Good afternoon, everybody. At the onset, I would like to thank the organizer for giving me this opportunity. So my responsibility today is to talk about ablation of perinodal and parathyzian arrhythmias. I have no disclosures, and my special thanks to my friend and colleague, Dr. Shomu Bora, for providing me the data and taking me through this very interesting and difficult topic. So as we know, the pathways, only the accessory pathways in strict sense, there are about 46 to 60% which are the left free wall pathway. 25% are present in the posteroseptal space, while 13 to 21% are present in the right free wall space. But 2% are within the antroseptal space. These are the most challenging pathways, and our ECG guide takes us through, before we can map these pathways in the cat lab, in the EP lab, the ECG guides us through the lead V1 and the inferior leads. And it also makes us to determine how we would aim at ablating these tachycardias and these pathways. For the left free wall or left lateral pathways, we take transeptal approach or retrograde approach, whatever we are comfortable with. For the right lateral pathways, it's a long sheath for the stability of the catheter that we use. For CSOS or distal CS pathways, we do use the irrigated catheters. And cryo is very important, and RF used in the titration of the energy is important for basically the antroseptal pathways. So once we see the ECGs like this, we know it's an antroseptal pathway. We look at the anatomy, and we see that where these antroseptal and midseptal pathways are located, they're very close to the non-coronary cusp of the aortic valve. And these pathways have been labeled in this area with a different nomenclature over the time. But this is very importantly correlated to the non-coronary cusp that this area of pathways can be tackled from there. And we have data in the Europace from Dr. Shomobara's group only to say that it is a very successful outcome with this mode. So there is a mass of histologically discrete myocardium within the interatrial wall directly inferior to the non-coronary cusp sinus. And it is separated from the compact AV node itself, and it is not insulated. So this approach can actually help us give the good results to this patient. The mapping is done in the aorta. Now once the pathway localization has been done, we can use the mapping in the aorta, and we can differentiate retrograde pathway and nodal conduction by earliest site of atrial activation near the hyst during the narrow complex tachycardia. There is a non-decremental conduction in most of these pathways. Parahysin pacing does come to our help. And we can try doing RB apical or base pacing. But very carefully, when we are aiming at ablating these pathways, bumping the pathway can occur very easily. So it should be done very gently. Otherwise, we are stuck up in the lab for 30, 40 minutes. We have to wait for the pathway to come back in case we are not very careful. Now once we have to decide the ablation site, ablation, if it is away from the hyst area anteriorly, then we can do safely. Preferably there should be a V more than A in our electrogram. And we prefer to ablate in tachycardia. Ablation if required to be done at the site of hyst, then ablation should always be done during tachycardia. And the ablation in the non-coronary sinus, even if the near field signal within 20 milliseconds of the far field signals are early, then we should take them. And it should have a large V with little or no atrial potential. That is very important. Other pointers that we can use are a patient can be taken under general anesthesia. And apnea can be set in for the stability of the catheter. You can take the jugular route, which hooks on the superior region and prevents any fall. And the curving of the catheter below the leaflet of the tricuspid valve in the RV, it does help. Let's discuss an example of the patient. This patient has an anteroceptal pathway. The ECG is pre-excited. So when the patient is taken on the table, the earliest A is in the hyst area. The mapping is done around the tricuspid annulus. And the best A is in the hyst. This is what the electrograms look like. Now we go to map the aorta in the non-coronary cusp. And here we find the signals in the non-coronary sinus in sinus rhythm. The A is more than V. And during tachycardia, it is around 20 milliseconds earliest of A in the hyst. So ablation is done during tachycardia. And it results in the successful ablation. And post-ablation, there is a demonstration of the VA block. Another example of a similar anteroceptal pathway where the pathway gets bumped. And there is no inducible tachycardia. Pre-excitation is intermittent, difficult to map. No inducibility of the tachycardia. And the hyst is now the most pre-excited EGM. So done through the aortic route in the non-coronary sinus, ablation done through the route, but the recurrence occurred. So hence the patient was mapped again in the RA with the anterior approach. And the post-ablation, this is the site of ablation, and it has been successful. So sometimes even non-coronary cusp doesn't work, the recurrence can happen. But it is still worth trying, it's with a good result. If the patient has incessant tachycardia, then these patients are taken for ablation. And the result of ablation can cause complete heart block. And patient may end up requiring a pacemaker. Despite good signal, while the best signal is at the hyst, so patient may require having a pacemaker. These are the couple of sites which have been defined where the AV block risk is high. So important points here are that unless incessant, do not ablate in the parahysian area during the first study. If the tachycardia is infrequent, let the patient ask for it. And the risk of the pacemaker, though is less, but is real, so has to be explained. We can play with the low energy of 30 watts and then upwards be titrated. Cryoablation, well, in India, we have a limited access to the cryoablation. So I have shared our experience, how we approach such patients. We have limited experience for cryoablation. In fact, the catheter of cryo, we do have balloon, but we don't have a catheter as yet available. So if you have cryo, yes, that is a preferred source. However, in cryo, the recurrence is higher compared to radiofrequency ablation. So when do you suspect parahysian atrial tachycardia? When the near simultaneous or not necessarily very early activation is noted at the several anatomical separate locations. Like simultaneous with P wave onset of 5 to 10 milliseconds earlier, maybe noted in the fast pathway region, backbend bundle, his bundle, roof of the coronary sinus, or in the anteroceptal mitral annulus. And of course, in the non-coronary