Thanks Nishant and thank Rod and Rishi, my colleagues, for sparing the evening to participate in this and certainly to all the fellows who have also joined in. So the subject that we're going to talk about, gastrointestinal papillary muscle ventricle arrhythmias. It is one of those subjects that has kind of become a little bit more interesting just because there are more and more cases that we are seeing of this particular arrhythmia. And so while a lot of the concepts that we use in cardiac electrophysiology with idiopathic ventricular arrhythmias apply to this particular group, there are certain unique features about the subset which we get into. So what I thought I would do is maybe start off by talking about some of these questions that I've put together to see what our background knowledge is of the group here and then we will build on that. So let's start with the first question. So what is the most common presentation of these arrhythmias? The choices are PVCs, non-sustained VT, sustained ventricular tachycardia, or polymorphic VT and VF. Okay. So, that's sort of a good answer. Most of you feel that premature ventricular complexes or isolated premises is the most common presentation, and that is correct. So then, the second question is, okay. So, the distinguishing ECG features of left ventricular capillaries, here are the choices. Right bundle branch block morphology, lack of precordial transition and left superior axis. Right bundle branch block morphology, lack of precordial transition and inferior axis. Right bundle branch block morphology, late precordial transition around V4 and the presence of an initial Q wave in V1. And then, the last choice is a left bundle branch block morphology with early precordial transition. Typically, anything that transits by about V2 is considered early. So, let's see what the group means. Okay, so again, some difference of opinion here, and obviously this is something that we talked about, so that's good to know. The third question is, during capture ablation of papillary muscle ventricular luteum, the target site, how do you identify that? So the choices are, at the earliest site, you should see a sharp opinion potential during sinus rhythm, which also is seen during the ventricular arrhythmia. Second choice is that the site of earliest activation doesn't need to be a protein gene potential, but it should precede the QRS complex for 20 to 40 milliseconds. The third option basically says that choices one and two are both correct, and then the fourth option is that really you should use face mapping and find an identical face match, and that should be the target site, and activation mapping is not as helpful. All right, so I think most of you got the correct answer, which means we have to find the site of earliest activation, to find a prokaryotic potential that's helpful but doesn't always have to be the case. All right, let's just go to the final question, which is when discussing management options for papillary, muscle, ventricle, and arrhythmias, which of the following is the most accurate statement? So the first one is that papillary, muscle, ventricle, and arrhythmias are benign and they don't require any treatment beyond reassurance. The second option reiterates the point that they are benign but allows physicians to use beta blockers or calcium channel blockers to treat patients. The third option advocates treatment for symptomatic patients or asymptomatic patients with a high arrhythmia burden, but the choice is a preference for antiarrhythmics or catheter ablation as the first option because catheter ablation is not very successful for these arrhythmias. And then the last option talks about treating highly symptomatic patients or patients with a high burden of arrhythmia and advocates for catheter ablation as the first choice because it's quite successful. It's a lot to read, so I'm trying to respond. Okay, very good. Okay, so that's an interesting, you know, response, and I think it's worthwhile clarifying the issue. So I think that's great. So let's now build on this. So let's get to the meat of the matter. So when we think about the capillary muscles, the way I imagine them, and I think that's really, you know, how these structures are, basically they are so-called complex pouching of the myocardial wall. And their primary purpose is to serve as supporting structures for the mitral and tricuspid valve. And so, because the mitral valve has two cusps and the tricuspid valve has three cusps, the left capillary muscle are typically grouped as anterolateral, posterior medial. The right ventricle of the capillary muscles, three of them, anterolateral, posterior medial, and septal. Now, the capillary muscle itself obviously has an interface of the muscle with the Purkinje fiber network within them. And many believe that the arrhythmogenic potential of these structures is as a result of this interplay of neural structures within the muscular bundles. So in terms of, you know, the mechanisms underlying cardiac arrhythmias as they relate to capillary muscle, and if you think about, you know, cardiac arrhythmias in just very generic terms, you can classify arrhythmogenesis into two broad categories. There are the abnormalities of impulse formation, and those can be either abnormal automaticity or trigger lactic tube. And then, of course, the second category of arrhythmogenesis is abnormalities of impulse conduction, which is another way to, you know, basically define reentry, how the impulse moves from point A to point B. So when you think about the capillary muscles and the Purkinje potentials and the Purkinje network within them, you can see how all of these mechanisms can potentially happen for arrhythmias that arise from these structures. So the fact that you have neural bundles existing between muscle fibers in relative isolation can cause resetting of the resting membrane potential, which would promote automaticity. The same reason could also lead to abnormalities of repolarization, which can then lead to trigger lactic tube. And certainly, if there is any disease process within the capillary muscles, which can cause delay in the conduction velocity, then that can actually also perpetuate reentry. So all of these mechanisms can be sustained by the capillary muscles. And so it's not a surprise that when you look at the manifestation of the arrhythmias, you can have premature ventricular complexes, isolated PVCs, which generally are the result of abnormalities of impulse conduction. Sometimes they can be isolated, sometimes you can have non-system. But then again, if the capillary muscles are incapable of slow conduction, there's an infarct, which is not an uncommon characteristic in inferior and posterior lactic infarcts of capillary muscles get involved. And that actually can lead to abnormalities of impulse conduction. And so you can