Chapters Transcript Aortic Valve Disease in Primary Care: What to know, what to do and when to get concerned Dr. Marc Sintek shared an overview of Aortic Valve Disease as it relates to patients presenting to a primary care practice. Uh, Doctor Mark Sentek received his medical degree from the University of Nebraska College of Medicine in Omaha, Nebraska. He then completed his residency in internal medicine, as well as his fellowships in both, or actually all cardiology, interventional cardiology, and structural interventional cardiology at Washington University School of Medicine. Doctor Sente is currently the director of the Adult cardiac catheterization. Laboratory and the Structural Heart Fellowship with the Washy Physicians and sees patients at Barnes Jewish West County Hospital in Cree Court. He specializes in valvular heart disease and complex coronary artery disease, care for patients with rheumatologic conditions, who also. have cardiovascular disease, aortic stenosis, coronary artery disease, angina, mitral regurgitation, and heart failure, coordinary stents, trans catheter valve replacement, and ASD and PFO closure. So thank you so much, Doctor Sente, for coming back again this year to present again, um, on aortic valve disease in primary care. What to know, what to do and when to get concerned. Oh, awesome. Thanks. That was way too lengthy of an introduction for sure. Um, so I, I was just scrolling through the list. I see some familiar names and stuff on there and, and thank you for joining this afternoon and, you know, thank you for, you know, doing all that you guys do as primary care physicians and, and whatnot, I mean. I always joke that It's the best thing in the world when I can say, yeah, you know, I, I just take care of your heart. So, uh, I really appreciate that. Um, please, you know, post questions in the chat, things like that. I, I got about 45 minutes or so, um, and then hopefully we can have some time for questions and, and discussions and, and feel free to ask kind of whatever you want. I do have some disclosures, none of this stuff is really necessarily what I'm talking about today, but I'm a consultant for a lot of device companies. So I thought um we'd start with the case cause I know this is always, you know, when you, especially if you've been on this all afternoon and kind of get your brain going a little bit. So this is a case from a few years ago, um, but I think it's a good one, for the topic today. So 86 year old lady has new onset, you know, shortness of breath and fatigue. She gets tired, you know, doing activities like laundry, going to church, um, doesn't have any chest pain or, you know, dizziness or lightheadedness. Has pretty bad chronic kidney disease with a creatinine clearance of less than 20. And then had intiro BMP that was pretty elevated at 1000. Um, we tested her for frailty, um, by walk, grip strength, other things, and she was pretty frail by all metrics. So I'm certain that you have many patients in your practice that are very similar to to Miss JS, um, 86 years old, having some symptoms, pretty frail, some coin illnesses. So, and we keep that kind of in the back of your mind and we'll kind of touch back on that case as we go through the next 45 minutes or so. But I wanted to really talk about, and we're gonna really, we said aortic valve disease, and I was trying to fit in aortic insufficiency in here, but it, it just didn't seem to fit with the time. Um, and, and truth is, the more common thing when we talk about aortic valve disease is aortic stenosis. So, I really want to talk about maybe the burden and impact of AS and remind you of some of those things that many of you know. Um, I think maybe the thing that may be new for a lot of people or at least to discuss is the different flavors of aortic stenosis, um. And I think this is really important when we start thinking about um treatments and undertreatment and things like that. And then we'll go over a little bit of treatment of aortic stenosis in 2025 and then, oh, you know, as time has gone on, I've compiled some frequently asked questions from different providers regarding aortic valve disease that that might be helpful and then I have time for questions and comments and all kinds of stuff. So, as many of you know, aortic stenosis is a progressive disease. Um, this is a pretty simple figure, but, but the idea is, is that, you know, we grade this based upon the degree of opening, and this is done via echo, um, and this is done, um, we'll go over this a little bit, how we make some of these measurements, but Suffice it to say we have arbitrarily sort of designated these different categories. We have taken a, you know, a disease that is continuous and bended into, you know, into these different categorical variables if you want to think about that, which we do all the time in medicine to help simplify things, but that isn't necessarily always the right way of doing things, and I think we figured that out more and more now that, you know, these are continuous disease processes and as we sort of make these distinctions, maybe it's not always working as we want. Um, as many of you know, uh, the most recent guidelines came out 4 or 5 years ago for valvular heart disease. Those are still the ones that we referenced. When we talk about severe symptomatic aortic stenosis, and this is a very frequent, um, sort of delineation of that of, of, uh, SASS. very symptomatic. You'll see that a lot in literature and things like that. Um, but a VAX greater than 4 m per second on the echo, a valve vary less than 1, or, uh, a mean pressure gradient across the valve of 40. And then again, a big emphasis on evaluated by the heart team. And, and this is sort of the Like, bla, this is the guidelines here, and we want to delve a little bit more into some of these things, uh, as we go through the presentation, but that's, that's sort of the 50,000 ft view of the guidelines. That's sever as you should send them to a heart team. Um, but I think we could do a little bit better than that, particularly this afternoon. So, how prevalent is this? Um, it's prevalent, um, some people say highly prevalent. I think that's sort of as a matter of perspective, um, but certainly there's a lot of it. Um, as the population ages, uh, we're expecting to see more and more of this with, you know, more than 16 million people to have AS by 2050. And then, um, we do think that. There are currently, you know, severe symptomatic AS patients greater than age 65, you know, several million of those. In the middle, uh, is a diagram from, um, uh, worldwide disease, uh, valvular heart disease. Um, and you can see here in the middle pane is calcic aortic valve disease. And certainly, we all know as patients get older, we have a more uh prevalence of this disease. Um, I would just like also to call your attention. We don't have time to talk about this today, but mitral valve disease is much, much more common than aortic valve