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Pulsed Field Ablation for Ventricular Tachycardia: ...
Pulsed Field Ablation for Ventricular Tachycardia: ...
Pulsed Field Ablation for Ventricular Tachycardia: Exploring A New World
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Good afternoon, yeah, now the microphone is working, welcome to this session, my name is Andrea Sarkozy, I'm from the University Hospital of Brussels from Belgium and I have the pleasure to chair this session together with Mohan Viswanathan from the Stanford University from the U.S. And I think because just to save some time we will immediately start with the best session of the afternoon, the session is going to be about pulse field ablation for ventricular tachycardia and exploring a new world and I have the pleasure to announce the first speaker, Dr. Arva Younis from Cleveland Clinic and he's going to talk about pulse field ablation for idiopathic VT substrates, preclinical evidence, please Dr. Younis. Thank you so much, dear esteemed panel, dear colleagues, thank you everyone, it's a great honor to be here. Today I will be sharing our experience with PFA for idiopathic VT substrates and showing some preclinical evidence. These are my conflict of interest. We all know that the outcomes of RF for VT substrates are not great, there is a lot of room for improvement and there are so many mechanisms to explain why are we limited with our results in RF because oftentimes we are able to map it and we know where is the circuit or we know where is the PVC but then we cannot penetrate, it's sometimes because of challenging locations, sometimes thicker tissue and oftentimes because of variable scarred tissue that we don't know what to deal with, with RF. Preclinical evidence from the PFA showed that we have a huge benefit as we've shown before and I know Dr. Carruth and Eddie have shown before that we can penetrate scar very well with PFA or much better than RF, we are able to penetrate below the scar and homogenize the scar much better than with RF but we also are able to create greater lesions, bigger lesions with a single shot, deeper and wider which may be beneficial when we ablate the ventricle. In contrast to what we do with the atria where PFA gained its great reputation because of safety where contact force may be not that important, we have shown that in the ventricle contact force is very important because with increasing contact force using a focal point catheter, we can increase our depth from a mean of 3-4 to a mean of 10 meaning that contact force is important, however we need to pay attention that at the end even with PFA we are still delivering high dose energy so thermal injury will be there with PFA if we get high dose or high contact force and high voltage we will have some sort of thermal injury. In the ventricle when we are ablating in the LV summit or septum and we have 1.5 centimeter then it is okay to have superficial thermal injury, it's less relevant than when we do in the atria but we have to keep this in mind that with increased contact force we will or we might have thermal injury as well. But what about also scarred and redo area because many of these patients have some sort of a scar that we often times don't understand, it's not always pure LED in fact but sometimes a mixed substrate and often times especially in bigger centers we see many patients that already have undergone an RF ablation, so how do we deal with these patients? To test this we had a study in which we randomized pigs to undergo an RF superficial ablation to try and create a redo environment and then go over and do RF or PF over the created scar before and then we survived the animals for two to five days and then we sacrificed and looked at the histology and as you can see on the right side the bar graphs the results for the PFA were the same meaning that if I have a mixed structure of scar or a redo environment that was caused by a prior RF my ability with the PFA to penetrate through and create was very similar to my ability when we did the lesion on a healthy myocardium whereas with RF, RF was very limited and often times we didn't even penetrate below the prior RF so you would see a superficial hemorrhage, you would see signs that you were at the right location but there was nothing below the previous scar. What about PVC because often times as we said before we find ourselves dealing with locations that are very challenging, moderator band, the PAP muscles, the LV summit where not only deep penetration is needed but the ability to maintain stability becomes extreme challenging and we know from RF studies that if we aim to get to six or seven or eight millimeter depth then with all the focal points, maybe with Q dot not but we would need to stay on the ablation for a long period of time. We would stay for two minutes, sometimes three minutes, monitor our impedance and be worried about the steam pups and monitoring everything for a very prolonged time. So can PFA answer this? Can PFA now with a single shot deliver better lesions? I removed my slides just now because Dr. Karuth will show some from his work about ablating in target areas and I don't want overlap but I will show our experience with a focal point catheter. The paper of Dr. Karuth was published in Circulation A&E last year. It's a very nice paper that discusses the faropulse catheter on these locations. We did something similar but using a focal point catheter in four different targets, the LV septum, the papillary muscle, the LV summit and the epicardium and then we survived the animals and we looked for safety as well as efficacy. Just because of the sake of time we'll advance. These are some images. Obviously we were guided by ice and we shoot the coronary for every animal before and after, monitored for ST elevations and for the LV summit we went from the CS. These are the results. In that study we had many lesions. We had a total of 10 animals. 37 lesions were delivered with RF. 48 lesions were delivered with PFA and these are the baseline characteristics of the ablations. When we go to the results we start with the LV summit and there's a bigger advantage for the PFA in terms of depth. RFA lesions were much, much smaller. Often times we couldn't even localize them. Again we are ablating from the CS with a focal point catheter. When we look at the papillary muscle there's a huge difference between when we delivered PF lesions in contrast to RF lesions and this is again because of the stability, because of the ability to deliver a better lesion in an adequate time with a greater contact that will give me a very similar lesion to everywhere else in the healthy myocardium. One thing, piggies are very sensitive to arrhythmia and every time you ablate in the ventricle you are prone to have a lot of arrhythmia and we have been seeing this with RF over the last five, six years. With PFA it wasn't like this. We did not see any VT or VF when we ablated on the pap muscle. On the epicardium both were lower, both PFA and RF were lower than on the endocardial side, but again PFA was able to create larger and bigger lesions than the RF. Obviously we avoided going near the coronaries, so we shot the coronaries, we marked where are the coronaries and we took at least a one and a half centimeter margin away from the coronaries. In this study we did not see ST changes, but