Thank You Nishant. Really just want to reiterate statements that have already been said but this has been just a really fabulous program for fellows especially in a time when social distancing has been so imperative. I'll start by I think introducing a case to talk about this topic because I think that's often the most illustrative. Okay disclosures and the case. So this is a 58 year old man with a history of coronary disease and associated cardiomyopathy that began when he had an anterior MI back in the 1990s. He eventually underwent CABG but with despite that as well as medical therapy his EF remained at 35% or less and he had this large apical aneurysm which made the likelihood of reversal less likely. He finally underwent single chamber ICD implantation for primary prevention purposes in 2002 and look at this time span here of more than a decade before then he presented with what was presumed to be BT. ICD shocks approximately 20 years after his initial anterior MI and that's a fairly maybe a little bit more prolonged time course but the usual kind of initial presentation of BT after an ischemic insult is around that range of you know a decade or more or so. It's not usually the first few years after an infarction unless there's some residual ischemia. Always exceptions but that's a kind of a rule to keep in mind. This patient despite continued treatment with amiodarone escalated treatment with amiodarone and lidocaine continued to have ICD therapies and then was transferred to our institution for further management. And so one thing that I always talk to my fellows about is you never just take what you're given in terms of information at face value. You actually have to confirm the information yourself. So there's always the chance that perhaps an assumption was made and it was wrong. So in this case this was the patient's telemetry as he was hooked up upon arrival to our facility. The telemetry labels it as VTAC but is it that? So this is the onset of the wide complex tachycardia. Fairly typical events representative of what he had been having that was treated. So the first poll question is what should be considered next for management? A is SVT ablation, B is reprogrammed the ICD, C admexilatine, D coronary angiography or revascularization, or E VT ablation. So those are the questions. Give a few minutes or sorry a few seconds for people to answer. Okay, I know it's early, but I'm up pretty early, so let's get some more responses in here. I usually end up giving them about a minute. Okay. That's about how long it usually takes to get. That's it. When it's anonymous, it's harder to, you know, pressure people on the answering. Okay. Okay. Great. We're going to walk through each of these answers and maybe explain why some might be more correct than others. Okay, so SVT ablation. None of you picked this option, which is good. So, if you look back at the tracing, you know, initially you might say, oh, it's white complex tachycardia. He's had an infarction. This is obviously VT. You don't know that for sure, except that what do you see here? This is a fusion beat, right? And then, if you look a little bit more closely, you can actually see P waves marching through and, you know, more evident VA dissociation. This one, of course, being the clincher, where you have a fusion beat between VT that's going through and a sinus beat that actually captures and conducts and a fusion of both sinus and VT. So, it's not SVT with aberrancy. How about reprogramming the ICD? It's not an unreasonable consideration, except that if you look at the baseline programming, which is already set fairly aggressively, meaning set to a high detection rate and treatment, which he has already failed multiple times, it's unlikely that alterating this much more, meaning withholding therapy even more, is going to dramatically improve the treatment course or prognosis. How about adding maxillitine? So, not a whole lot of data about this. Anecdotally, we do it all the time. You know, they've already failed amiodarone. Why don't we add another medication to at least buy a little bit more time? So, the existing data about this, as mentioned, is limited, but the best is from this study, the BANISH trial. So, ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. This was a study of a randomized trial of patients with post-infarction VT. What Dr. Sapp, the PI for this trial, has described as low-hanging fruit. So, these are the people that we see all the time in clinical practice. They have failed medical therapy, and the question is, do we finally offer ablation to them, or do we just further escalate the therapy medically? And so, many of these patients in this population either were treated with amiodarone at baseline or only Sotalol at baseline, and in each of those cases, amiodarone therapy was escalated if they were not on amio or if they were on amio at a low dose. In those patients in whom amiodarone was already at maximal dosing, maxillitine was added to those patients that were randomized to escalated therapy. And you can see that, regardless, this is like the overall outcome for the group as a whole, ablation versus escalated therapy, and in particular, those patients that already were using amiodarone at baseline comparatively did better with ablation compared to escalated therapy. When you look at just the patients that had max dose amiodarone and maxillitine added, which as you look at the number at risk is not a lot of patients, you can still see, though, that the performance of additional maxillitine on top of max dose amiodarone is pretty bad compared to just taking these patients to ablation. You