So, Dr. Devi Nair, I do not see yet, and we do not have files uploaded for her. So we are actually going to change the schedule up a little bit, and we may have her go a little bit later if she shows up. So our first speaker is actually Dr. Chad Gere from Northwestern, and he is going to be speaking about ex vivo evaluation of air intrusion into pulsed field ablation sheets during ablation and mapping catheter insertion. Chad, please. Good morning, everybody. Thank you all for waking up early on a Sunday morning after a long weekend to join us this morning. As you can probably tell, I'm not Devi Nair, so if you were expecting her, I'm sorry that you're stuck with me now. But my name is Chad Gere. I'm a first-year EP fellow at Northwestern Memorial Hospital, and today I will be presenting our study titled, An Ex Vivo Evaluation of Air Intrusion into Pulsed Field Ablation Sheets During Ablation and Mapping Catheter Insertion, quite the mouthful. I have no disclosures. So we have a brief 10 minutes together today, but during that time, I will review some background, background information, go over our study design, of course, show you our results, and briefly discuss some hypothesis as to why we think there's more or less air intrusion into specific sheets. We'll start by reviewing some background. Air embolism is a rare but serious complication that can arise during AF catheter ablation. Studies have estimated that air embolism occurs in 0.1 to 0.8% of AF ablation cases. Given the complexity of AF ablation procedures, many procedural aspects may contribute to the formation of air emboli, including catheter and sheath exchanges, improper infusion management, and negative left atrial pressure during spontaneous breathing during cases. And in my opinion, there's currently a heightened awareness of air intrusion in the sheets as some of the PFA sheets are transparent, and you can actually see the large air bubbles when you're inserting the catheters. Two prior ex vivo studies have evaluated air intrusion into previous generation sheaths. I wanted to highlight this one by Sukihara and colleagues that evaluated air intrusion into previous cryo ablation sheaths. They created a model that utilized the siphon principle to mimic negative left atrial pressure seen during anesthesia, and this is just a snapshot of their results, but to show you that they saw as much as 8 milliliters of air was entrained into these sheaths when estimated to have negative 20 left atrial pressure. However, at this time, no studies have evaluated air intrusion into the newer sheaths that have come to market to accommodate these larger PFA catheters. Therefore, the aim of our study was to evaluate the amount of air intrusion into these PFA sheets during ablation and mapping catheter insertion. Now that we've viewed the background, we'll move over to our study design. We evaluated three sheaths and four catheters. Each sheath and catheter was prepared using standard clinical techniques, including flushing, exercising, and inserting and removing the dilator. The three sheets that we evaluated included the two commercially available PFA-specific sheaths, the Boston Scientific Ferrodrive, and the Medtronic FlexCath Contour. We also evaluated the BioSense Webster Visigo for comparison. The four catheters included in our study were the Boston Scientific Ferrowave and the Medtronic Pulse Select, the two commercially available PFA catheters at the time when we performed our study. The other two remaining catheters were mapping catheters, including the Ava HD Grid and the Octaray. To simulate negative left atrial pressure under anesthesia, we again used the siphon principle to create negative pressure. This was achieved by submerging the tip of the sheath underwater and keeping the catheter handle at a pre-specified height that corresponded to a negative pressure of around 15 millimeters of mercury. Catheters were inserted in advance to the end of the sheath and then withdrawn while maintaining this negative pressure. And after insertion and removal of the catheters, air was withdrawn from the side port and measured to the nearest milliliter. So I'll show you our results. We completed a total of 40 trials, five trials for each combination of sheath and catheter. The average volume of air entrained was 9.9 milliliters. We found that the Boston Scientific Ferrodrive sheath entrained significantly more air when compared to the FlexCath Contour, 16.5 milliliters to 6.1 milliliters. We also found that the Ferrodrive sheath entrained significantly more air compared to the Visigo, again 16.5 milliliters compared to 5.8 milliliters. And again, this is just showing that there was a statistically significant difference between the Boston sheath versus the Medtronic or Johnson & Johnson sheath, but there was no significant difference between the Medtronic FlexCath Contour and the Visigo. Comparing mapping catheter to ablation catheter insertion with the Boston Scientific sheath, the mapping catheters entrained significantly more air compared to the ablation catheters, 18 milliliters compared to 13.6 milliliters. Similarly, mapping catheters entrained significantly more air than ablation catheters with the Medtronic sheath, 7.1 