MODERATOR: Stenosis, when angina, syncope and heart failure become evident the survival drops, and it's only at the late stages when the ejection fraction drops. And of course you know the spiral of death with aortic stenosis. These patients have chronic severe aortic stenosis and then something triggers them to spiral down and at least it leads to death. So they are a pretty sick population, especially those with low ejection fraction.
So we'll start with case one, a 92-year-old gentleman who presented with cardiogenic shock. His ejection fraction is 20% with an aortic valve area 0.5 and a mean gradient of 25. He was taken to the cath lab, and as you all know, he has a distal left mean bifurcation stenosis that is also significant. So he, during the ICU admission he had respiratory failure, cardiogenic shock, and renal failure. And we were consulted to see whether or not he would benefit from a percutaneous procedure. So I wanted to ask the audience, what would people do in the situation?
MALE SPEAKER: I think I would first of all see how functional he was as a 92-year-old prior to all this just to make sure things are very reasonable, then call our interventionists to see whether it'd be viable to do a left main stent and then percutaneous intervention or not. Obviously get a really close look at that valve as well, see how calcified it is, et cetera, see if it's viable, those are kind of things.
MODERATOR: Perfect, perfect. So as [INAUDIBLE] noted, there's a couple of facets that you're going to see the slide several times during this presentation. Those are the key points that we take into consideration when we're deciding whether or not we're proceeding with a percutaneous approach. First of all, what is the procedural feasibility and risk? Is it cost effective? And those are the risks of the procedure.
On the other hand, what is the patient's one-year outlook? Because as a rule of thumb any percutaneous-- any patient who does not have a one-year adequate one-year survival does not qualify for percutaneous structural intervention. And again, last but not least is what is the data supporting the decision, or meaning what does the data show regarding the benefit of this intervention?
So for this patient we'll start with the procedure feasibility and risk. In this day and age we can almost always push the envelope and come up with a creative way to challenge the anatomy that's in front of us and succeed in a procedure. There's always the logistics behind the TAVR here, including the coronary angiogram, the question of whether or not PCI is needed, the pre-TAVR CT scans, the surgical consultation.
In a critically ill patient some people would consider balloon valvuloplasty, but again there are several ways to approach this. So in this day and age this is almost always not a major issue. We can always find a technical way to get through things, aside from a few issues that would prohibit us from doing things.
Second question that arises is it cost effective? And the main purpose I say this is because some of these percutaneous procedures are not yet approved or covered. TAVR is, so the patient will be covered for it. But just remember that the way I understand is they give a lump sum of money, and then every time we do something it just gets subtracted from that lump sum of money. And so either the patient will be left with a bill at some point or-- and plus the program will lose money.
So again, that's not an issue. We always put the patients first. But the main concern for us is sometimes we do things, for example as you'll note later on tricuspid interventions, those are not covered yet and some patients will not be OK with having $100,000 bill. So that's something to keep in mind when we talk about considering structural interventions. Obviously in this case it's an emergency, so that doesn't even factor in our decision making.
What is the one-year outlook? So a 92-year-old with cardiogenic shock and multi-organ failure. And you're right [INAUDIBLE] what is his baseline functionality? He was frail, he wasn't mobile, so his one-year outlook was not great. What about the data? In aortic stenosis and heart failure what is the data? What is the benefit that we extract from doing TAVR on these patients?
So just a few things about the literature in this patient population. The first thing is all major trials excluded left ventricular ejection fraction less than 30%, so we're really left with registry data. And there's many registry data from what we call the TVT registry that looked at outcomes of TAVR in low flow, low grade, and severe aortic stenosis, in low flow and paradoxical low flow, low grade, and severe aortic stenosis, and all of them show that there's a benefit and it's safe to do this.
So really the envelope again has-- we've really stretched the boundaries of this field to the point where honestly many, many programs-- we don't do it here, but many programs-- for example, our approach for paradoxical-- or for low flow, low grade and severe aortic stenosis, meaning when the valve area is less than one and the gradient is less than 40, we usually do the butamine stress test to differentiate pseudo severe from true severe.
But you only need one out of the three criteria for TAVR, meaning you need either a valve of less than one, or a mean gradient more than 40, or a velocity, peak velocity of more than four. You don't need the three of those, you need just one of those to qualify for TAVR. So a lot of centers do TAVR on just low flow, low grade and severe aortic stenosis without even seeing if it's pseudo severe or true severe, and the registry data shows that it is safe and it's beneficial in these patients.
