Welcome, everybody. I'm Luigi de Biase from the Albert Einstein College of Medicine at the Montefiore Hospital in New York. And I'm the chair of the Global Relations Committee. And on behalf of the Global Relations Committee and the Digital Education Committee, I welcome everybody to the WEBIT webinar series. This time today, the BEAT webinar will be in partnership with the Japanese Hyderabid Society. I'm glad that this partnership is going to happen today. We have a series of cases that will be presented and a panel of experts that do not need any presentation because they are probably the most famous and expert on this topic that we're going to disclose today between Japan and the USA. As this is being said, I will give the word to the following speaker. Well, hello, and welcome to this webinar, which is a part of the BEAT webinar series. The topic, as Dr. de Biase said, is an uncommon case of idiopathic left fascicular tachycardia. I am Sana Al-Khatib. I'm an electrophysiologist at Duke University in Durham, North Carolina, and I'm here representing the Digital Education Committee. It is my absolute pleasure to be with you. We have excellent speakers and panelists, as Dr. de Biase said, who I would like to introduce to you before we start. Dr. de Biase, you heard from him. He's the head of the AP section and the director of arrhythmia services, a professor of medicine at Montefiore. In addition, he serves as a senior researcher at the Texas Cardiac Arrhythmia Institute. We have several presenters. The first presenter is Dr. Itsuru Morishima, who is the director of cardiology at Ogaki Municipal Hospital, as well as a clinical associate professor at the Nagoya University Graduate School of Medicine. We have the following panelists. The first is Dr. Mitsunori Maruyama, who is an associate professor of cardiovascular medicine at Nippon Medical School in Musashi Kosuke Hospital in Kanagawa, Japan. Another panelist is Dr. Hiroshi Nakagawa, who is a professor and an internationally recognized physician, teacher, and researcher, who holds several patents for a radiofrequency ablation catheter and mapping systems. He has been at the Cleveland Clinic since 2020. Then we have the pleasure of having with us Dr. Akihiko Nogami, who is a professor of cardiology at the University of Tsukuba Faculty of Medicine. He has great expertise in different areas and has done a lot of clinical research, mostly related to ventricular tachyarrhythmias. Then we have Dr. Kyoko Tsujima, who is a professor and a chair of the Department of Cardiovascular Medicine at Kyorin University in Tokyo. She specializes in the management of cardiac arrhythmias and sudden cardiac death prevention, as well as catheter ablation of complex arrhythmias and devices. Then last but not least is my colleague, Dr. Bill Stevenson, who is a professor of medicine at Vanderbilt University Medical School. Dr. Stevenson received his MD degree from Tulane University in Louisiana, completed his medicine cardiology training at UCLA, and he specializes in the management of cardiac arrhythmias, mostly ventricular arrhythmias, and the prevention of sudden cardiac death. We are delighted to have you all with us today. With this, I'll turn it over to the presenter. Good morning. I'm Dr. Morishima from Oguchi Municipal Hospital, Japan. First of all, I'm very honored to have the opportunity to speak at this webinar. I'll be presenting a case of idiopathic retroventricular vascular tachycardia, which has some atypical features. So I'm very happy to share the case and discuss about it. So I'll share my slides. The thread shows my COI. The patient is a 28-year-old male with no apparent structural heart disease. He was in fast-forward catheter ablation of recurrent wide QRS tachycardia with a light bundle bench block pattern, superior axis, and relatively short QRS duration of 120 millisecond. The EKG during sinus rhythm was unremarkable. The patient had undergone catheter ablation at another hospital, however, which was unsuccessful. So this EKG was included in the referral letter. Intravenous blood pumping slowed and terminated the tachycardia. Interestingly, you can appreciate a change in the QRS morphology in the last beats prior to termination. So we'll come back to this later. Based on the 12-lead EKG findings and weapon sensitivity, we thought that the tachycardia was likely to be a fast-forward tachycardia. So we brought the patient to the EP lab. We placed the electrocatheter at HLA. Here's RV and CS. During sinus rhythm, the HP interval was 55 millisecond, a little bit longer than the upper normal limit. So initially, we gave a program atrial pacing with a basic cycle length of 600. As we shortened the A2 interval