Thanks again, Nishant. I just want to also reiterate how impressive this series has been and the hard work Nishant's put in to do this for the fellows nationally and internationally. I know our fellows have greatly appreciated both the live sessions but also the online material as we all get back to work during COVID. I know a lot of the fellows can't be present at some of these live sessions but the extra work he's put on himself to do this for the fellows has been really impressive. So thank you all for being here and tuning in. I was asked to talk about outflow, PVCs, and VT. You're also going to have a number of lectures in this general arena on this topic. I think that the best way I can approach this topic for you is to explain the way we at UCLA approach these cases from the very beginning. Certainly show some examples but not spend the whole time just showing case after case of success. While that can be useful, I think we learn a lot in terms of how to do these cases, not just as fellows but when you become an attending. I know my techniques and strategies have changed over time. Anything I can help with your future assessment of these cases, I would love to do. I have no disclosures. Sort of an introduction or take home points, if you will, that I'll kind of address during the next hour are that the RBOT is a common side of these so-called idiopathic arrhythmias. But perhaps not as common as we've been led to believe. We should always consider whether there could be indolent structural heart disease in these patients. The majority of times, there's not. But in a percentage of patients, finding that indolent heart disease can drastically change their management. The anatomy and the physiology of the outflow tracts are perhaps more complex than is often considered. I know I've learned a great deal from my colleagues and from our use of the McAlpin Atlas at UCLA over the years, even as an attending, in terms of how I approach these cases and understand anatomy and physiology. Site of origin for these arrhythmias, which are predominantly focal or triggered, is an interesting concept because what defines the site of origin? Is it the termination site during an ablation? Is it the best pace map site? Is it the earliest activation site during mapping? The answer is it could be some combination thereof because there's no perfect definition of site of origin. And that may be what leads to some of the confusion about where these arrhythmias originate from. So you should always consider the interaction of this complex anatomy in the setting of the possibility of preferential conduction. So we'll talk a little bit about preferential conduction and outflow tracts and how that can fool you, if you will, when looking for pace maps and earliest sites of activation. And this is a quote that I enjoy and I think really is useful in EP in general, but also when it's specific to this topic, is that Eisenhower said, plans are useless, but planning is indispensable. So I think the way I interpret that is you should always have a plan for the case that you're starting, a general plan of how you're going to attack the particular arrhythmia. But as you gain more data, your plan should change and develop over time. And that changing of the plan as you get more information is really what defines EP and probably one of the reasons why a lot of us were drawn to EP in the first place. So when we talk about outflow ventricular arrhythmias, ventricular arrhythmias, in the perfect cases where we're mapping with electron atomic maps, as shown here in the REOT, we're looking for earliest sites of activation, either on a multipolar catheter or in this case, an ablation catheter. We're often pace mapping by pacing at different sites at the lowest output that captures the local myocardium to kind of generally triangulate where the best site may be. And ultimately we're defining the best site for ablation. And when things go well, we're seeing a lot of PVCs or VT, and then we're seeing termination of the arrhythmia. Unfortunately, things don't always go as perfectly and understanding the reasons why it may not go so perfectly will make you a better electrophysiologist and more successful. Because when we talk about idiopathic arrhythmias, it can be really frustrating if we're unsuccessful in these cases. If you ablate AFib, you can claim acute success in almost every case. Long-term success may be a different issue, but if you ablate structural VT, there are going to be times when you can't successfully ablate the VT, but those are complex cases. In these cases, we feel like we should be successful. And when we're not, we have to kind of reassess why we're not and what we can learn from those cases and how we can get better in the future. Because there's nothing worse than seeing a PVC that you think you got rid of, and then when they get to the recovery room, they're having PVCs again. At the bottom of this slide, a couple of nice reviews by Greg Marcus and by DJ Lacaretti's group that I think are nice references. So to start off, the first question I'll ask the group is, in what percentage of cases do you order preablation imaging or other than echocardiogram for your supposed idiopathic PVC or VT case? Never, 20%, 50%, or always? So it looks like Nishant's putting up the responses here. I'll give it 20 seconds. So it's an interesting mix and probably a little skewed towards the aggressive in terms of the always category. I don't think that all of these patients need imaging. I think we need to have a set of decision-making criteria in our mind that help lead us towards the necessity for further imaging. So the right answer is probably somewhere between B and C, but I think the answer is still to be determined. So the question is, when are MRI and PET