Okay, good morning. I'm Ryan Weispfenning, Vice President and Head of Medtronic Investor Relations. Thanks for joining us for our Structural Heart Analyst and Investor Briefing here live from the American College of Cardiology Scientific Sessions in Atlanta. It's great to see all of you in the room this morning, and I also want to welcome all those that are joining us online on the webcast today. During today's program, any of the statements we make may be considered forward-looking statements, and actual results might differ materially from those projected in the forward-looking statement. Additional information concerning factors that could cause actual results to differ is contained in our periodic filings and other reports that we make with the SEC, and we do not undertake to update any forward-looking statement. I encourage you to go back and read the slide. The slides that we're presenting today will be made available on our website at investorrelations.medtronic.com, and they should be there now or very shortly if you want to take a look at those. Included at the end of the presentation is a clinical citation slide with sources for the information that we're using during today's presentation. A replay of today's event will also be available for listening later today on our website at investorrelations.medtronic.com. We have a full program planned for you during the next hour. Joining me are Geoff Martha, Medtronic Chairman and CEO. We have Nina Goodheart, our Senior Vice President and President of our Structural Heart and Aortic Business. Dr. Jeffrey Popma, VP and Chief Medical Officer for our Structural Heart and Aortic Business, as well as our Coronary and Renal Denervation Business. And Sean Salmon, EVP and President of our Cardiovascular Portfolio. In addition, Dr. Laura Mauri, Senior Vice President and our Chief Scientific, Medical, and Regulatory Officer, is also with us today. Geoff will make some introductory remarks, and then Nina and Dr. Popma will discuss the results of the SMART trial, which were presented this morning and simultaneously published in the New England Journal of Medicine. Sean will close it out. I want to make sure we leave good time for Q&A today where Nina, Dr. Popma, and Sean will answer questions from the analysts that have joined us here in the room. So with that, I'll turn it over to Geoff for some opening remarks. Geoff. All right. Thank you, Ryan. All right. So good morning, everybody. Thanks for coming. It's good to see a lot of familiar faces here in the room. And thanks for those that are tuning in online or streaming. Look, this is a day that we've circled on our calendar for a long time. Really a monumental day for us. And it's not just for Medtronic and our TAVR program, but more importantly for clinicians and patients around the world. And before I turn it over to the distinguished panelists over here, a lot of firepower in the room here, so I'm not going to take up too much airtime. They're going to walk you through the results. So I do want to take a moment to remind everyone here that there are other things going on at Medtronic as well. A number of really exciting catalysts across the company. I've talked to you about this transformation that we've been undergoing for a while now, including differentially investing in secular high-growth segments like neurovascular, diabetes, surgical robotics, AFib, and of course, structural heart. So in these areas, we're really driving, continuing to invest in more technical innovation, but also developing additional clinical data to expand the market. But today we're here to talk about TAVR and our Evolut. You can move up a little bit here. Our Evolut platform. There's notes on here, but I've one-off script, obviously. But today our Evolut platform has already shown superior outcomes when it comes to surgery. You saw that in the fall at TCT with our low-risk data. But today's SMART results mark a really important moment in time here for us. And I don't want to mess this one up. Can you go a little further up there? There we go. Now we have direct head-to-head data here against Sapien. The results are clear and very compelling. Evolut provides superior valve performance without sacrificing any clinical outcomes. I've been reading. I do read your notes, and I've been reading the notes over the last couple of weeks. It appears coming into this, the consensus was that, hey, these results aren't going to really make a difference in terms of clinician choice and market share. Look, they are very compelling. Nina and the team are going to walk through. I think people underestimated just how strong the results are and the difference between us and our competitor here and some really simple messaging that we're going to make sure that clinicians and patients get this message and clearly understand the benefits. Today is really a validation of all the hard work put in by our structural heart team, some of which are in the room or here up on the podium here, in terms of bringing, like I said, a differentiated best-in-class solution to a really underrepresented patient population. I want to thank all of those involved for your leadership. This is a bold decision. You don't see many head-to-head trials in healthcare. We had that kind of confidence in the technology, but we also thought it was important to really highlight this underrepresented cohort of people. Before I turn it over to Nina, I want to close by saying that across Medtronic, we are laser-focused on delivering on our commitments, particularly the mid-single digit revenue growth and leverage down the P&L. So in addition to the innovation drive and the top-line growth, we're driving organizational efficiencies, aligning our incentives, and really instilling this performance-based culture, a more aggressive culture. And we expect all of this to lead to good returns, healthy returns for our shareholders. So I don't want to take up any more time with this. I want to turn it over to Nina, the star of the show here, to walk through the results. No, I'm not the star of the show, but thank you. Well, Geoff was exactly right. Of course, this is an amazing day for Medtronic. We have incredible innovation across the entire enterprise. But today in particular is really all about TAVR and all about Evolut TAVR. So what you saw today, I think, was a brilliant presentation by Dr. Herrmann about the SMART Trial. When we came into ACC, we were really focused on highlighting two things. One is Evolut FX +, which we just announced the approval of from the FDA. We'll be launching that. We'll be starting cases in the spring. We'll have full market release by this summer. And what that product does is it takes all of the benefits that you heard about today, all of the radial strength, all of the hemodynamics, keeps all of those in this platform. But what it does is it opens up the windows at the waist of the valve to address what some people have felt was a perceived issue with coronary access. And as we think about our patients, as they continue to get younger, physicians have said they want to be able to make sure that they can get to the coronary arteries. And there was a perception that it was a little bit harder to do it through this tall frame. We have fixed that. I think we have put that now to rest with FX +. The second thing we came into ACC with was, of course, the SMART trial. And we really had two goals when we started to think about the SMART trial. And Geoff is exactly right. It was a pretty bold decision because we don't see a lot of head-to-head trials. But we really had two goals for this trial. The first one was to take the two most commonly used valve platforms, the Evolut platform and the Sapien platform, and compare them in this very large patient population, this small annulus patient population, 90% of which are women, and see whether or not we could truly see significant benefit in that patient population. I think what you saw today, that the answer was unequivocally yes. The second thing we wanted to do was really to think about that small annulus patient and to think about women. Dr. Baron on the podium today talked about this critical question of this being a landmark trial that addressed an underrepresented, underdiagnosed, and undertreated population. Women present differently. When I think about somebody who looks like me, when somebody who looks like Dr. Mauri, and I think about my colleague in the back, Neil Yanke, who's 6'10" or 11, how could we possibly be treated the same way? But we had no data to show that there was an optimal treatment for somebody my size versus somebody Neil's size. We now have that with this trial. You heard that we met the primary endpoint of non-inferiority. Geoff Martha is going to talk about that, numerically higher, but non-inferior. That's a super positive thing. These valves are at least as good as they are together. They're at least as good. But they're