milliliters compared to 4 milliliters. When comparing mapping or ablation catheter insertion between PFA sheaths, significantly more air was entrained into the Boston Scientific sheath for mapping catheter or for ablation catheter insertion when compared to the Medtronic sheath. Now that I've showed you our results, we'll briefly discuss some factors that we think contribute to air intrusion into the sheaths. Air intrusion is likely a multifactorial process that we hypothesize has significant contributions from three factors, specifically sheath catheter size mismatch, catheter tip shape, and sheath hemostatic valve design. First we'll discuss the sheath catheter mismatch. So the Boston Scientific Faradive, it has a 13 French inner diameter compared to the Fairwave ablation catheter, which is 12 French, the HDGrid, which is 8 French, and the Octaride, which is also 8 French. As you can see, you can imagine that much more air is entrained when there's a larger size mismatch between the sheath and the catheter that you insert. Similarly, in the FlexiCath contour, it's a 12 French inner diameter with the Pulse Select being 10 French, again the HDGrid 8 French, and the Octaride 8 French. However, if you recall, the Medtronic sheath entrained significantly less air than the Boston sheath. However, as you can see, the Pulse Select catheter is smaller, there's more of a size difference between the sheath compared to the Boston sheath, which suggests that other factors must contribute to air intrusion. Which leads us to our next point, which is the catheter shape. So as you can see, each of the catheters we tested has a complex catheter tip shape. Due to these complex shapes, many of the catheters have an introducer tool that helps insert the catheter into the sheaths, and we believe that this may entrain less air, as many of us will fill the column with fluid to prevent air bubble when pushing in the catheter. However, the Fairwave catheter has this large pentaspline design, but does not have an introducer tool. And also, since it must be lead with a wire, if you withdraw the wire too far before pushing it forward, we've noticed that when you push the wire out, a large air bubble is often pushed out into the sheath as well. And lastly, we'll briefly discuss the hemostatic valve design. Each sheath has been engineered with different hemostatic valves to reduce air entry. The Boston Scientific Fairdrive has a dual seal design with a cat eye shape, which may lead to more air entrainment when catheters of smaller size are inserted. The cat eye design is different than the hemostatic valve design of the Medtronic Plex-Cath Contour or the Visigo. Each of these has a more complex seal design that resembles an asterisk, and may be better suited to accept smaller catheter sizes. Of course, our study must be interpreted with a few important limitations. Continuous negative pressure was used, which may overestimate air intrusion into the sheaths. And since continuous negative pressure was applied, this doesn't exactly mimic physiologic respiration. Again, we used water or saline, so this does not mimic the viscosity of blood, and that may have an effect as well. And because this is in our ex vivo model, this doesn't have anatomic realism. Some sheaths specifically have designs that mitigate a vacuum effect when the tip is occluded, when it's up against tissue. So to conclude, our study is the first to evaluate air intrusion into the larger bore PFA sheaths. We saw a high volume of air was entrained into these sheaths, with the Boston Scientific sheath entraining more air than the Medtronic sheath, and that mapping catheters, we saw higher volumes of air entrained compared to ablation catheters. Air intrusion is likely multifactorial, related to sheath and catheter design, and it's important to maintain meticulous sheath management to avoid air embolism. Thank you very much. Happy to take any questions. Best to come up to the microphone to ask questions, it's just easiest to hear. Is there any other mechanism of air intrusion, for example, what I've noted is that after the ablation, when I'm taking the ablation catheter out, I see distal to the tip, air columns are coming from the distal end. So is there any other way that electrolysis or whatever, the bubbles that you see during the ablation, it's coming through the sheath, backward? It's an excellent question. I think whenever you're withdrawing from the sheath, it creates a vacuum effect, and that may draw things in, and you're right. We have seen, when you're looking on ice, sometimes you see bubbles formation when you do ablation, and maybe you may be sucking that, that you're seeing that, but not sure. Maybe to ward off other questions, a lot of people had questioned me about the use of the new 13 French Agilis. This was not included in our original study, but we were fortunate enough to have one from Abbott, and with the 13 French Agilis, we saw less air intrusion compared to the Boston Scientific Sheath as well. Another quick question, Chad, so did you, you followed the IFU, did you also flush the sheaths continuously as they were going in to create kind of a positive pressure environment? Yeah, we actually didn't. We were concerned