imaging, those are the two most common imaging criteria, those are the two most common imaging modalities we use here at UCLA for our patients with VT or PVCs, when is it warranted? I would argue that if you're concerned about early ARVC or underlying inflammatory cardiomyopathy or cirrhidosis, then getting these imaging tests is very much warranted. And we'll talk a little bit about what leads us in that direction. The second topic about preablation workup that I won't talk about is Holter monitoring. We often think about Holter monitoring as simply a way to gauge PVC burden and to assess perhaps if their patients are at risk for PVC-induced cardiomyopathy based on that burden, to ensure that they're not having sustained ventricular arrhythmias. But there is additional information that you can get from those Holter monitors that we've found very useful, both for medical therapy decision-making, but also to understand what you're going to be up against in the EP lab in terms of responsiveness to drug challenges when they're not having enough of the arrhythmia to map. So we often think about MRI in structural heart disease, VT, and here's some images from our wideband sequence developed at UCLA, information on safety of MRI in patients with fibrillators and pacemakers from Magnesave. But in this patient population, what we're really doing is looking to see, is there some indolent disease that's causing the arrhythmia and what we're really doing is looking to see, is there some indolent disease? Obviously, if they have clear evidence of structural heart disease on echo or EKG criteria, then we might be going down a different direction. But if patients have generally normal ejection fractions, relatively benign looking EKGs, but have other suspicious findings, maybe borderline EKG findings, maybe PVCs that look less idiopathic than one might expect, and we can talk a little bit more about that, that's when MRI imaging additionally may be beneficial. This is a nice review by Daniel Muser and colleagues, and I won't go into great detail about this. The thing that I kind of start over here are two criteria that I often use that lead me down the path of looking for, considering MRI and PET scans in patients that were sent to me for so-called idiopathic ventricular arrhythmias. If they're having multiple PVC morphologies, that always raises my suspicion. So a single PVC morphology, outflow origin, oftentimes is just idiopathic VT. Multiple PVC morphologies, some with, and in particular, those that don't have morphologies that are typical of idiopathic arrhythmias. That can often be challenging to assess on a Holter monitor, unless you have a 12-lead EKG of it. But when I see things like superior access, it raises my suspicion. You can certainly have superior access idiopathic VTs, like from the vesicular system. But again, multiple PVC morphologies, morphologies that look a little atypical, raise my suspicion, and certainly lead me down the path of getting additional imaging. So what about PET scanning? We've done PET scanning in non-ischemic chromopathy patients and published in that regard. And we've also seen that there's a lot of disorders where PET scans may be abnormal that haven't really been described before. We've described it in Brigotta syndrome. We've described it in Chagas disease. So there is a component of that inflammatory chromopathy related to some of these disorders that's perhaps not been fully described. But when you look at the Maverick registry that Macaretti and Natale and others published for predominantly thought to be idiopathic VTs and PVCs, in that registry, about 50% of the patients had positive PET scans. So PET scans are, as with many nuclear studies, with significant limitations, right? Unclear medicine, as we sometimes call it, can often be hard to interpret. But when you have patients with multiple PVC morphologies, perhaps underlying rheumatologic disease, other findings that might suggest inflammation, PET scanning can often be beneficial. And I've seen two patients in the last few weeks where they were billed as idiopathic ventricular arrhythmias and their PET scans came back positive with findings consistent with sarcoidosis. So what about the Holter monitor? So when we looked at the Holter monitors done at UCLA, we found that patients fall into three general categories of PVCs. Fast heart rate response of patients where they have more PVCs with a faster heart rate, slow heart rate response patients where they have more PVCs at a slower heart rate, and independent PVC patients where there's no change in their PVC burden regardless of heart rate. And what we found is that this can be very useful in clinical practice because the patients that have fast heart rate responsive PVCs have more PVCs at a faster heart rate, typically during the day, so kind of a diurnal response, are the patients that have a chance to respond to beta blockers. Whereas slow heart rate responsive patients sometimes can even get worse and independent response, PVC response patients have no effect whatsoever. So if you're in one of these two groups, the likelihood that you're going to respond to beta blocker therapy, which is most of our first choice for relatively benign treatment of PVCs and idiopathic VT, is highly unlikely to work. Whereas at least you have a shot with fast heart rate responsive patients. And so assessing that on the monitor can be very useful clinically. Second point to be made is that when these patients do get brought to the lab for ablation, they've either failed medications or don't want medications, and we tend to give these patients either of those options in the clinic, or if they've had PVC and there's chromopathy and they need to need to have a potentially curative treatment for the chromopathy. The