do buy additional time maybe, you know, to kind of schedule more electively or what have you, but it really doesn't extend out to a year by much. Coronary angiography and revascularization is an option that many of you chose, which is not unreasonable. So this is not this patient, but this is someone that I got referred recently for VT ablation, whom the referring had told me had many, many monomorphic episodes of VT based on the ICD electrograms. This is, again, an example of where you must look at the primary data yourself. So this is the baseline printout of what the native conducted rhythm looks like. So that gives you a template to compare. This is the local bipolar electrogram. This is the far-field electrogram, typically the coil-to-can, which is a better approximation of a 12-lead, you know, surface ECG lead because sometimes the bipole doesn't provide enough kind of far-field information for global activation. These were the therapies. Now, if you only look at the local electrogram, you can see, okay, there's subtle variation in the bipolar on each of these tracings. Maybe it's monomorphic VT, but if you actually hone in on the far-field electrogram, you can see that it's all of these, all of these episodes are polymorphic, pleomorphic. And in fact, this person, I asked, have you done a coronary angiography on this person recently? No, no, but he's not having chest pain. True enough, he went forward, did an angiography there, and he had a tight proximal LED lesion, and once that was fixed, all of these episodes stopped happening. So it is, you know, important to consider that too in selected patients. In our patient, poor baseline chronic coronary disease, but no new lesions, no intervention. So then this last option, which is often considered, at least up until maybe recently, the treatment of last resort, VT ablation, probably an appropriate therapy to consider. So not many randomized trials have looked at this, but so far we have a total of four. The first three, these were all in post infarction substrates. So SMASH VT and VTAC were really the landmark trials that first introduced this concept of intervention earlier in the course of disease with ablation compared to just standard medical therapy. And standard medical therapy comprised ICD implantation and medical therapy. You can see in both of these initial trials that there was a clear difference in terms of VT-free survival in those patients that were randomized to ablation compared to control therapy. The VANISH study I already talked about a bit. This was a more recent study, again from that group in Germany, that was responsible for the VTAC study, the substrate modification study. These were patients who were a little bit more progressed in disease, perhaps, and presenting with unstable VT. So the difference between this and the VTAC trial was the VTAC trial enrolled only, quote, stable VT patients. So probably slightly different populations. This was the only one that didn't see a clear difference in terms of VT-free survival comparatively. And, you know, one could question about whether or not the patients were, how different the patients were in each of these populations. The overall concept, though, is ablation is at least not worse than medical therapy and is probably better in selected patients. Also important when looking at these types of Kaplan-Meier survival curves is an event is an event. So an ATP-treated, relatively asymptomatically and tolerated VT episode would be treated the same in each of these studies as a representation with ICD-STORM, which I think we all know has different clinical implications for patients. And in most of these trials, what they found was the ICD treatment rate was decreased substantially. There is this thought, too, that kind of emerged from those initial studies that the timing of ablation matters. So if you have steeped a patient for years and years and years in antiarrhythmic drugs and then finally consider ablation, perhaps, you know, the horse has left the barn. It's the disease process has progressed too much. So this observational retrospective analysis sort of looked at that question a little bit. So this is data from University of Pennsylvania looking at 98 patients in their cohort who were presenting with the first time ablation. And they separated the ablation timing into late and early. Late meaning they were presenting for ablation being considered after at least two VT episodes, more than one in the last month, and there were 62 patients in that arm. And early, so meeting less of that criteria in order to go forward with ablation. What you can see is those patients who were treated earlier in the disease course tended to do better than those who were treated late. So not a randomized trial, but certainly provocative in terms of asking the question of are we withholding an appropriate therapy for too long in these patients? This was a study from Europe, which again was not a randomized trial, but looked at a comparison of a similar concept except in primary prevention. So these are patients who met ICD indication for primary prevention ICD. Ended up being 38 patients who were studied. 