again we were away from the coronaries. The last project that we are working on and hopefully will be publishing soon is to try and titrate and create something similar to the ablation index for PFA using a focal point catheter. The idea is we don't always want to create larger lesions. If we have someone healthy 50 years old with a very localized PVC then obviously our target should be different than when we aim with an LVF of 20 and we want to do a scar homogenization. We want to be limited, we want to be precise and we want to be as small as possible yet deep. This is the aim that we want to be able to find an ablation index that we can, similar to with RF, say okay if I want a lesion that is three millimeter this is what we'll do and if I want a lesion of 12 millimeter this is what I need to do. This is a plot showing the performance of the ablation index method and we can see that with five, actually if we take the orientation, with five different parameters that are taken into the account of the formula, voltage, number of applications, the force, very important the catheter orientation which is measured by the focal point catheter and can be seen on the arrhythmia system and the multiplication between the voltage and the number of application. If we put all together in a formula then we can come with an ablation index that can give you a lesion depth from two millimeter to 12 millimeter and repetitively. So you say okay I want that high force and you can still get the 10 millimeter. I want to thank everyone. I'm the lucky one to present it but animal work takes a lot of work and thank you to all my friends, Dr. Wozniak, Dr. Santangeli, Kara from Boston Scientific and thank you for listening. In the interest of time we'll go ahead and move along. Our next speaker is Dr. Jacob Koruth coming from Mount Sinai Medical Center and today he'll be speaking on pulse field ablation for VT looking at scar based substrates. Thank you Dr. Koruth. Thank you chairpersons, thank you HRS for this invitation to speak about PFA and Dr. Yunus congratulations on your work. I read your papers. I'm a big fan of your work. My task is to talk about scar based VT and there's going to be some overlap because there is only so much work being done in the world of VT and PFA. These are my disclosures and importantly Drs. Watanabe, Shinohara and you are responsible for many of the pictures in this presentation and you see my disclosures. I'm going to step back a little bit because you may have heard similar talks on lesion depth and width and I want to just take a step back in an attempt to try and explain to all of you how best you should approach all these new catheters that are going to be coming into the world of VT PFA. The question you need to ask yourself is what is the electric field for that particular catheter? Now we are not going to be using multi-electrode catheters that are big in the ventricle. We are going to be using focal catheters. So you need to understand what the E field is. The next question you ask is show me the lesion so that you understand what the morphology of each catheter's footprint is going to look like. Is it going to be a homogenous ablation? Will there be hemorrhage in the center? Do these differences actually matter? And then we come to the important concept of contact. Now Dr. Yunus just showed that contact is important and I wanted to address this paper which is very important because it teaches us something about pulse field. This is a paper from Howard and Dr. Verma showing that even if you're offset from tissue, meaning you're not in contact, you can create a lesion. And that's just because pulse field creates lesions by electric field at a certain intensity. So if you're close enough and that tissue gets exposed, it will create a lesion. But remember, for making good effective lesions with current generation catheters, you have to stay in contact to make your best lesion. So contact is important. As Dr. Yunus just showed, Dr. Nakagawa also has shown that force makes a big difference. But the difference between force with RF and PF is that as force increases, it's the depth that's impacted the most and not the width. Something just to keep in mind. We know repetitions can make a big difference. That's the only tool that we have currently with the current generation focal catheters to make the depth go up. Now I want to share with you something more akin with an opinion not really supported by lots of data about how you should approach the concept of force with small footprint catheters and big footprint catheters. This is ventricular tissue. Remember, small footprint catheters are inherently unstable. And that's why force is important because as you increase force, you get improved stability, some improvement in coupling, coupling being the amount of electrode in contact with myocardium. But what you get in the myocardium and the ventricle is tissue compression, which is a significant factor that delivers these deep lesions with PF. You also get tenting and stretch in the thinner structures like the atrium. So keep that in mind. And that's why force, I believe, is important for these small focal catheters. When you come to large footprint catheters, the design of these catheters are that they're a little bit compressible. So they're inherently stable and force doesn't make such a big impact because you really can't compress tissue with these large surface area catheters. What you do get with increased force is the compression of the tissue and improvement in coupling, adding some depth but a bigger impact in width. Remember with all PFA, whether the idiopathic VTs, scar VTs, the area of pacing that comes with the ablative pulses is significant and you'll activate myocardium, something you won't appreciate in the atrium, something you'll appreciate in the ventricle only if you're looking in an arterial waveform or intracardiac echo. And remember, if it's not R-wave gated, every now and then you'll run into an issue with ventricular fibrillation, which in the world of VT and scar is not a big deal, but you should be aware of it. I'd also like to point out that when you pace during these pulse packets, sometimes the catheter gets even more stable when you're on top of a papillary muscle. So it's not always a bad thing. These are some of the slides that Dr. Yunus was referring to. And the point here is that for mobile structures like the papillary muscle and the moderator band that you see over here, it's a perfect tool to make lesions because you don't need prolonged, sustained, high-quality contact. Coming to scar, and this is work done by Dr. Gerstenfeld, Dr. Anter, Dr. Damian McLevich and our group, and what we are showing here is a porcine infarct, PFA applied endocardially, and you can see this area of lesion going right through the scar. The scar conducts, allows the E-field to go right through as opposed to thermal energies. This is an example of PFA-induced scar, something similar to what Dr. Yunus showed. You see the PF lesions going right through. This histology section, I guess you don't see my mouse, on the left top you see the PF on top and below. In the bottom you see an RF scar with PF going right through, but what I really want you to pay attention to is the right upper corner where you see those four black arrows. Now, everything dark pink on the epicardium is spared