So this is a relevant thing. I think I've learned a lot about this, actually, in the last few years, things that I just didn't imagine. And part of it's due to the mapping systems that are available now. I think we've learned some of the detail of the circuits, which we didn't understand before. And we used entrainment alone as quite helpful. But being able to visualize the circuits has really helped a lot. In terms of what you're going to see, it's good to anticipate what type of atrial tachycardia you might be facing when you go in to ablate that patient. Now, obviously, if you do the case, the first case, you're going to have a much better idea because you know what your lesion set was. Hopefully, you know you did a great job, so everything's blocked. And you know whether they had de novo fibrosis. Also, that if you did a PVI in a patient with normal left atrial voltage, the chances of them having AT are pretty low. And if it is, it's probably related to something right around the edges of the pulmonary vein. So there probably are two gaps in a pulmonary vein, and there's a little reentry. I'm not going to really talk about that. I'm going to give some examples of the cases that I think are a little more difficult to sort out and sort of what to look for. So the stepwise approach, so if you went, we used to do this actually a fair amount. This was the Bordeaux old approach where they went to try to ablate patients back to sinus rhythm. And that involved a number of lines. It involved doing CAFE ablation in the septum. When you use that approach, you see a lot of macro-reentrant ATs in follow-up. In fact, often, it was actually fairly uncommon to see AFib in our hands because we probably did even more extensive ablation. But at least 50% of the patients would come back with some form of AT as opposed to AF. And most of that, three-quarters of that, was a macro-reentrant arrhythmia, probably because they had done incomplete lines. And if you look at other approaches, double-lasso WACA, this was mostly focal, although, you know, I think if we went back and remapped a lot of these cases, they probably wouldn't be focal-focal. They would probably be some small reentry circuit. 80% macro-reentrant after you do the Paponi approach, which was anatomical rings without really checking for block. And then sort of Natamani using a CAFE approach where, again, similar to the Bordeaux approach, but not trying to isolate the veins or do lines, in particular, just ablating CAFEs until termination of the AFib. And then you'd start to see the worst ATs, actually, septal and free wall reentry, which can be probably one of the more challenging things because there's not necessarily a clear endpoint in those ablations. So this is literally a patient I did beginning of this week. When you see this, it's pretty much bad news. First of all, they're probably not going to do very well with any ablating you do. What do you ablate? I think I ablated that and that, maybe that, not really. But I think what we know is that when you see fibrosis, the chances of having an AT on coming back really high after ablation. This is extreme, but clearly this patient you have to worry about. You can actually predict somewhat what type of reentrant AT you're going to have as a function of where the fibrosis is. First of all, if you have low-voltage areas, this was a paper, a Japanese group, that looked at inducibility of atrial tachycardia at the time of ablation. And what they found was in patients who didn't really have low-voltage areas, you didn't really see left atrial flutter. You could induce AFib. You could induce common atrial flutter, but you couldn't induce macro-reentrant, root-dependent, perimitral, or other ATs very frequently without background fibrosis. With fibrosis, not only could you induce AFib, but you could induce multiple other left atrial, and everyone who knows this. So I always ask the fellows in our institution, when we see someone with de novo left atrial flutter, what's the one thing you're going to see when you go in that left atrium? You'll map it, you'll figure it out, but you're going to see fibrosis in that atrium. You just don't have de novo left atrial flutter in the absence of fibrosis. It's really just pretty much not going to happen. And the region of scar seems to also produce or predict the type of atrial tachycardia you might see. So perimitral ATs are associated with more septal fibrosis, roof-dependent, more posterior than septal. So not only does fibrosis predict that you're going to have AT, but where you have the fibrosis may actually predict the mechanism. So let's start with a case. And I tried to pick cases. They're not simple. I tried to pick cases where I was illustrating a point that I thought was particularly useful to know. And so there's essentially three cases, and then I had some bonus cases, depending on how things are going. So this is a 65-year-old man. It has a history of persistent AFib. He'd been in it for a year and a half, so almost a year and a half. He had prior ablation with pulmonary vein isolation. He had cafe ablation on the septum and in the anterior wall. Not something I would have done, but he came back to us. He presented for a second ablation with recurrent AT. We put a duodecopolar catheter. 