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Ann Thorac Surg 2009;88:830-838. doi:10.1016/j.athoracsur.2009.05.051
© 2009 The Society of Thoracic Surgeons
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Right arrow Congenital - cyanotic

Original Articles: Pediatric Cardiac

Management of a Stenotic Right Ventricle-Pulmonary Artery Shunt Early After the Norwood Procedure

Tain-Yen Hsia, MDa,*, Francesco Migliavacca, PhDb, Giancarlo Pennati, PhDb, Rossella Balossino, PhDb, Gabriele Dubini, PhDb, Marc R. de Leval, MDc, Scott M. Bradley, MDa, Edward L. Bove, MDd

a Section of Pediatric Cardiothoracic Surgery, Medical University of South Carolina, Charleston, South Carolina
b Laboratory of Biological Structure Mechanics, Politecnico di Milano, Milan, Italy
c International Congenital Cardiac Centre, London, United Kingdom
d Section of Cardiac Surgery, University of Michigan School of Medicine, Ann Arbor, Michigan

Accepted for publication May 15, 2009.

* Address correspondence to Dr Hsia, Cardiothoracic Surgery, Medical University of South Carolina, 96 Jonathan Lucas St, CSB 409, Charleston, SC 29425 (Email: hsiaty{at}musc.edu).

Presented at the Forty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Francisco, CA, Jan 26–28, 2009.


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 Reference
 
Background: Inadequate pulmonary blood flow through a right ventricle-to-pulmonary artery (RV-PA) shunt early after the Norwood operation can be remedied by adding a modified Blalock-Taussig (mBT) shunt. We used multiscale computational modeling to determine whether the stenotic RV-PA shunt should be left in situ or removed.

Methods: Models of the Norwood circulation were constructed with (1) a 5-mm RV-PA shunt, (2) a RV-PA shunt with 3- or 2-mm stenosis at the RV anastomosis, (3) a stenotic RV-PA shunt plus a 3.0- or 3.5-mm mBT shunt, or (4) a 3.5-mm mBT shunt. A hydraulic network that mathematically describes an entire circulatory system with pre-stage 2 hemodynamics was used to predict local dynamics within the Norwood circulation. Global variables including total cardiac output, mixed venous oxygen saturation, stroke work, and systemic oxygen delivery can be computed.

Results: Proximal stenosis of the RV-PA shunt results in decreased pulmonary blood flow, total cardiac output, mixed venous saturation, and oxygen delivery. Addition of a 3.0- or 3.5-mm mBT shunt leads to pulmonary overcirculation, lowers systemic oxygen delivery, and decreases coronary perfusion pressure. Diastolic runoff through the stenotic RV-PA shunt dramatically increases retrograde flow into the single ventricle. Removal of the stenotic RV-PA shunt balances systemic and pulmonary blood flow, eliminates regurgitant flow into the single ventricle, and improves systemic oxygen delivery.

Conclusions: Adding a mBT shunt to remedy a stenotic RV-PA shunt early after a Norwood operation can lead to pulmonary overcirculation and may decrease systemic oxygen delivery. The stenotic RV-PA shunt should be taken down. Conversion to an optimal mBT shunt is preferable to augmenting a stenotic RV-PA shunt with a smaller mBT shunt.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 Reference
 
Instead of a modified Blalock-Taussig (mBT) shunt, a right ventricle-to-pulmonary artery (RV-PA) shunt is an alternative source of pulmonary blood flow in the Norwood operation for hypoplastic left heart syndrome. By eliminating the obligatory diastolic runoff in the mBT shunt, the main proposed benefits of the RV-PA shunt include better coronary and systemic perfusion, more balanced and predictable pulmonary-to-systemic flow ratio, and decreased ventricular volume loading [1]. However, there are concerns of the consequences of the ventriculotomy and diastolic flow regurgitation on the single systemic RV. An ongoing randomized controlled trial aims to answer whether the theoretic advantages of the RV-PA shunt translate to improved clinical outcomes [2]. Controversies remain about which shunt strategy produces better postoperative hemodynamics, pulmonary arterial growth, and patient survival [3].

In the interim, there is a growing awareness that premature stenosis of the RV-PA shunt can lead to early oxygen desaturation and contribute to interstage morbidity and death [4–6]. Recognized initially by Sano and colleagues [5], early shunt obstruction is primarily due to proximal stenosis at the right ventricular anastomosis. Many centers are performing stage 2 palliation earlier in Norwood patients with RV-PA shunts, some as early as age 3 months, because of worsening cyanosis [7–9]. However, RV-PA shunt stenosis during or shortly after the Norwood operation, at a time when a superior cavopulmonary connection is not feasible, requires catheter intervention or surgical revision.

