So, I come from Jonesboro, Arkansas in the United States, and I will give a 20-minute session on appendage closure. Next slide, please. These are my disclosures. Next slide. So, the question is, you know, where are we with the Watchman device when it comes to safety, efficacy, leaks, implant success, device-related thrombus, et cetera. Next. So, this is the trial timeline. If you look at the Watchman trials, you can see that we started way early in 2002 with the pilot trials, and then moved on all the way up to 2020, where the Watchman Flex device was approved. And, more recently, in the United States, we had the Watchman Flex Pro device that got approved this year. Next. And, if you look at the Watchman Flex device, it's been a huge technological advancement compared to the Legacy device. There's significant difference between how the Legacy device worked and the Flex device works with its closed end, with its dual row anchors, its 18-strut frame, all of it allowing us to implant the device much safely and effectively. Next. If you look at the implant videos, this is an example of an appendage. I'll just keep advancing two more so the videos can play. You can see that the TE image shows the appendage. Next. And you can see the angiogram and the TE imaging showing the device being deployed. And, because it's so different from the Legacy device with that closed distal end, you can safely advance it into the appendage and deploy it in a much coaxial fashion, giving you much more contact points, especially because of that 18-strut frame. Next slide, please. And where did we get the data for the Flex device? It came from the Pinnacle Flex trial. This was a U.S.-only trial that looked at the safety and efficacy of the Flex device. Next. In the trial, about 400 patients were enrolled in about 29 sites, and these patients were followed for up to 24 months. Next. If you look at the success rate of the safety data, you'll see the event rates were as low as 0.5 percent. Let's go to the next slide. And this is looking at, compared to the other Watchman trials, so Protect, Prevail, Nested data, you can see this is the lowest safety data, lowest event rate that we saw compared to the other Legacy device, which was at 0.5 percent. If you look at the DOAC discontinuation rate, that was as high as 96 percent in the trial. Next. And looking at efficacy, so was the implant successful? You can see 98 percent of the implants were successful, and there was 100 percent closure. Now, if you looked at complete seal, that was at 90 percent at one year. Next. And this is in comparison. This is the implant success rate comparing to the previous trials, and you can see the implant success rates have always been good, but that stayed pretty high with the FLEX device as well. Next. This is looking at the 24-month secondary endpoint, which is stroke and systemic embolism, and the annualized stroke rate was 1.7 percent. Next. So this is a summary of the FLEX trial. You can see it had good safety, it had good efficacy, good OAC discontinuation rate, and good procedural success. Next. The 24-month data also was good with the annualized stroke rate of 1.7 percent and no additional DRT at 1.8 percent. Next. Now, if you look at the anatomies that were included, you know, with the advance with the technology with the FLEX allowed us to implant it into more challenging anatomies. About 21 percent of patients in the FLEX trial could not be implanted with a legacy device, and so that was also a huge technological advancement. Next. This is looking at the data from the U.S. NCDR registry. It's called the Surpass Registry, so this is real-world data, and if you can just kind of click through, you'll see that the implant success rate—next, please, and next, and these are all the highlights that you'll see. Next. You'll see the implant success rate, the safety data, the seal data, and one more. Next, please. All of them match in line with the IDE trial, so it was just as applicable in the real world as well. Next. This is flexibility data from the European registry, again, showing that we had good success rates and very, very good safety events. Next. Now, where do we go from the FLEX device? I mean, we already had a pretty good device, and the next device is the FLEX Pro device, and let's look into what that is and how it's different. Next. So the Pro device is based on the FLEX platform, so the structure of the device is still the same. Next. It has multiple additional features. One is it has a non-thrombogenic coating, so what that does is it allows for better hemo-compatibility, so it allows for better healing and less device-related thrombus. Next. You'll see a bigger size comes with this, so 40-millimeter size, which allows for much bigger anatomies that can be included. Next. And also, it has these radiopaque markers that allow for you to better see the device. Next. And if you look at those radiopaque markers, can you play that? Just advance it? Okay, that's all right. So you'll see that as you deploy the device, those radiopaque markers line at the level of where the maximum dimension is, so you can actually plan for those markers to land right at the osteum. And when you do a tug test, you can actually look at the relative position of those markers, and it'll tell you whether you have had any displacement. So it really lets you look at the device very well on fluoroscopy. Next. Go ahead and play that. Next, please. Just click next. Yeah. So this is a case of