Even in patients with contractile-- with no contractile reserve, meaning they have low flow, low gradient severe aortic stenosis, we do the dobutamine test and the stroke volume doesn't go up because their left ventricle doesn't have a reserve from, let's say, severe coronary disease. Even the registry data even supports that it's OK and it's safe and it shows favorable outcomes in doing TAVR in these patients. So the safety of TAVR has really again stretched the boundaries of what we can do and what we can offer with data showing benefit.
Now it's not clinical trial data, but it's at least some data. Even to the point where the next set of trials, particularly the TAVR UNLOAD trial, is looking at actually moderate aortic stenosis and doing TAVR in moderate aortic stenosis plus ejection fraction less than 50%. So a ventricle that is sick, we know that from recent studies that moderate stenosis, moderate aortic stenosis is not a benign entity. So an ejection fraction of less than 50%, a pump function that is not adequate, can have a composite poor outcome when it's facing even moderate aortic stenosis, so we're seeing whether or not TAVR benefits this patient population. So that's on the outlook and it's still enrolling patients.
Now we have also registry outcomes on patients who underwent urgent and emergent TAVR. It is feasible, again we can almost always get away and do things with acceptable outcomes in select patients with severe aortic stenosis. But in this patient, because of what we discussed we thought that the risks outweighed the benefit, and we actually went through a palliative approach.
His one-year outlook was dim, and so I think that that's what swayed the decision. Because and sometimes I don't know if you've seen this image before, but if we don't-- if we're not very careful about patient selection, we can inflict more harm. And this is a TAVR valve extracted from someone who had CPR. You saw how it becomes deformed, like a D-shape.
So the next case is-- and this case will highlight again the overlap between structural heart disease and heart failure. In a sense it's not per se valvular heart intervention, but these are techniques that we learned from aortic stenosis from TAVR that we can extrapolate to our heart failure population and use in our heart failure population.
So this is a 72-year-old male with peripheral heart disease, severe ischemic congestive heart disease, who presented with cardiogenic shock on inotropes. This is his CT. Now he was stabilized, he had a CT luckily and it shows a distal aortic iliac bifurcation stenosis on both sides. And what would people choose as a mechanical support device in this patient?
MALE SPEAKER: We can always try our axillary approach. We have done that for the past couple of years. Balloon pumps on Impellas in that so far if the anatomy's reasonable, then we can use the upper extremity approach for this.
MODERATOR: Perfect. So this patient had, let's say he had LIMA and RIMA, or he had calcification in the axillary arteries and there's no access up top. So this is-- that's perfect because, yes, axillary is the way to go in a lot of times. But there's this option that is nice and we haven't tried it here, but at some point we might need it because of the patient that I'm telling you about.
This is the IVC and this is the aorta. There's a calcium free window here, and the aorta and the IVC come in in close proximity. The pressure, we know from bench testing that the pressure in the IVC is lower than the pressure in the interstitium, which is lower than the pressure in the aorta, so there's always that pressure differential.
And that enabled what we call a transcaval approach where there's a snare that's put up in the arterial side and then a wire that we connect to a Bovie and cause electrocautery where we basically burn through the IVC into the aorta, snare it up, and then put the sheath up. And then towards the end, we pull the sheath and we put in a vascular closure device. This is an ADO device.
And so if the patient bled around it, there are multiple rescue. We can put a stent here. But just remember because of that pressure differential, it'll bleed into the IVC actually, a lot of times. Now if it's a major bleed, it'll bleed significantly and then we have to put a covered stent. But just because of the pressure differential that I told you about, it'll bleed into the IVC. But that's called a transcaval approach, and it has been used for Impella placement.
And so ideally we'd like to have a CT for these beforehand, but just to show you an example of how we can kind of extrapolate what we learned from TAVR to alternative access to the heart failure population. Also remember that the data on axillary alternative access right now is getting a little bit under scrutiny because of the stroke risk. So that's one thing just to keep in mind.