have sustained monomorphic reentry. And then we are all familiar with the arrhythmogenic potential of these structures that can actually trigger PVC-generated VF in polymorphic PT. And those have been well described, even in patients who lack spondyloarthritis. And so as a result of this diversity of the arrhythmia presentation, the patient's symptoms can also then mark it. You can have a lot of patients who just show up and the first time it's an incidentally recognized manifestation of the arrhythmia, and they have a very high PVC burden, but they're totally unaware of it. But other times, patients may notice palpitations. Depending on whether these arrhythmias are sustained, sometimes they can cause presyncope. And then certainly, sudden cardiac death has been described, particularly in population of patients with myocardial collapse, where PVC is originating from the posterior medial capillary muscle have been at least involved as one of the possible mechanisms. And then of course, depending on the burden of the arrhythmia, even isolated PVC is very high and certainly perpetually coming out. So, the presentation of these arrhythmias can be diverse. So, let's try to talk about individual groups. And so broadly, if you think about papillars, muscle ventricular arrhythmias, you can have left ventricular capillary muscle ventricular arrhythmias, and then you can have the right ventricular capillary muscle ventricular arrhythmias. So, we'll start with healthy capillary muscle ventricular arrhythmias, because between the two groups, this is certainly the more common presentation. So, the ECG features, and we had a question on this. So, the capillary muscles are in the left ventricle. Anything that's coming from the left ventricle, unless it's extremely subtle, should generate positive forces in the brain. And so, as a rule, capillary muscle ventricular arrhythmias originating in the left ventricle should have a right ventricular transport morphology of positive forces. Now, remember, the capillary muscles are sort of mid-cavitory. You can have the extent of the capillary muscle that we wrote in the base, which is near the apical aspect of the ventricle, towards the tip, which is closer to the valves, but the entire structure still is somewhat mid-cavitory. And so, anything that comes from the mid-cavity of the LV tends to have some pre-caudal transition. The only time you lack pre-caudal transition is in the source of the LV muscle, basically on the mitral valve, which is not the case with capillary muscles. And so, almost always, you have some pre-caudal transition. Typically, depending on whether the source is exiting near the base of the capillary muscle, then the pre-caudal transition can be early, or if it is exiting closer to the tip of the capillary muscle near the chordate, then the pre-caudal transition can be later. But there should be pre-caudal transition. So, those are the two unifying features. And then, depending on whether it's the anterolateral or the posterior medial capillary muscle, there are a few features that are unique to those. So, with the anterolateral capillary muscles, because it's situated somewhat higher up in the lateral wall of the LV, the inferior leads tend to have predominantly positive forces, but there can be some discordance between leads two and three, where three may be more positive than two. And then, of course, because it's a posterior lateral structure, it tends to manifest negative forces in leads one and eight. Now, compare that to the posterior medial capillary muscle. There, the forces are predominantly superior. So, you will not find this discordance between the forces in leads two versus three, that is the posterior medial capillary muscle. Also, for the posterior medial capillary muscle, when it's doing arrhythmias, typically, AVL should be positive. So, something is coming from the bottom of the heart, it tends to travel somewhat equally to the right and the left shoulders. AVL and AVL tend to manifest positive. If AVL is negative, it's unlikely to become posterior medial capillary muscle. Now, people have obviously studied the unique features of ECG for these arrhythmias because it's important to differentiate them from other arrhythmias that can be coming from the LV, such as the fascicular ventricular tachycardia, so ventricular tachycardia is coming from scar within the LV, and certainly, tachyarrhythmias that originate from around the LV are still in micro-valve. And so, this is a paper that was just published by our group, and this is looking at about 100 plus patients with capillary muscle ventricular arrhythmias, and comparing them to a control population of patients who also presented with predominantly right and we're not talking about the VT, which is positive forces in V1, but not in the capillary muscles. And the control group was diverse, including patients with fascicular VT, VT from the osteo-outflow tract, infero-basal VT, and of course, the apex. So, one of the features that, and again, you know, when you read through the literature, there are different varieties here that people have used. The point of this paper really was, are there a limited number of leads that can allow you to make a quick diagnosis? But yes, with some certainty, that it's a capillary muscle arrhythmias. So, one of the features that stood out is the morphology of the QRS complexes in V1. And so, there are three types that were found with capillary muscle ventricular arrhythmias, and those are shown here. The first couple is where you actually see a clear R, small notch, and R-prime, where the R-prime is shorter than the initial one. And this is, you know, has been described as the gravity or some other ECG patterns, but this is one manifestation. The second manifestation is where you don't quite see this RS-R prime pattern, but you see some slurring on the downstroke of the QRS complex in V1. It's predominantly positive, of course. And then the third morphology is where both the peaks, R and R-prime, are about the same height. Now, compare that to the rest of the PVCs, which are shown in the slide here, where you'll see that none of them actually have any of these, whether it's an RS-R prime or the slurring. So, that was lacking in this group. So, amongst the 111 patients in the control group, only two of them had anything similar to this. But all the patients in the capillary muscle group had this particular manifestation. That stood out as being almost pathognomonic of this particular pattern. Another thing that we looked at was the time that it takes from the beginning of the QRS to reach the first peak. And this was typically much shorter for capillary muscle groups than the remaining control group population. And you could actually use a cutoff value of 74 milliseconds to reach the first peak of the intrinsical deflection in V1, as being