from 390 to 380, the tachycardia was induced without AH jump. But during the tachycardia, we repeatedly saw a transformation between narrow and wide QRS tachycardias, a kind of confusing tachycardia. The QRS morphology of the wide QRS tachycardia was very similar to the clinical tachycardia. And the QRS morphology of the narrow QRS tachycardia is almost identical to that during sinus rhythm. The cycle length of tachycardia was around 370 millisecond during both the narrow and the wide tachycardia. However, there was a noticeable variation in the AH, AA, and PV intervals. The A sequence was always the same. You can see the earliest activation at the CS ostium. The HISS right bundle activation sequence looks the same during the narrow and wide QRS tachycardia, which is proximal to distal. The HISS right bundle activation sequence is the same. However, if you take a closer look, you can appreciate a subtle change in the sequence. During the narrow tachycardia, the signal goes from base to the apex from the proximal HISS to the distal right bundle. During the wide tachycardia, the proximal HISS activation is a little bit later than the distal HISS, indicating the retrograde activation of HISS bundle. The HV interval during the narrow tachycardia was the same as that during sinus rhythm. However, the HV interval during the wide QRS tachycardia was much shorter than that during sinus rhythm. So we diagnosed the narrow QRS tachycardia as SVT and the wide QRS tachycardia as VT. And they were competing each other. So in the meantime, the VT became sustainable with a gradual shortening of the cycle length of the VT. Then we mapped the LV with an ablation catheter during the VT. And we found these disordered Purkinje potentials going from base to apex. The Purkinje potentials preceded the QRS onset by 30 millisecond at distal and by 37 millisecond at the proximal. We attuned the tachycardia from the distal pair of the electrodes. This is almost selective capture or p-capture. As you can see some delay between the pacing spike and the local myocardial potentials. We saw a manifest diffusion, but the PPI minus VT cycle length was 25 millisecond. So this Purkinje potential was located on the VT exit. The diagnosis is made at the left plus the VT. We thought this was the spot to ablate and it started to burn. Then we saw something very interesting. We started ablation here. On the next bit, the VT was not terminated. However, there was a significant change in the VT morphology. The VT axis changed from superior to inferior with a slight increase in VT cycle length. This is the intercardiac recording. Again, we started ablation here and the VT morphology changed in the next bit. Although there was a transition in VT morphology from VT1 to VT2, the diastolic Purkinje potential could be seen continuously at the proximal electrode. Then we remapped the VT2 and gave another burn targeting Purkinje potential. You can see the Purkinje potential again going from base to apex. We also saw a change in the VT2 morphology and the VT2 morphology changed in the next bit. This is the intercardiac recording. Although there was a transition in VT2 morphology but again, the VT2 transformed to VT3 during ablation. We kept mapping and this is a success site to terminate the VT. Here you can appreciate tiny Purkinje potential which preceded the QRS by 65 millisecond. The ablation catheter was located not on the septum but somewhere laterally away from the septum. So we started ablation here. The VT was terminated but the SVT kept going. The HV interval during the VT was 15 millisecond. However, in the last two bit, the HV interval was identical to that during sinus rhythm. And more importantly, you can appreciate the obvious change in the HISS right bundle activation sequence as you did in the trace showing the transformation of the tachycardia before catheter ablation. So during the VT, HISS, and RB. So the timing is almost the same. However, during the SVT, you can appreciate the clear antigrade conduction from proximal HISS to RB. So this is SVT. So during the SVT, we gave a ventricular stimulus on the refractive period of HISS bundle. We did not reset the following A and HISS. In addition, the stimulus pulled the V which is the most closely located to the earliest A site. However, the A remained the same. So these findings made ORT unlikely. We diagnosed the SVT as fast, slow AVNRT. The slow pathway ablation made the SVT non-inducible. And we closed the session. This is a CT image to locate the ablation spot. You can appreciate that the ablation was done on the posterior papillary muscle. The present case, very sensitive idiopathic left vascular VT has two important characteristics. This