So AF ablation, there's not much to it. So really, we could do this probably in 15 minutes. Actually, that's a joke. It's very complicated. There's a lot of controversy in what you can do. And as a matter of fact, it's actually hard to test. So on the EP boards, for instance, there aren't that tons and tons of questions on this because there's not a lot of consensus or very straightforward things about AF ablation in general. And so it's actually hard to write a question that's unequivocal. But before you start, you have to know, well, who should you be doing catheter ablation in with atrial fibrillation? Well, first of all, Cabana helped to solidify this, I think. Mainly, we're looking at symptom relief for patients with atrial fibrillation. And so we're really looking at a group of patients who have symptoms related to AFib. Now, symptoms don't have to mean palpitations. They can mean fatigue and other types of symptoms. So you have to ask those questions. But symptoms are really mainly what we are targeting. So really, for paroxysmal AFib, there's pretty good evidence that once you've failed a drug, you're in a good position, class one indication for AFib ablation. Everything else is sort of 2A, 2B, but all with symptoms, whether you've failed a drug or not. Where we have more sort of squirrelly indications, but more and more evidence are those with congestive heart failure. We don't have a lot of data on very old or very young patients. Patients who are very affected by their AFib, such as hypertrophic cardiomyopathy, where the success rate's not very high, but the gain is quite high because those patients, if you can maintain sinus rhythm, do so much better. Tacky Brady, patients who, if you can get rid of their AFib, may not need a pacemaker. Athletes. So there are a bunch of other categories, including maybe even some patients who are asymptomatic, particularly if you're talking about younger patients, where we might stretch those indications a little bit. So the seminal observation concerning AFib ablation came from the Bordeaux group. And this is from the paper, the original paper, looking at where AF initiates. So I've heard Pierre-Jay tell the story of how they found this. They were initially mapping the right atrium, looking for triggers in a way they could, and they were in the left side through a PFO, and the catheter fell into a right pulmonary vein. And they saw AF initiate over and over again, right out of this vein. So similar to what you see here, where you have a right inferior pulmonary vein, and the very first thing that starts off AFib, the very first spike is within the pulmonary vein itself. And the pulmonary vein looks like it fibrillates first, and then it conducts out to the atrium and creates AFib. And when they looked at where triggers were, it turns out the pulmonary veins are the vast majority of initiation for patients with paroxysmal AFib. There are other places, but the pulmonary veins, by far, were more common. Here's an example of that as well, where we've got a 10-pole catheter in the coronary sinus. We have a circular mapping catheter in the left superior pulmonary vein. It's actually a catheter that's through a cryo-balloon. So it's poking out the end of the cryo-balloon. Getting ready to ablate, and here we have an episode of atrial fibrillation we were lucky enough to catch the onset of. And if you look at this, or this is where the P-wave envelope is, and then there's a new P-wave envelope for the onset of tachycardia. And you can see, outside of the P-wave that's produced on the surface and everywhere else, there's this early signal that comes. You can see it on the circular mapping catheter. So that precedes anything that's recorded in the atrium. And this is sort of what they saw in Bordeaux, and realized that if we could get rid of these triggers, we might fix atrial fibrillation. Just, I want to take advantage of this great slide for one other purpose, which is some people might say, well, these look early, but this one is even earlier. How come that in the distal coronary sinus, that's not the initiating atrial event? Well, if you go back to this, you can see that this is actually a V, probably. It's a far-field V, lines up with the ventricular electrogram here. You see it again here. So you could get fooled into thinking this is an initiating beat, but you have to go back. It's often useful to go back and look at beats you know what's going on, like a sinus beat, and see where that potential lies, and then you can figure it out on the one that starts. And this is sort of the onset of the P wave, where I drew a line down, which would be the beginning of the P wave envelope. And clearly, these are way out in front, and this is far-field. So there, I mean, I think these days we have choices. There's different technology, and maybe these will be replaced completely by electroporation, since it looks like potentially that energy source has a bigger therapeutic window, where you can damage myocardial cells without damaging nerves and the esophagus. But right now, we don't have that, so we can choose between fire or ice. And at least almost every study that's looked at this comes up with the same conclusion, that success rate with cryo or radiofrequency is really just about the same. And certainly, if you're facile with one or the other, your success rate might be higher using one technology over the other. If you've only done two cryo cases, and you've done a thousand RF, maybe you'd be better with RF than cryo. But my own feeling is I've done enough of these, of both forms. This is certainly simpler. It's faster. And so I tend to use cryo for paroxysmoiphib, where I'm only isolating the pulmonary veins. And I know the pulmonary veins' anatomy would be conducive to taking a balloon and doing that quickly. We have to realize that when we're, you know, quoting success rates, there's a couple of things I would tell fellows. Number one, this is not your success rate. This is the literature's success rate. And it's all over the map, partly because, you