the cutoff that you could use to separate the two. So, putting it all together, these are some of the different things that we looked at. And the ones that stood out was the time to intrinsical deflection, which, if it's less than 74 milliseconds, is highly predictive when it's coming from the capillary muscle. And another morphologic feature that was interesting was the presence of a small Q wave emission in V1, which was seen in 75% of the capillary muscle ventricular arrhythmias, which you could still see in about 25% of the non-capillary muscle ventricular arrhythmias. So it was not as defined. So, to summarize the ECG features, some folks have commented on the QRS duration, which for capillary muscle ventricular arrhythmias is typically longer than fascicular, but in our paper that I just shared with you, other than the fascicular VT, the rest of the LVVTs have a similar QRS duration as the capillary muscle ventricular arrhythmias. It's not very discriminating. Pre-cordial transition, we've talked about that. It's beyond V4. It is associated with this group, but it's again not diagnostic. Inferior lead discordance is helpful in distinguishing anterolateral and steromedial capillary muscles. The presence of a small Q in lead V1 is also seen in a lot of these. But again, the distinguishing features are the presence of this particular morphology that I showed you in lead V1, where it's either as an R-prime, which is smaller than the initial R or the same height as the initial R, or slurring on the downstroke. That had a sensitivity of 93% and specificity of 98%. Intrinsicoid deflection in lead V1 of less than 74 milliseconds, that also had a very good specificity. The sensitivity was not that great. But again, these two together can be helpful in discriminating capillary muscle ventricular arrhythmias and the rest of the body. Okay. So now moving on to what we can expect when we try to ablate. So a few things about the capillary muscle itself. Obviously, it's an intracavitary structure, so it juts out within the cavity of the left ventricle. Even though we think about capillary muscles as having a fairly well-defined anatomy with two heads for each of the capillary muscles, this is actually not always the case. The anatomy itself has a variable thickness and they are contractile structures that are fairly dynamic. And so they are hard to really balance your capture and map. And then of course, depending on how dense the network of the Purkinje network is and how diseased it is, you can have changing exits of the arrhythmia through this dense network. And of course, the mechanism of the arrhythmias can be variable. So there are a lot of potential challenges when you try to go after arrhythmias originating from the capillary muscles. And consistent with that, our evolution of the techniques has been sort of a work in progress. And so very early on, when we first started recognizing these arrhythmias, we sort of stumbled on it. So what I'm showing you here is a patient that I ablated in 2006, I believe. And if you look at the morphology based on what we just discussed, yes, it looks like it's coming from the anterolateral capillary muscles. But in those days, we weren't even aware that this structure was capable of arrhythmogenesis. We just expected this particular arrhythmia to be coming from some location in the mid-posterior LV, just based on the QRS morphology. And you can see the quality of the X-rays that were available to us were really not things that we have now. And with limited mapping points on the electron-atomic map, it looked like there was something coming from the mid-lateral LV. And sometimes you get lucky, and in this particular case, we found that this really, really early potential sharp receding QRS by about 40 milliseconds. We were successful here. But then again, as you go through some of these cases, it dawned on us, for example, this is another case where we have localized the source of this particular CVC, which again looks like it's from the anterolateral capillary muscle with the knowledge we have now. But at that point in time, we thought this was in the mid-lateral LV. But the interesting thing about this particular location was that when we had our catheter in that position, we just could never get the tip of the catheter out to the silhouette of the heart on an LV projection, which is what made us think that there is this structure that's prohibiting us from getting to the wall itself. And yes, we all know about the capillary muscle number, sort of stumbled upon the arrhythmia source. Then we kind of get innovative in mapping. So this is an example of how we first started mapping these structures, where using point-by-point mapping, we first create the LV shell. And then within the LV shell, we do point-by-point mapping using basically pneuro to sample different parts of the capillary muscle to create a structure within the cavity of the LV. And then doing that, now you can see you have a little bit more structure to the capillary muscle and now identify an area of early activation. We can see how challenging this whole exercise is if you use X-ray to guide yourself to creating an intraparticle structure. And you know, a lot of flow exposure, these procedures took a lot of time. And in that period, which is either the pre-ICE era or early-ICE era, the success rate that most of us had in tackling these arrhythmias was really not that great. So this was a paper from a group in Alabama, Dr. Yamada and colleagues. They did some of the early work in this particular area. And they defined in a small series of 19 patients, half of them from the posterior medial capillary muscle, half of them from the anterolateral capillary muscle, kind of talking about some of the observations. Sometimes you find an early potential, sometimes you don't. Sometimes you find a good baseline, but other times you don't. But the bottom line is that single-procedure efficacy in these small series for catheter ablation was about 40%. And that was, you know, shared experience. So this is the early success rate of capillary muscle ventricular arrhythmia ablation of 10. And you can see that from 2007 to 2010, these are really not good outcomes. But then in 2011, you see here, as I show in the slide, there is doubling of our success rate. Well, what was the reason for that? Turns out that somewhere around that era, we started using PI's a lot more consistently for all our ablations. And in doing that, we were able to really appreciate sort of the intra-cardiac anatomy and the disposition of the capillary muscles. And then so, you know, define some of the structural characteristics, which then allowed us to be a little bit more accurate in positioning our catheters and sampling the structure. And with that, we were able to define a little bit better the site of origin of the area. So this