the organizers for the invitation. Right, so I'm sharing with you a nice case that I picked up about a year ago in Dubai. This is a young girl, 12 years old. At the age of one year old in 2013, she was admitted to a hospital in Dubai with incessant SVT. She tried several antiarrhythmic agents and it was difficult to control, so she ended up traveling to India and getting an ablation there. I managed to get hold of the operative report of her EP study and ablation. Unfortunately, I don't have the ECGs from that time, but the EP study said no evidence of pre-excitation. AH and HV were within normal limits. Incessant narrow complex tachycardia with a rate of about 250 beats per minute. And they found that she has orthodromic AVRT, utilizing a concealed, slowly conducting posterior septal accessory pathway, and their diagnosis was PJRT. They ablated it with irrigated tip catheter, and at the end of it, they had a bit of a transient AV block which recovered within a few hours. And the ECG after the procedure, again the operative report says normal with a normal PR interval of about 180 milliseconds. Now fast forward, the kid was fine, didn't have any further arrhythmias after that, but was referred to me because she was seen by a pediatric cardiologist and who noticed that she has WPW now on her ECG. She has minor dizzy spells, but really no episodes of palpitations, no syncope, and nothing really suggestive of major arrhythmia there. This was the ECG that was shared by her pediatric cardiologist to me, and I looked at it, and it looks like a pattern of pre-excitation there, but again, like you see, sometimes the PR interval is a bit on the longer side, and the ECG didn't look right to me. I got her to the clinic and repeated her ECG, and again, the same pattern that you can see, for example, here, you can see the pre-excitation pattern is pretty much the same, but two different PR intervals. So I was thinking that this doesn't look like a straightforward pathway, and the family was very, very anxious and were very keen for her to be assessed again because they spent like three weeks when she was one year old in the hospital, and they didn't want a recurrence of that. So we took her to the EP, or actually we got some non-invasive work. So on a Holter monitor, you can see that in the middle of the night, she's getting times when she's getting high vagal tone, and you can see the sinus rate slows down, but also the AV conduction slows down, and the pre-excitation pattern remains. And again, the same thing. You see that sometimes you get a PVC, and again, you get this longer PR interval, but interestingly, in some of the cases, what we have seen is that after a very long pause, you get beats where you don't get any pre-excitation with those beats. We'll come to that later. So the differential diagnosis was, did she have just a funny-shaped QRS, and maybe they just got a bit of damage to the hysperkinesis system? Was it a classical AV accessory pathway? Was it a nodophysicular, nodoventricular accessory pathway, or was it a fascicular ventricular accessory pathway? So we took her to the lab, and that wasn't the easiest case. When she had her study, they did an ultrasound of the right groin, and the right femoral vein was thrombosed from that time. We went through the left femoral vein. We managed to put two catheters there, but it was already also stenosed. Didn't want to go through the neck unless I had to do an ablation for her. But anyway, we got a two-wire study, and we did get enough information. So with retrograde pacing, she had central and detrimental retrograde conduction, and that was fairly straightforward. With anti-grade curve, we had an HV interval of minus 25 milliseconds, and that HV interval was fairly fixed. So you can see here, the pre-excitation pattern didn't really change there. You can see the H is kind of hiding inside the QRS, and you can see this beat after the pause, which also kind of everything seems to normalize in that. And the HV interval is kind of fixed. So we continue with the anti-grade curve, and she actually had an AH jump and an echo beat. But again, the HV interval remains the same. And again, after the pause, you get normalization of everything. I gave her adenosine, I gave her 24 milligrams. I think because of the stenosis in the groin, we weren't getting an adenosine effect. So we end up pacing from the A until we got two to one block and again, the pre-excitation pattern is pretty much the same between those beats. She did get a junctional beat here, and with this junctional beat, the pre-excitation pattern is again, pretty much the same. And later on, we had, you know, with some isoprenium, we had some junctional beats, and again, the junctional beats had the same pattern of pre-excitation. So is it a funny pathway? It's not, so is it funny QRS? It's not a funny QRS because the HV interval was negative. Is it a straightforward AV accessory pathway? It isn't because you'd expect the pre-excitation to increase further. So the question to me is whether a nodoventricular or nodophysicular pathway, was it a physical ventricular accessory pathway? I'm not 100% certain, but I'm leaning more towards a physical ventricular. The reason is with both of these, the stim A to the V interval would increase, and that happened with both in our case. The HV interval tends to decrease with nodophysicular or nodoventricular, but in