It's a pleasure. Thank you so much, Nishant, for giving me this opportunity to talk with the fellows, which I always enjoy. And so, although, you know, the VA system has got, you know, mostly like a hardcore, you know, sick, older patients, as you know, I think this is one of the things which we need to keep in our mind, a potential problem which can arise, you know, on and off. So let me see here. Okay, these are my disclosures. So today, I will, the overview of my talk, we will be focusing entirely on the HPSD, the Hispokinja system related arrhythmias in general, because I'm just broadly clustering the whole concept of the vesicular VT along with other aspects. So just to have an idea, I think how much the ramifications of the HPS has on these arrhythmias, and one of them being the PVCs we often encounter, and also some of the papillary muscle PVCs often has got some ramification to vesicular, you know, system, and as well as some of the challenges what we encounter with induction and mapping and ablation strategies. So this is one of the papers published a while ago by Nogami, you know, and Kiko has published a lot on this aspect from Japan. The Purkinje related arrhythmias are, you know, broadly categorized into two, one is the monomorphic VT, and another one is the polymorphic VT and ventricular fibrillation. So the most common one, which is actually considered to be the case for a while, which is most exciting part, is the verapamil sensitive vesicular VT. And this is one group of categories. We'll get into the details later. That's probably the main part of the talk. And the next is the Purkinje fiber-mediated VT post-infarction, which is actually less spoken about these kind of scenarios, which actually is an important topic to talk about. Often it can also present with ventricular fibrillation as well. So then the bundle branch with re-entry and the inter-vesicular re-entry, I'm not going to be touching upon that because it by itself is a huge topic. And we'll talk a little bit on the focal Purkinje VT, which is another entity which can be mistaken for the vesicular VT in terms of verapamil sensitivity. And the polymorphic is short-coupled variant of the torsad versus ventricular fibrillation. And the VF in the ischemic cardiomyopathy may also be, you know, because of some incessant VF, especially when you're going in trying to do an ablation, you tend to see them. And there is a question whether this is a concept which is associated with the CP VT and the early repolarization syndrome. So let's talk about the vesicular VT, which is probably the meat of this particular talk. You know, the characteristics of the vesicular VT is interesting. The first state was actually described by Zipes back in 1979. And the most important part of the vesicular VT, it is seen in the patients without structural heart disease. That is one thing we need to keep in mind. I mean, that doesn't mean that it doesn't exist in patients with structural heart disease. It's just that it can be present in patients without structural heart disease. And later, Belhassen showed that it is sensitive to verapamil, and hence it becomes like a Belhassen type of a VT. It was described mainly because of the fact that it is sensitive to verapamil. So typically it is induced in the ventricular pacing, but the most important thing is like the bundle branch re-entry, it can also be induced from the atrial pacing. So that gives a little bit unique characteristic of being a vesicular VT with induction protocols can be from the atrium or the ventricle. So the right bundle branch block pattern with the left axis configuration, and I will talk about the different kinds later, is the characteristic morphological changes you see with the VT. So broadly, these are the three categories which are seen with the vesicular VT, which is the idiopathic left ventricular VT, in other words. The common ones is the one on the left side, which is the posterior vesicular VT, and it has got a characteristic feature of right bundle morphology with the left axis deviation. And they will get into the little details of the morphological findings in specific group of VTs. The anterior vesicular VT is the next category. Main difference is the axis is high to low as opposed to low to high. And the third category being the upper septal VT, this is often a kind of VT which can be completely mistaken as an SVT, and we need to keep an open mind to really look into this aspect. I mean, it is also true that I think sometimes all these VTs can be mistaken as SVT with aberrancy as well, but something we need to keep in mind. As electrophysiologists, I think we are dealing with something different. I think we obviously differentiate a lot more, but we need to still keep in our mind things can something be important to keep in mind. So this is the data come from one of the groups in Hyderabad in India. And the interesting data is because they have a lot of vesicular VTs they come through. And the distribution of this type of vesicular VTs among the patients in the three years what they had was about 57 patients out of which majority of them, as you can see in this