Hi everyone, my name is Joan Michaels, I'm the Director of the TBT Registry at the American College of Cardiology. Very excited to have the opportunity to introduce our speaker for this session, Dr. Brian O'Neill is a board certified interventional cardiologist of the Structural Heart Division of Henry Ford and he's also the Director of Interventional Cardiology Research at the Henry Ford System in Detroit. So without further delay, I'd like to introduce Dr. Brian O'Neill to speak to us today about tricuspid disease and tricuspid care in the transcatheter world. Thank you. Hello, my name is Brian O'Neill and it's my pleasure to talk about tricuspid valve disease. This has been a passion of mine for many years and so I'm really excited to be able to talk with the group today about where we've been, where we are, and where we're going in terms of the transcatheter treatment for tricuspid valve disease. So I want to talk and start a little bit about and talk about the anatomy of the tricuspid valve. Now, we initially thought when we were designing therapies for the aortic valve that the aortic valve was complicated. However, when we moved on to the mitral and the tricuspid valve, we realized that the valve complexity has increased by an order of magnitude and the reason for that is simple. It's because the anatomy of the tricuspid valve is very complex. So I have here on this slide a couple of pathologic images of the tricuspid valve during surgery and you can see that the tricuspid valve, first of all, is composed of three leaflets, the septal, anterior, and posterior leaflets. However, many tricuspid valves can have four leaflets. They may have a very small septal or very small posterior leaflet. So the anatomy itself, it can vary from person to person. Now, in addition to the varied leaflets, you can also have a variety of different insertions of papillary muscles and the chord tendon in the various valve leaflets as well. So again, this makes any consideration for potential therapies of the tricuspid valve much more complex than the aortic valve. Finally, another challenging aspect of the tricuspid valve is the tricuspid valve is not necessarily fixed in a fiber structure such as the aortic valve and that leads to the dilatation that we can see in patients with severe tricuspid valve disease. You can see in the cartoon on panel C that many times that the tricuspid valve annulus will dilate in the anterior-posterior segment. So any therapies that we design for the tricuspid valve has to take many of these into account. Now, tricuspid valve, tricuspid regurgitation can be thought, can be broken up into three main segments. The first of these, the first of these is primary tricuspid regurgitation. Now, this is from a issue with the valve leaflet itself. This can either be from a patient that's had a history of endocarditis and may have a perforation in the valve leaflet, it can be from a severe tricuspid valve prolapse, or it can be from an ininferior structure in the tricuspid valve such as a pacemaker. So that's, that really is kind of the primary leaflet abnormality. And it's important to know these different, these different types, because each of these types will have slightly different implications in terms of the designation of the particular therapy that one would like to pursue. The second is termed secondary or functional tricuspid regurgitation. What this is, is essentially the RV begins to dilate, and as the RV dilates, the annulus of the tricuspid valve itself also begins to dilate, and that leads to malcoaptation of the tricuspid valve leaflets, which can then lead to, which can then lead to tricuspid regurgitation, more volume coming backwards causes the RV to dilate, and so on and so forth. So that's kind of a, that kind of starts then a vicious cycle of tricuspid regurgitation. And finally, isolated tricuspid regurgitation. This is when the annulus of the tricuspid valve dilates itself, and this can be in the setting of patients that have long-standing atrial fibrillation where we see this dilatation occur, which can then lead to severe tricuspid regurgitation. This is a cartoon representation of the different types. In panel A, you can actually see a pacemaker lead that's impinging on the tricuspid valve leaflet, and this would be considered kind of the primary tricuspid regurgitation. In panel B, you can see that when there's color flow across that valve, that again, the RV itself is relatively small, but there is severe tricuspid regurgitation because of the malcoaptation caused by the impinging lead leaf, because of the lead impinging on the leaflet. In panel C, we can see that, we can see that annular dilatation that can occur as the, as the RV begins to dilate. And then finally, in panel D, we can see what that looks like in a cross-section, how the valve leaflets can no longer, can no longer co-opt with one another. This is one of the seminal papers, I think, that really kind of brought everyone's attention to the problem of tricuspid regurgitation. Now, if you know, this is from 2004, so we've really had an appreciation of, of how, of how severe and deadly tricuspid regurgitation can be for a long period of time. And this was a VA cohort study, essentially looked at 5,200 veterans that appeared with any sort of valve, any sort of valve problem along with tricuspid regurgitation. So it wasn't just isolated tricuspid regurgitation, it could be in the same