I think we will start for the sake of time. I'm Lena Riva from the Montreal Heart Institute, and it's my pleasure to chair the session on integrating PFA into our clinical practice. If you have not already done so, please download the app so you can answer, participate in the Q&A session. We will start with the first speaker, Dr. Oza Zorio from Florida, who will speak about should we apply PFA to all AF patients. Thank you. I'm honored to be here, and as it's been said, my topic is should we apply PFA to all patients, both de novo as well as redo AF ablations. Going through the history of atrial fibrillation ablation just briefly, in the early 90s, a lot of work was being done on the biophysics of RF ablation, work by Dr. Haynes. The first atrial fibrillation ablation, which was just an abstract in an AHA meeting, there was no publication or manuscript. This was by Dr. Schwartz in 1994, trying to replicate with a catheter what was done with a maze operation. This was 12-hour operations at that time, 1994. So remember the dates for a little bit as we go through this. In 1998, Bordeaux Group described the triggers, and then atrial fibrillation ablation really took off. And because of that, we saw a lot of changes in the technology and innovation for the ablation catheter as well, going from standard RF to irrigated catheters and then contact sensing catheters. And as the number of procedures increased, we started recognizing the complications with atrial esophageal fistula and PV stenosis becoming recognized complications of RF ablation. It wasn't until 2014 that we had commercially available contact for sensing catheters. This is really important because these catheters allowed us to start using index-guided ablation, which ultimately gave us a chance to standardize atrial fibrillation ablation. This was very important because now no longer only few highly experienced and high-volume centers really could achieve the best outcomes for our patients. And the VSTAC studies highlights that. So in our journey to improve radiofrequency AF ablation, it was 30 years for us to get to the current outcomes we are seeing. This study highlights Biosense Webster's clinical trials. The interesting part of it is because they're all similarly designed, and you can see a reduction in procedure times as well as improvement in outcomes over the decades, or about 15 years of clinical studies. And now we'll fast forward to pulse-fueled ablation. The first described ablation was in, I think, 2008 in an animal, epicardial-based ablations. And first in human studies published by Vivek Reddy was the Impulse PATHCAT 1 and 2. We're using the pentaspline catheter and highlighting how they were able to optimize the waveform with improvements in durable pulmonary vein isolation as well as long-term outcomes. Very quickly we realized that this was a technology that was sparing the esophagus, you know, the fear complication. This has impacts not just for our patients but for us practicing clinicians. The ADVENT trial showed really good outcomes. And perhaps the more important thing to highlight that this is 2023, five years after the first ablations performed in humans with the pentaspline, and we're seeing long-term outcomes similar to that of thermal ablation with the cryo-balloon or radiofrequency ablation. Several other companies have come to the field. The Afera catheter had a randomized trial of persistent AF ablation showing very good outcomes as well compared to radiofrequency. But the journey is far from perfect. We're still learning how to optimize these waveforms, and now we're dealing with catheters that unlike radiofrequency, which the form factor of the catheters were very similar, now you're dealing with different catheters, different electrodes, and different waveforms. And we're learning with time how to, how we can impact outcomes, lesion depth, or even complications by modulating the waveforms or better catheter design. So I think it's fair to say that today, with pulse field ablation, the clinical trials have shown significant improvements in efficiency, efficacy that is at least similar. And I think although it might be similar on an IDE study, it is fair to say that these catheters, it's so much easier to use them. So designing workflows and standardizing the procedure is easier as well. And because of that, I think for the community at large, we're going to be doing better patient care. The safety, although we've eliminated atrial esophageal officially virtually, as far as we know, and there's no PV stenosis, there are now recognized PF-related complications. So this is to say that for me, at least based on my practice, and I think the data supports for index ablations, I think we should be using pulse field ablation for all of our patients, as the question has been posed. What about for a redo? There's a few studies that I have found looking at redo. I'm going to talk about two animal studies and one clinical study. One of the studies did animal, six animals, with radiofrequency ablation. They created inter-caval lines leaving gaps, as well as ablation around pulmonary veins leaving gaps, and ablation in the ventricle with radiofrequency. And afterwards, used the pentaspline or focal PFA catheter to perform ablation on top of these areas that had been ablated before, and in the atria, they were able to isolate and achieve durable linear, not durable, I'm sorry, achieve a block across these lines. Interestingly, if you look at the ventricular ablation, however, when you use PFA in a lesion that had, over a lesion that had been ablated with RF before, it was much deeper lesions than if the repeat ablation was performed with RF. So perhaps a significant advantage for ventricular-based ablations with PFA. Another study looking at humans looked at redo procedures, patients that had the first ablation with either RF or a cryo balloon. And these patients were majority, I'm sorry, about 60, 40% paroxysmal, 50% persistent, and the repeat ablation was performed with pulse field ablation, and you see long-term outcomes that are quite similar to what we see with index ablations of paroxysmal or persistent in some of our well-monitored IDE studies. Another really well-designed study, animal study, they performed either infarct or ablation scar models in the ventricle in swine, in six animals, and afterwards performed pulse field ablation. I'm not sure if this projects well, but you can see that the PF lesions were, you were able to see them and they go beyond the scar area in this model, highlighting that you are indeed able to perform pulse field ablation over a previously RF or a scar myocardium from a chronic MI model. So now let's look about the journey