Dr. Fudim presents on the basics of heart failure, how patients present, and how to treat decompensation in those patients.
We have doctor uh coming to us from uh Duke University uh does a lot of work in the intersection between heart failure and the neurological system if you will. Um So we've asked him to uh give a discussion for us about volume over a load and distribution. Looking at mechanisms of the compensation and heart failure. I think what we learned from this will probably change how you view heart failure going forward. Thank you. Appreciate it. Thanks everybody. This weekend will be historic for two reasons. It will be in history books. One, you guys were able to pull off a magician twice in a row. Two years in a row had a heart failure at a cardiology meeting. That's quite impressive. And two, because there's a big event going on in Europe right now and there's a coup d'etat put in Russia. I don't know if you have been following your phone this morning, but Putin has left Moscow fled. So this will be probably the end of the Ukraine War. And you know, a lot of big things are coming good and bad. I've been monitoring, I've been monitoring Twitter for you all. I hope it's all true, right? So, but I will talk now a little bit about the basics of uh heart failure and the process of decompensation. I think you heard about advanced therapies for heart failure. You heard about uh specific forms of heart failure. But I wanna take a step back and just think about how do you actually patients present to the hospital and how do we target and treat heart failure and prevent heart fail de compensation? One and not um disclosure, I present data from one industry partner that I work with. So when we think of card compensation and I will uh put this to a vote here. Is that how often do we tell people following a heart failure compensation or we find them to be in a, in a worsen heart failure state? How often do we tell patients go ahead and watch your weight and call us when your weight is £3 and up and then attempt to prevent the cardia compensation and raise how often you tell patients monitor your weight. And that's in an attempt to identify cardio compensation. You see that on all the way, on the right side and orange wake in and symptoms tend to be very late in the course of cardio compensation. So if it occurs, often the train has left the station, you really have to identify patients in the process of de compensation a lot early here to the left as measured for example, by pressures, bio signs, vital signs. And this has been really demonstrated nicely in studies using endocar pressure sensors, endo pressure sensors. This is the same population shown here in pressures which is the invariable truth of decompensation started rising as early as 30 40 days prior to compensation. So prior to a decompensation precious rise millimeter every few days every week. At a time. At the same time, on the right side, the same patients have no significant weight gain when pre presenting to a hospitalization, in average half of them gains more than £3. Half of them does not. So using weight as a surrogate of cardio compensation is really a very bad way to try to catch them all because it really only applies probably in half of the population. So weight gain as a measure of salt and water retention that necessary not sufficient to explain cardio compensation. And a very way nice way to demonstrate. It was done by Cleveland from Scotland and colleagues. They took 20 patients with put them into an early phase unit. They locked them up, gave him dedicated amount of salt and water. Throughout the two days, withdrew all the medications and watched the output. And what I found is that these people had a worsening heart failure status. The nyh A scale increased by a point, the anti P doubled the blood pressure increased, that had more water on the lungs, the size of the increased classical card compensation over a short course of time frame. Yet, all in the absence of weight gain, if you and I would have told this patient to call us when your weight is up to £3 we would have missed this classical cardio. This is simply not sensitive enough for this process. So how can we explain that somebody might have elevated neck veins increase as of a hard amount of water on the lungs has increased. Yet all in the absence of water gain. And it's simply through the process of uh of redistribution, a shift of blood volume from the periphery. And this is now speaking to one of my interests of uh research and that's the abdominal cavity. I consider myself a heart failure doctor that does not care about the heart because I think a lot of the badness occurs below the diaphragm. And the reason for that is that because the sponge nick or the abdominal cavity really contains 30% of the total blood volume. Intra rascal blood volumes is 30% abdominal cavity, liver and spleen big sponges for blood, highly autonomic innovated, whether you believe in mother nature or God, they put 20 to 30 times the amount of nerve endings on the vaske of the gut as compared to the vaske of the arms and legs. So clearly, somebody wanted to control that area very tightly. And by doing so is what we can do with this bottle trick you know, I uh you know, Duke cannot afford fancy parties like this. We do not have magicians. So we have to resort to this cheap bottle tricks to demonstrate uh science. So