So moving along to secondary mitral regurgitation, which is a huge topic in the overlap between heart failure and structural heart disease. And I'll start with a 70-year-old gentleman with non-ischemic cardiomyopathy with worsening dyspnea and he had two heart failure admissions over the past one year. This is his echocardiogram, basically EF 16%, left ventricular end systolic damage of 72, and an ERO of 0.6 centimeters squared. This is his mitral valve regurgitation. So I'd like to ask, what would my colleagues do in this situation?
MALE SPEAKER: From a heart failure perspective, we like to always try to optimize in person thing that we have seen in the past couple of years, multiple patients that the first approach was to place a MitraClip without even attempting medical management. So we have been able to remodel many of these patients and reduce their MR substantially, but unfortunately sometimes they come already with a MitraClip. But then you still optimize them, but you wonder if you lost a window of avoiding a procedure.
MODERATOR: You're absolutely right. So the first step is to optimize them. This gentleman was on maximally-tolerated medications including, and I am going to repeat that, including Entresto. This is, some people call it the interventionless enemy because it gets rid of, it gets rid of secondary MR in many patients, so it's one of those miracle drugs that just worked beautifully in these patients. But this gentleman was on maximally-tolerated medical therapy, didn't need a device, his QRS wasn't widened.
So he presented to us for-- not here, it was when I was in Rochester-- presented for MitraClip consideration. So how do you approach this patient? From a procedural feasibility and risk, back to our, back to our balance here. Again, right now in this day and age we have many permutations of the clip, so that it gives us technical feasibility for different anatomies. So if there's enough, if there's enough, if the leaflets there's not a big gap, we can always get in and do it successfully.
We have now the new generation called the G4, which is a wide clip. It works beautifully for functional MR. As you know functional MR, there's dilatation and there's a crescent-shaped opening across the mitral valve between the leaflets, and so this has a wide gripper which can approximate the mitral valve beautifully. The biggest enemy right now, there are two things that I've noticed in heart failure population that makes mitral valve regurgitation technically challenging.
The first one is heavy calcium in the leaflets. If we don't have enough healthy tissue we won't be able to grasp it because it will avulse the leaflet. The second-- and it'll cause mitral stenosis. The second challenge is I've seen one case here where the ejection fraction was very low and the left ventricular chamber size was humongous that they didn't even see the leaflets on TEE, and that's before we understood more about the trends that I'm about to mention. So those are the two biggest challenges.
Now we can get an acute result, but the long term result-- again, the field is advancing. Because what ends up happening in a lot of times is we clip the middle line-- that's why I'll show you the trials later on-- but we clip down the middle, and then a few months later, a few years later, they come back with severe MR because the dilatation continues to go on the both sides, particularly in patients with ongoing atrial fibrillation where the annulus continues to dilate or the left ventricle continues to dilate.
The field is evolving. At some point we'll have annuloplasty rings. Again those are all investigational still, but that will be important to stabilize the annulus just like the surgeons do. And then we have the NeoChord system that there's now actually now a transseptal version of it that tacks on. So we'll see what the future holds. There are also transcatheter mitral valve replacement devices also in trial. So there are many, many things going on in the mitral field that could be potential benefit down the road.
So procedural feasibility and risk for the MitraClip again, the majority of patients there won't be any issues. Cost effectiveness, in select patients that meet the criteria that I'm about to mention that the CMS mandates, there is a cost-effective procedure for the patient and for the program. Again same thing, what about the one-year outlook? This patient was functional, but he had the low ejection fraction, he had two heart failure hospitalization, but I think it's a reasonable one-year outlook. And he is he's not very old, so something can be done to help him.
What about the data? This is where I think most of the focus will be on this stuff because this is important to understand the data and how we approach these patients. The two major trials, again MitraClip is the only FDA-approved device for mitral regurgitation right now. And in secondary mitral regurgitation, meaning mitral regurgitation that is due to annular dilatation from left atrial disease, left atrial enlargement, or left ventricular enlargement, the two trials that have been published and presented were the MITRA-FR and the COAPT trial.
So we'll start with the MITRA-FR trial. It was a trial that was done in France, or what we call France, included about 300 patients randomized one-to-one to MitraClip plus medical therapy versus medical therapy alone. Notice the inclusion criteria, the ejection fraction was 15% to 40%, the New York Heart Association was between two and four, and they had to have hospitalization within the previous 12 months, and they're not eligible for mitral surgery. They defined the mitral regurgitation as severe if the ERO is 20 or above, or the RV volume was more than 30.