other valve leaflet abnormalities as well. What we found is there was a very, there was a very good spread in the survival in these patients that had, that had severe, that had any degree of tricuspid regurgitation. This could be mild, mild, severe. You see, obviously those patients that have severe tricuspid regurgitation have the worst survival. However, there is even still some, some worsened survival in patients with monotricuspid regurgitation. So we've known for a while that this is, this is something that needs, that could potentially be addressed and that needs to be addressed. And for a long time, we only really had surgery as being the main option and surgery has been a great option. This is some data from 926 patients undergoing isolated tricuspid, undergoing tricuspid valve surgery. And the interesting point about this is that only about 126 of these patients underwent isolated valve surgery. And this really is, I think the problem with the current standard of surgery is that most of the time tricuspid valve intervention is performed with concomitant left heart, left sided surgery. In this particular cohort, you can see that only about 15% of patients underwent isolated tricuspid valve, isolated tricuspid valve surgery. And the reasons for this we'll get into, but that is one thing to keep in mind is that isolated tricuspid valve surgery doesn't really occur that often. Now the 10 year survival in both the repair and the placement groups was about 50, was about 50 and 38%. So over time this, the survival is, is good up front, but it does kind of start to tail off over time. But the important thing from this study is that tricuspid valve surgery is very effective in terms of symptom relief. If you look at here, the baseline, the vast majority of patients were an MIJ class three, four heart failure symptoms. And then after followup, we saw that many of these patients now moved to moved to one and two in terms of the MIJ classification. Unfortunately we found that one of the, one of the, one of the challenges that we faced again is recurrence of tricuspid regurgitation. So this, this is again, stratifies the patients into repair and replacement. And what we found is that in terms of correction of tricuspid regurgitation, that the tricuspid valve replacement is more effective than tricuspid valve repair. However, the authors concluded here that the surgery is associated with substantial early and late mortalities, but again, with functional improvements. So a challenging course for many of these patients that are actually referred. Here, if we look at the recurrence of tricuspid regurgitation, we see that this also is, this also is a challenge in terms of freedom from TR. If you look at tricuspid valve repair at 10 years, only about 40% of patients are still free from moderate tricuspid regurgitation. So what we learned from these initial surgical studies, the tricuspid valve replacement is probably more effective in terms of freedom from recurrence of tricuspid regurgitation. However, the mortality associated with these procedures remains regardless of the strategy. So it's really no wonder, based on some of this initial data, why we see so few patients undergoing tricuspid valve surgeries. Now, taking care of many of these patients, I think the onus is partly on the cardiology community as well, because we refer these patients late. You know, we diurese them for a long time. We really only start to refer the patients to surgery when they develop the renal insufficiency and the hepatic dysfunction, which can make them particularly high-risk surgical candidates. That combined with the fact that there is still mortality with this procedure, it's no wonder why this surgery is performed so infrequently amongst unindicated patients. This is some data from the National Inpatient Sample, and you can see 10-year trends in terms of tricuspid valve surgery. And one thing to note is that, over this time, that we did see some slight increases in the amount of patients undergoing tricuspid valve repair and replacement. However, unfortunately, the morbidity associated with this procedure remained pretty constant around this time, at about 8 or 9%. As we've become more adept at managing patients with percutaneous therapies in the aortic and mitral valve position, the spectra of tricuspid regurgitation continues to haunt us in our efforts to improve outcomes in these patients. This is a cohort study of 197 patients who underwent percutaneous mitral valve intervention. And what we saw is that those patients that had no TR at baseline did substantially better than those patients with moderate to severe TR. We also noted that those patients that had improvement in tricuspid regurgitation after mitral valve intervention actually did much better than those patients that didn't have any improvement in tricuspid regurgitation. So now, the reason this is important is because up to 40% of patients that present with mitral regurgitation will have concomitant severe tricuspid regurgitation. So the mitral valve and tricuspid valve really go hand in hand, and so it's important for us to be able to have therapies that can address each of these challenges. The same is true for patients that are undergoing TAVR. So this is data from the partner trial in the inoperable cohort, and you can see that those patients that had moderate to severe TR had much more substantial mortality than those patients that