know, people use different techniques. They use different technologies. And so you eventually will know your own success rate, but you're not going to know that the day you walk out and start doing afib ablation by yourself. Perhaps if you've done a ton during your fellowship, you'll have a pretty reasonable idea as you followed up those patients. But, I mean, again, you want to be honest with people. And it's not even the best labs are not going to quote 100% success rate. And you have to let your patients know that there's a reasonable chance that some of them might have to come back to do it again. And certainly for persistent afib, that's even more of a discussion. There's probably a large percentage of those may have to come back, particularly if they have some degree of structural heart disease that makes it even less likely you're going to get it in one shot. But in the absence of significant structural heart disease, probably you can approach 80% once you've done two procedures and kept some of them on antirhythmic drugs. So if we're being honest with ourselves, I think we really need to consider that success rate's not quite as good as we're doing for AB node reentry and WPW, etc. The other important point about this, we're going to go a little bit over how to recognize that a vein's isolated. But also that even if you do recognize that the vein is isolated, you're not done. There are other things you have to do in that procedure to make sure that that vein isn't going to recover. Just like Sonny talked about winging and stunning tissue, this is a huge problem for pulmonary veins. It's quite easy to stun a vein and cause it to isolate acutely. Long-term is a different story, and we've recognized that and made some changes that have made that better. So this is my setup, and I haven't changed this workflow much recently at all, where I take a 20-pole catheter that has 6-centimeter spacing, and I have an ice catheter, an ablation that's through a steerable catheter so I can maneuver in the left atrium and get good contact force, and then a multipolar catheter, and there's some kind of probe in the esophagus. The reason I like this catheter is it gives you information from both the right atrium and the coronary sinus, and by default, the left atrium. So this kind of gives you an idea of what's going on. So if there are triggers that are occurring outside of pulmonary veins, you have a more immediate look. You may not get many of those triggers. You have a good look at the right atrium at the same time. So the position of a circular mapping catheter is actually important. If you're going to put a catheter in the pulmonary veins, you would look at this and say, oh, these are far-field. This catheter, I've isolated this pulmonary vein. Well, I pull it back a little bit, and I see this. Does this look like an isolated pulmonary vein? No. So in every – when you get back towards the ostium of a pulmonary vein, you'll both record far-field things, and the far-field things depend on where – which vein you're in. So the far-field things for the right superior pulmonary vein can be what? Right atrium. They can be SVC. They can be the left atrium just adjacent to that pulmonary vein. For the left superior pulmonary vein, you could have appendage. You could have left atrium adjacent to it. Appendage is a big structure. It generates a lot of voltage, and so that's going to become a prominent far-field. So you can see that. As you shove it into the left superior pulmonary vein deeper and deeper, sometimes the signals get bigger and bigger because you start picking up larger potentials, far-field potentials of the appendage. So you have to be back at the ostium in order to record these because you go past the sleeve. The sleeve only goes so far into a pulmonary vein, and it's variable. Some people have sleeves that go way in, and some have sleeves that just barely go into the pulmonary vein. So you want to be back at the ostium to determine whether you're recording these kind of potentials. So you'll always see a far-field, and then you'll see a near-field, larger potential that looks sharp and local, like a pulmonary vein. And there you go. So again, this is a blow-up of the same thing, far-field potentials, PV potentials. When you isolate pulmonary veins, what we used to do is we used to pick them off inside the pulmonary vein, and that led to a lot of pulmonary vein stenosis. Not a good idea. So we've backed off and gone around the pulmonary veins. The problem with that is now you've got to make really good lesions because you're making a circle around the vein, and any one of those lesions recovers, and now you've got open for business, that pulmonary vein again. So it tends not to be that difficult to tell when you have pulmonary vein isolation. If you have a catheter in there at the same time, here you've got the far-field and the pulmonary vein potentials are all melded together here. And then as you start to ablate, you can see the far-field here of the left superior pulmonary vein. Now the vein potentials start to work their way away because now you're creating some degree of block. So it's taking longer to get into that vein, and now the vein potentials start to move out. And they move out and block. You're not going and picking off individual fibers within the vein. That whole pulmonary vein is now just moving. The potentials are moving farther and farther out. And here, even farther, until eventually it blocks. Now you're left with only the far-field and none. So that's a really pretty good way to do it. What you'll see is as you go along, the vein potentials move out, and it's very clear what the vein potentials are then and what the far-field is. Now when you want to try to separate that, there's pacing maneuvers you can also do to figure out whether it's far-field or near-field you're looking at. Well, again, you told me what's nearby these. So for the left pulmonary veins, the nearby structures are the left atrium itself. There's the appendage, which tends to overwhelm the