better when it comes to all of those secondary endpoints, things that really matter, like valve dysfunction. Nobody wants valve dysfunction. Why should you have to tolerate that when you have a treatment option that doesn't have it? Geoff's going to walk through all of the data that you saw in a little bit more detail that you saw from Dr. Herman this morning. Critical landmark trial. We know that because it was just published in the New England Journal of Medicine, and they really only take landmark trials. Very, very excited to see that there. Dr. Herman talked about the fact that this is the first randomized clinical trial that is primarily women. Just about 90% of the enrollees were women. We don't see that very often. That is hugely important, hugely impactful, and has to raise the question now in every heart team discussion. When a female patient is put up for a discussion about what TAVR valve to get, we now have answered the question of what's the optimal TAVR valve for this patient population. So we're going to walk through all of that. The other thing that we're going to talk about is the size of the market. We have been talking about for quite a while that we have modeled this market at about 40%. We believe 40% of patients have small annulus. We're going to talk about the fact that we have not only looked at our own modeling and our own data, but we look at Edwards' data as well. We looked at their product mix to see how many of their valves are put into small annulus. 35% of Edwards' valves are used for small annulus patients. That is a huge opportunity for us based on the data that we just presented. So we think that this, again, landmark trial tells us a couple of things. Just as good as the balloon expandable valves on those clinical endpoints, although Dr. Herman indicated he believes we're going to see improvement there. But on all of the secondary endpoints that Dr. Popmam is going to walk through, we saw significant superiority. I will be honest. We expected a positive trial. I think everyone expected a positive trial. As we were walking up here, what physicians have commented on, and especially physicians that we know slant heavily towards Edwards usage, what they were shocked about was the magnitude of that superiority. And I think that is going to make a significant difference as physicians on Monday have heart team discussions about what to do with these patients. So with that, I'm going to turn it over to Dr. Popmam. He's going to walk you through the data, and we'll go from there. All right. Thanks, Nina. Thanks, everybody. Good to see everybody. This is an important day for us for a lot of different reasons. But let me kind of tell you the history of why it's important to me. Because I was with Samine Sharma and Dave Adams for the first CoreValve implantation at Mount Sinai Hospital in December of 2010. At that time, we were three years behind the transformational therapy that Marty and Mike Mack put together with balloon expandable valves. And we said, we have something that's different. Why is it different? Because our valve design is very unique. It was designed by a heart surgeon, Jacques Seguin, for the purpose of providing better valve durability. The leaflets are high. They're long. They're made of porcine pericardium. The leaflet stress as a result of the reverse canting and the long leaflets is less than surgical valves. It's less than balloon expandable valves, which are annular. The valve apparatus is contained within the annulus. We had a theory. We said, this is a great idea. Everybody was very polite. They said, yeah, you may have something here, but nobody really knew. It's been 13 years that we've been collecting information to demonstrate that, in fact, valve design makes a difference in valve performance and affects clinical outcomes. When we first started thinking about this, it was a challenge. We said, how are we going to prove this to clinicians? We can no longer say, our valve does better than surgery. Another valve does the same as surgery. We're better than the other valve. That logic no longer held. What we had to do was to show it. We designed a trial that was big. It was 713 patients finally got in. It was multi-center. We had Sapien implanters. We had Evolut implanters. We had 83 sites across the globe. We had a total of 716 patients came in, one-to-one randomization. It was focused on those patients that had smaller annuli where we thought the benefit might be the biggest. Then, of course, we did a very meticulous follow-up. You'll see this data now for the next 5 years. The fundamental hypothesis was, is valve performance related to valve design? We had to prove it. I think we're getting very, very close to showing that that has the key effect. Now, when we talk to patients, and I still see patients at the VI, and I talk to them, I say, when you send them to aortic valve replacement, what do they want? They want a valve that performs well. I mean, at the end of the day, they want to have a valve that says it's going to work, and it's going to keep working, and I'm going to be able to do the stuff I want to do. As scientists and academics, we have to define it by something. The way we define this, valve performance, is by the absence of bad stuff that can happen to the valve. What are the bad stuff that can happen to a valve? First of all, on the left, you can develop structural valve deterioration over time, calcification, fibrosis, pannus formation fills up the leaflets of the valve, and the valve becomes stenotic. Then it comes back to where we refer to aortic stenosis. That occurs years after the AVR. What the focus on today was really on what happens early on. The essential component for that is the non-structural valve deterioration component, which is the valve big enough to do what the patient needs to live their life? The components of those are patient prosthesis mismatch. Another one in there is leaking around the valve. Is the valve maybe working fine, but is it big enough? And does it provide the patient what it needs in order to have a good, healthy life? And then the other ones are thrombosis, bad clot forms on the valve. We've seen that data presented at other symposiums. And endocarditis, which is something that can kind of occur unpredictably, randomly over time, but very important to the patient because the patient either gets an explant or they get a long-term antibiotic use and then maybe another TAVR valve. So these are big deals. And I think one of the things that you'll hear is that, hey, these indices of bioprosthetic valve dysfunction mean nothing. They're meaningless. They don't mean anything. That's crazy when you think about where we are today with our clinical track data. Howie Herman referenced some of this data, structural valve deterioration. Absolutely. That means that you have to have a valve reintervention, hospitalization, and death. The valve isn't big enough, Howie mentioned, patient prosthesis mismatch. That's the component. The valve isn't big enough to do what the patient needs to have done. That's a big deal. Lots of data in the surgical literature and in the TAVR literature support that. Thrombus on the valve can't be good. And the outcomes are such that even subclinical leaflet thrombosis, just seeing thrombus on the CT scan, bad stuff. In endocarditis, it's obvious, right? Because the valve actually has to take it out from the body. So these are the external literature that we have to support that all the components of bioprosthetic valve dysfunction are bad for the patient. That's how we picked them. So what is the data show from our stuff? I've given you what's shown in the literature, not us, but others. We have already published the importance of structural valve deterioration and clinical outcomes from our high-risk and intermediate-risk randomized trials. This was published by Dr. O'Hair in JAMA Cardiology. It's not often referenced, but it's incredibly important. And we need to talk about it more. And in this analysis at five years, the rate of structural valve deterioration was about half with CoreValve than it was with surgery, half. But that right forest plot, which seems a little bit scientific, a little bit overwhelming, it says some very important things. Any way you look at structural valve deterioration, any way you look at it, in SAVR patients, in TAVR patients, however you look at that, it's associated with a twofold increase, 100% increase in death, cardiovascular death, rehospitalization. You can't cut this any way, so it's not important. Every way you look at it, it's incredibly important. And that's structural valve deterioration. That's what we know. The valve fails, has to get retreated. It's bad news for the patient. We want to avoid that. What is new at this meeting is focusing now on something that occurs earlier, bioprosthetic valve dysfunction. The valve's too small for the patient. The valve has a high