category, were vesicular VTs coming from the posterior fascicle region. There was about 7% from the anterior fascicular group. And some group of patients had both anterior and posterior group in the two, 2%. And then the upper septal VT was about 2% in the one category. So the majority of the patients what we are dealing with is the posterior fascicular VT, which is the common kind of fascicular VT, which we encounter here as well. So the conceptual model of fascicular VT is as follows. And we'll go into the details a little bit later as well. So the important thing in order to have, this is the most important thing, this is a reentrant form of ventricular tachycardia. So when we talk about reentrant form, we always know there is an area of slow conduction that is very important. And in this case, this is the, this particular model is showing a area of slow conduction here. And there is a hinge point where it attaches to the fascicle of the patient's conduction system, which is the posterior fascicle in this region, which is depicted. It goes back around and comes, enters into this area of slow conduction and forms a reentrant limb. So it exits out further down into the myocardial exit comes somewhere more apically. So interesting thing aspect as it is revolving around in this region, there are two hinge points between the two zones are the zones where it is sensitive to verapamil. We'll actually show you how it can actually say that is the location, which is the verapamil sensitive. So typically when you keep your catheter somewhere in this region you can see the diastolic potential, which is actually this potential, which looks like a low frequency potential present somewhere there. And subsequently when it hits this area, you see this fascicular looking potential, which is a much more high frequency potential. And if you have a unipolar catheter sitting somewhere here, which is at the myocardial exit area, you see a QS pattern, but you don't see it when you have a catheter somewhere along the circuit, because we know that is not the site where it is exiting. So in this conceptual model, the patient has for some reason, this particular limb, which is actually mostly the functional limb, which is seeing area of slow conduction, like any other arrhythmias you see in patients without structural heart disease. Normally what happens, the conduction is going from proximal to distal conduction area. And then you have a conduction which is colliding both the anterograde and the posterograde fashion, and hence there is no VT. But we need to obviously perturb the circuit to induce the VT, which actually takes the anterograde limb going through the area of slow conduction, through this diastolic corridor, and it turns around in the posterior fascicle and makes this loop to form the common idiopathic left ventricular VT, which is the posterior fascicle fascicular VT. In the upper septal VT, which actually I will kind of combine with both of them from the anterior fascicle VT as well as the upper septal VT, it takes the same channel, but except what it is doing in this case, in the anterior fascicular, it goes retrograde and then comes down through the anterior fascicle as an anterograde limb. But in the case of upper septal VT, it is once again taking the anterograde going backwards in this area of slow conduction. It can exit either this way or that way, but it exits somewhere near the hisperkinetic system, and hence the QRS is super narrow looking and also, you know, it is confusing for a SVT kind of an arrhythmia. So classically, this is Nogami's very beautiful paper, several papers he has written in the past. You can see in patients with ventricular sinus rhythm, let's take a look at the sinus rhythm on the right panel. You always need to have a his catheter that is extremely valuable, and you have a his potential, and you have a fascicular potential going from proximal to distal, and that is depicted as P2, because this is the retrograde limb of most of the stachycardias anyway. The proximal, the anterograde limb, which is the P1, in the case of VT, is going anterograde in the case of the VT, and it turns around, retrograde through the fascicular conduction system and forms this reentrant loop, and this is the exit that is happening in the form of having a QRS, and it turns around, comes back through proximal to distal, and as you can see, this potential is rather low frequency potential in the diastolic corridor compared to the fascicular potential, which is a lot more sharper potential. So the spontaneous reset and decrement, that's an interesting aspect. So one of the things, interesting aspect is when you take a catheter, ablation catheter, you are mapping this one, and you have your catheter sitting in this area of slow conduction, when you pace, you can actually decrement. It almost behaves like an AV nodal conduction type of properties, although it is not quite the AV node, but except the conduction properties can behave like decrement. Now, when you have the measurements here in this upper panel, in this right figure, before administration of VERAPAML, you can actually see the timings. That is the P1 