was a double tachycardia with fast, slow AVNRT. And the success site was on the left posterior papillary muscle. Usually, the LV posterior septum is a common site of catheter ablation for the left vascular VT. Dr. Zipes first introduced this type of VT more than 50 years ago. One of the diagnostic trials proposed by Dr. Zipes is that the VT is inducible by HO stimulation as shown by this trace. So because of that, a double tachycardia with an ILVT and SVT is a possible condition, although it is rare. So this double tachycardia has been described in several case reports. So two cases of AVNRT plus left posterior vascular VT and a case of ORT plus left anterior vascular VT. So keeping this in mind may help you in performing an accurate diagnosis when you come across a kind of confusing tachycardia during the session. We recently proposed new classification of the ILVT. So in addition to the three classical types, which are left posterior and left anterior, excuse me, left posterior and left anterior and upper septal vascular VT, we have added two distinct types. One originated from the posterior papillary muscle and another originates from anterior papillary muscle. So each of the five forms has unique ECG calculistics and a specific area of catheter ablation. The posterior papillary muscle type has a right superior axis or horizontal axis deviation. So this is an example of a posterior papillary muscle vascular VT with a horizontal axis. You can see a clear P1 and a P2 potential at the success site, which is located not on the septum but on the posterior papillary muscle. The catheter position was further confirmed by endocardial echo during the session. Changes in the QR morphology during catheter ablation as you saw in this case is one of the unique characteristics of the papillary muscle type vascular VT. We saw the actual mode of termination by the intravenous VLA-PAML at the beginning. The VT changed from superior axis to inferior axis before termination. After the session, we noticed that the last three beats are very similar to VT3. So is it likely that the VLA-PAML induced transition from VT1 to VT3 before VT termination? So what is the mechanism? The left panel is an autopsy specimen of human hearts. You can appreciate the myocardial bridging so between the anterior and posterior papillary muscles. And a recent study using cardiac MRI showed the presence of anatomical connections between the papillary muscles and the ventricular myocardium in patient with a non-reentrant papillary muscle ventricular arrhythmias, suggesting that the number of anatomical connections is related to the number of variations in VT morphology. So therefore, these anatomical connections may also be related to the sudden change in the QRS morphology or the papillary muscle type of vascular VT. So in conclusion, I presented a case of VLA-PAML sensitive idiopathic left vascular VT. This was a double tachycardia with fast, slow AVNRT and the both were successfully ablated. The origin was located on the posterior papillary muscle. The dynamic change and the VT morphology were seen after VLA-PAML administration as well as during Purkinje guided catheter ablation. So this concludes my quick case presentation. Thank you. Thank you very much for this, I would say very complex and excellent case presentation. Before I hand over the word to the panelists, one clarification, you said this patient before the surgery you said this patient before going to the process you presented had a prior ablation. Can you comment on which type of ablation or what was the target of the procedure the first time? Yeah, go ahead, sorry. Okay, so actually they made a diagnosis. This is a vascular VT and the area they ablated was LV's posterior septum and the posterior papillary muscle. So they did a very similar procedure, but they were not able to achieve the termination of the VT. Yes, very good. Thank you for the clarification. The second one is when we say verapamil sensitive tachycardia, I saw you use five milligrams. Is five milligrams enough to define, is that termination of the VT due to the use of the verapamil or it's just by chance? What do you think about five milligrams? If anybody else wants to comment about the dosage utilized to make this type of ablation. Okay, see, I would say usually five milligrams of verapamil should be okay to terminate the VT, but in some cases we can terminate it with 2.5 milligrams. So, but in other case, sometimes five milligrams verapamil only longer, make the cycle length longer, but cannot terminate. Yes, so it varies with individuals. Thank you very much. So I see Dr. Stevenson has raised the hand as a first comment, please, Will. As one of the older