signal. So that's the most likely thing you'd see. The ligament of marshal runs right between – or the vein of marshal runs right between the appendage and the left superior and left inferior pulmonary vein. It goes right up through there, so you can get potentials from that. So where are you going to pace? You pace where the far-field is. So that pulls the far-field against your pacing spike and would separate it out from any pulmonary vein potential. So you can tell, and I'll show you an example of that. For the right pulmonary veins, what are the nearby structures? What are the possible far-field structures? Well, there, we've listed them. You told me them. Well, so what do you do? You go – you pace the far-field areas. And you pull those up against your pacing spike, and it gives you the answer. Here's an example. So we're wondering – we have a circular mapping catheter sitting in the right superior pulmonary vein. We have a catheter in the SVC. And we have a single electrode here of the CS. I've taken out most of the others just to unclutter. So is this pulmonary vein isolated or not? Yes or no? If you just looked at the electrograms itself, I guess people are voting, huh? Let's see what people think. Can we get an answer? It's only a yes-no, so just plug it in. 50-50. Okay. Right. Well, the reason is because it's hard to tell. There are some clues on that, actually, but it's 50-50. Good. Kind of what I expected, actually. So one of the things you can do is pace to figure this out. On the – I've lost my mouse. Where did it go? Oh, there it is. Okay. So here we have the signal in question. One of the clues that it might not be pulmonary vein, we've already tried to isolate. Look at the beginning of the P wave here. The beginning of the P wave is about right here. And the onset of this is right at the beginning of the P wave. So that makes it more likely that this could be something far-field. You go to the – and it lines up with the SVC potential. You pace the SVC, and what happens to this? It disappears. Why? You pulled it right against the pacing spike. So if you want to know if something's far-field, you go to that structure, you pace it, it gets sucked into the pacing stimulus, and you lose it. If this were a pulmonary vein potential, you'd see some conduction time to get to that from the SVC, and the vein potential would be out far removed from the pacing spike. So here's the other point. So there are ways that you can tell when a vein's isolated. Number two, what is another very important thing for you to understand is that when you're making lesions around pulmonary veins, there's a high chance, if you don't do it carefully, that you will isolate that vein acutely, and that that patient will come back with AFib, and you'll go back in, and you'll find the vein's not isolated anymore. That's a common problem. And it's becoming less common, but even now, having understood better how to make lesions, we still see people coming back. And so it still remains a problem. So in this case, this was a robotic ablation where they got pretty good, you know, contact on the wall way back when before we had contact force. And what they did was they brought everybody back three months after a successful PVI and looked at whether the veins were reconnected or not. And the truth was only a third of the patients had all four pulmonary veins isolated. And there were various percentages of one, two, three, and four veins, but only 30% had all four pulmonary veins isolated. And this was a common thing when you went back, and if you could have studied all your patients, this would have been a common theme at every lab, not just this lab. In fact, here's Natale's work looking at, you know, first, second, third, or the second procedure where initially they found 30% had veins reconnected. But after the second procedure, when they went back in the third, the veins are isolated. And if we could do that and follow people out 10 years, it looks like about a 75% success rate if you could get all four pulmonary veins isolated on the first procedure. You would have had a 75% 10-year success. That's sort of, you know, extrapolating this data. But that's pretty good. You know, I think we can expect a pretty good success if we could make pulmonary vein isolation durable on the first shot over a pretty long haul. What we did initially when we didn't have contact force catheters, we're trying to figure out a way. How do we tell whether we're making a good lesion? We could look at different things, but one of the things we used to do is pacing. So we would go on to the line that we just created and pace it. And if it captured, ablate it again until that local area that we were ablating no longer captured. So in other words, you can't pace dead meat. So hopefully, we haven't stunned it or we've made a bigger lesion at least in that location. And when we did that versus just looking at acutely isolating veins, patients did a lot better. And I know a lot of people who adopted this later said, oh, yeah, this definitely bumped my success rate up a good chunk by going back and doing this. It's just sort of a way of you didn't make a good lesion the first time, but now you can figure out where your poor lesions were by identifying which areas still pace. How much time do I have? Ten minutes. Okay. So I think this thing is off. Like this screen isn't showing with that screen. My mouse is moving over. Anyway. Extra challenge. Yeah. Is it possible to make the screens match up? The confidence screen is not showing the big screen. Thanks. Yeah, I'm looking down here. There, now it's matched. Okay. So I think the other thing that's made a big difference in afib ablation, particularly with RF, is that contact force correlates with lesion size. So if you look at lesion depth versus an index of force, power, and time all put together so you have important parameters, the most important parameters are how long you stay on, how much contact force you apply, and how much power you're applying or delivering into the tissue or current, really. And