And the way they optimized medical therapy was what we call quote unquote, I don't like the word, I never use it, I don't believe in something like this, but it's called "real world" heart failure meds, meaning it was just whatever they felt like treating the patient and call it optimizing medical therapy. So what they found was that there was no difference between both arms in terms of freedom from death or heart failure optimization, that was the composite endpoint. And so it was what we call a negative trial.
Around the same time the COAPT-- well sorry, around the same time the COAPT trial emerged and-- just here we go. So the COAPT trial was a little bit more stricter. And it was multicenter trial, included three plus, so moderate to severe or severe mitral regurgitation who remain symptomatic despite medical therapy. Now here there was actually there was stricter dimensions. I'll show you the exact differences between MITRA-FR and COAPT, but there are stricter selection, anatomic selection, and guideline-directed medical therapy was very strict, was very strict. They actually were calling the patients to make they were followed different protocols.
And then there was a steering committee that looked at whether or not this is a guideline directed medical therapy was implemented. So it was truly-- there was a high level of compliance that may be challenging to replicate, but that's why these things have to be done in a center of excellence where there's good collaboration between heart failure and structural interventions like we have here. And to your point one, this is what's not happening in the quote unquote "real world", where they put a clip before this happens. That shouldn't be happening.
So back to the COAPT trial, what they found in this trial is that there was tremendous response, all hospitalizations for heart failure within 24 months. So it was a two year follow up, heart failure hospitalization went down, went down, all cause mortality decreased as well tremendously. And then when they compared the treatment effect of MitraClip to guideline-directed medical therapy, just to show you, just to show you the scale of how effective MitraClip is compared to guideline-directed medical therapy plus other devices, so it really is a remarkable response.
Now the scrutiny was well, why did MITRA-FR, you know, why was it negative versus COAPT was positive? Well, there are big differences. Actually the trials complement each other, and I'll show you why. With MITRA-FR the severe-- remember that they included the ERO or the orifice of the mitral valve was 20, so there were some moderate mitral regurgitation in these patients, whereas in the COAPT trial it included more moderate to severe based on the ERO.
The LV end systolic dimensions, so here I don't see-- I see the end diastolic dimensions, but it's actually the end systolic dimensions. The MITRA-FR, I noticed that they included larger chambers compared to the COAPT trial. So the COAPT trial included more severe mitral regurgitation with smaller chamber sizes, whereas here it included kind of moderate range but larger chamber size. In fact the cut off that we use, that was used in the COAPT trial was an end systolic dimension of 70, anything above that was more or less excluded from the trial.
The second point that led to the difference between the two trials was the guideline-directed medical therapy protocol. It was loose in the MITRA-FR, whereas it was very strict in the COAPT trial, including Entresto which was which was initiated in these patients in this trial. Finally the results, the operators to be honest the operators in COAPT trial were better than in MITRA-FR trial. They got less residual severe MR, they had less procedural complications, and then that's why they had less residual MR down the road.
So that's the procedural and experience matters in MitraClip. Again it shouldn't be done by anyone, especially in these sick patients. So you really need to send-- these patients have to be tackled in a center where there's good heart failure and good structural interventions, or otherwise we're going to be in the MITRA-FR territory. So how do we put this together? Actually the-- you know [INAUDIBLE] you know Milton Packer from the days of UT Southwestern. You and I have overlapped, I think he was there when you were there too, right?
MALE SPEAKER: Yeah, he used to run our research conferences as fellows so--
MODERATOR: Yeah, you know, you know how he is. He's very critical and he scrutinized, but he put together this concept based on the two trials of what we call proportionate or disproportionate mitral regurgitation. So what does that mean? He calls proportionate MR is that the severity of the mitral regurgitation is proportionate to the left chamber dimension, meaning that the chamber dilates, the MR is severe because it's proportionate to the dilatation of the chamber.
Whereas disproportionate severe mitral regurgitation is the chamber, although there's heart failure but the chamber-- the mitral regurgitation is more severe than what would be expected from the chamber dilatation. And that is usually related to dyssynchrony in the ventricle, such as what we see in ischemic MR. So this is proportionate MR, again the ventricle is dilated and the MR is rightfully proportionate to the dilatation in the chamber. Whereas disproportionate MR, the chamber it's not extremely dilated, but the MR is severe.
