 I'm presenting this, I will confess the idea about the way we treat a orders fits this nice CLE, that's our Cleveland thing. Expeditious probably should go first, but I'm gonna be comprehensive here and I'm gonna move fast and really talk about the way I think about the aorta starting from the left and trick or outflow tract and working all the way through it and just share with you some of the things we're doing now and where I think we're gonna go in the near future, I don't claim to look too far along and I think it's dangerous if we try to get too far ahead of ourselves, so I have to use the arrows. Disclosures are shown here, I do work with a lot of companies and I've learned a lot from their research and development teams and I will talk about some off-label and investigational use of devices. I think it's important when we talk about any sort of intervention or any of the things that we practice that we really bring it back to the base of understanding the disease process. Lars Fensen and Renee Rodriguez pointed this out several years ago that the aortic disease and underappreciated epidemic and there's probably more than 40,000 deaths a year that are attributable to aortic disease. And data in other countries, it's this older but real study from the group in Sweden demonstrated increasing prevalence of aortic disease and increasing number of the operations that they do there and it's no surprise that if you look at the volume of cardiothoracic operations that we perform at the Cleveland Clinic last year over 5,000 operations, a fifth of what we do entails the aorta. It is really a critical part of what we do and as I know it is here and has been for many years of course with Dr. Koselli in the room, of course it always will be but it's really a trend that we're seeing across the whole practice, cardiovascular care. We did 1,441 aortic operations last year and even through the pandemic, we saw our volume rise and I think if what happens in Cleveland and Houston is a barometer of what happens in our fields and I think we have to appreciate the fact that in the near future we definitely will be treating the aorta more commonly at the very least. One of the reasons that we've built or the reasons we're seeing more of this is because of the way we've reorganized ourselves in Cleveland. When Toby Cosgrove took over in 2005, he changed the way the whole enterprise is organized from a conventional organization where we had divisions of surgery and medicine to a more radical disease and organ-based institute model and this quote from Toby really I think sort of characterizes the whole culture that we have there. We need to focus on the convenience of patients and families, not just what we do and that's a forward way of thinking of things because things move fast in medicine faster than ever and this busy slide just is a quick snapshot representation of what happens in our aorta center. It's a lot of different groups that come together around an individual patient with disease looking at it in a lot of different ways. We collaborate clinically, we collaborate in research and we collaborate in education and we have these other centers organized around other organ system or disease states like the aortic valve and adult congenital disease where there's a lot of cross pollination between what we do and this organization really fosters collaboration and allows us to do more. When Lars Fenson took over as the institute leader he gave me the job to be the aorta center head and I quickly realized that what we need to do instead of just having one surgeon at the head of everything is we need to create shared team leadership models. So I changed my title from the director to the surgical director and invited a cardiologist and a vascular surgeon to also be directors within the aorta center so we could really foster these ideals that you see on the right side so we can work together as much as possible. And when we did this, we sort of put our heads together and realized that we need to have a master plan of how we're gonna build our aorta center. It started with really focusing on those acute aortic syndrome patients, the patients that need us the most. We are their last resort, they get here, they get plugged into the system oftentimes in that desperate time of need. But if we really wanna treat that disease we need to understand it across the whole spectrum. And so we thought about how we have these different sort of buckets of where the patients come from. And by doing so, we've invited our cardiologist to sort of embrace this early phase of the disease and learn how to screen and find patients when they're in that sort of moderate phase and they can connect with someone on the medical side that can really teach them about, you know what they need to do looking forward the diagnosis of aneurysm or ectasia or dilatation doesn't have to be something scary and dangerous because they have a plan. And we meet people in the advanced stages who maybe had emergency surgery somewhere else and then were left to their devices or never really got good education about what was going on with them. We bring those patients in because of the broad spectrum of excellence that we can provide them. And we screen their family members. And now more than ever, we're actually finding a lot of people with disease in the early phases so we can get them on board because when you have aortic disease it's a problem for your entire life. And so how are we treating the aorta now? We're treating it together. We're like a special forces unit and we have a whole bunch of people with skill sets that tackle these problems at different phases along the way. We know that aortic disease is life-threatening. When we meet an aneurysm, we want to prevent it from becoming a dissection. However, sometimes it's not an aneurysm and it dissects anyway but the really only treatment that we have right now for this problem is prophylactic replacement. We don't have, I mean, we treat hypertension and that's really critical but we don't have medical therapy to stop the progression of degenerative disease of the aorta. You know, like we need to get better with that. I tell my patients all the time. Really the best time to fix your aorta is the day before it ruptures. And that's where we want to be. We want to be that good. We're not even close. But I think if we all work together and we think about this and we invite our cardiology team and our medical team to work with us on solving these problems. We work