Good morning, everyone. Thank you for being here so early this morning. It's my pleasure to welcome you to San Diego and Heart Rhythm 2025, 46th Annual Meeting of the Heart Rhythm Society. If you haven't already done so, download the app from the app store to participate in the live Q&A. Actually, you know what, I apologize for the Q&A for these sessions, we won't be using the app. But feel free to jump to the microphone if you have questions. Feel free to also, you know, raise your hand and ask a question as well. Please note that the visual reproduction of Heart Rhythm 2025 is strictly prohibited either by video or still photography. And now just to introduce myself in the session, I'm Andrea Kiethler, I will be your chair for today's session on novel mapping tech and ablation techniques for PT ablation and I have the pleasure of introducing our first speaker from the Montreal Heart Institute, Katcha Jirga, to talk about initial preclinical evaluation of ultra low temperature cryo ablation catheter for ventricular ablations. There, you saved me one minute of my presentation time by saying all that. The suspense, will it start? Good morning everybody. Thank you very much for being here so early in the morning. I am Katcha Jirga, I'm from the Montreal Heart Institute, but you will see on the slide a long list of co-authors who have been instrumental in realizing this work and all of the ongoing projects. You may have heard of ultra low temperature cryo ablation, in case you haven't. In a nutshell, we are working with nitrogen in a state where the combination of pressure and temperature suppresses the liquid gas phase transition. If you don't love physics, what it means is that we may get to maintain the viscosity and hydrodynamics resistance of a gas, however we have the density and the heat capacity of a liquid. Putting all those properties together, we have a free flowing substance in a vapor lock phase that allows us to get to very low temperatures, thereby reaching very rapidly the temperatures that we need to create intracellular damage and direct cell destruction and get much below those temperatures. If you're curious about more of the physics, then we can talk about it afterwards. The catheter that is currently in use, which was used for the CryoCure VT trial, which you will hear more about later in the session by Dr. Verma, and currently in the Fulcrum VT trial, is the one present on the screen. So it is a nine French bidirectional catheter, it's got a 15 millimeter element at the end. We have eight electrodes that allow us to do pacing and capture relatively high density signals and does not require irrigation, which is very useful for our low ejection traction patients who are volume sensitive. With this device, doing a freeze-thaw-freeze cycle, which is common with cryotherapy devices, we're able to reach with two times three minute lesion, applications, sorry, we can reach lesions of 10 millimeters and beyond in both width and depth. Now for electrophysiologists who like things to happen fast, these are very long and lengthy lesions, hence the idea behind the augmented ultra-low cryo temperature. Here we have pushed, well, I say we, I have used it, they have pushed the expansion of the cryogen within the distal tip of the catheter to allow us to yield even lower ablation temperatures. So you see on the right, the traditional catheter would reach around minus 145, and now with the newer catheter, you can get down to minus 170, 175. You see snapshots of the catheter in action, so you do not need this duration of time to actually reach the temperatures. This is just a typical lesion set that was done. The catheter has also been amended to allow a smaller diameter catheter. It is now an 8.5 French catheter, allowing it to fit in the traditional sheets that we love to use for our ablations. It is truly a bidirectional design, offering us a D and an F curve. We do have a shorter tip. It is now 12 millimeters instead of 15, making the curving at the end much easier in tight spaces. So if we want to curve in the aorta, if you want to curve in a small ventricle, the catheter is also more flexible, allowing us to buckle prolapse so that it can be in contact parallel to the wall of the ventricle. You want to avoid end-on lesions where you don't maximize the contact and you don't get the full size of lesions. We maintain a number of electrodes at 6, giving us enough signal density, but allowing the newer properties of the catheter. With this new device and new methodology to use the coolant, we studied four porcine subjects. The first two were used primarily to try different lesion durations and try multiple iterations of the newer catheter. So we don't have complete lesion sets to show you comparative data, but they allowed us to determine that using 30 seconds, 60 seconds, and 120 seconds gave us the maximum benefit. There was no additional advantage to going all the way to 180 seconds. We use electroanatomical mapping. We use fluoroscopy, which you can see in the top left corner of the panel. We use ice guidance, and then we have the information from the device itself. You see here, as you start applying a freeze, that yes, there is ice that forms at the tip of the catheter, bringing about noise. However, you do not see the distal tip, the ice forming on ice. You will see the movement of the tissue that is frozen change quite a bit. There's a bit of a rocking motion that can arise if