So, my topic is, you know, how to use hybrid ablation to treat those really complex patients. In the past, when I've spoken at conferences like this, a lot of my discussion points are program building. I started doing hybrid ablation, for me personally, 2016, when I was part of a big academic institution. I left in 2020 and joined a private practice group, and they had no hybrid ablation. And so I had to initiate that program, and so a lot of times I'll discuss, how do you do that? How do you approach your partners and referral docs, and how do you take a big practice of EPs and get them turned on to this concept of hybrid ablation? So I'm going to show you kind of our algorithmic approach, but across a landscape that includes multiple EPs and multiple hospitals, a little bit of the outcomes that we've gotten in our program, and then, again, building on what's already been spoken about by Kevin, some of the mechanistic background for that. So I work for an organization called Palo Alto Medical Foundation. It's part of a large healthcare system called Sutter Health. So in PAMF, we have these three EP groups that cover four hospitals doing procedures, 12 total electrophysiologists across that landscape. I actually don't know. 1,500 was kind of like calculating everybody's average annual cases, so I don't know the real number. But when I joined the practice, I knew that I had to try to introduce this very softly in terms of how I would encourage people to adopt a hybrid approach. So one of the hospitals I work at had doctors that were very impressed with the CONVERGE trial results. I had a very skilled thoracoscopic surgeon, and so we introduced CONVERGENT hybrid ablation there, and they picked up their program nicely, and we have a very good program going there. The hospital I primarily work at had a different type of experience in terms of those electrophysiologists. We're not as keen to refer patients for first-time hybrid approach for persistent AFib. So I introduced the TT, the totally thoracoscopic approach, to that hospital, and again, we're about even par in terms of how many cases we do per year. I started in 2020. Our first cases were at the end part of 2020 in both hospitals, and to date, all the EPs across the entire program are sending us patients, which I think is a reflection that we're getting good results. And just to give a little more background on what I was dealing with with my individual practice within that group, Roger Winkle, some people who are an EP have heard of him. He's been around doing catheter ablation for AFib since 2003. He's a well-known name. And one of the things our practice does is we've been published for a lot of our outcomes. So this is a paper we published in Heart Rhythm in 2020 on our individual practice results. And so part of what I want to demonstrate here is we talk about all the CAPLA, all these other results, but everybody has their own internal results, and if you've ever talked to an electrophysiologist, what they tell you they get in their case results never reflect what we see in these multicenter national trials. So you can see demonstrated here with our ablation attempts, the left-hand graphs there represent first-time single catheter ablation strategy based on type. Paroxysmal obviously does better. Persistent in them, we do divide them into persistent and long-standing persistent. Obviously, the single procedure success rates aren't as good. And I would argue that if you look at the long-standing persistent population, that's pretty similar to CAPLA. But nowadays, hybrid ablation is a two-stage procedure, and so a lot of electrophysiologists are going to push back on a single technique because they're going to say, well, if you get two procedures, I want two procedures. And so the right-hand column there is our two-procedure success rate or multiprocedure success rate for AFib. And this is, on the bottom, we're not talking months. I mean, that's years of follow-up data. And this is just so you know what follow-up data, because that's pushed back on that as well. This is two-week patch monitors, worn at three months post-ablation, then at one year, and then annually thereafter. And so our results don't look too bad, and in fact, they look fairly similar to what Convergent showed. So just recognizing there are challenges, and you've got to try to introduce these techniques to people, and you're going to run up against their biases. And this is just part of the equation. So when looking at our large hospital system or a large organization, two hospitals doing this procedure, this is kind of our breakdown since we started. So this was, again, starting at the end of 2020. The orange graph represents the totally thoracoscopic cases we do, blue being the Convergent. And we've been pretty steady. I will say, I lost my surgeon. So all of a sudden, the orange graph is getting shorter, but I'm working on fixing that problem. And so here's sort of our algorithmic tree on how we would do it. Again, it's not as clever as Kevin's, but it works under some of the same principles. And I think a lot of busy doctors just want to be simple anyway. So if you're looking at the paroxysmal population, I don't think