Dr Amin Yehya, Dr Matthew Summers and Dr Erich Kiehl present the workup for a patient with suspected hypertrophic cardiomyopathy.
Thank you for joining us, uh, to grand rounds today. Um, February is Heart Month and this week is Heart Failure Week, so I chose this case to highlight the importance of working among different subspecialties and the commitment and the expertise among different groups is the main reason uh for success to taking care of these critically ill, uh, patients. Um These are my disclosures. I will not discuss off label use of any of the drugs or devices. Uh, this is our, uh, team, as I mentioned, it's a Heart Month team, and, um, we're thankful for working with everybody and it's, uh, without you, um, our patients will not be getting the best care. So the outline of my talk, it's gonna be divided into uh the case presentation, a little overview about hypertrophic cardiomyopathy then we're gonna uh talk with uh Doctor Kiel and Doctor Summers about the care for this patient. So he is a 47 year old male. History of hypertrophic cardiomyopathy. He had an ICD as primary prevention. His EF has been chronically in the 15 to 20 range. He had an ICD initially on the left side, had a lead fracture. It was abandoned. Then he had a 2017, he had a right sided ICD and it complicated by SVC syndrome. His other comorbidities including atrial fibrillation, he had 3 afib ablations, uh, he had a moderate to severe mor regurgitation, moderate TR history of DVTs. He's on chronic anticoagulation, and when Doctor Kiel referred him to see me, the patient at that time had two different hospitalizations, uh, for heart failure exacerbation. So as I mentioned, he was referred uh to see me in the heart rate clinic by Doctor Keel, um, and when I saw him, the patient was volume overloaded. He was decompensated, symptomatic, um, we treated him in clinic with IV diuretics. We adjusted his regimen, um, knowing his history of hypertrophic cardiomyopathy, we obtained genetic testing on the patient and I scheduled him for a right heart cath to assess his hemodynamics and to plan the further care for him. And I told the patient most likely gonna be admitted uh after your cath knowing how symptomatic he was, um, so his testing results we did genetic testing, he came back positive for mycin binding protein C, which is one of the main, uh, mutations that have that in hypertrophic cardiomyopathy patients. His right heart cath, these are his numbers, his RA was 14, his wedge was 29, his index was 1.9, uh. So I admitted him for aggressive diuresis and knowing how bad his hemodynamics and he's kind of burnt out hypertrophic cardiomyopathy, we wanted to initiate some onotropes and evaluate for advanced heart failure or surgical options. So we're gonna see this later on. The patient was evaluated and at that time he was deemed not a candidate because of an SVC syndrome, as you all recall, he had, uh, multiple, he had two ICDs and had multiple leads and he didn't have um venous conduits for him to get at least safely transplanted. Um, this is one of, um, basically you can see there's not much Venus flow. So at that time a strategy was developed among multidisciplinary team approach between uh Doctor Kiel, Doctor Summers, and uh vascular surgery and also CT surgery to try to do lead extraction um and to dilate and stent his um vessels, um, and then to put a sub Q ICD. So that was the plan and we're gonna see what transpired out of it. But before going there, I just wanna give everybody a small background on hypertrophic cardiomyopathy and what's the workup for it. We're gonna go through it pretty fast but just for uh medical knowledge. So this is uh from the recent guidelines that was published around 6 months ago in Jack, um, which includes all the guidelines for management of patients with HCM and as you can see here for patients with suspected hypertrophic cardiomyopathy or have history, family history of hypertrophic cardiomyopathy. We look if the patients have the phenotype, which means if they have LVH, um, or if they have any obstructive symptoms, and this is kind of what we do, um, first thing if they have HCM with the phenotype, we have to assess the risk for sudden cardiac death because these patients, as you all see, probably patients, uh, or like football players just crashing on the field, they resuscitate them, they're young and they these patients have HCM and they're at higher risk for sudden cardiac death. So it's important to highlight and know what's the risk for it, and the follow-up usually every 1 or 2 years or if there's changes in their symptoms, and this follow-up will include echocardiogram, uh, ambulatory EKG monitor because we want to detect if these patients have VT and then also do cardiac MRI every 3 to 5 years to assess for uh scarring. And if their phenotype is negative, we do genetic testing and if the family has known history of pathogenic or likely pathogenic mutation. Um, we can also address that, um, based upon it if they have, um, the pathogenic mutation, we can screen these patients with an EKG, an echo, uh, especially if they don't have the mutations themselves. So this is technically uh this one of our patients with HCM this is not the patients we're talking about today we can see here how they have severe LVH and they have mor regurgitation and they have uh systolic anterior motion of the mitral valve and it's gonna be more prominent uh through this also the TE of one of the patients. This patient end up getting uh myectomy with Doctor Scortino as you can see here is significant LVH with a gradient. So what's the role of genetic testing as we were talking? I mean, if patients have a variant of unknown significance which could be likely benign or benign, um, you know, you survey, you know, if the patients have it, you can do clinical surveillance in the family if they are diagnosed with HCM just follow them regularly as they are if there's no evidence of HCM. Continue regular care, but if the patients have pathogenic mutation, you screen the family members for that mutation. If the family members do not have that