in the lab, we can do this because ultimately what we need to do is not provide care with average treatment effect. We need to provide care with precise, tailored, shared decision-making where we think about all these different characteristics that go into the decision. The disease specifics, the other comorbidities that the patient brings to us and then look internally at our own surgical experience and results so that we can really center any kind of decision around that specific patient and also appreciating their own preferences for things like avoiding surgery or anti-coagulation. Right now, we still use a model that's based on size and I always show this curve, which, you know, and I've even said it in front of John Elefteriades. I love the work he did, but this isn't really a curve. Any statistician in the audience would tell you, that's just sort of this jiggy little thing. And that's what we use. We decide to intervene around five and a half centimeters or less based on a feel. And it doesn't work because there's a large number of patients who present with acute aortic syndrome way below that threshold. We need to get better. Well, we've tried to figure out how we can do that by using some indexes, trying to sort of tailor it to a patient's body size. There's something that, you know, we refer to as the aortic area to height ratio. Some people call it the Svensson Index, where our Svensson really did this with a small amount of data. And then it's been explored a couple of times with Mace-Ree's written a couple of papers with Malin Desai and have demonstrated that it actually is a pretty good predictor of risk in our patients. At least we can tailor it a little bit to the individual when we're making these decisions. So we don't look at body surface area because people in Cleveland are heavy. They're heavier probably than even in Houston. So weight, gaining weight doesn't reduce your risk. It's the height that matters. And actually, interestingly in this, you can see that when we look at the diameter of the aortic root, the curve has probably shifted left a little bit. So now we're starting to gain an appreciation. It's sort of soft evidence, but we're gaining appreciation that the pattern of aneurysm probably makes a difference. So when the roots more dilated, we also tend to be a little more aggressive about repairing it. And even Dr. Elefteriati's team has looked at this and they've demonstrated in this paper that they also agree that height alone, better the body surface area is a good way to estimate risk. But really the whole idea size based on no disrespect to Sir Laplace, but based on this law of Laplace and wall stress is oversimplified because we're not dealing with man-made tubes. We're dealing with biologic structures and vascular tissue behaves in an anisotropic way. The characteristics of it change along the length of it. It deforms differently under the stresses. It is a very dynamic structure. And the forces upon that aorta also are dependent upon the disease states, not only how the heart functions, how the valve functions in the shape of the valve. You see these really fantastic looking MRI images that demonstrate normal laminar flow and how the stress is on the wall change depending on what type of bicuspid valve the patient has. And on the right, you add stenosis to the mix. It even gets more complicated. So we need to understand these details because what's happening in any individual patient is Sir Scott LaMarina's team can tell you is a whole lot of complex things at a microscopic level that are affected by the forces on the wall of that aorta and what's happening at a microbiologic level. And there's a strong interplay between those two. And we're trying to understand that better. My lab isn't as cool as the one that Scott showed me today, but we have a biomechanics lab and started this, what we call the Matador study, multi-disciplinary study, based on two characteristics and hemodynamics for development of non-hilarid sten grafts. Matador is much better. Where we use the standards of care for our patients with aortic disease, we enroll them prospectively. We do echocardiography as well as our cross-sectional imaging and all the clinical data. We get this specimen out, we test it in the lab, both in uniaxial and biaxial load, and we do a histologic assessment. We're also approved to look at other factors like blood, proteomics, genetics, and the entire thing. And you can see that with our partners from the imaging team and the anesthesiology imaging team, we can gather quite a bit of data, just again, using standard of care at the aortic ultrasound in the operating room in TEE to try and understand what happens to this tissue. And then we take those segments of the aortic tissue directly from the location where we've imaged it and we put it through load testing. And this is sort of the protocol we developed for tissue harvest. So this is a patient of mine with a root aneurysm. And I'm careful when I excise this aorta to keep it all intact. It takes a couple of extra minutes instead of just slicing it down the middle. I'm trying to take it out as a tube. And here you can see I'm taking out the non-pornary sinus down along the right side of this patient. So we maintain that within the specimen. This is a patient who's going to get a valve-sparing root replacement. About half of the patients in our protocol have bicuspid valves and about 15% have known connected tissue disorder, or genetic issues that are known, that are mapped. And then we take the specimen. I showed you some of the uniaxial load, but then we put these specimens on the different lengths of the aorta. You can see a couple of those specimens in the image in the corner. And we do this biaxial load testing where we look at speckle displacement. And this way we can gather a lot of information about tissue stress and strain from this experience. And then we look to correlate it with our clinical factors and we look to correlate it with the other information. And some of the things that we've learned is that the age and sort of the region of the aorta that's involved has a much bigger predictor of how much elastic energy is maintained in that structure. So again, lend some credence to our idea that a root aneurysm maybe is worse than an aneurysm along a different length of that zone zero. And also I think a little bit differently when I see an older patient with an aneurysm then I do a younger one because I know they don't have the same elastin structure in their aortic wall. They might be at risk for failure a little bit sooner. So I may be more aggressive about it. And we're certainly learning every day that thoracic aortic disease is familial. Not only these clinical syndromes that we've known about for a while because these patients look different on the outside, but a whole bunch of these other genetically triggered associations that we're just starting to learn about really quickly. 