myocardium. Everything light pink but surrounded by the yellow dotted lines is ablated with PFA. Everything in this dark black region is the ischemic scar. Now you see these three little islands marked PFA, PFA, PFA. These are islands of surviving myocardium within the scar that have been ablated by PF. And remember, PF has an affinity to build up the field at these interfaces of scar and healthy tissue, which is why I think PF is the best tool that'll get us the best results in any type of scarred environment. On the left over here you can see a small island of tissue with two little blood vessels that has not been ablated by PF, likely because we were not over that region. What about fat? Here you see an example of a lesion applied over epicardial fat and you do see the PF lesion extend somewhat. Now it will be impeded and if the field is big enough you probably can get a decent lesion. This is some modeling work by the group from Spain, Dr. Gonzalez-Suarez, who basically shows that based on modeling, if you have fat within the myocardium inside scars, something that we see in human infarcts, PF not always is a bad thing. In fact, in this particular model they showed that the depth of the lesion is actually enhanced a little bit. So maybe PF, even in fatty infiltrated scar regions, is the way to go. What about if you want to get a big lesion? You can use bipolar PF. Remember, PF, just like RF, can be applied across two catheters. You get edema. Whether it's across the septum or across the free wall, you can get really big transmural lesions. The advantage here is that you don't have to worry about steam pops, no char. You don't have to worry about the ventricular septum rupturing and causing a VSD. That can happen with radiofrequency because PF does not destroy the connective tissue. It will thin but likely not give way over time. If you decide to go to the epicardium, the same rules apply. Because PF is not lost to the blood pool, you get a slightly deeper lesion. But remember, every time you're in the epicardium, you need to ask yourself how much coronary spasm will that particular catheter cause and how far away do I need to be before I end up with spasm. If that's the case, you have to decide whether you want to switch to radiofrequency or premedicate with the right dose of nitroglycerin. An example of an application given right over the LAD, and yes, we do cause medial fibrosis and some intimal hyperplasia, but you will never acutely occlude the vessel with thrombus like you would with radiofrequency. And here you can see, despite applying over the fat pad, you see PF lesion going right through. What about RF and PF and PF before RF? This is Dr. Verma's data showing that it can add depth, although the sequence didn't make that much of a difference. I want to end with two more slides. This is an example of a catheter that has temperature sensors on the surface, the lattice-tip catheter. And as you deliver PF, it uses the temperature feedback that actually there's a small thermal effect with any PF. And it takes, it provides us that thermal feedback so you can qualitatively tell what lesion was good or bad. Here you see the temperature go up slightly. Here you see the temperature go up, then down, then up. And here you see a significant rise. And this means that this lesion is the best, this is the worst, and this somewhere in between. I'm going to end with what I really think is the future of BT ablation and PFA, is because PF is the right energy source for anything scarred, I think a powerful generator that can make a transmural lesion 15 to 20 millimeters is probably the easiest and best way to homogenize scars and target tissue that's important. This is an example of a catheter that will be presented as a late-breaking trial on Sunday by Dr. Reddy, it's an eight-point French deflectible force-sensing catheter that uses monophasic PFA, different from all the other catheters, with a blended micro-nanosecond pulse. Oops. And I skipped, how do I go back? Well, the point that I'm making is that this catheter can make these really large lesions, and to the point, I'll show you my backup slide, this is an application in the left ventricle causing epicardial spasm, and in the late-breaking trial that you will see, you will see examples of ET cases where endocardial applications take away signals on the epicardium. With that, I'll stop. Thank you. Thank you, Jacob, and we will come back with our questions after the next two talks, and the next speaker is Dr. Pannone, and he's going to talk about, from the University Hospital of Brussels, and he's going to talk about the early clinical experience with the large full pin catheter. Dear Chairman and dear colleagues, thank you for having me here today. I'm Luigi Pannone from University Hospital of Brussels in Belgium, and I will present about Passive Field Ablation for VT Substrates, Early Clinical Experience with the Lattice Tip Catheter. These are my disclosures. So this is our first experience on the use of Lattice Tip Catheter for Ventricular Tachycardia Ablation. And in this original paper, we included four patients, and we evaluated feasibility and safety of VT ablation with the new Sphere 9 catheter. As you can see on the right, we have pretty much different etiology. So we have one patient with Brugada syndrome, one arrhythmogenic cardiomyopathy, one patient with ischemic and non-ischemic cardiomyopathy. And we observed that both PF and RF are feasible, and we also observed that we describe a PF-first approach for the right ventricle and RF-first approach for the left ventricle. We used the ventricular PF pulse for the ventricle and also ventricular RF 30 to 60 seconds application. Since our first cases, we observed that it's actually a quite fast procedure compared to a standard VT ablation. It's around a three-hour procedure. And also, we observed that none of the past field applications induced any ventricular arrhythmia or ventricular fibrillation in our patients. Irritative firing is a new phenomenon that we described. Also, we observed a quite versatile tool. As you can see on the right, up, we treated with this patient, a patient with Brugada syndrome, and down, a patient with ischemic cardiomyopathy. And our experience has then been replicated also by the colleagues from Prague, Prof. Pekel and Prof. Kaltzner, in their paper. And actually, they confirmed our results observing a quite fast procedure. Also, they observed a good VT ablation outcome with the freedom from any VT of around 80% at the three months follow-up. And our colleagues described the PF ablation on the picardium with the spasm on the coronary that can be resolved by nitrates administration. And also, they described some kind of difficulty in reaching the posterior mitral valve region under the posterior mitral leaflet. And this sometimes needs to be overcome by a four-millimeter tip catheter. And I have the pleasure and the honor to present also the results of the ABA registry. This is a courtesy of Prof. Sacher that presented these results at AERA during a late-breaking clinical trial session. This is a multi-center registry, European Registry of AFERA in VT ablation. We participated together with other centers and also Prague. And we included all the patients treated with AFERA system and VT, VF ablation, or PVC ablation. We evaluated, of course, both safety outcomes