this case, it remained fixed. And every time we had the pre-excitation with atrial program stimulation, we end up with the same, about 20, 25 millisecond negative HV interval. And the pre-excitation can increase with nodophysicular or nodoventricular, but in our case, the pre-excitation remained the same. So no arrhythmia was induced despite really aggressive testing. The ERP for both the pathway and the pre-excitation was about 250 milliseconds. In my view, what the EP study was compatible with a physical ventricular accessory pathway, and we did not do any ablation in her case. The unusual aspects about this pathway for me, first of all, the negative HV interval. Normally, nodo, so the physical ventricular pathways tend to have an HV interval of roughly around 10 milliseconds, but I guess that's all related to where that physical ventricular pathway comes off from the hysperkinesis system. If it comes quite distal, then you're going to get the hys much earlier. And if it goes very proximal, then I think there would be, you know, potentially be negative. Why was there no pre-excitation as a baby? So she had a full EP study when she was one year old. I mean, she didn't just grow an accessory pathway. We must come up with an explanation for that. And why do we get those non-pre-excited beats after a pause? So this is the opposite of what you would normally expect. You know, if you're pacing normally faster, I would expect the pathway to block at the higher rates and conduct at lower rates, whereas in this case, every time I'm pacing faster and faster, the pre-excitation is there, it's always the same, but it only disappears after the very long pause. Now, the best explanation I could come up with is that as a baby, her heart was very, very small. And the conduction in the hysperkinesis system was fast, and this led to concealed penetration to the pathway, preventing the appearance of the delta wave. So if this was the accessory pathway, then he was just coming and managing to block the exit from that accessory pathway. And therefore, we're just not seeing it. So the accessory pathway was there, but on the ECG, it just wasn't apparent because the electrical impulse was not exiting from the pathway insertion point. And the QRS would be normal. As she grew up, the basal segments of the RV were becoming depolarized later and later. And this was allowing for pre-excitation to appear most of the time. So as the heart became bigger, it's taking longer and longer and that's allowing this pre-excitation to happen in the basal segments. And therefore, we would get the delta wave. As for why the pre-excitation would disappear only after the pause, my feeling was that at higher rates, the hysperkinesis system and the myocardium would decrement enough and the conduction throughout that hysperkinesis system was delayed just a little bit that would allow the delta wave to appear. However, after a long pause, the hysperkinesis system would have completely recovered and because of that, the electrical impulse would conduct very rapidly and again, it would block the impulse from coming out of the pathway for that beat after the pause. Now, at times, what I saw, and this would, the next slide would be my last slide, we could see the two wave of depolarization kind of competing with each other to activate in a manner very similar to latent pre-excitation. And this is like one of the traces where you can see that there's no significant change in the rate, but you can see that it's transitioning from having kind of a negative HV interval to having less pre-excitation and the HISS signal kind of coming earlier to no pre-excitation and coming first. So it seems like the two waves of depolarization were kind of competing with each other, depending predominantly on the electrical properties of the hysperkinesis system and how fast it was conducting. So after a pause, it would have a lot of time to recover and the conduction was very rapid and would not allow the electrical impulse to come out of the pathway. That was the best explanation I could come up with on the day. Followed up for more than a year now, she has not had any symptoms, she's doing very well, but she still had that pre-excitation on her ECG. Thank you very much. It's a great case and I think showing restraint and not ablating is really the right answer because you can actually hurt people with that syndrome. I'd like to invite our panelists if they have any thoughts on this case. If I can. Yeah, I think that's a really interesting case. I wonder if the two pathways were there in the beginning and if the ablation for the PJRT actually created some local conduction block and brought out the vesicular ventricular pathway, but I think your diagnosis is correct. I wonder if like one were to go there with like a multi-electrode mapping catheter and map her septum in a lot of detail, maybe you could see that there's like a little line of conduction block like near this coronary sinus os that might have played a role in the pre-excitation coming out. I agree with you. This was what I thought has happened there. Because as I said, the first slide I did say that they did develop a degree of avia block which took about five, six hours to recover during her procedure. Her HP interval when she gets that beat which conducts normally is actually within normal range, but it must be something which is affecting it at higher