you have a large area frozen. You see a little bit later in a lesion how you have reached significant temperatures. You see minus 172 here. However, the warming phase does occur quite rapidly. The bottom left panel here shows you the catheter. Catheter did not move during the application, but the representation of the catheter on the mapping system goes off the map during the application. This is important as we look at the electrograms a little bit later on in the presentation. From all of these applications that we did in these models, we looked at the gross necropsy, we did the histological analysis of the morphology and dimensions of the lesions, and then we looked at the EGMs to get further information about signal abolition during ablation. You can see right away that on gross imaging, we can see the lesions that are transmural. We see them both on the RV and on the LV. They show as circular, darker lesions. When we cut to the endocardial aspect of the ventricle, so the image, the second on the top, more on the right, you can see that we can easily find the corresponding endocardial side of our transmural lesion. When you cut through the lesion bottom right panel, you can see the typical characteristics that we expect to find in such cold cryo lesions with an aspect of hemorrhagic core and then a white, more fibrotic aspect border. The lesion morphology itself, if you look at it histologically, you can see the extracellular edema and you can see the coagulation necrosis within the core of the lesion, so that is the central part within the green line. We see that on the outside, the microfiber degeneration and the contraction band necrosis. These are expected finding that we do find despite only doing one rapid, very low temperature lesion. The lesion morphology is depth independent in that we maintain this architecture of lesion with the central core and then the contraction band on the outside, no matter how long the lesion is. You can see that it will get pushed to the other side of the wall, it will get pushed to the side as the lesion grows, but we maintain those two separate zones throughout the different durations of applications. I told you initially that the first two animals were used for catheter iterations, the second two animals were used for more rigorous lesions that we can compare and show you this data. You see on the panel on the left, the lesion depth analysis and on the right, the lesion width analysis. Typically, in the RV, we did 30 second lesions, allowing us a mean depth of six millimeter. In the LV, we did one or two minute lesions. The one minute gave us a mean of 8.2 millimeters, while the two minute lesions got up to 12.3. The width is slightly less than the depth, which is very useful for us to get lesions that are still controllable in size and we don't destroy too much myocardium in what are applications. We have 5, 7, and 9 millimeters respectively for the 30, 60, and 120 lesions. The EGM themselves, you can see that you will have good signal quality, bottom left of the left panel, prior to ablation. After the application, you see that the signals are completely gone. It may appear that the catheter has moved, but in fact, these snapshots were taken 10 seconds before and 10 seconds after the freeze, so the catheter has not returned to its exact position on the mapping system. It has not moved, but it's the representation on the mapping system that has not completely returned to position. Putting this in graph, you can see on the left that there is more and more signal abolition, so the percentage attenuation of the EGM grows with the depth of the lesion. The same thing occurs on the right with width. You see that there is more scatter in the 30-second freeze, and that is because lesions are much narrower, so lesions of 5 millimeters, and the catheter is 12 to 15 millimeters, so you actually get some far-field measurements, thus affecting the percentage that we calculate, but the local signal does truly disappear. In conclusion, this early preclinical work has shown that the augmented ultra-low temperature cryotherapy can be implemented in a smaller catheter, 8.5 French. It fits in the traditional sheets that we like to use, the deflectible ones. A single freeze with augmented technology produces acute lesions, titratable depth up to or greater than 10 millimeters. We have the tissue characteristics that we seek, the coagulation necrosis, the contraction band necrosis on the periphery. We are looking at the chronic studies to look at those lesions later on, see what happens and the further development of those lesions chronically. So in conclusion, the augmented ultra-low cryotherapy will allow for significant reduction in ablation times compared to the conventional catheter, which has already proven itself and different studies have been published, and you will hear more about it later on in this session. So I thank you for your time, and feel free to ask some questions. Everybody's too shy, because it wasn't all that clear. Thank you very much. I did actually, I wanted to ask, you know, looking at the depth, I think this can be a really powerful tool. Do you have any thoughts, you know, as far as when you're using this in the ventricle, you know, how this might penetrate through areas of scar and, you know, that and other things? There's actually a lot of data out there. We do have normograms telling us time and depth. We know that there's a little