mutation, the family members do not have hypertrophic cardiomyopathy. If the family members have that mutation and they don't have the phenotype or the uh. You know LVH or symptoms, you just do regular testing check on them every 2 to 3 years with an echocardiogram. So as I mentioned, the risk of sudden cardiac death is so important and it's very uh crucial that we assess it in our patients, and this is what the guidelines say the reason for ICD in these patients again, if any of the patients have history of sudden cardiac death if they were resuscitated before or history of VT or sustain sustained VT or VF, these patients qualify for an ICD. If they don't have that, this is how again, uh, from the recent guidelines, if they have severe LVH with the septal wall thickness more than 3 centimeters, if they have unexplained syncope or have less than 50%, or family history of sudden cardiac death, these patients also through shared decision making, they would benefit from an ICD. If they don't have that, you do non-stress, uh, um, you look at non-sustained VT. If they have non-sustained VT, if they're children, because they're gonna live longer, it is reasonable to do an ICD if they're older basically. It is OK to put an ICD, but it's not doesn't have a high level of evidence. Again, if they don't have non-sustained VT, you go, do they have scarring on their CMR and MRI? And the scarring usually it has to be more than 10+% on the scarring because the higher the scar burden, the higher risk for arrhythmias. ICD can be uh. Considered for these patients with high scar burden, but again this is technically what we look at and when we think about and we have a shared decision making with patients we assess the risk factors. This is a cardiac MRI where we can see um basically um enhancement which consistent with scar formation. And how to treat symptomatic patients with hypertrophic cardiomyopathy are also stray from the guidelines where we can see here we wanna know if they have obstructive physiology, if they have symptoms, you treat them with beta blockers or calcium channel blockers, uh, that are non-dihydropyridine such as verapamil or diltiazem, and if the symptoms persist, um, there are different options for it in the past that either alkyl septal ablation, which Doctor Summer does and his team. And uh you can do myectomy which uh our surgeons and other surgeons can do, um but now that was the only option before but now in the past couple of years we have min inhibitors which can talk a little bit about it, which is another option for these patients who are symptomatic. So alcohol septal ablation and surgical macectomies were kind of the standard of treatment for patients before who are symptomatic despite beta blockers or calcium channel blockers. Um, this is the pros and cons for, uh, each one of them. I mean, um, a septal ablation we kind of talked about it in the previous meeting, um, it's pretty like, you know, short length of stay, it's easier, less invasive than myectomy. Um, but there are some potentially adverse effects, you know, which can lead to pacemakers because they have right bundle branch block. There's potential scarring when they have scarring again, you can have arrhythmias. With myectomy it is an invasive and open heart surgery, as you can know, so the success rate is high, but it has to be done in experience centers. So what about the other options which is uh like Mavacamptin which is Camzaos, and it is a uh medicine that we are using in our clinic and other uh institutions as well. It is an inhibitor of the cardiacmycin and it reduces the binding between the uh myocin and actin across the bridges. Uh, one of the potential adverse effects of it is that this medicine you need to follow them, follow the patients with frequent echocardiogram because there is a risk that the ejection fraction will drop. Um, this medicine can make patients feel better but does not improve their survival or longevity. It can reduces the time to getting alcohol septal ablation or myectomy. So these are the options for our patients and this is the study, the Valor H uh HCM which showed that patients on Macatin have improved in their symptoms and less uh need for septal reduction. So back to our patients, what do the guidelines say in managing these patients? As you all remember, his EF was 15 to 20%. He had an ICD. He's symptomatic, MIA class 3 or 4, and these patients, you know, when they are burnt out, uh, hypertrophic cardiomyopathy, these patients are at increased risk of sudden cardiac death. So that's why we evaluate these patients for heart transplantation and this is what. End up with uh for our patients we evaluate him for heart transplant but again as we remember he was deemed not a heart transplant candidate because of his SVC syndro syndrome and lack of venous conduits. So, uh, on that I will, uh, do the Doctor Kiel tell us what happened to him from EP perspective. OK, sorry. So these are kind of some meshed together slides uh Matt and I presented this case in a national conference back in December. November I think in the snow in Colorado and so some of the slides are redundant we'll skip through those. I just wanted to add a couple points to the um ICD uh stratification um so. The guidelines are one thing and what we use are are another thing um so if you look at what's probably the most useful risk calculator, the European Society of Cardiology or ESC you can sit here if you want, Phil, there's another chair you can take mine. I'll I'll stand, um, there's a. There's the ESC has a really nice risk calculator. The the thing that the the guidelines that were shown kind of misses is obstruction. Um, and so although you can do alcohol septal ablation and you can do myectomy, some patients don't aren't actively being planned to get those things and so actually if you look at the two biggest risks of sudden death with patients, it's obstruction and ventricular arrhythmias and so in the ESC risk calculator you actually put in the resting gradient. So you know if you have somebody who has a resting grain of 80 you're probably sending