And this is where the COAPT falls, COAPT is a trial that showed that MitraClip is effective in this proportionate MR because they excluded anyone with LV end systolic dimension of more than 70. Whereas proportionate MR was more than MITRA-FR population, where there's these large chambers with moderate mitral regurgitation that didn't benefit much from clipping. So I love this chart. I use it actually in all patients with mitral valve regurgitation plus ejection, low ejection fraction.
And to put this in perspective, our patient back to our patient, and I'm going to go back to the echo just to show you, just to give you another look at it. Here we go. So the chamber was dilated more than what we expect in the COAPT trail. The EF was 16%, but the ERO always super high at 0.6. So if we plot it in the chart-- I'll go back to the chart here. If we plot it in the chart, that's going to be somewhere around here. So he's one of those patients that we don't know how he's going to respond, but he is a little bit on the disproportionate side of things, so we decided to do a clip on him.
This is the MitraClip. This is the TE, the left atrium, left ventricle, and here's the mitral valve. And notice the hemodynamics, this is the aortic pressure. That's the V-wave on the left atrial pressure. After clipping, the V-wave went down and the aortic pressure went up. This is a great sign that we would be very happy to see during these procedures.
We worry about the abrupt increase in the afterload in these patients, but he did well. Some of these patients just behave in a funny way. I know people have gone to the extreme of putting a balloon pump at the same time as doing a clip. Sometimes some people put an Impella in, but I think that's kind of stretching the envelope too much. But this patient did well.
And so now what is the data? What does the data show? So I showed you the COAPT trial and the MITRA-FR, but there are two more ongoing trials to kind of add to the concept of whether or not this disproportionate or proportionate MR is justifiable. And then there are multiple registries looking at now specific patient populations undergoing MitraClip. And forgive me for the next few slides, they look ugly, but literally the data was presented two days ago at TCT.
And the first one is called the MitraBridge Registry. It's relevant for the heart failure patients because in this patient population they basically took patients on an active heart transplant list as a pure bridge where the low likelihood to receive a donation shortly for body weight or blood group. And they also included patients waiting for clinical decision, bridge to decision, and patients not enlist for heart transplant bridge to candidacy with potentially reversible contraindications such as severe pulmonary hypertension or elevated PVR, and they clipped them and they saw the one-year outcome.
The selected use of MitraClip as a bridge to heart transplant was safe. 87.5% of them had procedural success and no death at 30 days, but keep that in mind. 2/3 of these patients remained free of development of composite adverse event at one year. 15.5% became eligible for transplantation. And nearly a quarter of these patients were removed from the heart transplant list because they had clinical improvement. However if we look closely at the results, 6% of them needed urgent heart transplantation, 80% of them needed urgent LVAD, and 4.5% died within a year.
And so again, I immediately got an email from our MitraClip rep, oh, look at how effective it is for the heart. Well, look at this too. So we got to be very careful about how we interpret this data. Again, it's one of those things that we need more data and we need to be very, very careful about how we select our patients. And again this is just a testament of how our program, the synergy between the transplant team and the structural team is so important because of how sick this population is.
All right, moving along to the next case of an 82-year-old with isolated severe TR and an enlarged right ventricle with lower extremity edema controlled with diuretics. This is a tricuspid valve, there's a prolapse here, and there's severe TR, and its symptoms ongoing despite medical therapy. Procedure feasibility and risk, the tricuspid valve is just-- previously the guidelines said tricuspid valve repair replacement in patients with persistent symptoms despite medical therapy, but now we're looking at the tricuspid valve differently.
What is the present and future holds to this, holds to this valve? We are now understanding more and more about the natural history because that's important, we need to know when do we interfere. But also the field is evolving from a percutaneous standpoint because it is a very tough valve, it is a very tough valve to treat percutaneously. It is the toughest valve to treat percutaneously.
From a natural history standpoint, we now know that severe TR ensues, then there's RV dilatation and dysfunction, then right-sided heart failure begins, and then there's end organ damage where there's now the liver gets affected, the renal the kidneys get affected, and that becomes irreversible and the patient just spirals down. So really pushing diuretics until they stop responding and having end organ damage is not ideal. So that's why it's important when we make decisions about percutaneous options to understand the natural history, to know when to intervene.