bit of difference between the penetration with healthy tissue versus scar tissue. So the data is out there, and we do have some normograms. We do use the ice to measure the thickness of the ventricle at the area where we wish to apply the lesion, and we try to aim for transmurality, but not overshoot too much so we don't cause any inflammation or damage to the surrounding structures. But I don't have time this morning to show you all of these datas, but it is out there, and if you're interested, please feel free to contact me, and we can look at it further. All right. So our next... If you introduce them, I'll work on it in the next lecture. Okay. Thank you. Our next speaker comes from Cleveland Clinic, Arway Eunice, to talk to us about pulse field ablation with a pencil-spine catheter for ventricular arrhythmias, a first U.S. series. Thank you for the kind introduction. Thank you, everyone, for being here. I will discuss our experience with a fire pulse catheter in the ventricle. This is all off-label, obviously, and bailout strategies and cases where we needed to use the PFA catheter. The idea to use PFA came from our bad experience with RF. We know that RF is extremely limited in the outcomes of treating ventricular tachyarrhythmias and PVCs, and oftentimes when you're in a referral center, you get cases where they already failed elsewhere, and then you need to think outside the box, how can we help these patients? How is PFA helpful? PFA helpful because of two things. First, the shape of the catheter is wide and allows you for better stability and quicker lesions. We also shown that it's better to penetrate scar tissue, mixed scar tissue, redo environment, which allows better penetration than RF. Similarly, in our lab, we have done a recent study with a focal point catheter, also from Boston Scientific, similar waveform to the one with the fire pulse, but a touch deeper. We have seen that in tough places, like the PAP muscle, LV summit, epicardium, and the LV septum, the catheter is able to give us better results without compromising the safety. In the current study, we took all consecutive patients undergoing PFA with a pentaspline catheter that are part from our VT registry from May to October, and then in October, once the Afera system came and became handy, then we moved to use Afera. PFA was utilized for large footprint VT substrate ablation, what we call substrate modifications, or as a bailout approach after acute RF failure. As I mentioned, we have 11 patients, all were male, mean age was 70. Nine patients were scar-related VT, and two patients were PVC. One of the scar-related, two were non-ischemic, seven were ischemic, the non-ischemic one was ARVC. So again, all patients, 11 patients, scar-related, nine patients, and then two patients with PVC. I'm going to go back to the procedure characteristics, and I don't know why is this here, I thought I updated it, I apologize about that. We look at the total irrigation and the total ablation time, and it's very minimal, and we all know that when you take these patients who failed RF and are in VT storm, then most of these procedures are four, six, five hours procedures with a lot of irrigation, and you wanna maintain, you don't wanna go high on the anesthesia, so it's very difficult to monitor the hemodynamics when we have a catheter that is flushing. And here, the irrigation was very minimal, and the total ablation time was also very minimal. These are the baseline characteristics of each patient, and as I said before, these are really sick patients. Most of them had already a previous prior VT ablation. The majority presented with a VT storm. Some of them had more than one VT already before entering the lab. Others had more than one VT during the case, and those with PVC were also tough areas, pub muscle in both of them, and one has already failed prior RF ablation. In two patients, we did not attempt RF. These were patients who already, one patient already failed two prior VT ablations elsewhere, presented with a VT storm, had three different VTs. We had great MRI imagings, and we knew where is the scar going to be, and then we thought that with PFA only, we might be able to terminate the VT. He was an incessant VT, came into the lab with VT, and we were able to terminate it with PFA, and I think this is important because once you, you need to know which strategy are you using to apply because once you, if you start with PFA, and it doesn't work, you may break the circuit just by delivering energy, doing cardioversion, and then you already applied energy, and then when you remap, the electrograms are different, and you don't know whether this is aturable lesions or not because when you deliver PFA, you have three zones. You have the irreversible zone, you have the reversible zone, and you have the healthy zone, and the partially reversible zone, you may be able to capture with a high output, but then you won't see the electrograms, so you need to know beforehand, okay, this is my strategy. I'm gonna go after the circuit, and if you think you're gonna go after the circuit, and you're having difficulty knowing where is your circuit, then what we recommend or what we are doing now also with the FERA is that you go with RF first, make sure you got the circuit, make sure you know where is your circuit, you know how to terminate it with RF, and then if you want, you can add PFA to do scar homogenization and modifying the substrate. The