that person for for some sort of procedural intervention if Mava Hampton doesn't work but say they're their grading is 30 you may not be considering that if they're not that symptomatic, but that actually does add significantly to their cardiac death risk. The other thing that's in the cardiac death risk and the ESC risk calculator is left atrial dilation. So patients who have left atrial dilation or increased risk of death with HCM and so when you put things into the risk calculator, it, it, it will stratify out are you 2A2B1 in terms of what your 5 year percentage risk is and you can have a really informed shared decision making with that patient based on what the other plans are in place for, you know, um. HCM management in terms of you know myectomy or or or septal ablation. The second thing I wanted to comment on, um, I don't know if I have my slides in, oh yeah, so from an Afib ablation perspective, uh, historically speaking, patients with, um, hypertrophic cardiomyopathy, if you look at the, the kind of older papers would suggest that the outcomes are worse with, uh, atrial fibrillation ablation compared to non HCM patients. That That probably is still true, but what I would say is that um the, the benefit is also significantly higher so patients with HCM in general have restrictive physiology, um, they are more reliant on their atrial kick and so symptomatically they benefit significantly more from being in sinus rhythm. So this particular patient just to provide you a little bit of backstory because I've, he was one of my first patients 6 years ago, um. So when he's doing poorly. He's class 3 to 4, but historically this is a guy who travels internationally. He's a sound guy um he's worked for Blackstreet, Mary J. Blige, um, he's, uh, so he, he does a lot of international travel and when he started becoming symptomatic was when he got atrial fibrillation the first time he'd be walking through the airport and he would need to get a wheelchair basically whereas historically if you look at this guy he's more muscular than me and and looks like he's in great shape so. I don't want to take credit for all the EP part of stuff because Doctor Patel also played a role in one of these, but these are, he had three different ablations I don't know if these will play, um, between 2022 and 2020, yeah, these aren't playing, but, um, so he had initial afib ablation and what you see here is some breakthrough in this mitral line here. He had a cava tracuspi dismus flutter. He had a roof dependent flutter that you can see kind of breakthrough here near the left superior pulmonary vein. Um, this is a reconnection of his pulmonary veins, I think, from his first ablation. What you see is that the tissue is thicker so it's harder to ablate it in a thermal this was all in a thermal ablation era. And so it sometimes will require more and more redos, but every time we could get him back in sinus rhythm, he felt dramatically better. So the time that I referred him, um, to Emin was the first time I saw him in the ER and he had terrible heart failure symptoms and he was in sinus rhythm. That's when I knew he was in trouble. Um, and so these are just some of his EKGs before and after, so you know, fib and flutter and then this is kind of what his EKG on the bottom, uh, looks like now in terms of he's got this long first degree AV block that's kind of what it looks like still now. You can see he does not have a left bundle branch block, um, as some patients do, having had some sort of surgical intervention. OK, so, so now we're back caught up and so, uh, we alluded a little bit earlier to, um, his venous conduits and why he wasn't a candidate, so. This is a big argument here for why you don't abandon ICD leads and pacing leads. So, um, his, his left sided lead was abandoned in 2017, uh, locally, not by any of us, um, and now you can see basically he's got this hemi azyous system on the right screen. You can see the extensive collateralization and so when we first actually discussed him in transplant committee. Um, Scortino was there. Dexter was there. Mean was there. I think Ed was on service that week. I was there. Um, we actually deemed him to be too high risk to extract him because he was actually doing, despite his indices, he was doing reasonably well, but about a week or two after his right sided ICD lead fractured. So now he's got two nonfunctional ICD leads. He's at super high risk for sudden death based on his EF and a variety of other things. So what we decided to do is go ahead and try and extract his systems and retain access. Um, so that we could hopefully make him a transplant candidate again. So this is again Um, kind of a, a melded, uh, presentation when we presented this last we were presenting to some people who knew things about lead extraction, some people who didn't, um, I said this at the time that I presented this, and I'll say it again, this is a really old slide. I don't agree with any of this stuff in contemporary, uh, times in terms of, um, what the risk of PCI and taver is. I think that's all completely wrong, but the, the point is. Uh, in the lexicon study, which is pretty old now for in, in high volume centers, uh, the risk of major adverse complications with lead extraction is very low, it's less than 1%, and this is data on the right out of Cleveland Clinic, um, over 2000 leads extracted from 2013 to 2017, 98% success, uh, need for cardiac surgery intervention, less than 1%, less than a 0.5% mortality. If you look at our numbers here we've done about 500 cases since I came in 2019 between myself, Doctor Patel, Doctor Hedley. And we've had one mortality 0.2%, um, and we've had, uh, I think three needs for open heart surgery, so we're, we're less than 1% there so very similar, uh, similar results. And the reality, you know, this is for infection, but if you don't extract patients. Um, and you try and treat it conservatively, the infection comes back and patients die, um, so even though you know it's a, uh, it's a procedure, um, that does carry risk and theoretically can can lead to very significant things actually the benefits