Percutaneous options, again there are many percutaneous options that are all experimental. There are the coaptation devices such as the clip, such as this FORMA device, which I was involved in when I was in Rochester as a fellow. This was put to a stop because this had a hook and it had a spacer where the leaflets coapt against, but there's a lot of perforations that happened with that because the RV is thin. The RV, the tricuspid, the thinness of the tricuspid valve leaflets, the difficulty with imaging the tricuspid valves, it is truly a very difficult structural intervention.
There are annuloplasty rings in the making. Some people put in transcatheter aortic valves in the IVC and as we see. But yeah, you're protecting the upstream and the upstream, but the right ventricle continues to dilate and you know when it dilates there will be ventricular arrhythmias, there will be-- I don't think it's an effective treatment. So same thing ring annuloplasty devices, and then dedicated tricuspid valve replacement devices, it is very tough. I don't think-- I mean, it's going to take years before. The most successful one so far has been the coaptation devices, but again everything is experimental.
Again, the only devices that we use off-label now, off-label, are the tricuspid clipping using the MitraClip device. So there will be a device dedicated to clipping the tricuspid valve in the making and in trials. But right now what we do usually for these patients is, any patient who undergoes a MitraClip, we can retract the MitraClip device and add a second MitraClip and try to clip the tricuspid valve using that.
Now we're clipping a tricuspid valve using a device dedicated to the mitral valve, so we actually make modifications that are a little bit clumsy sometimes in order to grasp any leaflets. And a lot of times we accept a torrential TR to severe TR result as a successful result. So again, it's not-- it is a field that is in a major need of more advances.
Now same thing, now the tricuspid valve-in-valve is a very quick and effective procedure, an old failed bioprostheses. Some people also put them in rings. The rings are a little bit tricky because almost always the tricuspid valve has an incomplete ring, and so anchoring might be an issue, and so we always are very careful about doing it in rings. But in failed bioprosthetic tricuspid valves it's still off-label, but a lot of times it is covered by-- it is covered and it's very effective, and quick, and very safe. And so we've done a couple here. It's been with really good successes.
The tricuspid valve on the other hand, this is one important caveat to know is if we just do tricuspid valve clipping now, it's off-label and it's not covered, so the patient has to pay out of pocket for a result of going from torrential TR to severe TR. If we're lucky we get moderate TR. That is if we're lucky. We almost always aim to clip two of the three leaflets and we would be celebrating in the cath lab, so from a cost-effective standpoint we have to bear that in mind.
If on the other hand we clip the mitral valve, if there's an indication to clip the mitral valve, clipping the tricuspid valve is for free because the company charges only for the guide and one clip. The remaining clips are actually not charged, so that's why we can clip the mitral valve, retract it, and clip the tricuspid valve. So from a cost effective standpoint for this patient it might not be an option. He might be left with $100,000 bill that he might not want, and so that's an important thing to discuss with the patient.
What is the one-year outlook? I think, I mean in this gentleman it's reasonable. But what is the data? We're limited, there are early feasibility trials for these devices. We're limited to registry data showing maybe there's a potential mortality benefit from these tricuspid valve interventions, but again it's only registry data.
So we're going to shift gears now to the role of the cath lab in optimizing heart failure patients, and we'll start with the LVAD patients. This is a 68-year-old with an LVAD presenting with dyspnea, severe MR on echocardiogram, otherwise poor echo windows. So in these patients we can-- and this is his echo. So in these patients we can offer a ramp study based on Atta Behfar's protocol in Rochester.
Traditionally a ramp study done by just doing a right-heart cath or an echocardiogram with increasing the speeds of the LVAD. But there's a limitation with that because we don't know what's happening on the left side a lot of times. We don't get all the data. So I love this protocol. He does left and right heart catheterization, and then increases the speed and looks at this parameter called the TAG, which is the difference between the aortic and the peak and the peak of the left ventricle.
And of course looks at the-- and what he found is that a TAG of 20 to 40, between 20 to 40 millimeters of mercury, or an LVEDP of less than 16 optimizes these patients, and they feel better, and optimizes their hemodynamics. And of course we also have simultaneous right-sided pressure to see what happens on the right side. We don't want the RA pressure to shoot up, because that is not good as well.