when we squeeze the bottle really, that refers to a construction visa construction is that process of volume recruitment. Note, everything about that yellow line we refer to as stress, blood volume or think of that central venus pressure, I can elevate the central Venus pressure or the distension of jug veins. I didn't have to give any water into that bottle to distend anything above the yellow line, simply distribution process. I think very trivial for the for the fans of Jean Claude Van Damme, I can't believe I had to put a movie reference down there, but I wanted to be academically correct. This is from blood sport. That's a concept. But now think about this, the recruitment primarily happens out of the abdominal cavity. Why I just told you the majority of blood volume recruit blood vol sits in the abdominal cavity and it's highly innovative. So that's how the body recruits that blood volume for daily activities such as exercise when we need to load the heart of blood. But unfortunately, in setting with heart failure, it might be detrimental. So a thought experiment, we took 20 patients and implanted them with cards and measured pressures at the same time and measured how much blood volume they actually had. These are people with worsening. Heart failure on the X axis is P A diol pressure. That's think of it as wedge pressure, everything outside of the green zone above 15 is abnormal about 15 or wedges abnormal. And on the Y axis, you have deviation from ideal, you wanna be in a green zone, you plus minus 8 to 10% of ideal for your age, gender, height and weight matched. So in you, if we're in red, you were wet. If you were in the white box, in the bottom, you are dry. So would you see that three out of 20 patients were in a yellow box, they had high pressures and high volumes. Well, that's that's unusual because you would have expected more patients to have that because the majority of patients, 60% were high pressures, blue box, high pressures but normal or low volumes. So the majority of patients running around with elevated neck veins, elevated filling pressures on uh on exam or with the cards in place do not have volume over load, the intravascular eic or dry. And the only way to explain that is that through the process of redistribution rather than volume gain. So pressures do not equal volume. We gotta be very careful about it. And in reverse, we don't treat every elevated filling pressures by having them diarrhea. And here another example from the real world, these are people on the left side of the mayo clinic on an outpatient basis where they measured patients that were either considered to be euvolemic and asymptomatic. And there was a very broad distribution of actual blood volume. Just look at the top row on the a there was a range between minus 20 to plus 40 in individual patients in the deviation of blood volume from ideal that will extend to some degree also to the edema status. But it's very important to note that these people were noted by the providers to be not volume overloaded based on physical exam. So your blood volume can be expanded and you still have no edema. And then you have a on the right side, it's actually Duke internal data where we gave everybody within 24 of admission, top row total blood volume, a blood volume analysis. And they have passed the emergency room at Duke. They have passed the general cardiology consult landed with us and we see that about 2030% of patients were within that green box or below to the left. They were either or dry yet they landed in our hospital service. What is the number one? Number two, number three, action we do for our patients that hit the hospital, we give them dia IV high dose. I'm telling you in 2030 40 50% might not need it. That's Duke and Mayo Clinic. Let's look at a community hospital from Jersey here. They have done the same analysis in 24 hours. They gave blood volume uh uh analysis done to patients. So it's a, it's a cumbersome test, but it was done here just to demonstrate your intravascular blood volume. And what I found is here in uh in the first red line, 50% of patients had UIA or hypovolemia but were anemic because the test can determine anemia, red blood cell status as well. And the second row was an additional 12% were also UIC hypovolemic but had no red blood cell abnormalities. If you do the simple math, 62% of people hitting this community hospital serial admissions were hypovolemic or volm. Why would you give these people diabetics? Why not focus on GDM TT vaso dilation IOS where needed. So concept number one shift can induce pressure elevation in the absence of volume gain. Could we then actually then target that process by reducing the stress in the recruitment of blood volume and prevent card compensation. So we have done it actually in the laboratories, we've done it in animals and also in humans where we stimulated sponge nerves to demonstrate that we can actually recruit this blood volume in healthy adults. We're able to demonstrate that when you turn on that nerve, the nerve, it's a bilateral structure that blood volume recruits quickly. You shift the blood volume within seconds within 30 seconds to reach peak, you turn off the simulation of pressures go down. That's arterial pressure, left atrial pressure, wedge pressure P A pressure. So we started blocking that nerve initially acutely to demonstrate to ourselves that acutely