to improve AF ablation. With radiofrequency, it took us 30 years to be where we are today, from understanding of biophysics to the first RF ablations, and then the multitude of trials and technology advancements we have seen. And with pulse field, with the first in human in 2018, five years later, we have 10 catheters, we have multitude of approved catheters, many clinical trials, understanding of complications. We in the U.S. were lucky to have European data, real-world data as we were applying. So I think the speed of technology advancement and the speed that we as a community are sharing knowledge really will make it such that it's easy to imagine that if you're not already using PF for your index procedures or your de novo pretty soon, that's what we're all going to be doing. So to summarize, should we apply PF to all atrial fibrillation ablations, both de novo and redo? My answer is yes. If you look at PFA, it's evolving very fast. It's far from perfect, but it is, it continues to get better. The learning curve is very short, allowing physicians with less volume, less experience to have success rates much closer to the IDE, something that was very challenging with radiofrequency point-by-point ablation. We are seeing progress in the mapping integration as well with new technologies being released. And I think if there's a reason for you not to use it on a redo, perhaps was the mapping integration in the past or the catheter form factor, but we are seeing really new technologies with good integration. So I think this should be what tips the scale for the redo cases as well. Very importantly, there's now animal and clinical data showing similar or better outcomes if you consider the data on lesion depth for PF on redo cases. And as we have more multitude of catheters available, large focal, single shot, or point-by-point, I think PF will be the tool of choice for our de novo and redo procedures. Thank you. We're going to skip Dr. Reddy. Maybe he'll make it on time. Next is Dr. Ed Gerstenfeld from UCSF. And he'll talk to us about how to avoid complications due to PFA, namely hemolysis and vasospasm. Thank you. I'm texting. I texted him. Restart. Afternoon. Pleasure to be here. Thanks. So I'm going to talk about how to avoid, or at least avoid, complications due to PFA. At least think about avoiding complications from PFA. We'll talk a bit about coronary artery spasm, hemolysis. I added in phrenic nerves as well. So this is the data. VIVIC published manifest 17K, so the first 17,000 ablations with the pentaspline PFA catheter, as we've heard. And now it's really up to 250,000 cases, but no esophageal injury, no PV stenosis, no persistent phrenic nerve injury. So hopefully these issues are a thing of the past. Coronary spasm, again, we know about now, but was one of the newer complications, but still not so frequent, 0.14%. We looked at this in a swine model initially using a focal pulse field ablation catheter. Pretty much, well, 100% of the time if we delivered PFA, this is epicardially through a sub-xiphoid approach, 100% of the time we would see coronary artery spasm. And this was quantified by Satoshi Higuchi, our research fellow, and on average he saw 47% narrowing. We did not intervene or give any nitroglycerin, and this does gradually resolve on its own over about 30 minutes. But perhaps equally concerning was that not just that there was spasm, but when we looked histologically at one month and two months, there was evidence of mild, but some, coronary artery injury consisting of neo-internal hyperplasia and tunica media fibrosis, you know, which is obviously concerning. But some people said, hey, maybe this is just pigs. We don't really see this in humans when I'm doing CTI with PFA. But this has now been presented in press by Mark Tam from Chinese University of Hong Kong, where he did OCT both during and then three months after CTI ablation using the pentaspline PFA catheter. They actually pre-treated with a mean of 800 mics of intracoronary nitroglycerins. They gave nitro down the RCA prior to PFA, and yet at three months they saw about a 10% luminal decrease in the RCA area, in one case 60%. So we may not want to recognize it, but we are causing some mild narrowing when we apply PFA near a coronary artery or over it. So how do we avoid it? Well, one way, as we know with RF, is just to don't ablate over the coronary artery. So Satoshi did this study where we measured the distance from the tip of the electrode to the most distal area of spasm. Mean was 5.3 millimeters with a standard deviation of 0.6, so if you take a mean plus two standard deviations. If you're six millimeters away, you're generally safe. Now there are some case reports even of PFA not on top of a coronary causing sort of a generalized coronary spasm, even VF, perhaps in a Prince Mendel's angiotype patient. But that's uncommon. But if you can avoid it, that is obviously the ideal. We know for CTI, which we didn't appreciate in the past, the RCA can be two to five millimeters under the endocardium. So sometimes it's hard to avoid, but at least recognizing when you're nearby is important. Vivek also published this example of pentospline causing spasm over the RCA coronary artery. And as he found, pre-treating with IV nitroglycerin, not necessarily post-treating, mitigated it most of the time, but there's still case reports of some spasm even after treating with nitroglycerin. And this is pretty large doses, so three milligrams IV usually through the sheath prior to ablation. You really have to give it prior. So whenever you are committed to giving PFA over a coronary, at least you want to pre-treat with nitroglycerin to limit the spasm and have perhaps colleagues around who can deal with it if it does occur. We also played with a PFCA catheter. So this is a catheter from Adagio Medical, not commercially available, but pre-treats with cryo before giving PFA with thoughts that this might both hold the coronary artery open as well as it gives lower current PFA because of the high impedance after cryo to see what that effect would be on coronary artery spasm. On the left is PFA alone, where you do see narrowing of the RCA, and with PFCA, where we pre-treat with cryo, we see maybe some mild wasting, but much less narrowing. There you can see the area there, but not as much narrowing when we pre-treat with cryo. And histologically, with PFCA alone, we see about two plus or mild neo-intima hyperplasia and tunica media fibrosis. With PFCA, it wasn't zero, but less, so no tunica media fibrosis, in this case, minimal neo-intima hyperplasia shown here in green. So we do still see some coronary effects, but less when we pre-treat with cryo. I'm not sure that's so