disease, um, and, and we still haven't addressed that sufficiently either. But, but needless to say, this is a disease of the elderly, um, and, um, it's going to become more prevalent. And of course, you guys know very well that our age greater than 65 population rise is happening and it's gonna happen more and more as time goes on. This is kind of an older slide. Um, but it, it feels as though whenever we normally used to look at these slides, we kind of feel like we're down here in this area, but, um, we're certainly more up in, up in the, the rapid steep incline, and we see this, we're seeing a lot more patients referred for aortic stenosis. But I think the point is, there is gonna be a lot of patients with aortic valve disease coming forward, along with a lot of other conditions as people age. And it it is important to understand how we can deal with this in an efficient process and treat these patients as quickly as possible. So this comes from uh Brumwald's um text. You guys may remember this from medical school. This is really old from You know, the 60s and 70s, and this was looking at, OK, you know, you have AS and as soon as you start having symptoms, then your survival decreases. And this has really been kind of our um paradigm for many years. Uh and there's a difference uh in survival based upon, you know, your symptoms, angina and could be your heart failure. Um, but again, this is relatively old data and believe it or not, this wasn't done in a lot of patients, um, but this, this was revolutionary and then it set the stage for when we should intervene. But I think, you know, we always talk about this because the intervention at the time was heart surgery, and heart surgery has come a long ways and it's still a very valuable therapy for aortic stenosis, but I think maybe this um decision paradigm might change if we have treatments, which we do now, uh, that are lower risk and high survivability. And if you see there's things such as Taver uh represent almost a 99% survivability at one year. And so the question then becomes, do we really need to wait for symptoms in order to treat this, um, or when is the right time to treat it? Uh, and that's uh currently uh an evolving, uh, recommendation and field, and we'll touch on that here in a little bit. But if you have symptoms, and uh I think the really revolutionary thing about Brunwald's is even today, it's associated with a very poor prognosis. Um, and I think this one on the left-hand side, uh, is really sort of eye-opening in that the 5 year survival of patients with severe symptomatic aortic stenosis is abysmal. It's much worse than many of the other cancers that we see on a regular basis, um, and certainly, um, You know, even if you look at 1 or 2 years survival, it's still not very good, um, 50% or so for severe symptomatic aortic stenosis. And so, um, this is a disease that not only causes people to feel bad, but also has a very high mortality. I think the other eye-opening thing is, is that um it's actually the, the mortality of it is also, it's not just severe or not. This gets at that idea of, you know, categorical versus continuous sort of disease process. And as the velocity, you can see here, this is the velocity going across the valve. As it goes up, your mortality goes up too. So, Uh, you know, having an abnormal valve, uh, is associated with, uh, uh, an increased mortality, and it's similar to some of the other diseases that we see. So diabetes, dementia, chronic kidney disease. If you look, you know, having an abnormality of that valve, even though it's not severe, is still associated with something that will happen to them later. And so, we're very keen on finding, you know, diabetes, A1C screening for these things, finding these things and monitoring and treating them, and you guys uh know more about this than I do on. And, and, and you see this every day, but we don't tend to think about aortic valve disease in that same way. We tend to think about it as severe or not, symptoms are not, treat or not. And I think this is a nice look at, it really is a chronic disease that we're looking at, not too dissimilar to some of the other ones that we see on a frequent basis. This came out a couple of years ago. This is a single center evaluation, a very big single center evaluation, and this really opened people's eyes because, although it's a little bit of old data over 17 years, um, it does suggest that we are not necessarily finding the patients that need to be treated. Um, I just showed you that it's associated with a high mortality, but yet the treatment rate is less than 50%. Uh, that's a little, uh, unnerving and um caught people's attention. I think there's some bias to this, and if you look at the date of the study, there that influences it some, but, but the truth is is that this has been reproduced in other areas too, and we are leaving a lot of uh what we call meat on the bone, I guess you might say, or disease out there that we're not treating. And some of it has to do with the different kinds, and this is the flavors, and I'm gonna go over this a little bit, but high gradient, normal EF, high gradient low EF, low gradient normal EF for this sort of paradoxical low flow low gradient AS and then low gradient low EF. And you can see that the rates of treatment vary based upon that. We're really good at this one, the high gradient normal EF. That's the VAX greater than 4, mean gradient greater than 40, Valva less than 1. That's this one. We're pretty good at finding those patients, but all the other groups um give us problems. And I hope today that I can kind of explain these different ones to you guys and see that and bring that to the forefront so that maybe we can work on getting some of these numbers down. Um, I think there has been a large push now amongst many valve programs and nationally to suggest that perhaps we ought to be thinking about referring patients or seeing patients more uh when they're moderate. And again, I think this gets out to the idea of this is a, you know, continuous disease process. But if you, if you look at the data, you can see that on here, what we call a sort of moderate to severe, or this sort of moderate AS is associated with a higher uh incidence of mortality over, over several years. Um, it's not a benign thing, none of them are, but, but you can see, particularly the moderate to severe. And that's where we're getting into this sort of hedging. I'm not sure if it is or not. Those tend to be tracking more with the severe aortic stenosis patients. And importantly, almost 40% of those patients go on to be treated uh in some respects in 4 years' time. So, the, the point is, is if we're seeing any abnormalities with the aortic valve that is other than very mild, that might be a patient that we need to uh treat differently. Um, we haven't quite figured out exactly the perfect sort of maybe paradigm for that, um, but I think it's somebody that we should treat