 Hi, thank you for having me. I'm actually very happy to be part of this conference. Now, I want to start my talk by first stating that my perspective is going to be as a cardiologist and how we work up patients with tricuspid regurgitation. And I will be showing transthoracic imaging as well as transsophageal imaging. And then the second thing is I would really encourage everyone to go and look at Max's talks. We actually coordinated and some of the topics he's covered, including tricuspid valve anatomy and mechanisms of secondary TR, I'm not actually going to spend too much time on. And then I'm going to direct you to go in and look at his talk. Here are my disclosures. So I'm going to start first with this first case. And this is a 54-year-old gentleman who actually presented about four or five years ago to his family doctor with right forearm pain. He was actually examined. And they did auscultation during the time, clearly pre-COVID when we were allowed to have stethoscopes. And he was actually found to have a murmur. They ordered the transthoracic echocardiogram and it reported severe TR, modern RV enlargement, and preserved RV systolic function. He was then referred to the Toronto General for an actual opinion on what to do about him. When you actually speak to him, he was New York Heart Association class one, as well as CCS class one. He had no significant past medical history. There's no history of rheumatic fever. And then his only other habits were smoking. And he was actually on no medications. So let's look at his echo. So this is a transthoracic echocardiogram. This is your apical four-chamber view over here. Here's your short axis view with the aortic valve over here. And then this is an RV inflow view. And the reason I'm showing these images is that first, you're going to have these to be able to compare with to the transesophageal echocardiogram graphic images that I'm going to show later. But what you want to notice is, first, the RV and RA are both dilated. There is actually a lot of tethering. And you can see these tethered cords on the leaflets. And that's causing a lot of problems. And it's tethering not only at the edges in the clear zones, but also in the rough zones that you can actually see on it. And there wasn't actually by, if you look on the apical four-chamber view, criteria met for ebstynes abnormally. So this wasn't an ebstynoid or an ebstyne, a frozen fruist of an ebstyne valve. But it was ended up being called a dysplastic valve. There's something congenitalia abnormal of this valve. And because we see an RV enlargement, our A enlargement wanted to make sure there was no shunt. He actually had a negative bubble study. Now, when you look at the quantification of the mitregratiation severity, the venicontractive was over 8 millimeters. You can see that there's triangularization of the inflow or the outflow, sorry, the RTR gradation. The density is actually quite dense. And then there's a dilated IVC and there's flow reversal in the paddock vein. Now, we don't normally do transesophageal echocardiograms. And part of the reason for that is the location of the tricuspid valve. The images on surface study tend to be much nicer than they are on transesophageal echocardiogram for most patients. So we actually, as cardiologists, tend to send people for transphabric agritation surgery to surgery with just a trans thoracic study. Now, our volumes of transesophageal echocardiograms for tricuspid valve assessment have actually increased because of the newer tricuspid clip, as well as tricuspid percutaneous valve assessment. So we're now doing more of them. But in reality, the imaging is actually much tougher for us to get the images. And some of the times when you do these transesophageal images, we spend a lot of time in the transgastric views to get good views of the anatomy and what's going on with the tricuspid valve. And when we're in the midisophageal views, because of that aortic valve sometimes shadows, that septal leaflet, what we end up doing is we end up doing these lowest-sophageal views instead of midisophageal views. And you can see this is one of them where you've lost the left atrium here, and you've got this coronary sinus, your very posterior, in order to bring out the anatomial leaflets and actually be able to see it much better. And so you can see here's the transgastric, the short-accessed view of the leaflet with the source of the regritation jet. Here's a long-accessed view of the leaflets. Once again, you can appreciate all the tethering and the extra cords and the abnormal cords, but it's much harder on this transgastric acrocardiogram than it is on the trans thoracic. And you can see these tethered cords, once again, on the lowest-sophageal views here. So one of the first questions I was going to ask is what is the more common primary or secondary TR, and the answer will come up later in my slides when we discuss this. And then the second thing is how many leaflets can a tricuspid valve have? My questions are two, three, four, or all of the above. So back to our case, though. His blood work was normal. Things that we follow up, including the liver function test, and that tends to be normal. BNP has not been demonstrated, but we used a