most frustrating thing we see is that PVCs have a mind of their own. Sometimes they're having bigeminy and sometimes you can't get the PVC to happen. And when that happens in the EP lab, it can be very frustrating. So what we looked at was how do those different categories of heart rate responsiveness in terms of PVCs on the Holter monitor correlate with response to the typical drugs we use in an EP study to induce the PVCs? Predominantly isopryl. So if you're a fast heart rate responsive patient, there's a pretty good chance if you're not having PVCs as a baseline that you can increase the PVC burden giving isopryl. Whereas if you're a slow heart rate responsive patient, you don't have a good response. And we've actually seen the opposite, that phenylephrine, which has a big olytic response, and even beta blockers can increase the PVCs, though that wasn't studied in this particular study to significant degree. The independent heart rate patients, no matter what you do with any of these drugs, isopryl, isopryl washout, phenylephrine, nothing seems to affect their PVC burden. And so if they're starting in a baseline without PVCs, you might as well call it a day at that point because you're unlikely to be able to induce the PVCs. And being able to induce the PVCs is important because if you look at patients that have spontaneous PVCs, they have a relatively high success rate of PVC ablation. And if you can induce their PVCs, the success rate is very similar. But if you can't induce their PVCs, obviously in large part because you can't find PVCs to map, success rates are incredibly low. So knowing which categories those patients fall into can help you plan for your procedure. So the second question I have is what percentage of cases originate from the RDOT in your individual centers? Jason, maybe while they're doing that, I can ask a question that came through here. Is there a percentage of PVC that you use as a cutoff to bring someone to the lab? Is there some number that you look for? Yeah, I mean, that's a good question. I usually tell patients that if their I usually tell patients that if their PVC burden is under 10%, that the chances of them having sufficient PVCs to map goes down substantially. If they are fast heart rate responsive patients, I have a little more flexibility because I know there's a decent chance they'll respond to isopryl. But while I don't have a hard cutoff, I tend to have that discussion with the patient because it's very frustrating for the patients to spend all that time coming to the EP lab and then being basically told we didn't do anything because you weren't having PVCs. So I find that above 10%, we have a pretty high likelihood of having a successful procedure. Below 10%, it's really hit or miss, and especially in the slow or independent patients, very unlikely. Okay, great. Here's the poll results. So I think those are excellent answers, and I would agree that it's probably in that range. I would say probably in that B-ish range, maybe slightly higher. The reason I put up this question is that if you read textbooks, I don't think fellows really read textbooks anymore, but if you read textbooks and early literature on PVCs, a lot of times the introduction talks about the percentage of idiopathic PVCs coming from the RVOT and how that percentage... I've seen some textbooks say as high as 70, 80% of cases are from the RVOT. The problem is most patients in the community, many of them don't come to clinical evaluation. We have no real sense of the incidence and prevalence of different PVC sites of origin. Further, early studies on PVC mapping and ablation probably were biased to more easily targeted PVCs in the RVOT. So I think a lot of the literature that doesn't give a lot of hard references makes it sound like RVOT is a little bit higher frequency than it actually is. Now, don't get me wrong. It's still the highest percentage, but especially I think in some of our centers with a little bit of a coordinated referral bias, it's certainly much lower than what may be reported. There was a recent multi-center collaboration that we were a part of that Frank Bogan led, where that percentage from the RVOT was around 40%, which I think is a little more accurate. Obviously, 12 ADKG assessment of location has its limitations. In this case, I just put it up because it's a V3 transition. So when you have an outflow left bundle V3 transition PVC, that can either be from RVOT or the LVOT. Jason, I'm not sure if it's just me or not, but I can't see your slide anymore for some reason. How about now? Yeah, it just turned into a gray bar. That's weird. Maybe you have to unshare and share again. I can see his mouse move when he did that. Yeah. Yeah, now it looks good. Okay. So, I think the way we think about PVCs and outflow VT is the importance of anatomy and really understanding anatomy and how much that helps you as a proceduralist. And again, I've learned a lot after fellowship in terms of being an attending and really studying the anatomic specimens and understanding the relatively complex relationship between the outflow tracks of the RVOT and the LVOT. And it's not nearly as simple as we want to give it credit for. I also think you kind of have to not just think about the outflow tracks, but understand the LV ostium as has been described, right? So the complex relationship between the valvular structures, the coronary artery and venous anatomy is all very highly relevant to the types of arrhythmias that we're dealing with, because these are really contiguous structures, right? So the valvular apparatuses, how are the fibrous and muscular components of the ostium interplay when you're targeting PVCs and VT from the region? We would argue that perhaps a better way to describe these regions, and we're