is just an example of what PI's can do for you. So here are two cases of an arrhythmia that was targeted from the anterobacterial muscle. And you'll appreciate that in the first example, the catheter, you can see it coming through and going under the anterolateral capillary muscle and it's extending into the depth of the capillary muscle, much near the base of the structure. In the second example, again, it's an anterolateral capillary muscle with two heads, but this time you can appreciate how this catheter is resting on the body of the capillary muscle. Just on the top of the superior. So this is what PI's was able to allow us to really refine our mapping techniques relative to the complex structure. The other thing that we were also able to do with subsequent iterations of PI's technology is the ability to actually use PI's to segment the catheter for a variety of arrhythmias this has now become sort of a standard approach. Didn't used to be that, but for the capillary muscles you can see how PI's segmented mapping can really allow you to identify unique features. So here is sort of a classic textbook representation of the anterolateral and posterior medial capillary muscles and both of them have two heads, which you can identify, you can define the apex of the capillary muscle, the tip of the capillary muscle, body of the capillary muscle. And doing that with PI's segmented mapping allowed you to do this actually very quickly. Now think about trying to do this using Loro and doing point by point mapping to characterize the structure versus ice and it really takes you one tenth of the time to do it and you have a much better representation. And then finally, the advent of contact or sensing technology then allowed us to really gauge just how well or poorly we were doing in achieving contact of our catheter structure. So here are two examples. First one you can see is where a catheter is resting on the body of the path, the vector is certainly not doing much and you can see the contact portion is about three to four. So when you're born here, you know that the region that you're creating is really not that great. Here's a second example where you can see the catheter is stuck under the papillomus and the vector is pointing upwards and the kind of force that you're generating here is so much better. And you know that for this particular region, if you are on the spot where the site of origin is, it's more likely to be successful. So those are some of the technological innovations that have really allowed us to do a better job and that reflects in outcome. So this is now the cumulative experience of Penn all the way to 2017. You can see the early experience where our success rates were not that great and then the advent of ice mapping to define our population technique and you can see there's doubling of the success rate. And then around 2015, we started incorporating some of the other tools that I shared with you, including ice segmented mapping together with contact force mapping and you can see now the success rate. So there's a similar procedure, drug-free survival after evasion. We're getting into the kind of numbers that allow us to advocate for catheter evasion as being the first choice. So we are seeing this now, but it's been a long and arduous process to get to where we are. And this is not our experience alone. So this is a small series that comes from a group in Argentina, about 50 some patients, and they looked at the success rate for papillomavirus and ventricular arrhythmias in three different scenarios. So one group of patients was treated using contact force sensing and ice segmented 3D anatomic mapping, kind of what I showed you previously. There's another group of patients where they actually used cryovlation after contact force mapping was not able to get you. And then the third group is where they did everything that they did in the group in red, but instead of contact force sensing, they had non-contact force sensing. So you can see that there is a significant difference in the success of the procedure where the non-contact force sensing group, these are half as successful. And this is somewhat similar to our experience, but those are the kind of success rates that we are looking at. So this is our most recent outcome analysis all the way to December of 2019. This is 137 patients. About 70% of whom were done using contact force sensing. And for these patients, our overall success rate, both in terms of acute procedural success, somewhat 95% and clinical success was upwards of 85, almost 90%. So that is sort of our experience using all the tools that I just shared with you in terms of what we were able to accomplish. Now, interestingly, for our series of 137 patients, where about 70% of them were done using contact force sensing but 30% were not, we did not find the difference in overall outcomes whether we were using contact force sensing. And that we attribute primarily to using ICE technology for mapping these areas. So I think ICE overcomes some of the limitations that non-contact force sensing has. You can really visualize the gap to tip and you don't always need contact force sensing to tell you whether you're in good contact or not. Okay, so this is sort of where we are and how we got to this point. So during the procedure itself, what are some of the observations? And so, when you're trying to go after these areas, generally activation mapping is the preferred tool. And using electro-atomic mapping together with ICE guidance, you really now have the ability to sample different aspects of the papillomavirus. And so here are three examples. The first case, what I'm trying to show you here is a phenomenon that you don't always see, but when you see it, it's helpful. So here is sinus rhythm QRS complex and then here is the clinical rhythm. So during the sinus rhythm QRS complex, you see this late potential, which reverses itself during the actual PVC. Here, it precedes the QRS complex for 30 milliseconds. Now the second example, here during sinus rhythm, we have an electrogram, but there's nothing really interesting about it. And the PVC, prior to that, the same site has something which precedes the QRS, for about 25 milliseconds. And this was a successful ablation site, but there's nothing very unique about this. And it's just good. And then the third scenario is an older patient where at the site where ablation was successful, you see this highly fractionated, long, somewhat small electrogram preceding this far larger electrogram. And this precedes the QRS complex for 15 milliseconds. And so again, there isn't an absolute criteria that you can say, well, if I have this, I'm successful. You just have to map and find the earliest location. Sometimes you will find a sharp electrogram and late potentials during sinus rhythm. Other times you will find a highly