With that, we'll go ahead and get started. My name's Jared Bunch. I'm from the University of Utah, the hospital in Salt Lake City, Utah. Yasuo Kuruma Yeah. I'm Yasuo Kuruma from Nihon University School of Medicine, Tokyo. Yeah. We also share this session, and we'll get started. The first, is that okay, ready to go? Yeah. The first presenter is Dr. Frederic and Francis Chee from the CHU, Timo, yeah. And the title is, so, First Electron Mapping and Monitoring of the Prostatectomy Frenic Nerve Policy in a Pulse Field Ablation Procedure. Let's get started. Go ahead. Thank you. So, presentation is 10 minutes, and so, three minutes, two minutes. That's right. My question. Yeah. Okay. It's a pleasure to be here and to give a talk on a subject I've been working on for a very long time. Indeed, our first publication in which we describe the concept of phrenic nerve monitoring with C-MAP in cryo-balloon procedures, dead bags, 15 years ago during my fellowship in the Montreal Heart Institute. Phrenic nerve palsy is a complication of PFA. In ADVENT, for example, 1% of patients had unresolved phrenic nerve injury at discharge, which recovered only before the end of the study at one year. They were not counted as complication and only reported in the supplementary appendix. A permanent case was even published in Manifest One Year. On this case, we have diagnosed without any dedicated monitoring, thus what is the real incidence of phrenic nerve palsy in PFA? In this case report, we described for the first time sequential phrenic nerve monitoring with C-MAP in PFA. We reported in particular the dose-response relationship. The more we ablate, the more the nerve is damaged. This work was continued and we are about to report a series of 64 patients. We wondered what happens during the procedure and can we see any consequences at discharge the day after. We recorded their phragmatic C-MAP with a catheter in the inferior vena cava and we measured the peak-to-peak amplitude. Phrenic nerve stimulation was performed at each right pulmonary vein at baseline and every two applications before moving the catheter. Two questions, has a complete phrenic nerve palsy occurred? And what was the C-MAP amplitude at the end of the procedure compared to baseline? Diaphragm contractions during PFA applications may be reassuring, suggesting the nerve is still functioning. But in reality, even in case of complete phrenic nerve palsy, diaphragmatic contractions remain the same during PFA application because the nerve is probably activated by PFA below the level of conduction block. For example, this patient has a complete phrenic nerve palsy, there is no diaphragmatic contraction with phrenic nerve pacing, no C-MAP after the spike, but during PFA application, the right diaphragm is still contracting. And here is the first misleading fact. In case of phrenic nerve palsy, diaphragmatic contractions persist during PFA applications. We have found that C-MAP can evolve in three different ways. It can remain stable, a palsy can occur, lasting from a few seconds up to 20 minutes. And there is a rapid recovery phase lasting one or two minutes until a complete recovery. The last possibility is a paralysis with incomplete C-MAP recovery. Interestingly, there was no additional gain after the rapid recovery phase, even after a long waiting period. Phrenic nerve palsy was observed in 40% of cases with incomplete C-MAP recovery at the end of the procedure in 18% of cases. One might say, I've paced the phrenic nerve many times and no palsy at the end of the procedure. And here is the second misleading fact. Even if C-MAP is significantly altered by half, for example, meaning that only 50% of the muscular fibers are still contracting, the diaphragmatic contraction perception with abdominal palpation remains identical. We've seen there was a lot of phrenic nerve palsy during the procedure, but can we observe any consequences the day after? If a palsy occurred during the procedure, we assessed diaphragmatic function performing chest X-ray, which were all normal. And this was unexpected, as many patients were far from having recovered at the end of the procedure. So is there a full recovery for all patients within 24 hours, or lack of sensitivity of the chest X-ray? We decided to perform a fluoroscopy in addition to the chest X-ray. It's a dynamic test, easy to make and easy to read. We obtained a simultaneous assessment of both diaphragmatic amplitudes, one side being the reference for the other. It's done in the supine position to avoid false negative. This is considered the gold standard for the diagnosis of unilateral palsies. This implemented approach was undertaken for the last 25 patients. Here is an example of a patient with incomplete CMAP recovery. On the left, chest X-ray were normal. On the right, the dynamic imaging shows that the movement of the right diaphragm is impaired. Almost by half, and it's easy to see. And here is a third misleading fact. In case of incomplete pharyngopalsy, chest X-rays are normal. A fluoroscopy is needed to make the diagnosis. This is another example. This fluoroscopy was performed because of a right pharyngopalsy during the procedure. Chest X-ray was normal. And here, we made an opportunistic diagnosis of a left pharyngopalsy. It was a surprise. Left diaphragmatic paralysis can occur during PFA procedures. Among these 25 patients, we found six unresolved pharyngopalsy injuries at discharge, four on the right side, and two on the left side. The incidence of incomplete pharyngopalsy at discharge the day after the procedure was 24%. Among these six patients, three had diaphragmatic motion impaired around 20%, and the three others more severely, up to 53%. The average CMAP at the end of the procedure was lower than in patients with normal fluoroscopy by about 20%. We were able to perform a follow-up in four patients. Three recovered, and one did not recover at three months. In conclusion, with CMAP monitoring, we were able to diagnose pharyngopalsy at the end of the procedure. And with fluoroscopy, we were able to diagnose incomplete pharyngopalsy the day after. The incidence of pharyngopalsy at discharge is not 1%, but 24%. And we found incomplete palsies. CMAP evolution may be predictive of pharyngopalsy at discharge. And even if these findings have to be confirmed in larger studies, our data probably