had either no or mild TR at baseline. So it really is, TR really is something that kind of goes across all boundaries in terms of the management of percutaneous therapies. This is a nice, I think this is a nice kind of summary of some of the data that I just presented. So in the upper left-hand corner, we see the all comers with tricuspid regurgitation. In panel B, we actually can see survival curves for those patients undergoing, or those patients with severe TR that's lead-induced. Again, those patients that have lead-induced TR do worse than those patients without it. In panel C, we see the TAVR data, and then in panel D, some interesting information looking at patients with isolated severe tricuspid regurgitation, which really no other valve of abnormalities, which again, I think is very similar to the data that we saw from MATH in 2004. So in summary, really, tricuspid regurgitation is something that cannot be ignored anymore. It does affect the outcomes of percutaneous therapies across all spectrums of left-sided heart disease. So if we really want to improve our outcomes across all of our transcatheter therapies, we have to be able to also improve outcomes in patients with tricuspid regurgitation. And so in 2015, I think the interventional community really began to kind of take notice of this. There were some articles from an editorial at that time that really called out the fact that we really need to get some percutaneous therapies for tricuspid regurgitation, given the fact that we, again, started to notice that those patients that had TR in our other left-sided interventional therapies weren't doing as well as those that did not. Now in order for us to be able to really understand tricuspid regurgitation, in addition to anatomy, it's also important to understand the natural history. So this is a cartoon slide that kind of demonstrates the stages of tricuspid regurgitation. And really it starts off with perhaps a very mild annular dilatation that causes some mild tricuspid regurgitation. Over time, we start to see that RV dysfunction, RV dilatation, that it can accompany this initial volume overload to the RV. And then over a long period of time, we really start to see what we're seeing, I think, now a lot of interventional communities, these patients that are really coming severely voluminous, severe RV dysfunction, really large right atriums, and massive or torrential tricuspid regurgitation. And really, if you look at the management forms of these patients, in the very beginning stages, medical therapy, I think, still has a role, but really anything beyond that, surgical evaluation is important. And then once we get in these patients that are really sick, these are the types of patients who are now seen as our initial patients in many of our clinical trials. If you can believe it, really, the percutaneous field in tricuspid regurgitation has really grown dramatically by leaps and bounds over the last five years. We've gone from really only one or two devices to now having almost a dozen devices. And each of these devices really kind of impacts the causative, the problem of the tricuspid regurgitation to start. And that's important as well, because as I mentioned, we have many different types of, we have many types of anatomical features of the tricuspid valve. The tricuspid valve has the unique distinction of many times having a pacemaker lead traversing it, which we have to consider when we're thinking about our therapies. So really, this will not be one size fits all, this will certainly be many different devices which are needed in order for us to, again, get the best outcomes for our patients. So I felt that this cartoon breaks things up into kind of good, into some categories to help us then determine who, when we use what for each therapy. So first of all, we have the leaflet coaptation devices. These are devices that will impact the valve leaflets directly. Currently the two main devices are the MitraClip device and the PASCAL device. The former device is no longer in clinical trials and has essentially been abandoned. The direct suture aneuplasty, this was with the TriLine device. This was kind of a great idea, really trying to shrink the coaptation distance of the valve leaflets in order to improve coaptation, decrease tricuspid regurgitation. Unfortunately, this technology is no longer being studied in clinical trials. The next kind of, the next therapy is a ring aneuplasty. And again, this is kind of mimicking the surgical technique for tricuspid repair over a long period of time. Again, many of these patients have this annular dilatation that leads to tricuspid valve leaflet malcoaptation. The thought process behind an aneuplasty, if you can reduce that coaptation, you can then restore the normal valve. You can then restore the normal leaflet coaptation, reduce the TR. So currently we have the CardioBand device, which places anchors around the tricuspid valve annulus. And then through tensioning, we'll decrease the size of the annulus to restore that coaptation. And we also have the TriSynch, the nillipede device, although those are currently in very early stages of testing. Finally, valve replacements. We have the Navigate and the Evoke device. The Evoke device is probably the furthest along and I think has some really exciting data, which I'll share with everyone. And then finally, heterotopic placement of valves. And this is cable valve implantation. And