practical other than with that catheter. The other data I presented here on Thursday is, you know, we looked at whether altering the waveform or the pulse field would affect, perhaps, or mitigate this coronary effect. So we looked at monopolar PFA with a lower energy, 1.4 kilovolts, monopolar with 2 kilovolts, bipolar with 2 kilovolts, or RF. We never really looked at RF, we've just been doing it for a long time. And it turns out, I mean, this is, you know, you don't see acute spasm with RF, you do with all the other modalities, really no difference among them. And all also had some evidence of injury, including RF. So in two out of three animals, we had evidence of, again, fibrosis and neo-intima hyperplasia. Kind of qualitatively, there's not enough animals to statistically look with bipolar PFA. It was only one out of three animals with minimal neo-intima hyperplasia, so it may be this is safest, but it's important to realize, even with RF, we're causing some coronary artery injury with CTI ablation. What about hemolysis, renal failure? So again, this came out of, I think, Manifest, where there were five patients, so 0.03 percent pretty infrequent, where they had evidence of renal failure needing transient hemodialysis. But if you look at the total number of lesions, it's 143 pentospline lesions, which is a lot of lesions. Were we doing this also with RF? Well, there was a study comparing RF to PFA. When you look at LDH, haptoglobin, really no changes with RF. Also RBC microparticles, which is the most sensitive, but you do see this consistently with PFA. So particularly when the electrodes aren't in contact, you'll get hemolysis when you're putting 2,000 volts into the blood pool. It's not so surprising. But this is dose-dependent. The more you put in, it'll accumulate. The more lesions you give, and the more your electrodes are not in contact. This is from Natali's group. So when they gave less than 70, it was about 4 percent incidence of acute kidney injury. This was defined as a 0.3 increase in creatinine. But over 100, you're getting about a 20 percent incidence. When they pre-treated with two liters of saline, they didn't see that anymore. So pre-treating with saline can be helpful. Honestly, I don't do this in all my patients, because one of the advantages I feel like of PFA is not having to put a Foley catheter in, no fluid. But again, if you have someone with pre-existing renal insufficiency, maybe they're persistent and you're thinking you're going to give a lot of lesions, that might be someone where you'd pre-treat them with saline and maybe watch them overnight afterwards for diuresis. Again, in my own practice, this is someone with persistent AF, where we did PVI and posterior wall. This was a total of 68 PFA deliveries. So I'm still not sure how people are giving 150. So by my practice, again, if you're under 70, rare things can happen. But I think it's actually a pretty minimal risk with general PFA, and we don't really pre-treat with saline. The last thing, again, there have been reports of acute phrenic paralysis, and I thought I'd introduce this. So, well, we know that, you know, there's a relative tissue selectivity of PFA, less for smooth muscle, but nerves have a higher threshold for injury, but not zero. And, in fact, if you ablate epicardially directly over nerves, you'll injure them. But we've had a few of these type of cases, I'm sure everyone's experienced this, of right atrial tachycardias, and you map it, and black is where we had phrenic nerve capture. And the focus was just right on top of the phrenic nerve, and we ended up having to treat them with drugs. One outside case actually got ablated and had phrenic nerve paralysis. And so we were able to get a compassionate use approval for this focal PFA catheter. And you can see here where basically where we applied 1.4 kilovolts directly over the phrenic, and we did lose phrenic capture for about three minutes, the first one, and four minutes for the second, but it always came back, and this patient was completely fixed and off drugs. So perhaps, you know, an advantage for some atrial tachycardias near the phrenic. So to summarize, PFA applied endocardially directly over coronary arteries leads to spasm, about 50% narrowing. You're not going to see ST changes in general, but it's happening. And mild coronary artery injury, even without clear ST changes. IV nitro, two to three milligrams of big doses prior to RF, attenuate spasm. But when we looked, there wasn't really a good relationship between the degree of spasm and coronary artery injury, so that just even if you mitigate spasm, you may not be mitigating this injury. Pre-treatment of PFA leads to hemolysis, more pronounced with poor electro-tissue contact, may lead to ATN in the setting of baseline renal insufficiency, as well as when you're getting to many PFA ablations, over 70 or over 100. Pre-treatment with saline may be helpful in patients with baseline renal insufficiency where more than just PVI is anticipated. PFA may cause transient but not permanent phrenic nerve injury, and that, again, gives it an advantage, perhaps useful for arrhythmias occurring in vicinity of the phrenic nerve for ATAC, AFib, or perhaps VT as well. Thank you. Thank you very much. We will be taking the question at the end, so feel free to send us the question by the app. Dr. Bain, from Australia, will present PFA-specific concern for anesthesia. By the way, Dr. Reddy is here. We're just giving him a break to catch his breath and cool down a little bit. So wait for his talk. Good afternoon. Thank you very much. Thank you, everybody. It's a great pleasure to be here today, and thanks to the faculty to present on this important topic from my perspective, perhaps as the only anesthetist here today or here at this meeting. I have no conflicts of interest to declare related to the specialty of cardiology or cardiac electrophysiology, and I acknowledge the support of the institutions listed below for my own research. So today, I'm going to cover specific concerns for anesthesia for PFA of AF related to cough, musculoskeletal stimulation, and vagal responses. And to me, this is really about addressing the important and changing question of which approach, really which approach, general anesthesia with muscle relaxation and full control of ventilation, or the various approaches to sedation, such as propofol-based deep sedation or conscious sedation with light sedatives and analgesics. And then conclude by summarizing with what I see as a patient-centered approach to anesthesia for AF ablation. So this brings me to my current practice at the Alfred Hospital in Melbourne, which is a major quaternary institution that specializes