shows the trend. We must understand what could be the long-term consequences of these injuries. In practice, let's pretend your patient has a complete pharyngopalsy after the second PFA application in the right superior pulmonary vein. What will you do? Would you change your approach? Or would you continue to block this vein, ignoring what happened? Dear colleagues, a lot of questions remain. And once again, we need more data from large-scale studies. But at this stage, we should observe three precautions. We need to perform pharyngeal monitoring during PFA procedures. We should be cautious in limiting PFA applications in case of paralysis, and CMAP could play a role. In case of paralysis, we need to perform a fluoroscopy before the patient leaves the hospital. Thank you for your attention. Thank you very much for the nice presentation, meaningful clinical presentation. And let's get some discussion about this. I have a question. So one patient had persistent pharyngeal injury after three months after the PFA operation. In that case, is he or she symptomatic or not symptomatic? To make a link between symptoms and pharyngopalsy can be tricky, as symptoms are not specific. So most patients won't have clear symptoms, even if they complete pharyngeopalsy. And in that case, this patient had no particular symptoms. But we cannot rely on symptoms to establish a diagnosis, in fact. Okay, thank you very much. I'm impressed with such a high percentage of incomplete pharyngeal injuries. I have a question, too. Did you see more of this in the basket configuration, where you may injure deeply versus the flower? Is that perhaps a configuration that we need to be more careful with? The way it happens can be variable, but the more often the palsy starts in the basket configuration. Not always the first application, sometimes it's the second or the third application. But yes, in most patients, when a palsy occurs, it occurs in the basket configuration. The distance from the pharyngeal nerve is the most important factor, I think. Should we avoid the basket? I don't know. Or just do the flower into the anteroom? I think pharyngeal nerve palsy is underdiagnosed, clearly, because we were looking for the complication we had with the cryo balloon. And the more often it's complete pharyngeal nerve palsy, we can see in the chest X-ray. Here, you don't see anything on the chest X-ray, because it's an incomplete palsy. But as you've seen, there is a real impairment of the diaphragm motion. I think we should make pharyngeal nerve monitoring. And in case of palsy, we probably should limit the amount of PFA we are going to deliver to the vein. Because we've seen that there is a dose-effect relationship. But we have to collect more data, on fluoro in particular, to really understand the incidence. But I think the incidence is huge, because in only 25 patients, I had 6 fluoro impairments. Great presentation. We don't pay attention to that, you're right. And the false impression about that, you have the contraction. This is really misleading. What do you think about the pathophysiology, like electroporation and non-thermal? To my mind, there is no inflammatory effect. There is nothing really encroaching on the nerve. What do you think about the pathophysiology of the pharyngeal nerve, and how we treat this? Honestly, I can only tell you what I think, but we don't know. I think we have two phenomena intricated. There is a purely electrical phenomena, that will recover fast before the end of the procedure. But what we see the day after, I don't think it's a hyperpolarization phenomenon. I think it's something else. But what it is, I don't know. Is it a traumatic phenomenon? Is it a thermal injury? Is it the ablation of the PFA on the nerve? Honestly, at this stage, we don't know. But I think we have to be cautious. We were looking for the complications we knew from thermal energies. Now we understand that there are other kinds of complications with PFA. Remember, it's a recent energy. I think there is a lot to say about the potential complications of this energy. Thank you very much for the great presentation. Let's go to the next speaker. Thank you very much. I forgot to mention that these articles were chosen from the most impactful for the year for heart rhythm case reports. They were chosen objectively based on how often they were downloaded, how often they were shared, and these metric scores of just impact in the world. These were all very well-received case reports that really helped in the education of heart rhythm disease. We're grateful for these authors for sharing. Our next presentation is Purkinje denetworking using a ripple map with novel multi-electrical mapping catheter for ventricular fibrillation storm in a patient supported by Impella device after acute coronary syndrome. This is from Yuhi Kasai from Soporto Cardiovascular Clinic. It's a great honor to be given this opportunity. I'm Yuhei Kasai from Sappo Cardiovascular Clinic. I'd like to present our recently published case report. The title is like this, non-disclosure, and let me begin with a simple question. How to treat VF storm? In the ideal scenario, a single morphology of PBC is present during the procedure and it appears frequently enough. We can recall the local potential that precise a QRS complex during triggered PBC, the site becomes the ideal target for operation. In the real-world practice, this ideal and the simple situation is relatively rare, so we often face some challenges in VF operation, especially for ischemic heart disease patients. Here are the three difficult situations, I think. First, a PBC is absent at the timing of catheter insertion. How to VF induce? Is VF induction necessary? Second, multiple morphologies of triggered PBCs are documented. How do we target all of them? Third, the patient is hemodynamically unstable due to recurrently, really recurrent VF. Is mechanical support necessary or how to optimize the impeller settings during the operation in impeller-supported cases? I explain the first two challenges, basically just like atrial fibrillation, VF is composed of a trigger and substrate and modulator. As I said before, the PBC is consistent and frequent during the procedure, as a triggered PBC operation can be effective. However, in the majority cases of VF storm cases, post-MI patients, the PBC is multiple or