that that would affect this kind of negative pressure model that we created, but that is, you know, certainly something to consider. And then, anything that you identified, like submerging under liquid, was there anything that you tried to identify to mitigate the bubble formation? That's kind of our next step. We're going to try to do some different techniques to see if we can mitigate the air that, you know, goes into the sheaths. Congratulations. No, great model, really good conclusions. Your hypotheses are great, they make a lot of sense to me. Thank you very much. Excellent. Excellent. Thank you. Perfect, thank you. So our next speaker is Yumei Shen, and Yumei is from Nanjing Medical University, and she is going to be speaking on prophylactic pulmonary vein isolation in patients with lone typical atrial flutter and heart failure. Welcome, Yumei. Here, let me help you with that. And it'll go up to the slide next. Okay. Good morning, everyone. I'm Yumei Shen from Nanjing Medical University. Today, I'm going to talk about prophylactic pulmonary vein isolation in patients with lone typical atrial flutter and heart failure. I would like to start my presentation with a simple case. So a 68-year-old female patient with typical atrial flutter presented to my clinic, and she has no history of atrial fibrillation, no atrial fibrillation recorded on the 48-hour portal monitoring. I would choose CTI ablation for this patient, because we know that that's a first-line treatment for typical atrial flutter. But when I read the clinical trials, I saw that there's a lot of atrial fibrillation incidents after the CTI ablation. So now I would be wondering, should I add the transceptor puncture and perform the prophylactic CPBI? So there are already some small RCTs showing that the prophylactic CPBI can improve the soft outcomes, reduce the post-ablation atrial fibrillation. But there is no such benefit in heart outcomes, such as death and heart failure events. So now I'm hesitating. I don't want to add increased procedure risk to my patient just to reduce AF occurrence. But in a slightly different situation, if this female patient has non-typical atrial flutter, but also with heart failure, I would still want to do the CTI ablation, of course, because they already show that by comparing the CTI ablation to drug treatment, the CTI ablation are superior in death and in heart failure admission at one year. But looking at this curve, I still saw that there were 10% in the half-life group and 11% in the half-life group. These patients still have heart failure rate admission at one year. Now, should I be adding the transeptal puncture and perform the prophylactic CPBI to this patient? Because I know that the post-heart failure rate admission might be associated with the atrial fibrillation occurrence. But I don't know for sure what's the answer to this question. That's why we designed this trial. The aim is to compare the effects of CTI ablation plus prophylactic CPBI versus CTI alone on all-cause death and hospitalization for worsening heart failure in patients with non-typical atrial flutter and heart failure. So, we included patients with typical atrial flutter referred for ablation, and they have no prior history of atrial fibrillation, fulfilled the criteria for heart failure, and they all received optimized medical therapy for heart failure for at least one month, history of worsening heart failure or hospitalization within one year before enrollment. We also excluded patients with any atrial fibrillation episode documented during the 48-hour heart monitoring. This is our study flow. So, we included 81 patients from nine centers in China. And in four of the centers, the CTI combined with the prophylactic CPBI was the standard practice. And in the other five centers, CTI alone was the standard practice. So, these are the two groups we have, CTI plus CPBI group and alone group. The primary endpoint is a time-to-composite of all-cause death or hospitalization for worsening heart failure. For the baseline characteristics, there was no significant difference between CTI alone group and the CTI plus CPBI group. We see that the mean age will be around 65 years old, and around 70% of the patients were male. Now, here's the outcome. After the mean follow-up of 14 months, the primary outcome occurred in 31% in the prophylactic CPBI group and 56% in the CTI alone group. The adjusted hazard ratio, 0.37. As for the secondary outcome, we also see there was less hospitalization for worsening heart failure and less atrial fibrillation occurrence in the prophylactic CPBI group. But there's no significant difference in the death from any cause. The prophylactic CPBI group also saw a lot more patients have the NYHA class improved compared with CTI alone group. So, our major findings are, after the CTI ablation alone, 56% of the atrial fibrillation patients with heart failure experienced either all-cause death or hospitalization for worsening heart failure over a median follow-up period of 14 months. Compared with CTI ablation alone, CTI ablation plus CPBI was associated with significant lower risk of composite of all-cause death or hospitalization for worsening heart failure, which was driven by a reduced