20 had never undergone a prior VT ablation, and those were called the, that was the non-catheter ablation group. There were 20 of those. And the remainder had previously undergone catheter ablation prior to implantation of primary prevent, of their ICD. So I guess it's, the concept is even in those patients who had never had a therapy. Sorry, to back up to clarify this. So it's primary prevention. So they did an EP study. If they were inducible, then they did a catheter ablation, even though they did not have any spontaneous events leading up to this. And you can see that those patients who were treated concomitantly with ablation as well as ICDs did better in terms of ICD-free survival compared to those in whom ICD only was the option. So we've decided, I think collectively as a group, that we're going to move forward with ablation. How should we ablate? So there are different strategies for doing this that are out there in the literature. Mapping and ablation during VT or entrainment mapping. Sorry. Mapping and ablation during sinus rhythm. So primarily looking at substrate and guided by pace mapping are the predominant approaches that are out there. Wendy, while they're looking at that, maybe I can ask a question. You know, that example you showed was polymorphic VT. Do you think there's a role for angiography or do you change your management with monomorphic VT for someone who has a positive cath? Yeah, that's a really good question. Many times if it's monomorphic VT and there's no other sign, you know, like no troponin elevation, what have you, I often will try to, if I'm convinced enough that it seems like it's scar mediated, try to get them not to get to that process. Now that being said, I've been burned that way too. A patient who had just straight up monomorphic VT, didn't really have any angina, actually did end up having some critical lesions that we found out unfortunately during the case. And so I've been, in general, even though I may not necessarily agree with every time it's done, I am okay if they haven't had a recent ischemic evaluation. Even if the presentation is with monomorphic VT because there is this concept that you have like ischemia provoked triggered activity, you know, PVCs that then, because there's a lot of substrate there, triggers the monomorphic VT. You know, I ideally want to make sure that both are sort of taken care of. Okay, so fairly even split, which is good because there's not really a one right answer here. Many times we do both. I would say that predominantly, as kind of goes with, you know, the predominant opinion of the group, we do more and more perform more and more mapping and ablation during sinus rhythm for good reasons. So when we talk about doing entrainment and inactivation mapping, that's, you know, really exciting stuff from a physiological standpoint. This is the kind of cartoon that we have come to understand based on work from Mark Josephson, Bill Stevenson, and many others. So the concept here is you've got this fixed scar and you've got some fixed anatomic boundaries and you have the potential for a circuit to exist throughout this region. When we perform entrainment mapping, what we're doing is, so imagine there's this VT that's ongoing, it's kind of circulating through here. When we try to overdrive pace to reset the tachycardia and then we observe the response of not only the return of the local signal after pacing has been stopped, but also the timing that it takes for that signal to to resume. This has several assumptions, of course, meaning that we don't really disturb the tachycardia much when we just slightly pace faster. And so the concept here is it takes time for the stimulus to get in to the tachycardia circuit, time to get around, which we approximate as the tachycardia cycle length, assuming that we haven't changed much with the overdrive pacing, and then there's time that it takes for the signal then to travel back to that site where pacing has occurred. So you could imagine that if you're pacing from a remote location, as this cartoon sort of shows, the PPI will, you know, exceed what the tachycardia cycle length will be by twice the distance that it takes or twice the time that it takes to get in and then back. So it would then, you know, reason that if you are within the circuit or very close to that circuit, the post-pacing interval will approximate the tachycardia cycle length, meaning when you stop pacing and the signal comes back, there's no need for additional time to take to return to that signal from that site of pacing, and so therefore the PPI approximates the tachycardia cycle length. So those are features that we look for when we're looking at potentially central isthmus locations. The isthmus contains actually an entrance as well as an exit. Anywhere along this corridor, at least the teaching has been, is that it is relatively protected on either side, either by scar or by relatively inexcitable tissue like an anatomic boundary. And the concept between going to the effort to find this out is to find the locations where you would have the most success in terms of terminating this tachycardia, preventing it from happening again. And so the isthmus features that were described are, with respect to timing, PPI is very close to the tachycardia cycle length, or the stem to QRS. So that means the time that it takes, so say you're pacing from within here, the pacing stimulus starts here, but it takes time for that wavefront of propagation to go out and then exit and then activate the rest of the myocardium. That's what produces the surface QRS. So the stem to the QRS, whatever reference you want to use that's relatively reproducible in terms of measurement, that timing, if you have captured the signal that you think is of greatest interest, should be the same as the time of that signal, that local EGM, to then that reference point in the QRS that you're measuring to. So that's what is meant by stem to QRS equals the EGM to QRS. And then this concept of concealed fusion. So that means when you are pacing during tachycardia and you're in a critical area, or a protected