this can be with a sapien valve, as well as some new technologies that I'll get into a little bit later in the talk. So I want to start off with the leaflet coaptation devices. So obviously, first of all, we have the MitraClip device. This is something that I think many people are familiar with from mitral valve repair. This device, however, now is being used in the tricuspid position. And we have much of our initial data from the Triluminate registry. This was a single-arm study of 85 patients with monitor-severe tricuspid regurgitation who were referred for TriClip. So this is kind of an interesting slide. We see here at baseline that 94% of these patients had at least severe tricuspid regurgitation. In this trial, I actually then divided these patients further into patients with torrential, massive, or severe tricuspid regurgitation. And I think this kind of illustrates the fact that not only are we still learning how to treat the tricuspid valve, we're actually still learning how to grade the severity of tricuspid regurgitation. So again, very early on in our experience in terms of how we can best serve these patients. But you can see at baseline, at 30 days and six months, really a really impressive decrease in the amount of severe tricuspid regurgitation amongst these patients. If you look at the panel B, we see of those patients that had severe tricuspid regurgitation to start, 86% had moderate or less at the end. So this is really, I think, a very exciting initial data for this technology. In addition, we also saw improvement in indices of RV function and size. On the left there, you can see that the RV diameters decreased, the TAPC improved, ready trill flow decreased, and really just the indices of function of the RV showed improvement. If you look at NYHA functional class, which obviously is incredibly important in many of these patients who are very miserable, very high degrees of NYHA class symptoms, we see that in the beginning, 75% of these patients were at three or four. And after tricup, they were able to reduce that to only about 20% of patients with severe NYHA class. So that's, I think, a really intriguing start to this technology. Now, the PASCAL device is another technology that's currently in clinical trials. This has a similar concept of the MitraClip in that it causes the clipping of the valve leaflets to decrease the tricuspid regurgitation. This device has independent class, which can help optimize leaflet capture, as well as a central spacer to help with tricuspid regurgitation. And this is just kind of a semi-fluoroscopy of what this looks like. Again, it looks similar to the MitraClip in similar concept in terms of grabbing the leaflets. And then you can see that the catheter is closed on the right-hand side there. And this particular patient really got a fantastic result. I mean, you can see this massive retraction on the left-hand side of the screen there. And then after the PASCAL device is placed, you can see that we were able to reduce that to just really mild tricuspid regurgitation. And the results from these initial 34 patients, I think, are very intriguing. 85% had at least one great reduction in TR, and 52% had moderate TR or less. So again, it's still early in these technologies, but I think we're making some great initial strides in terms of being able to help many of these patients. The next category of devices are the ring aneuplasty. And I'm going to talk mostly about the cardio band because I think the cardio band has the most data that's currently available. So this is a two-year follow-up from the tri-repair study. This was 30 patients in a single arm with at least moderate tricuspid regurgitation. And so again, as a reminder, this involves placing anchors around the tricuspid valve annulus, which then allows you to put tension on that to decrease the size of the annulus and improve the leaflet coaptation. And again, what we saw in these first 25 patients is many of them with MYJ class, or many of them with severe, moderate to severe tricuspid regurgitation to start. And if you look at a two-year follow-up, we have really great freedom from recurrence of TR. The same with the MYJ class heart failure symptoms, really great improvements over the two-year time period. So this data, this technology is going to continue to be modified, and I think we'll continue to see really exciting results from this technology. Now we can talk about the transcatheter valve replacement, and this is the orthotopic, meaning within the tricuspid valve annulus itself. And I'm going to talk mostly about the navigate, again, is kind of early on. So we have some, most data available with the Evoque device. This is what the Evoque device looks like on the left-hand panel here. You can see these tongs that will actually come up and grab the tricuspid valve leaflet, and then the valve itself is in the middle of the picture there. And this is what it looks like, this is what it looks like during the procedure. So again, the video on the left, unfortunately, it's not moving, but the patient had, oh, there it goes, had a moderate to severe tricuspid regurgitation. On the simian fluoroscopy on the right, we're doing an RV angiogram, and you can see a lot of reflux in the right atrium from the, across the tricuspid valve. Here we have a wire in the right ventricle, and we're just kind of slowly advancing the valve system into place. On the picture on the right, we