cusp. When such simultaneous activation is noted, the direct mapping should be in the NCC area. This is another study which have compiled to show that the mapping and ablation of the non-coronary cusp should be considered in patients who have atrial tachycardia originating from the his bundle region. In conclusion, non-coronary cusp has an advantage point for ablation for parahysian atrial tachycardias. Even if the LHC are rather on the RA side, ablation in NCC can be successfully completed in majority of the patient. NCC ablations are safe as compared to the right anteroceptal ablations. And AVBROC and recurrence are rare with the NCC ablation. The ablation of RA is to be done with care, especially that the A should be larger than the V. And the sheath can be used for stability in the right anteroceptal ablation region. Thank you so much for your patient hearing. We have a couple of minutes for questions. There are no questions. Can you tell us what type of sheath you like to use for these anteroceptal pathways from the femoral vein in particular sheath? So we do use ASLO sheaths and the long sheaths that are available. Most of the time I use the sheath we use for the transeptal ablations that we do. And they work good. The stability is there. But I do anteroceptal pathways with the retrograde approach in the non-coronary sinus. So there, no long sheath is required. A good catheter, a good placement, and a nice, good site has a good job for me. So, Dr. Benita, excellent talk. Do you use irrigation energy in the non-coronary cusp, or what do you do? I do use irrigation, yes. I do use that. Thank you for your excellent presentation. Thank you. I want to know about your experience about late complete heart block when ablation in the non-coronary or in the parahysian or anteroceptal area. Thank you. Yeah, kindly repeat the question. No, you repeat it. Okay, I will. Okay, I have heard it. Thank you. Thank you for the question. He wants me to tell him what is the experience with the non-coronary cusp ablation and anteroceptal ablation of the incidence of complete heart block. Yeah, the late, the late complete heart block. The late, yeah. Yeah, late, I have not come across with the non-coronary cusp. But in patients where I have done anteroceptal pathways, you know, related there, there I have seen even the late occurrence of complete heart block. One patient came to me almost after, I think, about three or four months later with a complete heart block. So I don't know, maybe it is the heat that we used. We do radiofrequency, we don't use cryo, so probably that is the reason for that delay. Just one more question. It becomes especially challenging for concealed pathways. So do you have any strategies for concealed pathways? Differential pacing in the ventricle? When you don't have overt pre-excitation. For mapping and ablating, do you pace at different regions? Yes, I do. Of course, the parahazine pacing helps there. The RV pacing from the apex and the base. You can do it separately, and that can help us to actually map the pathways in a better way. What I meant was looking at the atrial insertion, ventricle insertion, pacing from the paracepital region, and a slightly more 12 o'clock region, changing the direction of the wave front to bring out the pathway slightly away from the- Yeah, right. Thank you. Thank you, that was an excellent review. Thank you, that was an excellent review. The next speaker is going to talk about ablation of atrial flutters following catheter ablation or surgical ablation of atrial fibrillation, Mandeep Bhargava from the Cleveland Clinic. Thank you. Thank you, Dr. Ellen Bogan, Dr. Nayak. Good afternoon, everybody. So, I have no disclosures, but I'm gonna be talking about atrial flutters, and among all the talks that you hear, this is probably the most common, uncommon arrhythmia for the session. But the question is, now in this era where we have so many tools and gadgets to ablate atrial fibrillation into a maze, why should arrhythmias record? Well, obviously, it is either because of gaps in the lesion sets, or because of recovery of conduction, or whether you have missed epicardial connections, or you have triggers which are beyond the pulmonary veins, or just the general progressive nature of the disease. What we know already is that there are certain usual suspects, the most common being either the perimitral or the CT isthmus in different series, depending upon what workflow you use for your catheter ablation. And here you can see how the right atrium is passively activated, and any time you have a right atrial flutter, the left atrium is passively activated. But essentially, you either need some conduction gap, or you need an inert structure, or a scar tissue around which the whole macro reentry can occur. Now in many ways, we feel that prevention is the best cure. So when you do your ablation, just don't do the five things that we saw could cause recurrence of tachycardia. So our workflow is just demonstrated by this patient, where you see this patient has persistent atrial fibrillation and flutter that he came with. This is the voltage map of the PA view, and this is the septal view. And we did it with FaroPulse, and you can see that post ablation, we tend to ablate the posterior wall, we tend to ablate septally, almost one lasso length for many years that we've had as a habit and a practice. And you can see loss of voltages after the ablation, and hopefully that should not leave any gaps. We also ablated for the flutter, but the question is, is every AFib ablation the same? This is a patient who came to us with a cryo ablation, and as you can see, the veins are all isolated, but he continued to have arrhythmias, and all we did was just do the posterior wall, and after that, the patient did well. This is a patient who had an RF ablation, but you can see that there is a lot of work to be done, and after we did the FaroPulse, it is almost like he had his first ablation, so I'm not even sure whether it is reasonable to call it a recurrence. This is a patient that I want to use to show what, I'm gonna show a few patients to try and make some points about what are the important things to keep in mind as we do ablations for atrial flutters post-PVI or MACE. This is a patient who had atrial fibrillation, severe heart muscle dysfunction, ejection fraction of 20%, renal failure, and very large atrium, and we decided to do with this Afera, and you can see fair amount of scarring on the posterior wall, fair amount of viable tissue. This is the septal view, and this is where we decided to make the lines for the wide area ablation around the veins. This is the final lesion set that we had. You can see anteriorly going all the way to