to P2 interval is 18 milliseconds, and P2 to P1 interval is 287 milliseconds, and then the VT cycle length is 305. After injection of 1.5 milligrams IV of VERAPAML, you can see there is a decrement in P1, P2, and P2 to P1. Hence, the cycle length is actually, it is decrementing within the fascicular conduction system itself, but it is not decrementing from the QRS to the next signal, because there is compensatory slowing between the P1 and P2, and P2 to P1, it is not quite between the fascicular and the QRS, meaning it is not the decremental pore limb, which is at the exit area. So, that tells you the decrement happens within that zone, what I described earlier. So, the induction is a very tricky one. So, a lot of times, you may not be able to induce, that is one of the things that can happen. Spontaneously, if it happens, it happens in this particular cohort, 11% of the patients spontaneously, the VT came on. So, one thing to remember is, I think they're very sensitive to sedation, and sometimes you may have to bring the patient when the patient has many episodes of VT happening. That is one of the things, and medications have to be stopped, and all these preparations like any other arrhythmias, and this is particularly, is a very sensitive. So, you can induce, in this particular category, RV, they were able to induce in 42% of the time, which is actually good. Sometimes, it's just a very difficult one to do that. And as you can see, it was induced almost 30% of the patients from the high rate atrium. That means, we need to keep that in mind. This is one of the reasons, I think, we may ignore that this is a vesicular VT. If you don't know particularly, we are only suspecting this is a vesicular VT, we may think about it. This is something to keep in mind. Sometimes, you have to go to the left ventricular side. So, you need to use anything possible to really, in terms of location, where we want to pick to induce this VT. So, in pharmacological usage in the form of isopril, or sometimes even the phenylephrine seem to be very helpful in this group of patients to induce the VT. The other thing which has noticed, I think there is a paper published from the same group, is among the women in reproductive age group, although this is more commonly seen in men, it looks like it is hormonal dependent. And hence, they have even loaded progesterone to bring the patient during the time of induction of VT. It seems to be associated with cycles. I think history gives away some clues as far as what you can do in order to induce the VT in the laboratory. So, Suraj Kappa actually has shown in this particular, sometimes when you have the VT, you may actually end up on the false tendon on the LV. So, this tells you, we all know that false tendon is a structure where often there is a hysperkinesis system traversing through this bundle. And hence, an important thing to keep in mind, intracardiac echo may be beneficial in a case if there is any obvious false tendon as a potential target for ablation in this group of patients. So, just to give you what exactly the false tendon, how it looks like. So, it can be attached to the papillary muscle like this as a bridge. It can be attached to any structure from across the ventricle too. And you can see how this is there in one of our autopsy series. And this is to show in the intracardiac echo how it is extremely valuable to locate this particular false tendon in order to see and categorize so that you can actually target that specific site. It becomes easier often. It may be the reason why it may be difficult to ablate unless you find the structure. So, in this conceptual model by Nogami, once again, they have shown both the anterior fascicular and the posterior fascicular circuits. So, this is the circuit which is actually showing false tendon as a bridge between the slow and the fast conduction site. So, it could be this is location that we may have to ablate. But I think you can take this slow conduction zone where you can target this area, which is the diastolic corridor, in order to have the VT terminate. So, this is something we can keep that in mind. And it becomes a nice target, anatomical target, when you have a false tendon because you know I think that may be a part of it. And you can specifically visualize the target where you can actually go and do an ablation. So, this is, once again, the interesting concept what we described earlier between the sinus rhythm and the posterior fascicular VT. But in the case of upper septal, we kind of look, I was telling you about that it is going retrograde. The P1 is the area of the slow limb, which is going retrograde. And P2 is coming downwards, which is the antigrade limb. So, and hence, you can actually see the different type of VT. And the target in the case of the posterior fascicular VT is somewhere in this broad area in the basal. I will talk about the targets where else you can do in the RAO and the LAO view towards the septal area. On the other hand, the target for the upper septal VT can be anywhere in this region, where you can actually find this area of slow conduction. You can pretty much target in this very similar