lot of valve disease, and that was actually negative in this patient. And then the INR showing the liver function was actually normal within normal range, too. Given his asymptomatic status, he was actually followed clinically with serial echoes and cardiac MRI. And in 2016, his RV volumes were enlarged, if you look at it, it's about 171 milliliters per meter square, which is quite much larger than sort of the upper cutoff is about 90, 100 milliliters per meter square, depending on your gender and age. And then RV, ancestral volumes, once again, were large. And the RVEF was 57%. Now, I'm going to caution you that when you're similar to much regurgitation, an RVF of 57% is probably not normal in someone who has severe tri-cuspid regurgitation simply because of the offloading of the right ventricle. So we followed him up. He actually had our MRIs yearly, and actually his values are quite stable from 2016 to 2017. And then in 2018, there was further dilatation. So at that point, I had a discussion with the patient and said, listen, your function is probably not normal, mildly reduced, but you're starting to dilate again. At that point, he was open to going to surgery, and so we went to surgery. And if you see the images on the left are the transesophageal echo images that I had shown you previously, and then the images on the right are the images that he had enter off. And as you can see, he actually went and he didn't have a valve replacement. What he had was a repair of his valve and that there was probably at least a mild regurgitation in the post-op period. They went back on pump a couple of times to repair it, and this was the best that they could do for him. How's he doing right now? He's doing well. MRI was repeated after. And we could tell that there was an effective reduction in the regurgitation severity because the volumes actually decreased. Now, as I pointed out, the RVEF was probably not normal for his surgery. And you can see that after surgery, his MRI revealed that his RVF was truly about 39%. So he's been left with some RV dysfunction. But clinically, he's been doing well and has not actually had any signs or symptoms of right heart failure. So what are the key points I'm actually going to cover in my next two slides? Well, first, most TR is actually secondary, not primary, like this patient. And then, tracheosophal imaging, I'm going to make the argument that transtheracic echocardiogram is complementary and probably more informative for a clinical cardiologist instead of transophagealist. There's lots of challenges in doing transophageal because the location of the tracheosophal. And then quantification, one of the things you have to be careful about TR quantification is actually different from that used for mitral agitation. And then here's my slides going through some of these things. So first, most TR is actually secondary. So the case I presented is a minority of cases. About 25% of people will have primary leaflets abnormalities causing their trichesopteric agitation. And of those, a lot of them will be congenital. And then of those who have acquired primary leaflets, they're going to include patients with carcinoid and myxomonas disease. Endocarditis is a large one that we see nowadays. And then pacemaker leads are also increasing. And for the transplant population, RV biopsy. The secondary or functional regressions ones that you see a lot these patients who go in for their surgeries with mitral agitation plus trichuspid agitation or aortic stenosis with trichuspid agitation, those are the secondary or functionals. And then there's a category of others which are people who are post-op. Now, trichuspid valve assessment, when you're assessing it, it's sort of the breakdown for the major, the types of trichuspid agitation breakdowns to primary, secondary, and isolated trichuspid or agitation. And this is a nice table published in Jack that actually talks about the pathology that you actually want to look at in order to classify and identify what the mechanism of pathology is. History is going to help you with a lot of the types figuring out why the leaflets look the way they do. But things that you want to look at are leaflets, the sub-vabular pathology, the angular size, and function, what the leaflets themselves are doing, how they're tethered, and then what the RA and RV are actually, how they appear. Now, I've shown you before trichuspid valve imaging is probably transthoracic for most of that, and it can give you all this information on both the cause of it, you can see what the leaflets are doing, what the papillary muscles are doing, what the RA and RV are looking like. You can also get a good idea of assessment of severity of the trichuspid agitation. You're able to get measurements of the angular dimensions, the leaflet tethering, and also you get assessment of the pulmonary pressures and right ventricle function. And you can also look at what's going on with the left side of the heart. Now, one of the limitations of 2D echo assessment of the trichuspid valve is that your cut planes may be a bit misleading. So here is sort of a cartoon showing the aortic valve in the center with the trichuspid valve and the mitral valve up here. And you can actually get