fractionated electrogram and sometimes it may just be a regular electrogram. It's just the earliest. Now, face mapping can be helpful, but it's really not your primary tool. So here are two examples. And the first is the papillary muscle. It's a posterior medial papillary muscle, the catheter system right on the body of this man. That was the site of the earliest ablation. And the face map there, so this proprietary algorithm that Toccato has where they can actually do a match and give you a percentage of how close the match is to the native QRS is about 94% of this. Here's another example also of a posterior medial pap PVC where the catheter is nicely tucked onto this pap. There's a nice contact force here of 19 or so. And the basal match here is close to 99%. So this is a great match. This is a good match. But the bottom line is that we don't always get such good matches. And part of the reason is mechanism of these arrhythmias. Sometimes the Purkinje source is deep in the papillary muscle and the exit site for your catheter is you're capturing adjacent part of the papillary muscle and so the QRS complex is not really that great. So for a variety of reasons, pace mapping is really not a go-to tool. We all use it. So for the series that I showed you of 137 patients, in about 85% of them we did do pace mapping at the site of the reaction and the match was about 95%. But if the match is off and the site is still the earliest, then you wouldn't be able to do it. I guess that's the point I'm trying to make. The pace mapping is not consistent. Now, once you get to the earliest site and you're sure about that being the earliest location, then typically during power application, you can see a couple of things. In some cases, like for example, in panel A, you see the clinical PVC, you come on ablation at the earliest site and almost immediately there is abolition of the clinical. That's great. That happens. Our approach is to continue applying power there for 60 to 90 seconds and then give a few more lesions in that spot, which is oftentimes necessary to get an effective lesion. Now here's another scenario where when you come on ablation at the site of the earliest activation, you see a flurry of rapid monomorphic VT, which is very similar to the clinical VT. In fact, that's something that I tell my lab staff all the time, that as I'm coming on, I want somebody to be near the T-tube later, because this is not an uncommon observation. Sometimes there is the pro-arrhythmic effect of energy application, and you can see some patients who presented previously mediated ventricular fibrillation polymorphic VT, sometimes during energy application, which actually go into VF. So that's what we have to be cognizant of. But if you see something like this, this is a great sign too, just as good a sign as this one. So either of these scenarios, if you find this, either of these scenarios are approaches to continue with the power of polymerase 6297, and sometimes give additional lesions in and around that spot. Now, there are other observations that you can have, and so here's an example of PBC. So you can see here that this PBC has a superior axis, positive forces, in the AVL, bipolar block morphology, transition by molecule 4. So this is consistent with the posterior medial cytoplasm, and we mapped it there, and when we come on, we can see that this PBC goes away. But then just a few seconds into the lesion, you find this other PBC starting to break through, and this has got a totally different axis. It is inferiorly interactive, and AVL is negative. So you've transitioned during ovulation of the posterior medial papillary muscle to an anterior papillary muscle. And so in the series of 137 patients put together, which is currently under review, about 20% of the times the ventricular arrhythmias can have more than one morphology. Now another scenario that you can sometimes encounter is what I'm going to show you here. So this is the clinical arrhythmia, superiorly interactive, 2, 3, and AVL are negative, AVL is positive, transition is by V3, V1 is by V3. This is consistent with the posterior medial source, and in this particular case, using I-segmented anatomy to define the posterior medial pap, we identified a site of origin which was highly fractionated, catheter stuck under the papillary muscle, the rectum was looking up, and this is 50 milliseconds for each one of us. That's really great. So after we ablate there, that PVC changes, and it transitions into this PVC. As you can see now, there are several differences. 2, 3, and AVL are much more negative. They lack that initial arc. V1 looks very different than V3. So for this PVC, we continued mapping in the posterior medial pap because the other features suggest that it's still in the vicinity of the structure. And it turns out that this particular site was almost 90 millimeters away from the previous site, so it's more lateral and actually on top of the papillary muscle. And again, you can see this location is 45 milliseconds per QRS. So in this particular instance, we kind of went from this site where we ablated first and then we ablated in the opposite location on the lateral wall, and then we gave a few reinforcements in between, which you could argue that the source of this particular arrhythmia may have been somewhere in the center. And the first lesion clipped on this exit. It started exiting on the other side. And the reason why we did something in between is to really get a source because if we did not do that, there's a good possibility that it may find an exit elsewhere. It didn't happen during the case, but that's kind of what you have to imagine in terms of where the likely location of the source is if you're confronting this. Now, we're trying to understand how the papillary muscle and the anterior medial sources behave. And this is not an exact science. I mean, you're using the successful ablation site as the presumptive location of the source. And that is obviously erroneous in itself, that particular line of thinking, but that's the best that we can do. And so the way we tried to look at our own experience is to divide the papillary muscle into three segments. So the base of the papillary muscle is close to the LV apex. The tip of the papillary muscle is kind of where the cordy attached. Some people call it the head of the papillary muscle. And of course, the remaining segment is the body of the papillary muscle. So we looked at all the patients that we had ablated to characterize the distribution of the regions. And so in kind of putting it all together, there were some things that we summarized here, which is, as I told you earlier, for our series, we used contact force sensing about 70% of the times. And when we did use it, the typical force that we were able to achieve is about 10 to 11 grams. And again, that's not surprising, right? I