in the management of heart failure and is a leading center for ventricular assistance and heart transplantation. The electrophysiology service is integral, completing more than 500 AF ablations annually. And for AF ablation, 100% of the patients have their procedures under general anesthesia. And this is really consistent with worldwide trends. So between 2010 and 19, Garcia and colleagues showed that AF ablation procedures more than doubled with a trend of increasing use of general anesthesia and deep sedation and decreasing use or reliance on conscious sedation. This was a period when cryoablation was on the rise and patient comfort, reduced movement, facilitating improved catheter stability, and mapping accuracy facilitated the trend towards increasing general anesthesia and propofol-based deep sedation. What about outcomes? Again, general anesthesia is actually preferred. And this data, as I've seen presented several times recently, is from the Danish registry of nearly 8,000 patients, of patients having their first ablation for both persistent and paroxysmal AF from 2010 to 18, that compared general anesthesia, which was in approximately 20% of patients, to conscious sedation in 80% of the patients. And they demonstrated that the risk of AF recurrence at one in five years was 26% higher with ablation under conscious sedation when compared to general anesthesia. So what about PFA? From the first in human studies, that's impulse, monophasic PFA was conducted with general anesthesia and muscle relaxation to control the muscle contractions. However, the biphasic PEFCAT arm of the trial was conducted under conscious sedation with the commonly used opioid fentanyl and midazolam and the very potent hypnotic agent propofol without the use of general anesthesia or relaxants, a protocol that looks to me like really quite deep sedation rather than what I would necessarily call conscious sedation. And of course, the study did report issues of frequent phrenic nerve capture and intraprocedural cough. Five years on, and the manifest surveys provide us with very valuable insight into the direction that things are going with respect to general anesthesia and deep sedation. Manifest PF, 2022, 1,758 patients, 24 European centers, 90 operators, general anesthesia, 15%, deep sedation, 85%, no mention of conscious sedation. Manifest 17, published in 2024, over 17,000 patients, 116 centers, 400 operators, representing a very large percentage of the use of the Faro pulse catheter at that point in time. And with this, a rise in the use of general anesthesia to 44% compared to a reduction in deep sedation to 56%. That is thought to be due to increasing access to anesthesiology services and or a desire for better control of diaphragmatic stimulation and cough. From an Australian perspective, the authors of this small cohort outline why general anesthesia is preferred. Ability to perform transesophageal echocardiography, image-guided transeptal puncture, anteriorly-based transeptal puncture, improved access to right-sided pulmonary veins in the flower configuration, cost effective compared to intracardiac echo, reliable exclusion of left atrial appendage thrombus, and of course, neuromuscular block that really limits musculoskeletal stimulation and perhaps potentially significantly improves catheter stability. So I'm beginning to wonder whether the operators want the assurance provided by either very deep levels of sedation and or general anesthesia with muscle paralysis, being the absence of movement, the absence of cough, and of course, musculoskeletal stimulation. Because in the back of the mind, despite the clear safety and efficacy benefits of PFA, sits the concern about catheter control and movement, as always sits the concern about catheter control and movement and the potential issue of an injury that might precipitate cardiac perforation and tamponade. Studies of propofol-based deep sedation of AF for cryoablation, pulse field ablation, and RFA have demonstrated safety and suitability. But the issue of significant movement due to musculoskeletal stimulation or fasciculation remains. And this really raises questions about this approach for PFA, especially for systems such as the monopolar systems that are coming out and being used more frequently that are also integrated with 3D mapping. Propofol-based deep sedation for focal pulse ablation with 3D mapping has been shown to be possible. However, this involved adding the very potent short-acting opioid, remifentanil, and the potent hypnotic analgesic agent, ketamine, to suppress cough, pain, and agitation. There was also no comparison to general anesthesia, nor was there any measurement of patient cough, comfort, or satisfaction in the study. Another study did compare propofol-based deep sedation for monopolar PFA with general anesthesia using the lattice tip catheter and demonstrated no issues with 3D mapping. Feasibility was demonstrated, but again, there was no survey of patient comfort or satisfaction. And another group invested the utility of conscious sedation where the patients were conscious enough to be able to respond to the operator instructing them to breath hold for a few seconds. PFA with the acupulse system was then deployed at the end of expiration during the breath hold. And they demonstrated reduced measured diaphragmatic contraction and cough during PF deployment compared to the normal breathing group. However, again, there were no assessments of patient comfort, tolerability, or satisfaction. And finally, a pilot feasibility study by Calvert and colleagues elegantly describes patients' experiences of PFA under mild conscious sedation. A small study of less than 30 patients comparing PFA under mild conscious sedation to general anesthesia. And while it was feasible, high sedative doses were required, and procedural pain was a significant issue that limited tolerability. The authors conclude that the levels of pain being often much greater than expected underscores the need for general anesthesia or deep sedation for PFA. This brings me to the issue of vagal response, which is comparatively less controversial. Defined as an increase in the RR interval of greater than 50%, or transitory asystole and AV block, it occurs commonly during PVI utilizing PFA. And most frequently during ablation of the left superior pulmonary vein. It's due to the close proximity of the ganglionated plexi to the pulmonary veins. And it is not prevented by anesthesia and may require temporary pacing. And of course, the routine prophylactic administration of vagalitic medications, such as atropine and glycopyrolate. An interesting recent study by Delmont and colleagues takes advantage of the transient