an April 5 chamber view with the aortic valve or with the coronary sinus. And it can show you that the leaflets, and you're cutting through different parts of the leaflet whether it be the anterior septal or the posterior septal leaflets. And I'm going to show you using a 3D cut plane what that looks like. So here we have the short axis valve. Here's your mitral valve. And here's your trichuspid. The anterior posterior septal leaflets are all labeled. And here you're cutting through. This is going to give you a 4 chamber view. You're not too anterior or too posterior. You don't see coronary sinus and you don't see aortic or LVOG. And so you've got a 2-4 chamber view. But in here you're actually cutting through from the trichuspid valve. You're cutting through the septal and posterior leaflets. Once again, you do a different bit of anagulation here. You've got a 4 chamber view. Once again, there's no LVOG. There's no coronary sinus, not too anterior, not too posterior. But here you're cutting through the septal and anterior leaflets. So identification of the leaflets on 2D echo can actually be a little bit tricky. And this is where 3D echocardiography actually helps a lot because you can see all three leaflets. You know exactly where the pathology is. You can look at it from the RV perspective with the typically you're supposed to have the inter-hatral septum or the septal leaflet at 6 o'clock. And then you can identify your anterior posterior leaflets. And then you can look also from the right atrial perspective. And you can see your posterior leaflet and the anterior leaflets. And you can also cut through in a sort of a non-onfast view to actually see the leaflets themselves with 3D. And one of the things we have realized with 3D is that we actually don't really identify the number of leaflets very well with 2D. Here's an example of a valve that actually looks bi-cuspid or bi-leaflet. Here's one that traditionally the tri-leaflet valve. And this one could almost be argued that that might be a quadra-leaflet tricuspid valve. And in pathologic samples where they take serial patients and look at their tricuspid valves, it can be actually up to six leaflets seen on the tricuspid valve. And we really don't appreciate that when we're looking at a 2D image. And so I think one of the values of 3D is that we actually really understand the morphology of the tricuspid valve a little bit more. In addition to seeing the morphology, now similar to 2D planar imaging with 3D echocardiogram, 3D transthoracic, once again, is still better for identifying the or looking at the tricuspid valve compared to 2D. 3DTE, you can see the tricuspid valve anatomy with 85% to 90% of cases. With 2DTE, you're looking about 5% to 10% of cases. And then with 3DTE, you're looking about 65% to 70% to be able to clearly see it in an eye because there's issues with droplet. The leaflets tend to be much thinner and just the location makes it tough to get a clean image to get that volume set. Now, here are some examples with 3D echo about pathology here. So this is our patient that I showed you in our case showing the dysplastic valve. And you can see the different cords coming off the leaflet tips and where they're attached to. This is a carcinoid valve. You can see the thickening of the leaflets and you can see that the restricted motion here. This is a patient with functional. The annulus is dilated. The leaflets are all pulled apart. And then this is a patient with polymer hypertension where there's been remodeling and it almost looks like it's a bicuspid valve. There was a beautiful example of this in one of the morning talks on my trick or station about how you can take 3D echo and then you can use the multi-plane reconstructions to actually identify pathology. So this is a patient who actually has a septal leaflet flail and when you actually localize the 3D dataset you can actually identify where that flail is coming from and what that leaflet is looking like. One of the biggest things we have actually learned also is the appreciation of the role that pacemaker leads play in tricuspid or agitation. You can clearly see on this 3D image that the pacemaker lead is sitting in the commissure here and that there's no impingement on the leaflets and there's good co-optation here. You can see that pacemaker lead is going through. We're sitting in the right ventricle looking up here is the interatrial septum and you see that that's holding back that septal leaflet and the anterior and posterior leaflets are trying to co-opt there but you're gonna get a bit of a gap here and that's where you're gonna get tricuspid or agitation. You can also identify lead position in this nice study in about 90% of patients using 3D surface echo for identifying the cause of the tricuspid or agitation. Another thing is there's a lot of talk with much agitation when you go into the operating room you wanna know if the tricuspid annulus isn't large because you're gonna do an annual plastic at that time. One of the things is you can misidentify the size of the tricuspid annulus simply because of your cut plane. So here we've got a four chamber view and you're gonna measure that but if you look at the matching 2D echo you can see that you're