10 poles lie on the lateral RA and in the CS. We'll show you a picture of that. And then we overdrive pace, 20 milliseconds faster than the tachycardia cycle lane, from the distal coronary sinus. I'll show you the, first of all, the setup. So this is that duodecopolar catheter. What happens, you put it from the leg, and you loop it around the right atrium, and it goes out into the coronary sinus. There are 10 poles on the right atrium and 10 poles within the coronary sinus. Actually, and I think this is an important point, it's really useful when you're mapping these atrial tachycardias. And I know this is sort of maybe what the opposite of what Brad teaches of using fewer electrodes to diagnose things. But I find in these atrial tachycardia cases, frequently there's not only just one, there may be multiple. And it can be tough to tell changes in tachycardia mechanism even when you only have a coronary sinus catheter. And so when I get called in to help people, okay, well, I can't figure this out. I say, well, consider let's put up a catheter in the right atrium, and we can watch activation sequences. We get a much better idea of the mechanisms when you can see what's happening in both the right and the left atrium. So here's the tachycardia. And I'm gonna ask you a question about this pacing. And the question will be, based on the response to overdrive pacing, what is the most likely rhythm diagnosis? Is it macro-reentrant flutter involving the anterior wall of the left atrium, a focal AT from near the distal coronary sinus, perimitral flutter, or a focal AT from the left inferior pulmonary vein? So this is the, and I'll tell you that this, and there's a poll up with the different choices. And I'll tell you, this is, I'm not trying to fool you about whether we entrain this. It's entrained. This is entrained. This, we accelerated the atrial cycle length to the pacing cycle length. Okay, so we had a fair number of people. So there's the vast majority of people stop sharing. So the sharing results, great. So perimitral flutter, three quarters of people, and I think that that's the answer. Again, I said most likely, I didn't say this is definitely the diagnosis, but I'll show you why I think. So this is just an important pacing tip that can help you sort out arrhythmias. And this particular finding is really pretty good for perimitral flutter, which is, I think, the answer. And there's a couple of key observations. First, you always check to see whether you actually accelerated the tachycardia. So that's number one. And when you take the boards, that will be on there. They'll show you something that looks like you could interpret it, but then it turns out you can't interpret it because you never caught up to the tachycardia or you didn't capture. One of the tips for that, if I go back, is that just eyeballing it, you look and see that this pacing stimulus relationship to the previous beats, to all the tachycardia is fixed. So this is changing. The stimulus to that electrogram starts to change since you're not in a stable relationship with pacing. So that's one quick thing you can do to look at and tell whether you're in train. Now here's the other key observation. So first of all, the post-pacing interval is in. So when you're pacing from the distal coronary sinus and you see the return cycle, you can see that that's in. So the tachycardia, that particular electrode is in the circuit. The other key observation is that all the electrograms that are upstream are also in the circuit. So if you measure this cycle, that cycle, which I measured in blue, that cycle, those are all the pace cycle lengths. So this is going all the way around the circuit to get to these electrodes. So these are orthodromically activated. So you're pacing from an electrode that's just right next door. So how do you do that? Well, you have to be in a re-entry circuit and you have to be in it, dead in it, in order to see this sort of preserved orthodromic activation upstream. And so if the coronary sinus is in that circuit, chances are it's perimitral flutter. Left inferior pulmonary vein wouldn't preserve all of these electrograms orthodromically because the proximal part of the coronary sinus wouldn't be in that circuit. Nothing focal would look like this. So focal ATs don't behave like this, and I'll show you data on that. We looked at CTI dependent perimitral and focal ATs and some other macro like roof dependent. What we found was you see a very long stimulus to upstream electrogram, more than 75% of the tachycardia cycle length in every case. Every case where you're in the circuit or close to it, you'll see this same phenomenon. You'll see this phenomenon, long stim to upstream electrograms in every case. It's the nature of reentry when you're in or close to the circuit. Focal ATs, you never see that because there's no reentry circuit. There's no second wave front to collide with your pacing wave front. You can't set up the situation of constant fusion, and so you see a short stimulus to the formerly upstream electrograms, and so you get a short stimulus to electrogram time. And then if you're far away from a macro entrant circuit, you'll also see that sort of focal response. So this can be really useful. You can do the whole map and figure out where you want to ablate, but there are chances of this being perimitral flutter are extremely high. Now a lot of people would say, well, I don't like to pace tachycardias because I might change them or terminate them. First of all, it may be helpful to decide where you're going to map. So you could map both chambers, but you could decide, okay, well, I know this is in the right atrium because I just paced and it's out. The truth is that you will not terminate or alter tachycardia if the tachycardia cycle length is stable and you don't pace much faster than the tachycardia itself. The risk is only, there's a 99.5% chance you will not terminate or alter that tachycardia with a pacing train if you pace close to the tachycardia cycle length and you don't pace tachycardias that are quite unstable. The other key to remember, and this is probably half the reason that people terminate tachycardia, is you don't synchronize the pacing to a reliable atrial electrogram. So what we've done here on our mapping system is we pick an electrogram that it can sense. So usually we try to pick the catheter we're pacing from. In this case, it's the ablation catheter. And we make sure that this electrogram is being sensed reliably so that when you come on pacing, it's not going to pace here or here. If it comes in too early, it will terminate the tachycardia. If the first beat is synchronized, it comes in at almost the tachycardia cycle length and now it's slightly faster, and now