in HRS 2025, as we are all settling in, we hope you're as excited as we are. Start this joint session between HRS and EHRA, entitled Strategies for Managing Difficult VT Cases, What to Do for the Urgent Case. I'm Leonard Ilkenoff from Innova, Scharhart, and Vascular. I'm thrilled to be co-chairing this session with... Helmut. Thank you, Rafalina. We have four excellent talks from our speakers. We ask audience please to scan the QR code. Remember, just to forward your questions to the speakers through the automated system. We'll have a Q&A at the conclusion and last 15 minutes or so of this session, which will incorporate all of your questions. So please keep them coming forward. Without further delay, we have an all-star lineup today. Very excited to have these speakers with us. And to kick us off, I'd like to introduce Dr. Rado Lenarczyk from the Medical University of Silesia. His talk is entitled Management of Patients with Electrical Storm and Clustered Ventricular Arrhythmias. Good morning, ladies and gentlemen. Happy to be here. It's a great honor and pleasure to attend this HRS Congress and to have a speech on this joint HRS session. And the case I'm gonna present is a basis for the short discussion of some advice that has been included into this document. It's the era, the consensus document published last year in April, April last year, and is joint consensus endorsed also by CC societies including HRS. And it deals with management of patient ventricular storm and cluster ventricular arrhythmias. And the story follows as it's the story of 48 year old woman without cardiovascular history who totally unexpectedly suffered sudden cardiac death at home and was resuscitated and emerging ambulance crew found shockable rhythm either VF or polymorphic VT. We don't have ECG available and performed the defibrillation and CPR and transport her to our to our hospital. At the presentation she was already stable with ejection fraction of 32% on echo, silence, written nerve accuracies. We performed cardiac CMR and found active myocarditis. She was put on optimal medical treatment for heart failure, big force including beta blockade. However on hospital day two she had another polymorphic polymorphic VT which required defibrillation and we decided to perform coronary angiography but no stenotic coronaries were found and we switched selective beta blockers to non-selective ones and what would you do next? Observation, amiodarone, VT ablation, ICD, heart transplantation or wearable cardioverter defibrillator vest. I think there is no vote. Okay. I think. Loading now. So we equipped her with the wearable calibrator defibrillator vest keeping in mind that the reason for the arrhythmia or the origin of the arrhythmia may be reversible because it was the acute myocarditis. For the next few months she was fine. She reported no complaints during ambulatory settings. Then the vest recorded no arrhythmia at all. After three months she was in Neuro Class 2 on optimal medical treatment still sinus rhythm narrow QRSs. Ejection fraction similar to this on the acute presentation and repeated cardiac MRI and found no active myocarditis anymore but dilated left ventricle with diffuse LGE typical for non ischemic cardiomyopathy. And what would you do? The patient observation amiodarone transvenous ICD, a subcutaneous ICD heart transplantation. We decided to equip to equip her with subcutaneous ICD. There was no high high risk of infection of the device in the future but we kept in mind her young age and we wanted to preserve the vasculature for further procedures in the future. However after two weeks she was submitted again to our hospital with polymorphic DVF and numerous SICD shocks. She was unstable with ejection fraction lowered to 24% and she did develop another unstable arrhythmias with the same morphology during the hospitalization and we noted that they were always preceded or initiated by PVCs with the similar morphology. And the arrhythmia was refractory to all drugs we had including amiodarone, intravenous beta-blockades, short-acting beta-blockade, selective, non-selective and so on. What would you do? Drug challenge ovation, heart transplantation, denervation and MCS. Actually we did four out of those five options. We started with left Stanley ganglion blockade which was very effective in terminating arrhythmia acutely. However the effect was transient and after two or three days we observed arrhythmia again. However the burden of arrhythmia was lower so we decided to implant her with with Impel-ACP and then because the arrhythmia was always initiated by monomorphic VT with similar morphology we performed ablation focal PVCs with 3D system which was successful and we also put her on a waiting list for heart transplantation. And after two and a half years she's stable, no VTVS recorded by the SICD, no complaints. She's on optimal medical treatment including SGLT-2, ARNI and non-selective beta-blocker MRI. She's in with her ejection fractions. She's in stable New York class 2 and she's still on the observation not active list for heart transplantation. Our document, our consensus document addresses the problem or the issue of beta blockade and points out that amiodarone and beta blockers are usually the first-line treatment in majority of patients with electrical storm. It underscores also the fact that the non-selective beta blockers are more effective than selective ones in this group of patients and we know it from many, many studies including randomized ones. However, that was not the case in our patient. The beta blockade was only moderately effective probably because we are facing acute phase of myocarditis in the first stage and the very diffuse scarring and ectopy induced or relative to ectopy arrhythmia in the second stage. Our document addresses also the problem of autonomic denervation, pointing out that stelagangone block or thoracic epidural anesthesia may be very effective in acute phase and acutely terminating or lowering number of arrhythmias. However, their effects are transient and they are usually considered a bridge to more permanent treatment like ablation or heart transplantation or surgical denervation. Our document raises also the impact of ablation and in fact electrical storm is virtually the only indication where cataract