location. It's a broad area we can actually get into the details. There was one paper published by Ma just a couple of years ago. It's actually a very interesting paper for the fact they got into the details to see which is the best site to really go after the ablation. So, we all know one of the things that happened, we talked about the upper septal VT where because of the QRS gets very narrow as it is very proximal. If you just conceptualize the idea that as the fascicular system, the conduction through the fascicular system going downwards towards the exit area, if it's further distal, that means the myocardial involvement is further distal, the QRS tends to get wide. If you keep that in mind, proximal is narrow, distal is wide, that gets you an idea based on how the QRS is looking during the VT that you can potentially go towards a particular site. And as the HV, I mean his catheter is a very important catheter to have in this particular group of VTs. Let's say if it's a bundle branch re-entry VT, it is useful. You all know that HV gets really long. And on the contrary, in this case, the HV, if it is rather short, but even with the short HV, there is three categories they actually observed in this particular paper. And they found if the HV is greater than zero, in this case, it's eight milliseconds, as you can see here. And it falls into a very narrow group, which is a proximal site where you can actually consider doing an ablation. It's right there in that location. So there are several things you can see. Sorry for the, I think probably small picture that you're seeing here. The Purkinje potential to QRS interval is rather large compared to the middle portion, which is about 24 on an average, 34, 24, and 20 in the case of the smaller category. And if you index it to their HV interval, it is somewhat, you can see it gets smaller and smaller as you come down this path. So it's about 60%, 45%, and 30%. That's what it's going to look like. And the QRS duration is very narrow as you go in the proximal site and becomes about 128 milliseconds in the mid zone and becomes 140 milliseconds. So overall, the QRS tends to be less than 140 milliseconds in most of the fascicular VTs you can see. That's one of the classical descriptions, which is also been in the literature. So the lead one and V6 gives us some information, which is very important. As you are more proximal, you tend to have an RS ratio greater than one. And anywhere in the mid to distal location, it becomes less than one. So those are the classical features you see with this fascicular VT, apart from the fact that it is a right bundle morphology. In this case, as you can see, the HV is somewhere between zero and minus 15. In this case, it's minus six. And the PP QRS is about 28 milliseconds, falls in this middle category. And that's where the ablation will be successful to target. And as you can see, the QRS became wide in this case, which is much more distal location. And the HV is far less than about minus 33 milliseconds here in this case. And it's further distal, where it is at the site almost close to the site of exit, where you can target as the best outcome. So one of the observations done from this group in India, what they've seen is the exit as we know, it almost looks like a protected and exits out further down apart from the limb of the circuit, which is going around. This area of exit, if you keep your catheter somewhere in this region, the unipolar electrode shows a very nice QRS configuration. So is that a good site? Obviously, you are not really targeting the circuit itself and you are just trying to block the exit area. So it won't be successful. So unipolar in this case may not be very helpful. So what is important to target is this turnaround point either here or there, where you can actually see different forms of signal or even you can pretty much go anywhere. But I think this is a nice to really look at it and try to see if we can differentiate. In this case is shown, there is a tiny R. As you can see, the exit is further down there in the unipolar signal. And then the bipolar signal shows that Purkinje potential because it is the turnaround point And this is not as early compared to very proximal region if you go further down in this area The it will be a lot more early because that's where it actually the Purkinje potential will be seen like that Okay um, then in the case of the Slow conduction area if you keep your catheter down there, then you can see this diastolic potential which is farther out uh from The his Purkinje. I mean the Purkinje potential that's where it's been described by Nogami very nicely Ideally speaking. I think the best way to look at these particular arrhythmias is with having a multipolar catheter That is I think probably the ideal if you can have a catheter Going retrogradely along the septum and when you are ablating use your transeptal Catheter so that you don't accidentally bump one of the biggest problems with this particular one If you accidentally bump you may terminate and you don't you cannot induce it anymore That is one of the things you need to keep in mind. It has to be very slow I