Chapters Transcript Video Aortic Insufficiency: Review and Current Therapies Dr. Summers explores pathophysiology of chronic aortic insufficiency and other transcatheter therapies for AI. Welcome to uh the penultimate grand rounds um for the spring session here next week, we have uh doctor VV lines, um who's doing the evolving role of cardiac CT and clinical care. Um For those who haven't met, I'm Matt Summers. I'm the program director of Structural Heart. Uh I know I just presented, I think last week or the week before, that was a last minute substitution um where we talked about tricuspid regurgitation. This was a previously scheduled grand rounds um that I wanted to take the chance to show what what we're doing in structural heart. Doctor Kemp and myself uh with aortic insufficiency, particularly Gena valve. Uh and then also highlight some other cases or unique cases of aortic insufficient that comes up with structural heart and how we tackle those percutaneously. All right. So I like to showcases obviously to, to drive home the points and uh to sort of walk through our approach uh in handling folks. Um This is an 80 year old gentleman um that uh was an inpatient consults in December of last year, Coronary disease status post and RC A PC I in 2020 with an excellent result. Um A fib on a Doak currently in sinus rhythm A K A on CKD as a, uh, right nephrectomy from 2002. So his creatinine was 2.2 when he came in baseline is around 1.5 and then a prior small stroke, but he came in with progressive shortness of breath for three months. He enjoys, uh, hunting and was having difficulty with, with that and had a significant weight gain. Uh, despite, uh, the use of oral diuretics and this is his index tt E you can see, uh, in the parasternal la, I can often be difficult to see and can, can have quite a bit of eccentricity. We see it at its worst in the apical fives and apical threes. Um, you can start to appreciate the severity here and the eccentricity here. More importantly, this is a common thing we see is contamination by mitral inflow signals. This is a diastolic murmur, diastolic volume pathology. And so, um, a lot of times as you're trying to slice through this eccentric jet, you can get mitral inflow. Um, you can see this is from the, the index tt E it's a little bit difficult to see here, um, on the tee, um, which I'll show you in just a second. It was a little bit more clear, but this was labeled as, um, moderate, at least moderate aortic insufficiency based on that apical five. And we were consulted for moderate severe A R with decompensated heart failure. Um His right heart cath really showed pretty good biventricular filling pressures. Uh but with low cardiac indices, it was concerning in the context of his present presentation for volume overload and decompensated heart failure. This is the te which now shows it more clear, especially if, if you're comparing to that uh initial parasternal long axis and now with these signals te I did you, you can see that the true pressure half time, which is a little bit more dramatically declining um and fits more with the severe estimation of, of the valve disease. This is uh the best signal that I could get on a tee of diastolic flow reversal. And this was in the, the uh proximal descending aorta. So this is what uh doctor camp and I do on every patient with our surgical colleagues and our structural heart colleagues. This is what we do every Monday morning and again, just uh to uh promote that a bit. We, we invite everyone uh even referring um to, to see how we discuss valves, how we uh go through in detail. Uh someone's valve pathology in the context of their clinical scenario and uh incorporate all of the findings both on the iliofemoral imaging, uh echocardiography and annular uh imaging to make these decisions. So, this is what we did uh for this gentleman. Um We all agreed that he had significant aortic insufficiency at good uh iliofemoral access, annular anatomy most notably, uh was that we didn't have really any calcification on the valve at all. And that becomes an issue which we'll talk about when we're talking about trans catheter therapies. So we screened him for a trial that we're actively involved in called uh align A R and uh doctor Kemp and I have enrolled seven patients, uh actually treated seven patients up to this point. Um We're the only site really in the Mid Atlantic that has this only in Virginia. And we get a lot of referrals from U VA and other places to uh specifically for this therapy and, and folks that are not surgical candidates. Um This is a little bit of a long video showing all the technical aspects of it, but it's a two person operation. Um Doctor Kemp and I performed this operation. Um It's basically a, it's a hybrid between MitraClip where you're trying to capture leaflets and a tavern, traditional tower anchors to the calcium on the old valve. So we use the degenerated valve and the aortic sclerosis as our anchor point for a new stented valve. You can't do that if there's not calcification. So the way that this works is you isolate each, each cusp. So it has to be a tricuspid valve and then you're putting these uh cusp markers at the base of each cusp and you're using fluoroscopy to make sure that you have captured each of these three cusps that you're at the annular plane. Um and then the valve deploys with rapid ventricular pacing. There are a series of maneuvers on the delivery system and ultimately, you get a deployment of uh the valve during rapid ventricular deployment or rapid ventricular pacing. So this is the case for this gentleman, you can see the severe aortic insufficiency. We're in an lao view there. Uh just taking pictures, you can see that unlike other TORS, we bring the delivery system, the 16 French delivery system all the way to the S TJ and then unsheath the first part of this valve to um actually flare out the the cusp markers and the cusp capture uh components of the valve. This is the valve on the left. You can see as we do rapid ventricular placing, we're in a very precise location. After lots of cusp angiography, the valve deploys. This was a 27 GENO valve or trilogy. You can see afterwards, the immediate result