are significant, so these are a couple. Yeah I just showed you this this slide that shows you that relapse rates are high if you don't extract infected patients. This is a slide showing um what the real world world is doing and what we should be doing so. On the left is a study from Duke, uh, from, uh, Sean Pecorny where they basically looked through a Medicare database of about a million patients and they tried to figure out of the people who had in CIEDs and infections, what percentage of them got, um, class one indicated, uh, approach which is lead extraction, and what they found out is, uh, over 80% of patients did not get a lead extraction and those patients who didn't get a lead extraction had a 1 year mortality of 33%. Those who were promptly detected and were extracted within 7 days, uh, their mortality at 1 year was 18%, so that's a 14% um. One year mortality reduction that's a number needed to treat to save one life of 7. there are very few things in cardiology we do that have that high of an impact on the right, these are patients who have, uh, staph bacteremia, and there's no TEE showing they have infection. They just have staph bacteremia, empiric CIED removal, uh, in these patients reduce mortality by 72% relative at one year. So these are, these are life and death decisions so. So how do we, uh, how do we reduce the risk of complications during the lead extraction? So this is the bridge occlusion balloon which is placed through the right femoral vein. A wire is placed up into the um either the IJ or the right subclavian and basically you occlude and this is just another picture showing um just contrast and how it's occluding basically what happens if you tear in the SVC um you can inflate the balloon it tamponades from inside the bleeding, uh, in order for uh the surgeons to have time to isolate the tear and fix the patient. This is some data on real world uh experience with the bridge balloon. So in patients who, uh, this the left is just kind of modeling, but this is the amount of incremental blood loss you can save by having presaged the bridge balloon on the right, these are actual SVC tears across the US, so 65 cases without bridge balloon, 51 cases with bridge balloon, 88% of patients discharged with good neurologic outcome in the bridge arm. Uh, only 56% of patients discharged alive, um, so using the bridge balloon in patients that tear, which thankfully is a rare occurrence, saves, you know, an absolute, you know, mortality of 30% in this patient population, which is a huge amount. So what tools do we have to extract? um, we can use laser tools, uh, we can use mechanical tools, um, the one on the top right is a recalled one, so don't use that one, but, um, but in any event, uh, laser works well for fibrosis and, um, the mechanical tools work well for calcification. So this is not this patient, but it's, it just kind of shows you how we prep leads so we open up the incision. Uh, where, uh, where the leads in the battery sit and then what we're doing is we're basically, uh, cutting not all leads are the same, but for most leads there's a central lumen and so basically we're cutting, uh, the lead to open up, uh, the inside of it and then we're putting this locking stylelet down uh the lead. And what we're doing here is like if you try and write with a pencil and the pencils this long you don't grab it by the eraser right? it's a floppy noodle you want to be able to write with the tip so you put your hands down near the tip. So by introducing this locking style out all the way to the tip once you pull on the lead, you're not pulling on the back end you're pulling on the front end. Um, then, um, you know, that's the in central lumen of the lead, but there's also, um, there's also central insulation around there and one of the issues with lead extraction is that you're kind of pulling and pushing if things aren't all moving as one unit, you can get into problems we call it snow plowing. So here we're tying the outside you can't really see it because of the glare, but we're tying the outside of the lead with a suture. And then we're gonna attach it to the back end uh right here of the uh of the lead and so we're pulling on the unit all as one the lead, the insulation, um, and we'll be ready to extract here shortly. Um This is me actually putting the laser tool on and this is me almost dropping a $2500 piece of equipment, um, as you'll see here in a second but you can, yep there we go, uh, but you can see the red little glow that's the laser and then kind of getting ready to extract here. This is not this patient obviously you saw much more difficult case, but this is uh an example of using the tight rail which is the mechanical tool to get a lead out. That was a lot easier than normally is. This is, uh, using a laser uh in a patient who already has a free end of a lead, um, which is pertinent in this case this is the right atrial lead up here. And so, um, What you'll see here is, uh, you know, a fair amount of, uh, binding and the minute, the minute we try and get through the binding this ventricular lead frees up. So, uh, occlusion is a big indication for extraction to try and upgrade that's actually for those who are with me today. That's what my second case is. And in this case, remember that we're trying to get the nonfunctional pieces out for infection reasons, but the biggest reason is we're trying to maintain venous act. So, um, when this lead pops free in a patient who's occluded, we're not gonna just keep lazing out because the lead may just pull out now we haven't retained access. So what we're gonna do is we're gonna go through the groin, we're gonna take a little snare, gooseneck snare, we're gonna put it around the tip of the lead, which you'll see here in a second. Um, if you ever need this done, the best person to do this is Jeff Hedley. Um, you, you lasso around the lead, and then you can pull down. Now you have a rail, so you're not trying to laser over a, uh, a floppy noodle. So now that I'm pulling down with traction, I don't need to worry about pushing through the SVC um, whoever is with me