Two recent reports have documented an increased incidence of shunt intervention in Norwood patients with RV-PA shunts compared with patients with a mBT shunt [10, 11]. Stent placement can distort the RV-PA shunt, and many surgeons are reluctant to advocate catheter manipulation and stent deployment across a highly obstructed obligatory source of pulmonary blood flow [4, 12, 13]. Surgical revision of proximal RV-PA shunt stenosis requires rearresting the heart to prevent air embolism. The other two alternatives are conversion to a mBT shunt or augmenting the RV-PA shunt with an additional mBT shunt. The influence of either strategy on flow dynamics, such as diastolic runoff, and on systemic physiology, such as oxygen delivery and cardiac stroke work, is unknown.

This study was conducted to determine whether the stenotic RV-PA shunt should remain open as a source of pulmonary blood flow when a mBT shunt is used to remedy inadequate pulmonary blood flow early after a RV-PA Norwood operation. We used a recently introduced and validated multiscale computational modeling approach, where three-dimensional (3D) computational fluid dynamics (CFD) models of the Norwood reconstruction are coupled to a network description of the entire circulatory system, using clinical patient hemodynamic data [14, 15]. The multiscale computation quantifies the flow dynamics in the CFD model, such as pressures and flow in the Norwood circulation, as well as global variables such as systemic oxygen delivery [16, 17]. We studied various models of proximal RV-PA shunt stenosis, and their correction, by adding a mBT shunt or conversion to a mBT shunt as the sole source of pulmonary blood flow.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Discussion
 Acknowledgments
 References
 Reference
 
The mathematic equations and computational methodologies applied in our previous multiscale modeling studies were used in this study [14, 15, 17–19]. Briefly, the multiscale approach couples a 3D CFD model of the Norwood procedure to a 0D lumped parameter or hydraulic network description of the entire circulation outside of the surgical domain. Figure 1 depicts a multiscale model of a Norwood procedure with a RV-PA shunt. The multiscale simulation solves the flow and pressure dynamics at any part of the surgical domain of the Norwood procedure, such as flow regurgitation in the RV-PA shunt and coronary perfusion pressure. At the same time, physiologic variables such as systemic oxygen delivery and right ventricular stroke work can also be calculated.


Figure 1
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  		Fig 1. Schematics of the multiscale model of a 5-mm right ventricle to pulmonary artery shunt Norwood circulation that couples a 3-dimensional computational fluid dynamics model to the lumped parameter network of the entire circulation. (AO = aorta; ASD = atrial septal defect; CA1 = coronary artery 1; CA2 = coronary artery 2; CB = coronary bed; CV = coronary vein; LA = left atrium; LBA = lower body arteries; LBB = lower body bed; LVB = lower body veins; NEOAO = neoaorta; PAB = pulmonary arterial bed; PVB = pulmonary venous bed; RA = right atrium; SVP = single ventricle physiology; TRIC = tricuspid valve; UBA = upper body arteries; UBB = upper body bed; UBV = upper body veins.)

 
3D Models
Six different detailed 3D models of the Norwood procedure based on the finite volume method were developed. Figure 2A depicts a 5-mm RV-PA shunt with no proximal stenosis. Figure 2B depicts 5-mm RV-PA shunt models with either a 2- or 3-mm proximal stenosis (2 models). Figure 2C depicts the stenotic RV-PA shunt models plus a 3-mm mBT shunt between the innominate artery and right pulmonary artery (2 models). Figure 2D depicts a 3.5-mm mBT shunt Norwood.


Figure 2
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  		Fig 2. Three-dimensional computational fluid dynamics models of the various shunt configurations: (A) 5-mm right ventricular-pulmonary artery (RV-PA) shunt, (B) 5-mm RV-PA shunt with proximal stenosis, (C) 3-mm modified Blalock-Taussig shunt added to the stenotic RV-PA shunt, and (D) 3.5-mm Blalock-Taussig shunt only.