you can see you're accelerating. So syncing it is probably the most important thing, and many people forget to do that or don't even bother to try. And that's a big mistake, because you'll terminate a lot of tachycardias that way. This is sort of the idea of downstream pacing, where you've got a circuit like this. You've got electrodes upstream and electrodes downstream. If you have your electrodes here and you pace here, you get orthodromic activation of these upstream electrodes. If you pace way up here and all of your electrodes are downstream, you don't get that same effect. So one of the things that I always do is I try to pick an electrogram that's downstream so that I might observe this upstream pacing effect with re-entry. This is another cartoon to demonstrate the same thing, where we put a pen array into a circuit. Say here's a figure of eight circuit. We pace in an isthmus, and we have electrodes that are both downstream and upstream. I'm recording electrodes that are downstream and upstream from that pacing site. By coming in and pacing more downstream, and I have some upstream electrodes to look at, I can watch the whole circuit go around and get that long stimulus to upstream electrogram timing. That, number one, proves that I've got re-entry. And then second, can tell you whether you're close to the circuit or not. So here is another case where we bring a patient back, and we did activation and voltage mapping during sinus rhythm. And you can see on the anterior wall, there's a fair amount of scar around the pulmonary veins, but also sort of on the anterior wall of the left atrium. If you put this sort of early meets late indicator, you can kind of get this idea that there's potentially a line of block along the roof of the left atrium. Following the baseline mapping, which is misspelled, we found that the PVI in the posterior LA was isolated, CS musculature isolated. We created a mitral line in addition to isolating CS musculature, and then we induced atrial flutter with rapid pacing. Here it is. This is the pederates and the left atrial appendage. The CS looks, there's really no electrograms left in there, and this is the right atrium. We had done this lateral line here. So tell me if I play this, you can kind of tell from the activation, I'm sorry, I don't know why. I hope this isn't true of all these, don't know why this isn't playing for me, sorry about that. It was playing earlier and it was, trying to see, if I close it, it's a bummer. Hopefully not all of these will be like this, but I may have to go back to a previous version or something, sorry, Nishant. What we see here though, is that there's a, what looks like a focal source of tachycardia on this side of a line that had been created. Here's early spot. So this is activation. This is the voltage. And you can see here's early, and then here's late. So the activation breaks out in all directions here and goes around the valve. It'd be nice to look at the movie, but here's the activation map. If you had, so what's the best guess as to the mechanism here? Is this a focal AT at the base of the left atrial appendage? Is this a reentrant atrial tachycardia? Or is this a problem with mapping and we just need to remap? so the answers are coming in fast and furious. So focal AT wins and I would say you know yeah you'd think that in most cases because that's what it looks like. There's probably you know possibility is there's a line of block here already. There's a focal atrial tachycardia in this spot and it just looks like a reentrant arrhythmia because there's block here already. That's one possibility. The other possibility is that there's no electrograms that we can record here but there's a macro reentrant circuit going around and somehow it gets from here to here and you can't figure out where that is. You know you're not picking it up. What's between here and here that might be a bridge between this part of the atrium and that part of the atrium? Well the vein of Marshall and so I think you know this looks like a focal AT and I can't tell you by looking at this map per se what it is but one of the things you can do is you can train it and try to figure it out and what that's what we did. So this CTI was out. Deep in the left atrial appendage out. Lateral mitral valve annulus is in and the septal mitral valve annulus is in. If this were a focal tachycardia that would not be the case. So we have a macro reentrant arrhythmia and I can tell you I have seen this a million times. Now could you ablate this site and be successful? Yes but it's not the reason you think. You think well I diagnosed an atrial tachycardia that's focal and I ablate here. I got the focus. We're done. That's not what's going on. In this case actually it did terminate with ablation. It did terminate with ablation by pacing in this particular site. However one of the issues is what you did was you just dove into the vena marshal, went up some the ridge somewhere. You can't find it. It's somewhere epicardial and then where it touches down is one single spot. You've ablated away all the other potential touchdown points of this ligament except right here. And so what you're doing actually is you're ablating the last final return spot for the ligamental marshal. Now you could go in. There's different ways you could deal with this. You could go in and you could put alcohol if you could find the ligament. Put alcohol in there and that would have terminated this. You could go back into the CS and ablate around and look for connections either from the CS to the ligament or in this case what we did was found at least where the touchdown point was and this ablated and this created block. In sinus rhythm if you had paced down here you would have seen it break out in the same location. We didn't do that but I have done that in other cases and that's often what you see. You pace here. There's a long a fairly long delay and then it pops out somewhere around the edges of the appendage usually. But it can be up here. It's not