risk of worsening heart failure hospitalization. CTI ablation plus CPBI also reduced the incidence of atrial fibrillation and improved the NYHA function class, with no significant difference increase in the procedural complication compared to CTI alone. Only one case of growing hematoma in both groups. These findings provide preliminary evidence for considering prophylactic CPBI during the CTI ablation in patients with non-typical atrial fibrillation and heart failure. Thank you. Any questions at all from the group? I'll maybe ask a question. So, there was a study about five years ago. It wasn't in a heart failure population, done in the UK. They looked at doing CTI with radiofrequency and randomized them to pulmonary vein isolation for patients with just low and atrial flutter, no documented fib. And they showed that symptomatic recurrences were the same, and you don't do anything to the CTI. And with loop recorders, they actually had less asymptomatic recurrences of any atrial arrhythmia when they just did the pulmonary veins and not the CTI, compared to a group where they did the CTI. Now, do you think that in the heart failure population, would there ever be a time when someone would just do a PBI for low atrial flutter? And do you think there's a role for that? Sorry, you mean just CTI for low heart? Just PBI, not even touch the CTI. But it's typical atrial flutter. There was a study that showed you get less recurrences with pulmonary vein isolation. Yeah, yeah, I'm aware of that, like, there's, the theory is that the primary vein is providing some trigger to the atrial flutter, so that if you ablate the, isolate the PVI, maybe you can, like, stop the atrial flutter without touching the CTI. That's a very interesting study, and there's a theory, but I think, it's quite like CPVI, but I believe the cornerstone would be, like, CTI ablation, I would be, like, cannot go to sleep at night if I don't do the CTI ablation. I actually agree with you, I'm being provocative, but the tough thing in our practice now is that we have these tools now that can do a PVI really quickly and safely, and we don't have those same tools for CTI yet, they're coming, and so I'm sometimes faced with, do I just quickly do a PVI and leave the CTI alone, and someone with CTI flutter? But I agree, in a heart failure population, I don't think we're ready to do that yet. I think, I think we should be doing both, because I do think there's a subset of patients where there might be a non-pulmonary vein trigger for their flutter, a PAC or something, so I think, I, congratulations, really good study. Thank you. And our next speaker is Ali Rezak Rashid from King's College London. He is speaking about extra stimulus activation mapping that identifies functional VT substrate in normal voltage tissue proximal to fibrosis. Welcome, Ali. Okay, good morning, thank you all for attending, and I'd like to thank the abstract committee for this opportunity to present my research on using extra stimulus mapping to identify areas of functional conduction block within VT substrate. So, to start with some background, isochronal late activation mapping, or ILAM mapping, is a substrate-based mapping strategy to identify deceleration zones, which have been shown to be sensitive to highly arithmogenic regions within VT substrate. Another proposed strategy for refining ablation targets is to utilize extra stimulus mapping to unmask areas of functional substrate. Areas of substrate that exhibit decremental conduction, which is the delay of late electrogram components, have been shown to also be highly arithmogenic. These are two well-established techniques for VT substrate mapping. However, we've observed that as well as decrement into late activated areas, we also see functional block, and we hypothesize that this may also represent relevant substrate behavior. In this schematic of an area of substrate, we see a late potential on S1, and whilst we may see decrement in S2, we could also see the disappearance of the late component with extra stimulus, and this disappearance represents block into the late activated tissue. So we wanted to test the hypothesis that areas of block are also relevant substrate. So to do this, we undertook a mapping study including nine patients undergoing VT ablation. The cohort included six patients with ischemic cardiomyopathy and three patients with either non-ischemic or mixed cardiomyopathy. We acquired substrate maps during ventricular pacing at 600 milliseconds with extra stimulus at ventricular ERP plus 20. Electrograms were annotated according to the ILAM strategy, such that the last deflection on the bipolar electrogram was selected as local activation time. So using S1 and S2 electrograms, we constructed ILAM maps and identified deceleration zones according to the standard literature. We considered the primary deceleration zone to be the site with the greatest extent of isochronal crowding with the latest annotation relative to other deceleration zones. We undertook a comparison of the deceleration zones identified on S1 and S2 maps. We looked at the distance between primary deceleration zones, their relationship to low voltage areas, and the total number of deceleration zones. We then