area, protected corridor, and VT is ongoing, there's only one way for which the wavefront of activation to escape. And it's the same way that the VT is traveling. And so therefore, when you adequately entrain and you're in a central isthmus location, you will not only speed up visually what the tachycardia, you will reset the tachycardia. And with the paced complexes, what you'll see is a QRS complex that is identical to the VT. So that's what we call concealed fusion. Now you can be in a circuit location, for instance, here in an outer loop. And again, the qualities for determining exit versus entrance is based on the timing of that EGM of interest, as well as the stimulus capture to the onset of the... So imagine if you're looking at the entrance, it will take a long time, longer time, relatively speaking, for this activation to lead to activation of the global myocardium and the QRS complex. Same if you stimulate from that site. The opposite is true if you're pacing from this region here and you capture an electrogram that's very close to the onset of the next QRS. You pace that, you produce the same QRS complex, and that stimulus to EGM, electrogram to EGM time being the same, indicates that that's truly what you've captured and you're in a potentially important area. If you're in an outer loop, you're still in the circuit, but as you pace, you can capture more myocardium beyond what is in this protected corridor. And so therefore, you will get what's called manifest fusion. So that means the paced complex overtly looks different than the QRS complex during tachycardia. But the PPI in this instance is still important. So if you have a PPI that approximates the tachycardia cycling, it's still... you're getting close. You're like warm, you're just not hot. But you're close enough anatomically that you can explore a little bit further and find these elements. And then other kind of characteristics of kind of fake-outs include the adjacent bystander. So you say you have extensive scar here, lots of dead ends. So you can pace from within here, produced concealed fusion, because there's only one way for the wavefront of activation to go. But it's the same circumstances if when you're pacing remote from the circuit, it takes time for the stimulus here to go out to get to the circuit, to go all the way around and back. And so you'll actually have a PPI that far exceeds the tachycardia cycling in that circumstance. So why do we go to the... why do we go to the trouble of doing that? The idea is we can limit the ablation, relatively speaking, or focus ablation in this region of greatest importance to at least potentially diminish the likelihood that this particular tachycardia will occur. Limitations are that we assume, as previously stated, the conduction velocity doesn't change much with pacing. Multifractionated signals can often confound the interpretation. So you have a lot of little electrograms in there in the diastolic period, and it's sometimes difficult to tell which one you actually captured when you come off pacing. Most importantly, less than a third of patients who were referred for VT ablation have hemodynamically tolerated VTs that can be mapped endlessly in this fashion. And many times, the most that we're able to do is limited mapping, limited activation and entrainment mapping. It became recognized long ago that not only in post-infarction, but also in non-ischemic substrates with VT, that the underlying common denominator is the presence of scar. And keep in mind, too, that the scar itself is not what is arrhythmogenic. It is the abnormal tissue and abnormal myofibrils that survive within the scar that can still conduct, but conduct with different properties compared to the adjacent alive tissue that is adjacent to the scar that promotes re-entry, which is the predominant mechanism for VT in the setting of structural heart disease, and certainly in the setting of post-infarction VT. And this concept led to the way in which, you know, we've mostly adopted for doing VT ablation, and that is identification of substrate. The purest and simplest way to do it is to find scar as defined by low amplitude electrograms. And so, this coupled with electroanatomic mapping systems, which give us not only location information, but electrical information at the site at which the catheter has kind of roved, can allow us to produce maps that look like this. So, they're color-coded, and the standard has been that if the electrogram locally has an amplitude of less than 0.5 millivolts, then it's considered to be, quote, dense scar. Anything greater than 1.5 millivolts is considered to be normal tissue, and everything in between is border zone, so potentially abnormal tissue that can promote VT circuits. Now, when you look at this, this is a fairly large area of scar in a patient who's had a prior LAD infarction. When knowing how to ablate to target in this fashion, just based on sinus rhythm, you could end up ablating a fair amount, is one thing. The other thing is, just looking at the colors, and for fellows in particular, it's critical that you have to be critical about the points that are collected. You never trust only what the colors are that are displayed. You actually have to look at the quality of the electrograms that are being collected yourself, or you can get fooled, because this could be a very nice map of poor contact, because poor contact will produce low amplitude electrograms. But what you want to see is not only low amplitude electrograms, but really abnormal ones. So, this one, as you can see, is an example. Low amplitude, it's fractionated, it's long in