so we know that there's a pretty linear correlation if you take this index. So it's a very important thing to know these parameters as you're ablating. So the way you can figure out whether you've made a good lesion is to make an index. So you can look at mapping systems, and I'll do this for you. Different mapping systems have different calculations. But you can put something into that dot. So what we used to do is we'd say, I was here. I turned on power. I get a red dot. But a red dot didn't mean you made a lesion there. You might not have made a lesion at all. It might have been floating off the tissue, and you just turned on energy, and you get a red dot. So we had red dots all over the place. Those red dots didn't equal lesions. What we can do, though, is we can put lots of different things, lots of different pieces of information into those dots. We can put the time we spent there. We can put the power we delivered. We can put delta impedance, contact force. We can put all kinds of measures that take all of these parameters and mix them together and give you some kind of calculation that you can put into those dots. I think this is really helpful. Once you make lesions, you go back. You want something, and you're looking at a dot, to know, okay, I didn't isolate the vein on the first time around when I made all these dots. Where do I go back and look for a weak point? And so indexing them is really useful. There's no one index that's magic, but here's one way to do it. So this is automatic lesion indexing where it's giving you a mixture of contact force, the time you were on. We look at impedance quite carefully. But it's not just a number. Look at how the contact force is changing here. You can imagine that sometimes it could even be bouncing off the tissue and give you a number that looks like 15 grams, but it's 030, 030, 030. So the average number is not always what I want to see. I want to see the curves down here. And same thing with impedance. I don't want to just try to track a number that's flipping around on the generator. I want to watch the impedance curve. So it gives me way more information than looking at a single number bouncing around. What I do is I actually know the power I'm putting in. I know how long I'm giving the lesion. I put the impedance drop into the color coding. That's how I tell because we found that when we went back and looked at lesions that tended to recover at reduce, they had low impedance drops. So to just hit that point home, just to make sure everyone's following, it used to be the case that every single location where you did ablation was exactly the same color. But now whether you do it manually or automatically, you can say this was a good lesion where I had a really good impedance drop, and I made a lesion here. I didn't see as much of an impedance drop. What's your color code here? So for example, for you, what's pink and what's red? So pink is a low impedance. White would be really low, almost no impedance fall. Red is 10 ohms or more. Blue, so we had other tags as well. So we get pretty complicated about the colors. And Bill has worked out something where he's for VT ablation. He's got like 10 colors, like where it terminated, where, you know, all kinds of things. But generally speaking, what I tend to do now is I dark or lighter color for impedance. And then if I don't have irrigation on, which is another story altogether, I change the color and do dark and light for that. So if you were to go back here and say, oh, I went all the way around. I have dots all around, but I'm not isolated yet. You might say there was a cluster of white here, and presumably the reason there are more lesions here is the lesions weren't as effective in terms of impedance drop, so he kept trying to make more lesions, but for whatever reason, contact or whatever. So that might be a suspicious place that there was a connection in there. So it's helpful to kind of guide not just to say where did I ablate, but what was the effectiveness of each ablation lesion in each location. Another way you could do it is you go back and pace it. So what we used to do routinely was go back and pace every single location, and wherever it paced, we'd ablate again. Now I tend to do it only where I think it's suspicious because now when we have good power, good contact force, and we can stay on in that spot and it's stable, then it tends not to pace. So I don't look. Do you pace at 10 milliamps max output? Yeah, 10 mA and 2. And someone asked, can you pace while you're ablating at the same time? With one system and not the other. And I'm not sure what that means because we always looked at it after the lesion. And so if you lose capture, is that sufficient? In other words, do you need to stay on another 10 seconds? I don't really know the answer to that, so I couldn't tell you while you're pacing how much longer. If you're pacing and ablating at the same time, how much longer do you need to stay on after you lose capture? Another question. Sorry, one last one on the dots. People are asking. This is the holy grail, I guess. How do you decide how much distance between dots? Yeah, so another very important thing is, you know, the number that seems to pop out. We've done some animal studies. You know, the CLOS protocol was published recently. About 5 millimeter distance. So I've actually changed my dot size. I make it bigger now. And, you know, if you have, you want 5 millimeters between the center of lesions. Yeah, I had an idea a few years ago, many years ago. I wanted to actually randomize a trial to different sized dots. And I thought, because people basically want continuous dots so that there's no gray that you can see between the dots. Obviously, that's an artificial construct because all the dots are the same diameter, but your lesions are not all the same diameter. And my hypothesis was that the bigger the dots you used, the greater the likelihood for reconnection because people are going to overlap their dots and have more spacing between lesions. And if you made