that's a safe and we're able to lower our right and left side pressures dramatically. This was a bilateral block. This also resulted in a reduction in blood pressure, which certainly would not be tolerated in many of our heart failure patients. But this was a demonstration of proof that we actually can block that nerve, that we can lower feeling pressures. Then we went on to take sick patients that were undergoing transplant evaluation at our centers as this got early undergoing this tribunal. And one of the uh tests that we do, we act them, actually exercise them and do the CPAT test. And what we did is we exercise them black line and you see pressures go up as people exercise and comes down as a uh as they recover, we blocked them, waited an hour, repeated the test again. And we found that after nerve, there was a reduction in filling pressures, the exercise test in these predominant half patients. This study was then repeated in Europe where they cut one nerve and half patients, single arm studies. All here to be fully clear, demonstrated the nerve was extracted and demonstrated that we were able to lower filling pressures to some degree. I have to speed up a little bit. We now I have actually not shown you the shift of blood volume but you actually can track blood volume. There's some radiologists in the room that will like this, we can tag red blood cells with actual technetium. It's uh uh it's a test. You don't wanna do too many times because there's quite a bit of radiation. We examined them under the camera and what we saw there, you can actually see the counts shift from the abdominal cavity to the chest. So the ratio of thorax to optimum increases here in black rest to exercise. That's before the block, there was a slight shift and when we block the people with Botox and uh repeated the test in one month. And that's the bull dogs of the nerves were able to see that the rest and exercise. That was a lower amount of blood shifted from the abdominal cavity in the thoracic cavity. So just to demonstrate the mechanism of action of preventing blood actually shifting into the thorax. Ok. And last but not least now, we have actually dedicated therapy that's getting evaluated. That's a spongy nerve ab there's a a of one nerve because we have a couple of nerves that the bleeding, one of the nerves. And here we actually demonstrated in this unpublished data, we actually can stimulate the nerve to demonstrate that we're in the right place. This is what I've shown you earlier. But this is now in heart failure patients here on the top lip on the left, the X is a squash, but there was a 30% increase in arterial pressures. P a pressures and then when we block the nerve on the top, right, you see, post on the bottom that you cannot elicit you. So the nerve was that we can no longer elicit that shift of blood into the chest. So that's what's currently pursued by this therapy. And we have uh some uh some original uh open label data in uh about 20 plus patients. What we demonstrated with, at least with exercise, we are able to reduce card filling pressures in this population with he patients. There is an open label experiment. My clickers start working, we're now proceeding into going into randomized controlled studies and the initial study is over called rebalance. HF. We will be presenting it towards the end of the year. So stay tuned for that. And a large pivotal study will be initiated towards the end of this year to demonstrate that in the responder groups. OK. In conclusion, congestion is a complex concept. I'm not gonna take anything away from you. If you think that patient is congested, that's good. I'm not gonna argue with that but be careful to label every patient that is congested with also the label volume over it. That not, not, not be true. Distribution is one form of decompensation. You do not have to gain water, you can decom for shifting processes. I hopefully demonstrated to you in a fast fashion that the sponge nerve is a key contributor to cardio compensation. That's a recruitment mechanism trying to get rid of that nerve is what I made a life mission. Thank you very much. All right. Uh Thanks for that uh discussion. Uh We'll open it up to the audience and see if there's any questions for Mora or any other questions that may have come up with any of the other discussions. Hi. Uh Thank you for the excellent talk. I have a few questions. Would you routinely recommend a discharge anti BNP and all the patients? That would be the first one? Uh And second question I have is in patients with newly diagnosed uh systolic heart failure. Would you recommend starting all the guideline director therapy at the same time or start on a couple of them and then slowly up tight? Right. Right. I, I can take the, I can take this first step. So I think uh discharge anti BNP, I'm pretty sure that has been studied. I don't know that that's necessarily the best idea because the discharge anti BNP, uh you know, it's the marker has a half life of several days. So it's not gonna be very reflective of the volumes that right then and there and it still be a little bit down. It's not the, so even though the patient is, you will, an P is not back to normal in most cases because the average length of stay is four or five days in United States. So I think I personally use anti B MP on my 1st and 2nd clinic visit, even though that's not necessarily guidelines