people who has some experience with giving verapamil for SVTs, verapamil is very highly protein bound. So the effect depends a lot on how quickly you give it. You have to give it, if you give it very rapidly, you get much more of an effect than if you slowly push it in. Yes, thank you. I mean, I think, you know, younger generation, we have utilized these drugs much less because we were born in an era where the ablation is widely available, but I wanted to hear because I know that, you know, the way you deliver the medication also has an impact. So, any comment, Dr. Stephenson, on the case presented? Any question that you want to start? Yeah, well, thank you very much, Dr. Morishima. That's a beautiful case. You know, two tachycardias interacting makes a very long day usually in the EP lab. The first thing is you have to recognize that you have two tachycardias, and so congratulations on that, but then to have a type of VT that also has changing QRS morphologies really makes things quite difficult, and I think the fact that you had good HISS recordings throughout and right bundle recordings throughout really helped probably recognize what was going on relatively early. So, it's beautifully demonstrated, very challenging case. How did you decide to go after the VT first rather than the SVT? I would have thought it might be easier to go after the SVT and then that might make things a little simpler. Yes, okay. Yes, this is just because the VT became sustainable with the gradual shortening of the cycle length. So, yeah, so if the transformation continued, maybe we should have done SVT first, but just because we saw VT going on in front of us, so just because of that, we tried to avoid VT first. So, Jima, you have a question? Yeah, yeah. Thank you, Ueji. Thank you very much, Dr. Morishima. Wonderful case. I really enjoyed it. It's funny. I felt the same way, the SVT and VT simultaneous, like a double tachycardia. I would have ablated AVRMT, but I think as a mentioned, as VT became incessant, you'd proceed it with this challenging VT ablation first. My question to you is, before you start the EP study for this patient, why the QRS complex was identified prior to this? And the previous deferring physician gave you the diagnosis potential for this patient, but why the QRS complex was identified gave you the diagnosis potential for VT? Like a catheter preparation, you place the high RA hiss catheter, coronary sinus catheter, and RV catheter. Is this the normal setting for the vascular VT? I think it's one of the beautiful ECG recording, intracardiac recording, was because we had a nice multi-electrode catheter as a hiss bundle area, in addition to the right bundle area, we could observe the change, the very subtle change, of the hiss bundle and right bundle activation. I would have just placed a very simple, like a quadripolar hiss catheter, but this really made a big difference for this case. Any comments on the catheter preparation? Okay. Thank you very much for your comment. So this is the normal setting for us when we have the vascular VT. Yeah, so we always tried the EP study just as we do in the SVT cases, and we usually use the multi-electrode catheters for hiss and RV recordings. Yeah, so this is just a normal setting. So because we had another case which combined with SVT and vascular VT, so it's rare, but not very rare, so we usually do that. And another thing that we mentioned is that we do not enter the LV until we got the VT, yes, because this VT is easy to bump. Yeah, so if it occurs, yeah, it never comes back during the session. So yeah, that's what we do. Can I ask a very simple question as well? Could you go back to the slide six? It's just so beautiful tracing, and I think also you analyze just the one before that. This one? Okay. Yeah, so I think it's nice, you can see the narrow and wide back and forth, like a QRS change. And along that, you measure the HH interval at the top and AA interval in the coronary sinus and the VV interval. Do you think this is like HH is driving VV or some part, most of the part, I think it looks like HH is driving vice versa, AA is driving it. Yeah, so to be honest, it's very hard to tell. So that's why I print the exact number that I measured. So this could be 370 or 350, but it's very difficult for us to interpret. So the relation between these potentials. So I think sometimes the SVT drive, so VT, and sometimes like what you always drive the SVT. So yeah, so yeah, most of the part, it seems to be like, yeah, HH driving AA. But it's kind of go back and forth. But thank you very much. Yeah, thank you. I really enjoy the case. Thank you. Luigi? Go ahead. Yeah, this Hiroshima Cleveland Clinic. I was very happy