gradient at the end of the procedure. The valve develops thrombus. It gets endocarditis. All those things then are focusing on bioprosthetic valve dysfunction, which doesn't take years to develop. It takes 30 days to develop. That's what they get. Now, Steve Yakubov and Nicholas Omega have both published this data. This is now in preparation. You'll see it going soon. Hopefully, at one of our upcoming meetings, you'll see this. This is an analysis that we did. It's already been presented a couple of times, is that when we looked at bioprosthetic valve dysfunction in our randomized trials, there was a 50% increase in the 5-year death, cardiovascular death, or rehospitalization rates. So when Howie says what's going to happen over time, he's not just doing it saying, this is just what I think. He's doing it based on the fact we have some prelude into seeing exactly what's going to happen with the valves. Those valves that have dysfunction, bad valve performance, don't do as well from our data sets in 5,000 patients over time. That's what we're going to wait to see as we develop through the SMART Trial. I can't do anything better than Howie just did on the podium in terms of explaining this data. But I can give you some rationale about how we got there. We felt that we needed to prove two things. We needed to say, Evolut's as safe as Sapien. Procedural implant, one-year mortality, it's safe. I mean, we can put it in without any compromise to clinical outcomes. That was number one, non-inferiority. That made sense for us. Secondly, we want to say our valve's got to work better. So we did that through a whole series of endpoints. And any way you cut this, you come up with the same p < 0.001 answer, that is, our primary superiority in valve function was gradients over 20, non-structural valve deterioration, thrombosis, endocarditis, reintervention. I've explained the incredible prognostic importance of each one of those. Now, here's the statistical thing that you have to do, which is Howie didn't have time to go through. But it's pretty important from a design standpoint. One, once you meet your 2 primary endpoints, non-inferiority for clinical outcomes, which means we're as good or better than Sapien, and then superiority for valve performance, you get to test a series of other powered secondary endpoints sequentially. It's like going to Las Vegas and putting all in on each of your hands, right? You only get to move on to the next hand if you win on that hand. So you have to go sequentially through these. So the first one was bioprosthetic valve dysfunction in women, 1. Go on to the next one, hemodynamic structural valve deterioration, all subjects, 1. Go on to hemodynamic valve gradients as a continuous variable, 1, there. Superiority, effective or arbitrary, moderate to severe, walking down sequentially. You can't go on to the next one until you're superior to the one previous to that. So this is very sophisticated testing to say, we've powered these endpoints to say each one of these are an independent statement that we can make, and we believe in them, not through multiple testing and Bonferroni corrections. This is solid data that we can hang our hand on for each one of those. So you'll see us talk about each one of those components because they're independently powered. Now, look, I mean, all of us who see patients and you guys who have family members who come in, they say, what does this really mean? How do I put this in context? So the rates up here about bioprosthetic valve dysfunction, you've seen the data, 41.6% for Sapien and 9.4% for Evolut. It's a 4.4-fold reduction. It's a number needed to treat if you're a thrombolytic guru or a cholesterol guru that you saw in some of the earlier presentations today. The number needed to treat for clinical effectiveness is in the 40 and 50 range. We're three. Three. Well, what does that mean as you're trying to explain it to your patients? Say, for example, you treat 10 patients with a Sapien. We know from the data that four of them are going to catch bioprosthetic valve dysfunction. Of those 4 patients, you could have avoided bioprosthetic valve dysfunction in 3 of them had you used an Evolut. So that means that for every 10 patients treated for developed BVD, of those, 3 patients could have been avoided for BVD had you used an Evolut. It's a pretty powerful statement when you think about it. I mean, it's like you take away 3 of the 4 episodes just by going with Evolut rather than Sapien. And the numbers are kind of overwhelming. And sometimes they become a little less meaningful when you start to say, OK, there's a 2 x lower gradient, a 1.3 x higher effective valve rate. There's 10 x frequently less residual gradients over 20. These are huge numbers, right? 3.5 x less PPM, 5 times less bioprosthetic valve dysfunction. But this one at the bottom, Howie talked about, it's incredibly important because one of the things that has always been talked about is how well do valves reduce residual paravalvular regurgitation after you implant them? And we know that mild or greater has a prognostic implication. We've known that for a decade. What we found as a nonparadigm point was there's significantly less mild or greater aortic valve regurgitation with Evolut compared to, say, it's better. It's better. Howie showed you the quality of life, better with Evolut compared to Sapien. So not only are we just showing that there's mechanically something there, but it's also showing you that there's actually some other functional indices that you might not have guessed we would win on, but we did in a randomized clinical trial. So what did Howie say? So Howie said that it's the largest randomized trial, randomized to the two most widely used TAVR valves, largest trial ever to enroll women. This is going to be great for women in general because they're going to feel like it's safe to come in and get a TAVR. I mean, that's one of the things that can be very important as we talk to patients. And we've talked about the superior valve performance, as good or better clinical outcomes with Evolut than Sapien, numerically higher. And we'll watch that over time. Superior valve performance, 32% absolute lower incidence of BVD, 8 mm lower gradient, 5.5 cm greater effective orifice area, 0.2 larger Doppler, 6.8% absolute lower rates of severe PVL. You can't really beat that and less total AR and better quality of life. So when Howie was asked by Dr. Barron, the very important question, based on the large differences in valve performance, he expects that Evolut will demonstrate improved valve durability and outcomes in longer-term follow-up. He was asked when. He said, 2-4 years. Where did he get that from? Well, if we look back now at both PARTNER 2A and PARTNER 3, you know the data as well as anybody else, those curves cross for mortality at 3 years. Ours, as we've shown, continue to separate to 4 years. We're expecting that somewhere between 2 and 4 years, that there's going to be differences in outcomes based on these differences in valve performance. And that's where we get there. So look, Howie did a brilliant job. I mean, he can't do much better than that. I wanted to give you a little bit of background about how we got there and the fact that these are meaningful indices. The clinical as good or better with Evolut is hugely important for clinicians. But we get less residual AR. We get better quality of life. It sounds like a pretty good win for Evolut in patients with small annuli. So final point. You may hear people say, well, you just designed your trial, so you'll win. You picked the smaller valves, 23, 20, Sapien to go against. Well, in fact, the most frequently used valve in this series was 23 mm Sapien 90% of the time. As it turns out, we didn't know then, but we do now, the 23 mm valve was the best performing valve in the PARTNER 3 trial at five years, the best performing. So another way you can look at it if you're on our side is, look, we took on the best performing Sapien 3 valve that's available from long-term data. We took that on. And our randomized SMART Trial is in that set, the 23-millimeter valve, which has an 8.1% five-year mortality rate compared to the 26 and 29 at 10.1% and 12.9%. So this randomized trial was performed in the best of the best of the Sapien valves. And we won. So I think that's going to be a very, very important piece as we put this in context. This wasn't cherry-picked. We didn't design it so we'd win. As it turns out, we did that. And we won. We won it. But we won it going against the best performing of the Sapien series. So let me just turn this back over to you. Thanks. Do I talk to you? Do I believe? I don't know if I do. Yes, you believe. I think we should all believe now. So like I said earlier, one of the questions, so you've just heard the data twice now. You heard it this morning. Dr. Herman and Jeff just went through it in greater detail, which is great. The next