I just want to try to kick it off and get people kind of excited about what you're doing and why it's working. And then I think today we have just an excellent lineup of presentations that will help really build on that. And please feel free to ask questions at any time. So I wanted to talk about how the evidence supports epicardial left atrial ablation. And my main goal is just to make sure that everyone's on the same page about this continuum of atrial fibrillation. I think we all know that many people have early stage atrial fibrillation, which is a good time for us to be acting. Guidelines now encourage us to get on top of AFib at the earliest possible time. But of course, that same patient a year later could move down the continuum. Few years later, they go further. And often patients come to us at later stages, and we just have to deal with whatever stage of atrial fibrillation we're seeing. Think of the heart as starting off as this beautiful, pristine, structurally normal organ with very little abnormality. And then time is happening, and we get fibrosis, just like our hair is turning gray. Everything else is going downhill, too. And we're all sort of destined to get AFib. Very sad story. Hopefully, we can do something about that. This is a CT scan of the left atrium shown from behind with the four pulmonary veins. And the purple color refers to high voltage, normal voltage. It's a very normal-looking left atrium. It's small. The voltage is high. It's homogeneous, just like my atrium once was. But over time, this is going to change. In those early stages, we're going to just do pulmonary vein isolation in the quickest, safest, most efficient manner we can, because that's all that patient should get. We want to leave the heart unchanged. But this patient's left atrium is enlarged. They have long-standing, persistent AFib. The color gradations show evidence of fibrosis with reduced voltage, clustered around the posterior wall particularly. And there's just no way that isolating the pulmonary veins alone is going to help this patient. And that's why left atrial-posterior wall ablation has been a target. Now what supports isolating the posterior wall? Well, for the surgeons in the room, I think you know better than anybody that Cox showed years ago that if you don't isolate the posterior wall with a maze procedure, you're not going to get a good result. And I don't know how exactly he came to those conclusions, but it's brilliant. And it's, I think, still proven to be true. More recently, we have imaging studies like this MRI study from Bordeaux. And there are others just like this that show that fibrosis, the lighter colors you see there, cluster around the posterior wall. And they will begin in any patient at some point in time. There's healthy controls there. They have a little bit of fibrosis, often in the posterior vestibule near the left inferior pulmonary vein, which is a point of tension where the pericardial inflection wraps around. With all the beating of the heart 80 to 100,000 times a day, you have stretch and you get fibrosis. Well, if you have early AFib, you have more. If you have structural heart disease, you have more. If you have persistent AFib, you have more and more. And it really is clustered around the posterior wall. So when we talk about isolating the posterior wall, it's not just because it's a target we can get to or work on, it's because that's where the money is. That's where the problem is. So electrophysiologists, like the electrophysiologists in the room, we all want to isolate the posterior wall in patients with advanced AFib. But how do we do it? Here you see these endocardial lesions superimposed on CAT scans. You might do a single ring around everything. You might isolate the veins and then do the roof and floor lines. You see an A. You can do different things. Many people end up ablating a lot with endocardial lesions within the posterior wall itself trying to isolate the vein. It's not really very effective. It's not really isolation. It's sort of debulking because it's very hard to get to the epicardium from the endocardium safely in this region because the esophagus is laying right behind there. It's very hard to go across the roof reliably because it's very thick up there and there's interposed fat. And so we don't do very well. Here's a good example, just one of my cases. It's actually a very recent case. That's the map of this person with long-standing persistent AFib shown in our traditional view. Posterior wall's all patchy. Got a lot of fibrosis. Well, I love doing this single ring because when it works, it works and it's quick. But here's the problem. You isolate the veins. They're isolated. There's spontaneous firing going on in there. There's exit block. There's entrance block. I've isolated the posterior wall here. But 30 minutes later, the posterior wall is active and you see this sort of breakout point. And what's happening here, and we've all seen this a hundred times, is you see this point of activation in the posterior wall and physiologically what's going on is the roof line didn't quite get to the epicardium durably. And when you look along the endocardial surface, you can't see the point of connection. But epicardially, there are live fibers which are taking the impulse over the roof and then it just joins up on the endocardium at various points and that's what you see here. And