Good afternoon, everyone. Thank you for coming. I have an announcement to make regarding the general session, closing session, I should say, that is scheduled for 3 o'clock, but it will be now at 2.30. So please, and pardon me. I thought someone said something. So the closing session is now at 2.30 rather than 3. Okay. So my name is Patty Larkin. I'm the product manager for the EP, sorry, AFib Ablation Registry and the EP Device and Plan Registry, and welcome everyone here. As always, feel free to have questions submitted to us through the app, and we will answer those at the end of the session. So Dr. Igaru, welcome. She is an Associate Professor of the Division of Cardiology at McGovern Medical School, UT Health, University of Texas. After receiving her medical degree at Emory University, she received all her post-graduate training at UT Health and has remained there in the faculty. She's an experienced cardiac electrophysiologist. And she's excited about atrial fibrillation, relationships of arrhythmia to stroke and conduction system abnormalities seen in structural heart disease. She is also very interested in medical education and is heavily involved in the residency and fellowship program in her home institution. She is passionate about providing equitable healthcare and serves as a board member of the Cardiovascular Education Foundation, which is an organization dedicated to promoting cardiovascular education, research and patient care in underserved communities, especially in sub-Saharan Africa. In her free time, she cherishes lazy days enjoying the Houston heat with her husband and two children. So welcome, Dr. Rekharu. Well, thank you, everyone, for the warm welcome. I was here first last year. Last year was my first time coming to the ACC Quality Summit. And I was really, you know, excited. Everybody gave me a really warm welcome. And I'm really excited to talk today about paving the way to resolution for atrial fibrillation. So let me see how I can start this. Oh, you start this. I'm going to go back. So paving the way for resolution of atrial fibrillation from medication to ablation. And so if everybody knows me, you know, when I first started doing electrophysiology, I really didn't think that atrial fibrillation would be where my interest lies, you know, because atrial fibrillation is one of those things where either you have it or you don't. It's not really a mystery, at least so I thought. And then I started doing ablations. And then all of these things, you know, you start thinking about all the effects that atrial fibrillation has on the population. And that really got me interested. And so I'm going to talk a little bit about that today. So we'll talk a little bit about the background, you know, what we know about atrial fibrillation, what treatment strategies that we have, you know, both medical management and ablation, and then what we should do kind of moving forward all towards the goal of trying to see whether we can actually solve the problem that is atrial fibrillation. So what is it? Well, if anybody has heard anybody describing it, you'll hear it described as an irregularly irregular rhythm. So there are a few things that have to happen for you to be able to say that a patient has atrial fibrillation. The patient has to have an irregular rhythm. Sometimes they feel it, sometimes they don't. Sometimes they say they have the palpitations. About 50% of patients actually don't have any symptoms whatsoever. But you should be able to get an EKG. And on the EKG, you should see that there is no P wave organized contraction. So you shouldn't see a P wave there at all. So an example of an EKG is one that looks like this. Let's see. I'll use this. So one that looks like this, where, you know, as you can see, there's normally supposed to be a P wave right here that's supposed to be right before the QRS. And here you can't see any. You might think that you see one there, but you don't really see it here. It's irregular. A lot of times when the patient first comes to you, it's going very fast. But sometimes it's going slowly because you might be treating the patient for high blood pressure and might be putting them on a beta blocker. But either way, the lack of the P waves really tells you, hey, this is atrial fibrillation and the fact that it's irregular. And why does it look like that? Well, as you can see, you know, this is an electromagnetic, electroatomic representation of what atrial fibrillation is. And what normally is supposed to happen is that you're supposed to see this organized contraction that comes from the sinus node all the way down to all the areas of the heart. Well, you can see that instead of doing that, you actually just see like electrical signals just coming everywhere. So it's not going from one particular spot to the other. That's the left atrium. That's the right atrium. It's just basically everything is happening at the same time. Usually you should see it starting from up here and then going down. And this is not what happens here. So this is a representation of what your electrical signals are doing when you're in AFib. So clinically for diagnosis, you should have either an EKG, so 10 seconds of atrial fibrillation, or you should have a 30 second rhythm strip. Now today, you know, we have so many other ways of monitoring patients. And so we had to expand that definition further. So you might hear of things called AHRE, or atrial high rate episodes. This basically describes that electrical activity that happens for patients who have a lead in the atrium, and then you can tell that they have this really fast heart rhythm that's in the atrium. So this represents, you know, that. So it's not necessarily something that you're seeing on an EKG, but you can tell that on the device interrogation, they have atrial activity that's greater than 175 beats a minute. And usually it's pretty chaotic. So that's one. There's also subclinical atrial fibrillation. So this is for a patient who has atrial fibrillation, maybe has either a