What about the CRT devices? We can also optimize those in the cath lab. Again, this is also Atta Behfar's genius work that I learned from him. And he does left and right heart catheterization. And then he says, and his experience is that the AV delay is actually what does it. And in changing that parameter in these patients, for example for instance this patient, the LVEDP drifted a little bit downwards here. But what you notice is that the systolic pressure went up. And so with this optimization plus adding afterload reduction, you will improve the forward flow of this patient and decrease the failing pressure and they'll feel better. So that's one option for some of these patients.
Finally, I'll talk a little bit more about the LVAD outflow graft stenosis. Now outflow graft stenosis, especially the HeartMate II, they're not the best outflow grafts out there. We've seen outflow graft kinks and we've seen thrombosis or fibrosis. So I'll start with this case. This is you can see here, this is a patient who has had increased speeds in his LVAD, and so a CT scan was done and you can see in 90 degree kink here. What we can do for these patients is we can assess the kink actually hemodynamically.
So it's not only to treat the kinks, but also to assess them using pressure wires. We put two pressure wires across the kink and we can see here we can even change their positions because the kink can change with standing, or sitting, or laying flat. And so here with supine, the kink was worse, the gradient was 20. Now what is the optimal gradient? No one really knows yet, but if you extrapolate the coaptation gradient then 20 is your cutoff. But if you extract the aortic stenosis gradient and some people use a mean gradient of 40, but that shows you that there's a significant gradient when the patient is supine.
Here's another example, this is a patient who presented with significant hemolysis, and that's the outflow graft kink. We were able to put in a self-expanding valve across the kink. This is the ideal valve to use. I don't like to use balloon-- meaning that the stent comes in a sheath, and when we pull the sheath the stent expands and gets deployed, as opposed to inflating it with a balloon and deploying it. Because what happens is, if you use a balloon you're going to obstruct the flow to the LVAD then they can crash. It happened, it happened with me.
So that was a lesson learned. I'll show you that case. So what happened with this patient? The speeds went down immediately after we put the stent and then the hemoglobin stabilized, so it was effective. On the other hand, fibrosis or thrombosis. This is an LVAD fibrosis-- that's why a CT scan is very important to get in these patients with suspected obstruction, to understand what the mechanism is. Melissa, you have experience at Emory. Tell us about your experience with these.
FEMALE SPEAKER: Yes, yes, so we would see it quite frequently actually. And then they would come in with low flows and once we did the CT scan, identified that there was outflow graft obstruction, and then we would end up having our structuralist basically stent the entire outflow graft, and that was typically very effective in terms of restoring appropriate flow.
MODERATOR: Perfect, how many stents did you use?
FEMALE SPEAKER: So this one it would vary, but Dr. Bob [INAUDIBLE] would typically do at least six.
MODERATOR: Six stents. So to Melissa's point, we used one stent here and the thrombosis and the fibrosis shifted downwards. And what we learned from this case is one, using balloon expandable this was one of the rockiest cases I've ever been through to be honest, been through. Balloon expandable stents can lead to a hemodynamic-- now this guy tolerated it just fine, but we almost, we almost had a situation here because you're obstructing flow against the LVAD.
Lesson number two is when we plan these cases we have to make sure that we have enough reach to send the stent all the way from the access site down to the graft because we engage it in a retrograde fashion. So a lot of times we have to use the axillary artery to have enough reach. So for this patient we didn't have enough reach. And so, and we didn't-- we were initially in that early learning curve and we noticed that, like Melissa said, that the cloth shifted distally when we stented just at very proximal portion that was significantly stenosed. So I do agree with Melisa's input in terms of we need to probably stent the whole thing, because the whole thing, as you can see here, it just layers out with clot.
Other issues, you know aortic regurgitation with LVAD. We don't have good percutaneous therapies for native AR now, but some people are trying to put a stent in the aortic root and then deploying a TAVR valve in it. Other people, in some people who have-- in patients who have a park stitch, they can deploy vascular closure device across it. So there again, we can get creative but again we always try in order to provide the best care for our patients.
Severe TR is tricky again because of the matters that I mentioned to you. I know we had a recent case. The tricky part of it is we can always handle severe MR with an LVAD by increasing the speeds, but if there's concomitant severity TR what ends up happening is it unloads the left ventricle when we increase the speeds. It pulls the tricuspid annulus further and can worsen the TR. So not an ideal situation, but that's definitely a challenge when we're treating these patients.