10 years ago, if I wanted to do a genetic screen and maybe screen for three or four or five, now like an inventory panel is up to 37 genetic abnormalities. And yet only about 20% of families where we know it runs in the family do we identify the gene. So there's a bunch of variants of unknown significance we're learning about every day. The hope is that in the next decade or so we'll be able to tell a specific individual patient what their genetic make up is. Maybe we'll do something like wrapping their aorta like this Paris procedure with a robotic approach. I'm not gonna go too far on that discussion. We're not there yet, but we're gonna give them a better understanding of the genetics of what's going on with them. The pathophysiology that makes that connection between their extracellular matrix and their smooth muscle cells. And hopefully we're gonna discover some therapeutic targets. So maybe we can treat them with medical therapy before they need to go to the operating room with us. One of the things that we've learned is some discovery in our lab. We did mass spectroscopy to try to describe what's in that space where you see this degeneration. And we identified massive amounts of something called agri-can and Versa-can in the thoracic aorticanders and dissections and no one had ever defined that before. Agri-cans really common. They study it in cartilage and orthopedics forever. So there's simple assays that are out there that nobody uses because it's not that important for the cartilage. But we found was really interesting and we validated a data this in a mouse model where there was also some reduced Adam T.S. activity. The point is that there's probably many, many, many diseases that all filter down to this common fate of an aneurysm and dissection. Aneurysm and dissection are probably not unique disease states as much as they are complications of things that we're learning more about the causes of. And as we become more knowledgeable about it, we'll be able to tailor our therapy for patients. We certainly, again, going back to this idea that Laplace law of Laplace isn't so good. We actually found that thicker tissue did worse, had worse biomechanics than thinner tissue. So Laplace is kind of out of the water yet we're still using size. But maybe what we learned in some of this experience will help us create other ways to diagnose our patients. This group in Germany took our experience, I put it in the red box as they quoted our paper about the massive agri-can collection in that study that we wrote, and they actually used those commercially available assays and found that agri-can might be a new biomarker for acute type A aortic dissection in a small series of patients. We're looking at this in our own lab and we're trying to understand if we can maybe understand this better. It might really help us in the ICU. You've got someone that comes in with an IMH and you're wondering how important it is to treat it. Potentially you could use a biomarker to guide you. So when will we be treating they or in the near future? Definitely more sooner along the path of disease and more precisely to every individual. But for now, the treatment still is complex repair and reconstruction. I'm a surgeon, I'm gonna start talking about surgeon for a little bit this afternoon. We know that the more disease is involved in the aorta, the more complex the repair is, and then you add aortic dissection to the mix and it adds a whole nother level of complexity with what you deliver. We're able to still do this really well with our team. This is data from just this last year. Our ODE ratio is a third, it consistently has been and it's because we have this multidisciplinary team where we provide a lot of different modes of therapy. Acenaeortic replacement is still sort of the gold standard for acenaeortic disease. We've demonstrated before that we can do that well, even in multi-component operations and the paper on the right, we matched a bunch of patients undergoing cardiac plus aortic surgery with patients undergoing just cardiac surgery and found that you can add an acenaeortic replacement without any added risk in most of those patients. And so we're pretty aggressive about treating that aorta. And we'll do it minimally and basically as long as we think we can provide that same kind of outcome in this series where we demonstrated that we're able to do a lot of things including root replacement and acening plus valve or even hemiarchs through those many incisions and that still represents a portion of what we do. But we need to also understand that a lot of proximal aortic disease that involves the acening aorta also may involve the aortic root. And in fact, the bulk of the proximal aortic surgery that we're doing these days does involve the aortic root. It's typically for kind of operations that will do a mechanical and biological, dental procedure, homeograph or some form of valve-preserving root replacement. Most commonly is a re-implantation procedure. And it's important in an aortic center that you do it well. And I tell residents and fellows in training all the time no matter where you go, aortic root replacement can't be some sort of select operation. Everybody needs to know how to do this nowadays because that's what we're treating with surgery. Aortic valve disease is going towards TAVR. Aortic root disease needs to be really appreciated and it needs to be done really safely. This study from a few years ago showed that 25% of these operations on the aortic root or involving the ABR and the acening aorta were done at 3% of centers. I think we need to centralize this kind of care because you could see that volume had a big impact on outcomes going from a low volume center less than six of these cases a year to a high volume center greater than 30 cases a year. And that's not much volume for, you know a guy from Cleveland and talking to a group in Houston that cuts the mortality in half. At our center, we did over 500 room replacements and you can see kind of a good spread across the bentos, homographs, valve spring roots