mean, these are dynamic intracavitory structures. You apply too much force to the catheter, it's going to slide off. So if you get 10 to 11 grams, you'd be really happy. And typically to get success on an average, we have to give about 14 lesions, but about 20% of the times we could get by with five lesions or less, and about 20% of the time we had to get 20 plus lesions. And in terms of the distribution of the lesions, about a third of the lesions, or maybe even more, about 40% of the lesions were either near the tip or near the base. And only about 10 to 15% of the times did we have to ablate exclusively in the body of the catheter. So again, you can't really make much from your ablation point in terms of imagining that the source is necessarily there. But if we go with these observations that you had to either ablate the base or the tip, what you could probably hypothesize is that if you ablate near the base, then you're ablating the source. And if you ablate near the tip, then you're probably ablating the exit sites. Now that theory would bear out if you said, well, if you ablate near the base, you get by with a lot fewer lesions than if you ablate near the tip. But we weren't really able to sort that out because it was a retrospective analysis. We didn't have the granularity to be able to really sort it out. Because oftentimes, you get success, and you get a little bit more there. And so you get a cluster of lesions regardless if you ablate near the base or near the tip. But that's kind of what we found in that distribution. Now interestingly, in only a minority of cases, 15% of the times, did you have to ablate the entire extent of the pancreas. And that's a good thing. And of course, in our experience too, in about 12% of the cases, after RF ablation was not successful, we used adjuvant cryo ablation. We were successful in all those 15 patients where we did use cryo ablation. So I think that points not to the fact that cryo energy is more effective, but I think cryo ablation allows you to get stability. Because once you freeze beyond a certain temperature, the catheter sticks. And I think that may have been the reason why adjuvant cryo ablation was successful. This is that paper which describes our cryo ablation experience together with my colleague Rex Supper. 16 patients. It was a mix of anterolateral and posterior medial papillary muscle as well as right ventricular papillary muscle cases. But four of these patients actually had the PVC triggered VF. And all these patients' cryo ablation was able to get us lasting success after RF ablation. Okay. So that's sort of the narrative on LV papillary muscle ventricular arrhythmias. The RV papillary muscle ventricular arrhythmias, you really can use all the techniques that you use for LV papillary muscle ventricular arrhythmias to target the RV ones as well. The only thing you have to be cognizant of is that the RV papillary muscle ventricular arrhythmias are not confined to just the papillary muscles, but a large number of these cases actually tend to originate in the moderated band, which most of you know is the structure that connects the septal aspect of the ventricle to the anterolateral papillary muscle. And while it is an organ that provides some structural stability, it also permits the passage of prokaryotic fibers through. And so it's a source of ventricular arrhythmias. And again, the anatomy of the structure, you can use ice imaging and ice segmented anatomy to really bring out the different features. Oftentimes, the junction of the two structures can be the source of arrhythmias. Other times, you actually have to map each of these structures individually. And that's where ice guided mapping is just incredibly helpful. I don't know how people can do it without ice once you get used to it. And the features of ventricular arrhythmias originating from the right ventricular papillary muscle, particularly the moderated band, again, a series of patients put together by a group. So some of the common features, again, because it's coming from the right ventricle, the tachycardia tend to come from the left ventricle morphology, are predominantly negative. Because the moderated band connects with the muscle more closer to the pre-valve of the ventricle, the precordial transition for these arrhythmias, they tend to be late, beyond the V4. Again, because the structure connects closer to the inferior aspect of the ventricle, they tend to have predominant superior ventricle forces. And then there's positive complexes in the V1 and AV1. And of course, because it's coming close to the pre-valve, the QRS duration tends to be typically more than 180 milliseconds. So the unifying theme is left ventricular branch block, superior axis, and late precordial transition. And again, the point that I want to make is that the same tools and techniques that you use for mapping and ablating left ventricular capillary muscle and ventricular arrhythmias, the same principles apply here. And I use an electron-atomic guided catheter manipulation to identify the earliest site and using those approaches to really target the arrhythmia, in our experience, is quite efficacious. Okay. So in terms of some of the challenges, we talked about what the problem is with these structures, their anatomy, their dynamicity, variability, and the mechanisms underlying these changes. So it's not uncommon that oftentimes you have to map a lot and ablate extensively. In doing so, you have to be cognizant of where your catheter is. If you're sitting on the papillary muscle and your contact is not great, you can give pretty high power. It's not uncommon that when we know our contact on the papillary muscle is not great, we start with 50 watts of power with a coolant catheter. Now, that is a lot of power, but if you don't have great contact and the catheter literally is touching the papillary muscle and the contact force is four to five grams, that's okay. But if you are tucked into the papillary muscle and the catheter is at the base of the papillary muscle, you start off with power of 50 watts or something like that, and the coolant catheter, you're going to create such a good lesion, and that's not a good thing to do when you're tucked into the papillary muscle and close to the ventricular wall. So some of the potential complications that you can anticipate in mapping around these ruptures, catheter entrapment, the cordy, and if you are not aware of that, you don't pay attention to these things, move the catheter. If abandoned, you can cause cordy rupture. That obviously can be an emergency situation if you start free-form micro-regurgitation. Even if you don't cause foreign rupture, but you damage the papillary muscle, so I've seen papers from the early experiences where operators were talking about doing the equivalent of ablation-related isolation of the papillary muscle. So