have the system across the tricuspid valve annulus, and now we're going to get ready to kind of slowly unsheathe the device as we move forward there. So now we're beginning to kind of, we're beginning to release the device here. So now you can see the device slowly starts to expand right just below the level of the tricuspid valve annulus. And what it will essentially do is then kind of expand outward to sit both in the tricuspid valve annulus and the right atrium. And we're just kind of doing that in the second panel as well. And now we've kind of released the valve. So now the valve is sitting across the annulus and we still have a wire across to be able to capture it. And again, this is an RV angiogram and you can see afterwards, there's really no tricuspid regurgitation to speak of after evoke implantation versus the baseline with the rismatogist of your TR. I think this is kind of a cool echo image here. So on the left, you can see the tricuspid valve or you can see the evoke valve in place, the leaflets are opening and closing. And then a right there, you can see that there's really no tricuspid regurgitation whatsoever after implantation. And again, this kind of goes back to what we've learned from the surgical literature is that tricuspid valve replacement has lower amounts of TR recurrence than tricuspid valve repair. Here, I think the data is very impressive. Again, if you look at panel A on the left, the vast majority of patients in the first 25 had MYJ class three for heart failure symptoms, which improved. And then I think if you look on the right here in terms of residual TR, probably the most impressive results we've seen so far with more than half of patients having zero tricuspid regurgitation at one month. So really kind of, again, this valve now is currently undergoing the pivotal trial. So I think we'll hopefully have this valve available to patients the next few years. So finally, I wanna talk about tricuspid valve replacement in the heterotopy position. So this is cable valve implantation. Cable valve implantation has actually been around probably the longest of all of the therapies. And so what it involves is kind of really thinking about the symptoms of these patients. So these patients, as they progress in their symptoms, they develop lower extremity edema and hepato and spondyomegaly. That really causes a lot of the challenges that patients complain of, whether it be leg swelling, abdominal swelling, even paracentesis. So the thought behind this was, if you were to put a valve in the inferior vena cava and protect the IVC and the legs from this increased pressure, you could potentially help patients feel better. And so that's kind of what we've seen in the initial studies of these patients. So on the upper left-hand panel, you can see a hemodynamic tracing, which is looking at the RA and IVC pressure simultaneously. In the RA pressure, you can see a very large V-wave, but after valve implantation with a cable valve, you can see that there's really no V-wave at all on the IVC pressure tracing. So the thought behind this, again, is if you can protect the IVC and the hepatic veins from this volume overload, that you can help patients. On the CT scan there in panel B, you can see what it looks like. We have really a lot of contrast in the right atrium from the TR, but you don't see any contrast now going into the hepatic veins. And then in panels D and E, you can kind of see what the valve implantation looks like on an echocardiogram. And this is kind of what this procedure looks like. So one thing to notice, first of all, in this patient, again, this is the type of patient that we see quite often. You can see the sternal wires of the patient's post-surgical. It's kind of hard to see, but it looks like the patient's had both an eric anamitral valve replacement, has also had a clipping of the left atrial appendage. So we know this patient has a history of TR, I'm sorry, a history of atrial fibrillation. Again, something we see a lot in these TR patients. And with the catheter in the right atrium, you can see a lot of contrast that's going from the right atrium down into the hepatic veins and IVC. So what we do first is we place a stent in the IVC and this serves as a scaffold for the valve. And now we're expanding the valve here in the IVC. You can just kind of see it anchors really well as we expand. And now afterwards, we're doing an injection and digital subtraction. And you can see there's still a lot of contrast that fills up the right atrium, but you really see little to no contrast that's going on in the IVC. So this is really what we're looking for in terms of being able to kind of block that V wave down in the IVC to help these patients have improvement in their symptoms. Now, the majority of this data is just from registry studies. Here on the left, you see the U.S. capillary implantation, which I had the pleasure of leading with my colleagues across the United States. What we found is improvements in heart failure classification at follow-up. The graph on the right right there represents the European experience. And again, similar experience to what we found in the U.S. is that patients will have improvement in their heart failure classification. Now, for years, I've been talking with industry to kind of get involved in this space and to help us design some technology specifically dedicated to this technology or this concept. And industry has