differently. Um, I think many of you may remember Brian Lindman. Um, uh, he was here at our program at WashU for a long time. It's really kind of a thought leader in aortic stenosis, and particularly looking at, you know, the effects it has on the heart with remodeling and things like that. But um, he wrote this editorial uh for some for for that paper I just showed you about the undertreatment, um, and, and was talking a little bit more about, you know, why is this happening and and his thought and desire and I've talked to him about this quite a bit and um he's always such a thoughtful, nice guy, but, but the truth of the matter is he really does think it's a problem, and it's a problem not just of, it's a problem of the system. Uh, looking at how to treat these patients, it's not necessarily a problem of individual people or providers or things like that. It's a system-based problem as many of these things are. And so how can we address some of these deficiencies of finding these patients and seeing these patients and, and they Put out these kind of two states, um, the current state, you know, and I, and I think, you know, when you look at this, this is sort of, if you take a step back, this is maybe an implication of just our healthcare system in general, right? The current state and desired state, but Um, you know, we look at quality, you know, outcomes after we do a procedure, that's the quality that we measure. Um, and then, um, we basically rely on us to look at these tests and make the appropriate recommendation to, you know, usually in your guys' sense maybe a cardiologist, um, and then, you know, what are the results? Oh, you know, we make a phone call to the referring provider and says, hey, everything went great, we did a good job, and then, OK, happy you go about your business. But we could definitely do better than that, right? And that quality is not just about getting the procedure, but quality would be about You know, how are we following these patients beforehand? Are we getting them home after their procedure? You know, all of the things that go with that. Um, we have echoes now. There's no reason why we can't have some sort of automated alert for some of these things and, and get those patients to the right place. And then we really look at the comprehensive management and the outcomes, not just how they did on one sense, but You should know, if I refer this patient to this valve program, what are their outcomes? What do they look like? What are their, what are their quality improvement projects? What are they looking to, you know, improve upon? What's the technology going, all of those things. It's really a systems-based approach and a process-based approach to improving care. And I really think this is something that um you will see more and more of this sort of automated alerts um which I think will be incredibly helpful for bringing some of these subtleties to to top of mind. It doesn't mean we have to react to them, but at least it brings it top of mind, so it's easier to navigate the immense amount of information that we have in our health care system. And then, um, we do get a lot of questions about this. It just came out this past year. This is Early Tavern. Um, we did participate a little bit in this trial, though it was exceedingly difficult to enroll patients. Um, and so what they did is they took about 900 patients and they enrolled them either in clinical surveillance. They had severe AS. Uh, by definition, uh, most of them had high grade and severe as, and then the other part they treated with tabber beforehand. And what they found was pretty shocking and that there was a marked difference in outcomes if they treated those patients with tabber versus clinical surveillance. And um, you know, part of that, a lot of that was driven by um unplanned hospitalizations, um, not necessarily death. Um, the interesting part about it is the stroke. Um, there was a marked difference in stroke, which none of us can really get our brain around why that would have been such a big deal. But I think the thing that was significant of the combined endpoint was the unplanned hospitalizations. And so, uh, this is, you know, a a a a big study to suggest that maybe we don't need to wait until patients have symptoms to have benefit. Now, I started talking to patients about this, and most of the time they don't take that deal, which is why it was hard to enroll patients in this trial, cause if you really don't feel bad and you're doing everything you want to do, most people don't want to sign up for a procedure and to be fair, I mean, we're not perfect and so I always get a little bit nervous about treating asymptomatic patients because, you know, stuff does happen and, you know, I, I, I worry about making them worse. But I do think that you will see in the coming years, stronger and stronger recommendations regarding treatment of aortic stenosis. And, and, and part of this is probably our determination of symptoms is a little too obtuse. And I think once we start seeing more biomarker data. Much more functional testing, things like that incorporated in there, we probably are gonna uncover patients that aren't necessarily asymptomatic, and we're gonna see that benefit in those patients. But early Taver came out this year, uh, and did suggest some benefit, um, and so I'm certain we and you will get some questions about this. So, um, I wanna go back to the flavors of AS for a little bit and specifically talk about, um, you know, what some of these differences are. So again, I told you, um, echo is the standard, um, we do do cardiac cath for some of these cases where it's ambiguous, um, and we're really looking at aortic valve area less than 1 or index to body surface area 0.6. I get asked, well, when do you know the indexing and whatnot. I, nobody knows the answer to that. I, I don't know when. I mean, obviously our patient population in Missouri is a little on the larger side compared to other places, um, so it's always hard to know what to do with the index value. But truth be told, um, the area is a calculated value. It's not what we measure, and I think we measure gradients and flow to infer the area, and that's where we get some of these issues with the flavors of AS. And I think that's where we may be a little bit too prescriptive in our cut points uh for when patients have valve disease or not. So this is the way I like to think about this, so, um, you know. Journey with me here for a minute, anybody knows me knows that I'd like to speak in analogies, and I'm sure sometimes it's obnoxious to people, but, but this is the way I, I think of and explain these things, and this is what we've taught. The residents and house staff, and I think it makes sense. So when, when we have the system, and you think about the fire hydrant or the faucet, or the tap of your house is the heart, the hose is there, and then the valve is here, right? And so, when we look at calculating