effect of the pulse field energy on the ganglionated plexi. By targeting the right superior pulmonary vein first and the adjacent right anterior ganglionated plexus, temporarily modulating the function of that plexus first, they show a reduction in vagal responses during the procedure from 78% to 13%. So to begin to conclude, to me it's about remembering that the patients are at the center of all of this. And we need to seek an approach that balances patients' expectations and preferences, as well as creating conditions to maximize safety, comfort, and efficacy. Really, just as always, remember patient satisfaction is not solely dependent on procedural success or outcomes. So by conclusion, anesthesia or sedation is an essential component of patient-centered care for catheter ablation with pulse field ablation systems. Concerns surrounding musculoskeletal stimulation and cough are modified by the type of anesthesia care provided and the specific PFA system being used. Propofol-based deep sedation is safe and feasible. However, general anesthesia is increasingly preferred to enhance procedural conditions and ensure patient safety and comfort. Vagal responses are prevented by prophylactic vagalytics and or by starting from the right superior pulmonary vein first. And in the PFA era, close collaboration between electrophysiologists and anesthesiologists is essential to deliver patient-centered care and may improve procedural outcomes. Thank you. Thank you so much. Next is Dr. Vivek Reddy from Mount Sinai. He's going to talk to us about what do we do with atrial flutters when we're doing a PFA case. Thank you very much. Oh, I just did the wrong thing. Okay. So, again, I apologize for being late. It turns out that, you know, it turns out you can, when you're coming from the tent, you just take a quick right to get here. Or you could also take the left and run across that way and then all down this way and then down that way and come here. I also want to thank Osama for giving me an extra 10 minutes to catch my breath. Okay. So, I know I probably made things a little late, so I'm going to go through some of the slides a little quickly to catch up here. So, my goal is to discuss how to manage flutters. And I'm going to try to be a little practical, at least with the perspective, the U.S. perspective, because I want to talk mainly about devices that have FDA approval that we have available in our practice, with one exception. These are my disclosures as relevant to this presentation in yellow. I want to talk about the pentasiline catheter using with the CARDO system and the OPAL system. And I'm sorry, I'm going to use the trade names here, because otherwise people are going to get confused as to what exactly I'm using. And I also want to talk about the lattice-tip catheter with this associated FARA system. And I thought the best way to do this is to go through a number of cases. So, we have actually, in terms of atypical flutters, we have probably the most amount of experience using the fairwave catheter with the CARDO system. So, here, this is a patient with atypical flutter after prior PVI. And here we mapped it with the multipolar catheter. And you can see a couple of things. One, it looks like the vein's reconnected here. So, something needs to happen there. Number two, you see that there's a breakthrough right over here through the posterior wall. So, what would we do? We take the catheter and use the FLAIR configuration and ablate here on the posterior wall. I think that's relatively straightforward. This is what it looks like after the fact, ablating the posterior wall. We also isolated the veins completely. I think that's straightforward. And that's not really terribly interesting for most of you. We know that we can put it on the posterior wall. Here's another example, a little bit different. So, this is a patient also at a previous pulmonary vein isolation. And you can see the scar map on the right, an activation map on the left. And you can see that it seems to be going around this region. It's colliding here at the mitral angular region. And, again, there's no real scar here. And you also see, as this rotates posteriorly, hopefully, you know, there's some activation. It looks like collision. But there is some voltage here. Now, when we do this and we identify this, then what we typically do is do a couple of entrainments just to make sure that this makes sense. Do an entrainment on the posterior wall and make sure it's really far out. Entrainment anteriorly and posteriorly to this region. Then we prove the circuit. And then here we take the catheter again in flower configuration. The strategy I like here is to certainly incorporate that posterior voltage, but basically ablate to this scar region, this area block. I'm not particularly interested in bringing the line all the way down to the mitral angular unless I absolutely have to. And in this case, what we do is we ablate this. And then we do rapid stimulation to see if we do have another residual flutter or not. Why didn't I bring it all the way down? Well, with this catheter, I think positioning it as you get closer to the angular is increasingly difficult. You know, you have to get the catheter to be touching the tissue to get that electrical field to intersect with the tissue. It's not that easy at that location. But sometimes you have no choice. This is a patient with prior cardiac surgery, a maze procedure, and you can see a circuit that's going around and around. And by the way, that is the circuit because there's no other tissue left. So let's go back here. So here it is. Let me just freeze it right here. You can see there's a fair amount of scar. And there's a slower conduction here. And so this is where we're going to target this. Now, the question is in this kind of a situation, we have to ablate down to the annulus. And positioning the catheter sometimes can be challenging. And what we did here, certainly we did ablate. But the configuration we use is what we call the Powerball, where basically you take the catheter, put a basket configuration, advance the sheath over the back end to constrain this. There are a couple of reasons I want to do this. One, you can see that the ablation down here is getting closer to where the AV node would be. And that's the number one concern that I have is not to obviously cause AV nodal block. And this at least constrains this. By the way, I should note, this is off-label use, this catheter, as you can imagine. There's not a lot of preclinical data. We have some preclinical data. We can show that we make lesions at about three, four millimeters in the atrial tissue. I don't know if it's published yet, but it does appear to be a