a pro-device that was implanted recently. After the approval, you can see after the angiogram, we're going in with the device. You'll see those markers come out and how we align those markers to where that appendage needs to be occluded. And you can see that with single deployment, you can actually align those markers really well. Again, angiogram, all that is the same. Now this patient is also going to go home on DAPT therapy, so these patients are followed in a registry called the HEAL-LAA registry, where the patients actually go home on DAPT therapy for 45 days. Next, please. The other thing that is seen is the coating. And the advantage of the coating, which is a PVDF-HFP coating, which has been studied significantly in the drug-eluting stent world, what it is, it's an inactive coating that does not affect the mesh or the porosity of the Watchman device, but allows for quicker healing. Next. And how does it do that? This is K9 model. And you can see on the left is a coated device and on the right is uncoated device. You can see the amount of thrombus is less in the first two-week window. Next. This is looking at after they've been explanted at 45 days. You can see there's less thrombus on the coated device. And again, remember, these were K9 models that were not on any blood thinners, any DAPT, any oral anticoagulant. So these were challenging K9 models. And you can see the D-downward percent was also extremely low in the coated device. Next. And looking at the—this is looking at the fabric, the inflammatory markers on the fabric. You can see those are also extremely low on the control device or the coated device. Next. This is looking at albumin binding, which kind of suggests endothelialization. And there was more albumin binding on the coated device compared to the uncoated device. Next. This is looking at the inflammatory markers and plated addition, so less plated addition on the coated device, again, allowing for less DRT. Next. So combining the albumin binding, the less plated addition, all of this allowing for better healing and less DRT. Next. The other thing was the larger device that comes with the Pro. So you have a 40-millimeter device. And when you look at the registry, there is at least a 10 percent of patients that fall in this large appendage size. And now the extension is all the way up to 36 millimeters. Next please. Next. So if you—this is a case, you can see how big that appendage is. It measured at 33, which would not be accounted for the current 35-flex device. So here we are implanting the Pro device. And you can see the, you know, in those challenging big anatomies, it is definitely a useful addition. So allows us to get into the bigger anatomies as well. Next. So what are the other unmet needs? So if you think about imaging needs, device delivery, and let's look at post-implant regimen. Next. When you look at imaging, the things that we look for is you want to have some kind of pre-procedural imaging that is reliable and reproducible and is going to help you implant this device. Next. And CT is starting to image, you know, come up more and more into this imaging platform. You can go to next. And there are multiple 3D segmentation tools, and TruePlan is one of those proprietary softwares that allows you to have this automated 3D segmentation. Next. And what it does is it gives all this out, spits it out for you. It automatically identifies the appendage, gives out the measurements, sizes the device for you. Next. And it does the procedure extremely well, allows you to figure out what transeptal route you want, helps you figure out what it's going to look on fluoroscopy. Next. Helps you pick up a fluoroscopic angle. Next. Allows you to give TE simulation views so you can be prepared ahead of time and shows you the sheet. Next. And also gives you an idea of what the device is going to look like once you have implanted it. Next. So, you know, if you want to keep it simple, you can try to do it yourself, or it'll spit out the whole image in a PDF format for you. Next. And the newer versions, next please. The newer version of the TruePlan software even does the post-implant analysis. So if you do get a CT after, you can do post-implant analysis. You can look for thrombus. And also if you're planning on doing ice-based implants, it'll give you ice simulation views as well. Next. What are the other imaging things? 4D ice is coming up more and more. And you can, that's a new vision case with the 4D ice being used. Next. And that's a Philips Echo Navigator, which allows you to combine fluoroscopy and your 3D. Next. And one more, please. And you'll see that that still doesn't solve all the challenges. Next. It doesn't solve all the challenges. We still have to deal with leaks. We still have to deal with canted devices, and the deployment sometimes can be harder. Next. So the first thing is, you know, where have we come with the transeptal part? And the Bayless and the VersaCross systems have been a huge advantage when it comes to the structural world and allow us to do a much more seamless implants with, you know, no exchanges and stuff. Next, please. Then the question comes, okay, you've got a good transeptal, but do you still, you know, do you need steerable sheets? Because the current sheet is not steerable. And there are anatomies where it can be extremely challenging, and you saw that 40-millimeter implant that I showed you. It definitely, you know, it could have, you know, we could have been a little