ablation can be performed acutely. Apart from the mostly ablated monomorphic VT which is scar dependent especially in ischemic patients, we should keep in mind also that in rare cases like the patient I was talking about, the polymorphic VT can be evolved by monomorphic PVCs which can be ablated successfully. Last but not least, our document addresses the issue of mechanical cardiac support. We don't have many data for this, however, we do have randomized data which shows beneficial effect of MCS in patients in whom we want to achieve a stabilization and arrhythmias unstable. We also, the experts in this document also underscore or express their opinion because we have no data, not randomized data for this, that MCS can be beneficial in patients undergoing ablation when we expect that arrhythmia or ablation itself might decompensate the patient and even that the MCS can be can be used before the ablation just to just to protect the future the patient during the future procedure and when we assess the risk of the compensation that pain is ESD scale may be used and patient having 15 some say 17 points in this scale should be or may be considered to undergo MCS prior to ablation. Thank you for your attention. Thank you, we will discuss afterwards. The second presentation now is VT ablation during electrical storm. Should it be limited to tertiary centers given by Levalta, by Thorsten Levalta from Munich and we will discuss maybe the two presentations afterwards or at least yours because you have to leave as you said for the airport. So please. Mr. Chairman, ladies and gentlemen, my talk has the question is it VT ablation during electrical storm is it limited to tertiary centers and to be honest I think there is no real label up to now whether there is a primary, secondary, tertiary center which is which is used in practice in our country at least or in Europe I think. So I went to Wikipedia and and just checked what is a tertiary referral center. It is a level of health care obtained from specialist and large hospitals after referral from providers of primary or secondary care and I think most important is it is either a major hospital with full service or it's a smaller hospital but a specialized hospital dedicated to a subspecialty specialty care and I think at that point I would say yes electrical storm ablation should be done in in either large hospital with specialized departments or in smaller heart centers but with a high focus on arrhythmia care. I have a case to illustrate the need of let's say specialization. It is a it is a case 82 years old male at the moment of VT storm in 21. The patient had a history of complete heart block with permanent pacing DDD pacemaker, aortic dissection Stanford B in 92. He has a y-prothesis due to a bifemoral disease and he has an infrarenal aortic aneurysm. He underwent aortic bypass surgery. He had a check on of his bypasses in 2016 at that time in 21 and now it comes to the problem. He received a TAVI procedure due to significant aortic stenosis in a subclavian approach due to the limited approach from the femoral arteries and in 21 there was a device upgrade CITD to respond also to slow recurrent VTs at that point and in December he turned into a VT storm with recurrent symptomatic and hemodynamic relevant VTs. I'll show you this patient. This is a true story. He came into our hospital the day of a life course and we incorporate his case in that course and this was the x-ray which was taken and you see some form of dislocation. There is a left ventricular lead up here. There is an atrial lead up here. So I think we all agree this is a typical case of a Twittler syndrome. In addition, this is a patient with complete heart block. We had the option in a brief interval in sinus rhythm to check via TE the situation here. You see a TAVI. You see still relevant and good pump function and you see in the descending aorta this remaining dissection, Stanford B. So I think access-wise we all agree this is this is a challenge and the next point would be to ask what is your preferred way of getting access. This is the readout of the CRTD system. This is I think the last readout was done three days ago. So we had repetitive anti-techie pacing and repetitive VT which led to also hemodynamic unstable situation. So one question is how to get to the left ventricle in that situation. We have an aortic dissection, bifemoral bypass and we have a TAVI which is maybe the smallest problem but you could discuss going epicardially. Retrograde via aorta is I think really difficult. Transseptal per left atrium. Transapical was a discussion in a combined procedure in a hybrid operation room or using the arterial subclavia as the TAVI was implanted to get access to the left ventricle and we planned originally to take the transseptal approach through the left atrium to get in the left ventricle because that's where we thought this is an ischemic patient, old ischemic patient post TAVI where the problem is. But this was the incessant VT ECG and it was refractory to shocks, to amiodarone, ATP termination, it recurred immediately. But if you take a look to it, are there any thoughts about a potential origin? It looks, well Helmut you are a profi, it looks like ultratract. Simple, ultratract tachycardia. If you take a look to V1 which is now here the big and helping lead. The R in V1 is increasingly getting higher if you get more to the left ventricle and posterior wall. So there is a nearly no and only small R and if you go to more advanced algorithms and to make the story short, even if you use those advanced algorithms, the R wave duration index, amplitude ratio, everything here looks like a typical RVO2 septally located in that surrounding situation. And that's what we did. We went very simple transvenous to the RVO2 arena. We moved around the septal area. We didn't enter the pulmonary artery really but close and that was the spot of final successful ablation. It was on the septal, right septal side adjacent to the tarvy. At that time I think it was one of the first tarvy related incessant VTs which is now there are several case reports now presented. I show you the ECG at that point. This is the electrocrumb at that point and it was a single application to terminate this arrhythmia. After this we had to fix the dislocated