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Ann Thorac Surg 2009;88:170-176. doi:10.1016/j.athoracsur.2009.03.091
© 2009 The Society of Thoracic Surgeons
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Original Articles: Pediatric Cardiac

An Artificial Right Ventricle for Failing Fontan: In Vitro and Computational Study

François G. Lacour-Gayet, MDa,*, Craig J. Lanning, BSb, Serban Stoica, MDa, Rui Wang, PhDc, Bryan A. Rech, BSc, Steven Goldberg, MDa, Robin Shandas, PhDc,b

a Department of Pediatric Cardiac Surgery, University of Colorado Health Sciences Center, Denver
b Center for Bioengineering, University of Colorado Denver, Denver
c Department of Mechanical Engineering, University of Colorado Boulder, Boulder, Colorado

Accepted for publication March 31, 2009.

* Address correspondence to Dr Lacour-Gayet, Pediatric Cardiac Surgery Department, The Children's Hospital, 13123 E 16th Ave, Denver-Aurora, CO 80045 (Email: lacour-gayet.francois{at}tchden.org).

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


   Abstract
Top
 Abstract
Introduction
 Rationale for an Artificial...
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: The aim of this study is to develop a destination low-pressure artificial right ventricle (ARV) to correct the impaired hemodynamics in the failing Fontan circulation.

Methods: An in vitro model circuit of the Fontan circulation was created to reproduce the hemodynamics of the failing Fontan and test ARV performance under various central venous pressures (CVP) and flows. A novel geometry of the extracardiac conduit was designed to adapt to the need of the pump. The ARV was a low-pressure axial flow pump designed to produce a low suction inflow pressure and moderate outflow increase. With the power off, the passive forward gradient across the propeller is 2 mm Hg at 4.5 L/min. The ARV would require 4 watts at a rotation of 5000 rpm. To examine the shear loading on the red blood cells, virtual particles were injected upstream of the ARV inducer and tracked by computerized modeling.

Results: The effect of the ARV on the failing Fontan was studied at various CVP pressures and flows, and under constant values of lung resistances and left atrial pressure set respectively to 2.5 Woods Units and 7 mm Hg. The CVP pressures decreased respectively from 25, 22.5, 20, 17.5, 15, and 10 mm Hg to a minimal value of 2 to 5 mm Hg with a pump speed varying from 1700 to 4500 rpm. The pulmonary artery pressures increased moderately between 12.5 and 25 mm Hg at 4500 rpm. Cardiac output at 4500 rpm was increased by an average gain of 2 L/min. The average blood damage index was 0.92%, far below the 5% value considered to cause hemolysis. The flow structure produced by the pump was suitable.

Conclusions: The performance of this novel low-pressure ARV was satisfactory, showing good decrease of CVP pressures, a moderate increase of pulmonary artery pressures, adequate increase of cardiac output, and minimal hemolysis. The use of a mock Fontan model circuit facilitates device prototyping and design to a far greater extent than can be achieved using animal studies, and is an essential first step for rapid design iteration of a novel ARV device. The next steps are the manufacturing of this device, including an electromagnetic engine, a regulatory system, and further testing the device in a survival animal experiment.


   Introduction
Top
 Abstract
 Introduction
Rationale for an Artificial...
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The Fontan circulation, first described by Fontan and Baudet [1], is characterized by the absence of a subpulmonary ventricle and functions with unique hemodynamics. The absence of the subpulmonary ventricle induces an elevation of pressure in the systemic venous territory. The central venous pressure (CVP) rises to a mean pressure of about 12 mm Hg in the best cases to a mean ranging from 15 to eventually 20 mm Hg and further in the poor results.