the septum, but the bottom line was we achieved good isolation, but eight weeks later, the patient came back with atrial flutter. He did not have much choices in terms of antiarrhythmic drugs because of his comorbidities, and we decided to map it, and as part of just learning, we decided to first map with CARDO, although we knew that we might ablate with Afera. With CARDO mapping, this is the activation map that you can see. Posterior wall is fairly inactive. All voltages are gone, so we were happy, at least, that there was no recurrence of what we had done, but the activation map showed clearly that you had a counter-clocked perimetral flutter, which is not surprising. You see the whole cycle length complete in the atrium, and then we again mapped it with Afera. We were just trying to learn how these activation maps are. It's a new tool we like to learn, but you can clearly see the scar here. You can see it rotating through these two isthmus, and then we had to do an extensive ablation because this is an atrium which is almost seven centimeters, and as you can see here, the lesion set. In orange, you see the RF lesions. In green, you see the reinforcement with PFA, but finally, at this site, we finally had termination of flutter, but we ablated till we had bidirectional block, and the patient did fairly well after that, and we hope he continues to do well. This is, again, a post-map using CARDO, which shows that with pacing from the distal coronary sinus, you have the two wave fronts matching and colliding here, and you have loss of voltage showing you that you have a block, and conduction block is the goal, and that is important. So these are the few things that tell us that activation mapping, scar mapping, how they can be useful and important to make sure that you have conduction block. What about the MACE procedure? Now, we have different versions of the MACE procedure, but right from the very beginning, the effort in the MACE procedure has not only been to isolate the veins, but also the posterior wall, and depending upon your surgeon, he might do additional lines on the mitral and the tricuspid isthmus, or even from the SVC to the RA, but this is a case which shows you nothing but a perimitral flutter, which we mapped, and we found that it was perimitral flutter, but interestingly, you can see that in the posterior wall, when you have the grid catheter, it is showing a dissociated atrial fibrillation, which is going back and forth between a different flutter, and that is important to keep in mind as you annotate and do the activation map for these patients. So another interesting thing that you might see in these patients. This is a patient who came with multiple flutters post-MACE, and you can see that, again, the patient has kind of an eccentric activation in the coronary sinus. This is the activation in the right atrium, going from top to bottom. The patient was initially in this flutter. We did an activation map, but we also did an entrainment maps, and you can see that we had entrainment with concealed fusion all along the annulus, telling us that we are dealing with a typical counterclockwise perimitral flutter, and we ablated at the mitral isthmus, got rid of it, but then he, shortly after that, went into another flutter, and you can see here that the activation in the coronary sinus changed. It has become proximal to distal now. The change in the chevron pattern that you see in the right atrium, but again, what is interesting is that you see these signals which are very fractionated and showing almost a converse pattern in the coronary sinus. And that is something which is very meaningful. And now when we go to the entrainment map, all these areas had entrainment with manifest excitation and the PPI was very long. But again, continued to have good entrainment here, telling us that we had changed the circuit by this ablation line. And when we mapped further, both by entrainment and by activation mapping and tried to make sense of it, it clearly was showing us that the activation was happening within the left atrium and the sleeves of myocardium within the coronary sinus. And this is where the flutter was localized to. Same thing we found on activation mapping, an ablation in the coronary sinus got rid of the circuit. And this is important to know because many times when your surgeon does cryo in that area, it may cause partial damage, so the circuit is hurt but not killed, and that is an important thing to remember. This is again a different case to show the utility of activation mapping at times. So this is a patient who came with a myectomy and a maze and then had recurrent flutter. He was cardioverted, comes into the lab in sinus. We decided to see what we have. And if you look at it, you will say, oh my God, what a bad job that the surgeon has done. All the four veins look as if they have conduction. You can see this on the posterior wall. This is on the septum. But if you look at the activation map, it's very interesting. You have a block of the perimetral isthmus. And as you see the activation pattern, there is pretty much a block through most of it. It is just leaking through a small area, posterior to the left inferior, and also through a small area just anterior to the right superior. And that was causing the flutter and responsible for all his arrhythmias because of these two leaks. And then just a very targeted ablation in this area was enough to take care of that. And when this gap was taken care of, you can see we are pacing from the distal CS. We have the pentary catheter here. And you have loss of conduction as soon as you ablate here. So you did not have to do an extensive ablation all along the posterior wall. And that shows the utility of activation mapping in this patient where voltage mapping alone was not very helpful. This is another patient who came with flutter. And we mapped the right atrium. This is a map of the right atrium, covering only about 40% of the cycle length. This is the map of the left atrium. And again, covering just about 40, 50% of the cycle length. But then as you combine the two maps and you play an activation map, you see that it is going up the lateral wall. It comes here and then suddenly jumps to the SVC. And that tells you that this is a biatrial flutter which is using the Bachmann's bundle and moving from the left to right. And that is an important thing to keep in mind, especially when your cycle lengths are not making sense. So beware of that entity in these patients. So what has definitely impressed me in these very difficult cases in the last few years that we have come to be able to deal with all these tools is the advent and impact of high-density mapping. Fast anatomical mapping