the area, we have the flow in that we know, we have the velocity and the flow out that we know, and the pressure across there, and we and we sort of calculate this, this area based upon Um, this equation flow in and flow out and pressure gradient. And, and a lot of it is dependent on this diameter that I'm sort of circling here, um, which is a two dimensional representation and it's squared. So it's very easy to throw off the calculation of the area based upon this, right? The things that we're really measuring our velocity and the peak flow across there. And that's what we get. And this is done by sending sound waves off of the red blood cells as they exit. So it's also a technique driven thing. You have to have it at the right angle and things like that, and that can affect it, OK? So when we talk about high grading AS, what, what I think about and what I described to patients is, is the narrow or the valve here is narrow. The same way like if you had a garden hose at your house and you put your finger over the end of it, it squirts out really fast. That's what we see on the echo. We see high pressure gradient, we see high flow across the valve as it goes out. A Vmax greater than 5 m per second is considered very severe stenosis, and those ones we would treat even if you didn't have symptoms currently. But the point is, is that the flow is coming out of here, it's narrowed at the end, it's spraying out. High grade NS, this is very easy to understand. This is the one that we get right the most obvious. So what about the other ones, and this is where it gets a little bit tricky sometimes. So if you think about, if I have my finger over the hose, And the area of that, you know, exit of the hose or the area of this valve that's closed is the same. If I turn down the water, what's gonna happen? What's not gonna squirt out of there is fast, right? You kind of have this trickle of water, but the hole that the water's coming out of is the same as it was on the high gradient one. The amount of obstruction to the flow out of the faucet or my finger over the hose is the same. And so this is the idea behind this low flow, this low stroke volume. If I turn down the flow. I won't get the the blood exiting the the the ventricle as quickly, or the hoses quickly and so the pressure gradient will be low, but the stroke volume and this dimensionless index, which is normalizing kind of the stroke volume to pressure, will still be low. And this is what we always geek out about in cardiology. Uh, this is why we became cardiologists, is that pressure and flow are proportional, and that we really like this sort of relationship and understanding this. But the point of it is, is that if I have a sick heart that doesn't pump blood well, the pressure gradient will be low because the stroke volume will be low across it, right? This is the idea between turning the faucet down. Um, and I think this one's relatively easy to understand, but it gets more challenging when we have a normal pumping heart, a normal sort of, uh, ejection fraction, but we still have low flow. Um, and, and, and this is This is maybe looking more at the hose, um, and then this is where it gets a little bit hard to maybe put this in your mind, but The hardest pumping fine. But the flow out of the heart is not normal, and that could be because this hose is too small. If you think about if I have the faucet turned up, but the hose is very small, the amount of water coming out of that hose is gonna be less, the pressure across it will be less, but the, the hole across my finger will be the same. Um, this is where we get resistance. So we have a high resistance, either hypertension, we have something like that that is impacting the flow and therefore, the pressure is lower across that valve. OK, this is this paradoxical low flow, low gradient. And I'll show you an example of this a little bit more in hemodynamic tracings of what this is, but Um, it's the idea that the flow out of the heart is still low, despite having normal function, OK? And that reduces the amount of flow out of the valve, and we get this sort of low flow state. So this is um kind of what we mean. Um, and so at baseline, you can see there's a gradient of 28. Across this valve, because there is high resistance and there's low flow. In the setting of severe hypertension. And so we can in the cath lab, and these are pressure measurements. So one catheter is in the ventricle and one catheter is in the aorta, the green one is in the ventricle, the other one's in the aorta just to kind of orient you, right? And so there's a higher pressure in the ventricle, a lower pressure in the aorta that's consistent with AS. And as we increase the flow out of the heart, Then we should see a change in that, right? And if we have a fixed aortic stenosis and we increase the flow, we should see the gradient go up or stay the same. If we see that this um is a paradoxical state whereby we have a gradient because the flow is low. Because we have high resistance in series. If we take the resistance out, you will see less. And so this is the idea of reduced resistance, increased flow, and the gradient goes down. You can see we give nitropruide, the gradient comes down. So this is the pseudo severe aortic stenosis. This issue of the valve isn't opening by our measurements because of the flow out of it, but it's not because it's not because it's critically narrowed or because there's something wrong with the valve. Um, we do this not. Often, but uh sometimes and um it, it really does, uh, pretty amazing when you see it, when you increase the flow by giving nitropresside, reducing the resistance, therefore flow is more, you see a less of a gradient across the valve. The opposite is true too. So if we have a baseline gradient of 37, and we give nitropruite and increase the flow, the gradient goes up, or at least stays the same. And you can see here there is no difference. The this is the opposite now the green is the aorta and the purple, the blue is the LV. And so we have seen this, um, and to the point where I'll never forget a couple years ago, this lady had a mean gradient of around 20. Um, had a very small heart and, and had a lot of hypertension. Her blood pressure was like 180 or 190. It was very short of breath. And I gave nitropresside and brought her blood pressure down to like 110, but by giving nitroppresside, which is a very, very potent uh vasodilator, we, we doubled her cardiac output, and I took her, I took her gradient from like that 20 range all the way up to 40 by just increasing the flow. We did a taver on her and she felt like a whole new person, dramatically better, despite starting with a low gradient. And so this is, you know, and, and And my point of suggesting this is not to say that you need to be a master of all this, but it, it, it shows that this is a complicated system of interaction of flow and resistance, and that's probably why we're not always getting those