Holter monitor, or maybe they have an implantable loop recorder, and you can see that they have atrial fibrillation on the implantable loop recorder, but the patient doesn't have any symptoms. And so I actually had a patient who was convinced she had atrial fibrillation. Unfortunately, her husband had, and she kept on saying she has AFib, she has AFib, do you have palpitations? Yes. Every time we would put a Holter monitor, it would just show PVCs. I said, ma'am, you only have PVCs, you don't have AFib. She's like, I swear to you, I have AFib. I really, really need to be on anticoagulation. And I said, well, I can't give you anticoagulation until I see AFib. And finally, because she was so convinced, I said, okay, we're going to put in an implantable loop recorder. We did. And four months later, she had four hours of atrial fibrillation in the middle of the night. Okay. So that's how that can work sometimes. And so, you know, because of, you know, things like the Apple Watch and the Fitbit, you might see some of my colleagues say, well, you know, they don't really like it because patients come to them and say, oh, I have atrial fibrillation, and they don't, but I actually love it because, you know, information is always helpful. And if somebody comes in and says, you know what, my watch, you know, like the Apple Watch, they'll say something ominous like this, like your heart has shown signs of irregular rhythm suggestive of atrial fibrillation. And so everybody knows like, oh, I don't even know what AFib is, but my watch says something, you know, so they rush in to go see their doctor who sends them to see me. Sometimes this has, you know, the opposite effect because sometimes people say, oh, you know, the watches, they're not really accurate. I had a couple of patients, one of them who actually ended up having a stroke, and, you know, we put in an implantable loop recorder, find out she had AFib, I said, ma'am, you have AFib. She was like, oh, the watch was telling me the truth. And I said, the watch told you that? She was like, yeah, but I threw it away because my doctor said, don't listen to it. I was like, oh, no. So luckily, she didn't have a stroke that was too bad. But you know, that could have been a terrible story. So you know, whenever you hear stories like that, and then you see, you know, that folks have the Apple watches, they have the Fitbit watch, the ones that have EKGs on it, and then they even have, you know, Cardia, which is basically a small device that you can put your fingers on. The only thing bad about the Cardia is that you actually have to do it, right? So if you have symptoms and you have the Cardia and put your fingers on it, then, you know, you'd be able to find it. But what if you're asymptomatic? The Cardia really doesn't help. So, you know, the wearables that folks have, I actually have no problems with it. And I think it's great. So classification of atrial fibrillation, there are many different classes here. They can go from the first diagnosed, which means that basically, okay, somebody came into my clinic, and I know they have atrial fibrillation, or, you know, they had surgery, and I see it on their telemetry, you know, that's their only atrial fibrillation. I don't know if it's something as a result of stress. With COVID, we saw a lot of people who would go into AFib, really young patients go into AFib with COVID pneumonia, but never have it again. So we really don't know what to do with that information right now. But then you can also have the ones that we do know what to do with, your paroxysmal atrial fibrillation and your persistent AFib. Paroxysmal means that you have an episode, it terminates within seven days of onset. Persistent means it's longer than that. Or it's causing a great deal of symptoms, a great deal of hypotension, so much so that you have to cardiovert, that's still considered to be persistent. And longstanding persistent means that it's greater than a year. Now if you and the patient, so the caregiver and the patient decide, you know what, you're in atrial fibrillation, we're not going to do anything about it, you should, you know, we've tried cardioverting you, go straight back into AFib, your atrium is as big as my head, it's never going to come back, then sometimes we say, okay, you know what, you're in permanent atrial fibrillation, and we put that in the chart. So permanent AFib is really not something that somebody can say without having a conversation with the patient. You have to have the conversation with the patient, tell them this is the reason why you're calling them permanent AFib, and then you can say that. So that basically reflects a decision that was made. And so atrial fibrillation, like I mentioned before, it's a very complex thing. There are many different things that kind of interact to cause you to have atrial fib. Sometimes people ask me, well, why do I have it? It could be because of your high blood pressure. It could be because of genetics. It could be because of sleep apnea. It could be because of weight. Sometimes alcohol, you know, there are many different things that go into it. And so all of that basically also causes this endothelial dysfunction. And so, you know, the basic thing is that the atrium, anything that causes it to have increased pressure can increase that chaotic or abnormal rhythm coming from the backside of the heart, and then that would cause you to go into AFib. And so men and women have different occurrences of atrial fibrillation, mostly the highest risk patients are usually men greater than women, higher weight than not. And then also if you, more Caucasian patients than not, and we don't really know if that's because most Caucasian patients also live in areas that they diagnose it more. So that might be something to it. We don't really know. At least we know in the United States, it is more Caucasians than not, because everybody is hopefully getting screened at the same clip. But we do know that patients who are non-Caucasian actually have worse