reasonable lesion depth. Anyway, we use this Powerball configuration and ablate back. When we do this, we typically deliver three lesions per location. Now, here's another one. This is a right atrial flutter. And I'm not going to go through this in detail, but suffice it to say there was a fair amount of lateral scar. This is actually idiopathic atrial scar. We see these occasionally. These are very difficult cases, at least they used to be in the past for me, because you would oftentimes have multiple atrial flutters that are percolating through here with various cycle lengths. And mapping these is a nightmare. You start mapping and it changes to a different one. And anyway, the good news is now we can take a large area of ablation catheter and basically homogenize the area of scar. That really works quite well in these patients. The reason I want to show this is when you look at this, it's a very large atrium. Your catheter is going to be coming up here. You're deflecting laterally, but as it comes laterally, the problem is it's hard to get the catheter to be parallel to the tissue. You may have some spines touching, the others are floating in space. So the spines that are touching are ablating. The ones that are floating in space are just lysing red cells. So what we do in this case is we use one of our sheets that we actually like, this is actually developed for left atrial appendage closure. It has a proximal large deflection and a distal four quadrant deflection. So as it turns around, let me just pause it right here, the major deflection is coming out toward us and then you can vary the distal deflection to be more, well let's say, normal to the tissue. And so that's what we did and you saw the lesion set to ablate in this patient. Now this is, that was using the CARTA system. Now that we have the OPAL system, we're increasingly finding ourselves, well, using it for atypical flutter. So this is a patient who developed an atypical flutter in the middle of a PVI procedure, well, at the end of the PVI procedure. So you can see that it's percolating again down the posterior wall. We do one or two entrainments just to verify that this really is part of the circuit and deliver a bunch of lesions to homogenize this posterior wall and that treats the flutter. That's fairly vanilla. Let's look at something a little bit more interesting. So this is typical flutter. So after PVI, this patient developed typical flutter. This is the right atrium looking at LAO view here. This is the view I like. It's an inferior view where you go LAO and rotate it all the way up. So this is the valve and then the IVC will be somewhere over here. And anyway, so this is typical flutter. We proved that with entrainment. And this is the strategy that I like to use when I'm using this catheter because I don't want to open up another catheter. I use certainly this, the flower configuration to put it down on the annulus, but I also on the tricuspid end, I like to use it in a power wall configuration to get that tricuspid edge because oftentimes when you use just the flower, the pedal is floating away on top and not touching properly. Excuse me. There's an issue of spasm. I think Ed just talked about this. I'm going to go through this quickly. But I do want to talk about this. We just presented the Advantage AF data recently. This was using the Fairpoint catheter. But the reason I'm bringing it up is because it's 141 patients that underwent CTI ablation in a multi-center study using nitro protocol. And the protocol that we used, just to remind people, first you give a little bit of vasopressin, usually phenylephrine, 300 to 500 micrograms. Then we give three milligrams of nitro and the clock starts. You wait one minute and then you start ablating. And then every two minutes thereafter, you give another two milligrams and give additional pressures if you need. Usually you don't need to go through this whole thing. Usually after this and then a first dose, you're done. In this 150 or 140 patient series, the mean amount of nitro was four milligrams plus minus two. Half only received the three milligram initial bolus. There were no adverse events either from the nitro or the ablation. And we didn't shoot coronaries in these patients. This was a multi-center ID study. But we did not see any ST elevation. Skip the rest of this. Okay. There's also the issue of late coronary effects. And there's two studies. One that we published in 30 patients where we shot the coronaries 11 months after and there was no stenosis that we saw. So this is acutely, but chronically, we saw no evidence of stenosis. On the other hand, Mark Tam and his colleagues looked at 19 patients and they did see some luminal decrease, including one patient with a 61% decrease in luminal area using OCT. So I think certainly this is something we need to understand better. What are the chronic effects? I do want to point this out. This is a publication that we recently, this is a preclinical publication, where we looked acute and late after ablation near the coronary. So in the CTI, using the RF or PF. And here's what we're seeing. In terms of acute effects, not surprisingly, there's more spasm with PFA than with RFA. But chronically, actually the most amount of lesion that we saw or effect was actually with RF, not with PF. The point I'm trying to make is with RF or PF, these things can happen. And we have to be vigilant with both of them and try to understand this better. Okay. Let's do a few more examples. This is a patient with an atypical flutter, again, using the OPAL system. It's a little harder to see, but basically it was a flutter rotating here. Again, we ablate from here all the way down anteriorly because that turns out, well, this is where this is. You can see we use flower up here. And you can't tell, but this is actually a constrained basket. This is our so-called Powerball configuration. And there it is again. All of you know about the lattice tip catheter. It alternates between RF and PF. And let me just show you a case. This is a patient with atypical flutter. And you can see it's going around the mitral annulus. But it's actually percolating through here. This is a patient that had a previous mitral line. And obviously there's breakthrough here. So in this case, we decide to use RF. I honestly can't remember why. We certainly make sure that the esophagus is not near this location. I guess we decide to use RF. So we did. This patient also had some activity going through here where we're concerned. I don't believe we actually induced post-trial related flutter. But there was very low voltage. And so we decided to go ahead and homogenize this. And then the CTI line, you can see on the right