we use te with this more as an ancillary to isolate the cusps and make sure that we're centered in each cusp with all three of these markers, but he had no leak afterwards. He was discharged on hospital day number two, doing well and in follow up, uh this is him two weeks after uh the GENO valves of the day afterwards. And this was how big of a Turkey Mr Gibson £19.5. Excellent that we have a special guest uh, he was coming in, uh, today for, for other reasons and, uh, Emmy, one of our excellent care unit nurses, uh, it's her grandfather and so this, uh, this, uh, is closer to home with us at Centa because, uh, one of our nurses had a family member that needed this new therapy and didn't have any other surgical options. Mr Gibson was, was awfully sick in the fall. Uh, Doctor Kemp and myself and our team worked very, very hard to, to get him into this trial. Uh And ultimately, he's done tremendously well. Um Mr Gibson, I just wanted everyone on, on our teams to, to see you and see how well you're doing. So you're climbing up a tree stands to, to shoot those turkeys a couple weeks after the operation. He's still recovering, still in cardiac rehab, 12 ft high and so pretty remarkable from, from someone that wasn't, uh we, we wouldn't have been able to get you through surgery at 81 now. Um I think doctor camp and myself and our A PPS get to see patients through the entire course of when they're sick in the hospital and we're getting early consultations and decompensated heart failure all the way to the valve replacement, getting them through that in the perioperative period. And then afterwards, oftentimes we're the only ones that get to see the final product of that. All the, the, the fruit of our hard work. Did, did you hear I said an excellent result on the RC A PC I. Um but II I wanted particularly our Cath lab techs, um particularly the structural uh techs who work very, very, very hard day in day out, doing these cases over and over and over again, meeting the patients the day of when they're about to go to sleep and then their care really ends their, their critically important care to get them through this uh ends when they get wheeled out of the, the or or out of the Cath Lab. And so I, I think Mr Gibson is a perfect example of what we we can do and what the the actual payoff is for all that work that you all do from, from echo text to Cath Lab tech. Um and, and certainly for, for the doctors and nurses that also take care of you. So thank you for coming. We uh we appreciate you trusting us uh with this care and uh we're, we're glad you're doing so well. So a quick background um on chronic aortic insufficiency, this is common. Uh the uh best population based uh cohort we've looked at is from the Framing, Framingham Heart study. It's 2.3% of patients had at least moderate A I. And the prevalence goes up particularly with age and between 6070 the rate is around 0.5% but goes up to 2.3%. No difference between men and women uh once you become 70. So it's a disease, at least in this uh country of aortic dilation. Um some congenital issues if it's uh earlier point in time. Um but also the, the run of the mill aortic sclerosis generation that comes that we treat a lot of these folks with a traditional tabor internationally. Rheumatic disease is the most common. We obviously get endocarditis in younger folks. There's also rare causes that include trauma and some connective tissue disease. But uh the the main issues here is that you, you see uh the prevalence in in our biggest studies that are all, you know, more than 20 years ago at this point, um showing incidents in the general population of of almost 2.5%. And this is the path of physiology which I'm hoping to impart on, on folks today. I I view these as two different uh phenomenon and it all relates back to how our myofibril react to pressure and volume. And so there's two very important concepts and, and the uh the traditional one is aortic stenosis that we all know uh you have increased pressure requirements and after load on the ventricle and it responds and compensates by uh what we call concentric or pressure hypertrophy. And that's basically laying down the muscle cells in parallel such that you get thickening of the muscle that can then generate that extra pressure. So the ventricle becomes hypertrophy, you get diastolic dysfunction, you get a smaller LV cavity. Um and that ventricle is now conditioned to deal with the increased pressure requirement. When you get into aortic insufficiency, it's a volume dependent process, much like mi regurgitation or tricuspid regurgitation. And it's different. This is all based on what we know about Laplace's law. When you get regurgitant flow back into the ventricle from the AORTA, you have increased left ventricular and diastolic volumes. And then because of Laplace's law, you have increased wall stretch and the compensation there is by uh is to increase the diameter. So when you get a volume process, like much regurgitation or aortic insufficiency is the biggest of the volume processes or the most, most dramatic, you get dilation of the ventricle um to maintain wall stress. Um and you get basically de de decrease in your ejection fraction over time. And so aortic insufficiency is a volume remodeling process and aortic stenosis is a pressure remodeling process. And that's important for, for some of the concepts we're going to go through briefly today. The guidelines are pretty straightforward. If you're symptomatic, if you're symptomatic, you get a saber. So the vast majority of these patients uh go the way of Doctor Kemp and our surgical colleagues. I didn't get into the, the details of things like aortic valve repair, which we sometimes do. Traditionally, it's, it's uh typical ser they often do them in the context of uh abnormal roots is the, the most common ideology in these folks is an aortopathy and so they can be quite complex uh surgeries. Um I don't want to speak for doctor Kemp, but they often involve root replacements, coronary reimplantation, ascending grafts and things of that nature. Um The bigger issue is the asymptomatic criteria. And so when I think about all these valve guidelines, you can memorize all these