The elevated CVP is poorly tolerated with time in the inferior vena cava territory and has deleterious effects on the liver and the splanchnic circulation. Protein-losing enteropathy and plastic bronchitis [2] characterize the worst outcomes. At the liver level, the elevated CVP may induce complex liver dysfunction with a stimulation of angiogenesis factors [3] favoring venovenous anastomosis, pulmonary venous fistulas, and potentially, aortopulmonary collateral anastomoses (MAPCA). Liver carcinoma has also been reported [4]. At the lung level, the upper pulmonary artery (PA) branches are poorly or not perfused, and the lymphatic circulation is globally impaired [5]. The systemic single ventricle faces a significant increase in total systemic resistance because it needs to "push" against not only the usual systemic resistance but also the lung resistance. As a consequence, the systemic ventricle becomes hypertrophied, with elevated end-diastolic pressure, which diminishes its diastolic performance [6–8]. In addition, this "second portal circulation" decreases ventricular preload, which also affects diastolic performance.

There is a consensus in the literature that the most significant factor to predict the failure of the Fontan circulation is the time elapsed since the operation, given the regular attrition of the survival curve [9, 10]. However, it is also expected that performing the Fontan in the later years using an extracardiac conduit [10, 11] has a better anatomic geometry and should function better. There is nevertheless a general concern about the long-term performance of the Fontan circulation, particularly in single ventricles with a right ventricle anatomy, such as that found in hypoplastic left heart syndrome [10].

Unfortunately, medical treatments, which include systemic vasodilators (captopril) and pulmonary vasodilators (sildenafil), provide limited benefits under severe failure. Currently, surgical techniques can improve some Fontan heart failure by conversion to extracardiac conduit and correction of arrhythmias [11]. For most patients with failing Fontan, however, the only possible treatment is heart transplantation [12]. Considering the shortage of donor hearts and the unfavorable immunology due to an elevated level of pattern reactive antibodies, the survival of patients who receive a transplant for failing Fontan is expected to be quite limited [12].


   Rationale for an Artificial Right Ventricle in Failing Fontan
Top
 Abstract
 Introduction
 Rationale for an Artificial...
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
In patients with single ventricle, we hypothesize that the timely implantation of a permanent artificial right ventricle (ARV) should prevent or correct the failure of the single ventricle. The ARV, using axial flow pump technology, should restore together the diastolic and systolic function of the RV. The suctioning function of the machine should decrease CVP to a normal value and therefore decrease global systemic resistance. The increase in PA outflow and the generated pressure boost should normalize perfusion of the upper PA branches as well.

A few pioneering groups have tested different mechanical pumps as an optional treatment for the failing Fontan circulation. Rodefeld and colleagues [13] developed a cavopulmonary assist system using 2 axial flow pumps (Hemopump HP-24, 24F; Medtronic Inc, Minneapolis, MN) placed transcutaneously within both vena cavae of a sheep total cavopulmonary connection (TCPC) model. Riemer and colleagues [14] examined a sheep TCPC model with a single axial pump positioned within the inferior vena cava (IVC). Although promising results were found in cardiac output and arterial pressure, there was significant collapse in the IVC. More recently, Throckmorton and colleagues [15] have tested in vitro a 3-bladed propeller micropump to provide cavopulmonary assist as a bridge to transplantation.

Our goal in the present study is to develop a destination venous axial flow pump device with low inflow pressure and moderate outflow pressure boost that will normalize IVC and superior vena cava (SVC) venous pressures, improve lung circulation, and normalize cardiac output of patients living with a Fontan circulation.


   Material and Methods
Top
 Abstract
 Introduction
 Rationale for an Artificial...
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
ARV Design
Because of the dimensional and low-flow constraints found in Fontan patients, the axial type of flow pump appears most advantageous. Its compact tubular configuration can minimize pump dimension and reduce surgical invasiveness. It has favorable flow for low-pressure head applications and therefore is more appropriate to replace the missed RV function. As previously published [15], the axial flow pump was originally designed using computational techniques, after which several polymer ARV prototypes were manufactured using a 3-dimensional rapid-prototyping technique (Stratasys Inc, Eden Prairie, MN). The prototype used in the experiment had a 16-mm inner diameter. The resulting ARV blood pump unit (Fig 1) constitutes of inducer, rotor (or impeller), diffuser, pump housing, and coupling case.