and the guidelines say, assess congestion, it doesn't tell you how to assess it. But I think this IP is not very helpful um to GMT. Absolutely. I think there's very good rationale now to start GMT as soon as possible and then trade it as soon as possible. And most recently, the strong HF trial was a trial in Lancet uh a few months ago where you know, if you tight rate GMT within a month, you had better outcomes and that's including death and heart. When compared to standard of care, the problem with that becomes that if we want to titrate GMT, we often are not set up as systems to allow ourselves the resources to three GM at the speed that's really necessary because in a trial, for example, they rate it every week, week 12 and four or 12 and three, that's of course not sustainable in clinical practice. So we are working on solutions medication that clinic. Yeah, I think, I think that's right. I I might have a slightly differing opinion first about discharge and terminal Pro BNP. So we know from a fair amount of data that goes way back that the discharge and terminal PRO BNP is an extremely strong predictor of outcomes much better than the admission and terminal Pro BNP. So I think if you're trying to say, how is this patient going to do it won't be the final internal prob NP. But if it's markedly elevated on discharge, that's a patient that you better think about referring or hospice or something else because it's, it's really a fairly powerful predictor. And then I think the other thing that isn't certainly in the guidelines. But you think about what was your internal prob NP a year ago? And do you get back there with medicines? Because if you get back there, maybe we don't know this yet. But it's probably true. This was just a, a medication or a sodium, you know, uh uh not, not watching carefully with that. But if they're an internal Pro BNP, when you've got everything you can do, doesn't it gone up substantially from what it was a year ago? That patient is worsening for some reason and you know, you need to go back and say, is there a reason for their work for they not taking their medicines? Are they not, do they have, you know, increasing coronary disease? Do they have an, is there some other reason why they're not doing well? So I would say that about the UN terminal pro BNP. I think this question of guideline directed medical therapy. We want to get it started as soon as possible. But even in strong HF they were very careful about monitoring and they did terminal pro BNPs in that study and 15% of the patients based on the terminal pro BNP had to be stopped in their uptitration because it got worse. So we do need to do it, but we're going to be able to have these careful, you know, uh parameters and they're going to have to be paid for because many insurance we all know won't pay for those N terminal Pro bnps. But if you look at strong HF, you are going to see some data shortly that SGLT twos are appropriate to start immediately on the heart failure hospitalization. So we have a lot of things we can do to dire people, but you're going to see some data coming out at ESC that strongly suggests that they, they improve diar shorten hospital stay when you start them immediately and they are safe because that's been the big question to be started immediately. So that's one thing you can get started right away. But how we do this uptitration and how we get paid for it and how we get the people to do it is really AAA big procedural question. Thank you. I have one more question in younger patients with reversible causes of cardiomyopathy like the peripartum, alcohol or tachycardia mediator once the ef gets better, what makes us to wean up the medications or discontinue the medications? How should we do that? Go ahead. Ok. Well, I'll take a stab at that. So, so I think if you have a completely reversible cause of your cardiom like tacho cardio induced and that and it was clear and you're certain of that, that ultimately, you probably can reduce the medications with peripartum cardiomyopathy. If you go back to normal, many of those people have underlying genetic abnormalities. So we have to make sure that they don't have underlying genetic abnormalities before we think about withdrawing medicines in cases where you don't think it's completely reversible, then you're on medications for life because there was a very nice study that, that withdrew medications and showed at least half of people clinically worsened and many of the others look like they were going to start to worsen. So if you absolutely know it's reversible, yes. But in things that you think is are reversible, like per partum cardiom, you probably ought to understand if there's an underlying genetic abnormality in, in many of those patients before you withdraw medications. Uh, 11 quick question for all of the clinicians in the room. Take, taking a step back. You know, it's a very thought provoking lecture. So, you know, in clinical practice in the hospitals and the clinics in the primary care office, we're very, very bad at assessing congestion. All the trials are very bad. The exam is very bad. So a lot of times in clinical practice, we do these right heart cats to see how swollen they are quote unquote. So if we're bad at assessing congestion, how should we do that? Like, how do we know how much directs to give, how would other providers know the pressures are out if