finally heard both my call and the need from the physicians from some other options for these patients. And so there's actually a couple of devices in development. The TRIC valve, this actually is a valve that's placed in the SVC and the IBC, which really isolates the right atrium and does a similar concept of kind of decompressing the IBC. The Trillium device is another device. It also hangers in both the SVC and the IBC and has these valves that open and close, which will allow blood to return. This is kind of what it looks like in the cartoon demonstration. I mean, systole, you can see that as blood goes towards the Trillium device, the valves are closed, and then diastole, those valves open and allow blood return to the right atrium. So I think the concept or the theme behind all these devices, again, is that we're still very early on. However, we have some intriguing initial pilot data that supports that we're kind of on the right track in helping to find solutions for these patients. So in summary, a couple of important take-home points. It's important to have a high index of suspicion for tricuspid valve disease. In anyone that really presents with heart failure, I think an echocardiogram is important to look for both systolic and diastolic heart failure on the left side. However, particularly in those patients that manifest right-sided symptoms, we really want to see if they have any tricuspid regurgitation to start. I'm referring to valve centers as paramount to avoid some of this excess morbidity and mortality that we see with these patients. Most percutaneous therapies remain in early feasibility trials, but some are progressing to pivotal, so we should have some more data hopefully soon. And again, continued awareness of tricuspid regurgitation will allow us to not forget about the forgotten valve and it will no longer be forgotten. So I want to thank everyone for your time today and hope to see all of you in the real world soon. Thank you very much. Thank you, Dr. O'Neill. That was a fabulous presentation and I could listen to you all day. I've been involved with the TBT registry since nearly the beginning and as everyone knows, TAVR started and then we added mitral replacement, mitral repair. And back to your summary point, never thought about the tricuspid and the tricuspid valve was added as a module, you know, late, kind of as the caboose of the four-module experience in the TBT registry. And it had seemed to be more of a forgotten valve and not very important. It's, after hearing you speak, it seems like it could be the most important valve or the most tricky to diagnose. You know, with aortic, we sort of have a watch program. You look for the gradient, you assess the patient and you sort of know when they're ready. What makes you know that the patient is ready for tricuspid or are there some key points before they get into a lot of renal and liver involvement and the point of no return or, you know, and why is it no longer the forgotten valve? What, you know, where's it been? Any thoughts on that or why is it taking its place now behind mitral and aortic? I mean, is there any thought in the community as to why was it the forgotten valve? Well, you know, Joan, I obviously want to thank you because I've had the pleasure of working with you now for probably five or six years and work with you to kind of get the tricuspid registry up and rolling. And so kind of a plug for that, for all of you, you know, coordinators and physicians and everything out there, you know, we understand that, you know, a lot of patients are getting some sort of tricuspid valve therapies right now, whether it be CLIP or whether it be, you know, cable valve. And so I really would encourage all of you to submit those experiences to the TBT registry because really being able to kind of collect this initial data is going to help us a lot as we continue to move forward with the percutaneous therapies, because it's, I had mentioned, you know, where we were, where we are, where we're going. We really kind of have to know where we are right now. That's going to help us a lot in terms of figuring out where to go in the future. So, but Joan, I think back to some of your questions, they were all fantastic components, but the first question I get this a lot is when do you refer? When do you refer? How do I know that this patient needs something? So, and I think it's reasonable to send anyone with severe TR for a first initial evaluation to a valve center for just an initial consultation. We, a lot of times we'll see patients and say, you know what, you're doing fantastic. You're in a small amount of diuretic. You have no peripheral edema whatsoever and you're doing pretty well. But the question about timing in terms of when do you, when do you, you know, when is it, when is the TR becoming hemodynamically significant? I think if you look at the right atrium and you start to see right atrial dilatation, that is going to probably be the first sign of the volume overload. Because if you can imagine, particularly in those patients that have isolated tricuspid regurgitation, the RV is going to be okay. It's really just the annulus that's dilated and the volume is tolerated pretty well initially. But in the right, the right atrium seems to really be kind of the first structure that you see that gets kind of big before the RV will actually then start to fail. So in those patients in whom you see severe TR