Figure 1
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  		Fig 1. This schematic drawing of the artificial right ventricle blood pump model identifies the individual components. Geometric profiles are shown for the pump impeller and diffuser.

 
The In Vitro Model of the Fontan Circulation, Using A Novel Geometry
Despite many attempts, there has not been a successful survival animal model of the total Fontan circulation. In addition, testing prototypes in animals requires significant resources and logistics. A mock model of the systemic venous return and of the pulmonary circulation was designed at the Cardiovascular Flow and Imaging Research Laboratory within the Children's Hospital in Denver. The geometry of a classical TCPC with extracardiac Fontan conduit, associated with a bidirectional cavopulmonary anastomosis, makes it difficult to achieve optimal hemodynamics in both SVC and IVC with a single pump support because the outflow of the pump can generate a high retrograde flow within the SVC. A model with novel extracardiac conduit geometry was designed (Fig 2). The Glenn anastomosis is taken down and a conduit is used to connect the SVC connected to the IVC. The angle of the extra cardiac conduit with the caval veins is 45 degrees in this model, but can be varied over a wide range of angles.


Figure 2
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  		Fig 2. In this new geometry of the extracardiac conduit to prevent retrograde flow in the superior vena cava, the bidirectional Glenn is taken down, and the superior vena cava is connected to the inferior vena cava, using a Gore-Tex conduit (W. L. Gore and Associates, Flagstaff, Ariz). The angle between the caval veins and the extra cardiac conduit is about 45 degrees, but can be varied over a wide range of angles.

 
The Fontan circuit (Figs 3 and 4) Go is equipped with 18- to 20-mm diameter glass or silicone tubing to reproduce the high compliance of the venous walls, allowing collapse in case of negative pressure. We used water for this experiment, but blood or water plus glycerin could also be used. The circuit starts with a venous reservoir permanently filled. The height of the venous reservoir defines the CVP. IVC and SVC conduit follow the reservoir, and a differential valve sets the flows so that IVC/SVC flow is 2 to 1. The extracardiac conduit contains the ARV that is run using an external driver. The pulmonary arteries connect to a common tube equipped with a valve allowing the setting of lung resistances, which were set to 2.5 Wood Units (WU). Flow empties into a mock left atrial reservoir. The height of the left atrial reservoir defines left atrial pressure, which was set at 7 mm Hg. The flow and lung resistances are continuously monitored, as are pressures (Millar catheters) at multiple points along the circuit.


Figure 3
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  		Fig 3. Photograph shows the Fontan circuit in the Research Laboratory in the Children's Hospital in Denver. Notice the recipients and the red valve used to set up the pulmonary vascular resistances (PVR). (LA = left atrium.)

 

Figure 4
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  		Fig 4. Drawing of the circuit or the artificial right ventricle (ARV). (CV = central venous; IVC = inferior vena cava; LA = left atrium; LPA = left pulmonary artery; RPA = right pulmonary artery; SVC = superior vena cava; VC = vena cava.)

 

   Results
Top
 Abstract
 Introduction
 Rationale for an Artificial...
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
The performance of the axial flow pump, placed in the extra cardiac conduit of the mock Fontan circuit, was evaluated for hemodynamics and flow structure.

Hemodynamic Performance
The results obtained in using the new geometry (Figs 2 and 5)Go that prevents the SVC retrograde flow showed marked improvement compared with our previous model [16]. Pump performance was studied with rotational speeds of 1000 to 4000 rpm, and CVP from 10 to 25 mm Hg. The lung resistances were constant at 2.5 WU, with a left atrial pressure set at 7 mm Hg. The results are presented in Fig 6, 7, 8, and 9. Go Go Go


Figure 5
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  		Fig 5. In the new artificial right ventricle (ARV) model, the retrograde flow to the superior vena cava (SVC) is avoided. (A) Previous model. (B) New model. (IVC = inferior vena cava; LPA = left pulmonary artery; PA = pulmonary artery; RPA = right pulmonary artery; SVC = superior vena cava.)