rates and it's just kind of just ever so slightly reducing the speed of conduction in the hysperkinesis system and it's called allowing this interaction between the two pathways. Just for me in terms of nomenclature, so if a vesicular ventricular and you mentioned it as a possibly, I mean something to really explain a negative HV, how would you, how can this be a vesicular ventricular unless you're picking up a right bundle potential on your hys catheter and then you could actually have a negative right bundle potential to V. But a negative HV for me means that it's probably not a ventricular or something just above the node. But the junctional beats kind of exclude that it can be something connecting from the AV node so you have to be measuring something from the Purkinje system in another location. And also if you see on the slides, so the hys catheter was sitting appropriately in the hys position. You can see the beats where you get the pause and you get the block. You've got a normal HV interval. It wasn't the right bundle potential. And the beat before that had a negative HV. My feeling on that is that the pathway was very, very proximal close to the AV node and that as you said, there's a bit of a damage and delay in the conduction through that system a little bit and that's probably what allowed it to show its face. So what was the ERP of the pathway and what are your thoughts about it being sort of a phase four block with that sort of pause dependent loss of pre-excitation in the pathway? Yeah, it's, I personally, 15 is an EP. I haven't seen real kind of, you can always explain phase four blocks by other things in a lot of scenarios. It could be a phase four block but if you saw the last slide, it just looks like they're merging into each other. It didn't look like it was a sudden block. And that was, I mean, throughout the study, there's always been those beats where you would find, the HV interval was a little bit variable. It just looked like they're competing with each other rather than being true block. As I said, I can show you many of those but this one that I showed at the end is just three consecutive beats and the HV interval is just kind of merging between them. So it didn't look to me that it was a pathway block at per se. It was just like, looked like latent pre-excitation when you have a left lateral accessory pathway and then depending on how good your conduction through the AV node, you'd see a bigger or a smaller delta wave. I would think if you had complete heart block during the EP study that they were both injured in some way at some point. Yeah. Great. Adenosine, yeah, adenosine didn't block anything. These are really hard diagnoses to make. I had a case like this not long ago and we scratched our head and pulled out all the papers and is it noto or is it, you know, physical ventricular, it's not, these are not easy, but I think all in all, outstanding job. Let me invite our next speaker up. This is Dr. Alia Al-Muhanni from Egypt and Oman to show some challenging cases in wide complex tachycardia. I'll start with the first case. This is a case of tachycardia with white bundle branch block. I don't know what will come in your mind in such case. It's a young patient with no comorbidities with this type of tachycardia, and this is the baseline ECG. So what do you think? It could be supraventricular aberrancy or something else, yeah? Okay. What we go during the study in this case, because we are putting in our mind one of the diagnosis, that we do a stimulation, and once we see the hiss is becoming hidden with the white complex tachycardia that looks like left bundle, we are thinking about behind. So what we do, we start to have two strategies, either to induce the tachycardia and to see what is the earliest activation at the lateral tricusp annulus, or we go based on signal to see the hiss-like signal which is present at the lateral tricusp annulus. So this is a detailed map that we go after until we tag the signal which looks like hiss, and we identify our target, as we know the theory of the displacement of these hiss bundle to the lateral tricusp annulus that could be the cause of a MAHIM accessory pathway. Okay, so either in this way, if we pump and it's easy to pump such accessory pathway, we use usually long sheath, irrigated tip catheter, or we go during tachycardia like this, and we target to see the earliest activation at the tricusp annulus lateral, and we do the ablation. If we are lucky to have such tachycardia, we encountered a lot of cases that have been done as SBT, and already the slow path we have been modified, and one of the patient had already a basal right bundle branch block. Okay, this is an outflow BT in idiopathic. We go and map and see, and most of the cases that I can see after we exclude any myopathies with cardiac MRI, that these cases are related to the deep septum, and I will go to next case why I'm saying this, and sometimes the trabeculation that I feel it frequently is a cause of a reentry tachycardia, and that should be an easy case. I will show you a young patient. This is a patient who came, he was applying for military, and discovered has this palpitation. He was having frequently presyncope. He had this type of QRS, and we can see the P wave. I will show you the halter behavior, what's happening. We have like almost typical bundle with inferior axis, and I will show you the halter