can pull down as hard as they want on that snare the leads leads not going anywhere, and then you can break through the adhesions. Give it a second, you'll see the laser pop through. What type of energy you're using for 80 Hz, yeah this is this is real time. Like how you're casually showing that through a ring as well it's even more complex. So, so, so now we're past the occlusion which was up in the anoinate or the SBC. We Release our snare. You pull the lead out through the sheath which is now a tube back into the central lumen. You then put a wire down or 5 wires down if you want to, which I would usually put more than than 1, and now you can reimplant so that's, so that's kind of the concept of it so um this is a high risk enough patient that I didn't record all the different things but so remember I said you know the the bridge balloon helps you and you put it up in the IJ or the um. Or the uh or the right subclavian what do you do if they have SVC syndrome? You can't put it up there. So actually this is me putting my wire into his hemiiazous. So this wire here is going up through the occlusion and down the hemiiazagous. So the bridge balloon was staged there. You can see he's got a left sided dual coil ICD um, these are 2002, 2002, 2017, 2017, so 4 leads, um. You know, I think we extracted this in June of 24, so 22, 22, 7 and 7, so almost 60 years' worth of leads. High risk features for lead extraction, young aged implant, he was 25, highly likely to calcify multiple abandoned leads, bilateral leads, low EF everything you can think of that's high risk is this guy, but he has no other options, right? So, um. So the right side actually came out pretty easy. I don't have any videos to show you of that one. The left side was a little harder. What you can see halfway through. Here is there's this little fragment here, little fragment here, and we've still got one ICD lead from the left to go but we've gotten the atrial lead out and this is um. So, um, what you can see here. Versus before is now we've taken that wire we put it down the IVC and Doctor Rayhor from vascular surgery came in balloon, balloon, balloon, balloon. The data for SCC stenting is actually pretty bad, so you don't wanna try and do that. So you can still see whereas before the hemiiazyous comes down here. And here now you can see what wasn't present here before there's blood flow getting back to the heart so we've we've restored the conduit now this isn't particularly durable in a lot of patients, so you're still being followed by um Dexter, but. Um, but we now have restored him to potentially be a heart transplant candidate. Um, We still have these fragments we're not gonna leave behind so just kind of showing you an example of we're going down from a snare from below, um, using a bunch of other different tools and and grabbing the fragment into the into the uh sheath that's we kind of piecemeal removed all the other parts of the lead I think Doctor Hedley does half of them and I did the other half so so great success. Our goal is to get um. Get conduit we did that. This was his before this is his afters nothing in his vasculature, so, uh, we can all go home we can get a transplant happy story. Whoops. OK. Thank you for having me uh involved in this case. I think hypertrophic cardiomyopathy is the historic uh clinical example where we have multiple teams come together, uh, surgical for cardiac uh for uh extended septal myectomy, interventional cardiology for septal ablation. Uh, advanced heart failure to take care of all these really complex hemodynamics, uh, with outflow tract obstruction and and burn out situations, more advanced therapies, uh, for people that that absolutely need them, but this is a young sick patient population where historically we've come together in this fashion. I didn't perceive that we'd come together um as a multidisciplinary approach for tricuspid valves with hypertrophic cardiomyopathy, but, uh, this is one of the benefits to working in a place like this where you have such incredible collaboration. Is that we have the capacity and capabilities to do things uh when there are problems um but this patient absolutely needed these leads extracted and with the novel approaches uh um I'm by no means uh facile with with all the complexities of extraction. But I know that these kind of extractions are, are the ability to do them working in the tricuspid space is very limited. We're at when we're at uh meetings, um, it's rare to have, uh, programs that have uh such strength with heart failure and with uh lead extraction, but when things do happen, we have to be able to. Use tools that are available to us, uh, sometimes in novel fashions to get patients through and so first thing you'll see here is that uh we've got. Uh, a lead, um, obviously that's been the focus that Doctor Kiel's been talking about. 15 to 20% of our patients that we end up needing tricuspid valve therapies have uh cardiac leads. It's actually considered a type of tricuspid regurgitation, CID associated related TR. With TR therapies we gave a grand rounds uh on this last year are uh novel. Um, there, there really weren't any good therapies before last April. We had, uh, two clinical trials, uh, soon to be a third that we were heavily involved with both on replacement and repair, um. But surgical therapies have historically been very, very uh difficult uh because of RV dysfunction and getting people through pump, um, even though our surgeons are excellent at repairing these valves and have a variety of different approaches, predominantly tricuspid repairs and replacement is reserved for folks that are getting concomitant left-sided, uh, operations, um, but isolated uh TR, there were about 500 cases a year, 5000 over 10 years, um, and, and all of the register until this last year. We had access to this in April and I'll go through, but this is uh the picture after the extraction so pretty clear here what's going on. We have flail and torrential TR. Historically, the teaching is that acute TR doesn't necessarily lead to dramatic hemodynamic consequences, but physiologically