and geometry creation becomes the goal in this situation. You can map your pulmonary veins, make sure that your isolation from the previous procedure is still persistent. You can make a voltage map, find out your scars, and figure out where you can suspect the circuits can be. The activation maps allow for more targeted ablation rather than the conventional lines where you just go by point-to-point without any physiological basis. You can identify the epicardial connections as you saw in that patient, and it can help localize the leaks in the previous isthmus that has been ablated on previous lines. And again, very important tool to show that you have bidirectional block. Now this is a patient where you can see a figure-of-eight appearance. It is going around the roof, and the flutter is going around the perimetral line. And you can choose to do either an anterior line and get into a fight with the Backman bundle, or you can choose to do a lateral line and then get into a fight with the coronary sleeves, the myocardial sleeves in the coronary sinus. But you can also choose to just do a more targeted ablation in this patient who's having this figure-of-eight appearance and just get rid of the flutter with a more convenient line with less collateral damage. This is another patient who has a typical mitral flutter, but rather than doing the whole line, you can see that you have these very fractionated and slow conduction, which is just across this line, and just a single lesion there is good enough, and you cannot identify that easily without high-density mapping. This is a similar thing that you see in a patient with a previous CT isthmus ablation. You can see the leak through, and then subsequently, as you pace from the coronary sinus proximally, you can see that there is a wave front of activation coming here, and then turning around, and you have a clear line of block, and the patient has bidirectional block. So looking at all these examples, the few points that I want to bring home is that the basic mother arrhythmia is atrial fibrillation. So when you treat it, treat it well. If you have a recurrence, make sure you go back and treat it well. You can define what your boundaries are because a PVI is different for everybody, but whatever it is, reinforce the PVI and the other important parts of the substrate, both for the a-fib and the flutter. Find out which is the passive or the active atrium. Look for the usual suspects. You know where the usual suspects are. Don't ignore them. Define the voltage and activation maps, and study them closely because the computers can sometimes fool you, so make sure you annotate them correctly, and you're not being fooled by some automated algorithm. High-density mapping is the key. It increases speed, efficiency, and accuracy in these often frustrating and long cases, and target the ablation to localize isthmus that you can to prevent collateral damage. Don't forget entrainment mapping. That is the only thing that can tell you just before you're about to ablate that your activation map is wrong if it is not making sense. Don't settle for flutter termination. Ensure bidirectional block. Persistence is the key. We have so many tools these days that all of them can be used as and when needed all the way to alcohol ablation in very resistant flutters, and keep over-enthusiasm in check. Don't isolate the sinus node or the left atrium or disconnect the right and the left atrium because that is what happens in many of these patients where we ablate randomly without any physiological basis. Thank you so much. Thank you. Thank you, Mandeep. You've fit a lot of stuff into a short period of time. There's a question from somebody about if you're doing a mitral isthmus line, not an anterior line, a posterior lateral line, and you have to ablate in the coronary sinus, what power duration do you use for ablation in the coronary sinus? Thank you. So most often when we ablate in the coronary sinus, we are using an irrigative catheter. And many times, even when you start, sometimes the impedance may be higher than what you have in the tissue. So we would just watch the impedance. I rarely go above 25. Sometimes you may go to 30 if you're very sure that you're close to the ventricular myocardium with no associated collateral structure. But most often, 25 watts is what we keep at using radiofrequency, energy, contact force, either slow flow or regular flow, irrigation tip catheter. And watching the impedance very carefully so that we don't have a pop. Of course. But do you give for 15 or 20 seconds? Or do you look for maybe 10 on the impedance drop? I mean, most of these places, we are looking for disappearance of electrograms. And we might stay for about 10, 15 seconds beyond the disappearance of electrograms. People nowadays use different ablation indices, which you've used things like 450 in the atrium, but I'm not sure the same applies to the coronary sinus. So I usually go for disappearance of the electrograms and just about 10 seconds beyond that, I find that as useful tool. We have two more quick questions, so let's keep the answers short. So I'll ask this. That myocardial flutter was very fascinating. Do you have to ablate at a specific site or at a different site, different patients? Yeah, usually it depends, you know, like if you, you can see that this was using the mitral isthmus, but it was just propagating in a manner that unless you have that much delay that you go from the right to the left does not sustain. So many times, even if you get the lateral isthmus, you might get rid of it. Because you know, like any other re-entry, it needs a zone of slow conduction. But if you have just one single atrium, it is not sustaining because it is that fast. But when you have two atrium, then there is enough delay that it uses the other atrium to support that much delay and the persistence of the flutter happens. But many times, you just have to choose, or a lot also depends, like that patient specifically had a mitral valve surgery. So he had kind of, you know, a septal incision and we used that to connect it to the right superior pulmonary vein and we were fortunately able to do it. But otherwise, the Backman's bundle, you know, is thinnest and has most of its insertions very close to the base of the left atrial appendage. So in most such situations, we find it useful to make a line just on the base of the left atrial appendage because that is where you're likely to get it most easily without having to go epicardial or worrying about going epicardial. But sometimes you have to do, you know, martial injection with alcohol and get it perfect completely. Okay, thank you very much. Thank you. So let me invite Dr. Deepak Padmanabhan