really tiny dots, people would be more dense in their ablation. Maybe it's overkill, but I never did the study. Yeah, no, I think that's probably right. I used to use smaller dots for that reason. But now I want to, I think now that we have a better understanding of contact force, lesion size is more, I think we have a better idea of how uniform lesion size is when you meet certain parameters. So I made it bigger. But if you look at, so this is another important thing. What do you think happened to this catheter during this lesion? So this is a lesion. This is impedance. So here's the value. So it starts at 142, it's 128. We see it's dropping. So that's a property of tissue. When you heat it and you're actively heating that tissue, the impedance through that tissue will fall. And you get a lowering of the measured impedance there. What do you think happened to this catheter right here? It lost contact. It moved. So this is another reason to look at impedance curves. It actually tells you, I mean, you can see that there's respiration. Respiration made this catheter move a lot here. But it probably came back to the same spot. It's still on the general, generally it's falling at the same slope. But then here, something changes completely. This respiration kicks the catheter off, and it never comes back to the same location. So this would be an indication that this lesion was pretty unstable. Look at this one. What do you think happened between here and here at the same location? What did we do? This is something you can use that is really useful when you can't get the catheter to stay. We could have changed the sheath. But something simpler than that, something you tell your anesthesiologist to do. Apnea. Yeah, the pillow treatment. Pillow over the face. So once there's no respiration, you don't have this phenomenon where the catheter is being kicked off any longer. And you can see, and this is what happens. These are respirations. And you can see that in your impedance curve. And if every time a respiration occurs, that catheter moves, ask for a little bit of apnea. Three minutes of it never hurt anybody. Three minutes of apnea is fine as long as their SATs are up. Their CO2 won't get that high. You can do three minutes of apnea. And that's sort of the strategy that many people use of jet ventilation is doing very, very rapid shallow breathing, whether you actually use an actual ventilator and do more frequent shallower breaths or use a separate type of ventilator called a jet ventilator to minimize the respiratory excursions. Now, in the end, impedance-coded lesions are what I do. You don't have to do that. But you should put some information in that dot that gives you some idea of where to go back. The reason we did impedance is because we went back and looked at all of our redos. And what we found was that an impedance decrease less than 10 ohms during the initial procedure was present in 90% of the sites that had conduction recovery. So this, to us, was an important factor. And that usually it was not just that phenomenon, but when they were linked together. So there were a bunch of low impedance lesions all in the same region. So this is an example, right? These were all low impedance regions. We isolated this vein, but these were all low impedance. And look, right there is where the reconnection, and really a single burn re-isolated this vein. But this was the clue. And so we started going back and not allowing ourselves to have these low impedance. We would do it again until we got a decent impedance fall. This is – I have zero time. Should I – I can stop here. Well, we do want to finish up by noontime. So you have the option of stopping here or continuing or going to your workshop case. We're going to give you 10 more minutes, and then Son, you'll get 10 minutes. How's that? Okay. Yeah. This just brings home the point that stunning and edema are a common problem with pulmonary veins. We did a study where we went around and spared the posterior wall. We did that last. So we ablated the posterior wall last. And so we went around anterior, around anterior, and came back. And then we looked to see when the vein isolated. And what we found was that it isolated 60% of the time before you got – you completed your line on the posterior wall. And the mean gap size was something like 2 centimeters. So a pretty big distance between the two lesions. So you could say, well, maybe it's just because these lesions – this lesion coalesced with this lesion. No, because if you go right in between, there's normal voltage, and you can pace it. It's not. It's the – this is the problem, right? We go around the veins, and we isolate them without making a complete lesion set. And so this, to me, said, you know, this is the problem, and we have to do something about making individual lesions better. Here's an example where, yeah, we went all the way around a vein, paying very close attention to all the things that I talked about. Now you see the bigger dots. We made very close attention to these things, and we were able to isolate this gigantic ring around the – this was a patient with hypertrophic cardiomyopathy. I think this was a 20-centimeter line. But if you can pay attention to these details, you can actually get isolation. Now, I'm not sure I'd trust this single ring, but in this case, it clearly was isolated because we could pace the back wall of the left atrium, and it was completely dissociated. Here's sinus rhythm. Look in the background. Ignore the pacing spikes for a second. There's P waves. There's right atrial and CS electrograms. You pace, and now you've got this potential that's captured. Clearly, you're pacing faster, so it should conduct to the atrium, but it doesn't. You're pacing the posterior wall. It's exit block out of the posterior wall. So we've isolated that whole segment. What I do, and I tend not to trust that single ring, is I pepper the whole posterior wall so that anything that could potentially get out of here, if one or two of these lesions aren't very good, then there's