it's, it's clear why it does in scenarios like this. You have no volume remodeling or accommodation for that torrential TR and so you essentially get reversal flow and that's that's literally how this guy presented. um, we had started triclip two weeks before this and had done 2 cases, um. Tricuspid therapies were available starting commercially in February with TTVR, but they were very limited in their roll out, only rolling out to 5 centers for the 1st 6 months. Uh, T tier though, Triclip was available starting in April and when we had done our first cases just a few weeks before this, uh, when we currently have a problem, uh, as a consequence to a to an incredible extraction to to help save a patient's life and give him options for transplant. But now we have a problem that we historically don't have a fix for. We have a new therapy that has just come out. This is uh The anatomy of this just so you have a frame of reference, um for the echocardiographers and sonographers in the room you're very familiar with these uh. 3D uh uh pictures because you know, uh, Chris and Luke and Liu all helped with more than 80 tricuspid TEE studies that we did over the course of 2.5 years and contributed significantly to the field, allowing us to even take care of these patients and so you'll see the tricuspid valve, obviously 3 valve, 3 cusps in the valve. There's an anterior posterior septal. Um, I'll show you through some of the conventions, uh, as far as imaging in a little bit, but you can see here, uh, the anatomy that you have posterior flail. And so as a consequence of the extraction, um, this young gentleman was an acute RV shock as a consequence to posterior flail. Just a quick background on this, most people know what mitral clip is, but for a refresher, mira clip is based on an old surgical technique called alfier stitch. It's an edge to edge repair. That's what tear is trans catheter edge to edge repair. And there's a similar type of surgical approach, uh historically since the 60s on the Tricuspid gallery essentially. Take one of the commissures and you buy cuspidize it. What that does is it pinches it down here and also actually produces some annular reduction. So even in not even talking about the overall TR reduction, you're getting annular reduction with a successful tri-clip um based on this old case stitch technique. Most people understand, uh, mitral clip in general, but just so you have a frame of reference for what we're doing catheter wise with edge to edge repairs, this is a schematic. We've had MT commercially available since 2014, the year before last we were the 2nd highest volume center in the country, and last year we're the fifth highest volume center in the country. But what this is is a transcaheter approach. We go through the femoral vein. It's 24 French transeptal. We can very precisely orient the clip. To produce that effective stitch, there's two clip arms that independently grasp. This is an example of the clips coming down anterior leaflet posterior leaflet, aortic valve. You can see those leaflets draping very nicely over top of the clip arms. They pinch down with these grippers. We close And I tell folks, uh, you know, they have a double door and the door is swinging ajar, and what this does is creating a door, it creates a doorstop, um, with the catheter. It's effectively a small clothes pin that creates a double orifice. We always balance reduction and leak regurgitation with consequential at least from the the clip, uh, some elevation and trans mitral gradients. Uh, but incredibly effective therapy number needed to treat for mortality, um, mortality at 2 years for functional MR is 6. So every 6 patients we treat with functional MR, which is about 70% of our patients, um, we're literally saving their lives. This is what it looks like with 3D multiplanar reconstruction so you can see the clip clip, and now, uh, with Doctor Cohen and and how we're doing imaging. We are, we are literally doing the procedures in three dimension through the entire course of the procedure. So it is triclip, it's basically mitral clip on the right side. So we actually were using these in desperate patients with mitroclip systems before we had commercial triclip. Now it was out of just a necessity to try to get people treated. We can basically turn the mroclip system 180 degrees upside down. For us it's working literally it's like riding a bike backwards a little bit, but it's it's uh it's possible. Now that we have a dedicated system through triclip, this is sort of the orientation that we work and we keep the AS comma generally at 4 o'clock. You can see what we're doing here as far as the case stitch sort of similarity, but really what we're trying to target is into the deep AS commaer and work our way centrally, usually requiring 2, sometimes 3 clips. One thing that does happen is that when you cinch down the AS commissioner, you prop open. Uh, the posterior septal, what we call canyon, and so sometimes 1/4 clip is needed there, um, but this is a brand new therapy and it's being, uh. Applied to a vast array of patients nationally right now with good clinical data based on the trial of dramatic symptom reduction and in longer term data it will lead to reduced hospitalizations and things of that sort. TR is very difficult to show mortality benefit because mortality happens well after 2 years, but people struggle, jaundice, right? Heart failure, as you all know, is, is terrible, lower extremity edema, progressive liver, and renal dysfunction. Here they're showing a clip in the central AS comisher and now they're putting one in the deep AS comisher. These are the two trials we were involved in both of these at some of the highest levels. This KCCQ score improvement, Dr. Ye, I will tell you, is a dramatic one as far as what they see with advanced heart failure therapies. The most important thing is it's very safe. It's a right-sided procedure. It's a venous procedure. Our EP colleagues know how safe right sided procedures can be. You have 98% freedom from AC at 30 days and 49.7% of people had at least a 15% improvement. People can