leads. Please remember it's a patient with complete AV block. So the left side was I think access-wise a disaster. So we decided to move the device and all the lead access from the left to the right side and re-implanted CRTD system. Ladies and gentlemen, let me summarize. I think we have several requirements and challenges in VT ablation during electrical storm. I think we have a human factor. This case is, most of these cases, they need an experienced person, an experienced EP person. You don't have time, you don't need sometimes too much colorful pictures. You have to know what to do and you need to experience. You have surrounding diagnostic options. You need imaging echo CT as demonstrated, maybe MRI even. You need a good intensive unit care, even cardiac surgery backup is helpful in those cases. And you need device expertise and you need procedural environment and I fully agree you also need LV support in some cases like impeller or other devices. So my answer is yes, VT ablation during electrical storm should be done in specialized centers. Thank you for your attention. So there is room for questions. Let's start with the second presentation with this arrhythmia in the outflow tract. Any comments on that? There are a few questions from the audience. So one question was, is a specific type of TAVI valve more arrhythmogenic? What do you think the mechanism of the VT was in this case? I'm not aware. I think it is rare. It is not frequent but I think it's explained by the pressure. And then a follow-up question was, was there any concern ablating near the TAVI with respect to heating the valve, you know, getting secondary effects? That's a good point. Any other questions for Dr. Lewalter? He has to leave to catch a flight. I think maybe a comment from my side, doing ablations in VT now for many, many years, I have seen that they are getting more frequent as we are approaching elderly patients, and I think it's not only the valve itself that may be irritating this area, but also a degenerative process, so that some people you have for VT ablations without a valve have the same location there in the outflow tract. I think we have a real spectrum in the outflow tract of aging. One is the block, and the other one is the VT. I think that's what we learn more and more. Any comments on that? Any contradictory comments, or do we see the same? Okay, thank you. So then. There are a few questions for Rado. Why the use of Impella for the ablation? Sort of why did you need mechanical circulatory support? There are two questions. First of them is one, why did we use specifically Impella? And the second, why did we use MCSS at all? The patient was unstable and the arrhythmia was polymorphic. And when we calculate the pain ESD score, it was also roughly 15 or 16 as well as I remember so we expected also the problems during this procedure, so we expected the worst. That's why we used MCS at all. Why Impella? We know the data on Impella are scarce and even not very much in favor of this device, especially for older models like Impella 2.5. There is even a work from 2017, as far as I remember, which shows that the Impella use was independently associated with worse prognosis compared to patients with no MCS at all. However, it was observation study and the group that was comparator for MCS was less sick. So we don't know. From the majority of data on MCS are regarding ECMO. However, at the time, it was three or four years ago, our logistics did not allow to use ECMO. Probably today, we would think about ECMO. And then I had one question about your choice of autonomic modulation. first line before doing autonomic modulation. Yeah, that's a good question. ideal timing of ablation and we don't know it to be sure. What we know is that we should perform the ablation ideally during the hospital stay when the patient was admitted for electrical storm. However, we know also that the outcomes in patients who is ablated very acutely, like during the first days after the presentation and that those patients were worse. So we should ideally stabilize the patient for one or two days and then perform ablation. And that was our idea behind the MCS. Yeah, behind the ganglion block. Yeah, just to stabilize the patient. Perfect. All right, we'll conclude there and we'll move on to our third speaker. I have the honor of introducing Dr. Philip Kukulic from Washington University in St. Louis. His talk is entitled When VT Ablation Fails, Patient Selection, Substrate Delineation and Current Outcomes with Stereotactic Body Radiation. Great, good morning, everybody. My name is Philip Kukulic on behalf of my colleagues and collaborators at Washington University in St. Louis. It's my honor to be able to have this opportunity to speak about when VT ablation fails and when do we use Stereotactic Arrhythmia Radiotherapy or STAR. And I'm gonna highlight a bit of the EHRA HRS consensus statement document that recently came out. I have financial disclosures shown here. In particular, I'm going to talk about linear accelerators and these are outside of the current 510k cleared intended use. So what is Stereotactic Arrhythmia Radiotherapy? This is focused radiation that's delivered in thousands of different angles into the body. Each of those beamlets is very weak but where they coalesce and come together, create an ablative effect. By taking advantage of different angles and different modulation of the beam strength, you can really sculpt a volume of ablation. This technology has revolutionized cancer care around the world and it leverages workflows that are available in most of our hospitals in the basement. This has received cardiac STAR or cardiac radio ablation, has received FDA breakthrough designation and is currently in an accelerated phase of investigation. Now, I don't have to tell you, I can show you some important advantages. This is an entirely non-invasive therapy. A patient walks in, lays on the table, listens to music, no IVs, has the gantry move over him or her three or four or five times, and then the patient gets up and moves out and walks home within seven to 10 minutes. And so there's no anesthesia needed. It's entirely painless and it's entirely done as an outpatient these days. And I think importantly for us, the radiation that we deliver is full thickness. It's