you go around the base of the papillary muscle and you isolate it. First, I don't think it's possible to isolate the papillary muscle electrically, unless there is underlying scar or something like that, because to cause through and through burns in the ventricular myocardium around the papillary muscles, I just don't think that's feasible. But in trying to do that, you can certainly damage the papillary muscle, and that can cause problems with valve function. Certainly, myocardial perforation is a complication that can happen if you're not cognizant of where your catheter is and your power delivery. And then, of course, with any left ventricular or left-sided ablation, there's always the risk of thromboembolic complications, and certainly vascular access complications. But in our own experience, the incidence of complications is generally low. In our entire series of 127 patients, we had only five complications, which were basically two pericardial infusions that were treated with just pericardiocentesis, one case of pseudoaneurysm, and a groin hemorrhage. So it's uncommon if you're careful with your mapping and power delivery. Okay. So to summarize, papillary muscle ventricular arrhythmias, they are not an uncommon source. I mean, they're not the most common source. Our own incidence of all the arrhythmias from the ventricle that we ablate, papillary muscle ventricular arrhythmias, about 8%. They can have a diverse presentation, ranging all the way from isolated PVC, which you see 70% of the times, to polymorphic VT or VF triggered by them, which is less than 10% of the times. Because of their location, they manifest unique PCT features. We talked about that. Their management, of course, is based on clinical presentation. You certainly have the luxury to do a few things if the patient is presenting with isolated PCs, even if the burden is high, but they are asymptomatic, and the patient is preserved. You have the luxury to try different things. But the bottom line is that beta blockers, calcium channel blockers, are generally not effective for these arrhythmias. Antiarrhythmic drugs, also in our experience, really don't do much, maybe 40% success in reducing the burden, but again, not very effective. Precision therapy, in the present era, using all the tools that we've talked about, certainly for us, has been the go-to tool. We use it as a primary management option for treating these patients. I think with that, perhaps, Nishant, we can revisit the questions one more time? Yeah, sure. Maybe when we do that, I can ask you some of the questions that have come through on the chat function. Or we can defer those questions. Sure. I guess you guys serve as a kind of a quaternary referral for ventricular arrhythmias. In your opinion, what is the most common reason for failure when you guys are getting a redo case? Yeah, that's a great question. I mean, I think for us, looking back at why we were not successful early on, even after we started using ICE, I think it has to do with just the recognition that the source of the arrhythmia really has to be mapped very carefully. In doing that, you have to truly define the anatomy of the pathogen as best as possible using cartosan to create the structure. And then kind of really convincing yourself that you truly map the different aspects of that structure before you come on out. Because you want to identify the early site. And then once you do that, recognizing that depending on how old the contact is, if you are barely touching that structure, and sometimes I've had to admit literally resting my catheter on the cordy and the tip of the gland. And in that approach, if I start off with the traditional power settings of 15 to 20 watts and slowly increase the power, and the catheter is bound to get dislodged as the bubble starts coming out, that to me I think is the most important thing, is to really assess the source in terms of the earliest activation and then recognizing how your catheter is oriented relative to that source and then dialing in the power using those metrics. And then, you know, our comfort with power delivery I think has really also advanced our success rates. Because once you recognize that your catheter is in good contact, you can dial the power accordingly. If your catheter is not in great contact, you start off with high power setting. You stay for a little bit longer. Those, I think, are the reasons why you can be successful or not. Okay. And actually, that leads into a bunch of people have asked, you know, what your normal power settings are. How aggressive will you be? We hear about 50 watts, half normal saline, never-ending lesions. Yes. You know, how aggressive will you be if something's really deep? Right. That's a great question. So, just for the record, we don't use half normal saline for our operations. Actually, there's a paper from our group that's just come out in the most recent JAK-EP, which talks to, you know, what half normal saline, at least in the animal hospital, does. So, I urge the audience to read that. It's just come out. So, we don't use half normal saline for our operations. In terms of power delivery, so, like I said, if your catheter is in good contact, and I say good contact, 10 to 11 grams is plenty for these areas. If you're starting at 10 to 11 grams, you can start at about 20 watts with an irrigated catheter. And you're looking for about a 15-ohm drop. And if you can actually monitor the lesion with eyes, that adds another dimension to your ability to tell when the lesion is, you know, being created, because you can really watch that area become epigenic. And sometimes that preempts the bubble formation. You start seeing a lot of bubbles, and that's the beginning of what could become like a steam bomb, if you're not attentive. So, if your contact is about 10 grams plus, and your catheter is either tucked under the papillary muscle or resting between the heads of the papillary muscle, or the contact is showing you a good vector on top of the papillary muscle, the catheter is pushing it down well, you can start at 20 watts, dial up every 10 or so seconds to get about a 15-ohm drop. And typically, a lesion of 60 to 90 seconds should do the job. If you are very inside the papillary muscle, I think 15 to 20 watts is a good place to start, and you will see that lesion form. And again, 10 to 15-ohm drops is plenty, 60 seconds is plenty. When your catheter is resting on your hand, and you really have very poor contact, you can literally see your catheter bouncing back and forth, and if you have contact force sensing, you get 4 to 5 grams, you're lucky. In that setting, when you're really not ablating into the muscle, but you're literally ablating on top of the muscle, we start at 40 to 50 watts. Because you're very close to the exit site, the exit site seems to be very superficial, all you need is maybe