and we've gotten into doing some ROS procedures in young adults again over the last few years. It's not really for root disease but it is a root replacement operation and for elective operations their outcomes are excellent for emergencies. Now there's still emergencies but that represents a large volume of what happens in the country and compares I think excellent compared to the STS database and I do that maybe cause, you know Lars said I should come down here and brag about how we do but more so because I think it's important we understand how well we can do. These are should be our goals. Elective aortic root surgery should be the same kind of outcomes we strive for with isolated valve replacement needs to be done really safely because a lot of the patients that we see are patients with bicuspid valves, they're young. We see in this machine learning we kind of confirm what's sort of been known that a large proportion of patients bicuspid valve disease have root aneurysms that are often young and we need to provide good solutions to these patients because surgery is what they need and catheter advice is not gonna be it. Certainly a catheter device is never gonna fit well into a valve that looks like this, this severely diseased bicuspid valves or one like this that was repaired 18 years earlier I could hardly find the orifice in this thing I don't know how the patient tolerated eventually I scraped away some calcium and there was that little tiny hole in that valve but patients can tolerate a lot but they're not gonna do well over a tabber this patient needs a real operation. And then what do you do with a patient like this? This 40 year old who comes in with a bicuspid aortic valve, severe AI and AS mixed valve disease is common in these younger unicuspid type kind of valve patients and that aorta is dilated clear the ascending needs to be replaced it's over five centimeters but the roots that 4.2 by 4.4 ish kind of thing I don't know, do we replace that? Do we leave it alone? We might have to come back for it now that we have a trans catheter valves as an option we need to understand that even if the patient chooses a biologic prosthesis they might not wanna come back and just have another valve replaced when the bioprosthesis wears out they might wanna have tabbers so we have to think differently about how we managed to say aorta. We saw this data from Toronto that says certainly if you encounter an aorta that's greater than four and a half centimeters you should replace it but what do you do with the ones that are between four and four and a half? We don't have the data, we don't know. The same group from Toronto also told us that it doesn't need to be replaced when you replace bicuspid or tricuspid aortic valve it disagreed with them and let's look at their data and maybe explain why. You can see that their follow up was only, the mean imaging follow up time was only five and a half years you see the blue arrow down there but the patients who did fail and eventually needed to come back they all had that failure happen after about the eight year mark. This is true of almost everything we study in cardiovascular medicine we're getting so good at taking care of all these mechanical problems it's okay for data to share with the FDA to get something approved with five year outcome data but it's not really good enough for us to really understand the fate of what we're doing by following only five or 10 years. Our patients are living into that second decade and more and more surgical patients are young and we expect them to live into that second decade we need data to really understand what's happening in that second decade of follow up and so I would disagree with these guys I think that these patients are gonna come back or at least the significant portion are gonna come back with aortic disease later on we need a better way to determine how to do it maybe it's just imaging the aortic wall with some tool that Dr. Lamar is gonna provide us with to get an understanding of what their future is gonna look like or maybe it's just knowing we can do it safely and being more aggressive about it. Here's a patient that Toby Cosgrove operated on in 2002 he replaced the patient's aortic valve and left one of those kind of smallest roots alone and did it through a mini and it was great a mechanical valve the guy was doing fine. 17 years later he had this five and a half centimeter of aorta so we re-operated on it and we replaced his aorta should it have been done at the same time? I don't know it was a mechanical valve. This is a 46 year old who had an AVR in 2004 then came back eight years later now 55 years old had a moderately dilated aortic root that was left alone and replaced at a nearby hospital with a stentive prosthesis and thinking that that aortic root would be okay and then I saw the patient just about five years later and the root looks like this now 55 millimeters. So I think we have to appreciate that the size it's not a great predictor we have to look at that tissue probably a lot better and really appreciate the fact that the root will also grow and a lot of these patients are gonna live 10 or 20 years after an AVR. So that guy that I showed you earlier the 40 year old with the bicuspid valve and the small root, I replaced this guy's root he was bipolar and there was no way he was gonna take any coagulation when I got in there you can see down on the bottom right certainly half of this aortic root looked really thin walled I didn't trust it so I went ahead and did a lot of that on him. I think that's the right choice we'll see what happens down the road if it gets infected we have to re-operate on it's gonna be a little bit more difficult I suppose but we have to think about the choices as being informed choices that we should do with our patients and appreciate the fact that most patients don't want mechanical valve and a coagulation most of them want a minimally invasive approach. And if we can save that living valve and a lot of this root disease and get better at that then we'll be even better at providing what our patients need and providing some long-term solutions. So Lars Fenson taught me about this sort of class schema as the way to think about aortic valve function it's not just the cusps or it's really the commissures the leaflets, the annulus, the sinuses and the sinus tubular junction that all play an interactive role in the way that aortic valve functions. You see that cool 40 CT scan you can see how the LVOT expands in that