charts and you know that that's helpful to some extent. But I, I tell folks that there's, there's reasons to replace the valves just for symptoms. Um But we're also replacing the valve before symptoms before anything bad happens effectively. So that's that remodeling that we're talking about. And so really, the asymptomatic criteria are geared at the negative remodeling that occurs with each of these valve disease subsets. So for aortic insufficiency, any ef reduction, you, you go to saber or if you're doing surgery for another reason, more commonly, the aorta aortopathy, if the EF is normal, you still look for evidence of negative remodeling. And this is the traditional number that you hear about when people say there's a 5050 rule in ef less than 50 or left ventricular and systolic dimension of more than 50. That's in the Mayo Board review that this 5050 rule. It's, it's, it's a little bit more uh different than that. And, and current guidelines, indexed volumes tend to be more precise than just absolute paternal long axis, uh LVESD and then you can memorize all these things, but I've listed them sort of in the order of their importance and, and I'll, I'll give some tips and tricks on how I look at A I, but ultimately, we're placing these valves class one indication if you're symptomatic. If you're asymptomatic, there's a variety of asymptomatic criteria where you're looking for the consequences of the leak, which is negative remodeling LV, dilation. More than five if you can remember the number or ef less than 50 are the typical ones. And then this is what I remember studying uh A R as a medical student, having to memorize all these eponym which unless you're, you're um at trivia night at the bar. I, I don't think it's all that important. Um Only four of them have ever been validated. One of those is the Austin Flint murmur. The one that I got pimped on the most as a resident was the Hill sign. Uh I was in uh Tom Bay Sh um clinic as a resident at Duke and he would have the residents do this on every patient because it's the only one that has any validity whatsoever. Um But I remember doing these cuff uh pressures um on the uh popliteal versus the arm. So Hills sign, what you really need to remember is that these are consequences of wide pulse pressures. Um and diastolic murmurs. Those are the 22 main things that you look for on physical exam. When you look at this uh I I like this series a lot. I know people have seen this, this uh rational clinical exam. They have it for multiple different uh disease subsets, not just cardiac uh but does this patient have aortic regurgitation? So of all the validated things we can do in in exam listing for a diastolic murmur has the most positive likelihood ratio that's by a cardiologist. Even when there's wide variability in the ability to detect those diastolic murmurs. If you hear one that significantly increases the chances of aortic regurgitation. The biggest thing that I find helpful is just paying attention to the pulse pressure. Look at the diastolic pressure, especially when you're seeing patients with a diastolic murmur. If you're seeing a low diastolic pressure, that should be a flag to get more data on TT E I listed out all those uh numbers regurgitant fraction, regurgitant volume va contract, er oaar index, all of these things, what they fundamentally come down to is a sensitivity uh analysis which is basically what do I see visually as far as the severity and that's what they're getting at with the percentage of the LVOT with. So you can sit there and calculate out the LVOT percentage, but that's more of a visual test to screen for severe aortic insufficiency. And if you use it that way, you don't necessarily spend all your time focusing on the absolute absolute percentage of that LVOT. So it's a screening test. If you have more concerns that it's at least moderate. Then you can start measuring things like the vena contractor. It's very hard, often times to see an, er O A or measure a piece of the vena contractor is probably the best out of those. And then regurg in fraction regurg of volume isn't indexed. So it's probably the least reliable. But the thing I found is the most specific, remember all tests, we want to start with a screening test, a highly sensitive test and then move to a specific test uh which eliminates false, false positives. Um the diastolic flow reversal as you get further away from the, the aortic valve increases specificity. So the specificity in the ascending aorta is somewhere around 70%. As you get further down in the the descending aorta, it becomes even more specific. So this is what I do. When I look at A I, when I was looking at uh Mr Gibson's case, it was difficult to see on the TT E but he had a wide pulse, pulse pressure diastolic murmur. And then when we actually looked through his, his measurements that holo diastolic flow reversal was the signal for um the severity and the trigger for for us moving forward. The treatment as we mentioned is sr if you're high risk and there's enough calcification on the valve, we can do a tver tver for pure A I is off label. We often do it in the setting of combined aortic stenosis and aortic insufficiency because those patients have enough calcium to anchor A tver. Um or we do it through research like the geno valve trial. There's a lot of risks with doing these in pure A I without calcification. The PB L rates are 10 to 15% and valve embolization is the most feared consequence. The prognosis, I I tell folks, the improvement mirrors the decline. If you look at people and their decline in functional status, their LV volumes, all their parameters goes down, you get your valve replacement and the, the improvement mirrors almost identically the rate of decline. And so if you get to these people earlier, their, their improvement back to normal and LV volumes, the remodeling and their symptoms mirrors that it takes three months for you to remodel, then you should get three months to, to improve after fixing and vice versa. Some people can go a couple years of a slowly progressive, slowly worsening A I and, and the improvement often mirrors that on the back end as well. Symptomatic patients have a 25% 1 year