this is what leads to now starting to ablate in that posterior wall, peppering it with all these lesions trying to fix that up. And it adds risk for the esophageal damage and it is, of course, not really isolating the posterior wall. You're just trying to fix up something that just didn't work in the first place. And the reason is because of all the complex fiber architecture. This is a great study where that approach was used and then catheters were put in the pericardial space. And what you see is that the endocide, hey, it looks great. It's gray. There's no voltage. But on the epicardial side, there's still all this patchy surviving tissue that's being activated. It's being activated by epicardial fibers that are jumping over our lines. So when we talk about isolating the posterior wall, my message to all the surgeons is we're really relying on you to do something that we're just not able to consistently do safely and durably. And that's really what we're trying to get out of our surgical partners. Amongst other things, too, like clipping the appendage, as you well know. So what do we know about our studies, endocardial studies? Well, here's the three big ones, ERASE, STABLE, SR2, and CAPLA. ERASE and STABLE SR2 are almost identical studies. They have different outcomes, but they're essentially designed in the exact same way. They're about the same size. They're randomized studies. They're comparing isolation of the veins to isolation of the veins and low-voltage areas. CAPLA was an empiric posterior wall isolation study. What you can see is two of these three studies have absolutely no difference. CAPLA was, I think, one of the best ones. And what they did was they said, let's just do PVI and paste it with persistent AFib, or isolate the posterior wall by traditional means. They often had to do the same thing that we talked about, trying to pepper the posterior wall because the lines were incomplete, which is always a bad sign. And there was no difference. They followed them for 12 months, whether you just did the veins or empirically did the posterior wall. Now, why didn't it work? Well, maybe some of these patients don't need their posterior wall isolated, but the other problem is they didn't get posterior wall isolation in most patients, and there was a lot of recurrences. This study used a similar method. They did show a difference. They were isolating other areas of low voltage, so maybe it can work sometimes. They did the exact same trial, done differently. Another version of it, SR2, didn't show any difference. Here is a sub-study, and what it did show is that when the posterior wall is abnormal, it does help to get it isolated. So again, that's where we come in. We need to be able to do it reliably and safely, and if we can do that, we'll get good results for our patients. Okay. What about hybrid approaches? It's a totally different story. Every major trial that's been done using a hybrid approach, which involves a surgical or epicardial ablation of the posterior wall, is a positive trial, showing it's better than not. You're very familiar with the CONVERGE trial. It was my pleasure to lead that trial from a physician's perspective. The results are shown there for the entire population of persistent and long-standing persistent. It was actually much more dramatic in patients with more advanced AFib because the value of the posterior wall isolation really shines in patients who have a lot of structural heart disease. CEASE-AF is another example. It also had a very positive outcome using a different type of hybrid approach, again, involved with surgical isolation of the posterior wall, and HEART-CAP-AF as well. These are the hybrid trials, and they always come out positive. The CONVERGE procedure, you know, you'll see more about it, and you'll work with the tools. Our standard approach in the early days was just to do an epicardial or subxiphoid approach, and we didn't do any, in the CONVERGE trial, we didn't do any left atrial appendage management, no additional lesions. It was a very basic approach, just getting that posterior wall. So you had that single trocar approach, get the posterior wall isolated with the epicents, touch it up endocardially. In the CONVERGE trial, it was all done in the same day, same anesthesia run, showing that that is feasible. The results were great, as you saw. What's so different about it? Well, when you make an endocardial map, and this is an endocardial map of one of our CONVERGE patients done right after they've successfully had their posterior wall isolated, on the endocardial side, as you see in the map, it's totally grayed out. There's absolutely no voltage after we complete the hybrid procedure. When you ablate epicardially, and I measure endocardially, if you've ablated the tissue epicardially and there's no voltage endocardially, what have we done? We've proved transmurality. This is something we cannot do endocardially in a feasible way. Proving the transmurality of our lesions is so critical, and it's really the secret sauce of why the CONVERGEnt procedure works so well. So this is just something that we can rely on, that we always get these good maps. We're not getting firing in the posterior wall. We're not jumping over and activating the endocardium from the epicardium. None of that can happen when you've done these epicardial lesions. So just keep that in mind if you're doing one of