and a big right atrium, that's kind of the time to start thinking about, okay, I got to get this patient to a valve center. Got to start following more closely. Got to start getting my ducks in a row in terms of, it looks like it's becoming time to think about intervention. And it also counts in the patient as well. I think that that's an important thing. Joan, to your other question about, why has this valve been forgotten for so long? And that's such a complex question, but I think it can be broken down in a couple of different things. So first of all, you don't die suddenly from tricuspid valve disease. You really die very slowly. You're just kind of miserable and linger for a long time. Whereas with aortic stenosis, there's a lot higher incidence of sudden cardiac death from untreated aortic stenosis. I think that's why we kind of really focus on AS to start is because we got a big buck from a mortality standpoint in helping and fixing these patients. And we're not going to really get that from TR. I think that a lot of these trials, we're going to see improvements in the KCCQ scores, the heart failure classification, but we're not going to get a huge bang for our buck, my suspicion is, in this mortality because patients hang around for a long time before they unfortunately expire. So that's one of the reasons. And the second reason is because, you know, TR is hard. It's a hard surgery. You know, again, if we look back to who is being evaluated for surgery, it's patients that are really sick, really poor surgical candidates, and the surgeons really do not want to do much with them. So I think our surgical community is really behind us 100% in terms of finding these therapies that can help, the percutaneous therapies that can help, because many of them are such poor surgical candidates. So those, I think, are a couple of the reasons why we're kind of late to the game in terms of TR and really just have a very elementary understanding of the disease process itself. Thank you. Yes, I do want to thank you, too. You have been very helpful with developing the different data elements for the tricuspid module. Is torrential a word we will be hearing more within the tricuspid space, or is that nomenclature something that, I mean, when you're categorizing the severe, moderate, what's the difference between severe and torrential? And is that something we should be becoming more familiar with or asking our physicians to document in such a way? Are you seeing that more in echo reports? I think that we're going to be, I think that the reason that there's kind of massive in torrential is there's a recognition that some patients really have almost laminar flow across the tricuspid valve, meaning that there's really no obstruction to flow whatsoever from the valve. It's almost like you have a three-chambered heart in the fact that the RA and the RV are single conduit. There's no separation whatsoever. So I think that that distinction, and there are patients that have just such massive TR that there really is no obstruction of flow going back and forth whatsoever. So I think it is important to have that as a distinction because those are the patients in whom we really have to think, be very thoughtful in terms of when to intervene or whether or not we should intervene at all. So those are some of the, so I think that designation is important. I think we're still trying to find our way a little bit in how we can really grade that, really come up with a grading system for that. So I think, again, so, you know, kind of going back, again, there is this category that is beyond severe. You know, there certainly is. And then the next question is, is it important to have that category? Because if you reduce it from massive to moderate, are those patients still going to have kind of a benefit of the therapy? And they probably will, just because there's just so much fine going back and forth that if you can reduce it by half and half gets you to moderate, that may be better than if you have moderate to severe and go to moderate, you know, are they going to have a benefit? So, but I think it's still a little bit too early on. So I would be pressed to really push a lot of the centers that you're working with to start grading massive and torrential until we kind of see it in the guidelines a little bit more. Okay, maybe two more questions. When you see a patient that has both mitral and I think you touched on this earlier, but mitral and tricuspid, do you, what comes first? Is there a value in doing one or the other? Or are they both done at one table setting? I mean, how, what is involved in your thought process when you're looking at someone who has mitral disease and perhaps tricuspid disease? Is there a staging of that? Yeah, no, that's a really, and that's a really challenging question. And it's something that we face all the time. You know, we have, you know, I kind of threw that out there that about 40% of patients can have concomitant mitral and severe tricuspid valve disease. So they really do kind of come together. So we're getting pretty good at treating the mitral. And again, we're still kind of finding our way and treating the tricuspid. But what we do in our center clinically is if we get a patient that's referred for tricuspid regurgitation, we always do the mitral valve first. And that's because you can see an improvement in TR. I remember from the, if you remember from the mitral slide, the