think it's a good idea to use our ablation catheter to go through transeptal approach in my mind To minimize the chance it can happen even with a multipolar catheter but at least you know, if you can slowly get across the Where you know the aortic valve along the path and keep it I think that's probably the best way to handle this So this is just to show you the example of what we described earlier about Locating at the site of exit which is not the good site for ablation So you could you know What if you cannot induce in the lab so you can try to see if you can look for these diastolic potentials Or sometimes empirically you need to anatomically go in that area where you can ablate in the mid to posterior septal location Of this vt if you see the vt as we described in mass paper whether it is Qrs is fairly wide as opposed to Less wide it may give you some clue, you know Where you potentially want to anatomically target in a situation in a sinus rhythm where you cannot really induce the vt So, uh, this is the example for the successful ablation site once you have the successful ablation side You can actually see this the limb is actually has a broken circuit, which is the area of slow conduction It goes down p1. It is separated from The just before how it is present in the vt now it is actually kind of emerged within there and now it actually goes out uh independent, uh of the Uh, you know the normal sinus rhythm up to the ablation where the limb is actually broken then you can actually even demonstrate that This is a very interesting observation that we had we actually presented in the last heart rhythm society Um, you know in the online version of it. We observed a patient Who had a histoplasmosis of the proximal septum you can see a case here in granuloma I mean here right in this area and um, this patient kept having these arrhythmias, you know, unfortunately the Uh, you know, we were never called in the ep. They thought it was svt We can manage this patient was sick in the hospital in the icu And the echo actually ironically showed the same lesion what you're seeing right here And what we saw is all along was a fascicular vt which is actually ironically upper septal vt So the question comes up can it happen in a structurally abnormal heart? This is obviously structurally abnormal heart So whether whether or not this inflammation invoked this area rather whether it is involving this upper septal Hisperkinesis system is obviously debatable because we could not study but it's something to keep in mind That this can happen quite often where the vt can be quite mistaken Unless you know, you know, you can delve into looking into Why these arrhythmias are happening in a patient who has something? abnormal in the imaging um that you have obtained The other category is the purkinje mediated vt in ischemic scar This is something to keep in mind this particular patient. I will tell you very interesting was it's um after Modifying everything substrate. He had channels going through this There is repeatedly we saw this Pre-potential very sharp potential and that was the one as soon as you touch that he goes into incessant vt So it was uh, it was amazing the by the fact that this was so much for secular um associated type of vt and we had to Literally do an ablation, you know, they subsequently in this area Um, you know like a heavy lesion. So in order to actually terminate this particular vt This goes on to tell you that apart from the fact that we all know about mapping With late potential lavas and everything we need to keep in mind in patients with scar mediated vts You know the incessant nature of the vt whether it's a reentrant form or even ventricular fibrillation It may be a purkinje mediated Uh type of a phenomenon as well, so this has been observed by Many people and um nogami actually in one of the papers actually has also Um, you know categorized this particular group of patients as well So fascicular pvcs before we get into the details of the fascicular pvcs. It is good to really differentiate pvc You all know probably how to differentiate but I think it's a good idea to go through this exercise Between the aberrancy versus the pvc itself So you can see typical v1 morphology you see with an aberrancy in the form of a bundle branch block pattern and in this one a typical form you see with the case of a fascicular type of vt Um, the qrs is usually greater than 140 milliseconds because this doesn't really specifically involve Um, even if it involves the his purkinje system, it doesn't exit right at the proximal region it takes The normal path of the fascicles and as we saw that when it exits further down distally the qrs gets wide In this case it it passes through all through into the myocardium And there is no specific channel for exit and hence the qrs is greater than 140 milliseconds Whereas the qrs is far less than 140 milliseconds in the case of fascicular vt And the ratio here the v6rs ratio is greater than one As opposed to this one is less than one um, then Negative avr is seen because it is coming through the normal pathway in this case in the posterior fascicular being the commonest one