oxygen saturation after BDG, prevent formation of arteriovenous fistulas, and stimulate pulmonary artery growth [10–12]. However, APBF may raise upper central venous pressure, expose the patient to a higher risk of persistent pleural effusions, and may less effectively reduce the volume load on the single ventricle [13, 14]. Furthermore, antegrade APBF through a pulmonary artery may not have the same effects as through a patent BT shunt.

Here we report the short- and long-term effects of APBF and their differences according to the source of APBF in staged palliation of single-ventricle physiology based on a cohort of 106 patients operated on since 1996 at Marie Lannelongue.

	Material and Methods

Top Abstract Introduction Material and Methods Results Comment References

 
We retrospectively reviewed the clinical and surgical records of 106 patients with single-ventricle physiology who underwent BDG between January 1996 and December 2000. Patients were divided into three groups according to the presence of APBF. In group 1 (n = 54), BDG was the only source of pulmonary flow; in group 2 (n = 30), APBF through a natively stenosed (n = 17) or previously banded main pulmonary artery (n = 13); and in group 3 (n = 22), APBF through a patent BT shunt was present. Patient characteristics and previous surgical procedures are summarized in Table 1. Patients were followed up for 28 ± 29.7 months from the BDG (range, 0.03 to 146.2) until completion to TCPC or until December 31, 2000, the end of the observation period of this study. Data obtained at serial follow-up visits at the referring cardiologists included chest radiography, systemic arterial oxygen saturation obtained by pulse oxymetry on room air, and echocardiographic study, assessing ventricular function (fractional shortening) and atrioventricular valve regurgitation. Cardiac catheterization with assessment of oxygen saturations, superior vena cava and pulmonary artery pressures, systemic ventricular end diastolic pressure, pulmonary artery branch anatomy and size, and presence of aortopulmonary, cavocaval, or intrapulmonary arteriovenous collaterals was done in all patients before BDG and repeated in those scheduled for TCPC. Central pulmonary artery branch dimensions, measured directly proximal to the hilar bifurcation, were converted to z-values according to the normograms published by Slavik and coworkers [8]. During the observation period, a total of 28 of 90 patients (31.1%) underwent TCPC 3.4 ± 2.6 years (range, 0.9 to 9.5) after BDG, and 5 patients underwent successful biventricular repair. Indication for TCPC was deep cyanosis in 15 and programed completion in 12 patients.

Statistics
Data are presented as mean ± SD; percentages are given where appropriate. Statistical analysis was performed using Statview 4.57 for Windows (SAS Institute, Cary, NC). For continuous variables comparing serial values, repeated-measures analysis of variance was used. First, analysis of variance (ANOVA) was performed with the grouping variable APBF, namely, group 1 versus groups 2 plus 3, followed by a second analysis of all three separate groups. For within-group and between-group analysis, a Mann-Whitney U test and a Fisher's exact test were used, respectively. The Kaplan-Meier method and log-rank test were used for actuarial survival analysis. Univariate and multiple linear regression analyses were performed to investigate the relationships between various independent variables and early death. A p value of less than 0.05 or lower (according to Bonferroni correction where appropriate) was determined statistically significant.

	Results

Top Abstract Introduction Material and Methods Results Comment References

 
Outcome After Bidirectional Cavopulmonary Anastomosis
Early outcome after BDG is summarized in Table 2. Six patients (5.7%) died in the early postoperative period, 3 in group 1 (5.5%) of cardiac failure, 1 in group 2 (3.3%) of sepsis, and 2 in group 3 (9.1%) of multiorgan and cardiac failure. Twelve patients (11.3%) had their BDG anastomosis taken down, and 3 of these died postoperatively. The BDG take-down became necessary because of high pulmonary artery pressures in 5, low oxygen saturations in 2, a combination of both in 2, low output failure in 2, and pulmonary hypercirculation in 1. All but 1 of the 12 patients having their BDG taken down were borderline candidates with severe AV valve regurgitation (3 patients) or stenosis (1), pulmonary venous stenosis (1), high pulmonary pressures before BDG (2), very hypoplastic pulmonary arteries (2), or other reasons (2). There were significantly fewer cases of superior vena cava syndromes (defined as swelling and bluish color of head and neck with persistently elevated upper central venous pressure and cyanosis) in groups 1 and 3 and significantly more in group 2 than expected (p < 0.05). Clinically estimated low cardiac output was significantly more frequent in group 2 and less in group 3 than expected (p = 0.01). Other complications, namely, early reoperation for revision of the BDG (excluding take-down) or bleeding, prolonged pleural effusions (longer than 10 days), pulmonary artery branch thrombosis, renal failure (need for dialysis), infections (pulmonary, wound), and neurologic events (focal neurologic deficits, new seizures) were evenly distributed among the groups. Duration of ventilatory support, intensive care unit, and hospital stay were all similar in the groups. Univariate analysis identified smaller body surface area (p < 0.05) and single ventricle (p < 0.002), whereas logistic regression analysis identified smaller body surface area, single ventricle, and APBF through BT shunt as risk factors for early death after BDG (Table 3).