question is, so how many patients does this impact? And that's where, as I mentioned earlier, we've been modeling at 40%. We've been looking at the Edwards mix, which we looked at in the TVT Registry over time. So you can see here, 2011 to 2022, so that long period of time. And then most recently, in a paper by Dr. Stinis in 2024, again confirming that 35% mix. So again, huge opportunity for us as we continue to move forward. We're talking about this for small annulus patients. We're talking about this for women. Jeff, Sean, and I met with a physician this morning who had seen these results and said, if it works this well in small annuli, it should work even better in big annulus patients. So this is what we're talking about from this patient cohort. We think there's an enormous amount of opportunity here. This is the way we think about it, right? Women, we've talked a lot about women. We're going to continue to talk a lot about women. Again, underdiagnosed, underrepresented, and undertreated, 90% of our small annulus patients are women. We just fielded a study of 1,000 women over the age of 50. We asked them a lot of questions about their cardiovascular health. We put out a press release about that, I believe, yesterday. And what they told us is that if there was technology designed and proven to show benefit in women, they would talk to their doctors about that. I know I would, right? And so this is a huge opportunity going forward. We talk about patients of Asian descent. If you look here in Japan, 84% of that population have small annuli, smaller patient population, another big population for us to look at. And then as we think about valve-in-valve, 85% of those patients. And so we think that this is a huge opportunity for women, big opportunity, of course, for all patients with small annuli, and I would argue a big opportunity for all patients who are really looking for that increased blood flow. So we've already started to hear some pushback, as you would imagine. And we're just going to be really candid about that. Our field teams have already been hearing questions about what the anticipated responses were going to be. These are some of those questions. We thought it was important that you all heard what we were hearing, but also saw what the actual data says and what we understand. One pushback that we're getting is, yes, but you didn't do this against Resilia. I think two things we have to remember. There's no published data on Resilia, right? There's a lot of discussion about Resilia. But we've seen no data on Resilia. Second thing is, we did a post hoc analysis to see whether or not if we took what we know about Resilia and put it through the SMART Trial, there is no difference. We could go up against the most current Resilia valves. We will see no difference in this patient population. Jeff just talked a lot about BVD. It doesn't translate to mortality. I think he very effectively shows you that it does. It's important that physicians and patients need to think about this when they think about valve selection. We hear a lot about ease of use and pacemaker usage, that the Sapien valve technology is just easier to use. We have made, as you all know, significant improvements in the Evolut technology going from FX and now to FX + to improve that ease of use. Our pacemaker rates in the real world in the TVT registry, well under 10%, just about a parity with balloon expandable valves. We can continue to go on and on. I want to leave room for questions. We're happy to talk about any of these. But we know that we're going to get questions. But we also know that we have the answers. We're happy to share them with you. What does this all mean? When we put all of this together, what does this all mean? We have been publishing data over the last several years, but especially most recently at every major congress to talk about the benefits of the Evolut technology, most recently, of course, at TCT, where we showed our low-risk data, our four-year low-risk data, where we showed the superiority there. You can see the divergence of the curves. We saw crossing curves, as you know, in the Sapien data. Ours continued to diverge. We expect to see that going forward. We have continued to publish around valve dysfunction in pooled analyses. Of course, you know about our 10-year NOTION data, where we continue to follow patients now out to 10 years, where we continue to see less valve dysfunction out to 10 years. We are committed to data transparency. You will continue to see ongoing data releases from us on all of these trials as we go forward. We're going to be happy to share those with you. Today, of course, though, is all about SMART. We couldn't be more thrilled with the results than the results that we expected because we know the benefits of this technology. Of course, amazing to see this published in the New England Journal of Medicine. Then lastly, as we've talked about the FX + technology, which takes everything that we know about Evolut, takes all of the benefits that Jeff just talked about, that Dr. Herman talked about this morning, but widened that window in the middle of the valve, at the waist of the valve, to ensure that physicians who might have been nervous about coronary access can now access the coronaries. So a really great valve now as physicians think about younger patients and lifetime management. So great past data, great current data, incredible new technology. We're feeling really, really confident about the Evolut platform as we go forward. So with that, Sean, I will turn it to you to close. Thanks, Nina. I won't belabor too long here. Just congratulations to both Nina and Jeff here to have the courage or their convictions to take this population on. I imagine with a trial called SMART, that if it had gone badly, we would be having a lot of egg in our face. But clearly, this is a really important thing for us across this portfolio of important growth drivers we have. This is a big deal. And I agree with Nina. Today is about that. But I just want to remind you that this is just one of six major growth drivers that we have to continue to propel our portfolio and company forward, including our focal or single-shot pulsed field ablation, our point-by-point ablation, renal denervation, and our leadless technology that's both manifested in a pacemaker and now, for the first time, an ICD that can also pace the heart without having leads in the heart. The one thing I would like to point your attention to is on our pulsed field ablation, tomorrow at the EHRA meeting in Berlin, we're going to be presenting the first-in-human data on an upsized version of the PulseSelect catheter here, the Sphere 9, which is the anatomical catheter or single-shot catheter. Those first-in-human data will be presented tomorrow, as I said. And then HRS, our pivotal study, the IDE that will lead to the U.S. approval, the PER-AF trial done in paroxysmal AF patients, another head-to-head trial against another market leader, the SMART Touch Cool Biosense Webster product, we're head-to-head in that patient population. So suffice to say, we're really, really excited about today and every day that we're going to get the pleasure of selling all these wonderful products to help patients around the world. With that, I think I'm going to turn it over to Ryan to moderate the Q&A. And thank you all very much. All right. Thanks, Sean. Yes, we're going to move to Q&A. We're going to be taking questions just from the analysts and investors here in the room. As usual, we want to get to as many of your questions as possible. So we ask that you stick to one question, a related follow-up if you need that. If you have additional questions, once we've worked through the room, we can come back to you. Or you can reach out to us afterwards. And then just for the benefit of those on the webcast, we're going to come to you with a microphone, make sure you're speaking to the mic. And it's helpful if you give your name and firm as well before you ask your question. So let's start with Matt. Hey. Good morning. Thanks for taking the questions. Matt Miksic, Barclays. One pretty simple question. I'm sure there'll be a lot around the details of the study, which we're terrific. Congrats. But the opportunity for small annulus and moving the needle there over the next 12-18 months seems significant. Maybe if you could talk a little bit about where you're at in terms of share. Here's a question for Nina. What's a reasonable target to aim at as this goes from if it's 35-40? Is it 35-45? Just setting some expectation over the next couple of years about what this could mean. Thanks. I think the first thing that we're looking at is that 35% mix that we see with the Edwards valves, right? 