Dr Cynthia S. Herrington (Los Angeles, Calif). I just so happen to be your discussant, and I am not going to reiterate all the issues and problems of the Fontan circulation, because I feel that many other people want to come up to the mike and maybe ask questions, because that's the stage that you are in right now with the device, but I do have a number of questions.
First, do you have one of the flow videos for when the pump stops, what that looks like when the pump stops?
Dr Mark D. Rodefeld (Indianapolis, Ind). No, I don't. In the videos I showed, all the flow is induced by the pump. Although I can provide video showing passage of flow at 0 rpm, I don't have it for this presentation. Dr Herrington. It is not that I don't believe you, but I just would like to see what that looks like, being a visual person.
Dr Rodefeld. Agreed.
Dr Herrington. I know that you are aiming for an increase in downstream pressure about 4 to 6 mm Hg. What kind of a drop might we see in the central venous pressures with the device when it is running at the levels that you have it running at?
Dr Rodefeld. The pressure drop upstream should match the pressure increase downstream in the pulmonary arteries. So, if the pump is rated to provide a ΔP of 4 or 6 mm Hg, it should drop systemic venous pressure by 4 or 6 mm Hg and increase pulmonary artery pressure by 4 or 6 mm Hg. There will be additional pressure loss across the transpulmonary gradient, and therefore preload may increase by 1 to 3 mm Hg.
There is controversy about pulmonary resistance in Fontan circulations and whether higher pressure rise is needed from the device. Our target thus far has been to emulate normal circulatory physiology. It may be necessary to add a higher pressure rise with this device, and we are still at such an early stage that we don't know the answer to that.
Dr Herrington. I appreciated when I read your paper—and by the way, I commend you on your tenacity for hanging in, and I have been rooting for you for a very long time, so I am very excited that we are at least at this stage that we can discuss it. As I look at the way you presented it, it almost seems as though it is something that we would implant when we do the Fontan, or at the very early signs that we have an issue that in the later phases. Although it may work if you have retained systolic function, if you are having a true failing Fontan, I worry about that because I think the hearts turn into leather at that point; I think the lungs get in the center. But what you are basically saying is that this pump would not be able to push into a high-resistance lung?
Dr Rodefeld. It could be modified to do that, but I would echo your comment that it is probably better as a preemptive device and not an end-stage device. So, yes, this pump can be modified to generate higher pressure. That comes at the cost of obstruction risk; the higher the pressure rise, the more obstruction risk you have with the device. Depending on the situation of a particular patient, however, obstruction risk may not be as much of a concern.
Dr Herrington. I am going to ask one more question, so if anybody else has questions, you can jump up, because I think we do have a little bit of time.
With respect to imaging, maybe this is a downstream question, but I am going to want to know when the device is spinning and when it isn't spinning. So, what would imaging look like for this? Do you think it would be obvious by our standard imaging, by echocardiography and whatnot?
Dr Rodefeld. I think it will be. You will see flow effect from the spinning device, but in terms of seeing the device itself, I don't think that echocardiography will be able to image that. The device probably will have feedback sensors that will tell you if it is spinning or not.
Unidentified Speaker. [No audio]
Dr Rodefeld. In mock loops, you can put Penrose drains upstream and mimic a flaccid vena cava, for example. The inferior and superior venae cavae have a lot of structure around them. They are not necessarily dangling in the breeze, and not necessarily completely flaccid. All our work thus far has focused on hydraulics, motor performance, and electromechanical issues. We will do future analyses in a mock loop with distensible or compressible veins.
I can tell you that we have clamped inflow by 50%, and we saw a drop in pressure immediately before the pump, but it wasn't in the negative range. With complete occlusion, it will go negative, but physiologically complete occlusion of inflow should be transient. We have seen negative pressures as much as −13 mm Hg in a model. The good news is that at −13 mm Hg, the pump didn't cavitate; in other words, it didn't pull air out of solution. It was still spinning at the same speed, but it did not cavitate.
Unidentified Speaker. [No audio]
Dr Rodefeld. The current version you saw is at about 7 W power requirement. The HeartWare device runs at about 4 W, and with optimization, we are hoping that we will get it below 4 W. It should require less power input than a systemic ventricular assist device, so we hope that it will be less than that.
As far as power source goes, we hope that it can be a wireless system. A young, otherwise healthy patient with a Fontan circulation is not going to want to be plugged in and is not going to want to have to deal with driveline fractures and infections.
Unidentified Speaker. How close are you to trying this in an animal model?
Dr Rodefeld. It depends on funding. Potentially, it could be within 3 or 4 years.
Dr Yves d’Udekem d’Acoz (Melbourne, Victoria, Australia). With the very small clearance between the internal part and the spinning part and the very small orifice going in and coming out, one would expect a lot of turbulence and platelet fibrin deposition and clotting of this internal part of the pump. Would it not be worthwhile to put this pump in a vena cava in an animal model with anticoagulation and find out whether it clots off after a certain amount of time?
Dr Rodefeld. Absolutely, and we are not there yet with biocompatibility. And I didn't present shear rate data. We do have preliminary shear rate data, and they are in an acceptable range. But, yes, hemocompatibility and thrombogenicity testing is going to be the next step.
Dr David L. Morales (Cincinnati, Ohio). I just want to make one more comment. We keep talking about systolic dysfunction with Fontan failure, but we saw for those deaths it was only 25% to 30%, but it's diastolic dysfunction that is vastly underestimated, which is why I agree with Mark about this being a preemptive device. Once the Fontan circulation has really started to fail, forcing blood through an abnormal vasculature into a restrictive ventricle is probably not a long-term solution, and that's why this device preemptively could maybe affect this and not have a restrictive physiology that the ventricle has. It is not the systolic function mostly, it is the restrictive, I think.
Dr Rodefeld. Yes, I agree.
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Published online: September 26, 2019
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