you get blood? Well, II, I wish, but it's too complicated. I mean, the, the reality is that there's no perfect answer to ingestion. That's why we need cardiologists and, or I have to train other physicians to do. So, I think it's, uh, a myriad of things of physical exam will be indisposing. I mean, simply having a three plus edema. Of course, there's volume overload. At the same time, if somebody comes to you, I I always, I always call the little elderly ladies, you know, they come to the emergency room, the neck veins are elevated, there is not a single gram of water on these people. How can you think that they're volume overload? But that's what the neck exam would suggest, right? But that assuming that pressure equals volume, but it doesn't. So I think the first thing is to take a step back and differentiate between pressure overload and then volume of with our volume molo often leads also to pressure overload. So if you have volume overload, you often also pressure overloaded. But I think we need to differentiate our way of uh treatment. I think using radicalization, sometimes more liberally, uh remote monitoring continues, remote monitoring also is of course, uh you know, a step up to us relying on archaic stuff such as weight scales. But at the other end of the day, I don't have a perfect solution. All I'm all I'm pointing out is that it's a lot more complex than we often think. And which is why we often don't achieve the benefits we think we should be achieving is because we don't treat the things that probably was the problem in the first place. Um First of all, uh great to historical comments you made at the beginning of your talk. The only problem is I blanked out the first five minutes of your talk because I was looking at the Putin thing on my phone. But then when I recovered from that, I, I do think your your talk was um really very disruptive in many ways, right? Um that the separation of volume and pressure and the whole blank neck sort of capacitance if you would. Um I still, so, so I guess the question is if this blank neck vasculature is such a huge reservoir, right? And that it's a very sort of versatile reservoir in terms of pushing fluid into the circulation. And III I, I'm still trying to understand um how do you identify those patients clinically? Right. So whether you do a right heart Cath or whether you're checking edema peripherally, what I heard you say is that maybe the overall volume and almost two thirds of patients who present with elevated pressure is, is not the problem, it's not a volume problem. So what, what are the tools that help separate volume and pressure? Uh because as you say, um the therapy could be very different. Well, I think that is a very good question. I mean, I think we all will recognize phenotypes. I'm gonna give you the extremes the way we see them and I think we treat them accordingly already. I'm gonna give you the obese young man with three plus edema hitting the floor, clearly volume overloaded. And the little elderly lady, small frail also short of breath also can our life flat also has elevated neck veins but doesn't have edema. So those are the two extremes, how we can narrow down everybody in between into individual phenotypes. I think that's a lot harder. We try to get you some of those answers through the rebalance study. We're doing, we're trying to look now into phenotypes, how hemodynamic phenotypes translate back into um into clinical phenotypes. So I'm going to give you an example. If you to respond to the spongy nerve blockade, then you're probably gonna be some one of we call them shifters. You may be one of those shifters. If you don't respond, you may be not. So, in retrospect, we'll be hopefully able to answer some of your questions on the intermediate phenotypes, but uh I don't have that answer yet, but I'm I'm taking hypotheses. Um So I think it is really, really fascinating hearing Doctor Fu's uh comments. However, I think at the end of the day, we're still stuck with what's simple. Still, everybody has a scale and still as heart failure, persons that we create raisins for a living. Because if you make the patient dehydrated, whether by dire SGLT twos or even Entresto, which actually does a very good job of, of improving B MP. Uh PRO B MP, they get better. But it's fascinating to think that perhaps there may be ways in the future of uh of affecting things like blank faces or construction. Thank you. Any other questions? Yeah. Uh Just wondering a poor man's approach. What about liver size and congestion versus peripheral Dema? And does feeling liver edge help that you're central is discording with peripheral? It's interesting, we're actually looking into this, you know, uh all of us will clinical recognize there's always this patient that always tells you they congest in the belly only and those that only congest in the legs. I tell you those are two different phenotypes to begin with. Some of that will be related to this. I don't know how exactly, but we are trying to study, but it's not that easy because we really often have to rely on a patient's uh description and you know, it's a congested liver. Is this a sign of RV dysfunction or is this truly a sign of a local distribution process? I don't know. Um But that's that those are exactly the questions to ask, right. Any other questions? Go ahead. I just had a comment about this earlier debate between Dr