putting together a manuscript on this, is to think about it as this is sort of a slide I put together with a lot of the kind of key papers that have described different anatomic locations for ablation of PVCs and VT over the years, all excellent manuscripts describing locations in the coronary cusps and the thumb and et cetera, and how they relate to each other. But you can basically see that they all sort of correlate to what we would describe as a superior septal process for the majority of these types of arrhythmias that we're dealing with, or the so-called outflow arrhythmias, and some that are in the inferior septal process, so the crux, the ISP, as described by the Penn Group. So thinking about it as sort of the superior septal process and the associated arrhythmias in that region, and the inferior septal process has made sense to us, and anatomically, I think, is more attitudinally correct. But remember, all these structures are very fluid and contiguous, and so all those manuscripts that I just made mention of are excellent and help you kind of understand the classic description of a morphology that goes with a certain location, like the right-left cusp, you know, the triangle, the LV summit, right? Even the AMC, which, you know, I would dispute maybe is a, we'll talk about in a minute, may actually just be an extension of the LV summit. But the only way you really fully understand site of origin is to have detailed mapping, right? So if you only map the RVOT, you don't know what's going on in the Erechsinus pulsato, you don't know what's going on in the LVOT, and that doesn't mean that every case requires this complex of a mapping strategy, but understanding the different areas that could be mapped when you're confused or missing something can be highly valuable, and this is sort of our playbook, if you will, for mapping of these arrhythmias. So some examples, you know, the paper by Ouyang and Yamada looking at Erechusp PBCs and VTs and the right-left junction, again, I've read these papers over and over again, and they're excellent manuscripts, and they give you a roadmap for where to go, but they're not absolute. There can be variability between patients in terms of heart rotation and other subtleties, so they're not perfect. You need to understand, again, the anatomy, so of the coronary cusps and how that relates horoscopically and for your electroanatomic map, right? So a lot of times fellows will say, oh, I'm in the left cusp, but you have to remember the left cusp is a bit higher, if you will, than the right cusp, and so sometimes you're kind of stuck in that interleaflet triangle. You haven't fully engaged the left coronary cusp, which requires the catheter to raise up a bit and drop down into that left coronary cusp in an LAO view, as shown here. Hey Jason, sorry, sorry. I feel like your slides might have gotten frozen. I'm not sure. We're looking at the site of origin slide, and it's actually the presenter view of it. I have a feeling you're beyond that. Yeah, now I can see your mouse moving around. Are you still seeing the... Yeah, I'm seeing the site of origin. It's an anatomic slide with no labels. It's slide 19. Oh, okay. That's weird. Let's see if... is it moving now or not? No. That's weird. Sorry. It's okay. Let me stop sharing and re-share again. Now, it's the gray bar. Lost it again. Yeah, it's, I'm currently looking at a black screen. Maybe come out of presenter mode, because I think that gives you two monitors that you have to pick from. Okay. Or worst case scenario, maybe show your desktop and not the full slideshow, I don't know. It says that you're screen sharing, but nothing is, it hasn't changed. You see anything? I don't know. No, for some reason it's just giving me the screen sharing text, but it's not actually showing anything. I Wonder why that is I don't know. That's the first time I've had that issue Does it let you just display your whole desktop Or have you already tried that? It gives me screen one screen two or my PowerPoint and None of those are working right now I Tried all of them something happened because it was working fine the way, you know, and now you're not saying I think Yeah, it's just You started screen sharing but it won't actually switch over to show us your screen I Guess I could try to leave and come back but the The only other thing I could think is if you want you could email me the Presentation and I can try and share my screen and you can just tell me to advance Yeah, I think so big the shared on a box or something You want me to try let me try to let me try to leave and come back That's Probably the best way Now we can talk about him while he's gone. Yeah Well, I can provide some commentary. I think 10% PVC is a lot to use as a threshold. I Think someone told me a PVC per minute is kind of the cutoff for when they would bring someone to the lab Yeah, I know I don't know I've maybe I'm a little lower than 10% but if it's lower than 7 or 8 I definitely have a conversation with the patient that it might not be successful Yeah And then another point I would make you know with regard to how much comes from the RV versus other areas in the outflow I think early on we were doing I think early on we were doing sustained monomorphic VT and I do think that's more commonly from the right side I think once we started going after PBCs, it became more common than it was on the left side. I don't know Why but other people have noticed the difference in terms of origin based on sustained or single PVC's And The threshold to go to the left is so much lower now just to at least check so See if I can Says host disabled screen sharing. I just made you a co-host so it should let you do it now All right, let's try Screen Okay, I can see your screen now, yeah Okay, sorry, I'll try to