mortality. Um And, and uh if you get class four symptoms, like you're in the hospital for decompensated heart failure, it can be even higher and there's a 50% cardiovascular rent rate at one year if it's severe. This was the data from the align A R. So we, we uh uh worked on Mr Gibson through continued access registry. Uh but this trial which was published and presented at TCT last year was a prospective multi center single arm trial that had pre specified uh non inferior, non inferiority goals for both performance. Um As far as safety goes and performance, as far as um clinical outcomes go at one year and they pre specified these at a 40% performance goal for uh the non inferiority for safety and the 25% for the mace at one year, 100 and 80 patients were enrolled at 20 sites. Um We met both the safety and efficacy, non inferiority. Uh pretty significantly 40%. It was actually 27% had some composite measure of, of issues with safety versus 40%. Uh and 7.8% of patients uh had one year mace versus 25% was the performance goal. We had a moderate or more PV L rate of only 0.6% all cause mortality of 2.2%. 7.8% of patients had mild PV L, 0% had moderate. And importantly, the LV remodels uh within that time frame of the first year as well. There's excellent hemodynamics throughout and this is the more dramatic thing you can see that um a a vast majority of these patients uh at index have uh class three or four symptoms and 92% of patients uh at the end of this year have either one, class one or two symptoms. It's a pretty dramatic improvement in functional status. So that's the more common scenario that we face in structural heart, which is how to deal with aortic insufficiency in patients that are not surgical candidates. And again, it's often looking at a ate to quantify a little bit further and confirm that the severity is as severe as what the TT E um is signaling. And then a non contrast CT to look at the calcium of the valve and see if we can anchor a traditional tab or if we don't, we're obligated to go through clinical trials or do uh this, which is a case number two. So what do you do with, with patients that have exclusions to Gena valve? This is the next case is a case that uh Doctor Kemp and I and Doctor Talreja did. Um I think we were having a training session that day as well. So it was a very difficult case. Uh but a 67 year old with class three heart failure, symptoms had two prior ster anatomies, one for cabbage and then one for a physio, one ring in 2003. He now has at least three plus Mr through that ring, it's got severe tr he has an ef of 10%. His sts was over 20%. I mean he was excluded from miar they exclude patients with significant mi regurgitation. And so that's a very common uh coincident process of A I or A R and Mr because they're both volume dependent uh valvular lesions. This is how we implant. Um This is what's called a cusp overlap technique. So we're, this is the non coronary cusp isolated and this is the left and right. You can see we're trying to deploy the valve as close to the annular plane as possible, which is right here. Our pig tails in the non CSP and the uh left and right are isolated over here. This was after six recaptures because the valve continued, you know, sub millimeter placements continued to either migrate atrial or ventricular. Um your valves want to migrate the direction that they're in, in the closed position. So this is often misunderstood as well. But a valve and TVER is going to embolize ventricular, not aortic because when it's closed, it's feeling all the way to your diastolic pressure when it's open, which is cysto, there should be less than a 10 millimeter uh pressure differential. And so once this thing is implanted, the driving pressure is actually down. And so we watched this for a long time because of the movement. After six recaptured, we got it exactly where we wanted, which is a three millimeter depth um that gets us to single digit pacemaker rates if we can put these markers, which are at three at the bottom of the pig tail and the non CSP. And then after we released, it starts moving down, now it's 85 minutes later, it's 12. And now we're getting severe cellular A I, which means that our ceiling skirt is only 10 here. And so now we're getting leaks through the cells uh above the ceiling skirt. So this is a big problem. And obviously before we got to this point, once we released, after we watched this, probably half an hour, uh as we started noticing it migrate, uh we already were preparing the next valve. Looking back at the initial procedure though the the work up, there's there's basically trivial calcification on this, but there were absolutely no other options in this patient. And so I sneered the uh valve here to keep it from moving any further into the ventricle. And then this is a balloon expandable valve. A SAPIEN deployed uh inside at node six and that stabilized things. And you can see the final result here. There's trivial A I now next. And this gentleman who's only 67 again, we have to deal with his mi regurgitation in an old ring uh which uh may not be uh something his ventricle can tolerate with a true valve replacement like a valve and ring or a clip and ring, which is even more difficult um but may be necessary because uh of after L mismatch with that E fa 10% in LV dilation. Um and then, you know, if things continue to improve, uh we can talk about the Tricuspid valve, but that highlights the difficulty in a lot of these consultations we're getting in the patients that we're taking care of. Not all these patients, in fact, significant amount of them, uh don't have the ability to get through open heart surgery because the surgeries um are complex and extensive and uh often involve roots and ascending and things of that nature. And so we managed to take care of them through, through other means, but often difficult means because we don't have established purpose built therapies outside of clinical trials for aortic regurgitation. Third case is bioprosthetic A I. This is a 67 year old gentleman that's uh presenting with cardiogenic shock. He's got bic CPI aortic stenosis and had a sever in 2007, we didn't know which valve type and he had