not just endo, it's not just epi, and it's not limited by the anatomy. And I'm showing you an example here of a mid myocardial stripe, which I think you would say that's a very difficult catheter ablation procedure where we may have to come at that from multiple angles to try to be successful. Radiation can simply treat that entire area. Now, I think there's another important advance here. Catheter ablation for VT carries drama. You heard two very difficult cases, very difficult thought process. I want to show you what it's like to be an EP who's participating in radiotherapy. So somebody captured a video of me and I want to show you, you'll have to look closely. So this is the radiotherapist. The patient is on the table. There I am. Watch closely. And that's it. That's what I did. Want to see it again? That's it. So it's taken the drama out of this, right? It's easier for the patient. It's easier for us. We're doing this in a much more controlled standpoint. It captured me just two weeks ago. I bumped into our first patient in the halls of our hallway. And I didn't realize that we had hit our 10-year anniversary. So this is our first patient, Dr. John Sumi. He's an intrepid individual who was treated in April, 2015. And on the picture on the left is a picture of him in front of the treatment area that he received his treatment. This was written up in the New York Times in 2017. He and his wife bumped into me on that picture on the right. You can see that for being 10 years older, he looks much younger. So maybe radiation makes you look younger. Speaking of youth, this is that picture from that day when we treated Dr. Sumi. So the gentleman on the right here is Cliff Robinson. And Cliff is a radiation oncologist who I think took great professional risk to say yes to trying to intentionally radiate the heart when the entirety of radiation oncology field thought that that was too risky. So I wanna recognize his youthful. We look somewhat dorky as well. We don't look very cool. But radiation does give you an opportunity to look cool. So this is Cliff and I standing in front of a linear accelerator looking much cooler. And I know what you're asking. How can I too stand in front of one of these laser machines and look cool and sound cool? So I'm gonna teach you how to sound cool when we're talking about radio ablation. With a catheter, we talk about power. We talk about 30 watts. And radio ablation or radiotherapy, we talk about dose in gray. So think about 30 watts might be a 25 gray comparator. When we think about the generator that generates the heat or the electrical fields for RF or PF, we have a linear accelerator. Those are the words you need to learn. These are our industry partners and the tools, right? So we have J&J, Abbott, Bose Medtronic, and they have their ablation tools. We have Varian and Accurane Electa, and these are their ablation tools or linear accelerators, Truebeam for Varian. There's always discussions about photons and protons. And I'm trying to think about ways that we can equate that to EP. I think of photons as like RF or PF. It's widely available. In the United States, there's about 5,000 linear accelerators that can deliver photons. Protons are a specific type of energy that might have some value, particularly when delivered in a more intense way, like an RF needle ablation. There may be some specific ways, not widely available. There's about 50 proton centers in the United States. So kind of a different way to think about it. We have respiratory gating options. And importantly, I think from the EP community, we don't have catheter maps. We don't have the tools that we usually create with a catheter to guide our therapy. Now we can use those. That can be part of the planning, but it doesn't have to be part of the planning. In fact, as we've transitioned from invasive to non-invasive cardiac mapping, as we're starting to understand scar location and scar architecture, we've started to move away from the invasive catheter mapping and utilize off-the-shelf cardiac maps to identify where the scar is. Now, importantly, and I think this is the most important part of the learning that we've had for the last 10 years, when we put a catheter in the heart, we are trying to destroy things. We are trying to destroy circuits. We're trying to destroy myocardium. We're substrate homogenizing. Therapy with radiation is dose dependent. That is, we can modulate the dose to receive different effects in the heart. And importantly, we can adjust the dose to achieve different therapeutic effects in the heart without more destruction. And I'll show you a slide or two about that. Where do we stand with the clinical testing? Well, the first clinical in animal models was published in 2010. So we're roughly 15 years down the road. The first in humans was published here, Czech Republic, Stanford, and then R5 in St. Louis. We opened a formal phase one, phase two clinical trial, followed these patients very carefully over time called the ENCORE VT trial. This data has now replicated in over 25 centers across the world. We have a randomized clinical trial called RADIATE VT that's in progress, and I'm very proud of that. Now, along the way, we're learning about biology, and I'm highlighting some of the very important mechanistic studies, and I'm gonna share a slide or two with you. And I also wanna highlight the really important role of the StopStorm EU Consortium. That's over 30 centers across Europe, currently guided by Oliver Blanc, and really looking to harmonize and develop tools and pathways that are very consistent from one center to another, so that if a patient shows up to your center and you wanna try to do cardiac radio ablation, we'll have a set of tools that will help guide you and keep things very similar. We come together in an international meeting called the SnowStorm meeting. And I just wanna take maybe one slide to talk about the last SnowStorm meeting, and maybe a slide to show a little bit about the biology, and then I wanna brag about RADIATE VT and let you know about it. So let's start with SnowStorm. That was held in Amsterdam back in September. It was lovely. It was a three-day event, brought the world together. We voted on the name, and I lost. It's called Stereotactic Arrhythmia Radiotherapy, or STAR. So that's