and the behavior. So this what's happening for such case. He goes whenever he does exercise, he's pretty excited, he has some adrenaline surge. In this tachycardia-wide complex, and the same tachycardia, when it goes down, he start to resume his normal QRS when the sinus node takes over. Again, this was one of the challenging cases that we didn't know with what we are dealing, is it's automatic, VT, focal. In fact, we did a very detailed map of this case, and we ablated already above the HISS cloud, but where was the earliest activation, but it was not really very early. It was most of the time minus 20, the maximum. We went to the left side. We mapped even epicardial to see this triangle, and we from the aortic root, sorry, to the aortic root to find the earliest in such a VT, but at the end, after a few hours, this case was terminated from above the HISS with very deep lesions and long lesions with 55 watt and above with irrigated catheter. In fact, it was the challenge in this case that we have automated focal VT that's coming from above the HISS. It's behaving exactly like firing cells like the sinus node or AV node, but we didn't know it's like displaced firing cells above the HISS region that is causing this VT. You will see here the termination also after a while with these deep lesions, but we exhausted a lot of hours until we reached this theory and this, sorry, okay, and this was his baseline ECG. This was the two maps from RV and LV, and this was the ECG that continued to be with right bundle for all, and he was admitted to the military, and he's doing well with our precinct. In fact, even the blood pressure was dropping with any runs of VT from 120 suddenly to 80 with this run of adiabatic VT or focal automatic VT. This is another case that we had this tachycardia that looks as SVT. In fact, this patient was admitted at possible SVT, but once we went to the cath lab and did the EP study, we found the EP dissociation. See the baseline ECG. It's exactly like an SVT, but unfortunately, we found this case, this VT is coming from the membranous part below the bulb, but beyond the HISS cloud and was the earliest activation with avoiding also the conduction system in this case, and it was terminated and not inducible anymore. So this is a different scenario because these are the weird scenarios that we faced. I will show you, I want to show you another case. This is a case of 82 years old with wide complex tachycardia, right bundle atypical. It's for sure it's a VT. It's coming from a very frequent place in adiabatic or VT without examination, without scar. The MRI was clean. This patient was, once he's awake, he goes to VT. Once he is intubated and sedated, everything comes down. We went to the cath lab. The challenge in this case that we couldn't have, we did a detailed voltage map. The voltage map, in addition to the cardiac MRI, was quite normal. Sorry. Okay. In this case, what we do, I never consider mapping at baseline as enough. Usually I use all the challenges for the ventricle in any case, a type of case, including ischemic, including whatever, and we use the high doses of isopreniline until we started to isolate potentials at the posterior basal left ventricle, which is a common place for unexplained VT in some patients. And here we started to see delayed potentials with the same voltage map that we are doing. We do differential pacing, we do fast pacing, we do isopreniline, and we remap again to identify the late potentials in sinus rift, and then we start to induce the VT if it's inducible, and we ablate this target. In fact, in this case, the patient was plus minus ICD, he didn't put ICD, and he was doing well at the end. Okay. I'll go to different scenario of white complex tachycardia. Okay. This is another challenging case who have been already ablated two times abroad. And this case of, again, it's a weird axis, negative in V1, and early transition, and then again the axis changes. In fact, in this case, again, with consideration of imaging, the patient had something like a VSD, non-communicating, if you see here. Of course, here we have to consider the imaging intra-procedure, and this is what happened. In fact, this VT was coming by the hip of ice, was coming from the margin of this non-communicating VSD with the pouch going to the RV. And in this case, in particular, we were finding the earliest activation coming from inside the CS opposite to the LV at this position. So we went to the left side with the ice help, and we identified this margin to be stable on this margin to stop this VT. The girl had been doing very well for the next years. It's not moving. Okay. This is another nice case. He was a husband of a nurse that was working with us, and he had been arresting with recurrent VT at awake period, and he was calm only with intubation and antiarrhythmic. Of course, you know, between lidocaine and cordarone, and the patient was going on and off to this VT. The challenge in this case, of course, he has non-coronary artery disease, the challenge in this case that it could be epicardial. So this is fine as a challenge. So we went prepared from the beginning with the epicardial puncture, going to the LV epicardially to find the earliest activation, but I will show you what was the real challenge in this procedure. Can you wrap it up? Two minutes. I want to go ahead. It's not... Okay. Okay. The challenge in this case was, okay, we