to see Dr. Morishima using Octopora Hiscatherin. When I was at Oklahoma 28 years, all cases, almost all cases using Octopora Hiscatherin. When I moved to the Cleveland Clinic three years ago, you know, Dr. Suejima saying, usually people use Octopora Hiscatherin. And during a VT session, usually don't use Hiscatherin. But in this particular case, having even Dr. Morishima, they have Octopora Hiscatherin, which is very impressive. And they help a lot, you know, anti-glare, you know, case light bundle conduction or conduction. You have only like a four-pole electrode. It's very difficult to say anti-glare. So congratulations, Dr. Morishima using Decapora, even more than the current, you know, the Octopora Hiscatherin. So now even Cleveland Clinic, we're using Octopora Hiscatherin, you know, SVT, some VT cases as well. Thank you very much. It's beautiful. And then my question, the, like close to the end of the slide, you talk about some of the more likely false tandem between the papillary muscle or something, but did you have a chance to look at the intercalative echo relative to the ablation site? You assume the ablation site is more likely to locate the papillary muscle, but to be honest with that, it's amazing, sometimes difficult, you get on the papillary or, you know, you know, one still the between. Recently, like a Chinese group publications, they're looking for the false tandem from septum to the papillary muscle. They reported the, you know, insertion site of the false tandem site septum on the papillary muscle, sometimes successful ablation. So did you have a chance to cut by eyes during the procedure in this particular case? Oh, thank you very much. So I have never seen the connection between anterior and posterior papillary muscles on the eyes image, but I did have one case where the connection between LV septum to the posterior papillary muscle, and that case, two types of left vascular tachycardia. So which is a posterior vascular type, and the Xs are located on the LV septum, and another one, the Xs were located on the posterior papillary muscle. So I assume that the connection between the LV septum and the posterior papillary muscle did some role. How about this case? This case? No, because this case was very, very complex, and it took longer time than expected, so we are just happy when we terminate the tachycardia, so we forgot to see the papillary muscle by echo. Actually, we prepared the echo, but we did not do that, unfortunately. Thank you. Dr. Nogami? Yes, congratulations for the great case. Would you show me the entrainment? That is a manifest fusion, but I think that is a pseudo pseudo-manifest fusion because, no, entrainment. Prior slide, I think. You just passed it, I think. Oh, sorry. No, no, prior, prior. This is like a V entrainment, a little bit back, before that? Before RF1. Entrainment. Yeah. Okay, the QRS morphology changed, but I think that is a pseudo and pseudo-manifest fusion. The intracardiac electrode shows a beautiful selective Purkinje capture. However, QRS morphology changed. I think it's very long. Yeah, this one. Because the tachycardia itself is a fusion of the VT and SVT, so this is a change of the ratio of the fusion. So this slide is very beautiful, I think. Good example of the pseudo-manifest fusion. And I want to say something about the belapamyl sensitivity. This kind of papillary muscle task of VT is also belapamyl sensitive, but less sensitive compared to the regular type, septal type. Usually 5 milligrams of belapamyl terminate VT in the, just half of the, this kind of papillary muscle vascular VT. So this case is lucky because the 5 milligrams of belapamyl could terminate the VT. It is my comment. Thank you. Based on your experience, so I would like to give some, you know, take-home message for the audience here. So in this specific case, the operators, they knew probably it's a vesicular VT and they planned to place collators this way. The presenter clarified that this is the setup. But when you are going to do a complex VT-SVT ablation, which can be single, double tachycardia, what's the minimum number of characters, or there is no minimum character, what the number of characters that each of you would recommend for, you know, diagnosis at the beginning of the case. When I was an EP fellow in my second EP fellowship here in the US, at one of the fellow programs by Dr. Stevenson, he clearly told me, Luigi, if you don't have his bundle recording, you can't call yourself an electrophysiologist. So I like to remind always this comment to all the younger generation that approach complex cases like this one. So my question is for all the panel, we start again with Dr. Stevenson, is what is the setup that