infrequent, and any appearance of PBC immediately trigger VF. So this situation made a triggered PBC operation strategy nearly impossible. So we need to shift to a substrate-guided operation for VF storm. And the previous report says, shows 80% of triggered PBC in VF associated with ischemic heart disease originated in the scar border zone. So identifying the scar border zone using a substrate mapping helps estimate the origin of triggered PBC, even when the PBCs are not present during the procedure. In these complex situations, as the previous report shows, demonstrates, anatomical approach called Purkinje denetworking can be effective. I explain Purkinje denetworking specifically. We firstly create a LV substrate map, and we tag the left bundle branch and distal Purkinje potential to construct a virtual triangle, and operation is performed linearly along the base and along the axis of the triangle, while sparing the normal conduction system. So based on this information and these results, our hospital strategy for VF storm after acute or subacute MI involves two key components. First of all, we substrate, sorry, we create a substrate, LV detailed substrate map using a high-density mapping catheter. And the first key component is Purkinje denetworking as anatomical approach. The second key component is localized substrate debarking around the target area near the scar border zone. So let me show the, sorry, let me introduce the case we reported. An 80-year-old female with cardiogenic shock due to multivascular ischemic heart disease was transferred to our hospital, and she had VF storm, and we performed emergent PCI for both LAD and L6 under implicit support. After PCI, amiodarone and Lanziolol and deep sedation therapy was performed, but VF storm was, has recurred on day five, so we decided to perform emergent catheter abrasion for drug-refractory VF storm. At that time, she remains dependent on the impetus CP at P4 level in hemodynamics, and so we have to complete the procedure by only transceptor approach. Furthermore, there are multiple morphologies of triggered PBCs, and any appearance of PBC immediately triggered VF. So this situation made the triggered PBC abrasion nearly impossible. So following our strategy, we create a LV substrate map using octal-ray catheter, and this ripple map demonstrates, sorry, this ripple map can visualize the left main bundle and anterior fascia and posterior fascia, and bifurcation point, yellow circle. And yellow, left posterior fascia runs along the SCAR border zone, and this right side is a voltage map, and the posterior fascia runs along the SCAR border zone. So we perform the abrasion, we perform Parkinsonian networking, represents white line and localized substrate debarking in the SCAR border zone of the LPF region, including suspects that triggered PBC origin sites with good pace map matches. And the session was ended without any complications, including complete left bundle branch block. High-density mapping catheter is essential for creating substrate map efficiently, but also for obtaining local potentials around the target areas. Since panel A shows local parking potentials, during triggered PBC, local parking potential precise QRS onset, and during VF, the cycle length of local parking potentials is shorter than those of surrounding myocardium. So indicating that these sites might play an important role in VF maintenance. On the other hand, panel B, we thought this parking potential might be a passive, because of the cycle length of parking potential is the same as those of surrounding myocardium. Panel C and D highlights catheter-induced VF, originating from the suspects, originating from the sites that showed abnormal delayed parking potential during sinus rhythm. Conversely, during triggered PBC, the abnormal potential significantly precise QRS onset. The sites, we thought, the sites absolutely require ablation. So based on this information, we tailored our ablation to include these high-priority ablation points. On the day 8, implant CPU was successfully removed, and on the day 28, ICD was implanted. CRTD was not necessary, because the conduction system was preserved. So finally, on day 35, C could be discharged home. No episode of VF-BT or heart failure deterioration were observed during the two-year follow-up. Now regarding VF requiring mechanical support, this video shows LV cavity changes monitored by eyes during modulation of impeller flow. Increasing the impeller P-level reduced LV cavity like this, making mapping ablation difficult, you can easily imagine. Keeping the relatively low P-level constant during ablation is recommended. Increasing the P-level also raises the risk of EMI, electromagnetic interference, so it should be minimized during the procedure. P-level is reduced from P4 to P2 in this case. This video shows that ablation catheter appears to move on the carotid, but it's actually still constant. But reducing from P4 to P2, we are able to reflect the true position of the ablation catheter. We experienced 10 similar cases, VF storm post-EMI patients so far, and it becomes clear that anatomical ablation package, the networking alone is insufficient. Combined with localized substrate debarking and targeted catheter-induced VF sites is essential I think. But some challenges still remain unresolved. Defining the optimal ablation area is very difficult because the myocardial damage varies by the patient. So in two of our 10 cases, and the previous report demonstrates that VF recurrence has occurred due to insufficient ablation. So we advocate post-ablation high-density mapping in order to confirm success and ensure no catheter-induced VF remains. So to summarize using utility of high-density mapping catheter in VF ablation, first, ripple map helps identify the conduction system to guide safe package in the network without damaging the conduction system, like CRBB complications. Second, substrate evaluation identifies SCAR-Border Zone potential sites of triggered PV sheets. Third, by inducing VF, we can obtain the local package potential information and we can efficacy of the ablation procedure. So high-density mapping catheter is a player, very important role in VF ablation. And let me conclude. High-density mapping guided ablation incorporating package in the networking and local substrate debulking was effective management