and also efficacy outcome. And we included a population of 126 patients. And as you can see, it's quite a unique population, because up to 30% are non-ischemic patients. And two out of three patients are reduced. So only one out of three is a first VT ablation procedure. So it's a sick population. And it's a complex population. As you can see here, 20% of patients had the epicardial VT ablation. We used, in most of the patients, so 45% of patients, we used both PF and radiofrequency to target the substrate. And the acute success was around 80%. What about complications? So the complications, we observed the major bleeding in two, tamponade due to epicardial access in one, and the cardiogenic shock in one. Thromboembolic events in two, and VF in one. So for thromboembolic events, these were both after transeptal approach with ACT more than 350. And for the ventricular fibrillation event, it was caused by a breach in the catheter with a current leak to the patient. Actually, after this event, the catheter manufacturing was changed, and we didn't observe so far such an event. It was also a long procedure with a lot of catheter manipulation. We had plus cardiac transplant in 5% of patients, and the efficacy is promising. As you can see here, at six months follow-up, we have freedom from VT in 70% of patients. And if it's a de novo procedure, up to 80% of patients were free from any recurrence, and 68% for redo procedure. So in such sick population, it's a promising result. And I will present some cases that we performed in Brussels with Professor Cossi. So here you can see, this is our first commercial case ever with Afera. And this is a patient with Brugada syndrome and previous failed ablation. As you can see here, the toracoscopy image, we went in 2022 in for epicardial VT ablation, substrate ablation, because the patient had VF and shock of the defibrillator. But as you can see here, the huge, the thick epicardial fat prevented us from ablating the substrate. So the patient had a recurrence of VF and of also VT. So we went back in with the Afera catheter. And this is the video of the procedure. So we performed a substrate map of the right ventricle with the Afera catheter. As you can see here, it's a fast map. And so substrate map, voltage map on the left, activation map on the right. And as you can see here, of course, we have a activation delay in the RVOT, but also in the RV lateral. And we also observed these VT coming from the right lateral wall, where there is this scar region. So we homogenized both the scar on the lateral wall of the right ventricle and, of course, the scar on the RVOT. That is the typical region of Brogada syndrome. And actually, the final result is this. So as you can see on the left, the scar. And on the right, you can see the activation map. This is another case that we did. So our hemogenic cardiomyopathy patient with ICD and shock of monomorphic sustained VT. This is the activation map on the left and the voltage map on the right. You can see that, actually, we have a late activation in the lateral wall of the right ventricle and scar in the RVOT. And this is after our ablation. So we homogenized the RVOT and the RV lateral windows, this VT, that we could map completely in the right ventricle, as you can see, with an isthmus in the middle of the RV lateral wall. And I will show you. So these on the left are gorgeous middiastolic buffets. So you can see very nice definition with the unipolar signal on the afera system, the closest bipolar. So it's actually similar to unipolar. And also, what we did, as you can see down here in the slide, is we applied a reversible pulse. And we obtained the interruption of the tachycardia. So proving that in the green spot here, this was the isthmus. And of course, we consolidated with both PF and RF, and this is the final result. This is another patient with arrhythmogenic cardiomyopathy. This was a redo patient. So this patient had the previous ablation for monomorphic VT. It was only endocardial ablation. The patient went back to our lab with, again, a sustained VT. We did a redo endo-AP ablation. And this is the endocardial substrate map pre-ablation. As you can see, RVOT scar. And this is the epicardial substrate map pre-ablation. So as you can see, we have a huge epicardial substrate, both RVOT, RV lateral. And here up, we can see endocardial remap after epicardial ablation. So what we did is we performed PF applications on the epicardium, as you can see up on the left and up on the right. So we targeted the substrate in the epicardium. And after, we performed endocardial remap after epicardial ablation, as you can see down on the left and on the right. So the message is that, actually, PF epicardial is transmural only in the RVOT anterior, as you can see from the endocardial remap, but not on the RV lateral. Probably because the RV lateral is too thick. So we cannot reach transmurality from the epicardial side with the PF. So we had to complete the lesions from the endocardial side. In conclusion, so this is an early experience on sick population with the complex ventricular arrhythmias. Of course, the results are promising, both safety and efficacy. But we have limited data on optimal energy delivery, so both PF, RF, or both. And also, we are working on energy titration for transmurality. Thank you. Okay. Thank you very much, Luigi. We'll move on and save their questions for the talk from right after Peter's talk. So I'd like to introduce Dr. Peter Pichel from Prague, who'll be presenting his early experience pulse field ablation for VT substrates, early experience clinically with the focal tip catheter. Welcome. Thank you. Dear chairmen, ladies and gentlemen, thank you very much for the invitation. I would like to thank for the opportunity to present our experience. So my task is to talk about the focal catheter and just to bring up the topic of pulse field for VT. I believe the main advantage, once you look for the large lesions, you don't see images like this with the steampop. This is RF animal experiment. This is not a pulse field, and although there might be a lot of different applications, the pulse field, we've never seen anything like this, and I believe that should be one of the main reasons why we should also look into it. Just to remind the audience, I'm supposed to talk about the focal catheter, and there's been a recent paper that tries to harmonize definitions and nomenclature for these catheters because there will be many, many different catheters when we attend the pulse field day, and the focal catheters, according to this classification, should be the ones that are just the size of four millimeters, something that are conventional catheters that we are used to work with. So these are our data that we published. These were done in two centers, 44 patients, and what we used for the pulse field was available to us, which was the Centauri PL pulse field generator, which can be used with the catheters that are available for different manufacturers, so it can be used with Smartouch or with TactiCat or with the Intel-Enaf catheter for ablation, and so it's easy to integrate into your 3D mapping system, and we use it both for ventricular arrhythmias, for PVCs, and for structural heart disease, VT, and there seems to be a better outcome for a PVC, which I will come later on to. So although it was shown previously very