You have a positive avr when the three out of four criteria are present Then you know you're talking in terms of a fascicular vt Of course, one of the things you also may see is the va dissociation But you know this depends on the rate of the patient and many many factors you may or may not see it So something to keep in mind the morphological characteristics so um what the fascicular pvcs, um associated with the papular muscles, um is is another group of patients and You you all know that I think there is a challenge always fascicular pvcs are challenged for many reasons one thing anatomically, it can be challenging as far as where it seems to be arising from And the second thing is what are the real targets? So one of the things that I have noticed over a period of time as well as I think in the literature is also The case is the intrinsic heart deflection. We all know physiologically when you look into the intrinsic heart deflection It tells you that I think the origin to exit site. There is a delay in the conduction Okay, um, we are talking in terms of not a structurally abnormal heart, but it is just a papillary muscle associated um, so in that case if they Rather if it is brisk, you may be actually dealing with a fascicular mediated uh, you know, um type of pvc so in this case as you can see the there is a There is a pre potential which is a fascicular potential. You may have to target there interestingly enough. I have seen that quite often Uh the we are focusing on looking at the exit sites And it may not be the site where we need to ablate we may have to really track back Where it seems to to be the case you may burn and it may do the ablation. It may not Successfully terminate you may have to track back further down in order to find where exactly you want to ablate. So um, just keep in mind I think the intrinsic heart deflection may give some clue where sometimes it may be hard to find why we are unable to ablate this vts or pvcs In this particular patient that we had, uh very similar we looked at the exit site It is way down into the bay base of the papillary muscle and we started tracking back further and we found this fascicular potential And it was very interesting The unipolar was quite late as you can see that means that's not the site where the unipolar If you take the unipolar as the earliest then, you know, you look like you are not in the early spot But the fascicular potential was clearly the target and as soon as you ablated and the pvcs went away this tells you and also Sometimes you can invoke the vt at the time when you're actually ablating the fascicular um, you know mediated fascicular pvcs So in order to understand the difference between the fascicular Mediated papillary muscle vt versus the papillary muscle idiopathic pvcs Usually when whenever there is a fascicular mediated that means there is Some form of a limb that is coming in the form of a circuit So it's quite possible. You may end up seeing this reentrant i'm seeing i'm using the words carefully because there is another category as well reentrant form of vt, um, you know commonly present so the idiopathic the pvcs which are just primarily originating from the muscular component of the Papillary muscle are usually non-sustained And they are pvcs. They are not entrainable compared to the reentrant arrhythmias And they are not induced inducible by the programmed extra stimuli or the atrial pacing But anywhere if it is anywhere involving the hysperkinesis system You can do a program extra stimuli or the atrial pacing Let's give away in a way to look at it as a reentrant involving the fascicular conduction system And they may be responsive to verapamil because it's a fascicular mediated one as opposed to not sensitive with the fascicular pvc So outpatient it will give a little verapamil as a test and if it works It gives you a clue in a vt. It may be may be dealing in a patient. Otherwise in a normal You know, uh structurally normal heart So this is another morphological characteristics. We have seen this is i'm sorry for this particular tracing It's very small one just to give you a left posterior fascicle We kind of described middle fascicle, you know It's it's kind of a little bit in between a little bit the structure morphologically in between the two Antara fascicle is high to low and sometimes it can arise from the left bundle itself. It may take very similar looking morphology as the native conduction System, so whenever there is pvcs involving that, you know, you tend to match with What potentially it can look in that situation this is a little complicated algorithm which was published by zhang group and and you know, it's interesting is um, if you have the The potential what you are seeing is a fascicular potential to the qrs Timing and if you add the hv interval during the time during the sinus rhythm and then During the pvcs And if you actually add them and divide by two It will be the same as this one if those two match The site of ablation that's the site of ablation that you need to do you will have a very good very high success rate so it's kind of a Complicated algorithm that means that it doesn't tell