even 10 seconds, just like you're abolishing atrial tachycardia, you don't need a lot, you just need that short duration of good energy. I think that's kind of how we decide where to set the problem. And then, do you have any recommendations for increased stability, either using, also considering transeptal, or using a long sheath across the aortic valve? Yeah, so, you know, each of us has a preference, and I can tell you that 60% of our cases were done using the retrograde approach, 40% were done using the transeptal approach, and about 20% of the times we used both. My sense is that, you know, whatever is your comfort level. So for us, retrograde access is the preferred approach, and that's what we go with, generally. The transeptal approach can be helpful for the posterior medial papillary muscle, because coming through that valve, and with the long sheath, a deflectible sheath, you can really get your catheter onto the pap. But if you do that, you have to be very, very careful, because number one, if you're not watching the catheter dip on ice, the chances of the catheter slipping on the papillary muscle and getting into that inferior wall. So I've had one case of cardiac perforation with even just 20 watts of power for like 45 seconds, just because the catheter was so, almost like a harpoon, it was like so deep in that muscle, and if the muscle is healthy, you can really create a big lesion very quickly. So that's what you have to be careful with. But with posterior medial pap, the transeptal will be better. I have never had to use a long sheath retrograde to get across the aortic valve. Most of my partners have not had to do that either. The only time you may need to do that is if somebody's got like a really big aortic root, and you know, you're struggling with that, but I think it's mostly if you're oblating near the base of the left ventricle near the valve, and that's helpful. For the papillary muscles, I don't think so. And then, do you have any tricks, as sometimes it can be painful, and you try to avoid general anesthesia in these cases? So, any tricks to try and suppress the pain while you're ablating? Yeah, that's a good question. So I've got to tell you, I mean, these, you know, unlike your outflow tract ventricular arrhythmias, papillary muscle ventricular arrhythmias tend to be a lot more stubborn. So, I have actually done some of these cases under general anesthesia. I mean, you can always do the trial early on. You know, we tend to put a Foley catheter in most of our patients just because, you know, these cases can be long. You know, they're not like the ventricular outflow tract tachycardias. These can be more challenging. So, almost all our patients get done with Foley catheter, and when they're getting the Foley catheter, we try to give them propofol and give them sedation. So, that could be a test. If you're giving propofol and you're still having the PUCs, then you can keep this patient really deep. It's not going to impact you. Now, here's another interesting thing. I don't have data to necessarily prove what I'm going to say here, but it's just an observation. So, one of the things that I do at the end of papillary muscle ventricular arrhythmias, in fact, all of them, is we give isoproteranol. We're sure to kind of see the response. But it's not uncommon that sometimes these papillary muscle ventricular arrhythmias will come back at the washout phase of isoproteranol. So, you get up to, you know, 20 mics of isoproteranol, and you don't see anything. You're great. You're washing it off. And by that time, you say, okay, no papillary muscle ventricular arrhythmias, catheter's out. And as the isoproteranol is getting washed off, I've had cases where they've come back and yet still go back. Sometimes the sheets are almost gone. So, that's the one thing I would caution people to do is go through that whole phase of isoproteranol challenge to be sure that you've gotten it. And you wait a, what, full 30 minutes? 30 minutes or sometimes even an hour. Like, what I'll tell them is, you know, so the fellows, if they start taking sheets out, so I just leave the stuff in the right point until the patient is absolutely ready to get up. Okay. And then there are a couple questions here about mapping, I guess. So, in a foci where pacemap and activation are discordant, which one do you prefer? And if you're unsuccessful at your preferred one, do you empirically ablate at the other one? Well, so I guess the point I was trying to make in the approach is that activation mapping takes precedence over pacemapping. So, that's what we are looking for. Whenever we are sampling the papillary muscle to identify the site based on activation mapping. The only time we use pacemapping is when there's a paucity of the tachycardia. So, then you have only one PVC or two PVCs that you've been able to save on your review screen. So, you've pacemapped to perfection. But if the PVCs are happening enough that you can do activation mapping, then that's what we use. And if the activation mapping shows us the earliest point and the pacemap there is not good, that would still be our site. And then if there's divergence between the pacemap and the activation map, we continue to sample. But again, to be honest with you, I can't tell you if I've ever done or found a case where the pacemap was great at a location which was very far from where the activation map was. I don't see why that should happen unless you specifically capture just the fiber and the 3.5 millimeter thick catheter to capture just the fiber and get a great pacemap remote from the site of the activation, earliest activation. It just seems like it shouldn't happen. And then a tough scenario, PVC triggered VF cases where you don't have PVCs. What do you guys do in that situation? Great question. Great question. So there we kind of do a little bit of everything, which is we obviously try to put our catheter at the PVC site that we think it's coming from and then try to base from there to see if that triggers something. Sometimes we do program stimulation. Sometimes we give low energy from our catheter at that spot to see if RF energy can trigger PVC. But I got to tell you, I mean, our success rates for PVC mediated VF and polymorphic VT where we don't have objective evidence of that actually happening during the procedure, our outcomes are not that good. And do you guys consider autonomic modulation in those cases? Not as the first, second, or third option. Maybe after we've sort of failed many, many times might we do that. But no, not as the next option after the first failure.

Papillary muscle ventricular arrhythmias

symptoms

premature ventricular complexes

non-sustained ventricular tachycardia

ECG features

left ventricular capillary muscle ventricular arrhythmias

capture ablation

target site

management options

Catheter ablation