 
The geometric dimensions of the various vessels were obtained from angiograms of a group of patients before stage 2 palliation, as described previously. Other than the source(s) of pulmonary blood flow, all models were created with the same anatomy. Meshes were developed using approximately 130,000 4-node tetrahedral volumetric elements. The boundary conditions, segregated solvers, and the implicit backward Euler method used as the time integration technique were identical for the 6 models. Four cardiac cycles were simulated for each CFD model to ensure stable computational solution. The Fluent general-purpose fluid dynamic code (Fluent Inc. Lebanon, NH) was used for the finite volume calculations.

Lumped Parameter Network
All lumped parameter networks coupled to the 8 models are identical and describe the circulatory network of the entire body minus the 3D surgical domain. Data from 28 Norwood patients at the prestage 2 catheterization were used to construct the mathematic network [14, 19]. There were 4 subsystems: heart, systemic, pulmonary, and coronary circulations. A model defined in a previous study from our laboratory was used for the heart [20]. Time varying elastances were used to model the right and left atria, and the single RV. Nonlinear resistances were adopted to describe the ventricular inflow and outflow valves, whereas a linear term models a nonrestrictive atrial septal defect.

The systemic circulation is further divided into 7 arterial and venous compartments, and the pulmonary circulation into 4. Four compartments represent the coronary circulation, where a pressure generator controlled by the RV pressures reproduces the intramyocardial pressure. The main parametric values used in all the mathematic models are as follows: body surface area of 0.33 m2, pulmonary vascular resistance of 2.3 mm Hg · m–2 · L–1 · min–1, systemic vascular resistance of 21.6 mm Hg · m–2 · L–1 · min–1, heart rate of 120 beats/min, hemoglobin value of 16.52 g/dL, oxygen consumption of 156.83 mL/min/m2, and pulmonary venous oxygen saturation of 98%.

Multiscale Solution
The coupling between the 2 models described above (3D and lumped parameter), characterized by different levels of detail, was accomplished by means of interface conditions of flow rates and pressures [15]. The finite volume method, adopted for the 3D models, solves the mass and momentum conservation equations for an incompressible Newtonian fluid (ie, the Navier-Stokes equations). The lumped parameter network is described by a nonlinear algebraic differential equation system containing forcing terms derived from interface conditions with the 3D finite volume model.

According to the above interface conditions, uniform time-dependent pressures were imposed at the boundaries of the 3D model, while the local velocity profiles were not forced, but calculated, at each time instant. This allowed detection of possible reversal flows at the interfaces. Detailed sensitivity analysis to assess the validity and stability of the computational solutions, and to define proper mesh and time-step conditions, has been previously described in detail [16]. All simulations were done on a Pentium IV (Intel, Santa Clara, CA) 2.8-GHz personal computer. Time required for the simulation of 1 cardiac cycle was about 12 hours.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Discussion
 Acknowledgments
 References
 Reference
 
For each of the 6 models, the multiscale approach provides solutions to both pressure and flow dynamics within the 3D Norwood model and to physiologic variables from the lumped parameter network. Because of the large number of potential variables that can be generated with each simulation, only those that are most clinically relevant are presented. These data are summarized in Table 1. Variables derived from the 3D models include aortic and pulmonary arterial pressures and flow, coronary arterial flow and perfusion pressure, and retrograde flow through the RV-PA shunt. Cardiac output (CO) is the summation of flow between systemic blood flow (Qs) and pulmonary blood flow (Qp). RV performance can be evaluated from pressure-volume loops generated from the heart component of the lumped parameter network, including ejection fraction, stroke work, and mechanical efficiency (stroke work/total mechanical energy). Moreover, oxygen transport equations, combined with the multiscale approach, allow calculations of systemic and mixed venous oxygen saturations [14, 19]. Figures 3 and 4 Go graphically demonstrate systemic oxygen delivery and retrograde flow through the RV-PA shunt in 4 of the 6 models: (1) 5-mm RV-PA shunt, (2) 5-mm RV-PA shunt with a 3-mm proximal stenosis, (3) 3-mm mBT shunt added to the stenotic RV-PA shunt, and (4) 5-mm mBT shunt models.


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  		Table 1 Multiscale Modeling Results
 

Figure 3
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  		Fig 3. (A) Systemic oxygen delivery and (B) diastolic regurgitant flow through the right-ventricular-pulmonary artery (RV-PA) shunt as percentage of pulmonary blood flow (Qp) for 4 models: 5-mm RV-PA shunt, 5-mm RV-PA shunt with a 3-mm proximal stenosis, 3-mm modified Blalock-Taussig shunt added to the stenotic RV-PA shunt, and 3.5-mm modified Blalock-Taussig shunt only.