outcomes. And so that's something that some people that are smarter than me are doing a lot more investigation over. Now the global prevalence of atrial fibrillation, this is that. Basically what you'll find is that the areas that have so-called, I guess, I don't like using this term, but the colloquial term would be first world, I guess. The patients who are getting screened more, obviously you see more atrial fibrillation. And then so here, look at a whole continent here is green. I'm not sure if that's true, because I've been to Nigeria, there's a lot of atrial fibrillation. But we'll see how it goes as time goes on and as people begin to know a little bit more about AFib and the risks that come after that. I've shown this schematic before, a lot of atrial fibrillation. A lot of people in my field were like, yay, we're going to get rich. And then the government said, no, you're not. So there's that. In 2019, I'm sorry, 2023 recently, they looked at the global burden of atrial fibrillation and they saw that actually the burden of AFib is actually going up and it's growing faster than that schematic that I showed you, up to doubled in size and even in low to middle income countries. So that's a problem. And what we found is that obesity and alcohol use are replacing tobacco use as a risk factor for atrial fibrillation. So all of this is really a problem. Why do we care? Well, we care because it's more than just an abnormal rhythm. You do have that atrial fibrillation has been documented in all disease states to actually cause more mortality, more morbidity. It's disruptive to patients' lives. So for the patients who are symptomatic, even though it doesn't really kill you immediately, it does cause a great deal of discomfort. It can increase your risk for heart failure. Worst thing is it increases your risk for stroke. And it's a significant burden to healthcare systems. So we care. And it causes kind of all of these things, increased sickness, increased hospitalizations, increased disability, right? Because of the risk for stroke. Now what is the pathophysiology? Like I mentioned, we talked about genetics. We talked about high blood pressure. A lot of the theories, though, go around there being a trigger to atrial fibrillation. So there are two things that have to happen. You have to have a trigger and then you have to have what's called a substrate or an environment where the atrial fibrillation will thrive. As those two interact, you go from paroxysmal to persistent. There are some folks who have talked about this rotor theory where in the atrium there's this electrical activity that's greatly abnormal. And if we can find those abnormal drivers, then maybe we can get rid of atrial fibrillation. It was very popular a few years ago. Now it's kind of fallen by the wayside. Somebody got very rich, though, so that's good. What we do know is that for those patients who have, at least this theory holds true, that in the posterior wall of the left atrium where the pulmonary veins lie, where you have that embryonic tissue that's able to kind of conduct electricity really quickly, if you have PACs that come from there, you're more likely to go into atrial fibrillation. And so if we can isolate these areas, if we can do an ablation or we can do surgery to electrically isolate those areas, then you have a higher chance of not being in atrial fibrillation. The other thing that we know is that if you do have atrial fibrillation and you don't take care of it, then what you're going to do is going back to that theory where it increases the environment or it makes the environment better for atrial fibrillation. If we don't treat the atrial fibrillation, you have structural remodeling that basically perpetuates AFib. And basically that burden causes worsening of outcomes. So that's a problem. So if you consider, you have many different patients who come in with atrial fibrillation. Let's say you have patient A, 65-year-old man, has a history of hypertension, hyperlipidemia, diabetes. He has occasional fatigue, right? Or you have patient B, 25-year-old woman, severe palpitations, now post-hospital visit, you put them on metoprolol, they feel drained. And so they're very symptomatic. Let's say patient C, 72-year-old man, new diagnosis of obstructive aortic stenosis, post-aortic valve replacement, has no prior medical history, comes into your clinic with AFib. And then patient D, new history of COVID, that's supposed to be 19. Don't be afraid. That's not a new disease, sorry. Shortness of breath, has fatigue, and decreased exercise tolerance. So you see all of these patients, and all of these patients, I assure you, they'll have different ways of managing the atrial fibrillation, because it's not the same disease in all of these patients. So for the patient who has aortic stenosis, maybe treatment of the aortic stenosis, cardioverting the patient, and relieving that pressure on the left atrium would be enough for you to say, okay, you don't really have to do anything else. For that 25-year-old, though, you might want to do an ablation, because this patient is severely symptomatic. And if they continue, hopefully the 25-year-old has much longer to live, right? You don't want them to go into persistent atrial fibrillation, because then they could, with more atrial fibrillation, they're going to have more morbidity, more strokes, more heart failure. So you might want to take care of that earlier. Patient A, maybe you do something, maybe you wouldn't. That's the patient that I would say, look, I would love to do an ablation on you, however, we can make a decision, see how it goes. I definitely want you to be out of atrial fibrillation, so maybe we'll do a cardioversion. We don't necessarily have to do an ablation. For patient D, with this new COVID-10, maybe treatment of the respiratory disease is actually enough, and you wouldn't have to do anything else. So all of these patients, even though they all come in with atrial fibrillation, they're quite different, and so you treat them