more coaxial on that. Next, please. And you can kind of click through. Please. Next. Just keep going. So you'll see that the, this is not an approved sheet, but this is the true steer sheet that is being launched. Keep going. Next. You'll see that it has a handle that helps you rotate and get deflection, but also advantages that you will be able to steer it in the middle of a deployment. So not just in the, not just before implant, but in the middle of the deployment, you'll be able to steer it. Keep going. Next. It's a little bit bigger sheet. Next. It's about 17 French hour diameter. Again, it's not FDA approved currently, but is hopefully to be approved early 2024. Next. It will also be compatible with the RF Bayless transeptal system. So still be able to go a single transeptal. Next. The question comes, go ahead and yeah, play it. So what you, what happens with the steerable sheet is you can see, you know, that deployment with the non-steerable sheet, you can see how off axis that are the devices. And if you did have the steerable sheet, and if you were able to deploy it with steerability, you'll see how the device is being engaged into that model. And then as you're deploying, you apply the steering and you'll see how coaxial that device will land. And when the device lands coaxially, it helps with with less leaks. Next. Next. And next. Go ahead and click twice, please. You'll see that, you know, when you, when you have non-steerable sheets, sometimes what you see is you, you inject an angiogram and it's off axis and you don't get a good, you don't get a good angle shot because you have core wire bias and with the steerable sheets, you can actually reduce those core wire biases so you can get a good tug test, you can get a good angiogram. Next. Again, I told you that this will be compatible with the VersaCross system as well. Next. Now, how about upcoming future clinical trials? And I'll kind of summarize with this. There are trials that are looking, you know, I talked to you about the FlexPro device. There is a post-market registry. There are trials looking at concomitant procedures such as AF ablation and LAC. There are trials looking at optimizing therapy. The ICE LA trial had just been published and the, and Watchman got FDA approval for use of ICE in implantation. And then there are trials looking at appendage closure as first-line therapy. Next. The, the trial that, that we're looking forward to, to come out next year is the OPTION trial, which finished enrollment and is currently in follow-up. This was a trial that looked at appendage closure as first-line therapy in post-AF ablation patients. So these were patients that underwent AF ablation. They either got appendage closure at the time of the AF ablation or they got it three months later. Next. The CHAMPION trial is a trial that's looking at appendage closure as first-line therapy in all comers in non-valvulatory ablation. This current has, this trial has also finished enrollment and is currently in follow-up. And this is, this is going to open this therapy up to a huge range of patient populations if this trial turns positive. And again, we'll get a lot of data from this trial. Next. The, the, we all know about the, the LAOS-3 trial. This was a surgical trial that looked at appendage closure in patients who were going, undergoing cardiac surgery and they got appendage closure in addition to oral anticoagulation therapy. Next please. And there was a significant improvement in reduction in stroke in the, in the patients that were in, that got appendage closure and oral anticoagulation. So the LAOS-4 trial is being designed, which is going to look at percutaneous, which is the Watchman device, in addition to oral anticoagulation in this high stroke risk patient. So if there's a patient that has a CHATS VASc score of four or higher, we will look at this belt and suspend the therapy for those patients and randomize them to OAC versus the combined strategy. Next. The HEAL-LAA is the registry that is evaluating the Watchman FlexPro device that I just showed you and it's going to look at the use of DAPT for 45 days, so simplifying that post-thrombotic regimen. Next. We're looking at monotherapies, so this trial is being designed as well. So this is using the FlexPro device, so we're going to look at DAPT therapy as control and then look at if we could use just aspirin, which is single antiplatelet therapy, or maybe a low-dose DOAC as a post-implant regimen. Next. So I'll summarize that, you know, there have been significant improvements in the technology as such, especially with the new FlexPro device with its non-thrombogenic coating and its radiopaque markers and the larger device. We've come a long way for the device, but in addition, we have multiple trials that are ongoing, looking at how we can optimize post-implant therapy, how we can evaluate this new technology and also expand the patient populations that we can treat. Thank you very much. Next. Okay, I'm grateful that I have the opportunity to speak with you about clarity for complexity and some of the things that we've learned with high-resolution mapping, particularly with the arrhythmia system. Next. So these are my disclosures, if you could advance. Next. Is it working? Great. And then, next. So the evolution of high-density mapping is amazing. It's like television. And CARDO was validated with 75 points. And as we move forward, next, you can see that we started looking at the N-Site system. Next. And