 

Figure 4
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  		Fig 4. Simulated right ventricular pressure-volume loops for 3 models: 3-mm modified Blalock-Taussig (mBT) shunt added to a 5-mm right-ventricular-pulmonary artery (RV-PA) shunt with a 2-mm proximal stenosis, a 3-mm mBT shunt added to a 5-mm RV-PA shunt with 3-mm proximal stenosis, and a 3.5-mm mBT shunt only.

 
Model of 5-mm RV-PA Shunt With 2- or 3-mm Proximal Stenosis
As expected, proximal stenosis of the 5-mm RV-PA shunt leads to progressive loss of pulmonary blood flow and pressure, lower Qp/Qs, and decreased systemic oxygen delivery (Fig 3). There is associated drop of both arterial and mixed venous saturations. Because of higher Qs, coronary perfusion and pressure are both slightly increased. Ventricular mechanical efficiency is reduced, along with lower stroke work, as stroke volume is less. Retrograde flow through the RV-PA shunt becomes lower as there is less cardiac output (Fig 4).

Adding a 3-mm mBT Shunt to the Stenotic RV-PA Shunt
Adding a 3-mm mBT shunt to augment either of the 2 stenotic RV-PA shunts (3-mm and 2-mm proximal stenoses) leads to increased pulmonary blood flow, Qp/Qs, systemic and mixed venous saturations, and cardiac output. Despite increased ejection fraction and RV mechanical efficiency, both models resulted in higher stroke work than those without the mBT shunt, with markedly reduced coronary perfusion. In the model where a 3-mm mBT shunt was added to augment the 3-mm stenotic RV-PA shunt, there is pulmonary overcirculation (Qp/Qs = 1.4), and further reduction in oxygen delivery from 578.3 to 552.8 mL/min/m2 from that without the mBT shunt (Fig 3). In both models, adding a 3-mm mBT shunt dramatically increases retrograde flow through the RV-PA shunt into the single ventricle (Fig. 4).

Adding a 3.5-mm BT Shunt and Removal of the Stenotic RV-PA Shunt
Conversion to a 3.5-mm mBT shunt restores a more balanced Qp/Qs and improves systemic oxygen delivery (Fig 3). Both arterial and mixed venous oxygen saturations are slightly lower, but coronary arterial perfusion and pressure are higher. Despite lower ejection fraction and mechanical efficiency, the ventricular pressure-volume loop showed lower stroke work in the 3.5-mm mBT shunt model (Fig 4). By removing the stenotic RV-PA shunt, regurgitant flow into the RV is eliminated.


   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Discussion
 Acknowledgments
 References
 Reference
 
This mathematic modeling investigation demonstrates that when a mBT shunt is used to remedy inadequate pulmonary blood flow as a result of proximal RV-PA shunt stenosis, conversion to an optimal sized mBT shunt is preferable to augmenting the stenotic RV-PA shunt with a smaller mBT shunt. Adding a mBT shunt to the stenotic RV-PA shunt in the Norwood circulation leads to pulmonary overcirculation, decreased systemic oxygen delivery, significant increases in the diastolic regurgitant flow into the right ventricle through the RV-PA shunt, and reduced coronary perfusion. Moreover, by removing the stenotic RV-PA shunt, an improved RV stroke work in the mBT shunt-only simulation suggests that ventricular wall stress is lower at a given stroke volume or cardiac output. This study of the recently introduced and validated multiscale modeling approach to mathematically examine the hemodynamic and physiologic effects of RV-PA shunt stenosis answers a specific question of whether a stenotic RVPA shunt should be removed when a mBT shunt is added to the Norwood circulation.

The recent introduction of an RV-PA shunt in the Norwood operation has led to an ongoing debate regarding the optimal source of pulmonary blood flow. Armed with early reports of improved clinical outcomes and personal/institutional experiences many centers have elected an RV-PA shunt Norwood strategy [21–23]. In a survey of 38 international centers that perform the Norwood operation that are not participating in the National Institutes of Health-sponsored randomized controlled Single Ventricle Reconstruction trial, nearly 50% are preferentially using the RV-PA shunt during the Norwood operation [3].