differently. Main things that we think about when we're managing those patients are, what is the risk for stroke? Because the stroke is what is going to cause you the most problems, right? If you have somebody who has... When I tell somebody, oh, you've had a heart attack, now you have 40% of your heart working right instead of the normal 100%, they say, oh, gosh darn it, and then they walk away. But if I say, oh, you had a stroke, and you now have 40% of your brain working, they're just going to be like, oh, God, this is terrible, this is the worst thing I've ever heard. So even though I'd like to think that the heart is the most important, sometimes it's something else, a.k.a. the brain. And so that is really the thing I would want everyone to take away from this, where even though the patient comes in, and they say they have atrial fibrillation, but maybe they're not symptomatic, treatment and prevention of stroke is actually really high up there when we're talking about these patients. And the second thing is also the atrial fibrillation itself. Why? Because it does increase that risk for mortality, morbidity, but those things are far away. Coming closer, what are we worried about? We're worried about the risk of heart failure. So if you are in a higher rate, or even atrial fibrillation itself can actually put you into heart failure. So those are things that we worry about. And then also worsening of other conditions that you have. So what do we want to do about treatment? So there's the rate and rhythm control that we always talk about. For a long time, this has been, you know, a discussion that everybody's had. Do we go with rate control or rhythm control? Previously, before I would say 2010, this was more of a discussion because there weren't really easy ways of pursuing rhythm control. So in the 1960s, you know, when they first came out with the wavelet hypothesis, and then going up to the 1990s, where Hasagira came out with the, oh, no, it's coming from the pulmonary veins. You know, these surgeons actually came up with the maze procedure, where they basically cut the heart into pieces and then put it back together. And they found that in some patients, they were actually able to get rid of atrial fibrillation. The thing was, you know, what they were doing, and they didn't really know it at the time was, they were isolating the pulmonary veins. So when Hasagira came out with his theory, that was later on found to be actually pretty correct, then you could go back and say, oh, look, you know, in spite of them putting like all these scars and all these lines everywhere, the one thing that they always did was isolate the pulmonary veins. And so whenever they did that, the patients actually did much better. Now, any surgeon will tell you that actually doing a maze procedure, a true maze procedure, is really difficult, because you're literally taking the heart apart and then putting it back together. So nobody really does one anymore. They do have tools that they can use to isolate the patients, but of course, nobody wants to go through open heart surgery to do that. This is some of the results of surgery for atrial fibrillation in the past, where they ablated or they surgically ablated patients. But when they went further and did discrete intravascular ablation, we were able to get the same results. And they were able to find that, oh, we could actually take a patient from being in atrial fibrillation and put them back into sinus rhythm. So yay, everybody was happy. So now atrial fibrillation is cured, right? Of course, it's not that simple, because atrial fibrillation is not just like all other supraventricular tachycardias. Most supraventricular tachycardias, you have a reason, you have a focus. You get rid of it, it's gone. Atrial fibrillation is like, well, we have all these theories, but we really don't really, really know, right? So I've talked to you a lot about the posterior wall and how all of those you know rhythms are coming from the posterior wall that are causing AFib. Well there's some patients who after they've had atrial fibrillation for such a long time just isolating the posterior wall doesn't really help anymore and that's why you know what we would like to do is see about attacking it a little bit earlier on in the course. But before I get to that I do want to talk about you know this trial rate control and rhythm control the bane of my existence. This is what I would call it but I digress. It's not their fault right they did provide a really good trial. Basically the thought process was this was published in 2002 when I was thinking about becoming well not really thinking I was in medical school at the time and this was one of the first trials that I actually knew and I was like rate control is equal to rhythm control walking around. And the thought process was okay they would take patients who you know they concentrated on rate control and then gave them beta blockers and then they took other patients that they focused on rhythm control and remember this was in they were looking at patients in the 1990s right so they only had limited ways of actually taking care of these patients so the surgical processes that I was talking to you about they were in use but they were only in use unless if the patients were already going through surgery. So if the patients weren't going through surgery you know they were out of luck. And so what they would do is give the patients amiodarone or give the patients Sotalol another antiarrhythmic and when they would do that they would see if the patients would stay in sinus rhythm. And so they divided patients to either go through this rate control area or rhythm control and what they found was that you know with rhythm control well first of all with rhythm control if they wanted to cardiovert the patients they would cardiovert the patients and they would do everything that they could to put the patients into a sinus rhythm. For rate control all they did was give them beta blockers and this was from the time they