patient as well as the other changes in the aorta when that valve opens and closes. And we know how to do these operations. We've demonstrated certainly in patients with connective tissue disorders like Marfan syndrome that those repairs can be done really safely and they're very durable. And as we've gained experience with that our number of these operations performed has grown exponentially over the last 20 years where we now kind of appreciate the fact that while when I look at somebody like this 21 year old with really severe AI and a tricuspid aortic valve and a dilated left ventricle and I want to save his valve if I'm going to do a repair I got to do more than just something to the cusps of that valve I've got to address that dilated annulus even though he doesn't have a typical root aneurysm he's got really severe annular aortic contagion. And in this guy when we got in there that the sinuses weren't normal as well. And so we did a David re-implantation procedure in him even though it wasn't a typical patient that's part of the reason why the volume has increased. But you can see now I feel confident that we've stabilized that entire root and hopefully this repair will be as durable as possible for this young man. And then we've also expanded this sort of knowledge about how the root all interacts and has allowed us to use this operation expanded to patients with bicuspid valves that we want to save. So this is the typical way that I will do one of these operations in someone with a root phenotype aorticopathy and a severely leaking bicuspid aortic valve. We debride this fibrosis across this con joint cusp and clean that up. And you can see that there's a lot of good healthy valve tissue. And just to look at it, we see that eventually we can get that to come together in a nice way. That's a 30 millimeter hangar dilator just demonstrating this patient does have that annular aortic aphasia upper lumbar normals only 25. If we just did a leaflet repair that patient would be in trouble. This patient also had a dilated root. So we do this re-implantation procedure by securing that annulus with these interrupted sutures underneath after we've dissected everything out around that aortic root. And then I kind of can make a couple additional markings on my graph because I want to resuspend these two good commensures in this patient in 180 degree orientation so we can get real symmetry between this two bicuspid leaflets. And I spend a little bit of time sort of making sure that I'm going to be happy with how this thing looks. And then when we put those stitches under the annulus I'll often put more stitches in those patients as well to secure it more. And then we re-implant this valving and see when we're sewing this commissure in it's at that purple line kind of in between the two black marks because we want to get those posts lined up 180 degrees. And then after I get the valve re-implanted into this new root then we go ahead and do the cusp repair. And so we'll take that con joint cusp which has got that long free edge and we'll go ahead and pli-kate that valve and we'll close that with a running suture so that we have equal edges to those two cusps and I'll often carry that closure across the belly of that valve as well so that it doesn't prolapse or balloon out into left ventricular alfotrack and we get something that looks like this. And we've had good results with this of course they don't necessarily last as long as a normal tricuspid aortic valve but they seem to be pretty good option for a young patient with a living valve that we can keep it. And we've even used some of these principles about stabilizing that entire root to how we apply the ROS operation in adults. So some of our ROS patients might have a moderately dilated aortic annulus if it's really dilated we don't push it but a moderately dilated annulus we want to secure that and I'll put an annuloplasty band this is a mitral annuloplasty band around that ROS procedure to help stabilize that. And then we've also learned something else as we've looked closer at the imaging and the anatomy here here's a 29 year old with one of these root phenotype aneurysms is dilated annulus and learning what we've learned from the imaging aspects of looking at the mitral valve we've recognized what I call aortic annular disjunction. So we've heard about mitral annular disjunction or dislocation and we've recognized this process in our aortic patients and we have paper coming out soon about this but I've also developed a way to address this. So you can see in this video this patient with a bicuspid valve as you see the insertion of where the cusp is is really deep inside the lip ventricle and where the aorta and the ventricle come together is separated from that. So there's this aorta annular disjunction and we repair this by first bringing those two things together with a mattress suture that we run along the areas where there is that broad separation between the insertion of the cusp and the level of the aorta ventricular junction. And by doing that, we lift that leaflet that valve up into a more even plane and then we can go ahead and proceed with our re-implantation procedure, get the valve re-implanted. And when we do so, it comes on plane. You can see there's an application but you don't have the belly of that cusp that inserts really low in the ventricle falling sort of deep under the repair or having to put those sub annular sutures in some way where you're intruding in the right ventricle. This is a post operative assessment of this patient. We've got a few of these where we've been able to now recognize that sort of issue beforehand on the imaging. And then of course, there's some people that are the annulus just too darn big. This guy with a 41 millimeter annulus just needs a thing replaced. I don't think anything's gonna be durable in that situation. To spread all these attempts to do prophylactic repair, we still see patients who come in with a new dissection even after we've replaced their ascending aorta or that dissect at small sizes when we don't expect it. And a fifth of the aortic operations we do still our emergencies. Some of them are even in patients that we've been following. So, you know, as I said, we're falling short, but we know how to take care of them in these emergency situations. We've seen both in US and UK data that the more experience you have, the better you are at taking care of a patient in an emergency. We've demonstrated this with our own data. You see it next to