nicely, the large footprint catheter makes more sense for large lesions, there are areas that might be difficult to get to, so this was our case that we did ablation with a larger footprint catheter, and we somehow had a recurrence and we couldn't really suppress this arrhythmia until we got used to, we had a focal catheter just underneath the, this is tricuspid valve, so this is just underneath the inferior leaflet of the tricuspid valve, so what I'm trying to imply here, there are some locations that the large footprint catheter might be difficult to get to, for example, papillary muscles, if you really look for, to get deep beyond or behind or below, that might be difficult, so still, just we will use these focal catheters because there will be areas that will be easier to get to, and I will include some of the kind of situations and scenarios. So this was one case that actually changed our mind to think about this, so this was a patient with non-ischemic cardiomyopathy with multiple VT morphologies, they look more like something from the LV summit, although they were sustained, and when we mapped and looked at where's the earliest activation, the patient had there some PVC coming from that region, and the LV endo was quite late compared to the onset of the QRS, but what was strikingly early was, and very fragmented, was the distal CS, or great cardiac pain, somewhere in this region, and the problem is, we also could pacemap there, but the problem is, if you apply RF in that region, epicardial in the CS, you're usually limited by the power impedance increase or temperature, so the pulse field might be an additional way how to do it, so we did apply in the CS, we obviously applied also from the endocardium and worked for the patient for acute outcome, and there was no changes acutely on the coronary angiography. We looked more into it, and we gathered and published this 11 patients that mostly had a previous RF applications, and on purpose, we went to the CS with the pulse field catheter, and the acute success was not 100%, obviously, if you are there early on, like minus 30 milliseconds, the pulse field will do the job, if the prematurity is not that good, it might not work because it's farther away, obviously, what's endangered here is the coronary arteries, we never apply the pulse field on the top of the coronary artery, there was always some distance, and we shoot coronary prior and after, and there was surprisingly no real major spasms in this particular situation, it might come in this small series, it was not there, my kind of interpretation is that there might be this epicardial fat that is somehow protecting the vessels, and somehow prevents this to happen, and it's also small catheter focal ablation, it's not like a pentasplane on the capotrichospatism. The other, also used a similar, this is a subcephoid axis to the same location, LV summit, and for this kind of arrhythmia, and somehow, this was used to overcome the epicardial fat that is usually located in this location, which work, and after nitroglycerin pretreatment, there were no coronary artery spasms, obviously, the spasms may come, this is a case that we had, we had a RVOT ectopy coming out, it was a third procedure for the guy, for whatever reason, and that's why we decided to go with Pulsefield, hoping that we have a better chance to succeed, and the best kind of prematurity we found in the antireceptor RVOT, and if you look at there, what you find just underneath your catheter is this kind of black hole, which is the LID, and when we apply there, it worked for the ectopy, it was gone, but what we also saw is a spasm of the LID at that particular location, we moved the catheter, the ablation was somewhere there in the antireceptor RVOT, so we moved away after it, so we applied nitroglycerin, which just get rid of the spasms. It's something that does happen, you have to be prepared, you have to look for it, because there was no ECG changes for this, so unless you shoot the coronaries, you don't see that, but I still consider these spasms a lesser evil than the thrombotic occlusion, there is a paper that took or collected patients from different centers, that they apply their antireceptor RVOT close to the LID, and surprisingly, in four of them, they had using this power output, like 30, 40 watts probably, which is a normal setting, they found occlusion of LID, so if the RF, this is RF data, this is not pulse field, you can occlude thrombotically the artery, which has never been described with the pulse field, so this is a paper that looked at that, recently published in a small series of animals, and with pulse field, you may have more acute changes, like a narrowing spasms, but for chronic histological effect, there is more effect of the RF, because of the no intimal hyperplasia, or there may be also a thrombotic occlusion. What we also found, which was surprising to us, was this, and this was a bit scary, this was a patient with non ischemic cardiomyopathy, actually it was hypertrophic cardiomyopathy, it was a large lateral wall scar, the previous seven ablation procedures, a very desperate case, and we were ablating pulse field laterally, and surprisingly, when we did that, you can see the series of applications, so this is the 25 amps application, you have a complete AV block, so what's going on, we are very far away from the conduction system, it should not occur, so this would be the his region, this is the side, so what's going on? And it turned out to be a more technical problem, because when we use smart touch catheter, the catheter has on the top of the distal and proximal ring, these proximal ring electrodes which are used to locate the shaft of the catheter, and what the company didn't tell us, the centauri generator on purpose puts current into these electrodes that are on the proximal part, so this one actually is at the his position, and the reason why they put the energy there, or current there, because if they put 2000 volts into the distal electrode, and they put zero current into these proximal shafts, you have a risk of short cutting the wires inside the shaft, because the catheter was never made for such energies, so generally using the system centauri with this one, although it's off label, for whatever reason, you have to think about these two ring electrodes at additional ablating points, obviously the AV block recovered, because this was very small lesions, the patient two weeks later had a heart transplant, which was the solution for him, and for that, because we could harvest the heart, we could see the lesions that are up to 8 millimeters inside the scar tissue, so it is not like transmural, with this 4 millimeter tip, it's just up to 8 millimeter, mostly 6, 8 millimeters, what people have described in different series, this is from Belgium, they saw irritative firing after pulse field application, in many of those that they studied, to be honest, this is not something we've seen in a regular basis, usually when it comes, usually it's self terminating, I believe it's more to investigate about this, but generally it seems to be transient phenomenon, these are the outcome data for their series, 20 patients, and there are different kind of locations that can treat it with high acute and long term success, also targeting the papillary muscle, which the reason there is because the application time is