these cases as a surgeon and you're getting bored because it takes 90 seconds to put in a lesion, just remember it works. It's important what you're doing. Now this is a very recent trial, the four-year follow-up outcomes of the CONVERGEnt study. This is the spectrum trial. Preliminary results were made public at HRS in May, and it is available online. So these slides look a little funny because they're those kind of online slides. But the results were very good out to four years. You can see it starts to tail off, and I think that's typical of any kind of ablation, but still you have a good absolute result at four years. And if you look at the persistence for this long-standing persistence, they sort of track really nicely for the first three years. I mean, it's a pretty good result, and I think that really proves in this difficult-to-treat long-standing persistent group how effective the hybrid procedure is. And this, I think, is a big question for patient selection that everyone wants to know. A lot of people are reluctant to consider the CONVERGEnt procedure as a de novo approach. I feel very strongly, and this data supports it, that it really shines in a de novo approach. Why? You get that very consistent lesion set, it's controlled, it's veins and posterior wall, the right cable tricuspid isthmus, there's not a lot of other stuff, and it works great. By the time people are failing a bunch of ablation procedures endocardially, and then you do the hybrid procedure, it'll still work, it's just not quite as effective because who knows why those patients are failing their endocardial. They may have all kinds of other things we have to sort out that can't really be sorted out by CONVERGEnt alone. So always think about a de novo approach because I think you get a really good first stab at these patients with excellent long-term results. So CCAF we talked about, this was a randomized hybrid approach, and basically you got either the hybrid or the endocardial. I showed you the results, it's very effective. I love the design of the study, I just think, again, it's more randomized data for us. You can read that. There's the results. It's these major differences in outcomes, and it's very much like CONVERGE. I mean, these are large, large absolute and relative differences when you use the epicardial ablation. Heart cap also good. Heart cap involved posterior wall isolation in the endocardial arm, too. So some people have been critical, they're saying, well, if I do it endocardially, it's going to be just as good because I can do it good endocardially. But what you can see here is, again, it really makes a big difference when it's done surgically. It's just going to be more durable. So I want to plug the CONVERGE post-approval trials, my final slides here. And as a moderator, I'm taking liberties with the number of slides I show, and I apologize. But no one else is allowed to do that. So the post-approval study was mandated that we wanted more safety data, more long-term data. So we're enrolling the post-approval trial now. And I think that this is really important. There are some people in the room who are investigators, others who are not, who maybe can become investigators or refer patients into the trial. It's a very important trial, and it is expanded. It now allows enrollment. It is for long-standing persistent. You can do the appendage as part of this. They can have had up to two prior failed endocardial ablations. It really allows us to, and it can be staged. It doesn't have to be the same day like the original CONVERGE trial. Most people do them staged now. So you have a lot of freedom. Almost any patient you would consider for the CONVERGENT procedure could be a candidate to be in the post-approval study. So we really want you to keep that in mind because it's an important trial for us to get before the FDA. So in summary, CONVERGE provides a proof of concept that durable left atrial poster wall ablation, when added to PVI, improves outcomes. And it's dramatic, and it's been durable, as you saw in some of the other trials. So other hybrid therapies, as a surgeon, keep an open mind. There's a lot you can do with your electrophysiologist to control AFib. So we've seen that other types of approaches that are not just the CONVERGENT procedure are also effective. RF, radiofrequency catheter ablation, which is kind of a big thing for us, it is improving over time. And we've found that we can get more efficient work done. But we still haven't got to the point where we can really treat longstanding persistent AF effectively. And there are other things coming out, which you're going to hear next from Nitesh about pulse field ablation. Everyone wants to know, well, does pulse field ablation make everything obsolete? So we'll hear a lot about that. My only point that I'll make right now is that we really haven't studied advanced AF in pulse field ablation. So it is a leap of faith to think that that will be effective. I think substrate-guided approaches with endo-only technologies, we talked about some of those trials briefly, they haven't really panned out consistently to be effective in the advanced population. I do think that there is something there. We keep learning. But for right now, we know that the CONVERGENT approach is proven effective.

epicardial ablation

atrial fibrillation

hybrid approaches

pulmonary vein isolation

CONVERGE trial