went to the VT. We, of course, did the map endocardially, and we left the wire epicardial. The challenge in this case that endocardial, we found already late potentials after the QRS at the posterior lateral mid segment, but it was not enough to interrupt the VT. We, of course, ablated everything in the endocardial, but we shifted later epicardial. The funny thing, but unfortunately, I'm not well trained for the balloon to displace a phrenic nerve in this case, but what we had to do, I had my colleague at that time that helped me in displacing the phrenic nerve because once we found this substrate and we were very early in the pericardial space at the same opposite to the endocardial LV posterior substrate, what happened that we found the phrenic nerve capture. So what we did, we started to infuse some saline, 60 ml. Of course, the blood pressure was dropping for 20 mmHg, and we found a very early activation of this VT epicardially. So by infusing the saline, we were able to displace the phrenic nerve that was that, and we were pacing again to be sure that the phrenic is not anymore at the same place, and we started ablating until we terminated the VT and was not inducible with very aggressive protocol, including isopreniline for extra, and the case was done. Thank you. Thank you. Thank you very much, Dr. Aghalia. That's an impressive tour de force of cases. Very impressive. Maybe just one question from me. I know we have to keep moving, but do you do genetic testing on some of these patients with these weird VTs and normal LVs? What are you finding? Yes. If you have a normal VT, do you have some suspicion of any abnormality like adipogenic dysplasia, left ventricle involvement? Yes, of course, we go ahead. If we have already a family history, we go also ahead. But not in every case that showed that everything is normal. We consider it. Maybe we have to consider it as you. Any comments from the panelists? I would just put in a little plug. I really liked your epicardial case with where you need to deviate the phrenic nerve. One of our fellows, Mohammad Gaber, is presenting a poster where we actually use the grid catheter to displace the phrenic nerve. It's a lot easier. So you can double wire the pericardial space and just use the paddle itself to push the phrenic away and ablate underneath. HD grid. I'm sorry, we used any grid shaped catheter. So you could use the HD grid or you could use the optrel. We use the optrel catheter. But just if you double wire the pericardial space, especially in a case like this where it's a very limited area that you need to ablate, you can just push the phrenic away with that and ablate underneath. Oh, that's great. Thank you. The balloon can sometimes be difficult to position though because it and it also can affect your map so you might end up having to remap after the balloons in place. Thank you very much. I'd like to invite our next speaker Dr. Ahmed Talib from the Najaf Cardiac Center in Iraq and he'll be talking to us about challenging cases in fascicular video ablation. I would like to thank Amin and Marwan and the organizing committee for having this opportunity. So the case is a 30-year-old male presented with palpitation and structurally normal heart. He had this type of tachycardia. It was right mandoid, left X deviation with cycle length of 350 milliseconds. This is our traditional approach for these cases. We put multiple catheter, linear. We prefer linear catheter against the septum and we could record these potentials, what we call encyclopathy and on the left side you have A, his, after this we had the linear catheter having the P2 potential, that's prehistoric potential activated from proximal to distal septum and during VT or left posterior fascial VT, this potential was activated retrogradely from this. So this sharp potential was activated retrogradely where there is double potential, this diastolic we call it P1 potential, activated integrally and the target for ablating these cases is to get as low as possible of the fusion of P1 and P2 to avoid any left mandoid or a venodal block. So RF energy was applied at the site and the VT was no more inducible. However, another tachycardia was induced at the same session. So this is the sinus rhythm at the right side, on the left side this is the new tachycardia. Neurocurious tachycardia is similar to the sinus rhythm morphology and you can identify long RP interval indicating long VA interval with neurocurious tachycardia. The P waves are superiorly directed, so this means something from the posterior septum When we put the catheters there, there was one-to-one VA conduction, neurocurious tachycardia and the earliest retrograde activation of the atrium was at the posterior septum, just at the ocean of the coronary sinus and this was fast, slow AVNRT. So after we ablated the, by the way there is a common combination of idiopathic left ventricle tachycardia and AVNRT, this was known a long time ago and there are plenty of publications about this association. So we ablated the posterior septum and eliminated the retrograde slow pathway and both IL, left posterior fascial VT and SVT was no more inducible. However, the same patient five years later presented with neurocurious tachycardia. This tachycardia didn't respond to adenosine while it was slowed and then terminated by viropamine. And the tachycardia is again, was a neurocurious tachycardia, almost