View larger version (15K): [in this window] [in a new window]   Fig 1. Estimated Kaplan-Meyer survival curve for freedom of all events after bidirectional Glenn anastomosis, including total cavopulmonary connection outcome. Differences not significant (p = 0.96, Mantel-Cox) among groups 1, 2, and 3.

View larger version (21K): [in this window] [in a new window]   Fig 2. Repeated-measures analysis of variance; p values for group effect, time effect, and interaction are depicted. (A) Arterial oxygen saturations: *p < 0.01, group 1 versus 2; p = 0.005, group 1 versus 3; +p < 0.05, group 2 versus 3. (BDG = bidirectional Glenn anastomosis; open squares = group 2; solid squares = group 3; TCPC = total cavopulmonary connection; triangles = group 1.) (B) Pulmonary artery pressures: *p = 0.01, group 1 versus 3. (Open squares = group 2; solid squares = group 3; triangles = group 1.) Stratified by groups 1, 2, and 3.

Systemic Ventricle Function
Systemic ventricle fractional shortening before BDG was significantly higher in group 1 than group 2 (p < 0.005; Fig 3, A). Fractional shortening after BDG and before TCPC was not statistically different between the groups. Repeated-measures analysis of variance showed no relevant effect of APBF on fractional shortening. However, fractional shortening changed significantly during the observation period (p < 0.05), and showed a strong trend toward different changing patterns with or without APBF (p = 0.055). Fractional shortening changed also significantly during the observation period within groups 1, 2, and 3 (p < 0.05). Systemic ventricular end-diastolic diameter index was significantly greater in patients before isolated BDG (group 1) than before BDG with APBF (groups 2 and 3; p < 0.005) and in group 1 compared with group 3 (p = 0.001; Fig 3, B). End-diastolic diameter decreased in all groups (p = not significant) from before to early after BDG, but was still greater in isolated BDG (group 1) than in BDG with APBF (groups 2 and 3; p < 0.02). End-diastolic diameter increased in all groups between BDG and TCPC (p = not significant), and remained significantly larger in group 1 compared with group 3 (p < 0.01). Systemic ventricle end-diastolic pressures before BDG and TCPC were not statistically different between the groups. Repeated-measures ANOVA revealed no effect of APBF on end-diastolic pressure and no significant change during the observation period. Analysis of the three groups separately showed no difference between the groups as well (Fig 3, C). Similar proportions of patients of all groups showed abnormal AV valves (54%, 60%, 56% in groups 1, 2 and 3, respectively). Degrees of AV valve regurgitation were not statistically different between the groups before and early after BDG or before TCPC (Fig 3, D). Atrioventricular valve regurgitation decreased significantly from before to early after BDG in group 2 (p < 0.02), increased significantly from early after BDG to before TCPC in groups 1 (p < 0.05) and 2 (p < 0.05), whereas it remained unchanged in group 3. There was no significant difference of AV valve regurgitation from before BDG to before TCPC in any group. Repeated-measures ANOVA showed no effect of APBF on AV valve regurgitation. However, there were significant changes of AV valve regurgitation during the observation period (p = 0.0002) with similar changing pattern. Analysis of the three groups separately demonstrated significant changes over time (p < 0.0001) with significantly different changing patterns of the groups (p < 0.005). Atrioventricular valve regurgitation changed significantly from before BDG to before TCPC (p < 0.005) and from early after BDG to before TCPC (p < 0.0001).

View larger version (23K): [in this window] [in a new window]   Fig 3. Repeated-measures analysis of variance; p values for group effect, time effect, and interaction are depicted. (A) Systemic ventricle (SV) fractional shortening, obtained from cardiac catheterization: *p < 0.005, group 1 versus 2 and 3. (APBF = additional pulmonary blood flow; BDG = bidirectional Glenn anastomosis; solid squares = with APBF, groups 2 and 3; TCPC = total cavopulmonary connection; triangles = without APBF, group 1.) (B) Systemic ventricle end-diastolic diameter index (SVEDDI), obtained from cardiac catheterization (Fisher's exact test): *p = 0.001, group 1 versus 3; **p < 0.01, group 1 versus 3. (Open squares = group 2; solid squares = group 3; triangles = group 1.) (C) Systemic ventricle end-diastolic pressure (SVEDP), obtained from cardiac catheterization. (Open squares = group 2; solid squares = group 3; triangles = group 1.) (D) Atrioventricular valve (AV) regurgitation (grade 0 to 4), evaluated by serial echocardiography: *p < 0.02 for group 2; **p < 0.05 for groups 1 and 2. (Open squares = group 2; solid squares = group 3; triangles = group 1.) Stratified by groups 1, 2, and 3 (B–D).