post-MIV-STOM evening patient with requiring mechanical support. Thank you for your attention. It's now open for any questions or comments. I have one. How do you balance pro-arrhythmia from the multipolar catheter, particularly in these patients that are so irritable? And when I put a Nocturay into the ventricle, I get all sorts of PVCs. Do they have to be done on anti-arrhythmic drug therapy to stabilize pro-arrhythmia from the catheter? What's your approach? Thank you for your question. It's very difficult and I don't have a clear answer, but VF ablation, I think VF ablation is relatively less stressful than VT ablation, because VF ablation play a role, important role. Sorry. It's a package in the network plays an important role in VF trigger and maintenance. So in clinical experience, we performed amiodarone and Langevrol or something like anti-arrhythmic drug therapy and we, but we have some regard, we moved the catheter ablation and yeah, so, but I don't have a clear answer for that. Thank you. Thank you very much for the presentation. So my question goes, before the denetworking, when you're doing the mapping of the substrate and determining where these triggers are coming from, can you determine whether the trigger is more myocardial or from the Purkinje network itself, or is it just a PVC in general? Thank you. Thank you for your question. In our 10 experienced cases, the VF originate from the, all of the cases, the VF originate from the Purkinje fibers. So as a previous case studies or reports, the VF originate from the Purkinje network. So under the morphology of PVC, trigger PVC is relatively narrow and with a left anterior or posterior fascicle origin PVC. So I don't, I didn't experience trigger PVC is originate from the myocardium, not Purkinje potential, not Purkinje fiber. So we, yeah, so trigger PVC must be in, originate from the Purkinje, I think. Great presentation. If you map in that Hesper-Purkinje system and you find nothing there, what do you map next? Oh, thank you for your question. In my 10 cases, the catheter-induced VF occurred in all of the cases. But if no catheter-induced VF occurred, I analyzed the substrate map and we operated the SCAR border zone and base mapping was performed and we operated on the sites with good base map matches. But our 10 cases, if you use a high-density mapping catheter, the catheter-induced VF must be occurred. So next strategy is like this. Thank you for your insight. This is challenging and difficult, but we want to learn from you. Thank you. Thank you very much. Thank you very much for that excellent presentation. The next presenter is Florent Fnano from the Maastricht University Medical Center. The title is the focal point-by-point pulse field aberration for the treatment for atrial arrhythmia in patients who are challenging anatomy where radiofrequency aberration cannot be applied by the case series. Let's get started. Very long title, sorry. Okay, I would like to start by thanking the HRS for the invitation. It was a very long trip from Belgium for a 10-minute presentation, but I'm very happy to be here. I'm going to present you a series of three patients suffering from atrial tachyarrhythmia with complex anatomy at high risk for thermal ablation, for whom we performed ablation using a focal PFA system. I will start showing you the focal PFA system. So this is a focal PFA generator connected to conventional contact force enabled ablation catheter, focal catheter, and we used biphasic monopolar waveform using 22 and 25 amperes according to the optimized PFA protocol of the ECLIPSE-IF trial. Important question, why this series and why PFA? Because thermal ablation is associated with tissue heating, which is a nonspecific tissue lesioning mechanism. Heating the myocardium is what we want, but there is also a risk of heating surrounding anatomical structures through heat conduction. This can lead to dreadful side effects of thermal ablation, risk of phrenic nerve palsy, risk of digestive tissue heating, including atrioesophageal fistula, which is every electrophysiologist's nightmare. On this figure I've added the aorta, which is also just behind the left atrium, and we don't talk much about aorta because it doesn't seem relevant during conventional ablations, but we are not talking about conventional ablations here, and you will see it in a few minutes. On the other hand, we have now accumulated data regarding the excellent cardioselectivity of PFA. Among them, the manifest registry evaluating safety profile of PFA showed no esophageal event, no phrenic nerve paralysis, well, a few phrenic nerve paresis, as my colleague just said, no PV stenosis in more than 17,000 patients. As you can see, the aorta was not represented in the graph, but this is in general population and the inclusion of specific or high-risk patients was not specifically addressed, and that was one goal of this short series. So let's start with patient number one. It is a 64-year-old lady with risk factors and medical history of ischemic heart disease with reduced ejection fraction and undervascular aortic replacement of abdominal aortic aneurysm. The patient was referred to our clinic for management of symptomatic paroxysmal atrial fibrillation associated with tachycardiomyopathy. In our center, we systematically performed preoperative cardiac CT scan, and one of the reason is to assess the anatomy of the left atrium and surrounding structures, and in this case, we were very happy of doing this because this is what we found. You can see it. This is the left atrium. This is the aorta, and on the anterior portion of the aorta, you see a saccular aneurysm in very close contact with the left pulmonary vein, and this is just where you want to ablate. As you can imagine, we were not very comfortable with the idea of this ablation, and especially as the effect of ablation on the aorta have been relatively poorly evaluated in studies. We found this one, comparing the effect of ablation on the aorta using MRI depending on whether PFA, RF, or cryoablation was used, and the effect of ablation on the aorta seems to be less while using PFA, less but not zero, and this is the reason why we used PFA in this patient after a long discussion in heart team with a surgeon and including the patient in the decision-making process. This is the ablation integrated with the cardiac