from Bangalore. He's gonna speak on management of cardiac arrhythmias and granulomatous heart disease, approach and outcomes. We have a lot of this back in India and different manifestations, different ideologies. Dr. Deepak. Thank you for the opportunity to present and thanks to all of you for being inside the room rather than being outside. I mean, it's an amazing view, it's great weather, but thank you for being here. So I don't know if you can see this. Oh, okay. Perfect. So you have a question just in case somebody wants to try answering it. Which of the following statements is true regarding VT ablation and inflammatory cardiomyopathy? VT circuits are stable and well-defined during active inflammation. Bipolar ablation is avoided in septal involvement. Best outcomes observed when PET scan shows active inflammation. Our recurrence rates are lower when inflammation has subsided. So you could probably go on to the live content slide and see if we can get some answers. Huh, cool. That's easy, right? Great, so I'm just gonna use that opportunity to go on. What about this one? The setting of VT ablation during inflammatory cardiomyopathy which of the following suggests the need for bipolar ablation? Is it high amplitude unipolar signals with preserved bipolar voltage? Equal stimulus QRS intervals at endocardial and epicardial sites? Significant decrement during program stimulation at the deep septal site or a PPI-TCL difference of 30 milliseconds at the epicardial site? This is another one answer kind of thing. Nice. Ah. That's more interesting. Okay, so the objectives and if I may probably run out of time, my apologies. The objectives are essentially to understand the arrhythmogenic substrate in inflammatory granulomatous cardiomyopathy, review the approach to RFA in ventricular arrhythmias, examine outcomes based on the inflammatory activity and explore the ablation of atrial arrhythmias in this subset. As such, it includes cardiac sarcoidosis, tuberculosis, granulomatous inflammation leading to scarring, substrate for VT and atrial arrhythmias are commonly present. If you look at the pathophysiology, it's essentially reentrant VT from patchy scarring, patchy being the key word there. Active inflammation can trigger focal VTs and even VT storms and basal septal fibrosis is commonly involved. So it's the entire septum, free wall and sometimes even aneurysmal locations and patients can be in significant heart failure with mitral regurgitation also. Atrium is also known to be commonly involved in these patients. So the approach before you're trying to put a catheter in is to figure out whether you're in inflammation ongoing, whether it's the inflammation that's triggering the arrhythmia, knowing the substrate better versus where it's just scar mediated. So typical logic is to use cardiac MRI and an FDG PET to rule out active inflammation. You have the chitotriosidase, which is an active enzyme for inflammatory cardiomyopathy or inflammation throughout the body, which can actually tell you that and then evaluate the need for immunosuppression. So before we go in, which investigation do you want? Do you want to do the MRI first? Do you want to do the FDG first? Are they complementary? So a quick look at acute inflammatory conditions in the MRI, you look at the hiler lymphadenopathy with multiple liver lesions, sometimes the STIR phase actually shows you edema. T2 mapping can show you raised T2 values with inferior RV insertion points or the RV insertion site fibrosis can be present in acute myocarditis. Similarly, you can have diffused myocardial edema, diffused mid-myocardial to sub-epicardial. So essentially, take your pick. Everything can be seen in acute myocarditis. You can actually see hypokinesis of the basal septum with global hypokinesia. But what is critical is that how do you differentiate on the MRI report, whether it's acute myocarditis or chronic myocarditis and not rely just upon your radiologist to do so. The key is the STIR imaging, where you do not see edema on STIR imaging when you have chronic myocarditis. Acute one always will show, the STIR imaging will show you edema. Similarly, PET positivity will obviously show you improved lymph nodes. They'll show you localized abnormal uptake in the myocardium. And it will also show you prognostic value, especially when there's abnormal perfusion and FDG. This is something that we've already known. Additionally, focal RV FDG uptake can also signify poorer prognosis. It has a good pooled sensitivity of 89% for inflammation, as well as a specificity of close to 78%. Recently, there is the surge in the DOTONOC scans. And why the DOTONOC scan is important is unlike for the FDG PET for inflammatory cardiomyopathy, which includes a dietary restriction phase. This does not require a dietary restriction phase. It's a single stage. It's useful in critical patients. And it's less affected by those preparations. So it's a very critical scan, especially in patients who have active myocarditis leading to VT storms or ongoing arrhythmias. The role of the PET scan is useful to detect early cardiac involvement, select the site for biopsy in case you have an extracardiac site, and even assess the response to treatment to immunosuppression. So we had this small unpublished data which is under review right now, which looked at early myocarditis and looked at whether PET scan was better or MRI was better. It's actually, if you want to do one of them in acute inflammatory condition suspicion, you want to do the PET scan rather than doing the MRI. So when you go on to approach to ablation, you've decided that you want to ablate, whether it is the acute stage or the chronic stage. What is important to remember is a substrate-based ablation is usually better in these patients because you may eliminate the offending arrhythmia, but you want to basically target a lot of the substrate too. You want to avoid ablation during active inflammation and hence those tests before you do it. And you have to consider epicardial axis when necessary. You want to electroendymical map in the sinus rhythm, in pace rhythm, target low voltage zones, areas of late potentials, deep intramural and epicardial circuits and bipolar ablation if septal involvement is present. It's not uncommon for these arrhythmias to be hemodynamically unstable. Epicardial axis is usually required in close to 50% of cases. And avoiding ablation during active granuloma, especially if it's an active inflammation, you're unable to avoid the ablation, is very, very critical. You will see signals like these where entrainment during an ongoing VT will not capture everything. You'll see some signals which are not captured, suggesting that they come from a site that