catch up a little bit Yeah, it must have been a zoom problem looks great Yeah, except the slides get old Okay, let me get to this there we go Okay, so right left junction PVC's classically described with a W pattern and in the Kind of B1 B2 leads with an earlier transition I would say that this is the most common site that we see outside of the RVOT I like to joke that the summit is all we see in terms of PVC's these days I'm sure the Northwestern crew feels sort of the same way in terms of what we get referred But in reality, this is probably the place where we see the most common success outside of the RVOT Here's a an example of one recently that kind of met that perfect that matched criteria this kind of W shaped and B1 RVOT was minimally early kind of in the anterior septal region Coronary venous system the CS catheter was basically on time, but not particularly early Pace map from the left cusp. Actually, it wasn't really the inner leaflet triangle rather a little more leftward It was an excellent pace map not perfect, but pretty Actually, not a great pace map in this particular case And you know, we'll talk a little bit about why pace maps in that area aren't great Because of the anatomy and the preferential conduction So I don't put too much weight on the pace maps in this region and oftentimes you can't capture very well the myocardium But the timing here was good about 30 milliseconds early. A lot of people have described pre potentials in this area We don't see a lot of those really early pre potentials But maybe people with better eyes than I do it. But here's the map for that particular case. So right coronary cusp left Left main catheter. This is a stereotaxis case because the catheter actually went into the left main briefly Not recommended but a little less traumatic with a stereotaxis catheter. So you would expect it to be here It was actually a little more leftward than would be classically described in this case. So again Those those EKG criteria give you a good general concept of where you may want to go It's not exactly perfect all the time whenever I go left my Protocol is to shoot a root shot if the creatinine is okay not Not everybody does that some people do selective coronary angiography Other people feel comfortable enough with ice to just use the ice catheter to look for the for the Austin and the coronaries I think it's just nice for the fellows and to kind of overlay the root shot into the Electroanatomic map and have a better understanding of where everything is the For a while. We were without smaller catheters for the coronary sinus now with the refrench Mappet and then now there's a two French catheter as well that are nice that can get out distal into the AI be and highly useful for these type of cases This is the ablation site again with the stereotaxis catheter in this particular case and The Point I want to make is that These structures are fluid and really close to each other So this is a catheter at the left right junction going retrograde and this is a catheter in the rvot They really abut each other with a very small amount of tissue in between So if you ablate the catheter of patient from here and you're successful, you're gonna say that's an rvot PVC If I've laid it from here, I'm gonna call it a left right junction PVC who's right? Probably both of us. It's probably somewhere in between and success can be had from from either side Sometimes you can only get it from one side or the other But again understanding how close these structures are Really is important anatomically. This is a pathologic specimen that region So if you're at the left right junction that distance of a small amount of myocardium is here If the PVC is here, you may be able to get it from either side Obviously if you can get it from the rvot and avoid going into the arterial system, that's always nice But oftentimes you need to map on both sides and we'll show some examples of why This is a case Where yellow line came from the There were two PVCs in this case one that had subtle differences in the QRS morphology and they were coming intermittently But they both had they had different coupling intervals and slightly different QRS morphologies PVC one mapped earliest to the anterior septal rvot as shown here on the am PVC two mapped earliest to the kind of left right junction region Over here this left right cusp The termination site By ablating within at the left right junction, even though we were all we were early for the one PVC 20 milliseconds But actually late to the other PVC eliminated both PVC. So again, the muscular tissue in that region is thin It's likely that this could be one PVC exiting in two different directions It could be two different very closely associated PVCs either way in this particular case ablation at the left right junction was able to terminate and Have long-term success for both PVCs General catheter tips I would give is whenever possible using kind of a retroflex catheter position This is another left right junction case Is always useful And I think it's safer in a lot of ways You're not poking as much with the tip of the catheter. It also gives you a better Contact in a lot of cases obviously with contact force catheters And magnetically driven catheters contact can be perhaps better assessed Nowadays and then in the past, but this is often a very safe trajectory for a catheter for a number of reasons Whenever you're dealing with valvular structures, this isn't an outflow case per se, but this is the tricuspid valve, but Retroflexing under getting underneath the valve or between the valve and the myocardial tissue is preferable than trying to ablate through the valve tissue Not only to not damage the valve itself, but also Because you may not have success if the valve is in your way