side. The way I like to do the CTI line, I think this catheter is really nice for this. You start ablating here using PF. As you get to the back end, because the back end of the catheter is ablative, you can ablate there. And it's also nice after ablation, you see the vector activations proceeding in the opposite direction. I'm sorry. And finally, you see, you can see the catheter very nicely on ice for those of you that like to use ice. And with that, I think I'll stop. Thank you very much. All right. That was excellent. So we went over, should we use PFA in everybody? So Jose will start with you. Where is he? He's not here. Oh, he left. Well, he said, yes, you should use it in everybody. So I don't know. I mean, I think now with the newer form factors, there are other catheters that we can use. And I think companies are working on form factors for re-do's, for persistence. So I think, yes, potentially you can use PFA for everybody. Vivek, do you think you have a patient there where you don't want to use PFA and you want to use RF? Yeah, the two comments I would make are, number one, the very practical one, which is when you are near the AV node, then I think I don't fully understand exactly how close you can be yet. So I'm not sure that means you have to use RF. I think I'm more comfortable with it when I'm close to the AV node. I think with time, we'll understand better how close or how far away we need to be with PF. The other point I want to make is I do think we need to keep our eyes open. And I keep thinking about that article from the circuit dose investigators where they looked at long-term outcomes after cryo versus RF. And you know this. Acutely, there was no difference. If you looked, but long-term, there was also no difference in AF recurrence at three years. But there was a difference in the progression from paroxysmal to persistent AF, meaning the patients who received RF ablation had less progression of disease than the persistent. It was a statistically significant result. It's not a huge difference. But it does raise the question that there may be other things beyond isolation that are at play here, whether it's affecting the autonomics or affecting the stretch and whatever. So actually, we have a question about the GP impact. Can I just make one? Yeah, well, because the other group to think about, I don't know the right answer, is the tachybrady patients. I mean, I had someone recently who was actually like $0.45 for vasovagal syncope, cardioneural ablation, and we did a monitor and just having 3% AF. So we know there's some, but much less, autonomic denervation with PFA. If you have one of these people having 10-second conversion pauses and they have AF, is that someone where we'd go back and use RF for PBI? Or are you going to do PFA and then just add some RF to the GPs, but then you're opening two catheters? That's one where I kind of talk to patients and think about there might be some benefits to PF in terms of the RF, in terms of denervating the autonomics. I just want to make, I think that's a great comment. I also do want to point out, you just said it, that there is some effect with PF, which raises the possibility that if you, I don't want to use the word blast away, but if you ablate aggressively at that location, perhaps we get the same impact with PF as with RF. So somebody should do that study where you ablate aggressively at that location. Before we go to the mic, because this is related to your talk, Vivek, and I was going to ask you, you used PF with the SPHERE on the CTI line. So now we have a question on RF. Do you use nitro with the SPHERE 9 when you're doing PF on the CTI, or is it just the fire pulse? No, no, listen, any PF, every single PF technology, certainly that I've played with, that when you put it next to the corner and you deliver the energy, if that energy intersects with the vessel, it will spasm, period. Now, whether or not you appreciate the spasm, because whether or not that caused the ST elevation or it resolves quickly, those are somewhat chance events. Wonderful presentation, thank you very much. What about if you had a predominant atypical flutter only up front in that case? Are you gonna take, if you didn't have dual energy as an option, would you take pentaspline or would you take RF? I know there's some data that's a little bit mixed in terms of PFA versus RFA for atypical. Yeah, I mean, I assume you're talking, it doesn't have to be, let's pretend you're talking about a post-ablation patient, okay? I would still take PF because the big advantage of PF is some of the veins may be reconnected and it's easy to deal with that. Much of the area in the left atrium you can deal with with the pentaspline catheter. The areas I get start worrying, I start worrying about a little bit when you do the mitralismus, the posterolateral mitralismus, which is my preference. You can certainly get block. You really have to make sure, and my preference is to put an ice catheter in to really look at the location and make sure you're actually opposed to the tissue. Make sure that your splines are actually touching, that they're not just floating in space. At least some are not floating in space because some will be. The other point is that in those cases, sometimes you will have to open up an RF catheter and go in the CS to complete it. You do that with a? With a conventional catheter, yeah. Well, have you put the athera in the CS? Oh, yeah, yeah, no. So he was asking about the pentaspline. So yeah, with the lattice tip, you can put in the CS, again, off-label use. But the way you would do it if you were so inclined, there's two options. The way we initially started doing this is to put in a regular catheter, like a decapolar, through your sheath. Advance your sheath. Use a long crow sheath if you can. Advance the sheath distally into the CS, take it out, put in the lattice tip, and express it. So just pull it out. Once the lattice tip is in the CS, you really can't pull it or push it. Well, you probably shouldn't. I have never tried to do that. The other option, which I sometimes do because I get lazy, is in the right atrium, extrude just the tip of the lattice tip, just like a little bit, and then use that to enter the CS. You just do it very carefully so that. And just practically, we had a case a couple weeks ago, and I have been, up until now, pulling an RF catheter for mitral lines because I worry about the coronaries. So we did the PVI, mitral flutter. We did an anterior line. My partner did it with RF, and the flutter did not slow by a millisecond. And he called me for help, and we're like, well, let's go back to PFA. We put the pentispline in the roof, and we had done a lot of PFA in