IRAD with our multidisciplinary team. We've been able to keep the mortality from dissections in the single digits pretty much across the board, whether it's type A's or type B's and whether we're operating on them for type B's or not. And we've learned from that IRAD data that there's a multiple phases of hazard. So we're understanding aortic dissection a little bit better during the hyperacute phase. We get that information now sent to us as a page on our phone. There's an epic connection. One of our cardiovascular imaging specialists will get those images piped over, reviewed, and I can look at it on my phone while I'm laying in bed in the middle of the night if I have to before I go in to determine what my strategy is going to be like so we can mobilize our whole team so that when that patient arrives, we have a very good idea about what we're going to do and everybody's ready on the spot with all the different technology we need, whether it's a hybrid technique, a device, a RAD tech or just to even keep the anesthesia team up to speed and what they're dealing with. The typical repair is a conventional limited reconstruction and we still do a lot of these, certainly for Debakey type twos we do this. For a lot of Debakey type ones, we're doing more extended repairs now because we've learned that presentation predicts mortality. Certainly with really severe ischemia, the mortality is a lot higher, but even with imaging ischemia, those patients are at risk. And this unpublished data on the right shows that when we do an extended repair using a frozen elephant-type technique, which I'm going to show you in a minute how we do it, we've actually reduced kidney injury in these patients because we're getting their true lumen perfused better downstream. We know that a patent false lumen downstream from a repair is predictive of survival and also predict predictive of the need of late re-operation. And so I asked the question, is it enough to fix the ace in the aorta in 2022? Certainly it is if you're saving that patient's life, but if we can do more without compromising any of that early mortality, it sure would be nice. And so we've worked on that and I think there's some new technologies coming out. Dr. Kassellian is the national PI for the device you see in the middle. And I think we're going to hear probably at the ATS that it's going to get launched as a commercially available frozen elephant trunk device. I mean, there are some other devices that have been available in Europe and some graphs that reduce the number of anastomosis. But the problem with all of these devices and their current iterations is that they still require a lot of reconstruction. In an emergency situation, that's a lot to ask of anybody, even the most experienced surgeons. So there's been limited adoption of these techniques. In our center, using commercially available devices that have been modified in a bunch of different ways over the last really 12, 13 years or so, I've been working on changing and improving and evolving this procedure to what we do now is called a B-SAPER, a branched stent and an anastomosis frozen elephant trunk repair. And it's come to a point where that operation is pretty much standardized amongst our team. And we've got at least nine different surgeons that do this operation and it represents about 70 to 80% of the debakie type one repairs that we do in our center. As such, when I published this story of the evolution of this and there's only a handful of patients in that paper that actually got to B-SAPER in March of 2018. And again, it represents a large number of what we do over 130 elephant trunks. Just a little bit after that, maybe about six weeks after that I got this real nice email from the FDA. And they said, you know, we appreciate you looking at this a little bit closer because you're modifying a class three device that you're manufacturing. Well, it's not quite fair because it's still an open operation that we're doing but I got their point and I had talked to them about it and in many times different situations but it came pretty clear that we had to move along this path of developing a physician-sponsored IDE. And that's what we did and it took a couple of years for me to sort of put it together because this physician-sponsored IDE is not just to get something approved for industry where you can have very tight exclusion criteria. It's to study this procedure that we're doing and this device and I wanted it to be as inclusive as possible. So we developed an algorithm where we have sort of three groups of diverse groups of patients, those with aneurysms, those with acute dissections and then within those with aneurysms with or without chronic dissection and then some congenital patients. And it's a diverse group of procedures you can see sometimes we put multiple stents sometimes we'll do multiple and SMOs these but in all of these we're modifying a stent graph when we put it in the patient. And we shared some of this early data we had with the FDA and then on December 31st, 2020 we got approval for the FDA to proceed with this PS IDE. And after putting a few other things together like getting my team together around this and gathering a bunch of my co-surgeon investigators we started rolling in the middle of last year, May 27th, 2022. I'm sorry, that's 2021. We're not at May 27th, 2022 yet. May 27th, 2021, but in several months we've enrolled it was 81 as of March 10th I think we're up to 90 patients now. And you can see we've done them in all these sort of different iterations where we're always using a stent graph in a branch into typically the less of clavian artery but sometimes the carotid or otherwise. And we've had pretty good results in these first annual report analysis the acute mortality was less than 6% stroke rate was less than 10%. Some of these patients went on to have a second stage repair we've had no spinal cord injuries. And the circa rest time has consistently been under 45 minutes for these patients, the average is about 30. In parallel, we developed a device so we don't have to modify a class three device on the table and I was able to do this internally with the assistance of our innovation team. I'm sure that, you know, Billy Cohen was here he probably find a way to have developed this faster and I did, but I did have a good team we went pretty far along we went through multiple prototype designs and then we've got a business partner from industry used to be cryo life is now our TV on is working with us to develop