you recommend? And the second take-home message that I would like to get out of this is, when you are doing this type of ablation, what's the energy settings recommended and the duration of the application that are recommended for this fascicular papillary muscle VT? Dr. Stevenson first. Yeah, so, well, you said it, you need a hiss, you know, ideally a hiss in a right bundle recording for a complex Purkinje-related arrhythmia. So, and it's useful to be able to pace the atrium during a tachycardia when it involves the Purkinje system. And you've got to be able to pace the ventricle. So right there, you need three catheters on the right side, and then your mapping catheter as well. So we usually have four catheters with this sort of a case to start with. These are, as was mentioned, pretty easily bumpable and generally pretty superficial, so you don't need deep lesions. The problem often, though, is there is stability. And we also really prefer to have intracardiac ultrasound with these so that we can see these other structures, the papillary muscles, if there are any additional fibers that maybe are false tendons that we may be intermittently hitting, and the Purkinje potential is in that fiber, it's having stability on those to be able to ablate them. And because of that, we sometimes wind up using maximal output. But you can see that your contact is not great. And it's almost like duty-cycled RF. So imaging, I think, can be very helpful with these situations. Regarding this slide, during the entrainment from the ablation, this study, RF ablation, this site didn't terminate dicaria and change the aqueous morphology. And then, as Dr. Morishima said, the stimulus local V interval is similar to the potential, p-potential to the local V, suggesting you're capturing selectively Purkinje potential. However, showing the paste gas morphology, it's different from doing dicaria. So indicating also, this is not the earliest Purkinje potential site. It's more this study, close to the Purkinje junction. So therefore, you have some fusion, and then also do not terminate. So which makes sense, the reason not terminating, and also some fusion. So if this is the reentrant circuit, I'd like to know Dr. Stevenson's comment. This is related to the outer loop. Although, for the Berhelsen still, we don't know the entrant circuit, precisely where the circuit, but do you have any comment based on this entrainment response? Yeah, it seems like we often wind up capturing some of the myocardium adjacent to the Purkinje tissue, even though we're trying to capture the Purkinje tissue. And that myocardium very often behaves like you're close to the circuit, not quite in it, and you get a little bit of fusion. And even when we've tried to go up and down a little bit on the pacing output, I still find it hard to capture just the Purkinje tissue. Sometimes you can. Dr. Nogami probably has more experience with that than any of us. Do you routinely use entrainment for these, and are you able to capture the Purkinje tissue? Selective Purkinje capture is difficult, much easier to capture the myocardium cell. And the myocardial capturing, the PPA, is much closer to the BD cyclins. That means the ventricle muscle itself is an outer loop of the circuit. So, but in this case, intercardiac lobe shows the Plukinje selective capture. So, it is good, I think. I see Dr. Maruyama that has not spoken yet. Can I see the slide showing the VT termination? So, this one? Yes, yes, yes, this one. Actually, this successful site, you recorded the Parkinje potential during the diastolic phase. Do you consider this potential as a P1? Oh, which one? So, oh, this one, this one? Yes, yes. Um, so, I don't understand your question. So, this is a Plukinje potential, and we can see this at the diastolic phase. So, I think we can call it P1. My point- So, your question, this is not the specialized Plukinje tissue, but something, so, intermediate phascl or something like that? So, P1 represented critical slow pathway conduction, right? So, but when we look at the Parkinje potential after VT termination, that potential occur before the ventricle. Usually, the P1 potential is supposed to be seen after ventricle electrogram. So, I think this Parkinje potential was P2. So, you aborted the earliest P2. Actually, the Parkinje potential to ventricle electrogram interval was so long, but in this particular case, the previous ablation blocked the Parkinje ventricular interface at the posterior papillary muscle. So, the wavefront needs to travel to the anterior papillary muscle through a microwave breeze. So, it should take some time. So, I think that's why the Hb and this Parkinje 2b interval was wrong. So, in my opinion, you