CT scan, and we used PFA, and we used focal PFA. The reason for that is that we could tailor the ablation to the anatomy, and as you can see here, we ablated a little bit wider the left pulmonary vein to avoid ablation regarding the aneurysm. This created a narrow isthmus on the posterior wall, and that's why we made this additional line to overcome eventual further reentry. At six-month follow-up, the patient presented no recurrence of AF. That is a good point, and in terms of safety, follow-up CT scan showed no complication on the aneurysm, no rupture and officeration, no local clotting, and the patient presented no peripheral embolization of the lower line. The patient, too, is a different patient, but it's the same kind of story. It is a 63 years old man. Some risk factors refer to a center for paroxysmal and symptomatic atrial fibrillation with tachycardiomyopathy. Once again, preoperative CT scan, very useful, and revealed at this time it was no longer the aorta that was the problem, but the stomach, as the patient was suffering from a major aorta hernia with a compressive effect of the stomach on the left atrium, just here. That's where you want to ablate. As previously mentioned, digestive damage secondary to thermal ablation, including the atrioesophageal fistula, are among the most serious complications and represent every physiologist's nightmare. On the other hand, the selectivity of PFA on the myocardium sparing digestive tissue has been well demonstrated during ablation, and I already showed you this previously, and that's why we opted for PFA in this series. This is again a reconstruction, and you see the left atrium, you see the ablation points, and the blue shadow is the stomach. As you can see, we ablated a lot regarding the stomach in this case, because we didn't have choice. While focal, it was just a question of availability at that time. I think single shot was as good in this case. During follow-up, the patient had no recurrence of arrhythmia and normalization of the left ventricular ejection fraction, and regarding safety, the patient presented no symptoms of digestive origin. He didn't wish to undergo gastroscopy, which is a limitation here, but we performed an MRI, which showed no suspicious lesion in the stomach close to the left atrium. And third, last but not least, it is a young lady, 39 years old, no medical history, no medication, and referred to our institution's emergency department for palpitation. This is the ECG at admission. The quality is not very good. This is a narrow QRS complex tachycardia cycle length, about 210 beat per minute, so very fast. And if you take a close look at the inferior lead, you have two important information. It is a long RP tachycardia, and P waves are positive, which is a strong argument for atrial tachycardia. The patient first received adenosine with no effects, and then 10 milligram verapamil with conversion to sinus rhythm. We gave her the choice between medication or ablation, and she opted for ablation as she didn't wish to take long-term medication, and this is the EP study during tachycardia, several important points. The first point is we still have this positive P wave in inferior lead, and the cycle length is about the same as the clinical tachycardia. You can see there is a one-to-one VA relationship with a long VA interval longer than 70 milliseconds. You can also see that the activation on the CS is concentric, so you see it's concentric here, which is an argument for right-sided or septal atrial tachycardia. Finally, we made a ventricular overdrive pacing showing a reproducible dissociation of the V and the R with no change in atrial tachycardia when pacing was stopped. At this stage, we have enough evidence to suggest right atrial tachycardia that we decided to map. This is a posterolateral view of the left atrium. This is the activation map during atrial tachycardia, and as you can see, the earliest activation is located on the crista terminalis just here, and the gray shadow is the path of the phrenic nerve, so very highly problematic and high-risk situation regarding the phrenic nerve. Second point, this is an activation map during sinus rhythm. The sinus node is very close to the earliest activation during AT, so you need something safe for the phrenic nerve, and you need something very focal not to damage the sinus node in this young lady. At the time, I thought PFA was very safe, but today I'm not sure it's so safe. Focal PFA meets both these criteria, theoretically. After the first application, the patient converted to sinus rhythm, and we consolidated the ablation with two additional points, and the patient was non-inducible at the end of the procedure. She presented no AT recurrence, and most important, she presented no phrenic nerve lesion and no sinus node dysfunction at the end of the procedure, and regarding phrenic nerve, we used manual palpation and fluoroscopy control prior to ablation, after the ablation, and it was not different, so it's the gold standard, as said my colleagues, so it seems to be good. At the end of the series, we are happy because we had very high-risk patients, and it seems to be safe regarding the aorta, regarding the digestive tracts, and regarding the phrenic nerve, but it's only three patients, so what is the key teaching home points of the series? Pulse field ablation should be considered as an alternative to thermal ablation in patients with challenging or high-risk anatomies. Focal pulse field ablation allows the creation of tailored ablation sets for complex and targeted ablation procedures, and the safety and achievement of intra-procedural endpoints and short-term outcomes in patients with challenging anatomies are promising. You can find the full case report on the website of Heart with Case Reports, and I thank you very much for your attention. Yes, thank you very much for very informative three case studies. Let's open to the discussion. I have a last case that is very important. I think the origin of the HR tachycardia is very close to the sinus and also the phrenic nerve injury, but the former two cases, one-shot device, one-shot pulse field ablation would be maybe okay, one-shot, you know, like faraway ablation. Yes, for the first case, I think it's very useful to have a focal system. For the first case, I think it was useful because we made a map and