this device. Hopefully we'll have first in man early feasibility studies last summer we did the animal studies I think I was the first person to do arch replacements in sheep that almost killed me but what you can see the fluoroscopic images of that device in a sheep's arch and that proceeded along well and so hopefully we'll keep moving forward with that. And that was all done sort of in this spirit of what I've been really fortunate to be in the right place at the right time at the Cleveland Clinic and with my good friend Roy Greenberg I was looking for I wish I had that picture that Joe shows Roy where the two of them are giving each other a piggyback ride in China, it's a good image but Roy sort of taught me about always finding a better way to do things. We certainly all pay a lot of attention to the great work that's done here and the complex treatment of thoracolabdominal in order to handle this disease and we know that that one will never be duplicated but we follow your lead to make sure that we can do as well as we can when we do these open operations but Roy was able to find another way to take care of patients because you have to be really select when you do thoracolabdominal disease take care of some of these patients who didn't have great options and develop this technology, this branch technology which first started as sort of marrying a branch into an aortic device, something like this and then design these helical branches that come off of it and now there's these devices that have multiple of these branches built in them and now there's a lot of these different devices available from industry partners and a lot of teams out there have physician-sponsored IDEs where they're studying this and this branch endographed technology which certainly plays a role for a subset of patients who aren't great candidates for open surgery has been important but it's also led to the development of a bunch of other technologies there's now this imaging programs that automate the sizing in these devices there's imaging programs that limit the amount of radiation and contrast exposure both to the patient and the operators which is really critical to overall safety and it's also expanded this idea of putting endovascular devices in the more proximal order so we see a lot of these arch branch devices now available that have two or even three branches for treating the aorta and we're involved with several of these trials they've not progressed along super fast because stroke has been a real difficult problem to avoid no matter how you handle it with even these endovascular technologies but what we've learned from that has allowed us to come up with some other innovative approaches and this guy who was on oxygen had this horrible looking aneurysm after someone did a really limited ascending replacement for his acute dissection we de-branched him by making incision in the base of his neck at the top of his manubrium we put all of his head vessels coming off of his very large left of common carotid artery and I thought I was gonna get a branch device for him then the pandemic hit so we sat around trying to figure out what we were gonna do and we decided well, we're just gonna cover that arch with this device and I know this is gonna look really freaky this next image because there's actually no flow going off any branch vessels on this angiogram but we have a pump so we had him on axillary fem bypass that perfuses brain and then I went ahead and punctured his left common carotid artery with a spinal needle and you can see it's sort of pushing on the device and then sort of popping through there and that allowed us to get a wire across that and kind of on the table incite to creation of a branch device for this gentleman we're able to give him a branch device and it's worked really well and I just saw him recently for his one year follow up his lung disease is still horrible what hasn't progressed too bad and we're able to get him through this with this repair and that giant aneurysm is no longer an issue for him so I think we'll kind of continue to see this technology develop we certainly have seen it address some of the unmet need in the ascending award I showed you this curve before but there's these people that are turned down for type A dissections that we studied a few years ago and realized that even in our center where we thought we were aggressive with everything represented about 8% of the acute dissections that we saw they're older most of them weren't prohibitive risk like a person with dementia from a nursing home most of them they just didn't look good when they came in and we were comfortable operating on them but they were in their 80s but maybe they were pretty functional last summer cutting the grass and doing things and if we had an ascending device to treat them we could probably get them through it and we've done this in other situations where we've been desperate for a mechanical solution for a complex problem I have personal experience of over 70 of these T-VAR procedures and we learned a lot of details about what the challenges are from that experience like this guy, this 91-year-old who had a TAVR you can see his TAVR device sitting down there after the TAVR they realized he had this horrible dissection from the procedure his brain was being now perfused they quickly intubated him and called me and then I came in and put a commercially available stent graft in the guy and I thought we had a pretty good seal but realized that we had a ton of AI and I was like, oh man we gotta get that device off the valve so I did this, watch it, here it comes so we pulled the device back with a balloon by letting the heart eject against it and then the AI went away, which is cool but we really need a device that we can be coaxial at the sinus tubular junction with fortunately in this guy I kind of knew this time don't push it so far in and we were able to get this device second device deployed and get his ascending aorta treated and then we had to put some bare stents in his downstream aorta and he did really good I've seen him also a year later the guy looks fantastic and his valves working well, thank God but we thought that this idea of treating the ascending aorta with stent graft really have to think about this zone zero as being way more complex than just sort of zone nebulous zone zero and we've described sort of the difference between zero A, B and C and really need to sort of think about this short segment of the aorta as being really