always here. It can be on the top of the appendage. You can go all the way up the ridge and pop out on the roof. But what you have to understand is that these bridges over the vein of Marshall are very common and it's probably one of the reasons why you know we misdiagnosed some of these in the past if you didn't check with pacing or anything else you might have called this a focal tachycardia and ablation would have said well I know it was focal because I ablated it and it stopped but it wasn't. The mechanism was completely different. Nishant, are there any questions that are popping up? I'm not seeing them so maybe I could answer some some questions now. Yeah if anyone wants to ask questions you can either unmute or send it through the chat. There was also Greg the suggestion that if you come out of presenter view the videos may play. I don't know if you want to try that. Greg, other clues would be that you know the cycle length of that tachycardia is 304 and you have almost all of the cycle length so be if it was a focal tachycardia from that spot would be kind of a coincidence that you recorded timing so that's another clue that it's not focal. It could be it just may be by chance it takes that much time to get around the valve but it suggested right those are the same. Okay I can show you the here's the yeah this might work. Let me see if now it works. No, I really have to stay out of the presenter view, it looks like, for some reason. Okay, sorry about that. I don't know why that happens, but it did. Okay. What time is it? It's 7.30. So here's another case. Okay, so the other point I wanted to make was often you'll see some real slowing in a circuit, and it breaks out. Unlike this one where if you went along the endocardial surface where it was marked gray, we just couldn't find any potentials. I mean, there was nothing in this zone where we had ablated Zippo. Whereas what you find, and so you know that probably what's going on is that that circuit is diving somewhere else. So in this case, it was the vein of Marshall. It will go sometimes just to the epicardial surface of the atrium, and you won't see any endocardial potentials. If you're going to get it easily from the endocardial side, you often see something called what I call bridging potentials. Right in that slow zone, you see almost a very large portion of the tachycardia circuit in a small zone. So in this case, you can see there's these really fractionated, really long signals right in the zone. When you ablate these, and this is a macrorantrin circuit sneaking through this little area, and you see these bridging potentials, you know that probably within a few seconds of coming on, it's going to terminate because the circuit is actually endocardial. When it's epicardial, what you'll see is split potentials along what looks like a line of block. And what it's doing there is it's diving somewhere epicardial and then coming back to the endocardial surface somewhere else. And so look, that will give you a clue. If you see split potentials, it doesn't mean it's blocked. It means there's probably a portion of the circuit that you can't visualize. Did you want anything to that, Brad? No, that was good. How often do you have to go into the CS? Well, for that one, you know, frequently. Yeah, I mean, so I've changed the way, you know, if you look back and look at the way what this looks like a mess, but what's happening is this one was a difficult one to block. But what I do now is you can see the different colors of lesions here. I always, if I'm going to do a lateral mitral line, I always do the pulmonary vein side. And then I go to the other side of the ridge. I go all the way up to the top and I point in from the appendage along the ridge and drag it all the way down. It's amazing how many times mitral flutter, perimitral flutter will terminate, particularly if there's been a prior line. It will terminate when you just do the ridge right here, because the ligament or marshal is trying to touch down somewhere along this ridge. And if you ablate from the top to the bottom, you'll often break it. And often it'll be in the middle somewhere, not down here, sometimes even up at the top, but often right in the middle of the ridge as you're ablating, you'll see mitral flutter terminate. And then carry it to the valve. So that when I'm doing a mitral line, I'll do this, the PV side, the ridge side, carry it to the valve, and then go in the coronary sinus. And then I would give that even a separate color, like an orange color, to know that I've ablated along the epicardial surface from the coronary sinus. And pointing usually up and towards the atrium to get the atrial signals here from the other side. You often have to do that. It's difficult to get block without going into the coronary sinus and trying to interrupt, because that's another bridge. The vein of marshal itself is the bridge, but the coronary sinus is another bridge. So you can block everything else, and then the coronary sinus becomes your bridge to the vein of marshal, and then the vein of marshal back. So that's an important thing to know. Not something I think any of us really appreciated very well a few years back. But now, just knowing that, it's a lot easier to go and get some of these more difficult cases. So this case illustrates one of the reasons I don't like anterior mitral lines in general. And this is a 68-year-old woman who had three prior ablation attempts, including a PVI, a roof line, anterior mitral line, from the mitral valve annulus to the right inferior pulmonary vein. Again, I didn't do the first case. And she had recurrent atrial flutter associated with one-to-one conduction. Really symptomatic. One of the problems with ATs. So we checked, and her pulmonary veins were isolated, and the lines of conduction were blocked. So actually, this entire lesion set was blocked from the first ablation. We induced a focal AT, or a reentrant AT, you tell me. There's a reason I'm showing both atria here. And if you use Brad's