is far away from where your catheter is being placed. Going epicardially in these states might actually help you. And even better, if you are able to kind of wait for that extra second, you might get to golden spots like these. Going on from there, delineation of septal scar, especially in patients with unmappable VT is critical. Here, you need to not only ablate abnormal septal EGMs, but what you want to do is you want to pace the RV side of the septum and look at the LV septal signals. If it's greater than 40 milliseconds, that is an abnormal area. You want to ablate those areas also, even if they are not part of the VT. But critical, you need to figure out how to spare the conduction system and not keep ablating at sites where there are conduction system tissue. Another important thing, while using automated systems for mapping, is that this voltage is not calculated on the basis of the local EGM. The voltage is the largest signal at that particular location. So you can have a signal that is low voltage, but the system will pick it up as high voltage. So when you're actually doing an automated system of mapping, you might get normal sinus rhythm maps, normal RV-paced maps, but when you do decremental pacing at these sites, it'll actually push out by greater than 10 milliseconds. So using deep mapping liberally is actually a good strategy in these patients, especially if you're mapping in these patients. You might get these kind of arrhythmias where it's running all over, a PVC being triggered, looking at conduction system signals at that point in time with a 12-lead ECG to document the PVC that is triggering the arrhythmia. Suspecting that the conduction system will be involved is key to the successful ablation of these patients. Intracardiac echo does help you understand where your catheter is and the proximity to the conduction system in these patients. But ablation is not salvation in acute myocardial inflammation. You actually want to keep this right up your sleeve and pretty early before trying to ablate acute inflammation in these patients. You want to do cervical sympathectomy early and if resistant to that, then want to put your catheter in into these patients. It's clearly seen by this data by Kaur et al where they documented acute success rates of 70 to 80% with 30 to 60% recurrence of one year with a significant reduction in ICD shocks with multiple procedures, but only when it was chronic scar rather than acute inflammation. Higher recurrence rates were noted with lower complete success in acute inflammatory conditions, more unstable VT circuits, ablation itself causing more inflammation, substrate is poorly defined and dynamic and immunosuppression should precede ablation, especially if you can temporize it, stabilize the substrate and then try and ablate in these patients. Actually seen by this data by Lee et al too where cases of myocarditis where VT ablation was feasible had a better prognosis. But if you look at the independent risk factors for VT recurrence, you did have acute myocarditis as one of the cheap factors contributing to VT recurrence in these patients. Siontis also showed the same thing where outcomes during active inflammation did poorly as compared to outcomes during healed or stabilized inflammation conditions. Outcomes when inflammation has subsided has longer improved long-term freedom from VT, lower recurrence rates and the stable scar allows for precise substrate modification with best outcomes with the PET negative status. Our colleagues, Dr. Suresh is actually presenting this at HRS where he's looking at outcomes of ablation in patients with TB myocarditis and again once again in stabilized disease you do get good results but the inflammation has to subside. Adjunctive therapies role cannot be understated. Corticosteroids, methotrexate, antitubular therapy wherever indicated. Immunosuppressives stabilize the substrate, and this is not to take away from the role of ICD implantation. What happens on follow-up is the role of chylotrioxidase. This is an enzyme actively secreted by macrophages. Elevated levels indicate ongoing granulomatous inflammation. It is thought to be useful in sarcoidosis to monitor disease activity, especially when PET scans are not very easily available or may not be easily doable in these patients. It may correlate with PET activity and relapse risk. It is not disease-specific, but it's a useful adjunct to our armamentarium. Not to forget ablation of atrial arrhythmias in these patients. There is no reason why the atrium should not be involved, and especially in patients who do not have a significant risk factor for atrial arrhythmias or for atrial fibrillation itself, we have to rule out granulomatous myocarditis in these patients. Atrial fibrillation and flutter are common. It's usually substrate-based due to atrial scarring, pulmonary vein isolation with CTI ablation is usually enough in these patients without drawing a lot of lines, especially in acute inflammatory conditions. In summary, therefore, inflammatory granulomatous cardiomyopathy presents with complex arrhythmic substrate. Both the presence and absence of inflammation are very important to delineate before trying to ablate these patients. You can either do a PET or an MRI or chitotriazidase for the diagnosis of inflammation. Probably chitotriazidase followed by PET is a useful workflow. Multimodal management improves outcomes. Ablation is the last resort in acute stages. Stable non-inflammatory disease is amenable to ablation and has good results. Long-term follow-up is critical and it does not remove the need for an ICD implant. My thanks to my collaborators for all this work that we've been doing over a period of time. Thank you for your patient hearing. Thank you. Deepak, that was pretty comprehensive of a very complex disease, every year we are learning more. My question is, often it is difficult to differentiate between tuberculosis versus sarcoid versus overlaps. So how do you go about that? We usually like to use a MANTU. A positive MANTU can be suppressed in sarcoid, that's something that we have to remember. But a MANTU and a quantiferon gold are the two tests that we like to use. Any of them is positive, you know you are dealing with a complex substrate that may not be just tubercular. It could be tuberculosis sarcoid or it could just be tuberculosis. You already have to add on anti-tubercular treatment in these patients and only rifampin may not be the solution. Especially if you are trying to give immunosuppressive medication, you have to be very careful to not cause generalized tuberculosis. What do you typically do with these patients if they have electrical storm or they have active inflammation? While