Along with the broader application of the RV-PA shunt, and perhaps due to the associated learning curve, an increasing number of reports have described a higher incidence of early shunt stenosis [4, 21, 24, 25]. RV-PA shunt stenosis can occur at three levels: (1) proximal RV anastomosis, (2) within the shunt, and (3) distal pulmonary arterial connection. Proximal stenosis can be due to inadequate ventricular resection, myocardial hypertrophy, or fibrointimal hyperplasia [4, 24]. Intraluminal and distal stenosis are usually due to pseudointimal peel, tension, or kinking of the shunt. RV-PA shunt stenosis results in progressive oxygen desaturation, and can lead to sudden interstage death [14]. Several studies have shown lower interstage oxygen saturations in the RV-PA shunt Norwood patients and report the need for earlier second-stage superior cavopulmonary connection or aggressive medical therapy of increasing preload and β-blockade [6, 11, 25, 26].

RV-PA shunt stenosis recognized in the operating room or early in the postoperative period, or when a superior cavopulmonary connection is not feasible, required either surgical or catheter intervention. Significant higher incidence of shunt intervention has been reported in patients receiving the RV-PA shunt [10, 11]. Realized by Sano and colleagues [5] in their initial experience, and supported by subsequent reports, early RV-PA shunt stenosis occurs primarily at the proximal level [21, 24, 25, 27].

Catheter intervention with stent placement to relieve proximal stenosis requires intraluminal manipulation of the sole source of pulmonary perfusion, can result in shunt distortion, and increases the difficulty of RV-PA shunt takedown at the stage 2 operation. Most successful reports remain small series from expert interventionalists [24, 25, 28, 29]. Surgical revision of the proximal anastomosis necessitates cardiopulmonary bypass and may also require cardioplegic cardiac arrest to obtain adequate ventricular resection and to prevent systemic air embolism. Placing a mBT shunt is an effective alternative that can restore adequate pulmonary blood flow expeditiously without the need for cardiopulmonary bypass, or aortic cross-clamping. Of the 13 patients with a RV-PA shunt Norwood operation who required surgical intervention in the Children's Hospital of Philadelphia series, 8 were converted to a mBT shunt with RV-PA shunt removal.

By restoring a more balanced Qp/Qs, this study suggests removing the stenotic RV-PA shunt, after adding an optimal mBT shunt, increases systemic and coronary arterial perfusion and pressure. As a consequence, conversion to a mBT shunt as the sole source of pulmonary blood flow results in improved systemic oxygen delivery, which remains the primary physiologic goal of postoperative management of a Norwood patient [27]. The pressure-volume loops generated from the heart component of the multiscale model also predicted a lower stroke work when the stenotic RV-PA shunt is removed, suggesting a lower ventricular wall stress. A lower stroke work signifies that the single ventricle generates less power, or pressure, to eject an equivalent stroke volume, or cardiac output. Removing the stenotic RV-PA shunt may therefore benefit the ventricular performance and longevity of the systemic RV that has sustained a ventriculotomy incision, by decrease stroke work, increase coronary arterial perfusion, and eliminating regurgitant flow.

Furthermore, by eliminating the diastolic regurgitant flow through the RV-PA shunt, conversion to a mBT shunt removes a significant volume load on the RV. Continuous diastolic runoff through the mBT shunt is obligatory in the Norwood circulation, while regurgitant flow through the RV-PA shunt during diastole has been observed clinically [30]. However, when a mBT is added to augment the stenotic RV-PA shunt, the stenotic RV-PA shunt acts as a conduit to promote the diastolic runoff through the mBT shunt into the RV in a retrograde fashion. The resulting accentuated steal from the coronary circulation eliminates a main advantage of the RV-PA shunt, which is its superiority in coronary perfusion compared with a mBT shunt [1, 14]. Although the long term effect of the added volume load and ventriculotomy on the RV is unknown, there is recent evidence of reduced ventricular contractility after second- or third-stage palliations in those patients who had an initial RV-PA shunt Norwood procedure [9].

Despite the advantages of being able to correlate local pressure and flow effects of shunt strategies with systemic physiologic parameters, the multiscale modeling approach described in this report has several limitations. Present mathematic modeling studies, including ours, remain unable to completely account for biologic adaptation and cardiovascular autoregulation, including the coronary circulation. For example, the effect of cyanosis on myocardial function and vascular tone cannot be simulated. Also, physical growth and the accompanying physiologic maturation are not account for. Ventricular adaptation to different volume loading conditions is not well understood and may variably affect the resulting RV performance acutely and chronically. The hemodynamic variables used to construct the multiscale models are from clinical investigations of patients before superior cavopulmonary connections and, therefore, are not reflective of intraoperative or early postoperative conditions. However, by simulating late interstage conditions, the modeling examines the effects of various shunt configurations on hemodynamics and physiology before stage 2. The immediate goal of the Norwood operation is to optimize interstage physiology and limit morbidity and mortality before second-stage conversion.