another lesion around it. And so we do very short-duration lesions on the back wall, like five, six seconds, eight seconds at a time. There have been a number of questions along those lines. Okay. So I'll stop here. No, no, no. We can answer the questions. I was going to take the opportunity of you talking about duration of lesion to ask about power delivery and duration and what you use. And that's obviously a whole topic unto itself, especially nowadays with the high-power, short-duration concept. So this is what I do. So I don't know if we've figured out yet what optimal power duration. And irrigation. So irrigation is another factor that we haven't really thought about much because, you know, when we've used these catheters, they've had set sort of FDA-mandated irrigation rates for certain powers. The truth is that that probably doesn't make sense when you were trying to do very thin tissue and you're trying to do it quickly. So what I do and what I've worked out for myself is that I use a thermocool catheter, not an SF. And the reason is because I've worked out different irrigation settings for short duration lesions and I've only done it with the thermocool, so I'm not gonna switch catheters and chance that. What I'll do is 40 watt, 20 seconds with 30cc flow, that's anterior lesions. I'll turn this off earlier than 20 seconds if the impedance gets around 20 ohms. I'll do up to 50 watts for lower contact force. Again, looking at the impedance drop. 35 watts up to 10 seconds posterior, but six seconds if I'm over the esophagus. This is power control with a 50 degree cutoff. And then 20 to 30 grams anterior, 10 to 20 posterior. We already talked about this. Less than 10 ohm gets light tag higher. And 20 ohm impedance, because you have to worry about steam pops when you're using higher power. If you stay on long enough at high power, you will see a steam pop for sure. So I use the impedance drop, which is a pretty good way of heading that off. Thank you. Okay, well, Josh, with that, a number of questions have come in and we'll start with one of the one that really leaves off what Greg talked about, the impedance drop. And the question is, can you please explain the relationship between impedance changes and effective ablation? And the question is really directed at RF and with cryo. That comes from Dr. Sandoval. Yeah, so I'll just comment that one of the downsides of doing this virtual EP101 is the original program is three and a half days of material. And so there's a lot of content that we just were not able to include. Three and a half days in front of a computer is really too much for people's schedule eyes and attention span, I think. And one of the talks that unfortunately we haven't included this year was Ed Gerstenfeld's talk on biophysics of RF ablation. So much of what Dr. Michaud was just talking about really has to do with the biophysics of making a lesion. And that's critically important, especially when you're creating lines and long lines at that wanting to create permanent transmural block, but also not damage adjacent structures. The main issue with AFib ablation is that we want to create very aggressive full thickness lesions in atrial muscle, which varies in thickness from a millimeter or two in some places to a thicker muscle on the ridge between the left veins and the left atrial appendage. But the problem is, is that right contiguous with especially thin areas of atrium are critical structures that if we damage, you could have a serious or fatal outcome, the esophagus, the phrenic nerve, coronary vessels occasionally, things of that sort. And so you really have to understand exactly how radiofrequency ablation works from a biophysics standpoint. And it was a wonderful point that Dr. Michaud made at the end there, which is, if you are familiar and comfortable using a particular catheter, then don't mix things up too much. Certainly if a new technology comes, you can relearn, but there is a learning curve associated with switching even from a traditional thermocool catheter to an SF catheter, or just one brand, one company to another, and maintaining consistency allows you to get better and better and fine tune your RF delivery. So to answer the question, that when you heat up heart muscle, you are going to improve the electrical conduction of that tissue because you've heated it up, you've damaged cells, the electrolytes are perhaps more free to move. There are a number of changes that are happening. And so an impedance drop is one way to detect that you are making a lesion. And people generally use 10 ohms as a good indication. If you drop the impedance from start of RF application into the RF lesion by 10 ohms or more, you probably have changed the tissue and heated it enough to create a good lesion. If you're not seeing that drop, you may not be making a lesion. Using electrogram size and orientation may be helpful as well. Some people actually use a unipolar electrograms and look for a positive deflection only so that there's nothing moving away from the electrode. Different people have different tricks. But that's the short answer is, is that you look for an impedance drop usually around 10 ohms. If it's too high, you worry that you're heating tissue too much and you may cause damage beyond the bounds of what you're interested in doing or even cause a steam pop, create boiling of tissue water because you've exceeded 100 degrees centigrade or so. Joshua, a couple of questions that have come in really about WACA versus PVI as well. And I think in that respect, Greg referred to, and I think perhaps we'll just focus on the paroxysmal AFib patients. PVI alone with enthral, and the question came in is, how do you identify the enthral versus WACA versus cryo? How do you go about making those decisions? Greg alluded to some of the anatomic considerations. Yeah, the evolution of ablation for AFib has been fascinating to watch. When it was first discovered that there were origins of PACs and triggering spots for AFib inside the veins, the initial strategy was to simply go