 

Figure 6
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  		Fig 6. Notice the satisfactory decrease in the central venous (CV) pressure to 5 mm Hg. The blue curve represents the decrease for a CVP at 10 mm Hg. For this nonfailing Fontan value, there could be a risk of collapsing the caval veins.

 

Figure 7
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  		Fig 7. The increase of the pulmonary artery (PA) pressure is moderate.

 

Figure 8
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  		Fig 8. Increase in cardiac output gain is 2 L/min, depending on the initial central venous pressure (CVP).

 

Figure 9
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  		Fig 9. The gradient across the pump, when stopped, is 1.5 mm Hg at 4 liters, theoretically allowing a pump failure without important obstruction of the venous return to the lungs.

 
The CVP pressure (Fig 6) decreased respectively from 25, 22.5, 20, 17.5, 15, 12.5, and 10 mm Hg to a minimal value of 2 to 5 mm Hg with a pump speed varying from 3000 to 4500 rpm. When the CVP was set at 10 mm Hg (not a failing Fontan), the collapse of the caval veins occurred at 3000 rpm.

The PA pressures (Fig 7) increased moderately to a maximal value between 12.5 and 25 mm Hg at 4500 rpm. The cardiac output (Fig 8) increased by an average of 2 L/min, depending on the initial CVP pressures.

To quantify the obstruction generated by ARV pump, in vitro measurements of pressure drop under stall condition (pump failure) shows that pressure drop is nonlinearly proportional to overall cardiac output. The passive gradient across the axial flow pump, at a flow of 4 L/min, with the engine stopped, was 2 mm Hg (Fig 9).

Hemolysis
As previously described [16], we evaluated the shear loading on the red blood cells by injecting virtual particles upstream of the ARV inducer. Particle histories were tracked through the pump region by computerized modeling. The average blood damage index was quite low, only 0.92%, far below the 5% value considered causing hemolysis [17].

Flow Structure
Computational fluid dynamics was used to evaluate the flow field through the pump design. Figure 10 shows the midplane pressure contour plot on lumen and ARV pump surfaces from transient computational modeling. Within the PA trunk, the pressure increased downstream in the axial direction with the major suction (ie, minimum pressure) present at the impeller level. A pressure increase was evident as blood flow traveled from venous to PA flow pathways. The leading faces of the impeller vanes had higher pressures than their trailing sides, implying a smooth flow path and good pump performance.


Figure 10
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  		Fig 10. Computational results of pressure contour plot on lumen and artificial right ventricle (ARV) surfaces at (A) minimum flow and (B) peak flow. ARV pump is translated to the right and enlarged for clear view. (IVC = inferior vena cava; LPA = left pulmonary artery; RPA = right pulmonary artery; SVC = superior vena cava.)

 
Computed results for flow streamline plot at minimum flow is shown in Figure 11 After entering the ARV impeller region, flow suddenly accelerated and then slowed during its passage through the diffuser region, which produced the desired pressures. Although a streamlined flow path dominated in the venous flow pathway and the upstream region within the PA trunk, a strong helical flow pattern was present distal to the ARV pump. Furthermore, immediately downstream of the PA bifurcation, velocity profiles were skewed to the anterior-inferior side. Vortical flow rotating clockwise was also clearly evident in this region. Flow stagnation was absent in the vicinity of ARV components, but was notable near both venous conjunction and PA bifurcation regions, caused by impingement of the incoming IVC/SVC flows and the strike of outgoing flow on the PA wall.


Figure 11
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  		Fig 11. Computational results for flow streamline plot at minimum flow. Notice the flow acceleration at the entrance of the pump showing the suctioning function of the device. (IVC = inferior vena cava; LPA = left pulmonary artery; RPA = right pulmonary artery; SVC = superior vena cava.)