looking at a couple thousand points. And I remember when we called this ultra-high-density mapping from UCLA, because we didn't know what to call it, because it was more than high-density mapping. Next. And then the arrhythmia system really started taking, next, to another level, which was 8,000 or 10,000 points. But the real question is, does the density really mean anything? Is it just a pretty picture? Can we learn anything from higher-resolution mapping? Next. So I was first exposed to arrhythmia at the University of Chicago, and we already had the system. Next. And we really wanted to understand how it could be used for different arrhythmias. Next. And we started with sinus node mapping, next, and then AVNRT, and I'll show you a couple of those insights. Next. And then moving to the atrium, left atrial flutters, looking at the epicardium, the endocardium, and then finally ventricular tachycardia. So if you've never used arrhythmia, I always think it's very easy to start simple. Next. And next. So here would be an example, next, of understanding just principles of mapping. So here is a beautiful image of sinus node activation. And you can see that you have earliest activation at the terminal crest, sitting here in the SVC, where the anticipated sinus node is. Next. And what's important to emphasize for everyone in the room is mapping systems are nothing without electrograms. And now there is this tendency for all of us to map a lot and not look at electrograms as much, because there's so many. And what you see here is that the onset annotation, which is manual, looks very different than if you were to have automated annotation. And this is true for every mapping system. Every mapping system will annotate however it feels like it was designed to. But sometimes when you change the annotation, you can see the sinus node here, based on automated, is up in the SVC. But if you do an onset annotation, it's at the normal location where you expect in the sinus node. So this actually can be a difference of maybe a centimeter or two, depending on how things are annotated. Next. And then we started looking at AVNRT, and we published a paper of looking at retrograde fast pathway atrial nodal connections. Next. And what we were able to describe, next, is the idea that there is a lot of heterogeneity in AVNRT, and using the Rhythmia system and putting the basket and mapping the earliest atrial activation was something that was A, fun, and B, could really help us understand the differences in retrograde fast pathway activation. Next. And what we were able to demonstrate, and this is great for the fellows in the audience, is the difference between the slow and the fast. The fast pathway is typically immediately posterior to the HISS, which is antireceptal, and then the slow pathway, when you have a jump, is just anterior to the CS osteum. So that is the difference between the anatomic fast and the anatomic slow in very high resolution. Next. But what's really relevant is that there is a lot of special heterogeneity in AVNRT, and sometimes you have patients with retrograde fast at the anterior, sometimes you have it mid-septal, and sometimes you have it posterior, and this may have implications for the patients that have highest risk of AV block. You would imagine that posterior fast pathway might be the risk of AV block. Next. And then in this patient, we had simultaneous activation of the entire triangle of Koch within 10 milliseconds in this whole region. And this is really important, because maybe in these redo AVNRTs, you want to look in much closer to examine. So this, again, is a nice example of clarity for complexity. I'm not saying you need to use arrhythmia for every AVNRT, but it gives you an opportunity to really study basic electrophysiology and mechanisms. So is high resolution just a prettier picture? Well, I'm going to show you a pretty picture. Next. And this is a nice example of a Mahim pathway. Next. And what you have here is this beautiful, beautiful M potential in a Mahim pathway. And for those that haven't seen many Mahims, and you can go next and propagate this, this is exactly what Sonny Jackman has described, which is just an AV node that's on the free wall of the right atrium. Next. Propagate forward. And here you can see the activation coming from the tricuspid annulus going across the free wall and then breaking out. And this is Mahim activation. So I do believe there is beauty to looking at this in high resolution. You can look at the electrograms where the M spike is so large. And arrhythmia has this ability to show a trend plot. The trend plot is seen here in yellow, which shows you how many electrograms are actually consistent with the M potential or the Mahim potential. So it's not just one signal that is shown. It's almost like a signal average ECG of this area. So we've loved being able to investigate these mechanisms of unusual and very normal arrhythmias. Next. And then this is a great example of what looks like a two to one atrial tachycardia. And the first thing that we did is we put the arrhythmia catheter up into the SVC and we started mapping. Next. And what you see here is something quite beautiful. You don't always see this level of electrogram because one of the nice things about the arrhythmia system is it is printed microelectrodes. The frequency of what you're seeing is very different from a lot of the other catheters. And what you see here is very high frequency electrograms in extreme