we integrated the map in the CT scan, and it allowed us to make a wider ablation, not to ablate on the aneurysm, and I think with Farapulse, maybe it's less easy to ablate precisely where you want on the posterior wall, and to be honest, that was also a question of availability because we had the focal system, but we didn't have the single shot at the time, and for the second case, I fully agree PFA was important, I think, but focal PFA was not so important, I think, and as I said, I think a single-shot system could have done the job for patient number two. Okay. Thank you very much. Thank you. For our next talk, we have Dr. Tushar Pansuria from Michigan State University, and he'll speak to us today about full-thickness skin burn complicated by high-power radiofrequency ablation of persistent atrial fibrillation. Thank you for the invitation and for introduction. Good morning, everyone. I'm Tushar Pansuri, I'm a third year cardiology fellow at Michigan State University. I'm presenting this case, it's a full thickness skin burn complicating high power radiofrequency ablation of persistent atrial fibrillation. I don't have any disclosure. So introduction, even with emerging field of this pulse field ablation, radiofrequency ablation still remains primary modality of ablation. Radiofrequency ablation delivers high frequency current through the ablation catheter with heat dispersed via indifferent electrode, which is also known as a dispersive pad or grounding pad on the patient's skin. Skin burns at indifferent electrodes are very rare and is also underreported. So this case highlights a full thickness skin burn at indifferent electrode site during high power short duration radiofrequency ablation. So my case is about a 60-year-old female, morbidly obese, BMI around 38. She had a recurrent symptomatic atrial fibrillation. She had a prior to ablation, one was around five years ago and another one was two years ago and she developed a recurrence of atrial fibrillation. She was very symptomatic despite being on medical therapy. So team decided to underwent third ablation with patient's discussion as well. So procedure details, procedure was performed under general anesthesia and the tactic catheter, contact force ablation catheter was used for the ablation. One indifferent electrode was used. It was placed on the right lower back. And during ablation, they did reconnected right pulmonary vein and left it till posterior wall isolation as well during this third ablation. And the power settings, it was 50 watts. Each lesion was for 10 seconds and point-to-point techniques. Average temperature was around 32 centigrade and the average impedance was 140 ohm. Therapeutic time was around 11 minute and total radio frequency time was around 25 minute. And during this procedure, as per protocol, esophageal probe monitoring was also maintained. Immediately post-procedure, no visible skin changes were noted at the grounding pad site and patient also committed to sinus rhythm during ablation. But during the follow-up, patient did call on the second day and say that she's having some pain in erythema on the grounding pad site on the day two. And you can see in the image one. And the second image, patient was visited to office and it was noted to have a full thickness skin burn, which was treated with silver sulphur dyes and topical therapy. And you can see in the image C, within three months, patient did have a complete recovery with residual scar. And patient did maintain sinus rhythm. So discussion, why did this burn occur in this patient? There are some risk factors in this patient. Particularly, patient has high BMI. BMI is around 38. We can certainly increase the circuit impedance. So it can hit more heat concentrated in different electrode. And we also use only one electrode and so it can also have a more higher heat density at the same electrode. And there is a possible malattachment of the grounding pad as well during the ablation. So it can also have a more heat dispersion at the remaining pad. And our procedure also had a high radio frequency duration, around 25 minute. We certainly increased the high risk temperature in different electrode as well. And during general anaesthesia, there is no real-time feedback. So that doesn't help as well. So what does literature say about this complication? Average is around less than 0.3% reported skin burn during this radio frequency ablation. So it's very rare, but it's also underreported. So we don't know the actual how many prevalence is there. And the higher BMI patients certainly have a high risk of the skin burn, particularly because of the high impedance in the circuit. And the alternative strategy, according to literature, is to recommend multiple in different electrode used during the radio frequency ablation, which can reduce the circuit impedance as well as reduces the localized heat density. And optimal pad placement is very important. And they are considering mostly on the thigh or the chest to put the in different electrode. Or you can use alternative energy like cryo ablation or pulse-filled ablation nowadays. So there are some strategies also recommended, which is not practically possible sometimes. But real-time temperature at the in different electrode can also help. So I will go with the conclusion. So skin burn in different electrodes are very rare. But can we see this complication in radio frequency ablation? And most important risk factor is high BMI. And if we use prolonged RF ablation, and if you use only one in different electrode, or if there is a possible malattachment of the electrode during the ablation, these are the very possible risk factors to develop a skin burn. So preventive strategy-wise, optimal placement of the pad is very important. So it can have a uniform heat dispersion in the different electrodes. And I was also recommending multiple in different electrode use. And monitoring the skin side during ablation or after ablation is very important. And so certainly we need a better procedural protocol as well as the data to track and prevent skin burn in the future. And these are my references. Thank you so much. I'll take questions. It's open for questions. It's open for questions. Do you have a sense of the timed expiration of the pad? These pads tend to dehydrate, and that's one of the areas of scrutiny, at least for