first diagnosed atrial fibrillation. What they found was that in using all of these medications to provide rhythm control about 60% of the patients in both arms actually ended up being in sinus rhythm. So in the rhythm control arm you have 60% of patients but you're using these really hefty drugs right that have a lot of side effects. And in the rate control arm you're doing the same thing but with better drugs kind of right like beta blockers, calcium channel blockers. So there was that. When they finished and they looked at everything this was what everybody took away right and it's a very I guess nice thing to say right but there were there were all these other words in the conclusion that nobody seemed to read right. So everybody came out saying rate control is equal to rhythm control but really what they should have been saying is actually there were two things right that rhythm control and rate rhythm control with amiodarone and rate control there was no real difference. So if you used amio because of the adverse side effects because of the symptoms afterwards which were part of the conclusions or part of the endpoint you didn't really have a change. And then also remember both sides had 60% in a normal rhythm. The second thing was that anticoagulation they actually realized that anticoagulation should be continued in this group of high-risk patients. How did they discover that? Well for those patients who they were undergoing rhythm control they actually stopped their anticoagulation after they had been in sinus rhythm or they would say okay we're giving you all these meds you should be in sinus rhythm and they would stop their anticoagulation and those patients would come back with stroke. Further causing them to have you know worse outcomes right if you were randomized to the rhythm control arm. So it was a good study the conclusion just wasn't what it should have been. So since then we've had the cabana trial which basically looked at catheter ablation versus antiarrhythmic drug therapy and basically what they found you know it's pretty self-explanatory but what they found this was a really long trial you know looking at atrial fibrillation and within that time period from November 2009 to October 2017 you know the way that we were doing ablation actually changed a little bit. So we now have 3D mapping which is basically where we don't have to look at x-ray to actually you know do our ablations. So 3D mapping gave us the advantage of being able to see things a little bit bigger right. It's like a little video game you can kind of blow it up make it as big as you want and you can make these really small movements with the catheter that you're not really able to see when you do an under x-ray. So we're able to do that. Catheters were created that could actually tell you the force with which you are actually touching the wall so that was that and then the catheters also became better you know and the physicians also started to realize hey if we go into the pulmonary veins too much we might cause pulmonary stenosis maybe don't do that let's come out. So all of these things started to serve to actually give you better outcomes. So while all of this was happening the Cabana trial was going on and even though the primary endpoint really didn't show a difference you did see that the hospital there was ablation had superior efficacy to drug therapy and also there was significant reduction in death and cardiovascular hospitalization with ablation. So that was great. Another trial that came out soon after was the East AF trial the early rhythm control therapy in patients with atrial fibrillation and in this page in this group they actually did somewhat what a firm did in 2002 where they looked at two groups of patients one group they said okay we're going to do rate control the other group they said they would do rhythm control but not only they would do rhythm control they would do early rhythm control. So within the first three months they would make sure that the patient stayed in atrial fibrillation in sinus rhythm and what they found was actually those patients did better. So you can actually take a look this is the ablation arm over here and this is the rate control arm over there and actually I shouldn't say ablation arm this is the rhythm control arm this is the rate control arm. This is the number of ablations that happened. So actually over here they were using a lot of medications to keep the patients in sinus rhythm. Amiodarone was a little bit less than it was in the firm and so those patients did better and actually they had to stop the trial early because of it. And so what do we find? We find that okay putting the patients into a normal rhythm the heart likes a normal rhythm. So there is no such thing as oh you've been atrial fibrillation you're asymptomatic so therefore we should leave you in that because eventually the chickens will come home to roost. The heart likes being in a normal rhythm so if we can we should put the patients back in sinus rhythm as much as possible. Now once the patients have heart failure is the cat out of the bag already? Should we just leave them be? Well no. You know the CASTLE-AF trial showed us that if you see these patients you should actually do a pulmonary vein isolation and if the ejection fractions were greater than 20% they did much better. If it was less than 20% they did slightly worse but it was still worth it to put them in sinus rhythm and so ablation is recommended. So this is another example of the CASTLE-AF trial follow-up trial and that basically showed the same thing. So what should we do? Well I think that increased screening is definitely necessary. It does have the disadvantage of making people a little bit paranoid so there's some people who just check their watch all the time it's like oh my heart rate is fast. It's like ma'am you need to exercise like don't worry about it you're in sinus rhythm. And then you know so screening in these different areas whether it's you know if the patients have risk