you site specific where you are actually going But it tells you the site will be successful when you do an ablation But you could tie your algorithm to think about it that way where you want to really match that way um, but one thing we When you look back the morphological characteristics what we saw Where exactly the qrs and the hv interval fit in it gives you approximately very similar idea Whether you're in the proximal part of the septum middle part of the septum further distal down Then you know you may be able to You know Just to localize or regionalize that area and use the algorithm and then find these pvcs to ablate so We all know that sometimes it's been described that a pvc could be triggered for a polymorphic vtr ventricular Fibrillation. This is one of the categories. I think michelle hasger has described quite a bit and short coupled Fascicular pvc could be one of the targets So, you know in this case, you can see there is a clear evidence of a fascicular potential which actually mediates this particular pvc That's the one and causing this polymorphic Vtr vf so hence you target those you actually are you know helping this group of patients Who otherwise may have multiple icd shocks without any? Um help from any medications so that is that's the one we need to target in that situation so the other category the reason I mentioned earlier was uh, um that The reentrant is common lateral pacing but there is another category Which is a non-reentrant form of fascicular tachycardia in the form of an automatic focus Or a triggered focus if you pace your burst space and induce it becomes more like a triggered kind of activity But if you terminate with the burst spacing it could be automatic type of rhythm So you could base map and you can morphologically match in this case in a non-reentrant fascicular Because it's a local area what you are dealing and um that that group of arrhythmias are also known To occur in this particular group Um, they about approximately three percent of these fascicular vds could be in that category So the mapping and ablation, you know, you are targeting The same fascicular potential. So that's one of the things in this case what we have seen and if the other Criteria seems like it fits, you know, like a fascicular in the form of morphological characteristics QRS being relatively narrow compared to the myocardial origin of the pvcs and things like that then try to think about mapping for the fascicular potential Sometimes you may have to use a tight um, you know, um electrode uh in the form of a very short like one millimeter like a noga catheter or Some other catheter which actually has very short, uh holes in the way so you can actually target specific location to find this particular fascicular potential ablation catheters are good, but you know, I think most of them can pick up but I think if you don't I think that may be A good idea to think in terms of if your mind is thinking particularly you're targeting this fascicular uh pvcs are the non-rent re-entrant form of vt the etiology being a fascicular mediated ones so this is like the um in the Summarizing the verapamil sensitivity you can target the diastolic abnormal purkinje potential But as I said, you know, I think in that limb, it's a broad area you can actually um, you know, you can actually potentially look into Uh different parts of the limb, you know You may end up doing a poster fascicular ablation in a sinus rhythm where you cannot really get to it So sometimes you may have to do that so the other is the purkinje mediated Vt in a post infarction you look at the diastolic purkinje potential In the bundle branch re-entrant vt use specifically target right or the left bundle And the inter fascicular re-entry you can go to one of the fascicles and the focal purkinje Mediated vt you target the pre-systolic purkinje potential So the fascicular vt characteristics once again to recap The p1 and p2 recorded in a relatively large area in the mid-septal region That's one of the things that some things to keep in mind. Remember one thing Bumping and terminating is one of the big biggest problems You encounter and as gentle as possible as slow as possible to move the catheters will help you to record these particular group of potentials nicely the entrainment from the ventricle capturing Orthodromically and resetting the tachycardia gives away that one of the things that you see with particular slow limb because it's going orthodromically and You can have this decremental areas as we discussed earlier between the potential p1 p2 p2 p1 And and it is sensitive to verapamil and that gives you an idea But the interval is not the p2 qrs doesn't change anything We know that it is not that particular exit area where the problem is the problem of decrement is also seen With the verapamil within the limb itself. So that gives you some characteristics of the specific fascicular vt The success rates are very good you know if you ablate this and And you know, you you can be a lot more confident to say that the chance of recurrence is very small So, um the last conclusion being the these the pvcs and other group of other than