relatively new onset paroxysmal atrial fibrillation uh recently started on Doak. So he was walking two miles per day prior to his presentation with cardiogenic shock. Um He's a 67 year old guy. He's followed at an outside hospital for increasing trans prosthetic gradient um and some mild aortic insufficiency. Again, his valve is 2007. So he's, he's reaching the expiration date of the durability of his valve. Um And then uh the night of the 22 days uh prior to admission, he had coughing and phlegm which really in retrospect, sounds uh like orthopnea. And then he had a very, very abrupt and rapid decline the night of his admission. Uh had respiratory distress. N EMS was called um he was intubated before he ever got to the unit uh for overt hypoxemic respiratory failure and he was hypotensive in cardiogenic shock. His first labs, his lactate was 11.8 with a ph 7.1. His creatinine was 1.9. He had previously normal renal function. He was allegic and he had uh early shock liver as well. So he got to the unit had rapidly rising pressure on ionotropic requirements. He's on uh at 10, no, 30 vaso dope five and dobutamine five and he was on max vent settings um with essentially whited out lungs, uh very big a a gradient, um not oxygenating. Well, then his swan numbers put in at the bedside, you can see elevated biventricular filling pressures and a cardiac index of between 0.8 and 1.4. So, so literally as sick as he gets um I was not on call, it was four in the morning and I got called and came in and did this t to rule out endocarditis. Um It showed an injection fraction of 25% to 30%. These are some important key terms also for your, your trivia night at the bar. But some of the most severe manifestations of acute aortic insufficiency are diastolic Mr and pre closure of the mitral valve. So your filling pressures rise. So suddenly that you're starting to get diastolic mi regurgitation again, this is before the QR S. So all that flow is coming towards the probe. This is diastolic Mr and you're getting pre closure of the mitral valve. You can see that on M mode, we also saw this prolapsing bioprosthetic leaflet uh in the left cusp. Really, it's, it's more the non cusp but of the surgical prosthesis towards the left atrium. So we were convinced that we uh excluded endocarditis, which is a very common reason that people will come uh acutely declined like this after a prosthetic valve. Um but this was his TT E one week prior. And I think this is an important distinction for for when you see your patients uh with old surgical valves, he had some mild eaizf was 45% which was a little bit lower than his historic levels. And he had these increased trans prosthetic valve gradients. Um but minimally symptomatic, remember he was still walking two miles today. This is a routine screening. He became symptomatic after this echo. He came in at 430 to the C IC U shock alert was called at 445 did this t at 515. Got a non con ct, we know no valve details. And so on the CT we reconstructed very quickly. We could tell that he had uh good coronary heights and a big uh root and he probably had a magna 3000. This is, this is what I wanted to highlight here. There is nowhere else that I can imagine where we can see a patient at 430 in this kind of extremists and have a valve in them by 630. And this is the case in point of why I think what we do here is, is unique and special is that we're large enough to where we have access to all the therapies, all the research and can do really very cutting edge stuff for the folks in this community. But we're not big enough to where we can't be nimble and, and mobilize uh massive amounts of teams and team members to take care of problems like this. The entire hospital can pivot when we get someone that's sick. And it's shocking sometimes. Uh how at five in the morning, we can have two cardiothoracic surgeons, two interventional cardiologists, an IC U doctor all at the bedside and uh evaluating patients like this. And I don't know another place uh that exists where it's that uh collaborative and we can be that nimble. So that's exactly what happened. This is his emergent valve and valve tavern. You can see the big sinuses and we were trying to spare dye creatinine was 1.9 from normal EOL uric. This is 26 S3. See we're not really pacing there. It's because the pressures are so low to begin with. And this is a gentleman also. Uh this is a presentation from uh last year, but I asked if, if we could show a picture of him and follow up uh Mr Hunting and he agreed as, as long as we showed a picture of him in his normal street clothes and that I let everyone else know that he's doing well as uh as well. So at 830 this is his intra procedural hemodynamics. So this is what A I looks like. You can see the difference, this is your pulse pressure and aortic pressure and LVDP, your pulse pressure is actually here. But this difference is what we call our A R index. And so the LVDP is rising as the diastolic pressure is rapidly falling and they meet in the middle, we call it a triangle versus this is normal. You see that big separation, no pulse pressure. LVDP is low, aortic pressure is high. This is immediate results. So he came in with an index of 1.4 in LVDP of 40 he left the or with an led P of 10 and an index of 3.2. So dramatic turnaround. Um And he's done incredibly well since, but this is uh the, the point that I wanted to make about that case, in particular, when someone has bioprosthetic degeneration of their aortic valve, their ventricle has been preconditioned to deal with pressure and it's concentrically remodeled. So it's pressure hypertrophy, it's thicker, it's less of a chamber size. It's dealt, it's, it's meant to deal with future issues with over. Uh uh After load. So pressure process when the prosthetic valves start leaking, particularly older ones, even if you see mild, that should be the trigger to expedite work up for valve intervention. And that's because the valves can fail acutely like this. And the ventricle is not conditioned to deal with the volume of revered and flow. So instead of having time to remodel and dilate by Laplace's law, increase your diameter to decrease wall tension, you get in acute sudden