clarity. And what you see is reentry around the SVC. So this would be very easy to miss if you had low density mapping and you just went up and said, okay, this is probably some focal arrhythmia coming from SVC, but this really allows you to explore and unveil new mechanisms. Next. So this is a beautiful SVC reentry. One of the greatest challenges of mapping is how do you eliminate noise? The biggest problem with maps is you always want to take the highest amplitude. But we also understand that some of the most relevant electrograms are of the lowest amplitude or fractionated. And this is the problem we have with all mapping systems. One thing that this system does very well, it does not allow contamination of different isochrone colors when there is one point that does not match the other surroundings. So this is like voting. If you have a different opinion and you're in blue, but you don't see it, it doesn't allow one specific point to change the whole isochrone. Next. Go forward. So this blue does not contaminate the entire isochrone, whereas all the other mapping systems will do that. And this is the idea of using neighboring information. And many of the mapping systems now that we're seeing with BioSense and Abbott are starting to look at filtering mechanisms. Because when you look at this and every single point may change the isochrone, it looks very messy and looks very confusing. Next. And next. Great. And then one thing that's also very unique, which also is being done currently with the BioSense platform, is these trend plots and these skyline plots. Trend is showing you the local electrograms in one area, and then skyline is showing you all the mapping points within the entire map. So it's really beautiful to be able to aggregate all of the points with trend and skyline, which is something that we've never seen with other mapping systems. And then you can start looking for the valleys where skyline is missing some of the areas. And those regions tend to be very good sites for isthmuses that have fewer points, that have lower voltages and less representation. Next. So being able to find gaps is what we're always looking for in electrophysiology. And if you move forward and go next, you can see that any time we're looking for a gap, you want to find the regions. But the gap signals tend to be continuous signals and non-split potentials. Next. So these are wide splits when you're looking at a line. And when you're looking to get closer and closer to a gap, next, then you start seeing the regions that are continuous in activation. This occurs with PVI. This occurs with a lot of what we do with reentrant arrhythmias. Next. And then the most important signals are the ones that are purely continuous. And those are the ones that we look for. And arrhythmia allows you to be able to do that. Next. Here would be one example, next, of looking at gap signals in a redo PVI. You can go ahead and animate that. And you're trying to figure out, how do you get into this right-sided vein? Well, you have a very long component here, which appears that the posterior side is actually fine. With this roving electrode, what you can look at is the trend plot. And you can see that there's two populations as you're looking, which tells you there's a very wide split. As you start moving the roving catheter, then you're able to then narrow in on where the gap is. Move forward, next. And then when you're finding the gap, it's very easy to get single burn elimination with high degree of precision with gap mapping. Next. Great. Now this is a very humbling image because we always use large tip ablation catheters. There's no micro ablation catheters. I want to draw your attention to ablation distal. Ablation distal has two components. That's left atrial and PV. But embedded in this system, you have micro electrodes. And look at the difference between the MIFI and the ablation distal. The MIFI looks heavily fractionated and continuous between LA and PV. But the ablation signal is very large amplitude far field. So we say, oh, this is far field. It might be intramural. It might be something else. But it's really because the recording antenna is too large. The catheter is in the same location, but the MIFI looks near field. So be careful when you say near field and far field because nobody knows how near is and nobody knows how far is. And it's really relevant that depending on the antenna of how you're recording may make a difference in terms of how you look at the electrograms. One looks so beautiful. So imagine how many PVC cases you do with a large tip catheter that you say it's a far field signal. And you say, oh, this might be intramural. But if you were to use micro electrodes, you might say, oh, I found a beautiful prepotential. So this is very humbling. Next. Great. And next. So this is a beautiful example of a patient that was referred to us with continuous atrial fibrillation despite a surgical maze. We went into the SVC and we put the Orion catheter there. And you see something quite beautiful. You see SVC fibrillation in the Orion catheter with variable conduction to the coronary sinus. And this here is a great example of the rare 5% or 10% of patients where the SVC is the true driver for atrial fibrillation. Really nice to be able to show the high fidelity electrograms of SVC fibrillation. Next. And if I were to ask you a question of looking at redos, which we feel like is the best system for us, is the redo left atrial, if you were to look