how we're trying to use it in the literature. There were 10 more centers that contributed to the ongoing body of data showing reduction or elimination of VT. And we had our first presentation of low-dose treatments for cardiac inflammation. We built a consensus document, or at least talked about a consensus document which I'll share with you in a moment. And I'm particularly proud of these first two PhDs in cardiac radiotherapy. There was something very special about this moment. This is Martijn van der Ree, one of Peter Postema's PhDs. And it was a really special moment to see this field have a new group of learners and leaders. Now, I do wanna highlight this particular document. If you're like me, you download the document, you see that it's 55 pages, and you say, well, I just need to see the picture. Show me the first picture. So here's the main picture of this. And in that main picture, they actually talk about patient selection, substrate delineation, and outcomes. And those are the three main things I want to talk about. From a patient selection standpoint, we really think the right people are here. We have seen too often where EVCs, normal ejection fraction, that's probably not the right patient for cardiac rate ablation right now. We have patients who are on ECMO with VT storm who don't really have any other way out. That's very advanced heart failure. That's probably too sick to be considering for this. We'd like the patients where we have more VT than heart failure. And I would add, beware of the patients who are on inotropes or who have baseline hypotension. Those are markers of sick patients. As far as the substrate delineation goes, there's many different ways to do this. This document outlines a process that's very heavy in taking the electroanatomic maps and importing them into our treatment planning software. But I do think that there's many opportunities to bring other things like CT, MRI, and PET to help guide where the scar is. My team in particular is very strong about still leaving physiology and electrophysiology. And so we induce VTs, look at the 12 lead ECGs to help us understand where in the scar the ventricular tachycardia circuit may be exiting, and really focusing our radiation on those areas and not necessarily the entirety of some very large scars. So I think there's a lot of room for growth as we understand how to do this targeting process. And then outcomes become very important. What does it mean for a patient to undergo this and have a substantial outcome? I think we all push back on the atrial fibrillation guidelines these days to say 30 seconds of atrial fibrillation is probably not the right metric. Is time to first therapy the right metric for some of these advanced heart failure patients? I would argue no. If you've had 50 shocks and then you had two ATPs, from a patient standpoint, that's a very different experience and a very positive outcome. And so I think we need to be thoughtful about those endpoints. I wanted to just share with you a picture on the left was a radioblation patient that we did in 2017. That red target you can see on the apical septum, slightly inferior. This patient went on seven years later without any VT, developed VT, and went back to the lab. And I'm showing you then the catheter map of that target. And so again, seven years without VT, I'd probably call that a win. But it was recurrent, so we bring him back. But I think what's really interesting is you can see what looks like a reasonable scar modification, substrate ablation, but you can see just a little bit of survival. So this is where we stand in terms of the clinical care. I do really need to tell you, though, radiation is more than ablation. Different effects at different doses. We are using 25 gray to treat ventricular tachycardia. And more and more data is saying that that is effective at treating ventricular tachycardia without causing more scar. So let me say that again. We're able to modulate VT, reduce or eliminate VT without causing more destruction at these doses. Now, of course, if we turn it up, if we go to 40, 50, 60, 80, there can be more destruction. But there's a really important opportunity right now to take advantage of biology. What I think is really cool is that we can modulate the electrical properties at lower doses. So work from Stacey Rentschler and her team showing that lower doses of radiation actually can accelerate conduction by upregulating sodium channels and connexin 43. Really powerful stuff that with low dose radiation, we can actually be localized antiarrhythmic effect. And lastly, one of the new discoveries here is that low doses of radiation seems to modulate the inflammasome. And so in inflammatory cardiomyopathies, and I'm going to show you a picture is worth 1,000 words. On the left is a heart failure mouse. This is a mouse strain that is destined to have heart failure. And you see got a sham treatment. On the right is at the same heart failure mouse, litter mate, who received low dose radiation. Wrapping up, let me show you where we were 10 years ago. I showed you the picture of Cliff and I standing in front of that linear accelerator. Here is the seven patients that were treated in 2015, and here's where we stand in 2025. It is now a global experience with hundreds of patients that have been treated in a number of centers around the world. I am particularly proud to talk about the randomized clinical trial. We're putting the science behind this. It is a randomized clinical trial of redo catheter ablation. for patients who have scar in their heart, who have had a catheter ablation within the last couple of years and have failed in antiarrhythmic. So look forward to this. We have nine centers now open in the United States. So where can you learn more about the developments of Cardiac Star? When you think about Cardiac Star, I want you to be curious, not judgmental. Give us a chance to study this in very scientific, rigorous, slow but proven ways. Snowstorm 2024 was in Amsterdam. Snowstorm 2026 is actually going to be at Mont-Tremblant in Quebec. And so I open invitation to come to Snowstorm 2026, ski, and enjoy the learning environment. This is the team that does the work. This is our Center for Non-Invasive Cardiac Radiotherapy. Thank you very much for this opportunity. Look