influx of flow, your left ventricular and diastolic pressures rapidly rise and all that goes straight back to the lungs. This is why people come in, white it out. They don't have the time to accommodate for the new volume problem. So if there's one thing to take away from this, I would say that the only emergent towers that I can think of in the past five years were these their bros bioprosthetic aortic valves and, and people that had older ones that failed suddenly with, with aortic regurgitation. And if you look back on their echoes, the ones before they came in an extremist like this, they all had new aortic regurgitation even though it was mild. And so it should be a trigger, not just increased gradients or symptoms that trigger should be new leak on the valve. And if you have concerns about any of those folks send them our way, we can sort out whether it's necessary now or, or, or sort of dictate the, the cadence of follow up. Got two more very quick ones and then we'll take some questions. This is how we're managing PV L which is an entirely different process in, in our uh field for transcatheter valves. This is a 78 year old uh female that came in with uh volume overload. A £30 weight gain. She was admitted to the hospital. Um This was last, she had an interesting history. We had done her TVER in April of 2021 for run of the mill severe aortic stenosis. Um This was her index echocardiogram. You can see pretty typical scenario that we face that, that all of us face the severely narrowed valve with meeting all criteria for severity, peak velocity of 4.2 main grating of 46. This is the annular anatomy, nothing, nothing really out of the ordinary. This would be a pretty typical routine TF tower for us and it was uh in April of 21 we had an ef 45% which was a new reduction, slight reduction. There was mild PV L and a mean gradient of seven. After this, you can see there's no real leak on the aortogram to start. So this was like the vast majority of our 500 towers a year where they're doing well afterwards. This is the one month or sorry. This is the immediate post op TT E and we always get parasternal lungs obviously and, and TT es in inter procedurally uh and then a full one afterwards so that we can use that at 30 days uh to compare apples to apples mostly. Um But post have we, we had uh as I mentioned, you have 45% mild PB L and the mean gradient of seven, this is the one month echo. I mean gradient was 11 still some mild PV L. You can see it's very difficult to see in the typical views. If you saw an apical five, you'd start to appreciate some subtle A I uh but the symptoms are entirely resolved. So again, at this 0.1 month out, we're, we're uh we're happy, the patient's happy they're doing well, but came back um a year later with recurrence of mild dyspnea on exertion, the main gradient was still pretty similar as 12. They were still mild PB L. This is really all we could see and you can see it posterior here, but really hidden as I'll show you. So we said, you know, it's nothing to do that. The valve looks fine gradients are increasing a little bit. Let's have an interval visit to make sure this isn't halt or some reason that the trans prosthetic valve gradients are increasing. Um but came back four months later, even before that scheduled visit with even worse shortness of breath, almost class three symptoms. At this point, you can start to appreciate a little bit more leak and this severity of symptoms prompted a tee, you can see where that leak is posteriorly. Um, basically between the non and left coronary cusps, the left main is sitting over here, but it's actually a, a decent volume jet even here, it doesn't look all that bad. So the, the question all along was, you know, is this something that really needs to be done? Is this at least moderate A I is this leading to the symptoms? And that was very, very hotly debated, but her symptoms were so pronounced, um that we elected to post dilate this valve to try to eliminate the PV L as I'll show you in a minute, we know that after tver anything more than two plus two plus or more, uh PV L has a significant detriment, almost a two fold increase in mortality in the short term and the long term. And so we are looking for PV L and we do not accept anything more than mild uh as, as you all know in, in taverns. Um This was the planning any time we touch a valve, uh bioprosthetic valve. If you balloon a bioprosthetic valve, the risk of rupturing the leaflets is high. So you have to be prepared for a backup valve and valve. And that planning uh as we've talked about in the past is much more complex, um you can start to appreciate that how these comers splayed and where the calcium pattern was is right where that leak is occurring and this was uh a post dilation done in September of 2022. And this is the te afterwards some mild resolution. Really. We, we left this procedure thinking, you know, uh we're not quite sure that that's, that's what was driving this, but symptoms uh were really prompting us to treat a PV L that we thought was moderate. Um And this was the hemodynamics coming out. So nothing that would suggest uh a significant problem but she did well afterwards. So again, we we uh recycled and repeated the, the exact same process. Her main gradient was six. So it did go down. She had trivial PV L um and her symptoms completely resolved. This was at one month and then she came in last summer with 20 to £30 of fluid on her over die, uh heart failure, a volume overload. Um And uh an ef that had declined um as well, 35% again, had £20 severe lower extremity edema. And because this was hidden in the past, uh we went straight for A T and you can see recurrence of that leak right at 12 o'clock again, this is what's required to plan for these. And so this is the CT reconstruction to plan for a pari league closure. Um This is the evolut valve, this is the location of it. This is a virtual plug that you can create and embed in te recon and plan all your angles, how you're gonna engage the cusps, what size plug you're gonna use? It's quite complex, but it is something that we can do just with the CT scan as part of this work up and evaluation. And then this is the closure