at the CS activation, next, and you were to pull up the CS activation, and I asked you, which flutter is the least likely? There is a C-shaped activation of the coronary sinus. You would probably say the least likely is mitral flutter. Because usually this is linear, either proximal distal or distal to proximal. Move forward. So this is where we have a lot of, next, have a lot of ability to get humbled, next, next, great. And next, you can propagate this. And we started doing high resolution activation mapping. You can actually see there's a counterclockwise circuit that is turning around the mitral annulus. This is mitral flutter. But why does it give a C-shaped activation pattern, next? Because someone must have done, next, an inferior line, next, right here, which caused the activation to come around the line and back into it, which gives you a very strange coronary sinus activation. So high resolution mapping has become our gold standard. And in many laboratories, entrainment mapping is not used anymore. It's all high resolution that's more relevant. Great. And then this obviously allows us to be able to look at the localized nature of reentry. With high resolution mapping, the term localized reentry started coming out. And what is localized? Is that micro-reentrant? Nobody knows the size of localized, but it's not macro-reentry around the whole chamber. Next, right here, next. And Vishal Luther has often called this localized reentry, but you have to be aware of pseudo-reentry here as well. Next. And then it's important to understand that we still need humans with mapping. Next. Even one point can make it look like something has a jump. And even here you can see it's discontinuous. It activates up, there's silence, and then it jumps forward. But if you re-annotate it, it actually looks like it's quite smooth. So even one point in thousands of maps can change the way things look. Next. And this here looks like a very small figure of eight reentry on the anterior wall. What's really relevant here is everyone's wondering if you can use ILAM in the atrium, just like we use in the ventricle. Next. And you can see here, it looks like a very small figure of eight or a double loop pattern that goes counterclockwise around the anterior wall. Next. Well, what does this region look like in sinus rhythm? Well, there's actually low voltage on the anterior wall. Next. And then when you look here at the propagation, next, then you, and next, and propagate that, you can see there's an area of deceleration right where the critical site was. So we believe that in order to reduce localized reentries, using sinus rhythm isochronal light activation mapping and studying propagation may be the new PVI plus, and we're working on some new studies in proposing randomized trials of PVI plus deceleration zones, next. So those areas here where tachycardia breaks, next, really do correlate with functional abnormal propagation with wavefront discontinuities, next, next, next. And these are the areas with isochronal crowding, next. Great, next. Now the challenge with mitral flutter is like all of us, we either pick an anterior line or an inferior line. Regardless of what you choose, you have to transect transmirrorly, and we had a nice discussion about that yesterday, next. And if you do the inferior line, there's a coronary sinus that you have to deal with, next, if you do an anterior line, you have to deal with a Bachman bundle, if you do a superior lateral line, you have the vein of Marshall. So those are all epicardial bridges, and we've used high density to be able to account for a lot of this, these are all epicardial structures. And I just wanna show you two examples before we go to the ventricle and we wrap up. Next, next. We looked at the prevalence of epicardial bridging in the atrium, and how frequent we were seeing that it was requiring the outer portion with redo, and we found that 40% of the time in redos, there was often epicardial bridging, next. How do we show that there's epicardial bridging? Well, you look for activation gaps, when you don't see anything. Here is a beautiful circuit that comes around clockwise, but it doesn't look like it comes all the way around the annulus. You come down, and then it jumps out, and comes around, and it looks like it's partial reentry, but it also looks focal, so this is very confusing, next. When you start bringing in the other components of it, and you use the CS, you see this can be a coronary sinus bridge for mitral flutter that is clockwise mitral flutter, next. And next, and there's an activation gap, but when you bring the CS in, it actually makes the whole thing continuous. So this is a very classical example of inferior activation gap in the endocardium for a very typical clockwise mitral flutter, next. And then this would be another example of using the vein of Marshall, which is very popular with ethanol, but we actually do direct epicardial mapping, and we're able to find the missing components of this flutter that jumps from the inferior mitral all the way up to the roof, and it's using the vein of Marshall that goes in the ridge to activate. How do we prove that? Well, when you put a linear catheter, next, in the vein of Marshall, you can see that you have the epicardial catheter that completes the coronary sinus activation, which shows you that this is using epicardial structures to sustain reentry, next. And Dr. Cabrera has beautifully shown some different dissections of what this