computed delta S1, S2 maps to look at the change in local activation time that occurred between S1 and S2. The delta is computed as the S2 annotations subtract the S1 annotation, such that positive delta represents decrement and negative delta represents block. So this is a visual representation of a delta map in which the color reflects the change in activation time between S1 and S2. The blue region shows later activation following extra stimulus, and this is due to decremental conduction as seen on the electrogram schematic. In contrast, the areas in red are those in which the latest activation is earlier following the extra stimulus, which is the result of the absence of a late potential following the extra stimulus, and this indicates functional block into that area. So moving on to the results, we first looked at the number of deceleration zones identified in S1 and S2 maps. We saw a median of three deceleration zones in S1 and one deceleration zone in S2. However, this was a bit of a statistical quirk, and as you can see from the distribution, there's no significant difference between the number of deceleration zones identified in S1 and S2 maps. We then looked at the number of isochrones at the primary deceleration zone, and we also saw no significant difference. We examined the bipolar voltage in the region identified as the primary deceleration zone, and the majority of these were found in areas between 0.5 and 1.5 millivolts, with no significant difference between deceleration zone voltage in S1 and S2 maps. We then looked at the relationship of the deceleration zones identified to normal voltage myocardium, and as you can see, the majority of deceleration zones occurred close to the transition between normal and reduced voltage in both S1 and S2. So we've interpreted all of these distributions as indicating that individual deceleration zones identified on S1 and S2 were similar. So then we wanted to investigate the anatomic relationship between the deceleration zones identified to establish if they were identifying anatomically distinct regions of substrate. To do this, we looked at the distance between the deceleration zones, and we found that the deceleration zones identified on S1 and S2 maps were distinct. In seven of nine cases, there was greater than 20 millimeters of separation, suggesting that the S2 extra stimulus identifies different areas of substrate. In this example, the S2 primary deceleration zone, which is the yellow box, is on the other side of the inferior scar to the S1 deceleration zone, the red box, with a distance between them of 56 millimeters. Overall, the deceleration zone distance between S1 and S2 varied across the cohort from one millimeter to 68 millimeters, with a median of 38 millimeters. We also observed that S1 primary deceleration zones appear as deceleration zones on S2 maps in seven out of nine patients. S2 maps also contained a deceleration zone not identified on S1 in three out of nine patients. In this example, you can see the primary deceleration zone in S1 on the S2 map. However, the S2 primary deceleration zone is totally absent from the S1 map. Importantly to note is that S1 maps identified a deceleration zone not identified on the S2 maps in two out of nine patients, which I'll explain in a moment. Moving on to our delta map analysis, we saw that the majority of the chamber maps saw no significant delta. The majority of low voltage areas also saw no significant delta. However, areas of delta co-localized to areas of candidate relevant substrates within low voltage areas. The chambers maps saw no significant difference in the proportion of decrement to block that we saw. In other words, we saw a similar proportion of decrement and block on our delta maps. To link back to our hypothesis, when we examined the electrograms recorded at these areas of significant delta, we observed the phenomena that we expected. Areas of positive delta showed later annotation due to the decrement evoked potentials seen at these areas, and areas of negative delta showed earlier annotation due to block at these sites. Relating areas of delta to deceleration zones, we saw that the majority of primary deceleration zones localized to areas of delta. S1 primary deceleration zones most often co-localized to areas of block, whereas S2 deceleration zones most often co-localized to areas of decrement. You can see from the spread, the bar chart, the S1 deceleration zones are a bit more evenly distributed between block and decrement, whereas S2 deceleration zones, the vast majority, are seen in areas of decrement. This may indicate why S2 deceleration zones are on average closer to the transition between normal and low voltage, because the deeper into pathogenic tissue you are, the more opportunity the wavefront has to block into that area. And it's also important to highlight that two S1 deceleration zones that are absent on the corresponding S2 map, so this may be due to block into the extra stimulus occurring at the site of the S1 deceleration zone, proximal to the S2 deceleration zone. To conclude, extra stimulus pacing can uniquely identify areas of deceleration zones not seen on S1 maps, and this is already known, but what's new is that decrement and