factors for atrial fibrillation, if they have increased high blood pressure, if they have screening for obstructive sleep apnea, you know when the patient comes in for their physical telling the patient hey do you snore? Does anybody say you snore? Do they say that you could you know you're like a train and you know people can't sleep next to you? You know that's really important because if they do that does put them at an increased risk for AFib and that does come with all the risks following. Also looking at you know obviously the watches but sometimes you know just listening to the patient sometimes like my patient that I talked to you about earlier they say there's something wrong with my body and you can't really put your finger on it. There's nothing wrong with getting a Holter monitor or getting an event monitor or even if they report palpitations the implantable loop recorder is great. Five years, four to five years, we have three companies that have created an implantable loop recorder that's MRI conditional. You put it in underneath the skin and you can tell whether a patient has atrial fibrillation or not or any arrhythmia that you desire so to speak, right? And then the other thing is just taking care of all the other risk factors that go into causing atrial fibrillation or have a relationship with AFib. Now these are all the things that we know have a relationship with atrial fibrillation. COPD, the patient has valve disease. We've already talked about hypertension, talked about diabetes. Diabetes is the worst thing ever. You don't really think that it's doing anything and then it's just killing you one fingertip at a time. You know obesity, vascular access. Obesity is a really interesting thing because you know when we talk to our patients I think that a lot of, we haven't done a good job in medicine by not vilifying the patients who are obese, right? So a lot of patients don't want to come to the doctor when you tell them hey obesity is a problem they feel that you're judging them when it's really is just more the effects that it can have and we should be willing to have these discussions with patients and you know be able to encourage them in all the ways that they can lose weight. A lot of people talk very badly about you know the medications that have come out now with ozempic and everything that comes along with it. I have no problems with it. If ozempic is what gets you to lose weight, I mean more power to you. So we should make that all of our business, right? So that we can encourage the patients to be their healthier selves. So I'll come off my soapbox on that. But basically looking at you know a patient's lipid profile, their history of heart failure, high blood pressure, kidney disease, all of these things can actually go into causing atrial fibrillation. And so if we can attack all of that with a multidisciplinary team, cardiologists, primary care physicians, even sometimes rheumatology, a lot of inflammatory diseases have relationships to AFib, pulmonology, then maybe we can actually help solve it, solve the problem. Finally how do I take care of atrial fibrillation? Well we can do ablations if either we're burning or we're freezing or we're doing this fancy new thing called PFA. It still is not really well adopted yet. We're still going through trials for it, but it's very promising. But I don't want to do this, but sometimes I have to. And if we can take care of the patient looking at all these factors, these four factors, lifestyle modification, rate control, rhythm control, and reducing their stroke risk, I believe that we'll go a long way in getting rid of AFib. And thank you. »» Can you hear me? Okay. Great. Okay. A question that we received is, in an AFib ablation case via PVI isolation and confirmation is not documented, can it be assumed that entrance block is in all ways? »» So for atrial fibrillation, I mean, honestly, I would say that the way you're supposed to do an AFib ablation is you're supposed to isolate all the veins, you're supposed to make sure that there's entrance block, and you're also supposed to make sure that there's exit block. So even if they don't document it, it should be assumed. But you can't always, you never know what happens in cases sometimes, unfortunately. »» So true. Another question, no maze was done. But Hybrid 1, trans-thoracic and Hybrid 2 are done now. Not sure, that's a question, are they being done? »» Well, I would say that, at least in my institution, they don't do a full-on maze. So they will do, use implements called AtraCure where it's an epicardial ablation. They just take these two, this prong that's able to do radiofrequency ablation where they just grab the two pulmonary veins, close it up, and then it causes a scar on the outside of the heart. The issue with doing those sometimes is that what you want is a scar that goes through all the walls of the heart, so endocardium and epicardium. But unfortunately, sometimes it ends up being just epicardial. So sometimes it might actually cause atrial flutter. There is a convergent procedure that you can do. So for those patients who are persistent, they have a left atrium that is really big and they just look like, or you go in to do your ablation and you notice that the scar is all over the heart. Then sometimes you have folks doing a convergent procedure where the electrophysiologist will go on the inside and take care of a pulmonary vein ablation endocardially, and then the surgeon will actually do a thoracotomy and take care of the ablation epicardially. So there are sometimes where they do that. Thank you. How often do you ablate just the pulmonary veins versus PVI and a CTI line? So I personally, I don't do a CTI unless I have seen atrial flutter. Now there's some of my colleagues who just, as a matter of fact, they do CTI lines. The reason why I don't is because sometimes, you know, when you go into the heart, there is a possibility that atrial flutter was what caused the atrial fibrillation, right? Because a lot of times when