very short, so you are likely to be stable on papillary muscle compared to the RF, which takes forever to really create a lesion, and there's a third kind of series that was published, 35 patients, that actually somehow replicates this or confirms these data, in this particular study it was shown that for structural heart disease VT, the small tip and the pulse field might not be optimal because the recurrence was higher than expected, but maybe it's more about the strategy, how to ablate these things rather than the kind of failure of the pulse field. So let me conclude that when the focal catheter is used, it's definitely very effective for treatment PVCs. For VTEs, structure heart, large scars, probably we need to learn more how to use this focal one. I believe the large footprint is much better choice. Currently, the small focal catheter can be used in specific areas like the slow great cardiac veins, although we need to learn more how this will work. It's also probably safe to use it close to the cranial nerve because if you go epicardially, but we definitely need more data. Thank you for your attention. Thank you. Thank you, Petr, and then we can start with the discussion. And if you do have any questions, please submit to us with the QR code. And we also have one microphone there for the questions. And while you are thinking, maybe we can just start with the discussion. So my first question is to Dr. Yunus and to Dr. Koroutis, both about this distal cardiac vein PFA application. So I think, Petr, what you have showed was with the monopolar, with the cantilever system. I think, Yunus, you showed the data with the bipolar focal catheter in the distal CS. Do we really think this is safe to go ahead and just do PFA for some arrhythmias when we have also bipolar, when we have all collaboration? What's your opinion? So it looks to be safer and better than RF, yet it's still not great. Okay, it's very limited. When you ablate from the coronary sinus, the maximum lesions that we have been seeing is six to seven millimeter. This will not get you the LV summit if you're on the endocardial side. So the idea of sandwiching becomes handy if you go from the endocard and then do additional from the CS, this is where, but going starting from the CS, I don't think it's gonna get you transmural. It's still better than the RF. With the RF, what we saw, and we tried changing the solution, the irrigation, to try and improve our lesions, but there was a lot of variation, which may be to the lack of our understanding of how good the contact and how big the vessel is. You don't see it, and then you sometimes think the vector is showing you, and you have a good contact force, but the reality, once you dissect the heart, is that your lesion is two millimeter, and then you go and review everything, and you say, well, why is it two millimeter? Everything was okay. With PF, it was more reproducible than RF. That's, I think, one thing that we should. I'll just make one comment. I echo everything that you say, but the one thing that I would say is that when you're using a catheter that's designed to be bipolar across all four electrodes, your PF lesion is gonna be really wide. So if you have a coronary nearby, you're likely better of using a monopolar application with a smaller footprint, but equally deep. Okay. We do have one question. I'll just, somebody has asked a question for Dr. Koruth. What is the right dose for nitroglycerin when you are, presumably, proximity to a coronary? Yeah, so it's my fault for saying the right dose. We know there's a right dose for the Ferropulse catheter on the endocardium for CTI and mycolystimus ablation, and I'm referring to Vivek Reddy's publication in CERQ-EP that showed that if you give three milligrams of nitroglycerin once you support the blood pressure with phenylephrine, you wait a minute, then you give your PF applications, and then you repeat two milligrams every two minutes until you're far away from the coronary artery. So that's for one particular catheter with one dose. The assumption is most 2KB generators will behave the same way, but we won't know unless we check it for each catheter, and once you go into more powerful generators, maybe the doses are even bigger or may not work or may still work. Work needs to be done. Okay, then I have another question. So, Dr. Yunus, you said that about something about thermal effect with PFA, the thermal effect of PFA, and you said that if you increase the voltage, then it may lead to stacking of heat and maybe to steam pops. Now, I am not aware of any of this, at least with PFA in clinical scenario. I don't know if Patrick has ever any experience or anybody else, or what's your comment on that, that can you really pop now with a large footprint or focal PFA, only PFA I'm talking about? So we've never seen steam pops. You can, at the end, it's energy, and as Dr. Kourouth showed, actually now with Afera, the way we monitor how good the lesion is that you look at the thermal changes. So there is thermal energy that will be delivered to the cell. When you look at histo, even with very high contact force, I'm talking about 40, like 40 contact force, 40, 45, repetition for applications, on the endocardial side, we were able to see maximum of three millimeter. Very superficient. In the ventricle, that's safe, okay. However, I think the reason I say this is that, and I like your definition of the PFA, that we should know which tool are we working with when it comes to PFA, because you might find yourself using very high voltage and very high contact force, and you might reach some thermal energy if you did not test it in animal work before, and if you don't know the performance of this catheter, because at the end, it's energy. Okay, Petre, you have a comment, or I see that you're moving. Somebody put it, if you see one pulse-filled system, well, you've just seen one pulse-filled system. It's not a kind of generalized effect like we used to have with the radiofrequency. One point about the steam pump, what really is the scary steam pump, if the RF is the one that the energy is built, or temperature is built up deep inside a tissue, and suddenly, all of a sudden, you have a lot of blasts of gas. So there may be different steam pumps, some of them are very superficial that probably are not dangerous, but the really dangerous in the ventricle ones are the ones that you lose a lot of energy. On the surface, it's cool, but there's a kind of hotspot deep in the tissue which erupts, and if you're lucky, it goes endo. If you're unlucky, it goes epi, and you have a perforation. So I believe the pulse field should never do that, because even if you have some thermal effect, it's superficial, so you're probably safe and not reaching this, and we've tried to optimize or maximize the RF lesions for many years, and we know it's very difficult to predict what's deep inside the tissue temperature measuring on the surface, so that's probably the limit, and that's why the maximum RF lesion is so difficult. Go ahead. Nice work. I'm Takuro Shimura from Tokyo. I learned a lot this session, thank you, and I'm wondering, the pulse field operation is effective for Purkinje-related ventricular arrhythmia, because the pulse should be set for a specific myocardium, right? So I'm wondering why AV block occurred, that catheter, so I'm wondering. So generally, what I try