there's any equivocation here. Never been ablated before, do a catheter ablation. That seems to be standard recommendation. I don't think anyone's recommending hybrid for these patients. And I say less than two, because that's our program. In our program, we say give them a couple shots to see what happens. Now if they have failed multiple prior ablations and it is still paroxysmal, it doesn't mean it's not the same mechanism. So this goes back to the concept of non-PV-triggered ablation, right? So you've isolated the pulmonary veins, you've been in there a second time, you know their veins are isolated. So now what do you do? Now you can offer the hybrid approach. And so where I'm going to kind of shift and what I think is a big focus for me is that I always ask, are they having flutter? And I don't mean typical right-sided flutter, I mean flutter. And I will equivocate a little bit. We use mitral flutter all the time, and I'm going to show some images, and Kevin showed them too. I don't know why we say mitral, I mean, yes, left atrial, sometimes it's septal. You know, any of us that are EPs, you go in the lab, sometimes they follow the rules of entrainment on the mitral valve, but these are complex arrhythmias using these epicardial circuits. So the mitral valve just happens to be in the left atrium, but mechanistically, I don't know, the mitral valve doesn't seem to be contributing much to it. So then you can use the algorithm to say, well, if you're having atypical flutters, we don't have a convergent approach to manage atypical flutters. We use bilateral VATs to manage our atypical flutter. And so similar, persistent AFib, now you shunt your decision tree to include hybrid as the first procedure. And you can still go back to the same sort of question, are they having atypical flutters? And then in our case, we go to TT hybrid. So this was a different sort of cartoon version of what these epicardial circuits are, what are contributing to these atypical flutters in patients. And again, I mentioned in one of the earlier questions, when you look at a lot of these persistent AFib clinical trials and you look at what the recurrences are, these aren't 30% to 50% of patients coming back with atrial fibrillation. In fact, I would say we're pretty darn good with substrate ablation, eliminating AFib even after an initial procedure. But what you do get is a ton of complex atrial tachycardias, SVTs, and atrial flutters. And so these are the different ways in which we can get atrial flutter. So, and Kevin showed it, you've got ligament of Marshall, coronary sinus, probably an extension of the same mechanism. You've got Bachman's bundle, and you've got the posteroceptal bundles. Now, posteroceptal bundles are probably one of the main reasons why we target the posterior wall. It's certainly, in my opinion, why I think convergent is so effective, because I think those are the structures that are being addressed that we don't get with endocardial pulmonary wall isolation. This is a Rod Tong doing actual mapping, and I think one of these images was actually in Kevin's talk as well, and again, demonstrating the actual activation pathway of each of these different mechanisms of atrial flutter. But what you see is this is a epicardial disease. This is an epicardial mechanism. You know, I'm like every proceduralist out there. I've got a huge ego. I'm very arrogant. But I absolutely know I cannot fix this. I knew I couldn't fix this, because the number of hours I spent trying to fix this endocardially, and with all my God-given gifts, I just couldn't do it. And so some of the heart team approach of working closely with your surgeon, and you know, you see Andy and Kevin, how they work in a sandbox, even starting at a young age. They look very different now than they did when they were kids. You know, you can bounce these ideas off your surgeons, and you can come up with these creative ways. And it's an absolute honor to have Dr. Cox here in the audience. But you know, on the shoulders of giants, we know all of this, right? This is not new information. There are people who have proven over and over again mechanistically what's going on. As an endocardial ablationist, I just don't have the tools. I don't have the skill set. I can't do anything with it. But one of my tools is I can talk to somebody who does have that skill set, who does have that capability. So anyway, Dr. Dunnington, Dan Dunnington, and I were working doing these cases as part of my new program. And he mentioned the Dallas lesion set. We talked a lot about what had already been proven before. And we thought, well, maybe there's a better way to go after that. And there's certainly plenty of data that when you try to treat mitral flutters by doing maybe the original design by Dr. Cox, going on the posterior wall, doing the isthmus line, you're not getting the same good long-term results, whether it's challenges ablating in the coronary sinus or whatever. And here's a nice review, literature review, looking at all the available data showing that on every level that you could look at in terms of safety and efficacy of targeting a mitral-related flutter, that they all sort of actually favor going anteriorly