the common idiopathic type of Poster fascicular vt or the other groups of fascicular vts is to talk the targeting the Purkinje potential And the pvcs may also be triggering the ventricular fibrillation you can look at those particular group of Pvcs and also the ischemic as I mentioned I didn't I forgot to put it in that slide and the non-reentrant vt may arise From the his purkinje system as well as we you know, it is not necessarily always reentrant form of arrhythmia so I think I hope I kind of summarized and Help you to understand what? um I know, uh, this particular group of arrhythmias which um are Uh in a good group, you know, I see that dr. Talib is here You know, he's written a lot of papers on this aspect. That's amazing. Uh, it's a great honor to you know, uh talk about his papers in this presentation Thank you. That was great fantastic review. So maybe I can ask a few questions here There seems to be a sense that you know, non-inducibility can make some of this difficult so let me ask you sequentially a few things um in setting up the procedures Do you think about using general anesthesia or only conscious sedation for these? Yeah, I typically try to you know, you know have the anesthesiologist if you are thinking patient is very uncomfortable Available, but I would not possibly start with general anesthesia Keeping under conscious sedation is probably one of the uh best ways to approach this one, uh, it's rather short procedure because it's not like extensive and uh You might be able to get this done in a short time as a patient. It's our patient comfort Um, you know, I think will will not be a huge issue because of the fact that it is a short one Yeah, I would target more towards the conscious sedation And then um if it is non-inducible Um, I guess there's a couple questions you talked about Pace mapping for the non-reentrant variety for reentrant variety. Is there any utility for pace mapping? Yeah, that's a good question. There are some papers talk about the um, you know pace mapping But um, it is kind of a little questionable and I know that talib can give Um ideas about this, but I think you can anatomically target The posterior fascicle region because the commonest variety is this one if you have seen the vt How the morphology looks like you could do that. The other one is you could target the diastolic potentials Just the potential itself in this category. You can see it in the sinus rhythm You might be able to possibly target that particular area and if you capture very locally with This diastolic potential, um, you know, you may see the morphology similar to that. It's a very You know for refined way of you know doing the pacing thing and it requires patience But I think um, it is anatomical region in general targeting has been described for years I think in in the absence of induction of these areas and then for your end point if you do an anatomic line, it's what shift in access or Shift and access is uh is particularly if you're targeting the posterior fascicle You may change the shift and access but if you target the diastolic potential you may not um, and uh, once again, that's that's a tricky question mainly because of the fact that if you're particularly targeting the um Diastolic corridor you may not see that particular anatomical change and you know If you're not able to induce then, you know, we are in the same situation. I think Um overall it looks like even if you target those areas it appears like the outcomes are fairly good And then you mentioned this association with false tendons So do you recommend using ice for all of these procedures? Is that a potential target for non? Yeah, you know, I would rather consider that, you know, if you let's say if you do a An echo trans thoracic echo or and you see something ahead of time, you know You've done for various reason to assess for structural heart disease Uh, it gives you a clue if you don't see anything, you know, obviously you don't know what it is But if you do something, I think that particularly is a you know, the cost is an issue for using ice I think in that case, I think um, um, you know, pre-procedure Assessment is a good idea. But you know, if you routinely use ice for many You know ablations in that category. I think it'll be extremely valuable in my mind I use ice all the time mainly because of the fact, you know anatomically you can target where you're going And then um You know, you're looking for small diastolic potentials. Have you? seen any issues with everyone relying on these automap functions on the On the systems nowadays Yeah, no, I agree. I think this is one of the things I think We still need to keep our eyes open and because this is a unique group of patients Where um, you know, the primary targets is these these low frequency signals In that case, I think sometimes you have to really Because the algorithms have got their own problems, you know It may or may not it may filter out you have to really keep your eyes open to find these targets

arrhythmias

His-Purkinje system

fascicular ventricular tachycardia

reentry circuit

ablation strategies

verapamil

intracardiac echo

conscious sedation