In conclusion, the multiscale modeling approach indicates that when a mBT shunt is added to augment a stenotic RV-PA shunt in the Norwood circulation, pulmonary overcirculation and decreased systemic oxygen delivery can occur. Moreover, there is increased stroke work as well as significant accentuation of the diastolic regurgitant flow into the RV through the stenotic RV-PA shunt. Replacing the stenotic RV-PA shunt with an optimal mBT shunt restores a balanced Qp/Qs, improves systemic oxygen delivery, and removes the added diastolic volume load on the RV. These simulations suggest that conversion to an optimally sized mBT shunt is preferable to augmenting the stenotic RV-PA shunt with a smaller mBT shunt.


   Discussion
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
Acknowledgments
 References
 Reference
 
DR CHRISTIAN PIZARRO (Wilmington, DE): That was a beautiful presentation and a very elegant study. The essence of this model is that by adding a BT [Blalock-Taussig] shunt, regardless of the magnitude of the stenosis, is equivalent to creating neoaortic insufficiency. That is exactly what you have done. And therefore, can you think of any specific scenario where you would actually not ligate the conduit.

DR HSIA: No.

DR PIZARRO: Thank you.

DR CHRISTOPHER CALDARONE (Toronto, ON, Canada): That was very, very elegant. A question about your model in terms the comparison between a 5-mm RV-PA [right ventricular-pulmonary artery] conduit vs a 3.5-mm shunt. Just looking at that data, without the stenosis issue, was very interesting. The 5-mm RV-PA conduit had a Qp/Qs of 0.8 and an oxygen delivery of 640. A 3.5-mm BT shunt had a Qp/Qs of 1 and an oxygen delivery of 590. Based on that information, where the Qp/Qs is relatively low with the 5-mm conduit, should we not simply be using larger conduits to give us more reserve in case of some mild stenosis?

DR HSIA: This question was addressed at our group's 2004 AHA [American Heart Association] presentation, and subsequently published in the August 2008 issue of Journal of Thoracic and Cardiovascular Surgery [1]. The modeling results showed higher Qp/Qs with a large RV-PA shunt, but without significant change in systemic oxygen delivery. The retrograde flow through the RV-PA shunt is increased, however. The ultimate goal of Norwood palliation is to optimize systemic oxygen delivery. In terms of differences between the modified BT shunt and RV-PA shunt, at least mathematically, multiscale modeling results suggest that the RV-PA shunt would be more preferable.

However, as we know, this question will hopefully be answered with the outcome of the randomization trial. Computational modeling does not address some very important biological adaptive mechanisms, such as coronary autoregulation and myocardial response to cyanosis that affects hemodynamics and, ultimately, clinical outcome. Modeling studies, such as the multiscale approach used here, only offer a snapshot of some of the hemodynamic differences between different surgical strategies.

Specifically for this study, we had one simple question to answer: if you were using a BT shunt to remedy a stenotic RV-PA shunt in the operation room or early post-op, should the stenotic RV-PA shunt be removed? And I believe, at least mathematically speaking, the answer is clearly you should convert the source of pulmonary blood flow to an optimally sized modified BT shunt.

DR SHUNJI SANO (Okayama, Japan): We experienced the same situation. When the patients' pulmonary vascular resistance is very high, the RV-PA shunt does not work. So in this situation, I think it's better to put a BT shunt and also put the clip to the RV-PA shunt to prevent reverse flow from RV-PA graft. I heard from Tom Karl in UCSF [University of California, San Francisco] that he had the same experience. When he put an Ao-PA shunt in addition to RV-PA shunt, the situation got worse; therefore, he divided a shunt and the saturation improved.

I had similar reports from a few other surgeons. So I always suggest that it is better to divide or put a clip to RV-PA shunt if they put an additional Ao-PA shunt, rather than put a shunt in addition to RV-PA shunt open, if saturation is low.