So kind of sneaking in between the valve and the myocardial structure Is important Again this is an example of this going straight in versus retroflexed position that the tricuspid valve Others have described, and I didn't have time to find some of our cases like this, this kind of candy cane technique for Above the pulmonic valve, you know, you have to remember that these Myocardial extensions from below the valve occur and have been perhaps more described In the aortic root, but do occur in the RVOT as well, and this can be a useful strategy You just have to be careful obviously in the thin-walled RVOT in terms of bringing the catheter up into the PA and Flexing it down as you pull back As opposed to poking with the catheter When trying to make this maneuver any of these RVOT Interoceptal locations above or below the valve You have to remember are pretty darn close to the left main So you have, while we don't routinely shoot the coronaries Some people do and this is a paper from our group from a number of years ago showing the distances between RVOT sites and the coronary arteries and so you do have to be careful and at least consider the possibility of Damage, especially with extensive ablation in that region. Now, this is an issue for RVOT as well as in the coronary venous system Which is a little more obvious Another little take-home point for these cases is we use the word term septal a lot of times and the true septum is here But when you get out into the outflow tract when we say something is quote septal, there is no septum there This is a case from our center from a number of years ago where the catheter was quote pointing septal relative thought to be relatively safe, but Ended up in the pericardial space because there is no wall there and it's just the pericardium Newer Catheter designs and types are useful in a number of ways We mentioned contact force which certainly helps you understand whether you're having good contact Stereotaxis catheters sometimes are nice because when you're trying to get deep into the AIV for instance in this case A lot of times manual catheters are a challenge to get into a relatively small vessel Whereas these relatively floppy catheters Can safely be advanced without too much difficulty This is another case again talking about retroflex catheters Typically these outflow left ventricular outflow tract cases are addressed with a retrograde aortic approach But in some instances a transeptal approach is warranted. This is a case. We did not too long ago Where there was one PVC occurring at the left right junction Where we were about 40 milliseconds early and a more septal PVC number two That was closer to the kind of left bundle His region as you see on the proximal catheter here They require two separate ablations But we weren't able to get good contact and stability retrograde And so we ended up having to go transeptal to get better contact and Ouyang's group and others have talked about them the benefits in particular in the LV summit and region of the transeptal approach in some of these cases What's the definition of site of origin for PVC the next question Earliest site map, best pace map, site of termination, or whatever the tending of record says it is Ah Fellows are listening good. Oh, no, I thought we were going with the tending of record, but You know, I think the answer you're giving of the choices given is probably correct Activation generally is a better Indicator of site of origin, but it's not without its limitations And the reason I put this on here is it's it's really hard To know the true site of origin because all these things can help you triangulate the best site But we have to remember that preferential conduction and sort of dead-end Conducting tracks can can really alter the way activation maps look And this is just a pathologic specimen of the you know, showing the tricuspid valve and the coronary sinus The theoretical AV node and right bundle branch block You can get these kind of myocardial extensions and dead-end tracks that have been described And they've been described to facilitate ventricular arrhythmias they've been described to be involved in WPW and You know, you see these myocardial extensions above and above the pulmonic and aortic valve And through the leaflets and and what all that means and does from a clinical perspective is that a PVC originating from one site may exit in many different directions May preferentially conduct through fibers that make different sites look Relatively early on an activation map When in truth the actual site of origin is somewhere distant from that and so An example of that I believe is shown here. So this PVC was one we mapped a while back And we got you know, we went in and we said okay, this is a relatively, you know, it's a V2 to V3 Transition right relatively early it looked for all we thought to be potentially on the left side But as per our protocol we kind of start with RVOT mapping just to get a sense of Earliest site and we were really surprised to see this is kind of an REO view that that the earliest site Was in the right ventricular kind of posterior almost free wall And we were getting this kind of pre potential about 30 milliseconds before the QRS It didn't make any sense based on the 12 lead EKG And up to this point I had kind of told fellows, you know if you're if you're early on the free wall of RVOT, then then you don't really need to map the The LVOT because they're not next to each other or they don't not they don't you know We don't think of them as being next to each other And the pace map in this area wasn't great But the timing was weird, but we just were a little confused. And so we did a little what we decided to Map some more and we did a pace map on the more of the posterior septal region