other patient with the PPC where we did not try RF, it was a combined case. The patient was taken into the lab for AFib ablation. We've noticed at Huddle that the patient is having a lot of PVC, and then when we looked at the loop, the patient had 23% PVCs, so therefore we decided, okay, we will go with the PVC. We had already the pentaspline catheter in the atria, already cross-transceptal, so we went and did PVC ablation with the pentaspline without trying RF. This is some of the, that's an ischemic cardiomyopathy case. On the left side, we see a voltage map, and you can tell how big is the scar. These are sick patients with large scar, and in the era of RF, it's gonna take a lot of time, a lot of irrigation to do the case. I did this case with Dr. Higochi, so thank you, and then we started with RF after mapping the circuit. We identified the circuit. We were able to terminate it with RF, and then we said, okay, we're gonna do now the scar homogenization with PFA, and these are the shadows of the PFA, and you can just imagine how much time and irrigation did this spare the patient. Obviously, when you do something like this, then you have to make sure that you are continuously seeing and controlling your movement with the PFA catheter. It's a very large catheter. All the transitions between flower and basket should be done under ice, controlled ice, with Doppler, making sure you're not coming near the mitral apparatus. We can also see the scar. We can see the apical aneurysm, so it's a large substrate, and in this, that's an application with a basket, and that's another application in the flower shape. That's a very interesting case that takes us back to the era where surgeons in the 1980s and patients with ARVC, they would go and dissect the free wall to eliminate the epicardium from the endocardium, and that's a case that we saw, so we applied PFA from the endocardium side, and then the ECG is showing sinus, but our catheter on the epicardial side, showing that you still have VT ongoing into the epicardium, which was dissociated from the ventricle. So with further applications of PFA, we were able to eliminate both endocardially and epicardially, without the need to go and ablate in the epicardium. That's the case of the PAP muscle, and we all know how difficult it is to maintain catheter stability for two or three minutes when you are trying to perform RF ablation at the PAP head, and with the pinta spline, if you get it into the correct shape, and again, all the movements needs to be in the left atrium before you even try to, you don't wanna go and do basket and flower here in this area. This can end in a disaster, and we had a disaster that was referred to the clinic for cardiac surgery because the catheter was stuck in the valve. So you put your wire, you aim, you see where is your wire going, you do your basket, and then you advance the basket over the wire into between the heads of the PAP. During limited follow-up of a mean of around 220 days, the recurrence rate was a touch higher than what is reported for RF patients, sick RF patients, we're talking about 60% redo, 50% presenting with VT storm. So we had three cases of recurrence, one PVC, one that failed already two prior ablations and presented with three different VT morphologies with an EF of 15, very large scar, and the other one is also similar story, two VTs, prior VT ablation, and is chemicardiomyopathy. In conclusion, in this first US series, VT PVC ablation using a pentaspline PFA catheter for large VT substrate modification or following acute RF failure appears to be effective and safe. I did not discuss the safety. All ablations were done from the endocardial side, so we did not see any ST changes. When we did in the animal lab, the ability of the pentaspline, even with eight repetition, you cannot get deeper than five to five and a half millimeters so it's very shallow lesions. It's excellent for scar modifications when you have an apical aneurysm and you know on ice that it's five, four, six millimeter, that's ideal, but if you are aiming for an LV summit with this catheter, you're not gonna get it. And I wanna thank Dr. Santangeli, where is he? Dr. Santangeli, who is the head of our VT program for allowing me to be part of this. Thank you for listening. I don't know. I wasn't part of that case. That's a good question. I don't know. So oh, the question was in the case of the ARVC, did they try to pace from the epicardium to see that? Can you still capture endocardial? Is that what your question? Yeah. I don't know if they paced. That's a good question. But I can tell you that after the repeated PFA applications from the inside, all of the signals were gone. So there was no VT anymore in the epicardium. Yeah. So So yeah. So I'm going to repeat the question. The question is in an era of dual energy, when you have RF and PF, what's the workflow? And if you're going to use RF, then how is this going to affect your PF? Is that correct? So Atul Verma just recently published similar work that tested this hypothesis of acute RF and then acute PF. And what they show is that with acute RF and then followed by acute PF, you can penetrate a touch deeper. With the current technology that is available in the US, that's a little bit problematic. Why? Because when you switch from RF to PFA, there's a time that you need to wait. And then there's another time for the charge. The idea behind why does Afera require you to wait