cutting this way instead of the true long axis and you're probably under measuring how big it is and that may account for why in the ORs there's a 60 millimeter cutoff versus the 2.1 centimeters per meter square cutoff used on echo. 3D obviously can be measured and shows a little bit more accurate in terms of the size of the tricuspid annulus. I'm gonna briefly talk a little bit about TR severity assessment and as you look here it's actually a multi-parametric assessment of the cause of the tricuspid regurgitation. And if you can see here on the table that you're looking at many parameters and then you're integrating all of that to decide if there's severe or mild tier and then if you're not you're kind of in the probably moderate criteria. And when you look you're looking at the colored jet whether or not it's small if it's wide you're measuring the vena contracta width you're looking at the PISA if you measure it and then you're looking at the continuous waved tracing and then hepatic flows and inflows as flows RA and RV size. And then you try and sort of put all of that together to decide whether or not you've got mild, moderate or severe. But one of the things I wanna point out and it's a very small line at the bottom is that clinical experience in quantitative TR. So using the regurgitive volume, using EROA is actually much less than mitral and aortic regurgitation. And so a lot of this is actually not very well validated. But there is a bigger problem with how the guidelines are describing tricuspid regurgitation. There's a lot of assumptions made but and it's based on what we know about the mitral valve and we're adopting it to the tricuspid valve. And one of the things that we have realized with assessments for tricuspid clip procedures is that the tricuspid valve is not the same as the mitral valve. They have different orifice shapes in different sub-vabular apparatuses and they have different ventricular shapes. Yet we assess them the same way. So that's why a lot of the people who do a lot of tricuspid valve interventions such as Becky Hahn, they have recommended using this new criteria for where we include this beyond severe tricuspid regurgitation. We include definitions for massive and torrential tricuspid regurgitation because we know that those cut-offs actually have prognostic value and decreasing going from torrential to severe while it may seem counterintuitive actually makes a difference in how patients do. One of the last things I want to point out before I move on to the next case is that 2D echo underestimates the severity of tricuspid regurgitation compared to 3D and this is for a couple of reasons. First, it's rarely the regurgitation jet is a rounded shape because of the tri-leaflet co-optation. It may be elliptical or steelate in shape especially in secondary TR. The other thing is a lot of the cases in secondary TR result in tethering of leaflets which means that your PISA calculations actually have to have a correction for this leaflet tethering. TR often has eccentric jets. Volume status and respiratory variability actually affect your TR assessment and that being said, while 3D is more accurate they're still not ready for prime time and so there's still a lot of work that needs to be done on tricuspid regurgitation and assessment with 2D at 3D. So now I'm gonna move on to case number two here. This is a 71-year-old gentleman who has a two to three month history of increasing fatigue, shortness of breath on exertion. His past melgostasis for bypass surgery with aortic valve replacement in 2012. He also has chronic atrial fibrillation with a pacemaker and he's got adrenal insufficiency on cortisone. His medications are listed here. He's got atrial fibrillation as ECG and his blood work shows that his BNP is actually a little bit above our cutoff of 100 but it's not quite meeting criteria for heart failure which would be over 500. The hemoglobin is a little bit low, white count platelets are normal, his electrolytes are normal. More importantly, his creatinine is normal and his liver function tests are normal and because he's on warfarin, his iron and iron is a little bit elevated. Now here's his transtheracic echocardiogram and an image from his transthop gel so you can see that his RV is enlarged. His function actually is a little bit reduced so there's a mildly reduced TAPC as well as S-prime and if you look, there's on his transthop gel echocardiogram you can see there's a dilated right atrium. There's a pacer wire here. Here are his tricuspinal leaflets with a gap. If you look at his hepatic vein flow you can see that there is systolic flow reversal and then let's take a closer look at his transthop gel echocardiogram. So here's our low esophageal four chamber view. You can see that pacemaker lead is coming very close to that septal leaflet but the jet seems to be coming from a direction different from the lead itself and then here is a nice view we like using for the clip because it lets us see all three leaflets as sort of the equivalent of a bicom view on the mitral valve and you can actually see that we're cutting through and then getting these sort of, it's an apical four chamber view and we can see that this leaflet is not quite impinging that