trick, there's a little clue here that maybe this isn't focal. So the 12 of you said it was focal, you can change your answer if you want. So this is another, you know, another case where something looks like it could be focal, breaking out in the middle of the left atrium and up against the line of block and then spreading out and going out into the right atrium like you expect through connections. It can't make it through this line. You can see that when the activation comes, it hits this line and stops. So this line's blocked. This line's blocked. It doesn't get to the poster wall except going around and coming back the other way. So this is not, these lines are blocked. And this could just be a focal thing. Again, you have to realize though when you have all these lines, the chances of it being a focal thing are much less. So just from an odd standpoint, there's a good chance this is re-entering. Again, you've got the whole cycle length of the tachycardia pretty much here. And you've got this period where nothing's happening from here to here. Just what's going on here? So where do you think this is coming from? Nishan probably could tell you. How do you get from the right atrium to the middle of the left atrial wall? Well, it is Bachmann's bundle. So that's the other one. And this is one of the reasons I don't like anterior lines very much because what it, the one flutter that it can promote, particularly if it's to the lower part of the right of the veins, is it promotes a funny biatrial type of tachycardia where the circuit goes from left to right atrium or the other way around potentially, but I've usually seen it in this direction, around the valve. Can't make it back in the left atrium around to finish the circuit around the valve. So it goes through the CS here, breaks out into the right atrium, climbs up the septum, goes through this little channel here, disappears, and then pops out here. That's Bachmann's bundle. That's how it's getting there. So this circuit actually is using left atrium CS around the right atrium up the septum over Bachmann's bundle. So there's a couple ways you could go at this. You could go epicardial and try to ablate Bachmann's bundle. That's sort of the last resort kind of thing. You could try to get this touchdown. This, unlike the last case where that touchdown point was really small and looked much more focal, this is a very broad area and so it doesn't really look like a focal tachycardia necessarily because it has too broad an area of initial activation. And so if you ablate here, it's gonna move to here, to here, to here. You'd have to take a large amount of ablating and this is difficult to reach Bachmann's bundle. It just keeps moving where the touchdown point is. So I wouldn't necessarily advocate trying to ablate it on this side. What we did do was we ablated it right at that little choke point in the right atrium. We actually, with catheter pressure, before we even came on ablating, got it to terminate. We stuck it right there. Then we re-induced and then we re-ablated and it stopped again so it wasn't fortuitous. So we were able to break the... turned out that it had to get through this little zone right here to get on the Bachmann's bundle and over to the left atrium. So we actually ablated this tachycardia, which if you had entrained it, it would have been in this huge area in the left atrium from here all the way around. But this is where we ablated in this one little spot. We then induced the second one and there was another biatrial flutter. This is a ripple map if you prefer to look at that. Sort of a broad breakout on this side of Bachmann's bundle. It goes all the way around, comes through this little choke point right there, and then breaks out again. So just another way of looking at it. We did get another biatrial flutter and we found another biatrial connection just under the right pulmonary vein and this terminated that flutter and then she was no longer inducible. She's actually been pretty good. I haven't... she hasn't come back with further ATs or AFib since then. So we didn't actually do anything in the left atrium. All the... we cut these connections. Now what... if we had cut the connection in the CS somehow, then she would have dissociated her right... I think we cut every connection between her right and left atrium here and then the other one I showed on the right atrial side. I think we cut every connection in her right to left or left to right except the coronary sinus. So obviously we don't want to do that because then she'd have a completely dissociated left from right atrium, which has actually been reported. Hey Greg, can I ask a couple questions? Sure, absolutely. One was in terms of endpoints for ablation, aside from targeting the clinical, what do you try to get when you're done with these cases? Yeah, so it depends. So obviously the first case I'm trying to determine that there's lateral mitral block and I at the end I showed a case, I think, just trying how do you determine that. But do it mostly with, you know, putting a PEN array in the left atrial appendage and using ablation and using differential pacing. So I'm looking for block across that line. In the first case where that breakout was underneath the appendage, you would have seen that in sinus rhythm. You would have paced the endocardial surface and seen it break out on the other side and it wouldn't look blocked. So you have to look for differential pacing for block. One of the other problems with these anterior lines sometimes is you get really late left atrial. So this PEN array is in the left atrial appendage and you've got right atrium to CS. It can't make it over the septum to the left atrium anymore or to the left atrial appendage. So it's got to go all the way around the coronary sinus to activate the left atrial appendage. So the left atrial appendage is actually often activating within the QRS and that's not necessarily ideal. For this, for the anterior lines, that's what you look for. So I'm looking