DR HSIA: Thank you very much, Dr Sano. That is a very interesting observation. Of course, the initial observation that the Achilles' heel of the Sano shunt is early proximal stenosis was reported by Dr Sano. The impetus for this research project came from personal experiences having observed difficult clinical course in patients where a modified BT shunt was added to augment a stenotic RV-PA shunt.

Interestingly, I was unable to find manuscripts or reports of this strategy in literature. We hope, through this study, that the modeling data will highlight the potential unpleasant hemodynamics when a modified BT shunt is added to a stenotic RV-PA shunt, and point out to others that a stenotic RV-PA shunt is better taken down if a modified BT shunt is used to remedy the resultant inadequate pulmonary blood flow.

DR JOSEPH FORBESS (Dallas, TX): This has happened to me two times. Both were kids that presented with ductal closure and they developed very hypertrophied RVs. I would bet that, in the audience, there is a group that people have seen this problem in. I am just curious. This is a post-op day 1 to 2 time-frame problem you are envisioning, not immediately postcardiopulmonary bypass in the operating room?

DR HSIA: Correct. The scenario is for recognizing RV-PA shunt stenosis in the operating room, (ie, cyanosis) or for early in the postoperative period when a superior cavopulmonary connection is not possible.

DR FORBESS: In those kids I actually didn't clip either one of their conduits, and they were well balanced after the addition of a small diameter BT shunt. I would suggest that these, by definition, ill patients have a PVR [pulmonary vascular resistance] that is higher than normal, and their pulmonary vein saturations are lower than normal. There clearly had been some "water under the bridge" in the ICU [intensive care unit] before I made the adjustment. Clinical overcirculation was not evident for many, many days, and was easily manageable prior to second stage surgery. I would just say that if you are out a ways from the operation with a sick, blue patient, remain an empiricist. One may not want to take down the conduit right away.

DR JOHN HAWKINS (Salt Lake City, UT): Another approach—I will have to admit it has happened to me more than twice, and I won't say how many—but we have used the stent. And our cardiologists have just put a very short stent, wedged it at the ventriculotomy, and that has worked fairly well. We have not had good success with stenting the distal end, that usually requires surgical revision or ligation of the Sano and BT shunt. But for the proximal end, we have been very successful with the stent in the cath lab.

DR HSIA: Can I answer that real quickly. If you have difficulty coming off bypass because the patient is blue due to a stenotic RV-PA shunt, you are unlikely to proceed to the cath laboratory. However, early catheter intervention for proximal RV-PA shunt stenosis has been reported, and appears to be very successful in experienced hands. My personal fear is having interventionalists manipulate and periodically occlude the obligatory source of pulmonary blood flow in these patients, particularly in the early postoperative period.

The goal of this project is not to compare whether one method is better than the other in dealing with early RV-PA shunt stenosis. But it is to point out that if you are going to use a BT shunt, perhaps conversion is better than keeping a dual-source of pulmonary blood flow.

DR CALDARONE: I have to say we have stented them as well and it has worked reasonably well. Just because we all need some exercise, show of hands: Who would advocate the use of a stent—the patient is a week out and has proximal RV-PA conduit stenosis, would you replace the RV-PA shunt? Would you place an additional BT shunt? Or would you send him to the cath lab to be stented? So who would replace the RV-PA conduit?

(Show of hands.)

A few. Who would place a BT shunt?

(Show of hands.)

A few. And who would send them to the cath lab for a stent?

(Show of hands.)

I think the cath lab wins.

DR HAWKINS: There are some people who wouldn't do anything.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
References
 Reference
 
This work was supported in part by the Leducq Foundation through the Transatlantic Network of Excellence Award.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
Reference
 

  1. Aramburo A. Stage I palliation for hypoplastic left heart syndrome: is a right ventricle to pulmonary artery conduit associated with improved outcomes? Critical appraisal of Cua et al: Early postoperative outcomes in a series of infants with hypoplastic left heart syndrome undergoing stage I palliation operation with either modified Blalock-Taussig shunt or right ventricle to pulmonary artery conduit(Pediatr Crit Care Med 2006;7:238–244) Pediatr Crit Care Med 2008;9:438-440.[Medline]
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   Reference
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 Reference
 

1. Bove EL, Migliavacca F, de Leval MR, et al. Use of mathematic modeling to compare and predict hemodynamic effects of the modified Blalock-Taussig and right ventricle-pulmonary artery shunts for hypoplastic left heart syndrome J Thorac Cardiovasc Surg 2008;136:312-320.[Abstract/Free Full Text]




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