 

   Comment
Top
 Abstract
 Introduction
 Rationale for an Artificial...
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
Limitation of the Experimental Study
Despite the improvement made to the mock circuit, it cannot be totally superposed to a real total Fontan circulation. In particular, there is so far no systemic circulation in the model. The PVR values were set arbitrarily to 2.5 WU. It is important to note that the PVR will increase when the passive flow increases. To maintain a constant PVR at 2.5 WU, we had to open the valve (Figs 3 and 4) controlling the pulmonary afterload. We believe that in doing so, we were reproducing what the lung physiology does in recruiting more alveolar territory to decrease the PVR when the cardiac output increases. Similarly, the left atrial pressure was maintained at 7 mm Hg, which does not necessarily reflect the filing pressure of a failing single ventricle.

In using water in the circuit, we could not evaluate directly the risk of hemolysis and thrombolysis. The circuit is horizontal and thus does not reproduce the gravitational gradients seen in an upright human being. This limitation will be similar when using most animal models.

The acute angle between the SVC and the extracardiac conduit could generate turbulence. The computerized studies were not done on the real angle between the SVC and the extra cardiac conduit, but were based on a schematic approach.

New Acquisitions
The new connection and modified in vitro model showed clear improvements in our Fontan circuit. The new geometry prevents retrograde hypertension in the SVC territory. The placement of an occluding valve on the PA outflow allowed a constant PVR value of 2.5 WU.

The major result of this study lies in the satisfactory performance of the pump in vitro (Figs 6 to 9). The CVP pressure was reduced, as intended, to 5 mm Hg for values between 3000 and 4500 rpm, which is quite low for an axial flow pump, therefore limiting the energy consumption. PA pressures increased only modestly, while the pump can produce a cardiac output gain of an average of 2 L/min depending on the initial CVP.

The risk of collapse of the caval veins was almost avoided with this pump. It is noticeable that the collapse event, shown in Figure 6, occurred in "a good Fontan" model with a CVP at 10 mm Hg. On the contrary, when the CVP was high, above 15 mm Hg, there was no risk of collapse with a rotation between 3500 and 4500 rpm.

The axial flow pump is an occluded pump that presents a risk of obstruction when it stops rotating. The design of the device offers an interesting solution: When the pump stops, the passive flow gradient across the pump is about 2 mm Hg for a cardiac output of 4 L/min. This in vitro performance needs to be confirmed in vivo.

Future Directions
Our circuit will be used to test different prototypes with various hemodynamics and flow structure characteristics. Once the optimal performances are obtained, an implantable prototype will be manufactured for in vivo testing. An experimental sheep model of Fontan has already been studied at the Veterinarian School in Fort Collins (unpublished data), and the prototype will be implanted in this sheep model as soon as its hemodynamic performances are optimal.

Knowing the possibility of an epidemic of heart failure [18], that includes the failing Fontan, we assume that such an ARV applied to the failing Fontan would also contribute to the construction of the RV component of a destination biventricular artificial heart.

The final ARV will function with an electromagnetic coupling system that should provide 4 watts at its maximum rotation of 5000 rpm. The engine will be powered by a battery incorporated in the abdominal cavity and rechargeable by a skin contact extracorporeal electrical source. The battery should allow autonomy of 24 hours.

Conclusions
A low-pressure axial flow blood pump specifically designed for assisting Fontan hemodynamics has been developed. Meanwhile, an innovative Fontan model is proposed. In vitro and computational studies suggest that an ARV placed in the extracardiac conduit of a Fontan circulation produces promising outcomes for alleviating the downward hemodynamic spiral found in failing Fontan.


   Acknowledgments
Top
 Abstract
 Introduction
 Rationale for an Artificial...
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
This work was funded by grants from the University of Colorado Health Sciences Center, Denver, Colorado, and from the National Institute of Health (NIH HL 067393). We acknowledge the contribution of Dr Eric Monnet at the Veterinarian College of Medicine, University State of Colorado, for his contribution in developing the animal model that would receive the device in the next step of the experiment.