35% of their mix going to the S20 or the 23. That's a huge opportunity for us. That's going to be the first step. If we can capture that, we'll be on our way there. There's a market expansion opportunity here too. We talked about women are underdiagnosed, undertreated. And now we know the appropriate treatment for women. So there's that opportunity. And of course, the growth that we get in all small annuluses. And look, a lot of the valve benefits that we have here, this was the focus of this trial. But it's true across the valve range, as Jeff showed you. The best outcomes that you see in Sapien, we've vested those. We'll come back. Go to Chris. Thanks. Chris Pasquale in Nephron. Dr. Popma, two questions for you. One, just curious, you guys have a website where you can put in patient information, determine the risk of severe PPM. Is that entire 40% small annulus population really at risk? Or can physicians take a look at the baseline characteristics and sort of determine who's really the primary candidate here to potentially have a bad outcome? So yeah, it's a great question. I'm going to extend it to what a heart team does when they're evaluating a patient for valve selection. Let's put the matrix in there together. It's probably not going to be the right thing to do to plug in every value you have and say, OK, this is a go or no-go. It's a risk decision model that the smaller the annuli, the higher the risk for patient prosthesis mismatch. We know for whatever that annular size is, that we have a marked reduction, a large reduction in the risk of PPM if you use an Evolut compared to a Sapien. Just annular size is number one. But in full disclosure, that's not the only thing the heart team's thinking about. They're saying, where are the coronary arteries? How large are the sinuses? Is a valve that crosses over that really the best thing to do? And there's probably 5% of patients in that small annuli patient population where it's just not the right thing to put in for an Evolut valve. Then we think about the age of the patient. And certainly in a younger, I hope to be careful, younger. 74 was our low-risk trial age. We're not talking 55. So in that younger woman population, you want durability. You want a valve that's going to last longer as long as there's treatment options for both coronary access, which we have now, and in case there's a very, very small chance, less than 1%, of a valve failure. So I don't know that we'll get to the point where we actually plug in an algorithm and say, this one's a Sapien. And this one's an Evolut based on PPM risk alone. It's going to be an issue of what is the risk of valve dysfunction over time? What is the immediacy of how big a hole you can provide? We always know we can provide a larger hole with Evolut than with Sapien. And then is it safe to put the Evolut in? And I think that's going to be the matrix as clinicians think about how they're going to apply it. But absolutely, the annular size is right in the middle of that, as we showed with our data. When you talk about female patients, Asian patients going forward, the question is not why Evolut. Now it's like. Why not It's a shift of the paradigm here. Getting the message out to referring physicians and patients themselves, especially if you're a female or Asian, that you should be demanding this. If your physician isn't following the data, you've got to challenge them. An approach where you tailor it might be valid if we didn't see completely consistent outcomes across the board. But what we see is that it doesn't matter. Overall, the results are so striking with that 41% versus 9%. And a number needed to treat of only 3 patients is really dramatic. And so there's no reason to break it up into different groups that some may or may not benefit. There was really consistent finding. That's helpful. And then just to touch on that last point. So the 41% versus 9% was driven largely, it seemed, by acute hemodynamics, the increased gradient primarily. Rates of endocarditis, valve reintervention, and thrombosis were all pretty low and broadly similar between the two arms. So is there any particular link between long-term development of thrombosis and endocarditis and the acute hemodynamics that we're seeing? I think so. How do you think about how those numbers progress? Because you showed the kind of scary images of structural valve deterioration. Looks pretty nasty. But we're talking primarily about non-structural here. So a couple of things. One is the benefits are primarily for the acute hemodynamics. But that's the size of the hole. And what can we do and just consistent effect across all of that? Thrombosis is something that may occur later. We'll certainly see that over five years. And remember, in the PARTNER 3 data, you didn't actually see the higher thrombosis rates until after one year. So we're expecting to follow that. Absolutely, we think that it's related to hemodynamics. But that's not the only thing because even from valve size, thrombosis can occur across all the valve sizes. So we think we're going to be beneficial there. And endocarditis trended to be lower with the porcine pericardial than with the bovine pericardial material. I mean, it was a 0.06 in terms of a reduction in endocarditis risk. The thrombosis and the endocarditis, we know, are going to increase over time. We know that the SVD, the deterioration of the valve, is going to increase over time. The only thing that's going to stay the same, as you point out, is that acute hemodynamic effect, which is bad, and prognostic early on. So I think we're going to see more of that over time. And by the way, I think we're going to differentiate too. We're already seeing a little signal for differentiation from porcine versus bovine. We know that the thrombosis rates are different between the two valves after one year. And we know that the SVD rates are going to be different as well. Let's go to Patrick. Hey. It's Patrick Wood at Morgan Stanley. Thank you for putting this on. This is probably a stupid question. But given the very substantial differential on BVD and that set of things, why do you think in the field people haven't spotted this in practical terms already? Because it's a big gap, whether through mortality or whether it's just directly from the physician. It's a big gap between the valves. So why do you think it's taken this trial really versus anecdotally this kind of to appear at the time? Well, I said that I was with the first at Mount Sinai in 2010. And I've been talking about this for 13 years. I guess people don't listen. I mean, no, I'm just teasing. But we've been talking about this for a long, long time. We published almost three years ago the important relationship between SVD and mortality. And we've presented an abstract form at a couple of different meetings, this relationship between BVD and outcomes. So we have been talking about it. I think what it has to do is that clinicians have to feel as if there's a compelling reason, as Geoff and Laura have said. There's a compelling reason now. There may not have been felt like there's a compelling reason before. But if you look at patients' small annuli and you see the magnitude of these differences, it's a compelling difference. It's still going to be a discussion. But it's going to be a compelling, I think, like the way Jeff said, why not? And I think that's going to be the piece. We will continue to publish on this. I hope others will continue to publish on this. The surgeons have been publishing about this for years. Severe PPM has been a prognostic indicator for surgeons. And surgeons will take the patients back to the operating room if they get a bad surgical result because of that. So I think that it's just going to be a wave that's just going to continue. And we just have to have more people on podiums talking about it. I have a slightly more direct perspective too. Coming over from the neuroscience side, I was thinking spine. And we had no data, right? We had a lot of data. I was a cardiologist. Everybody follows the data. And then when I got involved with this space, I was really confused and frustrated because we're up against ease of use. Now, we've knocked down these ease of use. Nina walked through that. We've knocked down these things over time. But you're up against a confirmation bias. You're up against ease of use. And so even though people like Jeff are throwing all kinds of data and clinical, it's a tough one to overcome. It feels like this data is so compelling, though, that it's going to, it's like Nina said, you come in Monday morning with the heart team. You have to talk about this. It's going to change the discussion. And then we, we're conservative when it comes to marketing, all right? I get it. Now, even us, who are very conservative, this is the valve for women, full stop, period. This is the valve for Asians, full stop, period. We don't asterisk that. We get it out to the referrers. It's going to change the conversation. So the answer to your question from a non-clinical perspective, you're up against ease of use. Like I said, and I used to get mad, how can physicians do this? But look, they've got a crazy day. They've got a lot going on. And they have to check back in on any of these ease of use because it's gotten a lot better. And now this clinical data is just so compelling that if it's going to take an extra 4 minutes, you've got to do it. Let's go to Josh. Thanks. Good morning, Josh Jennings from TD Cowen. Great download. I wanted to focus just on the one slide where you talk about valve-in-valve and how most of those cases are basically small annuli cases. Is the market for that segment, is that about high single digits of the total TAVR cases, valve-in-valve? And how do you see this data being leveraged? Is it just intuitive? Or do you need more? And maybe what percentage does Medtronic have in that segment if you're willing to share? And then secondly, just great to hear just about lifetime management, what FX does in terms of the outlook for TAVR and valve-in-valve TAVR. And just any thoughts on how valve-in-valve TAVR lines are going to step up because that's another segment where, again, intuitively, small annuli cases. Thanks. Gotcha. Neil, 8%-10%? What's the TAVR and SAVR market? 