diagnoses on the echo as much as we should. And that's probably why we're seeing that signal of, oh, why are these patients aren't being treated. It's not because people don't want to, it's because it's sometimes More times than not, we're dealing in some of these gray areas of aortic stenosis. We're not dealing with high grade high-flow aortic stenosis. So this comes from um the, the um guidelines, um, and this has been the trend obviously for a lot of disease processes now to assign stages, um, but I do think this is helpful. It's helpful in a lot of things to call attention to things, and I, I, I try to do this as best as we can. In my general cardiology clinic, um, most of the patients we see in our structural clinic are, you know, symptomatic or stage C or D. But the point is, is if we can assign a risk to them, that puts them in a category, and that allows us to track or follow them more. Um, and importantly, This is where a lot of us, including here at WashU and and myself too, would really like to see these patients when they get into the stage B or moderate AS. Um, and, and that's where we want to start establishing this relationship. It may be that we see them once every couple of years or once a year. But I think this is the area where um we can sort through some of these nuances that they have. And I think if we start referring patients that are moderate, we probably are gonna capture more of those patients that are low flow, low grade that may be more severe than what they say on the echocardiogram. But these are the different stages, um, you know, and I think these are helpful to understand. You'll see this reference for papers and and things like that too to understand kind of where people are as far as their symptoms go. Like, for example, Early tavern. I mean, you didn't have stage D, you had C1 patients, um, where their LV and RV remains compensated, um, not C2 patients. Um, we just saw, I just saw a patient an hour ago by cuspid aortic valve, 66 years old, asymptomatic but has LV dysfunction. Um, so I don't really consider that asymptomatic, that's, you know, your LV starting to, to, to become dysfunctional. I think that's a problem and so we recommended treating it. Um, so back to our case. Um, this is our lady. You can see here's our, you know, echocardiogram on the left hand side. Uh, if you haven't seen many of these. This is a very thickened heart. You can see lots of thickening here. Um, as a side note, these are patients that many times we'll see with low flow low grading AS that have cardiac amyloid. Um, so it's something that we screen for on a fairly regular basis. But you can see thickened valve that doesn't open well. If you look here, her mean gradient is 14. And then this is her stroke volume here, which is 19, which is, which is low. So this would put her at sort of, uh, is this severe or not? It looks like it's pretty close. Um, many times when we're sort of equivocal, we'll do a cath and see. And so in this particular case, uh, I did a heart cath and I'll kind of point you up here in this direction here. You can see that the mean gradient. Um, across her valve was, where do I have it, um, was 27, so a little bit higher than our calf, and her valve area was calculated out at 0.6 to 0.89 depending on the cardiac output that we measured, which is consistent with severe S. She also unfortunately had pretty severe coronary artery disease with a severe lesion in her proximal ID and a heavily calcified severe narrowing of her proximal right coronary artery. So, Our little old lady who's having symptoms, who's frail, who has CKD, has severe AS and also has severe two vessel coronary artery disease. Um, and the way that we interpret this to be is that her stroke volume is low because she has severe LVH. Her LV cavity size is small because of that. Therefore, her stroke volume is low in this particular case. OK, so to change gears and talk about treatment a little bit, um, you know, Taver, uh, is approved for age 65 or older and suitable anatomy. Um, patients that are less than 50 should be considered for a mechanical or the Ross procedure. Um, if we have time at the end, I can kind of explain that a little bit, but that's a really nice therapy that, uh, at WaU we have taken a keen interest in over the last several years. Um, but those younger patients, it comes down to this idea of lifetime management, which I'll touch on here in a second. The long term durability of taver is still largely unknown, although the the data that's come out so far shows that it's excellent. And the only way that we're gonna be able to put something on the slide that says it's known is when I'm giving this talk 15 years from now, which that that's just not, I mean, sure, we'll do that when that happens, but that's not really a feasible way to make medical decisions, I don't think. Um, taver in taver is the thing now, um, and that's become a topic that we've discussed a lot, um, you know, doing a tavern, then doing another taver later, uh, again, another unproven strategy. And then we've really focused on the last several years, this idea of lifetime management, and that is, you know, what are we gonna do not just for one time, but other times. If you're 90 years old, I don't think there's much to discuss lifetime management. Maybe even in your 80s, there's not much to discuss lifetime management, but if you're 65 years old, there's a lot to discuss with lifetime management because the expected life, you know, span of those people is much higher, and you probably are gonna have to do something else to your valve later. So does that mean you do surgery in those patients in Taver later? Does that mean you do Tavern now and Taver later? These are all the things that we think about. And the problem here is, and not to get too technical, but I think this is helpful to understand this idea of lifetime management, is that when you put a valve in, it's not necessarily certain that you can put another one in afterwards. So this is a surgical valve. Um, you can see here in the middle, uh, uh, hopefully my pointer is showing up, but you can see here in the middle or on the left hand side, these, these purple circles, that's, that's the valve, the surgical valve or the trans catheter valve that we've modeled or mocked to put inside there. And what you see is, is that these little measurements, that's the distance from our valve that we would put in there in the surgical valve to the coronaries, and also the distance to the aorta. And so, if you look here, here's a picture of it at the bottom, you can see this valve coming up, and the post coming up. And so if I stick a valve in there, I might completely shut off the sinuses and have no blood flow down the coronary arteries. And this is a real problem of coronary artery obstruction when we do a valve in valve procedure, both for taver and in this case, a surgical valve that we put a tavern in later. And so, um, if we knew this up front, we