   References
Top
 Abstract
 Introduction
 Rationale for an Artificial...
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Fontan F, Baudet E. Surgical repair of tricuspid atresia Thorax 1971;26:240-248.[Abstract/Free Full Text]
  2. Feldt RH, Driscoll DJ, Offord KP, et al. Protein-losing enteropathy after the Fontan operation J Thorac Cardiovasc Surg 1996;112:672-680.[Abstract/Free Full Text]
  3. Starnes SL, Duncan BW, Kneebone JM, et al. Angiogenic proteins in the lungs of children after cavopulmonary anastomosis J Thorac Cardiovasc Surg 2001;122:518-523.[Abstract/Free Full Text]
  4. Ghaferi AA, Hutchins GM. Progression of liver pathology in patients undergoing the Fontan procedure: Chronic passive congestion, cardiac cirrhosis, hepatic adenoma, and hepatocellular carcinoma J Thorac Cardiovasc Surg 2005;129:1348-1352.[Abstract/Free Full Text]
  5. Matthews IL, Fredriksen PM, Bjørnstad PG, Thaulow E, Gronn M. Reduced pulmonary function in children with the Fontan circulation affects their exercise capacity Cardiol Young 2006;16:261-267.[Medline]
  6. Gewillig M. The Fontan circulation Heart 2005;91:839-846.[Free Full Text]
  7. Deleval MR. The Fontan circulation: what have we learned?. What to expect?. Pediatr Cardiol 1998;19:316-320.[Medline]
  8. Cheung YF, Penny DJ, Redington AN. Serial assessment of left ventricular diastolic function after Fontan procedure Heart 2000;83:420-424.[Abstract/Free Full Text]
  9. Fontan F, Kirklin JW, Fernandez G, et al. Outcome after a "perfect" Fontan operation Circulation 1990;81:1520-1536.[Abstract/Free Full Text]
  10. Khairy P, Fernandes SM, Mayer Jr JE, et al. Long-term survival, modes of death, and predictors of mortality in patients with Fontan surgery Circulation 2008;117:85-92.[Abstract/Free Full Text]
  11. Mavroudis C, Deal BJ, Backer CL. The beneficial effects of cavopulmonary conversion and arrhythmia surgery for the failed Fontan Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2002;5:12-24.[Medline]
  12. Mitchell MB, Campbell DN, Boucek MM. Heart transplantation for the failing Fontan circulation Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2004;7:56-64.[Medline]
  13. Rodefeld MD, Boyd JH, Myers CD, et al. Cavopulmonary assist: circulatory support for the univentricular Fontan circulation Ann Thorac Surg 2003;76:1911-1916.[Abstract/Free Full Text]
  14. Riemer RK, Amir G, Reichenbach SH, Reinhartz O. Mechanical support of total cavopulmonary connection with an axial flow pump J Thorac Cardiovasc Surg 2005;130:351-354.[Abstract/Free Full Text]
  15. Throckmorton AL, Ballman KK, Myers CD, Frankel SH, Brown JW, Rodefeld, MD. Performance of a 3-bladed propeller pump to provide cavopulmonary assist in the failing Fontan circulation Ann Thorac Surg 2008;86:1343-1347.[Abstract/Free Full Text]
  16. Wang R, Lacour-Gayet FG, Lanning CJ, Rech BA, Hertzberg J, Shandas R. Initial experience with the development and numerical in vitro studies of a novel low-pressure artificial right ventricle for pediatric Fontan patients ASAIO J 2006;52:682-692.[Medline]
  17. Song XW, Wood HG, Olsen D. Computational fluid dynamics (CFD) study of the 4th generation prototype of a continuous flow ventricular assist device (VAD) J Biomech Eng Trans ASME 2004;126:180-187.[Medline]
  18. Redfield MM. Heart failure. An epidemic of uncertain proportions. N Engl J Med 2002;347:1442-1444.[Medline]

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