other areas, and in the first one, it terminated, and we had block. So it does seem to have advantages for depth, but I have heard some late recurrences, so I think that's the concern. So there's a question online on the rate of recurrence after PFA using for the left anemones. So after the mitral line, what is the? Well, so acutely, the thing you have to remember, if you only use RF after PF, when you deliver PF, you're gonna get relatively quick tissue edema. So that's just a distance issue that you're gonna be fighting. Now, if you're talking about, then as I said, go into the CS and a blade from the other side, no problem. If you're talking about doing RF late after PF, so in a discrete procedure, that's also no problem, because PF tends to thin the tissue quite substantially. So question for Dr. Bain, because we have to finish at 2.45, and we have other places to go to, but so, I mean, what I got from your talk, and what we've been doing is just use general anesthesia for everybody. Is there something else that the panel, I mean, Vivek, you get to work in Europe a lot, so you've seen it all, but let's give Dr. Bain some more of an idea. But I wanna ask specifically that question. For those people that can't use GA for any reason, can you just give us some idea of hints of things we could use, and particularly talk about ketamine, talk about dextromethamidate, and talk also about inhaled lidocaine. Does that, do any of these things make sense? And just a caveat to that, the thing we care about the most, of course, we want patients to be comfortable. We really don't want them to cough and move around. Can you hear me there? Yep, so look, I personally, I think that all of the discussions that I'm listening to today are all about increasing attention to accuracy and precision with everything you do, and that the delivery, the power and the energy that you're delivering is extraordinary. So the only conditions, in my opinion, that can really achieve that are general anesthesia with a muscle relaxer. And I don't know whether you've tried doing this work with the focus that you need to put on what you're doing without that. That's a really, not necessarily a reasonable thing to say because that's a very resource-dependent issue for many places. So then, I can see, looking at the literature, that they're using different attempts, and essentially, it's just adding more potent drugs that are shorter-acting, where patients will be temporarily deeply anesthetized, and then they'll wear off quickly, and you haven't necessarily utilised the resources of an anesthesiologist to achieve that. But effectively, it's the same principle, and that's why I mentioned drugs like ketamine, where they try to use it to manage agitation and discomfort over and above propofol, plus remifentanil, which is an extremely potent drug, and if you overdose someone with remifentanil, you're very quickly gonna have someone who's not breathing. So personally, I do believe general anesthesia is the way to go, and it's not necessarily gonna be feasible for all centres, and I think a lot's been achieved without it, but the direction we're going with these catheters that are linked up with mapping systems seems to me like, the ultimate point is that I think the role of anesthesiology, working closely with electrophysiologists, is only going to grow as this technology becomes more advanced, and also, the type of patients that are coming to the cath labs these days are increasingly more dependent on quite significant experience of anesthesiologists in the rooms, because you're also now dealing with patients with redo, redo, heart failure, and so on. All right, we'll just do one last question. So there is a question, difficult one, about the risk of stiff LA syndromes with all the amount of ablation we're putting. I think PFA actually has some advantages that way. It doesn't create the same fibrotic myopathy as RF, so I think you have to be wary about anticoagulation, because the HM's not contracting if you do a lot of extensive ablation, but if I haven't seen the stiff LA syndrome that we saw with maze or a lot of RF with PF, I think it's less likely, if you agree. Yeah, 100% agree. We have an abstract here at HR as a case. It's an interesting case for me, which was the patient that we did PBI and posterior wall ablation, relatively a vanilla case, I thought, and then, and I don't remember exactly why, but the patient stopped taking anticoagulation, okay? And then, I think we were doing a Watchman or something, but the patient ended up getting a TE a couple months later, and there was a massive clot on the posterior wall, just a big posterior wall adherent clot about the area that we ablated. So it's the opposite of the stiff. It's the flabby left atrium, posterior left atrium. Again, this is an N of one, you know, whatever, but still, it was, it made me. No, so that's a good cautionary tale because we just had a few patients, younger patients, who thought that when you use PFA, you don't need anticoagulation after ablation, even though we told them you take your anticoagulation non-interrupted, and then, in follow-up, it's like, oh, I stopped it the next day. I was like, who told you to stop it the next day? So I thought this is what pulse field ablation is supposed to do, so please remind your patients that they should continue taking anticoagulation for at least two to three months after the ablation. That's very, very important. And some of these where the atrium is red, I think, you know, they have to take that into consideration. I put it in the chart that you're not gonna stop anticoagulation long-term when there's not motion. The other one quick point, maybe just for safety, when you're using the Powerball by the annulus, you have the wire, because I know early on, there was some perfs with the basket configuration alone, I thought, moving the pentaspline around. So do you always have the wire out, or? I'm not aware of perfs, maybe there are, I have no idea. But certainly, your point is well taken. And what we typically do is extend the wire at least a few millimeter, like a centimeter or so, because if it's then bent in a non, let's say normal way, then you know you really pushed against the tip with the actual tip. Look, this is a temporary thing that we do, because this is what we can do with the catheter that we have. I'm not saying it's ideal. So I think we arrive at the end of the session. Thank you very much for all the speakers. Very interesting session. Thank you all. Thank you.

Pulse Field Ablation

atrial fibrillation

clinical practice

procedure times

catheter design

waveform modulation

general anesthesia

patient outcomes

technological advancements