as opposed to laterally or posteriorly. So this is the lesion set from January 2021 to today. Every single one of my totally thoracic hybrid cases has had this lesion set. So it's very similar to what Andy and Kevin showed in terms of, yes, we come from that left upper vein near the base where the clip has been placed, ablating towards the mitral annulus. And obviously, we're not using the epicenters. We're using an MLP. What I also include going from the right upper vein also towards the mitral annulus kind of makes a V. Now, one of the things about the story with GERDISH and getting into these incessant arrhythmias, and I am not a surgeon, I see the camera the way everybody else does, but I don't understand the anatomy the way a surgeon does. There seems to be a gap between where the aortic root is and where the mitral annulus is that the surgeons, at least through a thoracoscopic approach, just can't reach. So there's always that little band of tissue that does have to be ablated. So this is a common case where this is after stage one. So Gann has done roof and floor, pulmonary veins, and these anterior lines. And so this is what I get when I come into the lab. And I would argue his ablation was phenomenal, but clearly, it's not precisely obvious where their lines are. Now, I've done a lot of these cases. I've done 120 plus of these cases, so I know where they are. But ultimately, the V that's demonstrated in the very left-hand image, this is looking at the front side of the heart now, right? I've talked a lot about posterior wall, but looking at the front side of the heart, I can find that point where these two lesion sets overlap. And similar to what Kevin and Andy do, that last little tail that gets you from where that crossover point of those epicardiosurgical spots to the mitral annulus, that's really easy. And similar to the experience discussed, I would say more than half of the patients that have undergone stage one, they come in in a flutter. And I don't even treat them. I'm like, let's just rate control them in between the two stages. I'm just going to figure out what it is. And I would say 90% of those cases, when I'm ablating, I start at the mitral annulus and work my way up towards the right superior pulmonary vein. And usually, the lesion that I do that hits the most distal point where the surgeon was able to reach, we terminate. And I said 90% of the time. And these are patients who, they're tough cases, right? So we've got a long history of doing ablation. We've got something like 9,000 to 10,000 case history in our practice. So a lot of people who were ablated decades ago, they are going to come back for recurrences. Unfortunately, I haven't updated my data. I apologize for that. But this was the first 50 patients who had more than a year follow-up data on. It was 3.3 average prior ablations. And so the other unique part of them is that they were not coming back with AFib. These were just these complex AT, atrial flutter patients. And we did this and wasn't really clear how it was going to turn out. And it's been very successful. I would say that the numbers have shifted quite a bit. I would say the number of prior ablations is starting to creep down because people aren't waiting. They're not struggling and failing three to four times before they send me patients now. I get them earlier. I would say the number of patients presenting with complex flutter is going up. So it's probably 80% of my referral patients now. And the success rates are sustaining so far. I mean, it's easily above 80%. One of the things I tell people is that this is the one procedure I do. And obviously, it's not just me. It's everybody involved. But this is the one procedure I do where at the one-year follow-up, these patients just cry. I mean, they come in, and they talk to you. It's like, how are you doing? Oh, I'm great. I'm back to my golf. And you're just chit-chatting with them. It's like, great. Well, you don't need to see me anymore. And then they just break down crying because these are the patients. These are that last little tail of that Gaussian curve where they debilitated, not responding to any therapy. Forget about t-cassin. It didn't touch them. Forget about any prior catheter ablation. And they've never experienced 12 months continuously without any AFib or any arrhythmias. And so it's a very powerful approach. And I apologize. I don't have a thank you slide. No, thanks. Hey, can we go back? Just go back to your lesion set slide. So explain your two anterior lines. Where are they going? So this is looking from the backside or from the top down on the atrium. So you can see anterior wall. You can see posterior wall. And so the encircling, let's see. Well, four is probably the one lesion you're talking about. Yeah, four and six. So four is coming from the left upper pulmonary artery. So four is coming from the left upper pulmonary vein roof line junction, right? So he's done roof with MLP. He's clamped for the veins. He's already clipped the appendage. And now he's going to tie in sort of that roof LSPB and then head down towards a mitral annulus. And then six is the same from the right side. So sort of dissecting down, getting where the