could make better recommendations, and we've just started over the last 4 years, really started to become keen to this and trying to model this and trying to figure out ways in order to set people up for success in the future. Um, this is an example of Tavern Tavern. And the problem with the second valve. You can see here, this is the taver valve that was put in that failed, and you can see how it's just kind of plastered in there, and then over here, there's the sinuses that stick out. Um, the problem, if you look down here, if we put a valve inside there, it pushes the old surgical leaflets up. And so it creates a tube graph, and that tube graph extends up to what we call the neo skirt height or up towards the top here, and that's what this purple line shows. So if my coronary is sitting here, or in this particular case, if I stick a valve in and completely created tube graft from here to here, there will be no flow in those sinuses and no flow in the coronaries. This particular lady, um, we saw, we couldn't treat and she ended up passing away because she wasn't a surgical candidate and there was no treatment for this, unfortunately. The chance of her having an outcome was too high, uh, a bad outcome was too high. So this is a problem that we need to be mindful of when we go forward. Um, to give you kind of another example, this was a, a case that we did. Um, this was a, uh, Medtronic evolute, you can see here, and this is us deploying a Edwards or balloon expandable valve within there, and you can see at the bottom there. And then this is uh us protecting the left coronary because it got so close and you'll see if you watch here in the middle, uh, where my pointer is, you'll see when we inflate this balloon, it pushes this sort of catheter that's in the left main up. If you watch the balloon and everything pushes it up. You see that? And so there is an impingement here, and then afterwards we take a picture and measure and you can see it, it looks OK and it's fine, but everything is very close. We're talking about millimeters there. And so if we don't do some of these steps, we can include that coronary artery and cause major problems. And so this is the stuff that we're trying to figure out and we say, oh yeah, just have a table when you're 65, and then when you're 85, we'll just do another one. If we don't plan for this up front, we could lead to real problems for these patients down the road. And this is an example, 67 year old gentleman. This is what his valve looks like here. It's a tri-leaflet valve, not a bicus, but he's got a little bit of calcium here on the bottom part you can see. And then, um, his mean grading was 60, yeah, for 20%, really bad. But if we model the valve here on the side, what you see is, is that it would look like he would get one valve, and that would be it. You get your one tavern and that's it. Well he's 67, he said, well, I don't want to do that. I would rather have, you know, uh, surgery then. He had surgery, he did great. His LV function perked up. Um, they did a root enlargement for him, so now he could have another valve in there later if need be. So, just kind of in summary, you know, tower valves will fail. We're gonna see that. We do now more trans catheter valve replacements and surgical valves and I've done that for years, and we're gonna see them fail. Younger lower risk patients are more likely to need a second valve, and so we have to be thinking about that when we talk about lifetime management. And sometimes that's why we might recommend surgery over Tavern. Um, there is an issue with coronary access when we put these valves in, and there's been iterations on all of these valves to allow better alignments and easier access to the coronaries. And we traditionally have not planned for the second taver when the first is done, but we do do that, uh, pretty extensively now. So, um, this is our lady to kind of come back to our case. Um, this is the angiogram, you can see here. There's a very severe lesion in our proximal LAD and you can see here a very severe lesion in our proximal right. We have gotten away this, we don't have time to talk about coronary disease treatment in, in Taverb, we've kind of gotten away from doing a lot of coronary artery disease treatment now, but in this particular case, this is a lot of ischemia that she has and so um it, uh, we felt it was important to treat this. Uh, I won't bore you with all the interventional details, but the point is, is we use some of these fancy devices, we put a stent in with IIS. You can see that looks really good here. And in this particular case here, she has a nice stent there. We only use 60 mL of contrast by doing these things, and both of these devices are fairly complicated, but by using intravascular ultrasound, we can use less contrast, so that's not very much at all. And then um in her particular case, we didn't get a CT, we got a 3DTE to size it, and here's that picture. And then here's her valve replacement. We started doing this what we call non-corary isolation technique. Which we use very little contrast, and you can see here this is a pretty classic valve deployment. We pace the heart really quickly as the heart is pacing, we go up slowly on this balloon, and it pushes the old valve aside, and then the new ones in there doing this trick. I'll play it again for you. You can see here pacing, and then the valve goes up. We let the balloon down. Uh, we then close up the groin with some stitches, and this is what you have afterwards, a brand new valve, and this is what you have 2+ years later. You can see here, valve is still working great. You can see her heart is still thick, um, and in this particular case, no leak around the valve and the gradient is still quite low. You may not be able to see it, but it's 4 or 5 across her valve. She felt markedly better after this. Um, and believe it or not, it's still alive and it's still doing reasonably well. I see her every few years, uh, in this, in clinic and things like that. So, um, in the last maybe a couple of minutes, so we have time for questions. Um, I just thought maybe some frequently asked questions, um. And so, you know, I sort of hear this all the time. Should I directly refer to a cardiologist or the heart surgeon? Um, which one should I send it to? Um, and this is a little bit of the old paradigm, right? Is that we used to have our person. So I have my person that I referred to for cardiology, and that person has a surgeon that they like to refer to, and it just kind of goes through that. And that person you may know or talk to or kids play baseball together, or whatever it might be. And that's great. But I do think that having a more, you know, sort of programmatic approach is important, and I think if you refer to a structural heart disease program or a valvular heart disease program, you get both. And I think that's the, the real distinct advantage to it, right? And that's why it's a class one A