septal leaflet and then we cut it through both the anterior and the posterior leaflet as well as the septal leaflet to get an idea of what's going on in this long axis, apical view for the leaflet. So you can see that this is very challenging to see these thin leaflets in these dilated hearts and what's going on and you can see that there's a pacer lead going through but it's not really, there are views where you can see that there's a gap and there might be a possibility that we could actually clip the leaflets on these views. Now here's a 3D echocardiographic image from TEE showing the pacer lead and a lot of times when we take these leads out in the OR you can see that they're wrapped around a little bit and you can see here's the pacer lead. It's actually mostly in that commissure here so this is the RV perspective, you're sitting here on the septum, there's your pacer lead and then your anterior and posterior leaflets here and then this is a right atrial lead and you can see that curve of the leaflet as it goes down into the tricuspid valve. So next question is gonna be what is the operative mortality rate for isolated TR? And then I'm gonna go forward to, he was actually declined to go for surgery, he wasn't very interested, he has been assessed for tricuspid clip and he's going to be going forward with that and he hasn't had his procedure yet because that was deferred because of COVID. The key points here is late TR post-left heart surgery actually occurs frequently, it's something we see and mortality for tricuspid valve surgery is higher than other valves and I'm gonna show you the data now and so I'm gonna review all of these. So we have appreciated over the last five to 10 years that TR is actually bad isolated TR in particular. We used to think that it wasn't something to be concerned about but we know that independent age function of the ventricles it actually has a poor prognostic, is a poor prognostic sign and one of the things we are more appreciative now that we have interventions, non-surgical interventions for tricuspid valve is that actually can develop over time. So here's a study looking at mitral valve repair patients and you can see this also in theortic valve literature that tricuspid recretation that wasn't soon at the time the surgery can develop and if you look at this long issue of follow-up of over 20 years of patients who went over and had mitral valve that at one year there's about 5% who have moderate or severe tricuspid recretation but by 20 years almost 21% of patients in this group had tricuspid recretation. And risk factors for this include time, age and atrial fibrillation which is a major cause and preoperative heart block and then the New York Heart Association functional class before surgery actually is predictive of this. What is the mechanism? Well, in patients who've had previous left heart surgery they may have mild RV-RA dilatation secondary to pulmonary hypertension which leads to annular dilatation and remodeling that remodeling of the annulus as well as the left right ventricle then distorts the tricuspid valve anatomy the cords and papillary muscles you end up with more tricuspid recretation this volume overload from TR then creates a cycle where you get more RV and RA dilatation and then you go into this negative cycle and I just wanna point out that whether or not you have a primary tricuspid valve abnormality or secondary you end up in this negative cycle of RV volume overload and more TR. Now, TR after left heart surgery, the results are mixed but most of the conclusion has been that it's actually poor tense, poor prognosis even in the micro clip literature we're now seeing that if you have residual TR or develop TR after your procedure you do actually have a worse prognosis from it and there is still some contradictory literature suggesting that it's actually maybe not tricuspid recretation but the RV dysfunction that's actually more predictive of survival this is one study that was published showing this but there are a lot of people criticize the study beyond the fact that it's a single center observational study but there wasn't actually information or accurate echo data on the timing or appearance or degree of TR and the determination of RV dysfunction in the setting of significant TR is also difficult to assess as we've covered before and the ideologies of the left heart surgery was unclear in these patients. Now back to the guidelines. So what do the guidelines say for patients who have TR after left heart surgery? Well, it's a 2B indication so not a very strong indication recommending it and part of the reason for this is because you have to not have severe pulmonary hypertension or RV systolic dysfunction. Now we go, my last few slides are just gonna talk about tricuspid valve surgery. First of all, isolated tricuspid recretation surgery is rare. If you look at the numbers of mitronaortic surgeries they're much higher compared to tricuspid surgery and most of the surgery is actually tricuspid repair and in the context of having mitral valve operations it's rarely performed by itself. Now what is the mortality for isolated tricuspid surgery? So in the STS database it's still eight percent and if you do replacement for tricuspid