patients that improvement in TR did better than the patients that didn't have improvement in TR. So sometimes we'll get lucky, we'll fix the mitral valve and lo and behold, the tricuspid regurgitation actually gets better as well. More often than not though, we have a competent mitral valve and we still have tricuspid valve disease. So that's when we'll start to evaluate for therapies for the tricuspid valve. And I think we'll probably see that once we have all of our therapies, once we have multiple therapies available for both the mitral and tricuspid, is we'll still probably see mitral first and then the tricuspid second. Thanks. Is there, I mean, this might be difficult to answer. Are there any adverse events that you look out for or that you see most commonly after a tricuspid patient or any worry points, bleeding, detachment? Is there anything that's on your worry list more so than with the mitral or in the ORDiC case? One of the really nice things about, and this is kind of, we kind of exhale a little bit when working the tricuspid valve because the right side is just so much more forgiving than the left side. So I think to be honest that you'll see similar types of events that we're seeing on the mitral side right now in that, if we look at aortic mitral tricuspid, we certainly have less adverse events when we're doing mitral interventions than we do with aortic interventions. And I think we'll see kind of a similar rate at the end of the day with tricuspid or maybe even lower. So I think that once we have these therapies down, that this is gonna be a really safe therapy, a really effective therapy. And I think that we'll see really some of the most, some of the most dramatic improvements in quality of life that we'll see across all the different valve interventions. One last comment maybe, you know, we hear these miraculous stories with a patient with AS and they pretty much jump off the table and get on the plane and go home, you know, day after procedure. I'm hearing that, I'm hearing you say, I think that's really not what you see in a successful tricuspid case, but what's your best tricuspid story? I mean, do they go home the next day or what does that success, what does that positive experience look like for you at the tricuspid patient? Well, when we, you know, when we get really good at this, I can easily see us doing same day tricuspid valve interventions. You know, patient comes in the morning, gets their valve or, you know, gets either repair or replacement of their valve and then goes home later on in the day. I think we don't see that dramatic effects initially, but we have had certainly multiple cases of patients that come back at 30 days and the edema is completely gone and they're feeling great. And so I think, and, you know, a lot of it too, and a lot of the companies are asking me this is, you know, when can we expect improvement? When can we expect improvement? And it's variable, it's variable. I think you'll see some patients that get an improvement in 30 days, you'll see some patients that continue to get improvement after six months. So it's gonna be a little bit of a slower process. You will have those patients, again, that have great, you know, great, great improvements at 30 days, but for the tricuspid side, I think that you'll need a little bit longer to do it. And one thing too, that I would point out is that it's been our practice now with our tricuspid patients that we don't do anything to the diuretics until 30 days. So I think in the very beginning, we were just so enthusiastic about this that, you know, we do our valve intervention and then take them off all their diuretics and say, you're gonna feel great, you know, bring it back in a month. And they come back in a month, like, no, I still don't feel very well. And so many of these patients are just so chronically congested that they still need some time to diurese even after the valve intervention. So I would really, really encourage all of your sites and all of your coordinators to work with your, work with your physician colleagues and your surgical colleagues to keep them on their diuretics until you see them in a month and then you can kind of make some adjustments. And these don't have to be dramatic adjustments, little tuning here and there because, you know, heart failure re-hospitalization is a huge problem in the tricuspid valve space. And so we really wanna try to kind of keep these patients out of the hospital and we can do that by keeping them on diuretics for 30 days. So I wanna thank you, Dr. O'Neill, very much for this presentation. And your last parting words really gave the TBT registry the charge that we're looking for. We didn't plan it this way, but certainly the value of that 30 day and one year follow-up is even going to be very much more of an important factor in tricuspid than maybe the aortic and mitral. So I appreciate you saying that. And on behalf of all of the TBT sites and myself and the team at ACC, I wanna thank you for all the work you've done in helping us put the TBT 3.0 modules together, specifically tricuspid, and for also working on all our work groups with our risk models and all the other work you do. Thank you. Thank you very much. I'm just a soldier in your army.

tricuspid valve disease

tricuspid care

transcatheter world

tricuspid regurgitation

percutaneous therapies

leaflet coaptation devices

ring anuloplasty devices

valve replacements