anatomy looks like. And this is very relevant for anyone that does any atrial fibrillation ablation or atrial flutter ablation, next. 2D gaps are obvious, next. And if you propagate this, you can see, next, and you can see that you can propagate this, and you can see where it squeezes out. This is very obvious to everyone, where there's a gap. That's not the concern, next. This is the problem, when you have activation, and then you have another activation in the center, which is like an island that gets activated, and this is a three-dimensional gap. It must be using other epicardial structures to arrive to this region, next. And it's important that this is the septal pulmonary bundle activation that we understand in atrial fibrillation, next. And this here is the first high-resolution mapping, where we went to the epicardium to explain why box isolation doesn't work. This is why Andrea Natale likes to ablate everything in the middle, because it increases the chances of eliminating the epicardial components, next. If you look on the screen right, and you look at all the different fibers in the epicardium, and then you map the epicardium, next, then you can see, next, when we pace from the epicardium, next, I want you to focus your attention on the vestibular region that activates. It's all intact on the epicardium, but you don't see it on the endocardium. So this is what is happening in the 3D left atrium. Anytime you see focal activation in the endocardium, usually there is some epicardial bridge. In this case, this is why posterior wall is so challenging, next, and next, next. And then this is a typical Bachman-Mundell activation with biatrial flutter moving over and jumping across an anterior line in the SPC. Many of you have seen this, many of you have recognized this. This did not exist before high-resolution mapping in terms of the descriptions. The first descriptions were from Bordeaux, next. And this is just using epicardial bridges, next, next, and next, great, next. And then this would be the beautiful anatomy highlighting next, that when you transect across, next, you have to use Bachman's bundle, next, and you have to come across this very thick region. Note that the anterior wall is transiluminated and very thin, and that's really relevant. So you can see all of this with high-density mapping. Next, next, and next. Next, and next. And I just wanna get to the intelligent annotation, next. Great, the most important thing to understand with ventricular tachycardia is the isthmus is the little local electrogram that is the smallest component. Most mapping systems wanna annotate the largest component. That is a problem, next, because when you look at the diastolic corridor, that is the true isthmus, and the large components are the outer loop and the QRS, next, so when you look here, the true channel, they are the lowest voltages, next, and then the electrograms in sinus rhythm, they always annotate next to the largest component, and that's a problem because that would be 1.8, next, and no mapping system wants to annotate to the smallest component. So everything you've read about voltage mapping where there's different isthmuses, it's all potentially wrong because it's not annotating the local electrogram, which is the Holy Grail, but if you were to annotate the local electrogram in the smallest, you would annotate a lot of noise potentially as well, next. So this is one final example of a ventricular tachycardia circuit that appears to you and me as focal. This looks like there's focal activation, and you should never be satisfied with just saying, oh, it looks focal. You must look at the electrograms and say, what about in diastole? And this allows a dynamic window of interest to try to highlight areas, and when you highlight areas, you see, wow, there is diastole. It just was annotating the largest components and missing diastole. So then when you re-annotate this, and you make sure with LumaPoint feature, they all get annotated, which is automated, you have a beautiful re-entrant circuit. So this happens all the time, that you're allowing the mapping system to take control, but you must control the mapping system of what is going in. It's not focal, it's re-entrant, but you have to annotate the local electrograms, next. And these are the beautiful signals that they're always annotating the largest component and missing the smallest component, next. Next, and next. This is a VT, single lesion, and the other thing that's a huge advancement is using local impedance for ablation, next. Great, next. And we're finding a late potential, and we're ablating a late potential that you can see on ablation. Note that with MiFi, with the microelectrodes, it looks much more near field. This is something, again, that we have problems with large tip catheters. You ablate a late potential, and it looks like it's already gone, next. This is also very humbling, because, next, it looks like on the distal ablation, the signal is eliminated, but the system impedance drops only by eight, but the local impedance drops by 21, and this is a new feature, that looking at local impedance reduction may be better, because it's more sensitive than anything else, and we're always looking at system impedance, rather than local tissue impedance for biophysics, next. So, next here. Great, so this is a very modest reduction in local impedance, in system impedance, but a huge reduction in system impedance, in local impedance, next. So lessons from one