block are seen to occur at similar rates during extra stimulus pacing on delta maps. Conduction block following the extra stimulus pacing can mask relevant substrate on the S2 map, therefore it can only be identified on S1 maps. Consequently, consideration of both S1 and S2 maps may be necessary to comprehensively identify ventricular substrate, and delta maps may help in visualizing the changes in activation time following extra stimulus to identify these areas of relevant substrate. I'd like to thank my collaborators for their contributions to this project, I'd like to thank the chair for hosting the session, and if you have any questions, feel free to ask. Any questions from the group at all? Excellent. So, my one question is, from a research perspective, this is great, and I actually do something similar in patients where I cannot induce, but how much time would this add to a clinical case if you did this in every single patient? A lot, yeah. Extra stimulus mapping is much more time consuming, of course. It depends on the extent of the substrate as well, because you don't necessarily have to map the entire chamber, and also with high-density catheters it may reduce the procedure time, but it's still much more time consuming than just regular S1 mapping. The trade-off is then, do you get better VT termination, and do you get lower recurrence, which currently we're not sure, but... And just a rough estimate on minutes, how many minutes would it take to, if I had someone do this for me? I'm really not sure. I'm really not sure. It might take maybe even as long as double the time. That's kind of my experience when you're doing these S2 maps, it takes them a while to do the annotation to the S2 points and then process everything, and it does add sometimes 20 minutes to the case, but it can be, if it helps you find a spot in the two to nine patients, then I think it's worth it. Yeah, well done. Thank you. Congratulations. Thank you. Excellent. And our next speaker is Dr. Soren Popescu from the University of Schleswig-Holstein in Lubeck, and talking about esophageal fistula following cryo-balloon-based pulmonary vein isolation, a sub-analysis from the Potter AF2 study. So thank you, dear chairman, dear ladies and gentlemen. I think I should open my slides. I'm just going to start and then go through your disclosures. I'm going to start this up. So these are my disclosures. So, dear ladies and gentlemen, it's an honor for me to be here today and to present our results from a Potter AF2 sub-analysis. This is called esophageal fistula following cryo-balloon-based pulmonary vein isolation. And this results from a worldwide FDA database, it's the MODI database. First of all, regarding the background, we all know esophageal fistula is a rare but dreadful complication following catheter ablation for atrial fibrillation. We have conducted the Potter AF study, which was published in 2023 in the European Heart Journal. This was the biggest study to date to analyze the incidence of esophageal fistula following catheter ablation for atrial fibrillation. More than 500,000 patients were analyzed, and we found an incidence of 0.025% in the general population, but significantly higher, more than 20 times higher in the radiofrequency ablated patients compared to the cryo-balloon patients. It's important to note that the prognosis of these patients is extremely poor with mortality of 66%, but significantly better survival in patients undergoing invasive treatment. Last year, we conducted a subsequent study, this was the Potter AF2 study, where we looked for the esophageal fistula following catheter ablation for atrial fibrillation, reported in the MODI database of FDA. Here we analyzed more than 1,200 reports, and we identified 47 patients with atrial esophageal fistula, but considerably more patients undergoing cryo-balloon-based ablation and having fistulas. One third of the population had fistula following cryo-balloon-based ablation. The mortality was similarly high, and we also published last year and presented a late-breaking clinical trial, the Potter AF3 study, where we compared the two populations from the Potter 1 and Potter 2 for the same time interval, and we found a major, massive underreporting in the MODI database regarding such dreadful complications. Now regarding the current study, as I said, this is a sub-analysis of the Potter AF2 study. The original study looked for esophageal fistula and esophageal injury complicating atrial fibrillation, catheter ablation, in the MODI database from FDA. This is a mandatory database where all the manufacturers and physicians should actually report all these dreadful complications or the severe complications following or possibly related to medical devices. And we looked into this complication between August 2009 and August 2019. The current study is a sub-analysis of the patients undergoing cryo-balloon-based catheter ablation, and we aim to investigate the clinical characteristics of these patients, the management, the outcome, and also the quality of the reports in the MODI database. As we mentioned, we had 47 cases of atrial esophageal fistula in the original population. 