is because that they don't want, even with PFA, the way you monitor the lesion is by monitoring the thermal injury. Correct? So there is thermal increase with PFA as well. So Afera was designed for the atria and they didn't want you to stack the lesion immediately after the RF to avoid heating the esophagus. But when you wait for the PFA after the RF, you see it on ice that now you are getting to the zone of edema. And edema is going to push your catheter away from your target. The ideal workflow is to have a catheter where you don't need to wait if you are planning to do a ventricular lesion where you apply RF and then immediately go after PF. This is where RF will allow you to lower the impedance which will allow better penetrations of the PF. Currently, that's not what we have. So we are forced to wait. We would still rather do RF but not because of the deeper penetration but rather because of the maintenance of the electrograms and the circuit. With PFA, you're going to screw the circuit and you're going to have false or pseudo electrograms that might not be of interest. So these patients are like the penta spline was done for scar homogenization. These areas are not moving. You're not going to have more stunning than something that is already scarred and aneurysmatic. I'm sorry to cut you off but we're out of time and I want to make sure we give our subsequent speakers adequate time to speak as well. Thank you so much. That was really an interesting discussion of those cases. Next, I have from Vanderbilt University, Daisuke Togashi to talk to us about peak frequency map to guide ablation in ARVC. Hi, good morning. Happy to be here today to present our finding peak frequency mapping to guide ablation in arrhythmogenic right ventricular cardiomyopathy. As we know, there are several strategies for mapping and ablation in VT. So in patients with hemodynamically unstable VTs, we perform a sub-cellulite based on ablation in sinus rhythm. This includes a rate potential, desalination zones, and low voltage, fractionated potential, and scar homogenization. Recently, peak frequency mapping has gained attention for scar-based arrhythmias. What is peak frequency mapping? An insight mapping system automatically measures and annotates the highest frequency associated with mapped inter-cardiome EGMs. While dominant frequency annotates signal energy and frequency, peak frequency mapping only high-frequency alone. This technique identifies area of slow conduction and it can also discriminate near field from far field components. Peak frequency mapping is automatic and highly reproducible. It has been applied to ischemic VT substrate. Highlighted peak frequency often co-localized with desalination zone and VT is smooth and it may predict potential ablation site. So we sought to assess value of PF mapping in ARVC originating from the thin-walled RV. And we sought to evaluate the relationship of this PF map and electro-anatomic mapping in both endocardium and epicardium. A total of 20 ARVC patients with VT were analyzed. And the relationship between frequency, more than 220 hertz, versus desalination zone, bipolar voltage, and successful ablation site were evaluated. This is the baseline and procedure characteristics. Mean age was 36 years and 60% were male. And prior ablation was two times and 90% received prior ICD implantation. Medium VT cycle lengths are 290 milisecond and on average two types of VT were induced. The most common critical site was RV basal free wall followed by RVOT and RV basal inferior. Bipolar scale in endocardium was 3.6 square centimeter and the unipolar was 42 square centimeter. In epicardium, bipolar scale area was 35 square centimeter and the unipolar scale was 55 square centimeter. This is an example for electro-anatomic mapping on the epicardium. The low voltage area on voltage map corresponded to desalination zone, ice current rate activation map, and furthermore overlapped the high frequency area, more than 220 hertz. A total of 14 desalination zones were identified, and 12 of them were concordant with high-frequency region. This figure shows relationship between frequency and bipolar voltage. There are no correlation frequency and bipolar voltage, but highlighted red mark, the point within deceleration zone were located on lower bipolar voltage and high-frequency area, both in endocardium and epicordium. The cutoff value of frequency within deceleration zone were 208 hertz in epicordium, and 289 in endocardium. So deceleration zones were characterized by low bipolar voltage and high-frequency electrograms. So 18% out of 20 patients' successful aberration sites showed peak frequency more than 220 hertz. 