for, particularly the ones where you draw from the valve to the left superior pulmonary vein, the left atrial appendage will always be late. So in that case you're looking to see it comes after the distal coronary sinus. If it's equal with or before the distal coronary sinus, you haven't blocked it. And so the anterior lines are pretty easy to figure out, but usually it takes, it's much easier if you have two catheters. And here after block, this was before block, so it's almost simultaneous and here it's moved much later. But it's not a, it's not ideal probably to have the left atrial appendage that late. So this is one more case. Sorry, before we move on, one other question. If you could just clarify, I think they're trying to figure out why you chose to ablate that last case in the, near the SVC or on the right atrium rather than a lateral line. Yeah, so you could have. I think a lateral line was possible when we mapped it out and saw that it was in the right atrium and when I put the catheter and we saw that little choke point and I put the catheter on that choke point. So let's go back to that. Here there was this choke point near the SVC where the circuit kind of came and squeezed through this little spot. When I put the catheter there, it actually terminated tachycardia. So just catheter pressure there terminated one lesion. And so we reinduced it and then ablated it and it terminated again. So we knew kind of a single lesion there was probably going to prevent this particular flutter. Then there was a new one that broke from lower on the septum to the right veins and we did that. The lateral lines, it's a lot more, you know, it's a lot of work. You're talking about again doing the other side of the ridge down to the valve in the CS and she already had a blocked anterior mitral line. So what's the other thing that would have happened with the lateral line? Potentially. We blocked off, you might isolate the entire left atrium. So I mean that you're at risk of that certainly. I mean there are right to left connections still before we did that. But if you did a lateral line with a line of block anterior, you always have to be careful. There's a chance you might isolate that whole chunk of atrium. So that's another potential reason. I don't think that would have happened in this case because above this line of block there were still roots from right to left but they were pretty potentially tenuous. And if you made another line you have the scenario where you might end up isolating. Does that make sense? Yeah I think it does and someone wrote through the chat rather than unmuting with concern about isolating the appendage. I have a case exactly like this where that happened. Yeah it probably wouldn't happen with a line this low because there are ways to get over to the left atrium that are above this line as we showed. So here and then on the septum. But if your line is from here to here for instance or here to here you may have cut off all the right to left connections to the left atrial appendage. And so if you were to complete and you had a complete line here then you went to the lateral line and did that you could easily isolate the whole left atrial appendage. And I know the German Karl Heinz Koch group or I think it was his group was using that as a strategy to isolate the appendage and they had an extremely high rate of left atrial appendage thrombus even in sinus rhythm. So it's one of those things where if you're going to do that you better be prepared to probably to ligate the left atrial appendage in some form or fashion. So because they're going to be very high risk for a stroke. Okay do we have a few minutes left or I can show. Yeah you want to go through another one of your cases? Yeah I have another one. So this would indicate a little bit about how you know I said how do you tell you have blocks. So this is aimed at that. So during if you can put up the poll that'd be great because then I can move to the figure quicker. During RF catheter ablation perimitral flutter occurs. There's wide enteral PVI and isolation of the posterior left atrium. After conversion to sinus rhythm a multipolar catheter is placed in the left atrial appendage and the electrograms shown in the figure are recorded in sinus rhythm after a line of ablation from the anterior mitral valve annulus to the left superior pulmonary vein. Based on the activation sequence I'm about to show you, you can draw the following conclusion to what you're on the poll. So here's the signal here's the line we tried to that was drawn left from the mitral valve annulus back to the left superior pulmonary vein. We put the penta ray catheter sitting in the appendage so that's here and this is the right atrium and coronary sinus. So based on this you can answer what you think is going on. And I'd say that this is probably too strongly worded, can draw the following conclusion. It's probably more most likely scenario. So yeah, it's difficult. I know from experience what the answer is here. Even in sinus rhythm, when if you've drawn this line and you have simultaneous activation of the appendage and the distal coronary sinus, it's not blocked. It doesn't matter. You can go pace right up against the line, you'll see the same thing. And what's happening is the wavefront, again, there's right to left activation of the septum. And so when that happens, you get activation here and you always see sort of simultaneous activation of the appendage and the coronary sinus. Sometimes the appendage will even be earlier than the distal coronary sinus because activation is coming around the coronary sinus and it's also coming through the septum, over the septum to the appendage. When they're tied, this line is not blocked because what has to happen if it's blocked is activation comes up to this line and is halted completely. You have to get to the appendage. The only way you can do that is to go around the valve and get to the appendage. Now it could be over Bachman's bundle, it could be, who knows where