you are waiting for the steroids or methotrexate to kick in, do you treat them with amiodarone, IV amiodarone and then just bring them back when they have fibrosis or the VT ablation or how do you manage that at a tricky time? That's a challenge. That's an absolute challenge. What Dr. Ellenbogen is saying is when you have active inflammation, you have an ongoing VT storm. You treat it like a VT storm, forget about the inflammation. You do have the suspicion for the presence of inflammation that should prompt you to go very, very hard at trying to prove the inflammation as soon as possible. Maybe the dotonox scan is a great possibility there. But treat it like a VT storm first and active inflammation later. Use your steroids fast, block the cervical ganglia, do an emergent sympathectomy with your thoracoscopic colleagues, take them on ECMO if required and you can actually do sympathectomies on ECMO. If your thoracic colleague is your friend, he will actually do that for you. But it is basically all hands on deck. It's an active fire going on. Don't try and put your catheter in and increase the fire. You want to suppress the inflammation as much as possible and use ablation as your last resort when you're suspecting an active inflammation leading to a VT storm. Perfect. Perfect. Thank you so much. Thank you. Our last speaker for this session is Dr. Yung-Ko Lin on high-risk PVCs and non-sustained VT, how to recognize and management from the Taipei Municipal Wonton Hospital. Thank you for the invitation. It's my honor and privilege to be here. This is a topic of high-risk PBC and non-sustained VT, how to recognize and management. This is my outline today. First, I will start with the case. We can see this is a complicated EKG. The patient had baseline pacemaker region and atrial fibrillation. And you can see multiple VPC with different morphology. The patient had multiple VPC. And there are also the short-run polymorphic VT. And we can see the two VPC, the first, the couple interval 328 and the second has shorter couple interval, initiated ventricular fibrillation. And in this patient, the shorter couple interval, only one VPC can initiate the ventricular fibrillation. We can see the dominant VPC is RBBB superior axis and the very long QIS duration, 174 millisecond. Dominant R in V1, IS in V5 and 6. So we suspect this is from the posterior fascicle. And we can see the posterior fascicle. We can recall the potential preceding the VPC and also the fascicular blocked potential. The operation started with the Purkinje potential. We can see the operation induced the polymorphic VT. In this patient, he had a multiform VPC. It means he had multiple focus to initiate the polymorphic VT and VF. So we must take care of many, many sources of VPC. For the VPC and the non-sustained VT, it might be a primary arrhythmia or primary cardiomyopathy-induced arrhythmia. So PVC means from the ventricle and the non-sustained means more than three consecutive PVC in the less than 30 seconds. And this is we frequently encountered in our clinical practice. Back to the 2010, we can see the ischemic heart disease. The ventricular otomosity had been identified as a predictor of sudden cardiac death. This is a long classification. Depends on the frequency of the PVC, multiform PVC or the repetitive PVC or the coupling interval of PVC, we can identify the potential risk factor contributed to the VT or VF. However, when we record the PVC every day, it's a day-to-day variation. So sometimes it's difficult because a patient may present with frequent VPC or they can prevent very rare PVC. We cannot identify this burden with only single recording. How about asymptomatic patient? With frequent and complex PVC. In 1980s, we can see the report from NEJM. The report 73 asymptomatic patient with 24-hour EKG shows a very frequent PVC, multiform PVC and non-sustained VT. And the long-term prognosis follow-up for 10 years shows similar to the healthy population and suggests no increased risk of death. However, subsequent studies show that there are long-term clinical impact of PVC. This study enrolled more than 5,000 subject. Of course, this included symptomatic and asymptomatic patients. We can see about the all-cause deaths or hospitalization or heart failure is increased in patient with PVC. For the non-sustained VT in structured normal heart, this group enrolled more than 5,000 patients asymptomatic. We can see the patient with non-sustained VT had the worst outcome in terms of survival, CV hospitalization, CVA and heart failure. For the non-sustained polymorphic VT, only short duration of non-sustained VT or polymorphic VT can induce syncope. So in patient with ICT, we need to appropriate a programming to let the time of VF below 10 seconds to avoid a syncope. For the major concern regarding the presence of PVC and the non-sustained VT, the major concern is the patient had a substrate for the developing VT or VF or the VPC is short-coupled to induce VF or VT. Sometimes we can find the source of malignant PVC and most frequently we will find the burden of PVC. If the PVC burden is large enough to induce tachycardia-induced cardiomyopathy, then we will try to treat the PVC or non-sustained VT. The approach including EKG holter, echo, MRI, signal EKG or EP study or some blood sampling in case we suspect some chanopathy or genetic suspect cardiomyopathy. In baseline EKG, we can find if the old myocardial infarction this substrate for VT, but sometimes we can find a fractionation of QRS or delayed activation indicate there are some fibrosis or slow conduction or the EKG of cardiomyopathy. In case of determined necrosis or myocardial fibrosis, the cardiomyopathy provide the best resolution for the fibrosis with the leg cut or linear enhancement image. For the holter monitor, we can identify the PVC burden and the morphology of PVC or coupling interval. A PVC burden more than 10% generally consider high risk for the PVC-induced cardiomyopathy, but as low as 60% had probability to cause cardiomyopathy. If the burden is less than 5%, then the patient without a short couple with PVC, then the risk is low. Usually, where PVC from the common outflow tract from LVOT or RVOT is benign, and if they are not high burden, and coupling interval less than 300 millisecond are considered short coupled. This is a long-term outcome of multiple PVC reported with 3,000 patient perinormal heart with EKG monitor shows. If the patient had multiple PVC showing green and uniform PVC in blue and no PVC in red, we can see in terms of survival or hospitalization with CV hospitalization or heart failure hospitalization or the TIA-free survival or AF-free survival, all the company endpoint, all kind of endpoint showing the