lesion is the large tip ablation catheter doesn't always see what you wanna see. The local impedance is much more sensitive than system impedance, and the MiFi shows the efficacy better than the large tip. So in conclusion, ladies and gentlemen, next. Next. We have high resolution mapping that really allows us to identify gaps. It allows us to explore everything from sinusoidal activation, AVNRT, Maheim, flutters, and VT. So hopefully I was showing you the variety of what we studied with this. It's important to understand annotation is everything, regardless of what mapping system you use, and we're always very humbled by what electrograms look like, and what their automated annotation is, but this allows you to do dynamic windows of interest, and re-annotate with this arrhythmia system. Just remember that mapping systems are nothing but a lot of electrograms, and we must be able to control what goes into the mapping system, and not be told by the mapping system what the arrhythmias are. Thank you very much. Dr. Jose Llorente and Dr. Juan Carlos Diaz please come with us and Dr. Miguel Valderraba I don't know Greetings Milton, can you hear me? Hello, how are you? Yes, we can hear you Hello, I'm Dr. Ortega I'm here in the room of Hospital 20 de Noviembre del Iste Can you hear me well? Yes, and loud Perfect, very good Greetings to all the panelists We are going to talk about a case of a 76-year-old male patient who has a persistent hearing loss diagnosis and has a step-mark implant outside the unit in 2020 The patient presented a cerebrovascular event in 2022 and had previously presented some transitory cerebrovascular events The patient was anticoagulated with warfarin and despite that, he did these two events so he was replaced by Rivero Xaban He is a patient who has a CHAS-VAS of 4 points and a HAS-BLESS of 3 points He is currently being treated with Rivero Xaban The patient was considered a candidate for ear occlusion and pulmonary vein ablation We discussed with the patient and as you know, patients are very afraid of the cerebrovascular event and the patient wanted only the occlusion implant We will see if we can convince him to do the ablation but for now, he got an occlusion implant with the antecedents that we have there Next He is a patient who has a 50% hearing loss and has a slightly dilated left auricle with a Lavi of 38 and an AP of 38 mm and the left ventricle is not dilated So, it has an outside tomography, we don't have the images, but it says in the tomography that it has a diameter of 27 at the entrance and a depth of 22, with an area of 5 and a perimeter of 80, but here we have above all the diameter that says 27 and the depth of 22, the one that follows is in auricular fibrillation as we see and that is our case. Fingers. I want comments from the table, I want comments from the speakers, from the panelists. Any comments from the panel? I wanted to ask you, Martin, the planning that you did for the ear closure, since it is a patient who has a very large auricle, has permanent FA and everything else, and really, if we get the indication of the ablation of the pulmonary veins, in itself the indication alone of placing the ear closure with all the planning that you did, is there any difference to what you are going to do? Because you have a large auricle, right? Yes, look, we normally do a study for the patients, because the institute requests a tomography study or transesophagic to be able to update it, there is a national platform that authorizes them. So, for it to be authorized, it has to have one or the other. In this case, that is the study I had and it was authorized with this. We usually put the patients, most of the time we have done it with transesophagic echo, and we have evolved little by little to put more and more cases with intracardiac echocardiogram, as is this case. In this case, we have the patient, we try to use practically zero fluids, right now we are going to have in some small videos that we are going to show you right now, what is the workflow that we initially did to do the zero-fluid pulsation, to do the determination. Normally we use only this, and we proceed to the angiographic measurements, and by ultrasound at the time of the room, and we decide the implant of the device. In this case, by teaching, we did something else that we are going to show right now. There is a question from Dr. René Martín. Hello Martín, good morning, can you hear me? Greetings René. I am Dr. René Jiménez, good, an excellent case, good indication, a four-point CHAS-VAS is an adequate indication. And my question would be, they decided to do it with transesophagic echo or intracardiac echo, and the second question is, if they have the patient with intubation, general sedation or is it only with superficial sedation? Yes, I tell you that in this case the patient is sedated, sometimes because he is an older patient and very nervous, because he did not accept the ablation when he was told about the benefits and all this, and then he is sedated. Normally, when we do transesophagic, if the patient is very calm, we do only local anesthesia and we work very few people in the room. When you already know, when you have the transesophagic, the echocardiographer and his machine have to come and when the patient is intubated.

persistent atrial fibrillation

cerebrovascular events

anticoagulation therapy

atrial appendage closure

pulmonary vein ablation

rivaroxaban

intracardiac echocardiography

patient preferences