of RVOT And that started to get a little bit better in terms of the morphology Started to look a little nicer in terms of the pace map. So the pace map was better septally But the activation time was much better on the free wall posterior free wall so we decided to Map in the aortic route and it turned out that at the left right junction We were about 30 milliseconds early with this nice fractionated signal And what was happening was that the site of origin was probably here, but you had preferential conduction Through this posterior aspect of RVOT that was entering over here on the posterior posterior free wall of RVOT So if we had ablated here, it likely would have done nothing To the arrhythmia and here with one burn the tachycardia or the PBC went away So the other area again, that's probably a topic in itself and because of some of our delays I'll try to So go through these relatively quickly and they'll be online But the LV summit is an area that you know, especially a coronary care centers We're seeing all the time right something that before about 10 years ago when Yamada Described it in that from a clinical standpoint. We weren't really talking about these LV summit BTs and PBCs, but now they seem to be everywhere And it's a complex area of the thickest part of the myocardium it's Protected by coronary vasculature and epicardial fat and and often is very complex to ablate It's defined by the LAD and the circumflex and this triangle here And I like to when I'm talking about the LV summit sort of include intraceptal BTs one while they are not the same they're sort of an extension of the summit and Fall into the same category because of how complex they are to ablate because they're often deep in the myocardium and we have to often have creative Concepts that we utilize to target these arrhythmias. So this is a CT scan from Shunpei Mori Are one of our excellent Colleagues showing some of the venous branches that are often targeted the communicating vein the summit vein the supple branches with a RVOT removed here showing The kind of complex anatomy that can be targeted for these arrhythmias Epicardial ablation so percutaneous epicardial. This is a percutaneous epicardial sheath coming in here Is rarely useful in these cases This catheter is in the aorta because of the epicardial fat and the coronary arteries that we just show the picture of so You're really protected epicardially by these vasculature and unless you target within the vasculature itself it's rare that a percutaneous approach is beneficial both because of those coronaries and because of the epicardial fat that underlies it I Think some of our nomenclature Probably will change over time The AMC is a region described for idiopathic PVCs and VT But the AMC itself is really a fiber structure. So my cardio there's really no myocardial component to the AMC and so my personal opinion is that these PVCs are likely just in the kind of a Slightly more posterior extension of the LV summit and then what we're really seeing is LV summit PVCs through that fibrous tissue Often in this region again, you're going retrograde and coming underneath the left coronary cusp If you to target these endocardially or within the cusp itself Or within the venous system. So in this case you have a right bundle PVC with a relatively slurred initial component Inferior access relatively negative mostly negative and leave one because it's so interior And you can often map within the coronary venous system to target these rhythms so again coronary venous PVCs and VTs have been described as an independent entity and the summit PVCs and VTs have been described But this is a continuous area and a lot of times we're targeting so-called summit PVCs from the venous system or Or from endocardial locations because we can't target them from the coronary venous system due to risk profiles location next to coronary arteries, etc in this particular So again, I'm just going to skip through in this particular case Within the venous system we had this is before we had the more recent smaller three and two French catheters But you had a four French catheter deep in the CS and you kind of see this a little bit of a reversal of polarity here at the GCVA IV junction And that's often a good target But again when that doesn't work or it can't be done other techniques like ablating within the coronary cusps or in the endocardium Across from that region is often necessary. This was a paper by the Penn Group looking at the targeting these challenging cases from this left sinus above salva and showing that basically You could use a ratio of abl to avr, but in reality if you are a certain distance If you were within a certain distance from the anatomic so-called side of origin, which is here You could often get the ablation successfully done endocardially And Frank Bogan has a paper coming out and Jackie P that has a nice protocol for that in terms of targeting endocardial sites by anatomy as opposed to by timing and how and so Oftentimes it's trying to get to the closest anatomic site as opposed to the earliest activation site When you can't ablate at the site of origin I'm in this case endocardially coming under the valve Terminated the PVC that was previously in by Germany Final question and I'll try to keep things moving I feel comfortable with alternative techniques for PVC and VT ablation, wire mapping, bipolar ablation, alcohol ablation, coil embolization A yes, B no, C. This is just a bunch of people showing off and putting their stuff on Twitter Jason there was a question about settings in the outflow tracks How high are you comfortable going on the wattage and what type of catheter would you use? Yeah, I mean, I've mostly moved to using all irrigated catheters I mean, I think there was a time when we were