	Comment

Top Abstract Introduction Material and Methods Results Comment References

Previous studies demonstrated higher oxygen saturation and lower hospital mortality rates among patients with APBF compared with patients in whom bidirectional cavopulmonary anastomosis was the only source of pulmonary blood flow [9, 15, 16]. The present experience supports these findings in terms of significantly higher oxygen saturations after bidirectional cavopulmonary anastomosis with APBF.

Although some studies did not demonstrate increased rates of persistent pleural effusions and development of superior vena cava syndrome [10], we and others [13, 14] have found significantly higher rates of superior vena cava syndrome, cardiac low output, and arrhythmias after creation of the bidirectional cavopulmonary anastomosis in the presence of APBF through the main pulmonary artery. These complications, however, did not entail longer intensive care unit or hospital stay after bidirectional cavopulmonary anastomosis, as shown by others [5, 9, 17, 18]. In contrast, APBF through a BT shunt showed significantly less superior vena cava syndrome, cardiac low output, and arrhythmias than expected, but was an independent risk factor for death after bidirectional cavopulmonary anastomosis in logistic regression analysis.

Some reports have shown increased pulmonary pressures in patients with APBF compared with isolated BDG [12–14, 17, 18]. We, like others [3, 10], could not corroborate these findings, as pulmonary artery pressures were unaffected by APBF. Interestingly, pressures were significantly lower with APBF through an open pulmonary artery than through the BT shunt.

Exclusion of all other sources of pulmonary blood flow at the time of BDG is aimed at volume unloading the single ventricle, improving its function and reducing AV valve regurgitation [14]. We, like others [10, 11], cannot share concerns about incomplete unloading with consecutive worsening of systemic ventricular function and AV valve regurgitation in the presence of APBF. Ventricular function, as assessed by serial measurements of fractional shortening, end-diastolic diameter, and end-diastolic pressure, remained unaffected by the presence of APBF in our series. On the contrary, although in patients without APBF, fractional shortening was significantly better before BDG, it significantly decreased until TCPC and was finally not better than in patients with APBF. Furthermore, repeated-measures analysis of variance showed a strong trend toward a significantly more stable course of systemic ventricle fractional shortening with than without APBF. Atrioventricular valve regurgitation also seemed not to be negatively influenced by APBF and even showed a significant decrease in patients with APBF through an open pulmonary artery early after the BDG. Reduction in AV valve regurgitation was a temporary effect in these patients, however, as it returned to previous bidirectional cavopulmonary anastomosis levels on follow-up. Patients with isolated BDG even showed significant worsening of AV valve regurgitation until TCPC. In contrast, AV valve function remained stable after the BDG in patients with APBF through BT shunt. The findings of others [10, 11], showing no adverse effect of APBF through the main pulmonary artery on late AV valve regurgitation, are therefore supported by ours.

The potential for growth of the pulmonary arteries after BDG with or without APBF still remains controversial. While Mendelsohn and coworkers [7] questioned the adequacy of pulmonary artery growth, Reddy and colleagues [6] demonstrated no reduced growth after isolated BDG. Others suggested increased pulmonary artery growth in the presence of APBF through the main pulmonary artery [3, 10], whereas others did not [11, 16]. Our results also demonstrate growth of the pulmonary arteries, albeit unaffected by the presence of APBF. However, growth of the right pulmonary artery was best in the presence of APBF through the main pulmonary artery, whereas the left pulmonary artery showed impaired growth in the presence of APBF through the BT shunt. One may speculate that rigidity of the BT shunt and scar formation at the anastomotic site or decreased flow in the central part of the left pulmonary artery may negatively affect pulmonary artery development.

Several previous reports have suggested that APBF may prevent development of intrapulmonary arteriovenous malformations late after BDG [10–12]. Similarly, we have not seen any late development of these vascular malformations in our series during follow-up.