multiple PVC patient had the worst outcome. For the coupling interval, short coupling interval means it's a very high risk to have R on T. R on T is induced polymorphic VT, VF, and you can divide it into the R to T or R from T. In R from T, it's a long QT with VPC originated from the previous QS. And R after T means even with the long coupling interval, if the patient had post-reparation reflaternitis or slow sync mismatch, acute myocardial ischemia or carcinocyclic instability, they still have chance to develop ventricular tachycardia or ventricular fibrillation. So it's become difficult. If the patient had a short coupling interval, yes, it's at risk. But in long coupling interval, you cannot exclude the possibility of developing VT, VF. So we can see the clinical setting and the R on T. Most patient, yes, R on T, short coupling interval is dangerous. But however, in some clinical condition, the long coupling interval still have a chance to develop the VT, VF. And we must identify some source of malignant VPC easy to trigger polymorphic VT or VF. In the malignant PVC, it might originate from the Purkinje origin. You will have coupling interval less than 300 millisecond. However, if this is myocardial origin, you will have a longer coupling interval, greater than 300 millisecond, usually from the RVOT or RVOT. It will become very difficult to distinguish. So how to distinguish the malignant from the benign from the RVOT? Because RVOT VT is the most common since the benign ventricular tachycardia. So the study shows that short coupling interval of initiating VPC or the long QIS duration, shorter cycle length of VT, and previous history of symptom help us to identify the malignant form of RVOT VT. And if the patient had the non-sustained VT, then the second coupling interval of VPC help us to identify the malignant from the benign form of OT ventricular tachycardia. We can see if we use less than 317 millisecond, we have 58% sensitivity and more than 87% specificity. And the tachycardia cycle length of VT, if we use the 294 millisecond, we had a 75% sensitivity and more than 82% specificity. So in clinical practice, if the patient had a frequent VPC or attack of VT, it's a problem for the patient, but it's good for the doctor to have a correct diagnosis and a measurement, especially in EP lab. However, sometimes the patient had, they had a idiopathic VF, but they had a very rare occurring of a PVC or VF, then it might be a problem. So at the moment, the 12-lead whole hormone will provide a very good support for the identification of potential target. And this kind of arrhythmia may happen in the structural normal heart or structural heart disease. And the Japan group and the French group, they reported the triggers of VF in patient with infrared J-wave syndrome, very similar to the molecular origin of PVC. You can see the Purkinje origin, they have originated from the Purkinje, from the pumping muscle or moderate bend, or other myocardial triggers from the lateral wall of myocardium, usually in the epicardial, located epicardially. This Purkinje triggers, we can see this left Purkinje and this right Purkinje, usually they have RS-wave in the inferior lead, a tau R-wave in lead one, and a narrow QS duration compared to myocardial origin. You can see the mean QS duration is 161, and in myocardial origin, there is longer than 180. But compared to the normal benign RVOT, usually there's less than 120 to 140. This is also, it's a longer duration than the benign ventricular tachycardia. This is a case provided by Professor Nogami. This is a 24-year female patient, had multiple syncope. You can see the baseline had a 2-3 AVF, had a J-wave. And before the onset of ventricular fibrillation, there is elevation of J-wave. And the PVC operation, we can, they identified the operation site. They had Purkinje potential, 133 millisecond preceded the PVC. Before operation, you can find the J-wave, and after operation, the J-wave disappeared. And the triggers from myocardium, we can see the RBB type and the LBB type. The QRS duration is generally longer than the triggers from the Purkinje potential. And you can see the QRS duration is about, average is 188 millisecond. And you can see a specific W-wave morphology in two and three, and M-wave morphology in AVR, in RBB type. This is triggers from the posterior lateral LV apicardium. At sinusoidal, you can see the fractionated, separated split potential. And the VF trigger from the posterior lateral LV apicardium. This is another case, a 30-year-old male patient with J-wave syndrome, frequent VF. Also, you can identify the W-wave in the two and three, and M-shape in AVR. This is baseline, the TEFL-EKG. But in case with subcutaneous ICD, you can use secondary sensing to find the EKG morphology. If there is a W-wave, it means the patient at high risk of VF attack. Dr. Lin, we are exceeding the time. It's very fascinating, but could you mind? Yeah, this last two, and we can go to the next slide. This take-home message. For the sudden patient with PVC and NS non-sustained VT, first we must do the list stratification and identify the history of syncope or some family history. And treat the patient according to the PVC burden, morphology, and the symptom status, or any structural heart disease. For the idiopathic focal VPC symptom and potentially ectopic mediated cardiomyopathy is very important. Some malignant PVC, if we identify it, we must treat. And in symptomatic patient, we must go Holter and echo follow-up for symptomatic treatment, medical, and a case elaboration. ICT is rarely used, but in certain polymorphic VT and VF, we need the ICT support. This is my last slide. Thank you. Thank you very much. Those were great slides of polymorphic PVC induced polymorphic VT. We have time for just one question, if there's anyone in the audience who has a question. We'll have the last word. Thank you. I think it's a fascinating topic and it's very difficult to decide when to intervene. And is family history a very important thing when you decide whether you want to give a trial of drugs or do you want to go ahead and have it? Yes, but apart from the family history, the personal history, especially syncope, is very, very important. Because when the patient had syncope, sometimes patient will not aware of it, especially in the very old patient. They will consider that just have a nap. So carefully interview with the patient and the family is very important. Thank you. And this closes this really great session. Thank you for your patience.

cardiac arrhythmias

treatment strategies

perinodal arrhythmias

granulomatous heart disease

immunosuppressive therapies

ventricular arrhythmias

PVCs management

EKG analysis

advanced mapping