to say is a specific design of the catheter, it's a smart-touch catheter, but it's never designed to be used at the pulse field, and Centauri came and put 2,000 volts, and for each level, they show that can be done, but what they didn't tell us is that just for some technical reasons, they also put some electrical current into this proximal pole, so what I was trying to show, the very proximal pole, which was about six centimeters from the tip, was actually at the HISS region, and that's created a temporary AV block, even, that was the catheter design. For example, if you use Centauri with Tactica, there are no proximal ring electrodes to show visualization of the, they used for impedance-based visualization of the shaft of the catheter, the 3D mapping system, so it's a specific, for a certain catheter, for, that is used in a manner that was never designed with a different generator, because obviously, since smart-touch was supposed to be used with the biosensor, J&J, Medtech, up later. The other question is how, what's the effect of the pulse field on the parking G? So generally, if you start to use it, what you find out, it's the conduction system quite sensitive to the pulse field system. The question is how much durability you also get, so we, if you really ablate a little bit far away from the conduction system, you may have some effect, but the question is whether this is a really permanent effect, or is this only kind of more susceptibility to be stumped, and there is a higher chance of reconduction, because this is something we need to learn, so there might be different effects that have acute, and the kind of durability effect on the conduction system, so be careful, just to say that if the conduction system is very sensitive to pulse field, you should ablate the pulse field, if the conduction system is pulse field, there might be some discrepancies. I'll just add a comment. The AV node is very sensitive to PF, in the sense that you'll see AV block and it'll recover, so you can be six millimeters away from the AV node, and you'll get AV block, so that's well documented, and I think that should be remembered. The question is how does the His bundle behave, and how does the Purkinje fibers in the myocardium behave? I think there's data from the Mayo Group saying that Purkinje fibers can be ablated superficially on the endocardium. The His bundle, which is a structure that I'm a little bit confused about, we have data saying that if your Purkinje fiber's deep in the porcine myocardium, it's spared, and there's data from a Chinese group that was a preclinical study showing that the His bundle can be ablated. My sense is at the right dose, you can ablate all these structures. Thank you. I wanted to ask a quick question to the whole group. Few of you have shown the prior use of RF and then PF on top of that, and you show the depth of lesion penetrates. I wanted to see what your thoughts are on, we all have done repeated RF ablation within the same hospitalization for VT, and we wonder about thermal energy, deeper thermal energy. Is that a concern? How acutely can you go with PF after a recent RF ablation and be safe, and what is the impact of the thermal effect of PF when you've just recently done an RF ablation? I'll take a stab at it. So, RF and PF can be done simultaneously, and there's a CERQ-EP paper from Dr. Verma showing that it adds a little bit. The sequence didn't make that big a difference. Logically, RF followed by PF makes a little bit more sense. The only thing that you need to remember is with RF, you get edema, so your target, if it's deep, can get further away when you come back, and I think that's the same issue with RF. When you go back a second time, but in any setting, whether it's scar, edema, fat, I still think PF is a better option than current generation RF catheters. Yeah, so Luigi, I have a question to you. So, because you mentioned that we started in the right ventricle first PFA and left ventricle RF, so what do you think, when should we start with PF and when should we start with RF? Yeah, thank you. Indeed, in our paper, we described this first approach with PF in the right ventricle and then RF on top, and then RF first in the left ventricle and then PF on top. As, yeah, Prof. Korut was mentioning, actually, it makes more sense to start with RF and then to go PF on top. The point is that when you do PF first and then RF on top, after PF, you will not see anything anymore, so you will have a complete wipe out of the electrograms, and this can be a problem, especially in VT, when you want to see the small fraction of the electrograms under the isthmus, so that's why we are now doing RF and then PF on top, especially after the data from Atul Verma about the combination of the two that can reach more depth. On the right ventricle, we start with this PF first approach, actually, because we believe that it's transmural in RVOT anterior, so if it's not so thick, and so we can reach more transmurality and then apply RF on top, and also, of course, for safety concerns. As we know, the right ventricle is more thin than the left ventricle, so that's why we describe this approach, but this is all a matter of further research. So if I make a comment about the epicardial mapping, I believe it's still important to consider it, especially for non-ischemic cardiomyopathies, because if you just do endomap, and some people hope that if you have a possible bigger weapon that you can prevent epicardial access. Generally, it's a bit dangerous there, because if you have a non-ischemic cardiomyopathy and you just map the endocardial breakthrough in the endocardial kind of surface, and you apply a lot of energy there to get something small, epicardial circuit, you may actually not get the slowest conducting zone. You just slow down the VT, we saw that. So we started with 160 beats per minute, then we went down to 120 beats per minute, then we go to 90 beats per minute, same VT. It's not VT by definition, but with the same tachycardia, just ablating a lot of myocytes from endo, and then we went epi, and we saw a small kind of circuit there, just goes up, and that was it. The problem is also the epi slow conduction may be a little bit away from the endocardial breakthrough, so you don't see the epi substrate or slow conduction from endo, because it's a normal voltage. So I believe we should also emphasize that still, for the mapping purposes, just to do as minimal damage as needed, the epicardial mapping should be part of our momentarium. Yeah, thank you, Petr, that's a right comment. And Jacob, just one last question. Regarding that capture with irreversible PFA, so I still struggle with this, what's exactly capturing. Do you really think that we are capturing under the electrode, or do you think it's a farther zone away, so the irreversible zone around the, I'm sorry, the reversible zone around the electroperation, or do you really think that we are capturing the, do you have any information that the tissue under the? Yeah, I only have data from engineers who've shown me models that show you if the IRE zone under a catheter is maybe five millimeters across, the zone of myocardial capture is like two inches wide. So these pulses are so powerful that you can capture myocardium from a huge area. So loss of capture from a PF application may not really mean anything. It may mean that you killed