8%-10%, something like that. See, I'm learning how to do this. So 8%-10% is the market. There's a randomized trial called the LYTEN Trial that was presented and published, a randomized trial of balloon expandable versus Evolut in patients with surgical valve failures. Small study, stopped because of futility, I guess. Huge difference in gradients in those patients that had a Sapien in the surgical valve versus those that had Evolut in the surgical valve. The data is there that a supra-annular is potentially preferred in that situation. And so this is a very, very important area. It's something we need to focus on. And this is where there's going to be an amazing benefit. And I hope SMART extrapolates to that. Your second question about TAVR and TAVR, now how do we manage transcatheter bioprosthetic valve failures, is a very, very important one. Vini Bapat came by with an amazingly important app just released three days ago called the Redo TAVR app, which you can download on your iPhone free. That guides clinicians to the very complex process about how you effectively treat a Sapien failure, an Evolut failure, maintaining one thing, access to coronaries, coronary perfusion. We've changed the script over the last several months, last years, saying that, yes, you can treat an Evolut failure with a, unfortunately, balloon expandable is where we are right now, balloon expandable, and still preserve coronary access and coronary perfusion. It's a complicated scenario. Docs are going to have to learn it. The app that Vini Bapat's given is going to help us. But I think we're learning what that means. It also means that we're under responsibility to really understand what leaflet management's all about. And of course, none of that's approved or on label right now. But we are working very hard on our preclinical models to show for all valves what exactly does leaflet management mean. The final point I'll make is FX has made a difference with the treatment of TAVR and SAVR and TAVR and TAVR because the commissural markers allow us to do commissural alignment. Can't do that with the Edwards valve right now. So commissural alignment is going to be very, very important as we think about how to keep the leaflets out of the front of the coronaries so we can have perfusion and gain access. So I think those are the growth areas, Josh, that we need to come back around. I think that that's an area that we should be able to do well in. Larry. Thanks a lot. Larry Biegelsen and Wells Fargo, congratulations on the trial results. So Jeff, on the PVL, I was surprised that, a little surprised to see that result, that Evolut was superior. ALFA- TAVI was just published a couple of weeks ago, actually showed the reversed result. Why do you think we saw that here or the difference with AlFA- TAVI? And Nina, do you think, can you set expectations for what you think your share capture could be? I'm not asking for a number. But do you think you need to show a clinical benefit to really maximize the share capture? Or between now and when you do see a clinical benefit, if you do, do you think you can show some meaningful share capture even before that? Thank you. Yeah, Larry, I'll go first. I think data is important to clinicians. And we know that it is. This is now irrefutable data, right? Before, we had to extrapolate how these valves performed in these patient populations. But when I look at the small annuli population, when we think about the underrepresented population of women, as we think about our patients of Asian descent, and we now have, for the first time, head-to-head data with the valves that people are using right now, if that data is important, there is no way that we don't move share because every physician has to start their heart team meetings next week asking to Jeff's question, in this patient, based on this randomized clinical trial, a landmark trial, why would you not put Evolut in? And physicians are going to have to rationalize that. It's going to be hard to rationalize after we see this data. So do I think we're going to see some meaningful shifting? Yes. Do I think it's going to take some time? Of course, right? We know that clinical practice doesn't change overnight. But this is pretty amazing data, specifically head-to-head in the valves that they have in their hands right now. So I think we're going to see it even before that 2, 3, 4-year period. AlFA-T AVI is a study that was a non-randomized comparison with propensity matching. I think that, similar to all the propensity matching studies we've seen, they're all limited by the unmeasured confounders that come into the study. What I mean by that is patients didn't randomly get an Evolut or a Sapien in that registry analysis. They got them for a reason. They may have gotten them for left ventricular outflow tract calcification and wanted to avoid a rupture. They may have gotten it because of a bicuspid disease. So there is no amount of propensity matching that we've been able to identify that actually gets you to the truth, which is really what we want to get to. That's why we made the decision to move to a randomized clinical trial, which equalizes the distribution of the unmeasured confounders and says, look, these groups are identical. It's a randomization process. All those are the things that physicians may use to select one device or the other. They're not here. They were suitable for both. And we randomized them. That's one reason. The second reason is that we trained all of our clinicians about using the Cusp Overlap Technique. We've technically talked about all of that, that the pacemaker rate's got down. But it also means that we have a higher implant and that we can use more of the real estate of the inflow of the valve to seal the valve. So we have seen consistently lower rates over time of paravalvular regurgitation. And you'll see more of this data at SCAI with Hemal Gada when he does our Optimized PRO FX analysis. So I think that we got better. Our self-expanding valve continues to expand. It's not balloon expandable. It's plastically deformable and sits. We continue to expand and continue to remodel. These data are wonderful to see. They're not surprising because we've changed so much over the last couple, three years in terms of heart implantation. Rich. Hi. Rich Newitter from Truist Securities. Congrats on the data sets, guys. Wanted to ask just, since TCT, when you really had the opportunity to begin marketing the data that you have right there, the 4-year Evolut data versus Sapien 3, 5-year, I'm just curious, what have you seen in terms of market share or receptivity from that data set? And then I'm just curious to hear, even if qualitatively, how you see this data set and your ability to market around it comparing to what transpired since the presentation since TCT. And then I'll follow up. So let me start. But I want Nina to talk about market share here. This was the limitation of all the trials we've done before. It was Sapien versus surgery. It was Evolut versus surgery. And so when you go to the heart team meetings, what does that mean in terms of Sapien versus Evolut? You can't really make a judgment. You have to do something inferential. And it may not be as convincing from inferential data as it is from randomized clinical trial data. So this is why we made the decision three years ago or so that we just can't keep comparing the Edwards trial results with our trial results and having any meaningful statements. The only way to do that is perform the randomized clinical trial. So Nina's going to tell about market share and see what's changed. But from my perspective, it's a very confusing conversation in the heart team. I've mentioned the heart team. That's where these discussions happen. And what was the number one conclusion, appropriately, from PARTNER 