RSPB, much more septally. So you see it drawn there, because that's actually the quest of mine, is to try to come from that side of it, RSPB between the SVC in it, and then, again, extending down towards the mitral annulus. Yeah. So you've basically isolated the anterior aspect of the... So you see in the final picture, RSPB down to the junction, LSPB down. So this is where they tend to get their ablation down to. And if I go back, you can see this is kind of the tail of their scar. This is just mitral annulus. This is not like ablation scar or anything like that. So this tends to be every single case where I pick up where their lesion set is. And I think that's a lot of what Dr. Cox was referencing, is that that little gap between where they can reach and the mitral valve is now going to set up for what is, in my opinion, the actual true mitral-dependent flutter at that point. Got it. So actually, you're not really isolating the whole anterior wall, you're doing a triangle and it meets at something. One of my objectives is that, obviously, the right atrium is over here somewhere, and I want to maintain this conduction pathway that can actually come from the right atrium down along the back and then still contract laterally in the left atrium. I mean, you want to see contraction. It's another criticism that we get. There's not much functional, structural, atrial contractilities remaining after you do one of these big, aggressive ablations. And so I like to demonstrate my maps and show, hey, this is what I leave. And I would say most of what's been ablated is not contributing much to contractility. And in fact, the cases that are my failures are because somebody else went hog wild and ablated everything. And there's just not enough preserved tissue to maintain normal conduction after that. What does number six add for it? So I don't know. I don't know. I don't have an answer for this. Other than when you do, and just as anyone who knows anything about endocardial mapping, I was at a critical institution that did firm mapping, if you've ever heard of it. And so this is the idea that you can map it in a complex arrhythmia, focal impulse, rotor modulation mapping. And so you would find these critical sites that would pop out here. So there's a focal site here. There's a focal site here. This one we actually deemed eponymously the area of Chad. And so I did build the lesion set a little bit off of this informed experience. And so knowing that this is almost certainly one of the Bachman insertion sites over here. And then obviously we know Bachman extends out and connects to the appendage. Okay. We take care of that. There's another nice deposition site. Plus the ligament of Marshall activation can come through there. So in a way, I was just trying to take out as many of those known mechanistic sites as possible. But have I done anything to compare eliminating one of those two? No, I haven't. So Chad, are you, the four and the six epicardially, are you completing the triangle endocardially? Is that what you're doing? Yeah. Okay. Yeah. Let me ask it to you. I don't mess around. I just, even if there's part of it that looks good, I ablate the entire line. And I don't know if you can see. So we call this the SAMI, which was deemed by an Atricure employee, Tom Loman. And so it stands for sequoia anterior mitral Y, because it looks like a Y when we're done. And I even do this little caterpillar walk. Actually, you guys start seeing what I'm doing. I do this caterpillar walk. So I'm really worried about the thickness of that tissue and making sure, since I don't know exactly where their line is, I got to make sure that's transmural, there can't be any gas there. And then this one, for whatever reason, it's an easier line to do. And then I'll pace around everywhere in here just to confirm that nothing captures, nothing's exiting. Yeah. So we've been very pleased with our results. But in terms of hybrid programs, I would just demonstrate that you can do what no one else can do. I mean, no matter how good the ablationist is, I mean, there's just so many more options when you get into that epicardial space. And when you think back to some of those anatomic images that were shown in other people's presentations, there's a lot going on. And a lot of these epicardial circuits are for fast, rapid conduction, right? So if sinus node is kicking things off, you don't want there to be tremendous delay between right atrial and left atrial contractility. It's the same principle as synchronizing the ventricles, right? And so Bachmann's post-receptal bundle, that's what they're there for. I mean, these are some of the original progenitor cells originating from the sinus node that create these tracks. And they're fundamentally different in terms of how they do conduct. They're fundamentally different in terms of how they interact with the surrounding tissue. And so they cannot be dealt with the same way we do isolating veins and posterior wall. They have to be dealt with through this epicardial strategy, or at least that's my opinion.

hybrid ablation

atrial fibrillation

Palo Alto Medical Foundation

Convergent approach

thoracoscopic ablation

multidisciplinary collaboration