forward to questions. Thank you. Thank you, Dr. Kukulich. All right, we'll reserve questions until the very end. We'll bring up our last speaker, who's Dr. Joshua Moss from UCSF. His talk is entitled, New Energy Sources for VT Ability. Okay, so I'm gonna start this with a couple of disclaimers. First of all, I'm going to assume that the audience is comfortable with the fact that VT carries significant morbidity mortality, that catheter ablation is an important treatment for VT, and that catheter ablation is not 100% effective, at least in part due to ineffective or inadequate lesions. And unfortunately, there isn't time in this session to discuss really what is still my favorite energy source, which is radiofrequency, and using techniques like low osmolality irrigation or bipolar ablation, RF needle ablation, ways to enhance RF delivery. I left some references for you there, but I'm not gonna have time to talk about that. Not all of the energy sources I'm gonna discuss are new per se, but their use in VT ablation remains in the early stages. So to kind of summarize these into two categories, we have thermal sources of energy, RF cryo, high-intensity ultrasound, for example, and there are non-thermal sources such as pulse field ablation, chemical ablation like alcohol, radio therapy, which, you know, without any pre-planning, I want you to know that I chose this picture from the web thinking, well, this is the coolest one of Phil. So, I guess I got lucky there. Or shockwave therapy. So I'm gonna pick a couple of these. It's a short talk, so we're gonna kind of fly through a few of them just to give you a general overview. So everyone's familiar with cryo ablation using nitrous oxide, which is the typical source that we're using for these focal catheters and for cryo balloon. Here you can see just a regular radio frequency ablation catheter kind of flipping around on the moderator band, papillary muscle complex on the right ventricle, tough to get good stability there, but with cryo ablation, it does offer that advantage of being able to kind of freeze to the tissue, especially target areas that are very mobile and give you a chance to ablate there without sliding around. And here you can see on the left, the fluoroscopic image of that ablation and the catheter just moving with the heart stuck to that papillary muscle. Well, we can also do ultra low temperature cryo ablation, which uses liquid nitrogen instead of nitrous oxide. And that has a boiling point of negative 196 versus that for nitrous oxide, which is negative 89. So it's quite, it gets quite a bit colder. And this is from Adagio Medical. It's a nine French catheter with a 15 millimeter long ablation element as well as electrodes for electroanatomic mapping. And without surprise, this can make some pretty big lesions. So 16 millimeter lesion here. There has been some human work already. The Cryo Cure VT study was just published this past year as the first in human multicenter experience using ultra low temperature cryo ablation. It was 64 patients at multiple centers, mostly ischemic cardiomyopathy. Most of them, it was their first ablation. It was a median of about eight lesions per patient, most using a two minute protocol. And that's based on the preclinical data showing a two minute freeze time giving about a seven and a half millimeter lesion depth. And the procedural times were as expected for a VT ablation, a few hours with 40 minutes or so of ablation time, 19 minutes of thoroscopy time. And what they showed were results very similar to a lot of other VT ablation trials. So it's effective, 60% freedom from any VT at 25 weeks and 81% freedom from an ICD shock. And more importantly, as Phil alluded to, just the reduction in overall burden, which is really what is important to the patients. So median of four events versus zero events post ablation. So this is early stages, but effective. It was safe, a couple of small pericardial effusions and one asymptomatic false aneurysm. Going on to kind of a non-thermal, obviously pulse field ablation is kind of the star of the show at HRS here, but we had early potential applications for pulse field in the ventricle. This was Mount Sinai group and kind of an early basket catheter from TheraPulse showing transmural lesions and sparing arterioles and sparing nerves. And animal data has shown really that there is more effective scar penetration than RF. This is from Ed Gerstenfeld's group with us at UCSF. Looking at the TheraPulse catheters and what they showed was that in scar, you could get ablation to surviving tissue that was both endocardial and epicardial to the scar up to about seven milliliters deep and also ablate islands of surviving tissue with PFA. And when they looked at lesion depth in healthy tissue, they did not see a significant difference between PFA and RFA, but when they looked at the depth in scar based on histologic measurements, indeed, they were able to get deeper lesions in scar than could be achieved with RF. And RF was also associated with arterial evacuation and venous thrombosis, nerve evacuation, so potentially safer as well. Elad Anters' group did a similar type of studies with the Sphere 9 catheter and also showed deeper lesions, higher percentage of wall depth penetration, wider lesions, more transmurality with PFA compared to radiofrequency. And again, similarly, you can see here irreversible injury to cardiomyocyte bundles that were separated from the catheter despite being separated from the catheter by collagen and fat the PFA was nevertheless able to reach those as well as these islands of surviving tissue within scar. So this may be a good tool. Early clinical use, the first in-human study published online in 2022, a prior anterior MI with frequent VT, and they were able to, as you can see here, kind of eliminate the isochronal crowding after seven overlapping lesions, and that patient did well. There had also been some case series. This was a three-case series using, again, the pentospline catheter. And the example here was kind of a focal VT that they were able to very rapidly eliminate, and you can see the scar created there. This is from one of my colleagues, Matt Hutchinson actually sent me this the other day, just coincidentally, a case that he had done, difficult patient having VT storm