argue about subjective end points and things like that. That's great, but there's very rare things in medicine that have that dramatic impact on people's symptoms. TTVR is a little bit more complex, it's a little bit clunky, uh, it's not difficult to deploy, but it's, uh, it's imaging intensive, uh, and as we're finding out, a lot of patients have some degree of RV dysfunction or pulmonary hypertension that make it to where completely treating the tricuspid valve and eliminating the leak that produces something called afterload mismatch so and it, uh, induces and uh. Untoward uh amount of uh after load onto an already weakened ventricle. Can you click the uh uh valve with a in there we have the concern there and, and so I'll get to this in a second, but the reason this is so important to have, uh, folks like Doctor Keel who is a representation, uh, representative on the Multidisciplinary heart team as far as Valve conference and Dr. Yaya is because 15 to 20% of the ones we're coming across have leads. So it requires very, very precise imaging to look at the location of the lead. Most of the time they're buried in the posterior septal commasure if they have enough slack. We've seen some though that developed quite a bit of slack and then go across the annulus way down the anterior septal leaflets. It's a variety of things, but if they're buried into the PS commisure we can generally clip and jail them. The problem is there's a lot of concern with the EP colleagues about what that does to the insulation. Well, if you, you've been at these national meetings so, so the, uh, the Miami lead extraction symposium which I go to every March, drafted a letter and sent it to the ACC and all the insurance companies basically saying that that there needs to be EP involvement on care teams, which we already did, right, so we don't need somebody to tell us that, uh, just because this is more a triuminate the the valve replacement, um. Late lead failures are pretty high um in some of those patients you develop new conduction abnormalities which mean you're gonna pace more and then you've disrupted the lead a little bit um once the lead is jailed, you cannot get it out um and so for infection reasons it's, it's tricky and so I think that the right way to approach this is though it may be feasible, uh, to clip around it to have a discussion about the risks and benefits of potentially extracting the leads if you can replacing them with a leadless system and then clipping. We've done that what 3 or 4 times now thus far combined in combined procedures and, and I think that the reality is the results may be better for both if you do it that way. You also consolidate anesthesia and higher risk procedures as far as uh getting through general anesthesia, that's the biggest biggest part for these folks with tricuspi regurgitation. That's incredibly unique. I, I don't know anyone else who's doing combined procedures with their EP colleagues to make sure that we're getting that specific, uh, question answered correctly, which is what do we do about leads. This is back to our patient. TR is graded on a scale of 5. This is, no question 5. There's flail. We understand the anatomy. Um, we're very lucky to have a lot of, uh, good images. This was last, uh, was last May, uh, into June, um, and I called Doctor Cerris, who, uh, came from Ose and helped with this, uh, procedure. Otherwise, you know, we, we found out about it at 4 o'clock on a Tuesday, um, and did this first case on a Wednesday. So not only do we find an excellent imager to help us with 3 multiplanar reconstruction, the entire hospital uh uh pivoted so that we could accomplish this procedure uh literally the next morning. You can see in 3D multiplaer where the leak is coming from. We're positioning ourselves over the posterior septal commiser again, the AS commissure is at 4 o'clock, so we're orienting this clip appropriately. This is where it's at in relation to the leak. This is the schematic of what we're looking at on uh Echo and trying to compare, we're trying to clip that posterior septal commiser more in a central location but leaving a little bit of room in the commiser um. So we get the main pathology which is this flail here. You can see after uh one clip we still have a leak and so we can place that second clip. This is what we call tricommissional view, but basically it's looking down the commiss like a equivalent would be a 60 degree for a mitral and this is the intent to clip view which is a steep um angulation, uh, showing the posterior and septal commiss or posterior encetal leaflets. And this is a reduction afterwards. That's the TTE the uh 3 months afterwards is trivial TR. I didn't pick the best picture. I know it would be eccentric, but that is the worst we could make it look. So what about ice um. This requires uh images with really really advanced uh training that you can work through a lot of the challenges that come inherently with the fact that the tricuspid valve is an annular is an anterior structure and so it often requires adjuvant imaging, intracardiac imaging, and that's where 4D ice comes into play. We've used ice for years, um. But you cannot use ice in two planes and by plane. So if when we were doing these before 40 ice, we'd literally have to take the ice catheter into the ventricle, pull it to the leaflets, and look up to get our intent to clip views, which is you're knocking clips off, you're potentially damaging the tricuspid valve further. Now that we have 4 dimensional ice, we can literally go back and forth between TEE and ice with 3D multiplanar reconstruction and so we can get. Uh, important information from both of those two mo modalities. We start in TEE, Doctor Cohen, we can get most of, most of these with TEE now, um, but if we have difficulty looking at leaflet insertion. We can often get that extra information with ice. Now you can see the quality relative to TEE. It's not quite there yet. Actually a simple software upgrade improves this substantially, which we've been working very diligently to get done. We're using ICE in about 60% of our tri-clip