approval pads, that they can dehydrate in a pattern that's asymmetric. Did you look at the pad or anything to see? So during the ablation, the pad was placed in the back, and it was very properly attached. But certainly we are thinking that there is a malattachment. You can see that a skin burn is not throughout the pad, it's only in a certain portion of the pad. So during the ablation, BMOs 30, and even during the moving, she might have sweating underneath that, there is a possible malattachment of the pad. And that would cause a skin burn most likely. So, yeah. All right. Thank you very much. Really enjoyed that. So the last speaker is Dr. Robert Manning from the Niagara Great Metropolitan Hospital. The title is a pulse-filled ablation of the persistent left superior vena cava in recurrent pulmonary atrial fibrillation, and its effect on the mitral arrhythmias, a case report. Let's go ahead. Dear colleagues, I'd like to start by thanking the scientific committee and the moderators for inviting me today to talk to you about this case I have seen during my fellowship in France. It is the case of a 60-year-old male with multiple cardiovascular risk factors that had been referred to our Center for Symptomatic Recurrent Paroxysmal Atrial Fibrillation that was impacting his quality of life by limiting exercise capacity. He had normal left ventricular function and a severely dilated left atrium. His history in the EP lab starts back in 2010, when he received the first cryo-balloon pulmonary vein isolation. Already at that time, the persistent left superior vena cava was reported, but was not ablated. In the few following years, he experienced asymptomatic recurrence, so he was brought back to the EP lab for a first radiofrequency redo in 2016, where a gap at the level of the right inferior pulmonary vein was noted and ablated with radiofrequency. Shortly thereafter, he experienced another symptomatic recurrence, so he was brought again to the EP lab for a second radiofrequency redo. At that time, the operator found no gaps. He performed a more untraveled pulmonary vein ablation, but reported a very electrically active persistent left vena cava that he decided not to ablate, judging it too risky for venous perforation and cardiac tamponade. Unfortunately, the patient experienced another symptomatic recurrence, and for that reason, he was referred at our center. And at that time, we had a new tool available, compared to 2020, that is PFA, that we deemed to be ideal for managing this case. So before the case, this routine at the center, the patient underwent a CT scan. Here you see the 3D reconstruction of the atrial anatomy and of the venous anatomy, with the left superior persistent vena cava joining the coronary sinus. We also performed a venography to better delineate the anatomy and the size of the vena cava that had a maximal diameter of 35 millimeters. We started by performing an endocardial voltage map of the left atrium that confirmed the electrical isolation of the four pulmonary veins with a very untrue ablation, minimal substrate disease on the anterior wall, and at the level of the posterior mitral isthmus. Here we can also appreciate the anatomy of the persistent left superior vena cava that, just a quick reminder, is an embryological remnant of the left cardinal vein. So it starts from the left subclavian vein, runs down over the coumadin ridge anterior to the left pulmonary veins and posterior to the left atrial appendage, passes over the posterior mitral isthmus to join the coronary sinus. We then performed a mapping of the left superior vena cava, which revealed a very electrically active vein with a high voltage, high frequency signals all over the course of the vein from the coronary sinus ostium up to the most distal portion on both the anterior, lateral, and posterior aspect of the vein. We also performed a left coronary angiography to better delineate the anatomical relationship between the circumflex artery here and the persistent left superior vena cava. And as we already knew, we would have delivered several PF applications close to the coronary artery. We decided to administer one milligram of isosorbidin nitrate preventively to prevent coronary spasm. We then advanced the far wave catheter into the left vena cava with the classic over the wire technique under fluoroscopic guidance and under guidance with a CARTO system. At the time, the far view model was not available yet, so we only have the representation here as a multipolar catheter seen in the distal portion of the left vena cava. And by starting from the most distal portion in the vein with a routine scheme, we performed two PF application per position. We then rotated the catheter, other two application, and retracted the catheter more proximal into the vein until no electrical signal was recorded anymore. What was the effect of this ablation? Here you see again the baseline voltage map, and this is the voltage map taken 20 minutes after the last application. So a very reassuring red homogeneous, no voltage in the left vena cava. We then decided to move back to the left atrium and perform a second mapping after the applications in the vena cava. This again is the baseline voltage map, and this is the voltage map following applications on the epicardium. And we can see how the area of low voltage is close to the mitral valve is considerably larger. It almost reaches the mitral valve, and now a small corridor of slow conduction between the inferior pulmonary vein and the mitral valve has appeared. As we deemed that corridor to be too high risk of becoming a possible future substrate for a potential perimitral flutter, we decided to also perform an endocardial ablation of the mitral isthmus, always with a faraway catheter in the flower configuration. Here you see under fluoroscopic guidance, the fusion with a 3D reconstruction of the CT images to guide the ablation. We also used the electrical signals as a reference to locate the mitral isthmus, finding a balanced signal between atrial and ventricular signal, and we performed endocardial ablation of the mitral isthmus. Finally, this is the left atrial map at the end of the procedure, where we can appreciate the presence of a complete line of conduction block at the level of the posterior mitral isthmus. A brief discussion, the persistent left superior vena cava