technique. There's very little written about these when you have to do them. It's usually quite complex. Um There's not a standard way to do it. I think most people take a glide cath. It's based on how we, we typically treat uh surgical, post surgical PV LS. We'll take a glide cath a little long guide. Um And we'll try to wire that with an 035 stiff angled glide wire and then you cross through it, advance the glide cath and deploy a vascular plug. This is the technique I came up with and we've subsequently treated six patients post uh tab or PB L in similar scenarios. Um using coronary equipment and CTO equipment uh that, that we adopted. And so what I do here is isolate based on that t uh on that CT scan, the leak, you can see it's much more significant when we actually do a cus gram. And then I use an aspiration catheter that we use for stems which has an 038 lumen to aspirate and, and hook up to the vacuum. I wire this with CTO wires which are much more nimble and much more precise than an 035 angled glide catheter. And I can actually use the CTO wires that I use in CTO S the most advanced wire technology that we have. I can use that to cross the defect with smaller wire, maintain wire access because this is an Rx port, this is an Rx delivery, but the aspiration port has an 038 LU and that we can then deploy an A VP for vascular plug through. And so that's what we did in this scenario, you can see the plug straddling both sides here. Uh Deepak and I did uh one of these in an avatar last week. Again, the the total is up to six. But uh these patients actually do phenomenally. Well, afterwards, um the risks obviously are, if you, if the defect is too large, the largest device we have is an A bavp uh four, that's eight millimeters, but this is the pre te and this was the most convincing thing. These are images by Schinder Le, which somehow I've been lucky enough to get in each one of these cases. And he's, he's doing uh abdominal aortic uh flow and and pulse wave. But this was pre you can see the leak there and there it looks a little bit more significant interop we have diastolic flow reversal and this was immediately post closure. So no more leak at all. And you've got immediate change in the diastolic uh flow pattern and the descending aorta. And more importantly, the f improved and has had no symptoms since last summer. So I mentioned this uh T or PV L two or plus more is associated with significant or tid decrement. So you'll see us post dilating, taking repeat aortogram, repeat echoes. It's one of the main reasons that we have echo texts uh that have to be able to put the probe on the chest immediately and get good information for us. So it is awfully difficult from their position. But we're looking at effusions and sort of immediate complications. But one of the biggest parameters of completeness are being done is our trans prosthetic valve gradient, which we try to shoot for less than 10 and nothing more than one plus PV L. Our approach here is not data based um because there is no data on this fact, there's only a few papers that even describe uh techniques on how to close these, but they, they can be fairly common especially late after the fact in self expanding valves. Um And that's the predominant valve pathology that we've seen or the valve subtypes that we've seen has been self expanding valves. If you're within six months, anecdotally, you're probably safe to post dilate. It's enough intraoperatively uh close to the intraoperative period that your risk of tearing the leaflets is left less, but you should have a backup plan for redo ta. These are all done in the uh hybrid operating room, even if we dilate the valve and it's just a typical bav. Uh it's not a typical bav because of the risk of rupture if you're over six months. Um And it is truly paravalvular and there's anatomy such that you have the calcium on either side of the commissary as it got pushed out. Um We should consider PB L closures. Um uh they, they do improve symptoms. And as you can see in this last case, continuing to post dilate doesn't have a durable result when the calcium pattern is what's causing the PV L and the self expanding valve in the first place. And then the last one before questions, uh this will, this will be quick, but this is the extreme end of, of what we do. Um And this is really AAA dramatic case. But one that shows again what, what we have the capabilities of here at Centa with the team approach that we have with taking care of these patients. This is a compassionate use. Uh uh PA case I petitioned the FDA for and had to write letters. There's a tremendous amount of people in the background from administration and research that were involved in getting this through. Uh But this was a 38 year old female that had pretty advanced congenital heart disease, multiple stronomy. And you have a 30% we, we met in the IC U um where she was nearing intubation for hypoxemic respiratory failure. Uh She was not a surgical candidate. Her sts was calculated way above 20% even though she was uh 38. Um she had some mild cognitive things, but she was otherwise very fun. She lived at home with her mom. Uh A lot of the cognitive stuff was related to her congenital heart disease. Um But her primary problem was was uh uh an ascending aorta that was large at 5.8. Um and severe aortic insufficiency. It was leading to a progressive decline in her ef and in this setting, more uh rapid hypoxemic respiratory failure, she has a completely horizontal right sided arch. So you can see the angle of the pig tail here and you can see the size of the sinuses. This is the largest valve that they've ever attempted uh from the Gena valve trial, 0% oversized. But one of the things that's nice about that company and then working here as well is when we have a patient in front of us like this and they don't have an answer. We can, we can use the resources available to us. And GENO Valve, uh That company is actually very, very uh quick to say, let's try to take care of the patient. We have these devices won't be through the trial. They're excluded. But uh they, they're very much in favor of compassionate use cases which helped this patient. Now anatomically and