Ben and Dr Lindon. I'm sorry if I'm pronouncing your name. Don't worry, everybody does. So in defense of Dr Ben, because he's been beaten so badly by her. She forgot to list a six check or not. So check mark about cost of transplantation for life saved. So I don't think she showed the data. So maybe Doctor Ben can point it out to her as maybe a plus for LVAD. I don't know what the answer is. It's, it's a very good question. So I don't know whether ventricular cys device over the long term is cost-effective compared to transplant because they're really sort of apples and oranges, right? So in fairness, the over the for now, certainly an insurer would say that they both have a significant cost, the the cost of transplantation in terms of the monitoring and other things you need and medications is quite a lot. But Doctor Lin Feld is exactly correct as we both take care of patients. It's not that you get the VD. And as simple as the debate makes it that you get the VAD and you're fine. Um, readmissions are a big issue, but it, I would say this, it transplanted V both have different phenotypes and you don't know when you go in. I have one young lady who took care of when I was in Newark. This you oftentimes see her at conferences sponsored by Abbott. She's now 12 or 14 years out on original heart made two, which would have clotted off years ago. And for whatever reason, it's been perfectly fine and same as you see, transplants who are 20 years out and they're perfectly fine on two meds. On the other hand, you also see the opposite, see somebody who would have done well after a van and just has a miserable time. And at the end of the year says, please turn off make me hospice and transplants that should have done well. And on the other hand, every conceivable problem happens. So I don't know the statistics about which is more cost-effective. I think there's clearly a role for both. The one thing I would take away is that still, even if you say 14,000 transplants a year, there's still hundreds of thousands of patients to get neither and give your patient a transplant or a ad. But don't let them die when you see them, you know, and people often say, well, ok, I got one moment. Tell me, what is the one thing you want me to do? Who do you want to send? It's the patient that comes in over and over and over and over again. More than one emergency room visit or admission for heart failure, you have a problem. You have to do something because that patient's going to die. So if you remember nothing else from what I said, please remember if the patient is constantly in the er um you need to instead of just copying and pasting. The note. Think about, gee do I have to refer them because something bad is happening, the house is on fire now that I agree with all of that totally. And that it's a really insightful question. One of the reasons we have so much trouble getting at this cost thing is it isn't just the cost of the procedure and the hospitalizations and the medicines. It's can that person go back to work and we don't know the relative. We don't have a study that says relatively to, to you know, these patients who goes back to work. But we know a lot about transplant and that a very large number of patients who don't go back to work, post transplant don't go back because they can't get insurance that the the workplace won't, they won't get insured. So if we could change that, is that a misguided therapy then and people could go back to work, then we, we change a little bit that balance of how cost-effective is something that people can go back and, and, and work and, and do the things that they want to do. So it's a very, it's a really important question but it's a very difficult thing to get at the total cost. But in our institution, the one year cost of transplant versus bad is very similar at Vanderbilt, taking everything, medications, hospitalizations, everything. All right. Any final questions? Just, just quick. Final II, I know you have an EP and a structuralist there and, and I know we didn't focus very much on sort of the, the ep and structural aspects of heart failure. Um And I, I'm wondering if, if, if, if you could just um address that because I think it is a multidisciplinary team. The, the one thing I'll say briefly is IC DS and L ads equals nightmare. And I would love to take advantage of the power of this panel and ask them if I am a monster for not being aggressive about exchanging batteries and defibrillators and dealing with all these problems with IC DS and L ads. Yes. No. Yeah, I just, sorry, you just set that one up. So, I mean, I think that's one of the things we didn't discuss is that the problems with ad that I told you were adverse effects are chronic adverse effects. You start having arrhythmias and they are really, really hard to get rid of. So I don't know what the right answer to that is. It's something we're gonna have to address as a community, I think. Yeah. And so it, it, the issue is with IC DS and L ads is definitely a real issue. But I think the question is if you have uh if you don't have a rhythm as before, if you come in very ill heart failure and decide to put a ad in, there's a lot of evidence that probably don't need to put A I CD in after the LVD. If they didn't have arrhythmias before, on the other hand, the converse is also true. If they have rhythmic like crazy, you put an L vet and you'll have the