patients come in with AFib, we weren't there at the beginning of the AFib. So there are a few patients of mine where I do the AFib ablation and then probably like six months later I have to do a flutter ablation. However, it's never a good sign when you do a CTI line and the patient does not have what we call the substrate for atrial flutter, and I'll tell you why. So typically the CTI line is this pathway between the tricuspid valve and the IVC, and typically it's pretty thick. When you have atrial flutter, it's because you already have somewhat of a scar there. So somehow you have your body created a scar there and you have this substrate that will support an atrial flutter if you have like a premature beat. If you don't have that substrate, then all you're doing is trying to burn this really thick healthy tissue and then you create the substrate for atrial flutter. So I typically don't, but I know that there are some of my colleagues who end up doing that. Great, thank you. Can you speak a little about pulsed field ablation and what it is and where it may be going? So it is, I can't speak too much about it just because there's still so much that we're learning about it. So it's basically this type of energy where we're able to cause cellular death. And so the idea is that it only causes cardiac cellular death, which sounds great in theory, but then at the same time it's kind of like, well, this throws all our prior theories out of the water. Because we do say that this is, you know, atrial fibrillation and sometimes atrial flutter is caused by not just the scar in the heart and problems with the tissue, but it's also caused by these, sometimes it can be because of electrical connections, abnormal electrical connections that you do have to separate. So if you use pulsed field ablation and it only affects cardiac tissue and causes cellular death, and it doesn't really cause nerve tissue death, then maybe it's not really going to be as good. Having said that, a lot of the studies that have come out have been very promising. I think the longest that they have follow-up has been a couple, I think one year. And in the last study that was published, I believe it was in HRS this year, they said that it was at least equal to pulmonary vein exhalation. So it's going to take a long time before we are able to say definitively whether it's better or not. It is looking more promising than cryoablation, and I think that what folks are looking for is this way of doing an ablation where you don't have to go point by point. So the atrial fibrillation ablation with radiofrequency ablation that we do now, it's very technically challenging where for you to have a good scar, you have to go point by point, those points have to touch each other. And so it does take a fair amount of learning for you to get to be able to do that. And so a lot of folks are looking for an easier way to do a pulmonary vein exhalation. Cryoablation was that for a little bit. But cryoablation, the only thing about cold is that the lesions sometimes are not as long lasting. And so PFA might solve that issue where you have this catheter, you just put it up there, and it's able to take care of the entire pulmonary vein without you having to go point by point. So that is the reason why I believe a lot of people are trying to look towards that as being the next thing. »» Great. Thank you. Why would a provider choose to do a PVI and WAC? »» PVI and what? »» WAC. W-A-C. »» Oh, so a WACA is basically, so a pulmonary vein isolation is you isolating the pulmonary vein. The WACA is basically you're doing a wide circular ablation. So a WACA is basically you're just describing the pulmonary vein isolation. So instead of ablating inside of the vein or really close to the vein, which can put the patient at risk for pulmonary stenosis, which is miserable, then you do a WACA, which is basically the way that we do the pulmonary vein isolation. So everybody who's doing pulmonary vein isolations now is doing a WACA. Yes. Yes. So the whole idea, so the WACA is basically saying that, okay, instead of going into the ostium of the pulmonary vein, you're actually going to go at least half a centimeter, if not a centimeter, outside of the pulmonary veins. So that's basically what it's describing. »» Okay. I wanted to address the question on presentation slides. They will be uploaded. For some reason they're not right now. But I'll make sure I will go to our people and let them know they're not uploaded. So it might be just a technical issue. It takes a little bit longer. Okay. Any other questions? I don't see any more in the app. Did someone just say they had one? Oh, Matthew. Okay. Okay. I did see one here while he's typing in. Does a box lesion always include a PVI? »» Yes. So a box lesion basically means that on the posterior wall you are trying to isolate the posterior wall as well. So there are different levels to pulmonary vein isolations. There have been a couple of studies that have basically said, you know, just doing a pulmonary vein isolation is the only thing that's necessary. Any other ablations that you're doing are not necessary at all. Having said that, nobody believes that. And so everybody does whatever it is that they're going to do. So this is my approach. Typically if a patient comes in, left atrium is a normal size. They're coming in with paroxysmal AFib. Maybe they are, I've cardioverted them a couple of times or the patient is symptomatic. I just do a pulmonary vein isolation and I see where it goes. Now if the patient has an enlarged left atrium or I actually do electroanatomic mapping, which is basically where we're mapping the voltage of the chamber in sinus rhythm, and I notice that there's a lot of scar in the posterior wall, then I'll do a box lesion, which is basically where you isolate the posterior wall. There are a few different ways about trying to do this. Typically people will form a line between the upper veins and the lower veins, and that's why it's called a box lesion. The folks in Austin, Dr. Natale