technically, the difficult part here is the horizontal right sided arch. We can't navigate this very Well, Kemp will tell you, we often times have to snare nose cones of the evolut and pull them across the valve because your force when you're pushing the tavern in makes you dive into the scutter uh of the non coronary cusp. And that was the case here. You can see the valve deployment on the left. We actually got a good result, 0% oversized. They were shocked up to that point that we even could deliver the valve and then the immediate result was pretty good. There's a little bit of leak here which had torrential A I before this was an acceptable result. Um But getting the delivery system out is harder than getting the delivery system in, even in a completely horizontal aorta. So our next picture is maybe this is the worst day someone like me or Doctor Kemp or Doctor Talreja can have. Um So this is the valve we're trying to very carefully um push this wire to centralize the nose cone and keep this from scraping on the inner curve and something that's 0% oversized. So it's, it's hanging in there. It needs to heal, it probably will. Here. The driving force is ventricular, but we cannot have anything, anything touch that on the way out. And you can see despite us doing that very carefully navigating with the wires, this is a critical portion for our EPPS. They do this tremendously. Well, there's just as much importance on the back side of the tower, um controlling the wire and centralizing the nose cone uh as there is on the front two positions. And so this is the worst kind of thing that can happen in any valve procedure, especially compassionate use where there's no surgical back up. And so this is what we had immediately afterwards, we snared the GENO valve and pushed it into the root. It's an now watch, this is us putting in an evolut. You can see now just not a snare pushing the valve, lower this horizontal aorta with a 34 evolut. We're having to pull on the snare. We, we actually wire it in the uh descending aorta and bring the entire system up with a snare and we pull on that snare covered by AJ R four on the valve as we advance it across. So this is me and Kemp pushing, pulling together and we're able to get the valve down to the correct position. What we effectively did again is the Gena valve. Now that it's aortic wants to embolize aortic. So it wants to migrate north. The reason we couldn't use the evolut in the first place is because there's no calcification. It wants to drive south, it wants to go to the ventricle. We've got a scenario now where we've got one valve wanting to do one thing on, on one side of the valve and another valve wanting to do another thing on the other side of the valve. So it essentially creates a Chinese finger trap right at the annulus, the cage of the evolut is anchored by the Gena valve which is positioned in the aortic route and that keeps it from migrating further up. And the Gena valve itself uh is holding on to the cage and preventing the evolut from migrating. And this is the immediate post tee image, this girls at home doing incredibly well. Um And so in, in summary, uh most of this is chronic aortic insufficiency that the take homes. Uh here is uh don't necessarily get inundated with uh memorizing flow charts and algorithms and regurg infractions. Uh Although it's important, it's easy to reference if you have a borderline cases, ef is less than 50 or LV dimensions are more than 50. That should be a signal to, to think about referring T is possible if they're not surgical candidates either through an off label approach by using some calcification on the valve to anchor a tab or valve or through a line A R. Um We are planning on starting the intermediate risk phase of that later in the fall. Clinically. If you hear a diastolic murmur and you have wide pulse pressure, that should be a signal to get more data. Even if you don't see on the TT E necessarily a significant leak, start looking for other things. Look for the diastolic flow reversal which may be more subtle. Um Your screening test is visual assessment of the LV outflow tract and how much of that leak is occupying the outflow track. Your specific test is the diastolic flow reversal as you get further away from the aorta. Another take home point here for, for me. Uh and, and from our team to, to the rest of folks is if you see an old valve, our median time to valve and valve reintervention across the country now that we have TVER is eight years. If you get a sa or valve, the median time to reinvention is eight years, the average time of valve durability for a saber. And again, there's a ton of different types, but the average is 13 years. So if you see a valve over 10 years and it's starting to leak, just send to us, they can present more dramatically. The ventricles are not tolerant of the volume and have not been preconditioned to deal with that volume. And a Tara can be a life saving thing even when patients come in and extremists like this. And then TVER PV L is something that we focus on every single day and, and all of our tas and are relentless in trying to improve but can occur after the fact, it's one of the complications in the short and intermediate term for these valves that we do have to deal with. It leads to symptoms and the symptoms can be dramatic. Uh like this lady that had £30 of fluid on her and they can often be subtle missed on TT ES. So if you have a clinical scenario where someone has had a tab or, and they're not getting better uh a year out, they're kind of languishing clinically. They're not expecting the improvement or they improved and are starting to decline the two things to think about. What is their conduction. So do they have a left bundle afterwards? And a and a declining ef do they need uh resynchronization or do they have a hidden PB L? And so if you see Patara patients in the, the after uh period, we stop seeing them after a year. That should be a trigger to get more information. Thank you. I'll take any questions. Published May 21, 2024 Created by Related Presenters Matthew Summers, M.D. Sentara Cardiology Specialists View full profile
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