3, which was a landmark trial, like ours was a landmark trial? It's reassuring that it's not worse than surgery. It's reassuring it's not worse than surgery. So when you're heart team meeting, you're making that decision. Now, it's a much more binary decision, okay, I'm going to go to a transcatheter. Which valve am I going to choose? So I think it's going to be a different conversation now than it was after TCT. And the reason is because we have randomized clinical trial data to show this. Yeah. I think that's exactly right. I think if you think about the questions that physicians have asked over time, those questions have changed. So when we first came out with TAVR, the question was, how does it compare to surgery in the sickest patients, right? And so we did trials against the sickest patients. And we saw the benefits of TAVR. We then worked down the risk scenarios till we got to low risk, right? So compare it to surgery. How does Evolut do? How does Sapien do? And to the point that came out at TCT, essentially, was this was a good day for TAVR. Those were essentially the headlines. We think it was a better day for Evolut given the fact that our curves did not cross. And those are conversations we continue to have with physicians as they have their heart team meetings. They still couldn't answer the question, though, which is the question they ask now, which valve, now that I believe TAVR is better than surgery in the right patients, right, better than surgery, which valve do I use of the TAVR valves? And we've had no data, no randomized data, to be able to answer that question. So now that we have that, as we were saying before, we've got a lot of populations to address. And I believe we will see market share change. What do you think, what would you say to the physicians that we all have been speaking to that say that they're doing Evolut in the maximum number or optimal number of eligible small annulus patients already? Therefore, there's not much more room to go beyond. I guess, how do we reconcile that with this percentage of patients that you're identifying in Edwards camp that are kind of now jump-ball opportunities? Well, based on the Edwards product mix, 35% of those are still getting an S20 or an S23. This data says that all of those patients, essentially, should be moving, should have gotten an Evolut, right? And so clearly, we're not getting all of them because there's 35% that are still getting Edwards valves that are absolutely considered small annulus. We also think about women, right? 50% of the population are women. They're not getting either they're not getting valves, right, or they may be getting a mix of Sapien and Evolut valves. So two big areas, I think. Is it possibly a definitional difference? And everyone's small annulus, that 35% is overstating potentially where the doctors are seeing? So that's a great point, a great presentation because I talk to docs the same thing. And really, what it means is I don't use 20 Sapien anymore, right? Small annulus was 23 Evolut versus 20 Sapien. I use a 23 Evolut in every one of the cases rather than use a 20 Sapien. This trial defines what small annulus is from a data perspective, right? So now we pick the bar of saying, if you go to Japan, a small annulus for them isn't 430. It's 350. I mean, to them, that's a small annulus because the entire Asia population has smaller annulus. So for them, 430 is huge. So we've done a randomized clinical trial. And what we're defining small annulus, which is specifically defined as the use of a 23 Sapien. So we're redefining what small annulus is. I think, to Nina's point, that's where the 35% is coming from because the docs you talk to don't consider a 23 a small annulus. I think that that shift now, at least we have data, randomized data, in what we're defining a small annulus, which is 430 or less, comparable to a 23 Sapien. I don't know if that makes sense. But I think you're right that in terms of it's all definitional. David. Thanks, Dave Rescott with Baird. A little bit of a follow-up on the prior question as well. But I'm wondering if you have a sense for what your share of that small annulus patient is today. If you look at 35% of Edwards implants in this specific patient population, the market's 40% would suggest that you theoretically have a lower portion of the small annulus patient market than what you do in the overall U.S. market. And so I'm trying to understand what a baseline is, maybe, especially just following up on the prior question around whether or not there is peaking penetration or peaked penetration in this small annulus patient population, specifically for the self-expanding valve. Well, we don't have 35% share. You can see here that we still have room where we can grow in this small annulus population. I think we still have a lot of runway here. David. Thank you, David Roman from Goldman Sachs. Nina, you made a comment in your remarks that, well, if this works in small annulus, this should work in large annulus populations, effectively saying you can extrapolate these results to the entire population. Maybe talk to us a little bit more about the go-to-market strategy for how you might execute at this. And maybe this fits also into Jeff's comments earlier and other forums about a more aggressive approach with Medtronic and less conservative marketing. But how do you think that plays out from an operational perspective? So let me just clarify that. So thanks for asking the questions if I have to clarify it. When I said the benefit extends to large annuli, I didn't mean the magnitude of the benefit. It's just that there's a reduction of BVD. And you'll see more data you saw it on the abstract presentations that these reductions in BVD also hold true versus surgery and larger annuli. We need to study those, right? We're not there yet. We've just studied the small annuli. But what we're going to say is that there's still, from the data we have from our versus surgical literature, there's still a reduction, significant reduction in BVD with CoreValve compared to surgery. But we need to go study that more. But we do know that the smaller annuli magnifies that effect. And that's what we studied in the SMART Trial. So it's more BVD. But our preliminary data says that that magnitude of BVD will also be present in larger valve annuli. So is the right way for us to think about it then, the SMART Trial makes a clear statement around small annuli? But at the same time, if you believe the BVD correlation with outcomes, it makes a statement about the entire population from the BVD perspective. And that's really where we could see the benefit that you might be able to extract from the data beyond just the small annuli, but an entire opportunity to capture more share than what CoreValve has broadly now. I mean, you just taught me something. So yes, that's how we have to say that because the BVD that I showed you was all annular sizes. We did split up saying how frequent is BVD in that larger data set of 5,000 patients, less than 23, greater than 23. The magnitude of the reduction in BVD was greater in the smaller ones. But it was still present in larger ones. But you're absolutely correct. That correlation model that we did was for all valve sizes. So BVD is bad, whether you get it from a small annulus or a large annulus. Yeah, that totally supports that inferential. Yeah. Yeah. Time for me to have a few more. Lilia, go to you. And then Shagan. And then we can come back and wrap up now. Thank you. Maybe just on quality of life, I think the results were pretty similar across both arms on that metric. So can you talk a little bit more about that and why there wasn't a more meaningful difference? Well, if you just look at the absolute mean levels, those look pretty similar. It was a little bit lower quality of life to start with for our Evolut. But they're pretty close together. It's hard to interpret what those numbers mean. What does 41 mean versus 35? So the Valve Academic Research Consortium, VARC-3, put together some more meaningful qualitative statements about what quality of life means and graded it by you didn't have much improvement. You had a little bit of improvement. You had moderate improvement or had substantial improvement. And how we showed with the metric and the categorization established by the convention of VARC-3 was that there was better improvement with Evolut than there was with Sapien. And as you pointed out in the presentation, the gap was about 10 percentage points in those patients with substantial improvement. So it's always tricky to look at the number bars because what does that 42 mean? What does 43? What does 52 mean? It's hard to know what that means. That's why the VARC consortium said, well, let's talk about the changing gradient. And are they better? And what we saw in this study was that 10 percentage points better for substantial improvement in the Evolut group versus the Sapien group. I