and his group will say that, well, nature abhors order, and so you shouldn't just do a line. You should actually, I guess, throw a pellet gun at the posterior wall and burn everywhere. I've tried to do it their way and all I've done by doing that is causing flutter. So I'm sticking to my lines. And so we go from there. Yes. Yes. Yes. So I don't know what people are saying when they're saying segmental. There was a time we used to do it around each vein. Now most people actually just go around both veins in a circle. Maybe when they were saying segmental is because they were doing both veins and then a line in between for both. But that's not in the common lexicon anymore. And did you have a second question that I didn't address? No. So that is considered to be, that's actually an ablation, an additional line that you're doing for atrial flutter. And so the justification for that is that, oh, you induce the left atrial flutter. So remember for the lines that you do anterior, the posterior wall is pretty thin. So you getting a transmural scar is actually easier. If you do an anterior line and you don't have a flutter or something that's going around anteriorly, then you actually have a higher risk of causing flutter. Because remember the anterior walls are thicker. And so it's harder to have that transmural scar. So when you have flutter, that means you already have some sort of abnormal conduction. You have an area of slow conduction that you can basically homogenize by doing ablation. But if you just do it, then you'll cause an area for flutter to arise. »» Matthew, many of the modes have been discussed. Do you have a specific mode that you would like? »» The empirical linear lesions, so we don't do those anymore. There are some people, so there was a time when people would just, a patient would come in the same way that people would do the CTI line, just empirically. Some people would do upper roof line and a floor line just because as part of their ablation. But studies have shown that you can actually cause flutter by doing that. And so I would say that for you to get paid for doing that, you have to say in your note that there was a reason why you did it. And so most people would say, oh, you know, we saw fractionation or there has to be a reason for you to say that you're doing it. Now, you know, if people still continue doing it and they don't really have a reason, I can't really speak to that. But that's really the thought process is, you know, after STAR-AF where we saw that there really wasn't that much of a difference in outcomes than where most people are going towards the less is more approach. Well we don't throw it out. It's still a tool. The rotor base, so the rotors, rotors have really just kind of fallen by the wayside. And the reason why is because for rotors, for you to actually map a rotor, you actually have to buy their program. And so it's kind of like it's not that effective for you to invest that much money in buying the program. So for you to say that you're mapping a rotor, you'd actually have to buy the program for you to be able to do it. And then what ended up happening is, you know, when they were doing the rotors, when they finished the blading, you looked at it and you were like, well, this looks like a WACA with a posterior leg. So why am I investing all this money to buy this when I could just do it and just be done? So we didn't throw it away. The thing, like I say, you know, atrial fibrillation, yes, we have all these theories, but we really don't know. And even there's sometimes when patients will ask me, okay, well, you know, for atrial fibrillation, is it just caused by these, you know, fast PACs that are coming from the posterior wall? Well, what about the patients who are young and don't have that problem? Where did it come from then? And you'll see drivers for AFib, you know, really if you pace the atrium fast enough, you can cause atrial fibrillation. It doesn't necessarily have to come from the posterior wall, but the posterior wall is where we see it most of the time. There's sometimes that you'll see fast heartbeats coming from the SVC. Sometimes you see it coming from the CS. And so you might have to ablate in other places, but in about, I would say 80% of patients is coming from the posterior wall. And so anything that you can do to isolate that posterior wall, whether it just be the pulmonary veins, or you have to also add the posterior wall to that, then, you know, that would be a plus. It's just that we have just become a little bit quicker about making decisions. So whereas before we would go and map and see, oh, do we see problems with the fractionation, looking for CAFAs, now we don't do that anymore. We say, okay, most of the CAFAs, they come from the posterior wall, we're just going to ablate the posterior wall because the patient is still going into AFib after I've done a pulmonary vein isolation. Most of the time you see it when the patient has persistent. I have seen some cases where the patient has paroxysmal atrial fibrillation and you just do pulmonary veins and then usually we'll put them on some medication like isopril or adenosine and then they keep on going into AFib. Then you realize, oh, they do have a driver from the posterior wall. So it's rare that that happens, but that does happen enough times that I test everyone. So there's nobody that I'll say, oh, paroxysmal AFib, I'm just doing the pulmonary veins and then I'm not even going to test, I'm going to let it go. I typically won't do that. »» We don't have any more questions through the app? Anyone else? »» My problem is the doctors don't appreciate the system. »» They don't? »» That's another problem. That's another issue. Thank you, Dr. Ecker. We really appreciate it. Wonderful presentation. »» Thank you. Thank you, guys. »» And don't forget that the closing session is now at 2.30 rather than 3.

atrial fibrillation

AFib

treatment options

cardiology

irregularly irregular rhythm

diagnosis

rate control

rhythm control

ablation