might need the earliest P2 ablation, but not P1 potential. What do you think? Okay, thank you very much. So, actually, I noticed, so you mentioned this potential. So, this one, yeah. So, it seems this potential comes from his, yeah, but you can see that the, you can see this only this beat? I think the next beat also has a Parkinje potential before the ventricular electrogram. Okay. So, actually, to be honest, I think this vascular VT has atypical findings. So, for instance, that his, so usually his does not precede the QRS onset in a common type of vascular VT, but in this case, he's preceding the QRS onset. So, that means maybe a paternal under the VT is very close to the his. So, this is unusual for the, so typical case of vascular VT. So, yeah. So, the circuit may not have been typical one, but I cannot say this is, the posterior fascicle. And you mentioned there was a block in the left posterior fascicle, but it seems this goes anti-gradually from prosthema to distal. And the catheter was not on the septum. So, I think it's unlikely this was the LPF. Can I comment on that? According to the Chinese paper, if the HV interval during the VT is positive, the successful visual site might be the earliest P2. So, Dr. Mariam's hypothesis is right. But the another explanation of this tracing is during the VT, the spiky potential is a P1, but during the SVT, the spiky potential before the onset of QRS is a P2, just a regular erythrogram of the left posterior fascicle near the papillary muscle. Dr. Sojima wanted to say something more, I think. No, not related with this tracing, but is it okay to comment? Yeah, just, I think for the education purpose, I think it's very important to see the first initial ablation. It wasn't applied at the earliest site. Can you show us the first ablation site, Dr. Morishima? So, I think we discuss all the time like a P1 and P2, and I think you start with the earliest, the closest to P1, P2 interval. But in this case, yes. So, it looks like ablation catheter 1, 2, where you ablate is a later, the P potential, P1 potential, right? And the proximal portion of the ablation has an earlier P1 potential. But I don't know how extensively mapped, but you studied ablation from this point. And based on the CT image, which you showed in the following slide, you applied, I think after you applied out of here, you come back more proximal and terminated as the more proximal site. Is this the regular way you do this for the fascicular VT or a safety issue, or what was the reason to ablate this site? Okay, thank you very much. So, several reasons. So, as you mentioned, safety reason. So, we usually try to ablate distally, try to minimize the risk of creating a conduction block, a major conduction block. And secondly, in this case, at this point, we were able to hold the catheter. So, this is a idiopathic VT. So, the LV chamber is very small and the LV will rapidly moving. So, it's sometimes very difficult for us to hold the catheter at the basal site of the LV during the tachycardia. And again, so the tachycardia is easy to bump. So, because of that, we just did not want to move the catheter within the LV chamber during the VT. So, that's why we start the ablation here. I see. Just a quick question. I think you mapped with ablation catheter in this case. Is that always you do? Or I think Dr. Nogami always like to use like a multi electrode catheter in trying to kind of cover the whole area of the entrance circuit. Was this because of the concern for the bumping and also prior failed ablation? If you can mention about the reason. Okay. So, we usually do multiple electrode catheters to locate the P1 potential first. Then we switch the catheter to ablation catheter. But again, I say for sure, why we only chose the ablation catheter to map maybe because the VT was there and we think we were able to map and ablate the VT with only an ablation catheter. Yeah. Can I comment shortly? Go ahead, Dr. Nakazawa. Okay. Anyway, as Kyoko, you know, talking about the... So, you know, this is a specter analysis, but ablating modistile goes to the exit site. You don't time it. And the QS morphology keep changing from VT1 to VT4 indicating the specter analysis we should ablate more earlier proximal site. Even proximal site, it's not very basal. So, therefore, in terms of the risk of AV block, you know, it's not really, you know, it's not really to be high. So, therefore, and this particular slide showing the ablating ablation 1, 2, eliminate local Purkinje potential, but no impact for the proximal, you know, Purkinje potential recorded ablation 3, 4. So, you know, if you ablate it for the first time, you know, ablation 3, 4 area, we don't know, but you may time that