patient with an LVE in I CD and miserable because they keep having shocks and you'll probably be asked to abate near places. You probably would rather not go. Yeah. It, it may be worth just explaining to the audience exactly why that is, is it actually the, the trauma around the A, what is it that makes the LV patients be more arithmetic? Uh I, I think it's, it's just the, if you get a patient who's sick enough to need an LVAD, the overall myocardium is bad, just like the atrium and said in a fib patients with uh amyloid is overall very, very bad. So it's not that, you know, you carve a piece out, you put the vat and that's usually not where the trouble is. It's all the rest of the heart and some people are those who have lots of rhythm as and others are not, the VD doesn't protect you except that you may not be symptomatic. I've had patients come in, in ventricular fibrillation and they just feel a little unwell because their right ventricle is in fib and you do an EKG and they would otherwise be dead. And I, I think you make a critically important point that heart failure has become, um a team approach. I think that's been said several times today and I was just in a symposium about um implantable device, defibrillators and, and IC DS and stuff causing tricuspid regurgitation and severe right heart failure. And it's very clear that the guidelines for that will come out. And this is a team decision that involves the structural guys, the EP guys and the heart failure, folks about how to treat that. They're very difficult decisions. We're learning a huge amount about that. Um But I think it's become a, a team, a real team effort just like we thought that we think nowadays, valves are, but I think more so how has become a team, a really huge team effort and ep and structural are just a huge part of that, especially now as we get into the earlier um addressing mit mit regurgitation earlier. And it's especially tricuspid regurgitation, which is the most common valve lesion. So, yeah, exactly. You know, we talked about val therapies yesterday and, you know, Ronnie and I, and, and all the team, we got to decide, you know, for all these devices and tear therapies for tricuspid valve microvalve when it's a, a bowel problem and when's a uh a functional problem and you know, we're doing these for functional conditions, but timing and patient selection is going to be very, very paramount. Yeah. All right. That's uh I would say uh just add another thing I think for functional patients making sure that they stay on medical therapy after tr is very important. Right. Because we've seen a lot of patients where they're functional, you get a great result. They do come back later with because the process is really the, and if, if they're not on medical therapy because they feel better on, they come off of therapy, then the process will continue and they come back with, uh, with more and more and more and they're sick again. But definitely, I think it's, it's one of those, you know, for us in a structural kind of a field, it's very important to have that strong collaboration with, with our heart failure docs. Um And I think that's what really makes, you know, patient care successful and program successful. Uh we've had situations where patients, you know, were referred to us because they could not tolerate medical therapy, right? You want to put them on GDMT and they just couldn't. Um And, you know, thinking maybe if we do an intervention, could that make them tolerate therapy? And, you know, I think from our experience, it, it really has uh the other um I think tricky part for us that we have been seeing a lot. And I'm just curious um what the rest of the panelists think uh the patient population of, you know, cardiogenic shock, right? Trying to do you know MitraClip or Tricuspid in the hospital to get him out of inotropes. I mean, that's I know, there's a lot of data on this where uh there's some positive uh retrospective data, but it's obviously it's kind of a tricky situation as well as the transplant, right? Patients who are waiting transplant. And can you if you do for MitraClip, for example, data showing that some of those patients actually might end up um not needing one. So I'm just curious what your your kind of thoughts are on, on that type of patient population. We have just quick comments because we're away over time and just quickly important point. I think there was a nice study that suggested that you might get patients who were waiting for a transplant or waiting for a decision off the list with the micro clip. And I, I think the problem with that publication is there was no comparison to the demographics of the patients that came off and on. So you don't know if they were the least sick patients in the study. But that said you could say if we do a micro clip, we know it doesn't resolve heart failure. They still all die of heart failure. It's a progressive disease. But could you give them enough time? Which we know it does reduce mortality? So, can you give them enough time to wait for a heart transplant instead of to have a bad and the answer to that is probably yes. All right. All right. Well, thanks everyone for this uh lovely discussion. Um So just remind everyone, uh, there's lunch outside these doors. So as soon as you open, there'll be food available for you to partake in.
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