31 of them underwent radiofrequency-based ablation, 15 of them cryo-balloon-based ablation, and only one patient underwent laser-based ablation. And I would like to point out in the first study, in the Potter AF study where we had more than 500,000 catheter ablations, we had only 3 patients with cryo-balloon-based ablation, so significantly more patients in this population. This is our population for the current study. Regarding the reporting, so only 20% of the reports were found in the literature, and the other 80% were reported directly from the manufacturers. And regarding the location of the reports, so this is a worldwide database, this should work actually worldwide for all the manufacturers. Actually, this was available for 87% of the patients, and all the reports came from the United States. So this speaks for the massive underreporting in this database. Regarding the catheter ablation characteristics, 4 patients, 27% of them had additional radiofrequency-based ablation, 2 of them underwent touch-up ablation, one patient underwent atrial flutter, typical flutter ablation, and in one patient what's not clear, it was not specified in the report. Regarding the device to use, until 2019 we only had the Medtronic balloons, 27% of them were with the Arctic Front cryo-balloon, and 73% with the Arctic Front Advanced cryo-balloon. An important finding is the number of cryo-balloon applications, so this was available in 60% of the patients, with a median value of 11 applications for patients, but up to 30 applications for one patient, so this is enormous. And also the temperature, considering that we are talking about the Medtronic balloon, the minimal temperature that was reported was minus 75 degrees Celsius, with a median of, with a mean of minus 60 degrees Celsius. Regarding the symptoms and the presentations, so the mean time to presentation was 24 days late after the catheter ablation, and regarding the symptoms, most of the patients presented with neurological events, followed by fever, dysphagia, and thorax pain. Regarding the diagnostic methods, most of the patients underwent the CT scan of the thorax, this was used in 75% of the patients, followed by a magnetic resonance imaging, echocardiography, exploratory surgery, and as you can see here, endoscopy was also used in one patient. I would like to point out, this should be avoided, actually, in patients where we suspect an esophageal fistula to avoid air inflation and air embolism. Regarding the treatment, the majority of the patients underwent surgery, 88.9% of the patients were treated surgically, and 11.1% of the patients were treated invasively, endoscopically, but not surgically, and no patient in this population was treated conservatively. Regarding the mortality, this was extremely high, 87% of the patients died, only 13 of them survived, and this data were available for the entire population. So dear ladies and gentlemen, I would like to come to my conclusions. First of all, esophageal fistula is not uncommon among patients that are going cryo-balloon based ablation for atrial fibrillation, and this is something that we all have to take into account. 31.9% of the patients in this population underwent cryo-balloon based ablation, and I think this is even more important considering the new Argent Field safety notice released by Boston Scientific regarding the extremely high incidence of esophageal fistula with the Polar X balloon, which was not available at the time when we performed this analysis. I think the number of applications and the minimal temperature, the minimal esophageal temperature plays an important role in developing this complication. As you saw here, we had a median of 11 applications for each patient, but with a maximum of 30 applications for one patient, and the minimal temperature was in minus 60 degrees Celsius, with a minimum of minus 75 degrees. Regarding the symptoms, we have to take into account this patient will come late in the hospital after a median of three weeks following the catheter ablation, so we have to make our colleagues aware of these complications. They will probably not come in the original clinic who performed the ablation, but will go to the, I don't know, emergency department, or to the cardiologist, or to the family care physician, so we have to make them aware of this complication. And of course, esophageal fistula is associated with an extremely high mortality, and the treatment can save lives. We had other, some analysis of these populations where we've shown that the invasive treatment, either surgically or by means of endoscopy, can save lives, so this is associated with a reduced mortality. I would like to thank you for attending this session, and I would also, I'm happy to announce that this abstract was awarded with the Eric Prystowski Award yesterday during the award session, and I would like to take this opportunity to thank the selection committee for choosing this work, to all the collaborators, Professor Roland Tills, my mentor from Lubeck, and also John Catanzaro from East Carolina University for supporting this work, and thank you all for being here today.

esophageal fistula

cryo-balloon

pulmonary vein isolation

atrial fibrillation

catheter ablation

mortality rates

FDA MODI database

procedural parameters