type carrier without changing the exit site. Again, this is a specter analysis. It's not fair to say at this moment, but, you know, that's my suggestion. Thank you. I agree with you. Thank you. And Dr. Maruyama, you had another question? Yeah, in this slide, this Purkinje potential was annotated as P1. So, theoretically, we can ablate the Pascal VT anywhere the P1 can be recorded. But if this is P2, it should be the earliest. Otherwise, the VT does not terminate, or QRIS monophagy may change. I think, actually, the sequence of this Purkinje potential seems prox to distal, so it looks like P1. But this was recorded at the papillary muscle. So, distal Purkinje fiber inserting into the papillary muscle maybe have the other direction. I mean, the proximal Purkinje was at the base of the papillary muscle, and distal Purkinje at the apex of the papillary muscle. So, this type of recording can be seen if this potential was P2. Does it make sense? I don't know. Okay, so thank you very much for another critical comment. So, yeah, but we're not sure that the electrode, the direction of the electrode catheters were parallel to the direction of the P1 potential, even in the posterior papillary muscle. So, yeah, you could be right, but it's very difficult for us to show the compelling evidence to that. So, maybe I think I can ask Dr. Nogami for the answer. So, I don't know. I don't know, but I recommend for mapping, I prefer the multipolar electrode catheter. Ablation catheter is not good for the recording of the Purkinje potential because the tip of the electrode is big. So, I recommend the multipolar electrode catheter with a small electrode. I usually do that kind of way. Yeah, with ice. Yeah, with ice. Thank you. Dr. Morishima, which type of power do you use for this when you turn the ablation on? Usually 30 watts. 30 watts. I think 30 watts is enough to terminate the PT because the Purkinje is located very superficial. So, as Dr. Stevenson said before. So, the last thing before we hand it to the conclusion is Dr. Nakagawa said, oh, when I was not in Cleveland, I was using, you know, decapolar for the His bundle, but do we think that for this type of fascicular, you know, having a multipolar catheter for the His bundle is necessary, or, you know, with the standard His bundle recording, you can make it happen? Quick answer from everybody, please. I'm in the Oklahoma bias. I live in Oklahoma too long. I love the octopolar His catheter. I'm sorry. I'm minority. I know that. Thank you. Dr. Nogami? Yes, but I'm not always using decapolar. Dr. Sojima? I think it's probably seen this case. It's nice to have multi-electrode catheter, I think. Dr. Stevenson, I think you already said before something, but... Yeah, well, this was a particularly complex case. So, the more electrograms you have, the better, but for the usual thing, if you just have one VT morphology and you know it's VT, I think that we could use the lessons that Dr. Nogami has taught us to probably do it with two catheters. So, at this point, I think I congratulate the presenter for this, I would say, very unique case, well presented with a lot of slides with teaching points. Each of these slides can be reviewed, I think, one by one by all the audience. And there is probably something to learn in each of these slides. And we can spend probably a lot of time on reanalyzing this case. So, I congratulate him for this well-presented case. And I pass the word to Dr. Al-Khatib for the conclusion. Thank you very much for all of you. I also want to thank the presenter for sharing with us this great case. The moderator, Dr. DiBiase, for keeping us all engaged and all panelists for sharing their excellent insights. Please be reminded that ACE credit is available for this presentation. To claim your credit, please complete the session evaluation, which will be available after you have reviewed the content of this presentation. Upon completion of the evaluation, you'll be able to view and download your certificate for your records. This will also appear in your transcript, which can be accessed at any time by selecting transcript from the left-hand navigation menu within HRS 365. I hope you all have found this webinar as interesting and insightful as I did. Thank you so much for watching. And again, thank you very much for this collaboration between the Japanese Haridom Society and Haridom Society. And again, thank you to all the participants for the contribution. Thank you very much. Thank you.

idiopathic left fascicular tachycardia

atypical features

catheter ablation

double tachycardia

verapamil-sensitive idiopathic VT

posterior papillary muscle

QRS morphology changes

multiple electrode catheters

challenges