12 out of 14 deceleration zones corresponded to peak frequency more than 220 hertz. However, many peak frequency sites were noted that did not correspond with this circuit. So like this figure, which is successful zone overlapped high-frequency zone and corresponded to deceleration zone and the low-voltage area, but high-frequency area was diffusely distributed, so we can't specify British successful aberration site by only high-frequency area. This figure shows frequency and the unipolar voltage of aberration point. Totally, seven patients required endocardium aberration. We compared endocardium aberration versus only epicordium aberration. Blue mark successful aberration site in endocardium. Red mark opposite site to successful epicordium aberration site. So endocardium frequency are similar in both endocardium and only epicordium aberration group, but endocardium unipolar voltage is lower in required endocardium aberration group. So although PF mapping alone on the endocardium may be insufficient to determine the necessary of endocardium aberration, unipolar voltage may be useful. In summary, 85% of deceleration zones were concordant with high-frequency region, more than 220 hertz, and EZMs of deceleration zones rate potential were low bipolar voltage and high-frequency. In patients who required endocardium aberration, unipolar voltage was significantly reduced while frequency didn't prove to be useful indicator. PF appears to be sensitive, but not specific to BT circuit. The interrogation of PF maps with deceleration zone low-voltage area were useful in distinguish near-field potential even in the epicordium. However, frequency alone didn't correlate with electrogram amplitude in either endocardium or epicordium. Thus, even when high-frequency potentials are present, they should be interpreted in conjunction with abnormal electrogram characteristics and underlying cardiomyopathic substrate. Thank you for your attention. We are running a little behind, but we could take one quick question if there are any questions. So, a question about the cutoff value of the frequency, so I referred 220, the previous report, so I ran on LV, that's cutoff value, clearly described as ground deceleration matched the high frequency area, so I referred this frequency area, but actually I adjusted more than 300 hertz, but it exceeded more than 300, deceleration zone disappeared, so I adjusted 220 hertz. Thank you very much. I have next from McGill University at Tulverma to talk with us about the long term outcomes of ultra-low temperature cryoablation for monomorphic BT. Thanks very much for the opportunity to present to you the longer term outcomes, and I'll just wait for my slides to come up, but, there we go, so first of all I'd like to just show you my disclosures, and you probably are aware already that there's been a lot of literature on using the ultra-low cryo catheter for BT, there have been case studies, there have been smaller cohort studies, but then we did publish the cryo-cure BT study last year as a late breaker at ERA, which showed the full cohort at six months. Katya already explained to you the fundamentals of ultra-low cryo, so I'm not going to go into all of those details, other than to say that depending on the length of the freeze, you can really titrate from four millimeter depths all the way to plus 11, 12 millimeter depths, allowing you to really go transmural for ventricular tachycardia substrates. The cryo-cure BT trial, just to remind you about some of the acute results, we were able to eliminate the clinical BT in about 97% of patients, and all BTs at the end of the procedure in about 85% of patients. Now in these Kaplan-Meier curves, you are seeing this dark line in the middle. The dark line in the middle represents the six-month outcomes that we reported in the cryo-cure BT study, and now we've extended that follow-up for another six months, and what you see is that when you look at all events, there is a progressive decline, and that's not surprising given the fact that we know that ventricular tachycardia tends to be a bit of a progressive disease. What I want you to focus on is the freedom from ICD shock, because those are the numbers that historically have been reported by other trials, and you can see that at the end of that follow-up, the non-ischemic still had a success rate of about 60%, and the ischemic patients at 12 months still had a success rate of about 76%. And just to put that into context of other trials, you can see here that in this first in human study, we were getting both an acute and chronic effectiveness that was really numerically anyway superior to many of the other BT trials that had been published in the past. But of course, looking at any episode of VT greater than 30 seconds, we know is not an appropriate endpoint, just like it's not appropriate for atrial fibrillation, and all of these patients have devices, so it is actually possible to look at burden, and this is really where I want you to focus your attention. From six to 12 months, this was the incremental increase in VT burden for the patients. You can see that it wasn't very much at all, and so enduring success is possible, and what was actually very interesting is that nearly 30% of all the recurrences that we saw over this 12-month period consisted of fewer than three ATP events and no shocks. Furthermore, there was a 12-month sustained decrease in the use of antiarrhythmics, in particular amiodarone. If you look at harder outcomes like freedom from hospitalization or a combination of freedom from hospitalization or reablation, you see that over the 12 months, nearly 90% of patients were staying out of hospital because of VT and were not getting reablated because of VT. So again, very impressive enduring results. We did a few statistical analysis for predictors of recurrence, and what was really very interesting is, and this is no surprise I'm sure to any of you, that ejection fraction was clearly the biggest predictor for recurrence. So if you had an ejection fraction that was 20 to 30%, you saw that those patients really did the poorest, whereas those patients with ejection fractions of greater than 30% were really the ones who had more enduring