too much tissue, but I don't think it has a lot of prognostic value in my mind. I think more work needs to be done, but noticing that is still important, because catheter stability and stuff like that matters. Yeah, maybe. I agree with Dr. Koroth. That's an excellent point. In my mind, it's similar to the pacemakers, when you have absolute and then relative. Same with PFA. So you have an area of complete irreversible, and then you have an area which is somewhere between, because if you look at the lesions at one day, two days, three days, four days, the histology, then you will see some areas where the cardiac pathologist was telling us, ah, I'm not sure this will be scar or not scar. I'm not sure. And this membrane, you may be able, with high output, to capture. And this varies between catheter to catheter. So I think we are looking into it with cardiac imaging to try and define what are the borders for the reversible versus irreversible zone, because the partially reversible zone, you will be able to capture. We have one more question from the audience. Can you share any information you might have about the amount of thinning of the wall long-term that occurs with RF versus PF, in particular, like how that might affect redo procedures and so on? You know, I think what needs to be, I mean, I don't think we have that much clear data. It's very dramatic to see a swine tissue that's been ablated with PF, because the tissue really thins out. What we need to understand is thinning will occur with RF also if it's equally effective. But the amount of fibrosis and the kind of fibrosis is a little bit different. RF causes a more contracting, denser fibrosis than PF. So the tissue may be equally thin, but thicker structurally is my imagination. I don't think there's been any detailed study looking at what kind of collagen and elasticity there is between the two technologies. But PF scar typically, in healthy tissue, doesn't fall apart. It always retains a structural integrity. With radiofrequency, if there's enough liquefactive necrosis, some structures will occasionally give way, although it's quite rare. So let me just comment to this. If you're working with the post-venous structure heart disease, which is probably the scenario, you always ablate in the scar. I mean, there's not much reason to ablate in the normal myocardium, because you kill a lot of myocytes. So you're ablating over pre-existing fibrose scar, which is the pus and my, whatever it is. So I wouldn't really expect that much change in the structure of the tissue, because there is something pre-existing. If you do it in the normal myocardium, then there might be some changes later on, and this is something we probably haven't done, because it would kill a lot of myocytes for a human with one doo-doo. I just want a little comment. I'm still following on the right ventricle of my patient. I'm looking at the echoes very carefully, especially when we do an extensive substrate modification. I really still worry. I want to be sure we won't have any aneurysms and any wall thinning in. I think long-term effects, we still need to wait and see. And Dr. Viswanathan, maybe it's time to close this session. I think so. I think so. I was going to ask one final thing. Do you think that, what do you think will be the optimum catheter for VT ablation with PFA? Will it be a focal? Will it be a regional? You know, will it be as wide as a parapulse catheter? What are your thoughts? I think it's a little bit unfair to put everything under VT. So the way we see it at the Cleveland Clinic is there are two different groups. You have mostly healthy myocardium and then some focal. And you have scarred, whether ischemic or non-ischemic, it's still at the end scar that we target. And the catheter design should be completely different because also when we tried with larger focal catheters, I'm not talking about the parapulse. Some things are smaller. You will see heart failure in the swine model. You will see immediately on ice. You'll see lack of contractility, blood pressure drops. So you don't want to substitute one disease with another. So I think it's that we should have two catheters. One would be focal to target PVC, penetrate deep. And then one should be large, but not too large for scar homogenization and to target scars. Yeah, it's for ischemic VT. I mean, the ischemic scar is usually flat and it's a thinning of the wall and it's a smooth surface. So for that, I mean, it's, for example, sphere nine works pretty nicely because you can have good contact. But if you go into non-ischemic cardiomyopathy and some of the kind of spongios remodeling of the ventricle, there are a lot of these recesses and these larger tip catheters might have a problem to get into it. And also if you go into this coronary sinus, for example, locations or some areas, so that for that, you still probably may need both. I mean, for the large footprint, it's very nice because you can do the job very quickly. But for the smaller one, you need to do a much more number of lesions. It goes like the question whether you need a single-shot device for the PV isolation or it's just the need a little bit more applications around the osteocytes. Generally, both will have their role. We will see which will in the end. Okay, really appreciate everyone's, all the panelists and all the talks today. Appreciate your perseverance. It's 5.05 for the first day of HRS. So with this, we will close the session today. Thank you very much. Thank you.
Video Summary
In this HRS session, multiple speakers discuss the use of pulse field ablation (PFA) for ventricular tachycardia (VT), highlighting its benefits, challenges, and findings from recent studies. Dr. Andrea Sarkozy from the University Hospital of Brussels and Dr. Mohan Viswanathan from Stanford University co-chair the session. Dr. Arva Younis from Cleveland Clinic presents initial preclinical evidence that PFA can create deeper and larger lesions compared to radiofrequency (RF) ablation, suggesting improved outcomes for idiopathic VT substrates.<br /><br />Dr. Jacob Koruth from Mount Sinai Medical Center explores scar-based VT substrates, emphasizing the distinct advantage of PFA in creating effective lesions through scar tissue, which is hard to penetrate with RF. He also notes the potential for contact force to influence lesion depth significantly with focal catheters. Dr. Luigi Pannone shares clinical experiences from Brussels using the Sphere 9 (lattice-tip catheter) for VT ablation, reporting promising results and fast procedures with manageable complications.<br /><br />The session also includes insights into safe and effective PFA applications, like those in the coronary sinus for challenging substrate areas, and the potential for new catheters that balance lesion depth and safety. Overall, the speakers underscore that while PFA shows significant promise, particularly for complex VT and scarred tissue, more research is needed to optimize catheter design and application strategies. The discussions also touch on the potential for epicardial approaches and considerations for myocardial thinning post-ablation.
Keywords
Pulse Field Ablation
Ventricular Tachycardia
Radiofrequency Ablation
Idiopathic VT
Scar-based VT
Sphere 9 Catheter
Lesion Depth
Epicardial Approaches
Myocardial Thinning
Catheter Design
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