exactly the same morphology of the sinusoidal and you can identify dissociation of the V and the A's and there is PR dissociation. So now the question, is it atrial tachycardia, AVNRT, is junctional or VT? And when we put the multiple, the HISS catheter, it is very important to identify that. The earless side to be activated is the HISS and the HISS is activated way before the ventricles and there is V-A dissociation and the, when we compare the HV interval during sinusodium to that during tachycardia, the HV interval was 25 during neurocurious tachycardia while it was 55. So this is similar to what we see in bundle branch reentry where we have the sinusodium HV interval is longer than the tachycardia HV interval and this was actually upper receptor VT. So this is, let's say, iatrogenic type of VT. We ablated the left posterior fascicle, fascicle type VT, then the patient came with a left upper receptor VT. Again when we put a multipolar catheter again in the septum and during sinusodium, we can identify the left posterior fascicle activated from proximal to distal with the ventricle fusion at the distal part of the ventricle. However, during tachycardia, this potential was exactly the same. That's why this is mirror image of the left, of the left common VT. So the QRS almost the same. The diastolic potential is activated, systolic is anti-gradually while the diastolic is retrogradually. That's why it explains neurocurious tachycardia with almost similar morphology to the sinusodium. And it responds to verapamil. That's why we always advise, please at the ER start with adenosine to avoid confusion with the verapamil sensitive VT. So if you compare the potentials between the first tachycardia and the third one, the P1 potential was anti-gradually activated from proximal to distal, however, during the left upper septal, it was the reverse type. And interestingly, the left bundle was the first to be activated, followed by his, then right bundle, then the ventricle. This means that the left bundle, I mean, the left posterior fascicle or the left fascicle is the main area of interest, where the his bundle and right bundle are just bystander. And to prove that, we did pacing maneuvers from the right bundle. And you can see here, basic from right bundle, the PPI was way longer than the tachycycline with manifest entrainment, while down the left posterior fascicle entrainment showed also manifest entrainment. However, when we paced from the P1 potential, we could identify exactly the same, almost similar PPI to tachycycline with the stimulus to QRS exactly the same as P1 to QRS complex. And if you divide it, it's almost entrance of the ventricle tachycardia and concealed entrainment at the site, where ablation could slow the tachycardia and then was terminated. And all these tachycardias were non-inducible. So this is a schematic presentation of the tachycardias. The left posterior fascicle type was activated by diastolic potential from up to down. However, the mirror image was seen during the left upper septal, and we do believe that P1 is the main target for these tachycardias to be cured. And when we reviewed these cases, we found that after ablation of the left common type, we could identify small deepening of the S wave in lead I AVL, small new Q waves in lead and inferior leads, indicating that we created some substrates, some blocks that could induce or could be a new substrate even a long time later on. So the question is, are all our VTs are iatrogenic? So we collected almost 150 cases, and we found that half of the cases were really de novo left upper septal types, while half of these cases had already had a session of ablation of left posterior fascicle VT. So whether iatrogenic or idiopathic, these ablations could create a substrate for, or these patients had already a substrate for these lesions. So in conclusion, the upper septal type is a very rare type, however, it shares common characteristics of reentrant VT. These are inducible by ventricular or arterial stimulation, can be entrained, and most importantly, they are sensitive to verapamil. The problem is, it's confusing, because similar to the QRS, which can be terminated by verapamil, so it really fools us that this is simple as VT. Thank you very much, and I would like to acknowledge this important work was run by a mentor, Dr. Nogami, who created this schematic presentation. Thank you very much. Thank you, Dr. Taleb, for a great presentation. I want to ask a question regarding the energy settings when you ablated those upper septal. Can you tell us more what settings and how did you ablate? We just go, we just go, as usual, 30 watts, but it's important to start it in sinus rhythm. So in these 12 cases, we have only one transient left on the branch block, and then once we stopped energy, it returned back. So once we are sure of diagnosis, if you see, oh, I cannot see this light. We are not really high. It's midway between the hiss and the apex, so it's not really high, but the important is to identify the diastolic potential, make sure to stop the tachycardia and ablate during sinus rhythm. So whatever the energy you have, 30 watts, one minute, we have no problem. I'll ask our panelists if they have any questions from our panelists. That's very nice. So I'm just wondering, the AVNRT that you induced, could this have been also left upper septal VT with one-to-one conduction? So you