valve it's even higher, it's about 13% versus 9.5% and these are the numbers for what the mortality rate for mitral valve repair surgery or replacement versus repair are for mortality rates. So you can see that it's significantly higher and if you have a re-operation for tricuspid recretation after left your mortality is about 9% blood studies. So overall this is a case of late TR due to RV and RA remodeling and mortality for re-operation is very significant. And so the question then is gonna be that you may end up seeing these patients earlier in these processes to try and reduce this and for other non-certical procedures. Thank you. Thank you for that outstanding presentation and beautiful for the images that you share with us. And there's a couple of questions from the audience versus what's your point of view for indication for tricuspid valve intervention in TR secondary to left heart disease? So Max was gonna talk about that and actually show a case example of that. So the literature right now is arguing that especially out of the European studies is arguing that you should fix the tricuspid valve at the same time as you do mitra clip procedures. And in the ORs, there's a large NIH funded trial that's doing mitra that is looking specifically at how you should fix the tricuspid valve with mitra recretation. Now after left heart surgery, when should you fix the tricuspid valve? That was the question they asked. In our assessment, we tend to be I think more aggressive. If you wait till they have liver dysfunction, if you wait till they have renal dysfunction, it's too late, the mortality is already gonna be very high. We are very bad at estimating what RV function is. The Europeans are probably more advanced than the American guidelines in that they recommend as a almost a, if I recall correctly, a class one indication. If you have RV enlargement, you should consider fixing it. So they're not even talking about RV failure or assessing function. They're just saying RV enlargement. And I think we're leaning towards that, especially now that we have triclip available and percutaneous tricuspid valve. So we're tending to become more aggressive on that. Okay, and the second question is, can you comment on the long-term outcomes post tricuspid valve repair versus replacement and what are the major risk factors and common issues? So I think it depends on why you're having your tricuspid valve done. So a lot of the patients we see tend to be the young IV drug users, and they are given if they're, they may be repaired, sometimes they're because of the extensive nature of the vegetations that actually get them to surgery, they're replaced. And a tissue valve prosthetic valve on the tricuspid side is actually not very good. It will probably degenerate very quickly is the feeling of our, a lot of our interventional colleagues that we've talked to about this. But so we try to delay people as much as we can, but once again, then they get to surgery and they have RV dysfunction after surgery. So there's a fine balancing act, but I think part of the high mortality that you see those 8, 10% mortality ranges are because we belong when we're looking for this, when you wait for it and you see this renal dysfunction, you see this liver dysfunction, we're probably waiting too long for a lot of these patients. And so I think for both a surgical side as well as the percutaneous side, we're taking them earlier. And I think I saw a question flash out. So what exactly, when would you actually take someone? If they do not have symptoms, but they have RV enlargement and I confirm it with MRI if possible, I would probably prefer them or intervention if they're willing. Okay, and in that first patient that I showed that had the dysplastic valve, he had already had a dilated RV when I met him. He wanted to wait and see what happened. And then the minute continued to dilate, we said we should go and that's why he went. But there are some patients I have who they come in and they don't wanna wait because we were waiting for it to get bigger and you don't know if they'll come back. Sorry to interrupt. Do you think there's a bit of a strict reasoning because we often see people hesitant to intervene on tricuspid valves because of the poor outcomes, but that we're kind of creating those poor outcomes by waiting too long. Right, so the liver dysfunction, a lot of the times if they get liver dysfunctions, the surgeons do not wanna operate on that because of the high mortality with liver dysfunction and then renal dysfunction and permanent dialysis afterwards. So it becomes this negative cycle. I have a lady that I followed who had tricuspid valve repair, but the problem is hers was in the setting of atrial fibrillation and we waited. And she only had mild heart failure and the argument was that we should continue to wait, but then she ended up with significant RV dysfunction after we had surgery. But then people who are more aggressive wanna go, you see they come back and their RVs are nice and their volumes come down. So I think we tend to wait too long. But it's hard to argue because the mortality data with a patient and say, I think you really should go. Another question just came in. When should we intervene