the line, it's a long line. So where one of these lesions is not creating block or maybe multiple. But if this is blocked in sinus rhythm, you'll see it'll go around the coronary sinus and activate the appendage late. In fact, the posterior part of the left atrial appendage will be the earliest part that activates. And so I can tell you that more ablation is going to be necessary. And here is when we, the moment we get blocked. So here's the current condition. You drop a line and you see the distal coronary sinus and the left atrial appendage are pretty much simultaneous. This electrode here is posterior. And so the other thing you notice is that the anterior part of the appendage is activated first. The posterior part of the appendage is activated later. When you get blocked, and so it's from this beat to this beat, block was achieved. The posterior part of the left atrial appendage is now early and the anterior part's late and they are after the coronary sinus. So it's got to come all the way around, go through the coronary sinus and come up posterior to the appendage and then activate the anterior portion. So this is what you see when you get blocked in this particular line. Now the lower the line, sorry, where is it? The lower this line, the more you have to kind of put catheters on either side to tell what's going on. So you always want to, the nice thing about this is the left atrial appendage is sitting right next to your line. So that's why this works. If the line's down here, sinus rhythm, it may be difficult to tell. So what you want to do is put a catheter right on the other side of the line and pace this side. Sinus rhythm, if you put your catheter right next to the line, is a pretty good indicator. But we do always check. So we will put a catheter here and see that this relationship is the same. But I can tell you in sinus rhythm, you already know this isn't blocked. We will pace just on the other side of the line and you'll see the same relationship. This posterior part will be early as part of the activation sequence being posterior to anterior in the appendage. This is sort of, I think, a final example of a lesion set where you make this line of ablation. It has to come all the way around and activate the posterior left atrial appendage first. I wanted to just go a second, because people ask this question, what are we doing for our persistent AF lesion set in terms of settings for RF? I've changed this over time, gradually been creeping up on power with the idea that you cut down the duration and we use certain safety checks. So in the anterior left atrium, I've moved up to 50 watts. I will set a actual time, maximum of 20 seconds. So if the contact force is low and the impedance hasn't approached 20 ohms, I'll go a full 20 seconds at 50 watts. You can use ablation index, and when it gets around 500 to 550, that's another reasonable end point. I've gone actually from 30 watts posteriorly, I went to 35 for a while, and now 40 watts, but the maximum of 10 seconds at 2cc flow with a thermocool, not a thermocool SF. So I rarely actually go 10 seconds, it's more like 6 to 8 in most cases. If I'm over the esophagus, 6 to 8 seconds, if I'm away from the esophagus, maybe 10 seconds at 40 watts 2cc flow, never seen char. We have a large experience that we'll publish soon that shows you've never seen a stroke using 2cc flow and limiting the duration and using the thermocool catheter, not the thermocool SF catheter on the posterior wall. And then within the coronary sinus, I cut the power to 30 watts, maximum 20, but often we do about 10 seconds. We found that pops seem to occur as you get close to 20 ohm drops in the ventricle. We've seen that repeatedly. When we get close to 20 ohm drops, so around 18 ohms, I'll come off ablating. I put the... So when we're showing the cardio, we always have this screen up so that we can see impedance, and we'll watch the curve. We'll have our cartographers set an upper bar at the beginning impedance and then drop it down 20 ohms so that we can see when the curve comes close to the 20 ohm bar, we'll come off. So we'll stop earlier than the preset. But we do have a fail safe on the posterior wall to set it for 10 seconds max so you don't go over that 10 second limit. When you're going at 40 watts, for instance, and on the posterior LA at 2cc flow, with the concern that longer duration may lead to char formation potentially, but at that short duration, I think it's quite safe. Although I do have less data for 40 watts, lots of data for 30 to 35 watts. Greg, there was just a question if you could clarify about using the 2cc flow, how do you do that? Yeah, you have to, it's sort of an off-label thing, you need, so first of all, I don't use the SF, let me repeat that, I don't use the SF, I use the Thermocool. I don't know whether you could get away with the same settings with the SF. You have to tell the system, the Smart-O-Blade, which happens to not be so smart in this case because it doesn't know the difference. You can tell it that it's a four millimeter tip catheter, and so the background flow won't change. So you're going at 2cc, you come on ablating, it doesn't turn on the pump because it thinks it's a four millimeter solid tip catheter, and so it will then ablate at 40 watts with 2cc flow. I set a temperature limit of like 50 degrees, and it never really gets there. Even with 2cc flow, the temperature's always maybe in the low 40s at the most, but that's how you have to do it. And that's only with Cardo. I don't really, I haven't really done this with other mapping systems because they're not as easy to fool, I think. Greg, recall we also had to switch over to a power-controlled mode instead of a two. Yeah, yeah. So for the four millimeter tip, you switch to a power-controlled mode, 40 watts, with a cutoff temperature of 50, and basically, you know, 10 seconds, 10 seconds max. If I'm over the esophagus, I'll try to do six to eight. There I'm looking at electrograms too, so the electrogram's gone, six seconds, I