recommendation, and that's why we're really pushing this is that when we, when we see patients that are treated in this way, via a team approach, their outcomes are better, um, their surgical outcomes are better, their trans catheter outcomes are better, everything seems to be better when we do it that way. Uh, so, taver is only for people who cannot have surgery, right? This is a bit of an old question, but still sort of lingers. Um, that's not really true anymore. We actually for the last several years have done way more trans catheter treatments for aortic valve disease than surgical ones. Both Saver and Taver are important therapies for aortic valve disease for all people. And so I showed you a case of a young guy with low EF. That most people are like, oh, you should definitely not do heart surgery on that guy. Well, he did fine. We've had patients that have been 85 years old, who have had bad taverna you've done great with surgery. So I think it's not necessarily like a hard cut point, it's understanding what is the best therapy for that person and Just a couple minutes ago, I talked to a person and we sort of say the same thing. We'll look at the CT scan, we'll look to see what your anatomy is. If it looks like we can do a good job with Taver, well, that's what we'll do. And if it looks like we're gonna do a bad job with Taver, well, you wouldn't want that, right? And they say, oh no, I don't want that. So then there you go. I mean, that's and that's really how I phrase it and how I how I suggest it to people, and it seems to work out fine. Um, you can't exercise if you have severe. I hear this a lot. We're following patients who have symptoms or they have moderate AS or people like, you'll die if you exercise. That's not true. Um, as a matter of fact, one of the things that we utilize frequently is if patients have severe AS and we don't know if they're having symptoms or they're, they're not, they tell me they're not having symptoms. I make them walk on a treadmill and there's a class 2A indication that you can do that. You can measure the amount of exercise they can do. You can see if they get symptomatic, and then you have a starting point. Let's say I put you on a treadmill, you walk for 8 minutes, that's a lot on a Bruce protocol. Uh, that's great. And then next year you come back and say, I feel OK, but I'm a little bit more tired. We put you on that treadmill again, and now you can only do 4 minutes. That's a problem. Sometimes we'll see their blood pressure drop when we exercise them. That's a problem. And I think what occurred to me several years ago, and this is what I tell patients, um, if you're limiting your activities, So that you're not doing anything. Well then, are you asymptomatic? I don't know. And if we're limiting your activities, then we really should be treating your mouth. For that worried for you to be doing something, then we should treat your mouth. And if we're not worried about your mouth, then you should be able to do whatever you want. Now, some exceptions, um, there was a guy, uh, several years ago that competed in like um decathlons. Uh, and I said, you can't do that. If you want to compete in a decathlon or a strenuous, you know. The activity like that, we need to fix your valve and things like that. But, but outside of that, normal activities, you know, exercise, all those things, people should still continue to do that's not a risk. Um, do you have to take Dap after tab or aspirin and Plavix or tagor and Plavix? No. There's been no proven benefit to Dapp over aspirin only, um, as far as, you know, valve thrombosis or Holt or any of those things. Um, there is also limited benefit to systemic anticoagulation with Doax. Um, and so what we recommend is aspirin 81 mg daily. If someone is taking in a Coumadin or a Doak for Afib or whatnot, I would have them continue that. I would only do aspirin for a few weeks, you know, borrowing from the stent sort of world, and then they should just do their regular um anticoagulation. So if you see patients that are on for Taver, that's not a usual thing anymore, at least with our program, there's probably not much benefit to that, um, that needs to be. What about endocarditis prophylaxis? Yes, I give it to everyone post taver. Um, it's a real problem if someone gets endocarditis when they've had taver for a lot of reasons, but, you know, traditionally we've done it in higher risk surgical patients, so. I give it to everyone, and I tell them to do that, so that would be my recommendation. And then how often do we get echoes post taver? We usually do them yearly. Um, I think you will see this change, but traditionally it's been done yearly, particularly for the first, you know, several years after the valve replacement. So you will see yearly echoes. That's not true for surgical valves. Uh, correct. Uh, can you do Taver for aortic insufficiency? Um, yes, as a matter of fact, that's what we didn't have time to talk about today, but there's two ongoing clinical trials for TaverR with dedicated devices that really work well. You will probably see in the next year or two FDA approval for these devices. The ones that I showed you with the Medtronic or valve and the Edward splint expandable valve, those don't do very well for treating insufficiency. And so we really need these dedicated devices. But if there are patients, send them to us, we can get them in these clinical trials. It really works great and they've done fantastic. We've had really good results. So just to conclude, and then I'll be happy to take some questions, um. AS is common. It's under-recognized and therefore undertreated. Um, and, um, a lot of that is not anyone's fault. It's just related to the complexity of this disease. And I think if we can get in our minds that it's more of a continuous disease, instead of, you know, breaking it up into categorical bends, that might help a little bit. Um, it's deadly, it's, you know, associated with a lot of symptoms. I would, we would really, and I think there's gonna be a big national push, you might see more of this to refer patients with moderate valve disease to a valve center or valve team to follow those patients. Um, and Savr is still around, it's not going anywhere. It's a great tool. Uh, Taver is not the right choice for many patients, and so, um, I think that's the other part of this too. You're not referring the patient for Taver, you're referring the patient for aortic valve management, and sometimes that might mean that saber is the best option. Um, you know, there is never a person that says, oh please, I would love to have surgery. That's never what anyone says. I wouldn't say that either. But similarly, no one ever says, I wanna have a subpar therapy or a crappy therapy. Nobody raises their hand for that one. And so that's what I try to tell people is that we want the best treatment for you, and that can mean a lot of things. It could mean, you know, the person that's Younger, but