cases, but this is an absolutely essential modality that we need to do tricuspid valve therapy. So if you think about all the things that had to align for this gentleman to have a chance when he was quite literally. Dying in RV shot, we had to have a brand new ice catheter get through all of you know sort of the normal hurdles that come with new device therapies on top of having tricuspid therapies that have no national coverage decision even now. So the hospital is uh working with us so that we can help take care of these patients even though reimbursement is still a little bit unclear now everyone knows it's going to be reimbursed the same way as Mitroclip. But these are incredible sort of barriers that that are are not feasible or possible at most places, uh, much more to mention that the collaboration uh that's possible here. This was the first acute tri-clip in the world that we did because it was 2 weeks after um commercial release and so quite literally one of the first procedures for a scenario like this was done here in this hospital, and we are currently the number 3 program for tri-clip in the country as well. We've done 32 cases, um, we're behind Minneapolis Heart which their PI is their person is the PI of the trial in Swedish in uh Seattle. We get on average almost a 3 grade reduction in our TR. This is adjudicated by Abbott themselves, so they give us this data feedback. So it's not us saying we've reduced that by 2 grades. 3 grade reduction is dramatic and it's more than what we saw in the clinical trials. We have an average time of 85 minutes. That's where this is a little bit onerous. It requires a lot of time for our texts, a lot of time for our imagers, sonographers, etc. Um, but we are quite literally leading the way in this and it's allowing us to treat people in unconventional fashions when they, uh, the need arises. This is a key. We we were way ahead of this, as Doctor Keel said it's now becoming a guideline sort of statement and and position that, yeah, we should have multiple people besides just uh heart surgeons and interventional cardiologists on a valve team. We've known that for a while and so before we even got to Triclip. Uh, Doctor Eggert was helping with, uh, helping me work through some of the pulmonary hypertension issues. Doctor Yea, it, it comes to every one of our, uh, valve conferences every Monday and helps us with GDMT and making sure we're doing everything we possibly can for the functional MR and TR patients, not great medical therapies for TR. They're inundated with an incredible amount of other advanced heart failure therapies that are necessary throughout the hospital system, but they're seeing a lot of our patients for diuretics and things just because. The coverage, uh, and, and, uh, national decision coverage on on this is still unclear, and we want to make sure we're doing everything 100% by the book. Doctor Keel, uh, Doctor Patel, Doctor Hedley have have also contributed significantly to making sure that we're we're managing leads and setting of TR effectively. One of the big things that that we look at here is the balance between RV dysfunction and pulmonary hypertension. I think that's probably why triclip is gonna be a more effective therapy up front. It's similar to what we do in microclips, so it's reproducible and people that have done, you know, in operators that have uh used and done mitro clip. It's also a little bit more forgiving in the fact that. Um, you know, you have less pacemaker issues that come with that. uh TTVR the the Evoke can have late complete R block. We've seen that more than 2 weeks out, and the, the big issue with, uh, tricuspid valve replacement right now is, is that if you have degrees of RV dysfunction or pulmonary hypertension, it's incredibly difficult to get people not just tuned up but through the the procedure and afterwards getting their their RV to to uh adapt to the new scenario so it requires this sort of workup and comprehensive evaluation. I included this just from a frame of reference last year we talked about some of the tips and tricks of how to visualize uh TR and tricuspid valves. Uh, really what you need to know is that if you have concerns about the complexity of the leak, if it's a new leak, if it's something you've been watching for a long time, hasn't gotten any worse, you know, that's one thing you just follow with TTEs and clinically. But if you have concern for eccentricity or think you need a dedicated TEE. That's really something that that we need to to narrow down and isolate into the, the hands of our advanced imagers, Doctor Saros, folks like that, that, that, uh, understand that what we need to see to determine whether someone is even a candidate anatomically uh for tricuspid therapies or not. So in summary, uh, TR is super common. We we are viewing it and, and treating it in the in the scenario of patients that have chronic right heart failure symptoms, but we have options when people come in acutely like this with atypical presentations, uh, to use this therapy in novel ways. Um, we let in trial participation. We're continuing to lead in. Um, at the national level on volumes and you know, outcomes that are not compromised by those volumes, and I would just like to point out this for heart month, uh, being able to work in an environment where you have incredible collaborative colleagues like this and the ability to to use these therapies in unique ways to help people that desperately need them and don't have any other options. If we wouldn't have gotten tricuspid therapies, ice, all of these things that are interconnected, we didn't have that collaboration, this this gentleman was a day or two away from not being around and he had his daughter's graduation to go to that weekend. It was incredibly powerful to see that the um the consequence of all of this collaboration leading to a patient that was able to see his daughter's graduation is doing, you know, 100% OK now. Um, and I think that's unique and that's something that that we have here that that most places don't.
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