on ECMO. And you can see the sinus rhythm activation map and scar here. And what he did was target the channels with radiofrequency and then went back with PFA to reinforce the rest of the scar. And you can see how effectively that was able to eliminate that. You can also combine cryoablation with pulsed field ablation, and this is PFCA, so ultra-low temperature ablation with PFA. This is Adagio again. And potential advantages here include countering the incidental heating effects. Here you can see this turbulent convective flow from PFA from heating, and no turbulent flow with this ice that's formed around the catheter just prior to delivery of PFA. There's also less microbubble generation, which you can see here, PFA on the left versus PFCA on the right. Possibly less coronary spasm or injury, and my colleague, Tommy Doolin at UCSF has been looking at this in the animal lab. I'll direct you to the abstract that he presented on Thursday showing less coronary spasm with PFCA versus PFA alone. And there may be this insulation effect of frozen tissue that confines the PFA field to the area of interest, so here you can see a PFCA lesion with very smooth boundaries versus just a PFA lesion with more heterogeneous boundaries. Briefly, I wanna just mention high-intensity ultrasound as another thermal technique. This is from Bob Ignazer, the Sonavera catheter, an 18 French catheter with a ultrasound transducer that's internally irrigated, and let's see if I can make that play correctly. Nope, it's not going to. But you can see a lesion being created here in this gel when this restarts, but yet sparing, here it comes, sparing the area just next to the catheter so it's a bit more focused. And how that kind of translates clinically is these large transmural lesions that still spare the subendocardium, which could be a way to protect the conduction system on the septum. And with this type of ablation, looking at 30 days later, he was able to demonstrate septal thinning, and so this is actually now being studied for use in hypertrophic cardiomyopathy for reduction in septal thickness. Here's an example on MRI. You can see immediately post-ablation. You can see the LGE that's generated from the ablation, but normal wall thickness still, but at one month, due to fibrotic remodeling, you can actually see how the septum is thinned after delivery of these ultrasound lesions. And then just lastly, earlier in development, there's studies of this laser catheter and lesions that it's able to make. Shockwave ablation by pulsing a laser into a chamber of water and creating shockwaves the same way you would for lithotripsy, but incorporated into a catheter. This is an area of research and focused electrical field. So using kind of a different shaped electrode, this toroidal conducting surface, this is really just stuck right on to the end of a laser catheter to increase the depth of resistive heating using radio frequency, allowing you to make a larger lesion without the risk of steam pops. So to conclude, we know there's a need in the VT ablation space for larger and deeper lesions that we can achieve with traditional RF. And larger lesions are possible with alternative energy sources like pulse field ablation, like ultra low temperature cryo ablation, pulse field combined with cryo ablation, high intensity therapeutic ultrasound. But there are important factors that are still being studied and optimized safety titratability. And obviously radio ablation, chemical ablation are already in use at select centers. Thank you. Thank you, Mos. So there is now around six to seven minutes for questions. Please come up with questions. Yeah, if you feel comfortable moving to the mics, you're welcome to ask question. There's several that came through the portal here. So I'll start, I'll reserve some. There were many for Dr. Kukulich here. So we'll hold off on that for a second. So first question for Dr. Mos, there's a question about where do you see RFA VT ablation in the next five to 10 years? Will these new technologies sort of begin to supplant RF ablation? And how do you think about using these newer technologies sort of as an upfront strategy, perhaps rather than RF energy? Are there particular substrates or particular patients rather than using it as an initial strategy? Are you thinking about it more as a, if you can't get the VT, you bring them back with an alternative energy source? Yeah, it's a good question. I wonder how people would have answered the question of whether or not RF was gonna be supplanted for AFib ablation even a year ago. And here we are. So I'd like to think that RF is gonna maintain an important place in VT ablation. And I think it will, particularly for focal VT, for conduction system based VT, certainly PVCs, focal PVCs. But I would not be surprised if over the next five years, we see some of these new technologies start to supplant RF. When we're using a strategy of substrate homogenization, so often now, particularly for patients with non ischemic cardiomyopathy. And the ability to make larger lesions over larger areas faster and potentially more safely is gonna be hard to deny. Similarly, as it has been with AFib ablation. And I do think that some of these will probably end up supplanting RF. But RF won't go away entirely. Question from the floor. Great session. I just, in terms of dual energy delivery, thinking of RF and PFA, in terms of sequencing, I think the example you gave was RF first, followed up by PFA. There seemed to be conceptual reasons why you might favor either order. I just wondered if the panel have a view on that. The technique that I actually showed was cryo and PFA combined, not RF and PFA. And the idea there, I believe, is more cryo first, again, to sort of create that zone in which you might be able to sort of confine the PF field, in addition to increase the safety factor around the PFA by reducing the micro bubble generation, by having the catheter be more stable, by potentially protecting the surrounding or nearby arteries from some of the spasm effects. And also, I didn't mention it, it was on the slide, but I didn't say it, reducing the skeletal and phrenic muscle contraction as well. One of the limitations, as I'm sure you know, with PFA, a lot of times, is if you don't have a patient who's paralyzed or