caring for, you know, their loved one that has dementia, and they say, listen, I just can't have surgery because I can't be out for very long periods of time, then that's fine. The best therapy for that patient is the least invasive, you know, tavern, and then we'll deal with whatever, deal with, uh, later. And so I think there's a lot of nuances to that, but it really is about picking the best therapy for each individual patient, and, and that's really what I think a hard team does for a lot of your patients. Um, I am happy to answer questions. Um. Actually are some questions. Hey, there we go. All right, so, um, early Taver slide showed that death from any cause was nearly incidental between treated and untreated groups, or nearly identical, sorry, between treated and untreated groups. Um, and then after that, in my experience, aortic stenosis, and this is the same provider. In my experience, aortic stenosis always seems to be very well tolerated by patients until it becomes severe, whereas mitral valve disease can seem to deteriorate much more rapidly. Is that a correct observation? Um, so, uh, No. And I can read it again if you want to answer the first one. So I, I think, um, so first of all, regurgitant lesions are always more well tolerated than stenotic lesions. That's true for mitral stenosis, that's true for aoric stenosis, aortic insufficiency, all of those things. Um, and so, um, you know, uh, mitral valve disease is even more complicated than aortic valve disease, and that mitral valve disease is a lot of times a problem of the ventricle, not necessarily of the valve, and You know, maybe one of these times we could, we could cover that too for everybody cause it, it's, it's, it's fascinating and also complicated, um, but, um, I would say that mitral regurgitation is more well tolerated than aortic stenosis. Mitral stenosis, and maybe that's what they're thinking about, um, yeah, that's kind of the same vein as aortic stenosis and that You know that's another one that's a mechanical problem that it doesn't do well. Many times in something like mitral valve disease, particularly mitral regurgitation, they will respond to medical therapy, uh, and that can get better. They will never respond to medical therapy for mitral stenosis or stenosis. So those are ones that require an intervention. Um, to your point of death for many causes is no different, that is correct, um, but please remember, it was not powered specifically for death, it was powered for the combined endpoint of all of these, and so you probably don't have enough power to detect a meaningful difference between death only in the study. So I would caution you on that one, but that's why we haven't been saying. That's why the recommendations haven't changed is that there's this is the beginning of this evidence. This isn't like, if we don't treat everybody with SuS they're gonna die. That's not true. Like I said, I talked to my patients about this, and a lot of them are like, I'm good, doc. I'll just see you in 6 months or 3 months or whatever it is, and that's fine. What I traditionally do is just so, this is my thing and You know, it doesn't mean that's the only way to do it, but when I see somebody for the first time and they're asymptomatic, if they tell me I'm farming, I run 5 miles a day, I'm very active, and I'm not having any symptoms, fine. I don't put them on a treadmill. I check an NTR BMP if that is low, and they're having no symptoms, that's fine. I have them come back and usually 3 to 6 months with a repeat echo and a repeat NTR BMP and a repeat clinic visit. And then I can see the change in time, the progression, to make sure that their LV function isn't getting worse, or that that valve isn't rapidly progressing, or that NTO BMP is not going up as a marker of heart failure and things like that. And then if they're fine at that point, I just usually see them every 6 months with the yearly echo, and every 6 months I do the NT Pro BMP and I talk to them about, are they having symptoms and we go over everything. If people were not sure about the exercise they do, then that's when we put them on the um treadmill and have them exercise and see what they do and use that as a marker. But that's what I do, and I still do that for a lot of patients, even in light of early tavern. I think I hopefully I answered everything. What else you got? OK, so here's one that was in the chat. What is the risk of stroke with Taver? How often do you see problems with artherosclerotic aortic lesions causing embolic stroke? It's a very good question. So the overall incidence of stroke for Tavern in particular our program is under 2%. Um, and that's kind of what it's been nationally. Um, that's clinic, clinically meaningful stroke. Um, if you look at some of the MRI studies and things like that after Taver, I mean, there probably is a lot of incidental, you know, showering of debris and things like that that occur. There have been numerous trials, um, particularly with these baskets that catch things and, um, we're, we're in the process of, you know, trialing two more, uh, because this is a concern, uh, to catch these things, but at least the earlier trials with all this stuff have not shown a benefit in reducing stroke. So it intuitively. You know, you have all this atherosclerosis, you have all these things, you're inflating balloons, you sort of think about shattering of glass and stuff going everywhere. It just doesn't seem like that is happening as much as we think. Um, these newer devices are a lot more effective at catching these things and are covering the whole body, so we'll see what ends up happening with those. But it's under 2%. It really stinks when it happens. Um, it's like my least favorite complication. Uh, when someone has a pretty bad stroke after a taver, uh, and they generally don't do great with that, um, so. Yeah, it would be nice to prevent that even though it's a rare event. Other questions. I am not seeing any other questions at this moment, so, is it OK if I put, I do a follow up email and is it OK if I put your email address on there. Always happy, you know, if you, again, I, I think the point is, is, you know, we're here to a resource if you have questions or things like that, please send them to us. Um, you know, if you have patients that aren't getting what you need or you're having issues, please reach out. I'm happy to try to help as best as I can with that. Um, you know, I, I, I. I think the idea here is to do the best job we can take care of patients and doing it the most efficient way possible. And I know sometimes we don't always do that. So if that's happening, let us know, and, you know, if, if there's things that you need, please let us know. We're always happy to help. Thank you very much Created by Presenters Marc Allen Sintek, MD Associate Professor of MedicineAssociate Director, Adult Cardiac Catheterization LaboratoryDirector, Structural Heart Fellowship View full profile