It is important to consider the source of APBF, since we, like others [12, 19], have found relevant differences between APBF through the main pulmonary artery compared with APBF through the BT shunt. Additional pulmonary blood flow through the main pulmonary artery shows significantly lower pulmonary artery pressures than with APBF through the BT shunt and may increase the risks for superior vena cava syndrome, cardiac arrhythmias, and low output after BDG, which all may be the consequences of the more difficult control of pulmonary blood flow through an open pulmonary trunk. Nevertheless, this type of APBF stimulates right pulmonary artery growth. In contrast, APBF through a BT shunt may reduce the risks of superior vena cava syndrome and cardiac complications after BDG, but it negatively affects left pulmonary artery growth and is an independent risk factor for early death after BDG. Although pulmonary artery pressures were lower with APBF through the main pulmonary artery than with a BT shunt, superior vena cava syndrome was more frequent in group 2. The reasons for this paradoxic finding remain speculative. A BT shunt on the contralateral pulmonary artery may not increase pulmonary artery pressures on the side of the BDG, owing to the preferential flow to the contralateral lung, while blood flow across the main pulmonary artery may be evenly distributed between left and right or even show preferential flow to the right side. Furthermore, in this study mean pulmonary pressures were analyzed. However, with APBF through the main pulmonary artery, systolic pressures and the pulsatile nature of pulmonary blood flow may be more important than mean pressure for superior vena cava syndrome to occur. One may also speculate that a wider range of pressures and flows across the main pulmonary artery, due to a more difficult process of pressure and flow calibration with the banding and a less fixed gradient than across a BT shunt, may favor the development of superior vena cava syndrome.

Having identified the presence of a BT shunt as an independent risk factor for death is concerning, and the reasons for that are not obvious. Impeded pulmonary artery growth, altered patterns of flow with the shunt physiology, and acute shunt complications may play a role. Furthermore, the need for a BT shunt may be a surrogate marker for a borderline candidate for BDG, having a shunt added at the time of the BDG procedure because of poor saturations or poor hemodynamics with a BDG alone. Additionally, patients coming to BDG with a BT shunt previously placed may have an abnormal pulmonary vascular bed due to pulmonary atresia or pulmonary artery distortion, and therefore may be less ideal candidates.

Whether adding a source of pulmonary blood flow to the BDG and delaying TCPC is a better strategy than isolated BDG and earlier TCPC is presently not clear. Early TCPC at the age of 2 to 4 years is advocated to shorten the period of hypoxemia and volume overload and reduce the need for additional shunt procedures before TCPC [20]. However, very young infants have shown higher pulmonary vascular resistance, lower oxygen saturations, and more arrhythmias after TCPC than older ones [20]. Furthermore, placement of adequately sized Gore-Tex grafts to perform an extracardiac TCPC, the preferred method of many surgeons today, may be difficult in small infants and may entail the need for later replacement or anticoagulation. On the other hand, APBF offers a pulsatile pulmonary blood flow, which may reduce endothelial dysfunction and favor growth of the pulmonary vascular bed and avoid development of pulmonary arteriovenous malformations. It may also allow recruitment of borderline candidates and potentially longer intervals to TCPC. However, calibrating the additional blood flow to the lungs may be difficult and necessitate repeat interventions. Furthermore, APBF through BT shunt exposes the patient to its inherent risks of long-term complications. Additionally, early morbidity after BDG with APBF may be increased. Taken together, the decision to use an additional source of pulmonary blood flow depends on the purpose it should serve: Should it be added to recruit also borderline candidates for a potential staged palliation of single-ventricle physiology, or is it merely an escape route in the setting of low oxygen saturations or poor hemodynamics in the presence of a new BDG? Should it allow for longer intervals to TCPC or even avoid TCPC in patients who would probably never qualify? We believe that the present study may not give the answer to all these questions, however, it shows what risks and benefits may be anticipated with APBF. It may or may not be a good thing to leave patients for longer periods of time on BDG, irrespective of the presence or absence of APBF. However, our data suggest that there are no apparent shortcomings of APBF on hemodynamics or saturation levels, at least in the intermediate term.

We conclude that APBF combined with a bidirectional Glenn anastomosis has no adverse effect on outcome after cavopulmonary anastomosis in patients with staged palliation of single-ventricle physiology. Oxygen saturation is higher than without APBF, cardiac function is preserved, and ventricular unloading is not impaired. Additional pulmonary blood flow has no rising effect on pulmonary pressures, and changes in AV valve function may depend more on its performance before BDG than the presence of APBF. However, APBF through the main pulmonary artery offers different advantages and disadvantages concerning perioperative complications and pulmonary artery growth compared with APBF through a BT shunt.

Study Limitations
The power of the present study is limited in that it is not a randomized study. Our control population, patients without APBF, is therefore not matched; and the present differences in baseline characteristics, with significantly younger patients with better ventricular function in this group, that are the consequences of selection bias may potentially have influenced the outcome measures. Despite these imperfections, our findings appear to be generally applicable, as they are in close concordance with those of recently published studies [10]. It also offers more detailed information on differences between various sources of APBF.

	References

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