up in the veins and ablate those spots. And the appreciation came in two ways that that wasn't the right strategy. One, there were typically multiple spots in multiple veins. So you'd miss things if you were trying to sniper off individual spots. The other is you could damage the very thin walled vein tissue and cause shriveling up of the diameter of the vein, cause pulmonary vein stenosis. And so then the next philosophy was to move a little bit further out near the mouth of each individual vein. But because sometimes the sleeves of muscle that extend up into the veins are finger-like projections and not circumferential, you could ablate only focal spots around the circumference just inside the vein and isolate the tissue beyond that. But again, pulmonary vein stenosis was a problem as were foci that were just outside of the ostium. So then people moved to four veins, isolating one at a time, but just outside the ostium, and then further doing two veins on block, the left veins together and the right veins together. And the upside of having migrated further out to what's called the antrum, the sort of component just outside the veins themselves, the advantage is you're not going to cause pulmonary vein stenosis if you're not ablating right at the vein. And you're incorporating more critical tissue, both in terms of substrate and triggers, within your circle of isolation. The downside is that you now have a bigger circle and you have to be darn sure that you have contiguous lesions that are full thickness. Because if you are incorporating more tissue into your lesion set, you have a single point of failure, then everything inside of that is going to regain connection to the rest of the left atrium. So in terms of defining the antrum, it's really if you were to do a CT scan, probably that would allow you sort of visually to assess the best place of where you think sort of the common part of the left atrium is where it's feeding into the veins. But honestly, it's a little bit of semantics and you'll have different people pointing to different locations. You really wanna balance effectiveness of your circle and making sure that it isn't too big, that you're not going to get contiguous lesions, but not too small that you're getting too close to the veins. And then there's also the debate about the posterior wall in between the two pairs of veins, whether that's relevant or not. That debate is ongoing. Some people incorporate that in different ways and some people don't and they just do the veins usually in two large circles nowadays. That's terrific. And Josh, there's a question that really comes in. And again, I think it's important we define patient population here. So let's just address this to the paroxysmal AFib. Is there any value in doing anything beyond pulmonary vein isolation, roof lines, posterior wall, firm, cafes? And let's deal not just with what you do, but perhaps the evidence on the paroxysmal AFib. What's the key thing that we achieve and what are the risks and benefits of going beyond that? Yeah, and let me pick up on a previous point I didn't mention with the last question also, which is the cryo issue. With cryo balloon technology, the pattern of migrating outward toward the antrum has kind of gradually moved a little bit back into the veins depending on the shape and size of the balloon and how it snugs into the vein ostium. So there's been a little bit of regression in terms of our lesion location, going to cryo balloon technology as compared with point by point RF. Although it is faster, there's a shorter learning curve and you can isolate the veins quickly. But getting to the question of veins only versus doing other things in paroxysmal AFib, in my mind, and I think the general understanding is that if somebody goes into AFib and then they automatically pop back out to sinus rhythm in a matter of minutes or hours, they probably don't have as much scarring which can maintain the fibrillatory activity. And therefore your strategy really should focus in on the triggers of AFib. And so that really is most people's focus with the paroxysmal patients, younger patients, normal sized atrium, and triggers are really your target. And because the lion's share of them, 90, 95% often appear in the veins, then pulmonary vein isolation alone should really manage things in the vast majority of patients. There are many programs who will look for non-pulmonary vein triggers after they've isolated the veins by giving high dose isoproteranol. Usually higher doses are needed under general anesthesia or heavy sedation in order to get those spots to fire. And they typically come from common locations, the left atrial appendage, the SVC, the coronary sinus, the mitral annulus, the crista sometimes, sometimes the fossa ovalis, and looking for those and then focally targeting those as well tends to be the strategy that some will use on top of pulmonary vein isolation for our paroxysmal patients. Great. And then, you know, again, just focusing perhaps on the paroxysmal patients and we'll get to the permanence in just a brief moment here, but a couple of questions about complications. What's the best way to protect the esophagus? The best way to protect the vagus nerve? What's the best way to prevent LA wall perforation with full thickness burns when you're doing that pulmonary vein isolation in the paroxysmals? Yeah, if I knew the answers to all those definitively, then we wouldn't have so much controversy about how to make lesions and where, and we wouldn't have complications anymore. The problem is that everybody's a little bit different in terms of their anatomy, their wall thickness, where the esophagus is located, which may move throughout the case. I think the key points are to, number one, be aware of anatomy. So you need to know what is where, where it is the phrenic nerve run, where it is the esophagus run on average, and be aware of all the possibilities. And then knowing your biophysics is important. What does it mean when I see the impedance is dropping or isn't dropping? How am