has a prevalence of almost 1% in the general population, and when it is present in a patient with atrial fibrillation, it has been estimated that it can be responsible for driver triggers or fast electrical activity in up to 50% of the cases. For this reason, different ablation strategies have been proposed, each one with its strengths and drawbacks. Radiofrequency for sure is the one that is better known. It has the advantage, especially with the last generation catheter, of having the possibility to modulate the energy and irrigation output with specific protocols for the coronary sinus, but still the first pass efficacy in isolating the persistent vena cava is very low, as low as 30%, and it still carries a considerable risk of sympopsis and perforation with potential cardiac tamponade during an ablation of a persistent vena cava. Also in a case such as ours with a widespread distribution of electrical signals, point-by-point radiofrequency would be a very long procedure. For this reason, some center reported their experiences with a cryo balloon that has the advantage of having no risk of sympopsis and perforation, that can be a very short and straightforward procedure, but in these patients, a very high risk of phrenic nerve palsy has been reported. Interestingly, not of the left phrenic nerve, but of the right phrenic nerve. Lastly, we reported the first experience of PFA ablation of the left vena cava, and again, here it says no risk of phrenic nerve palsy. Probably I have to correct this slide after the presentation we have seen today, but for sure is a lower risk of phrenic nerve palsy compared to cryo balloon. It has no risk of sympop of perforation and is a very straightforward procedure, especially if performed with a large interface regional catheter such as the far wave. On the other hand, we have to keep in mind that the risk of coronary spasm is present, but the literature tells us it can be effectively prevented with preventive nitrates, and here I put it under PFA only, but actually the risk of incomplete mitral isthmus block, arrhythmogenic mitral isthmus block, is present with all the energy sources that can have a transmural effect when ablating from the epicardium. So my take-home message is that our persistent left superior vena cava is a common anatomic variant and is associated to an increased risk of AF. PFA may be a safe, fast, and effective strategy to ablate the persistent vena cava, but this approach may result in a potential arrhythmogenic incomplete line of block at the level of the mitral isthmus, and thus endocardial mapping and eventual touch-ups of the applications are needed. All the details of this case are presented in the related publication of our Arrhythm case reports. Thank you very much for your attention. Thank you very much for a very challenging case, and let's open the discussion, and I have a question, the strategy, the ablation strategy, during the PFA ablation, you use a continuous nitrogen injection in this case, no? No, just a single dose, one milligram, not of nitroglycerin, but of isosorbic denitrate, which has a longer half-life compared to nitroglycerin. So we expected it to give a full coverage throughout all the procedure, which in this case was really, really fast, because in total we applied 12 applications. So I don't have a time, but it would have been, I think, a couple of minutes from when we administered nitrates to the end of the ablation, the same protocol of one to two milligram of isosorbic denitrate. We also used it for all the cases we did of endocardial mitral isthmus ablation, which were considerably longer, and we had procedures with up to 40, 50 applications only on the endocardium of the mitral isthmus, so 20, 25 minutes of applications, and just with abolus at the beginning of the, before the first application, we always had a full coverage throughout the procedure with no clinically relevant spasm. Okay, thank you very much. Go ahead, one question. People who propose, like, instead of like isolating the whole persistent, just go to the lower part and isolate it, but I think all of us, you know, there's epicardial-endocardial, you know, connection, and it would be better to do that, you know. Some other people will do, after you do the ablation, try to induce a perimitral atrial flutter, you know, dependent atrial flutter, but the map, it was so perfect, it showed that there's an area of leakage in that area. We have cases with venom marshal, actually, after we did the alcohol ablation, and endocardially, and then we induced mitral isthmus dependent atrial flutter, which was, like, for us, like, unusual, and when we have inside, we have incomplete circuit, but we found remnant, even after alcohol ablation, remnant of connection epicardial, and we have to go inside and put, like, some lesion to terminate it. So the question for you, after you do this, you did not do induce, try to induce any perimitral endometrial flutter? You did not do it, just did the voltage map it and see if there's any area of connection and just go ahead and ablate it, you know? Exactly, just by looking at the voltage map, we decided that the passage was too narrow, and also, I didn't mention it during the presentation, but also, the corridor on the posterior wall that I've shown you before, resulting from the previous atrial ablation, was very small, so we not only performed the ablation of the mitral isthmus, but also of the posterior wall, also, probably with the faraway catheter, in order to block the two most likely potential circuits for a recurrence in a patient that was already at the third redo procedure. So we really wanted to try to eliminate all potential arrhythmogenic circuit, even without trying to induce the flutter. You're a gutsy man. You did the one PFA in the liposystem, I will do RF from inside, but you have bigger biceps than mine. Great case, thank you. Thank you very much for the great presentation and the challenging case, and that's all. Time is passing, so we have to wrap up this session, and so thank you for joining this session, and so valuable presentation, and thank you for audience, and thank you very much. Thank you.

electrophysiology

pulse field ablation

PFA

arrhythmias

phrenic nerve palsy

high-density mapping

ventricular fibrillation

thermal ablation

cardiac intervention

clinical case studies