see a nice impedance fall, then I'm done with that lesion. It works pretty well, and sort of, the other thing that, this is sort of our current persistent AF lesion set, particularly when they have scar like this. So patients who have no scar, we might just do the PV. But many patients we see have a fair amount of low voltage in the left atrium. What we do is veins, the posterior LA, this patient had already had the veins done and came back with AFib, so we did the posterior wall. And then what we do is this thing I talked about, the ridge had already been done on the prior ablation, so we did the anterior side of the ridge, carried it down to the valve, and then go in the coronary sinus and try to eliminate local coronary sinus potentials. So sort of more or less isolate musculature in the coronary sinus. So this is kind of what we've worked at. This lesion set has worked, you know, I've been impressed at how well people have done with this. I think this idea of creating a more durable lateral mitral line is the key, and taking out some CS, potential CS triggers, and the posterior LA has worked for us anyway. I mean, we'll have some data published at some point, but I think this is what we are doing currently. At least Travis and I are doing it. All right, I know it's getting real close to 8 o'clock. Are there any other questions? Yeah, maybe I can ask one or two more. So this was a question about epicardial connections, because we know there are some. Have you come up with any tricks to make sure that your lines are transmural aside from pacing? Do you do high output pacing on the line, make sure it doesn't capture anything along those lines? Yes. So one of the things for the posterior LA is it's very common to have epicardial sheet that's still active. You can ablate the endocardium, and you'll often find something that captures in here. So the way we finally go about this is we'll go in and we'll apace back and forth across the wall in this entire box region, and any place it captures, if we can do it safely, we will reablate it until nothing captures at high output. So that is one thing we do for the posterior wall. For these other lines, you know, again, we've done a lot here. I will pace along the endocardial aspect to see if anything captures, and then make real sure that I pace close to the line and record all along the edges of this line to make sure there's no leak along there. It's really easy to fool yourself that you have block in these scenarios. The first thing I'll do is put in a catheter here and look to see that the CS is reversed, but then I'll go along the line and make sure there's nothing else that might be leaking through there. It's not easy though. I mean, I think I look forward to the day when we have potentially an energy source like electroporation that could, you know, reliably give transmural lesions without worrying about damaging arteries and veins and nerves and the esophagus. Maybe then we'll take the next leap in terms of, you know, these kind of lesion sets then might be perfect because you know that the durability is really high. And then you can start to test these lesion sets more accurately. I mean, you test strategies, but you don't know whether any of this is blocked, right? I mean, so, but what we do do is those tricks to try to make sure. We've had pretty good success. I mean, these are posterior wall, if not completely isolated, almost never has, you know, the equivalent of leak all the way through the posterior wall when they come back. So there's always like the equivalent of a roof line. And most, if not all of the posterior wall is pretty well isolated when they come back. And this actually helps improve the pulmonary vein isolation as well, I think, from RF. Do you have any thoughts on the combined surgical and EP approach, you know, involving your surgeons at some point? We have one operator who likes to do that and has been doing it for a long time. I'm not that impressed with it, honestly. I think what they do, it depends on the surgeon. We have some surgeons that seem to take out like this little spot here on the posterior wall, you know, and, you know, if that's all they're contributing, I don't see the real advantage of that. You know, again, you could say doing the posterior wall epicardial, and then you being able to do the endocardial may improve the durability. That's really the, I think that's really probably what they contribute to the posterior wall part. But then again, you know, if they can manage the appendage. So that may be another advantage to doing that, where if you can manage the appendage at the time of that combined procedure, and, you know, we'll see the results of May's trial and some suggestion that if you can take out the appendage safely, that may be something else they can add that we can't do easily. So most of the published data that came out of our group here on the hybrid approach is not exactly the same hybrid approach we're able to do now, I think, because we're using a new end contact catheter, and having kind of seen both, I think the one thing with the approach now is, you know, now most of our group is doing these, this type of posterior wall lesion set, and we haven't seen that much esophageal heating. So if we're able to isolate the posterior wall, there's just the patients tend to do better. Most of the patients who get the hybrid, they've got chest tubes in, they have a drain, their recovery seems to take longer. I think the only benefit to that is they've been doing combined lariat through the epicardial access. So for those patients that we've decided to take out the appendage, you know, by a lariat, and then they'll do the combined, but yeah, it just seems like the post-op course for those patients is definitely more challenging. Hi, Sharon, how are you? Good. Nice to see you guys. Great.

catheter ablation

atrial tachycardia

mapping systems

circuits

visualization

ablation approaches

challenging cases

entrainment

pacing

radiofrequency ablation