using non-irrigated in the RVOT and then if we had to switch to the LVOT using an irrigated catheter, but I think because we're often in the LVOT and just to avoid having to switch over and to get a solid lesion We pretty much use exclusively irrigation In the RVOT, I tend to start just timidly start a little bit, you know lower around 30 watts and gently titrate up if I if I need to. In the LVOT endocardially, I basically just start at 50 watts like I would for structural heart disease case. In the coronary cusps sinus of valsalva, I tend to start a little bit lower and titrate up again Usually I can get away with, you know, a little less wattage in the sinuses because you have such good contact Whereas when you're endocardially and you're trying to make a little bit bigger lesion, you kind of need the 50 watt All right, here's the results Okay. So yeah, I think you know, I wanted to in this and this talk with some, you know more complex concepts and and rightly so Fellows shouldn't be real comfortable with these techniques I think like many things in EPE like epicardial ablation and things you get a certain amount of exposure as a fellow But you only develop some of these skills as you develop your career and hopefully have some senior mentorship in your practice Wire mapping and surgical ablation is something that we we enjoy doing and in septal substrates for non-ischemic cardiomyopathy certainly Finding these Special techniques for difficult to ablate Patients is sort of what led to a lot of these cases But you can in any even in endopathic cases you can put wires So this is a these are wires into two septal branches coronary branches Where you can put normal diagnostic or coronary wires with a balloon Covering most of the wire so that you're just the wires exposed and attach that to an alligator clip Or you can use a pre pre-made wire like the biotronic vision wire and put those in And you can record electrograms from within the septum itself as you see here and Even in structural VT again, this is a structural case, but two different structural cases, but you see these diastolic potentials In these two cases, these are from wires in the coronary vasculature The final case I'll leave you with so we don't keep you guys too long is a surgical case. So this is a patient that had PVC induced cardiomyopathy Failed multiple drugs, failed endocardial ablation, I believe on the East Coast somewhere, failed epicardial ablation With some tamponade afterwards and was sent to us To deal with To deal with It was not felt to be a candidate for percutaneous epi after the hemopericardium We took him to the lab to get one shot at endo before the consideration for surgical Which is really what he was sent for which again is a rare thing in our idiopathic, so-called idiopathic populations We do it all the time in structural heart disease patients, but for idiopathics, it's very rare This patient we mapped in the venous system, we mapped in the LV endo and You know, this is PVC that you see here. So somewhere in the summit region We have a nice Three friends down into the AIV here and we can get moderately early in a lot of different locations Which is kind of a sign that it's something deep intramyocardial We wire mapped all the septals into the LAD into the septal branches Everywhere we can get into we took a point and basically you see that kind of diffusely Minimally early or even a little bit late in some of these locations And so we actually took him to the lab Playing I'm hearing the volume, but I'm not actually So we actually Opened them up and this is the summit here and the LAD coming down this way and We put in a couple needles into the LV summit and attached alligator clips to get bipolar Signals from the LV summit here. We actually tried To do cryo ablation epicardially here, but were unsuccessful And in the only case that I can remember us doing this for we actually put the patient on pump You can see the surgeon has the cryo probe through their valve here Cryo-ing endocardially on pump to allow for a deeper lesion on pump And we were obviously all very nervous That he would have a response because God forbid he Were to go through all this and not have a response And you can see the lesion in the post ablation state in the LV summit here And he actually did great. He's about a year out LV function has improved and he's done very well So in conclusion, I think the value of pre-procedure imaging in certain clinical situation is becoming more clear More data is needed We're hoping to contribute to that in the upcoming future Comprehensive mapping and anatomic understanding is really the key to a successful ablation in this region But always consider in the back of your mind Things that can confuse you like preferential conduction The frequency of RVOT as the site of origin is likely somewhat overestimated in the literature And RVOT ablation is not without risk Ablating in the coronary venous system can have some limitations both due to risk, but also due to technologic limitations And if you're deep within the LV summit, it may require ablation for multiple sites so In any of these cases and I would say an EP in general Set a plan For your case, but be continuously reappraising your plan and planning Throughout the case to have the best outcomes. I want to again thank Nishant and Brad and the team for inviting me and I apologize for the technical difficulties I'm not sure what that's about or why these yellow things are on my screen, but Zoom

Dr. Jason Bradfield

outflow ventricular arrhythmias

premature ventricular contractions

ventricular tachycardia

comprehensive mapping

anatomy of outflow tracts

successful ablation procedure

right ventricular outflow tract

structural heart disease

complexity of anatomy and physiology