under general anesthesia, it can be a pretty disruptive type of technology. Particularly as you're using larger and larger energies, and it's possible that combining the cryo with it could reduce that effect, such that you might even be able to do it in an awake patient, not under paralysis. Okay, I'll move on to some questions for Dr. Kukulich here. Does radiotherapy compromise a patient's future candidacy for heart transplantation? Yeah, terrific question. And we really wanna have all those options available for these advanced cardiomyopathic patients. The short answer is no. Several centers have had patients now who have had radiotherapy, who have survived long enough through their VT storm to then get a cardiac transplant. The explanted hearts and the quality of the inflammation in the chest, I think is surprisingly low. I think there is, the term is hostile chest or hostile chest that we sometimes think about when you are a 25 or 30 year survivor of cancer that received high doses of radiation to the chest. But we have not seen that with focused radiation at these more moderate doses and shorter follow-up. So the answer is that cardiac transplantation is very much on the table for these patients. And then two related questions. What is the VT recurrence rate after cardiac radiotherapy? And if there is, how many sessions of radiotherapy can one get? Yeah, great question. Again, short answer of does VT return? The answer is yes. Not for all patients, but I would say at least half of, when you pool all of the data, it's about a 50% recurrence rate over the course of the patient's survival. Some centers have reported higher, some centers have reported lower. But when VT comes back, it tends to be more ATP terminated as opposed to requiring ICD shocks. So there's something about the modulation of that scar that allows ATP to work better. If you look at the shock burden, that tends to be dramatically reduced. Whereas the VT burden alone or time to first VT recurrences is a modest event. Can people receive multiple rounds of radiotherapy? The answer is yes, but I think we know even less about the biology of receiving multiple doses. The radiation oncology world has significant concerns about re-irradiating at these moderate doses for the type of destruction that may come from that. We can take advantage of radiation and biology sometimes if you think about, for example, prostate cancer is oftentimes delivered in 30 fractions. So one gray in a day and that you come back the next day and you get one gray and you come back the next day and you get one gray. Now you get 30 gray, but it's now extended over the course of multiple weeks. And that's a different biology and that's taking advantage of the rapidly reproducing cancer cells. Now we don't have that in cardiac myocytes which are relatively dormant, right? So there doesn't seem to make a lot of sense to think about fractionating the dose. We're not really taking advantage of any biology that way. So I wanna congratulate you for this amazing work you've done. I think I saw one of your first talks on this topic. You've been following these patients for many, many years now. Have there been any surprises with respect to collateral issues, device-related questions, other things that come along with getting radiotherapy? Yeah, I think one of the important things that was both in the EHRA document that I showed as well as just about every talk that we have which is we really need careful longitudinal follow-up on these patients, right? They're receiving the benefit of a non-invasive therapy on the front end. So they have a less risky exposure, a lower risk exposure on the front end for the first weeks and months. But should we expect some changes longitudinally? So the ONCOR VT trial carefully followed these patients. Now we're out past seven years. We reported the five-year longitudinal concerns at HRRS two years ago. And we do follow these. In short, about 5% to 10% of patients will have a pericardial effusion which is usually not symptomatic but that's the most common thing that we've seen. We're keeping a close eye for LV function, making sure that heart failure doesn't develop. We're really trying to bring the cardiac volumes that we're radiating smaller to try to reduce those risks. I think, and then lastly, I think the importance of being close to luminal structure, so esophagus and stomach, radiation can have a very sensitive effect. Those are very radio-sensitive structures. And so figuring out ways to mitigate those risks is important. Okay, one last question here. Michael Caine, Buffalo. Phil, again, congratulations on a great volume of material. The comment you made just a few minutes ago about the recurrences that you are observing and that they may be easier to pace terminate than before, are you doing any planned randomized trial as part of this that if people do recur that some get on drugs to see if they work better now versus some get a re-catheter ablation versus they get ATP, or is it still not at that point yet? Oh, thank you for that question, Dr. Caine. I think that's a really, that's a curious idea. So the answer I would say is no, we don't have anything planned for that. We are bringing together the global community's experience with remapping. So when people do have a VT catheter ablation after radio ablation, the overarching theme seems to be that the scar is relatively homogenized, it's a single circuit that we're dealing with, that it's very easy to map and ablate. One of the posters yesterday called it a hybrid VT ablation. That is, you radiate it first, whatever is left you clean up with a catheter afterwards. And I think that's what people are seeing as a way to simplify the complexity of some of these catheter ablation procedures that we've seen today. Some more to come on that. That was a good finishing statement. Dear colleagues, thank you for attending this joint session between HRS and IHRA. I wish you a good Congress, and of course, thanks all the presenters for their fabulous presentations. Thank you, have a nice day.

VT management

electrical storms

ventricular arrhythmias

non-selective beta-blockers

Stereotactic Arrhythmia Radiotherapy

heart transplantation

specialized centers

pulse field ablation

wearable cardioverter defibrillator

myocarditis