looked at the hiss activation, was it integrated as proximate to this bit? So that's another, I mean, you could be confusing it. If you have a left upper septal VT, that could be a diagnosis. This was clear one-to-one conduction, and the posterior septum atrial potential was a less one, and this was just a typical type of ventricle. Entrainment from the RV would tell you, right? Sure. Absolutely. Dr. Habeshi, you had a question? I think it has to do with how high it is. Okay. I'm not sure what it is now. So I actually didn't, because it was not the, it was easy thing, so I didn't prepare all the slides. I see. So in the same session, this is the training. Did you do it with the... We did, of course. We did all the maneuvers, of course. We did all maneuvers. Yes. So it's one-to-one conduction, yeah. Because sometimes we get confused when we have one-to-one conduction of the common type, and once we put A, you will have A-V-V-A response, or you just pay, especially in these young boys, they have really good V-A conduction. So you really get one-to-one V-A conduction during upper septal type or during left common type. But once we explore all maneuvers during entrainment, A pays, they will dissociate at some point. This was not dissociated, and the posterior septum was ablated, and this almost absolutely it was atypical A-V-R-T. Yeah. Yes, exactly. Exactly. Yeah, Dr. Aghalia has a question, yeah, great. This was published by a Chinese group that they identified what they called late something LAP, late something potential, where they found abnormal Purkinje potential after the QRS, and they updated. We tried this, but it didn't work very well. The problem is this is very sensitive, can be easily traumatized. That's why we don't really go to map all the Purkinje, because we will get confused, because we will traumatize the circuits. So we just gently put the linear catheter against the septum and do stereocardia. Before ablating anything, do atrial overdrive pacing, ventricle overdrive pacing, just make sure this is fascia type, and then we can manipulate. I had one comment, just that I had a case similar to the first part of this, where we kept getting different forms of interfascicular reentry, and the patient we thought had structurally normal heart, but he turned out to have myotonic dystrophy, actually. So maybe for some of the de novo cases, it might be worth considering more structural underlying disease. This left upper septum is also described to cause polymorphic fascicular, and even cause VF. So in some cases, that could be a source of malignancy as well. It's really elegant to watch the linear catheter, and I have to say, I've never used it. I usually do multipolar mapping, and I agree with you, it's easy, very sensitive to bump things. It traumatize a lot. I know, and then I feel like an idiot, but that's the world we live in now, is mapping. Any questions? Yeah, Dr. Sabah. Thank you. Really, really nice to see this. In our experience, I have to say, we get very lucky if you can keep this tachycardia going. You get sometimes just 10 seconds of it, you can't do anything with it, and you know it's fascicular, but you really can't find P1. And I have to say, in, I don't know, 20 cases or so, I've seen P1 maybe twice. I work in the UK, so we can't really see P1, P2, and all that beautiful stuff that Nogami shows. So we end up relying on the LPF, that fractionated junky electrogram, you know, pre-QRS, pre-local B, and we do what David Wilber taught us, which is just take a line straight down the septum halfway, two-thirds of the way down, and it's very effective. If you just target that tissue, you almost always get it. Thank you. So we do this approach for non-inducible types, and mostly, when we, this is interesting, let's have some, many maneuvers, and it ends in non-inducible. In that case, I mean, we can use whatever you can, because it's no more inducible. And we target the best, the open approach, we do the best base map type, and then we go up. Interestingly, like what we have in AVNRTs, once you ablate it, it becomes irritable, but you'll have the tachycardia again. You just go up on transects, and it will be the same. So the P1, even in the first tachycardia, you induce the left posterior fascicular, you always look for this low area of contraction that's orthodromic, but that could still be the left upper septum. Sure. Do you believe that was the same substrate for left upper septum, once orthodromic, once ... This is really complex. This is nice work done by Scheinman and the organic group, they said probably every human being have upper septal fascicles. It's really, there's a huge variation between individuals. And here's the difference between the other strategy, you don't need to ablate the left posterior fascicle, you just ablate the anterior to it. You do not give the patient a hemifascicular block, and then you just eliminate the ... Thank you. Fantastic cases. Just want to, first of all, thank our speakers for really giving us fantastic cases, a lot of food for thought, and thank our panelists for all the comments and insight, and thank all of the audience for joining us, and see you next year, hopefully, for another joint session. Thank you.

cardiac arrhythmias

electrophysiological studies

catheter ablation

WPW pattern

ventricular tachycardia

Purkinje network

pre-procedural assessment

electrophysiology strategies