success. Not surprising at all. The low ejection fraction means more sicker patients, more severe disease, and probably more progressive disease. If we look at this data here, this was a 2023-era survey, and actually, it's funny because this has nothing to do with the acute results or the longer term results, but look at this. When would you perform VT ablation in first due procedures in patients with ischemic and non-ischemic cardiomyopathy? And you can see here that the blue bars are ischemic, the red bars are non-ischemic, and look at this. After the first shock, people are not very excited about ablating their patients. After multiple shocks, maybe they'll consider it for the non-ischemic, but some people are waiting for incessant VT or incessant ATP episodes before they're ablating their patients. So what this is saying is VT ablation is still problematic, it's still difficult, and people are not super happy about doing it, with the exception, perhaps, of Bill Stevenson and the group at Vanderbilt. But if you look at where we need to go, we need to develop tools that are going to make this procedure more democratic so that the people who are not the Bill Stevensons of the world can actually do these procedures. And so that's why we've now moved into the Fulcrum VT US Pivotal trial. It's basically happening at 20 sites, 206 patients will be enrolled, we're already well into that enrollment, you can see the patient population, and this is really the next step from the CryoCure VT study, and I think it's going to be really interesting to see what these results are. So in conclusion, a comparison of 6-12 months post-ablation versus the initial 6-month period showed a reduced rate of VT recurrences and ICD shocks, a persistently low VT burden, with a further persistent reduction in the use of amiodarone, and continuing equivalency between the outcomes, particularly the hard outcomes for non-ischemic and ischemic cardiomyopathy, some encouraging signals about the fact that most of these patients are staying out of the hospital, they're not getting reablated, and furthermore, we saw that very, very interesting enduring result with respect to burden. Fulcrum VT will be the next step, and hoping that we can present that at the next HRS. Thank you very much. I was just wondering about the relationship that is less of a contact force is less of a factor as to the length of time that's spent on the VT. I mean, so, a lot of people VT, you know, some of them are contact force, some of them are troubleshooter. So I was wondering if, with the VT, you were talking about the contact force is less of a factor. Yeah, so the question here was, contact force seems to be less of a factor for this catheter than, let's say, radiofrequency, and you're absolutely right. It's really about being in contact with the tissue, but not necessarily pushing the catheter against the tissue. In fact, you get a more optimal lesion when you place the catheter parallel to the tissue rather than perpendicular, although you get lesions in both directions. So, no, contact force is not important. It's the duration of the freeze. And what's interesting is when you're actually doing these ablations and you're looking on ice, you'll sometimes see the catheter moving a little bit with the heart, and then as soon as you start to freeze, that catheter is stuck, and it's not moving anywhere. That actually helps with the contact as well. Any other questions? The floor is yours. I have a question. Oh, oh, sorry, sorry. Yes, yeah. Did you observe any coronary injury during the dialysis? Because the lesion is very deep. Yeah, so did you observe any coronary injury given the fact that you can develop such deep lesions? That's a great question. The answer is no, we've not observed that. In the preclinical data in animals, it appears that this ultra-low cryo does not do any significant coronary damage. And certainly in the patients that we have done, we have not seen any evidence of this. What's interesting is that in a couple of cases, we have seen a very small, tiny little pericardial effusion indicating that you've really gone transmural, and that effusion disappears within a few hours. But just like if you're really going transmural in the ventricle and doing extensive lesions, it means you're going through, and yet you're not injuring the coronary arteries. So we haven't seen that clinically at all. Thank you. Yeah, so what is the procedure time looking like for ultra-low cryo versus other modalities? So the average procedure time in the CryoCure VT study was just about three hours, which for VT ablation in a first-in-human study is pretty good. But, you know, Katia presented on a more efficient form of the freezing, and so I anticipate that that's going to get even less. So again, talking about democratizing the procedure and allowing people to do procedures in a reasonable time frame, that's not going to keep them away from their families. Thank you. Thank you all so much for being here this morning. We've had four really great presentations talking about new mapping and ablation techniques for VT, and appreciate all of your attention. If you have any other questions, then please feel free to engage the speakers on your own.

ventricular tachycardia

cryoablation catheter

ultra-low temperature

pulse field ablation

electro-anatomical mapping

CryoCure VT trial

Fulcrum VT US Pivotal trial

novel mapping technologies

ablation techniques