complex if we're gonna develop devices for it we need to understand the nuances of it and I showed you, we'd been looking at the tissue but we also need to know clinically it's important as well the person on the upper right that had this little pseudoanderism that we could sneak a device above some coronary bypass and seal it off is gonna do great based on the bottom right that has a tab or a bunch of other stuff going on we put a bunch of hardware in there they survived that but I don't know how long that's gonna last the cool thing is we got industry partners now that realized there was a place for this technology the gore device, this ASG arise study we enrolled 19 patients in this early feasibility study and this is a device that's steerable so not only do we get it into the ascending aorta and partially deploy it which allows us the ability to mobilize and position it a little bit better after that partial deployment and you can see that sort of on the angiographic image as well we can then go ahead and shape the device so by turning that dial that you see on the bottom right we're turning and shaping and shortening the lesser curve of that device so we can pull the edge away from the left main coronary artery and really get this thing lined up super precisely along the sign of tubular junction for these patients before we fully completely expand it as you see in the images here there's a fluoroscopy image and it pops open completely we do that typically with rapid ventricular pacing and there's an option to then again dial it and scoot it up a little bit more if we find on the angiography it's still too close so we can get precise within a millimeter or two all the coronary arteries of this device and we've had good experience with it so far we're gonna see a pivotal trial coming out and we're learning how this technology interacts with the disease like this is the one case where I thought we had a great result but on the early post op CT you see some flow still there in the false lumen but six months later they're totally resorbed and that's like a real nice 3D image of how we treated that the Bakey type II dissection in this 80 year old lady that was on dialysis but still pretty functional that did great one home after a couple of days this whole idea that of course opens the eyes to the world of maybe adding it to TAVR and doing endo-ventals amazingly this was done in 2020 by this group down in Brazil they were really smart about how they did this to treat this really unique complex patient that they came up with this device for and it worked they spent hours doing it I don't think we're gonna see a lot of this yet because there's a lot of issues to address we have to remember that TAVR valves still have a little bit of leak around them even in the best situation and that's a bad endo-leak if we're treating an aneurysm but and select patients we might see these technologies married together in the future certainly we think about ascending stent graft as part of our treatment paradigm for acute proximal aortic dissection you can see it's not just OR or nothing now we think about whether we have an endo solution if we don't have a broader open solution and we have a much lower threshold to extend the repair with these be safer procedure in our patients we've also learned a couple other things and I'm gonna go kind of fast through these last few slides for the interest of time but I think we have to appreciate that we need lifelong care for these people it used to be again I was talking earlier about this incomplete follow-up we operate on them we hope that like they're gonna do okay now in Stanley Crawford knew at a long time ago these people shouldn't be considered cured of their disease when they have an aortic dissection now we've developed clinics where cardiologists faster surgeons, cardiac surgeons we all see these people we invite them back we all see them we all kind of educate them with our different perspectives about what to do they'll often see multiple of us at one of those visits and the patients welcome that because their doctors at home are scared of aortic disease and what we've seen and this is old data but it's significantly increased the number of office visits so it's good for the business of our cardio aortic cardiology specialists it's a great area to specialize in so these patients will keep coming back to you and they're very grateful our outcomes are a little less than ideal when we get these people through the acute phase the average age is 59 and three or survival 60% that's not nearly good enough so we've been a little more aggressive about treating type B's with T-VAR sooner knowing even knowing that this repairs are incomplete but we developed a whole bunch of these other strategies to try and address these chronic dissections some of them are shown on this slide there's this new technology with some bare stenting to optimize flow and the true lumen and with new problems we find new solutions so we are doing more open repairs in patients that have a previous T-VAR than ever it's about half of our thoracodominals have a T-VAR in place this graft on the right I call it the Roselli-Coselli because the team helped me add a cuff to the Dr. Caselli graft that we use all the time for thoracodominals and all the nurses call it the Roselli-Coselli but anyway we're going to get that soon and this is kind of what we do for a patient this patient had a thoraflex device then came back had a T-VAR and then an open thoracodominal repair we left the iliacs alone because it was kind of a mess down there and then my partner from Vascular Surgery put one of these branch graft devices in and we got this whole aorta treated in multiple stages and got this patient through it safely and this is the kind of crazy schema we have when we see a chronic dissection lots of options so we need lots of people to come together to make these decisions about what to do for our patients because we're going to see more survivors that need late treatment especially after dissection they do better with earlier proactive treatment we know that endovascular solutions can be safe and expand treatment options but we have to understand they have a complementary role to open and hybrid repair we're going to continue to get better devices and we need to understand the natural history of this disease and the causes of it and hopefully in the future when we're treating aortic disease we'll be doing it both collaboratively and more precisely thank you very much