in the tricuspid valve and pulmonary handkerchief and darthorectomies? Now that's a little bit outside of, I don't actually know the data on that, but I would say that with pulmonary hypertension, in patients who get treated, I have a series of patients I share with the pulmonary hypertensive clinic here. You have to, because the RV is very sensitive to pressure and changes in volume status, you have to wait to see if they can bring down those pressures with treating the endarderectomy with endarderectomy or anticoagulation because when the pulmonary pressures come down, the RV is sometimes very responsive and remodels in a positive way. And then when the RV remodels, the TR goes away. So you don't want to intervene when you don't have to. So my argument is that I would wait to see if they're responsive to treatment and then go in. And I think this is especially true as the tricuspid technology develops for percutaneous interventions and we have more options. Thank you very much again for your participation. It seems that there's no more questions. So, oh, there's one. One last question, Wendy. What's the role of RV strain right now in assessing these patients? Where are we at? So RV strain, RV strain is still, I think, more of a research tool than we use it regularly. I think for left-sided disease, there's a lot more literature supporting its use. And I suspect either this next coming AHA guideline the one after that is going to recommend using strain for your mitral valve disease. But in terms of tricuspid valve disease, it is still probably not enough data to recommend its use. And I think that data will eventually probably get there. We just got one more and then we'll move. So there is any specific selection criteria for triclips or any functional TR can go for triclips? Right, so Max was going to cover this. But in the triclips, we do, first of all, you have to be able to image the tricuspid valve with TEE imaging because that's what's going to guide your procedure. So I think if you can't get good images with trisapodial echocardiogram, it's probably not going to be a very doable procedure for the tricuspid clip. And I think that's just one of the challenges you have because of the location and the imaging. And that is also why there's a lot of transgastric views that are done, as well as the lowest apatial views. Now, in terms of the imaging or the actual criteria, that is still being developed. But the major one is that you don't want to gap greater than seven millimeters, okay? Because the arms of the clip are about a centimeter. So you have to be able to have long enough that you can pull things together. Now, you can clip from a commissure and move inward. So as long as you have a view that you can see that it's not so big, you can start clipping from the side and move towards the center and close off a commissure. And sometimes you bicuspidize a valve to do that, okay? The second thing is if you have a pacerleaf because a lot of these patients that are being referred are because they have pacerleafs going through. If you have color jet coming from an area where there is not the pacerleaf going through the valve, okay? So you don't want to jail the lead, okay? And then you want to see then what the anatomy looks like where that jet is coming from. That is away from the lead, okay? In some patients we have, if they are accepted, we actually put in an epicardial pacemaker lead system. We take out the transvenous lead and we put in an epicardial system and then send them forward for clip, okay? The criteria, the views that you kind of want to do are you're going to need this short axis view where you have the aortic spout soil between 40 to 60 degrees. You have the short axis aortic valve at the level of the cusp where you can see all three cusps and then you have the bicommissural view and then you biplane through each of those leaflets as I showed you. And then you want to have this almost this inflow view where you see IVC coming into the right atrium and then the tricuspid valve. It's kind of like between a, not quite the short axis, not quite the four chamber at zero, it's about 30 degrees. And the reason you want that is that's a delivery view. Okay, so you want to get that view also. So those are the views that you need to do it. And then when you're in those views, swing in and swing out, sweep through the valves to find where the jet is coming from away from any pacemaker leads and looking for the leaflets themselves that you can grab it. And then one last thing I've talked a lot about the triclip. We do percutaneous or in Toronto, there is percutaneous valves. We have jailed ICD leads with these percutaneous valves. Literature shows so far that in a hundred patients done that there's no misfunction to the ICDs or pacemaker leads that are jailed by these percutaneous valves. However, help us if there's ever an infective endocarditis on a pacemaker lead because we would not be able to take those patients at those leads out, right? So that's one of the things that hasn't come out in that literature yet but it's similar to TAVR valves that get infected. It's a massive re-operation to do that in someone who's already not been a candidate for something else, right? So.