I using my contact force to best advantage, things of that sort, and understanding the anatomy of where tissue is thicker and thinner. So people have used strategies of looking at temperature in the lumen of the esophagus using a one thermocouple versus multiple in the esophagus. So you can detect heating in the esophagus and maybe curtail your lesion formation at that point, although it may be too late and you may be not taking temperature at the hottest part of the esophagus. People are looking at cooling the esophagus by putting in some kind of saline in a bag of some sort and trying to cool the esophagus itself. Some people move the esophagus away using a tool that can deform and kind of pull the esophagus in one direction or another. Whether you put the esophagus at risk for damage during that is a question. And whether you have your instrument, the esophagus, can you damage it just from the instrumentation? And if there's metal there, might you actually focus the RF energy into that metal component, whether it's a TEE probe or a temperature probe that's not protected in terms of the electrode? Could you in fact shunt current into the esophagus and conversely increase the risk of esophageal injury? People usually though will try to use lower power and shorter duration on the posterior wall. I think the duration is important because the lesion depth increases with longer lesions. So I think that's important to keep in mind. So some people, regardless of temperature monitoring, will be very careful on the back wall where the esophagus is and just deliver shorter lesions. In terms of the phrenic nerve, especially with cryoballoon, people will generally pace the phrenic nerve and look for loss of attenuation in the diaphragm contraction during continuous and repeated pacing with the phrenic nerve during cryoballoon of the right veins in particular to avoid damaging the right phrenic nerve. So there are different strategies depending on what complication you're looking to avoid. Terrific. You know, the remaining three minutes here, a couple of questions come in, and you did indicate that you can tell the difference between the antrum and the pulmonary vein itself based on the CT scan, based on the fluoroscopic. But what about the electrogram signatures too, which are useful? And then another question after that, what about the value of ablating a CTI, cable tricuspidismus for flutter ablation, routinely at the time of atrial ablation? Yeah, so in terms of the electrograms, if you are on atrial tissue, you're going to see a healthy electrogram. And I'm not sure the electrograms only will be successful in telling you when you're at quote, the antrum versus the true or rest of the LA, because really the tissue is going to be similar. That said, if you fall into the vein, you may see smaller signals and certainly you may see a higher impedance. If you have a RF generator that shows you impedance when you're not on RF and finding that point where you go from higher impedance to lower, as you withdraw your catheter from the vein, may in fact show you at least the vein atrial junction, although not necessarily where people would call the antrum, which is yet further out. And what was the other question again that you asked? CTI ablation routinely. A lot of controversy there because many people are starting to understand and believe that atrial flutter typically starts with pulmonary vein firing. So in fact, conversely, there are some people who feel that if you have atrial flutter, you could potentially solve that problem by doing a pulmonary vein isolation if you got rid of the trigger. That said, most people don't do that for flutter and they do a flutter line, which eliminates the circuit because we can do that safely and effectively. But do people who have AFib also have flutter? It's possible. And there are definitely some people who routinely will do a right atrial flutter line on their way out or even on their way in while they're waiting for heparin to achieve its full therapeutic level. And other people will say, look, I'm not gonna ablate flutter unless I've seen it or if I'm able to induce it in EP lab, some people will only do it then. So there is a variety of opinions and I'm not sure that I know of any outcome data to support one or the other strategy. So in the remaining few seconds, Josh, the other end of the spectrum, the more permanent AFib. We have good data with the STAR-AF2 looking at PVI versus PVI plus CAFAs versus PVI plus Rufline and Mitraline, no difference in the outcomes. So is there any consensus on the best way to approach the permanent AFibs currently? Yeah, no. The longer answer is that when you have persistent AFib, generally those patients have more scarring and that can be anywhere in both atria, usually left greater than right. So people generally in their mind feel that doing just the trigger targeting with the pulmonary veins may not be sufficient in some people, although many purists will say, well, let's start with that. And if they still have AFib, we'll bring them back and maybe do more. What is more, usually it involves trying to find areas of slow conduction, areas of scarring, things of that sort, whether that's empirically isolating the whole posterior wall, whether that's empirically isolating the left atrial appendage, which may have both substrate and triggers, whether that means going after fractionated electrograms. The problem with the trials is, is that everybody does these differently and our lesions are not necessarily effective. So if you have two different arms that don't show a difference, the question is, was it the strategy that was faulty or was it your ability to execute that strategy in a durable fashion? And we haven't been able to sort that out yet because really the difficulty of creating lesions and achieving a durable result for something complicated like substrate, we have not yet achieved.

AF ablation

atrial fibrillation

symptoms

pulmonary veins

controversy

success rates

complications

repeat procedures

permanent AFib