don't know if that helps. But the VARC criteria that you saw on the right side of the screen, that was what the criteria came back and says, let's just put the numbers into something that's meaningful to the patients. So we can say, you're going to feel substantially improved after your TAVR. And that happened for 10 percentage points more in Evolut than it did with Sapien. Shagun. Shagun Singh RBC Capital, just a quick one from me. What do you think the expectation was for BVD through 12 months versus what we saw in the trial today? I mean, the expectation was that the results would be positive. How much of a difference do you think we have seen here? I would say when I first saw the data, I looked at it and said, oh my god. So that was my initial reaction to it. I had no idea the magnitude was going to be that big. We knew it was going to be different. You're absolutely correct about that. I just didn't know it was I didn't expect the magnitude. And look, these are measured by an independent core laboratory. They're measured by any criteria that you put together. They're not us measuring them. It's an independent core laboratory who reads all the echoes sequentially and will read the echoes over five years, didn't know the clinical outcomes of patients. So the magnitude of difference, to me, when I first looked at it was I was shocked by how much the magnitude was, understanding what I knew about the fact it was going to be a positive trial. I don't know. Nina, I don't know if you feel. I think we heard a bit of a collective gasp in the audience, actually, when Dr. Herman presented because I think that, to Jeff's point, most people would have said, this trial will be positive. They did not expect the magnitude of positivity, if you will, on those criteria. So I think they're dramatic. And I think they're going to be meaningful. So much so that when we saw those, I said, oh my god. I got a little nervous, right? Because you try to be an academic and certain things. I said, oh my god. Are these right? I don't know if they're right or not. Could you just help me check the code? Sometimes in trials. But then we went and checked all those other criteria for all the other different ways that you could potentially measure BVD and how we showed that slide. It doesn't matter what criteria you use. It's a p=0.001 superior no matter what criteria you use. So the ones that we selected as the primary endpoint were dramatically different. But then we applied all the other potential criteria, definitions that we possibly could. They were all dramatically different, too. So I think we did check and double-check and then externally validated the fact that, look, these numbers are real, however you define them. I think no matter what, we thought we'd see a significant difference. But I think what's striking is all these binary means of greater than 20, greater than 22 millimeters; those are really large differences. And that's where you get the large magnitude of that number needed to treat between the two groups that prevents the bad outcomes. But to, I think, Rich, your earlier question about how the data from SMART in small annulus patients might then be extended to the broader patient population, I think it's really putting it all together in context, which is that we keep seeing and we know from prior literature in the cardiac surgical space as well that high gradients lead to bad outcomes in the future. And that's why we see the differentiation in the low-risk data across the different programs. And so I think this is another part of the data set that show that hemodynamics do matter. And these large differences in hemodynamics matter even more. And that compounded with the fact that the 23 millimeter valve that's represented with Sapien was the most common valve used. And that is highly represented in the broader patient population, not just the small annulus. So by extension, it has an impact beyond what we classically might think of as a small annulus population. It's unusual in clinical trials to roll through all of your powered secondary hierarchical endpoints all the way to the bottom and still have a p0.001. You remember I showed you that list? It didn't matter how you looked at it. It was p0.001 better, however you looked at it, whatever lens you used. And that's why we did all those powered secondary endpoints just from a hierarchical fashion, keep testing until the very bottom of that list. Okay. We're going to just go to Chris and then Matt for the quick follow-ups here. Then we'll wrap up after that. Thanks. Chris Pasquale, Nephron. I appreciate you taking the follow-up question. Jeff, you talked about some of the clinical data around the consequences of BVD and PPM. There is some lack of consensus around PPM in particular. There was analysis PARTNER 2A and I think the Sapien 3 intermediate risk registry, which did not find a difference associated with either moderate or severe PPM. Why do you think that was? And is it possible that the clinical sequelae of these issues are different between the balloon expandable and self-expanding platforms? Yeah. No, that's a great question. Of course, you're going to hear that for the rest of the meeting, that we did the analysis. There's 2 factors, numbers of patients and time to follow up. So I would even say in the PARTNER analysis so far, I would ask, just do the analysis like we did it and follow up for everybody for 5 years and see if there's going to be a correlation between the two. And I suspect that there's going to be. So a lot of these ones, if you only do 1,000 patients, then the effect of PPM may not overwhelm the comorbidities of the patients who are all 80 years old. They have other reasons to die. It may not be that. But if you take it to 5,000 patients to find truth, which is what we did, follow the patients out to 5 years, there's a very strong correlation between that, as have been in all the surgical series. As you follow this out, just a recent meta-analysis was published of 250,000 patients followed out to 20 years, absolutely severe PPM affected the prognosis of patients. It's kind of hard to say that one orifice size done surgically and another one done in terms of transcatheter is going to have a different prognostic impact. They've got to be the same. So I would say that a lot of the other analyses have been limited by not having enough patients and not having enough time. This trial is smaller. So does that. No. I'm just talking about yeah. But the delta effects are so much more dramatic. They're so much more dramatic. And now we're going to be measuring them. So we're expecting to see those play out in a randomized trial where the differentials are accentuated. Last question, Matt. Sure. Thanks. Just quick follow-up on coronary access. We've talked a lot about the big headline differences here. But FX+ is obviously important. You mentioned the perception of making those coronaries. So maybe if you could any sense of how big of an opportunity that is, what that could do over the next year or two as docs are more comfortable avoiding that perception, if you will. I'll just speak to this real quick because I know we're over time, Ryan, is that in our low-risk trial, great trial, following patients out to 4 years, 40% of the time, we had the commissural post right smack in front of the coronary, right smack in front of the coronary. That's not great to try to re-access coronaries. And that's where a lot of bad rap happens. Then we learned that doing the cusp overlap technique, figuring out how we're going to do commissural alignment, we got to 80% with FX now. We have commissural alignment now in 97% of patients, 97% of patients. Guy Attizzani has done a study out of University Hospitals in Cleveland where in 100 consecutive patients, he was able to cannulate the coronaries with optimal alignment, concerned for the CT. So there is a little bit of a problem that we did have that we think we've now fixed. Now, FX+ is going to open up that cell right where it's supposed to be because we've got commissural alignment. And boom, that's right where the coronary is. And that's where the cell opens up. So I do think we have to drill huge concern for docs. I think the data is much, much better. And now it's going to be intuitive by being able to look, commissural alignment, that cell from the coronaries. All right. I want to thank everyone for their questions. If anyone has any follow-up questions, including those online, those that are listening online, please reach out to me or a member of my IR team. The slides that you saw today are already up on our website, investorrelations.medtronic.com, including a citation slide so you can see all the clinical references there at the end of the deck. A replay will be available later today on our website as well. Thanks, everyone, for your continued support and interest in Medtronic. And with that, we'll conclude today's event. Thanks.