duration. This is the reference surface lead here, and you can see that the activity locally continues well after the activation of the rest of the myocardium has occurred. Locally, the conduction here is very slow, so these are so-called late potentials found at critical central isthmus sites, including the very central isthmus itself, as well as the entrance and exits. And then, in this kind of model, this construct, we fish around, we find electrograms that look like this. If we have a surface 12-lead ECG of the clinical VT, which is always a goal, if it's not available before coming to the lab, we will often, after acquiring a voltage map and sinus rhythm, induce VT in the lab to try to see what we're dealing with, at least in terms of easy inducibility. And what you can do, then, is take this ECG and estimate where this exit might be, because that's what the surface QRS represents, is the exit from the circuit. The exit is then what promotes the depolarization of the rest of the ventricle. And so, in this case, we have a right bundle, right inferior axis VT, with a relatively early transition. So, based on the vectors here, you can estimate that the site of interest is probably here, in the anterolateral portion of this infarcted region. In the perfect scenario, you'll pace there and you'll get a nearly perfect pace map to the clinical VT, which suggests you're actually pacing in a relatively protected area of dense scar, truly, but it's still electrically excitable. And it mimics the exit of the clinical VT. So, keep in mind here, when you pace map and you get a good pace map, you're just identifying, basically, where the exit of the tachycardia might be, especially if the stimulus to the onset of the QRS is relatively short. But the exit is what is attached to the rest of the critical circuitry elements. And so, that's kind of what you want to know, is the latter. And then you can know where you can focus efforts. The problem with pace mapping is that it's also not perfect. So, this is a cartoon of why that might be. So, this illustration here, again, inexcitable scar here, boundaries, and tachycardia is ongoing here. So, trying to overdrive pace during tachycardia and train, as mentioned or shown in the prior cartoon, even, you have this wavefront of activation that's propagating through all of these potential channels of conduction in sinus rhythm. When you are pacing from this same location during VT, again, because of the wavefronts of propagation that are coming here, these wavefronts that are going in these directions are extinguished. And the only way in which the wavefront can then propagate is out, because these areas here are extinguished. And so, you get an identical QRS complex to the VT morphology. When you are pacing in sinus rhythm in that same spot, these channels of conduction are now accessible. And so, pacing there, you might actually get a fusion of activation, comparatively, when compared to pacing in VT, because you have these other areas that are no longer being activated by another arrhythmia, and therefore, a relative fusion is produced. In this study here, which, again, is an oldie but a goodie, less than 30 percent had perfect pace maps at likely circuit sites, and only nine percent with perfect pace maps had actually termination with ablation applied to those sites. What was more informative about the importance of a site was the stimulus to QRS of greater than 40 milliseconds. So, a long stim to QRS time, sort of what I was alluding to before. If it takes time from pacing from within here to activate the rest of normal myocardium, then that suggests that you're in an area of delay. And if you produce a pace map that looks perfect to the VT, and it's a long stim to QRS, that's a little bit more exciting than if you just have a good pace map. This is a nice example of the concept of pacing and producing alternating exits. So, in this case, this patient, dense inferior scar, pacing at this single site produced alternating exits here that were very close in vector and morphology to the two clinical VTs that the patient had. This suggests that, you know, there's the potential for a dual loop circuits going on here, or alternating exits of VT that would produce two distinct QRS morphologies. Give the impression that you actually have more than one VT, when in fact you just have a very large area of substrate that must be addressed. Okay, so advantages of mapping and ablating during VT is the mechanisms that are able to be obtained. There's potentially greater precision and knowing where to kind of target energy. And it's also very satisfying if you've mapped carefully and you can get to a spot that you think is an isthmus and you actually terminate the VT rapidly with ablation. The disadvantage is that, you know, most VTs, as mentioned, can't be mapped in this fashion because they're not hemodynamically tolerated. And you can get into a situation where you get yourself and the patient into trouble. Repeated inductions and shocks can then produce hemodynamic collapse, particularly in patients who already have very low reserve at baseline. You can make that worse. And the outcomes, importantly, are not better when you do it this way compared to that one. Even use support like mechanical circulatory support to support these cases, the outcomes in terms of VT-free survival are not improved. The advantages of mapping in sinus rhythm and ablating sinus rhythm, of course, patients are more hemodynamically stable. Usually more comprehensive ablation is required in order to do this, but it has been associated with better long-term outcomes. Disadvantages are that, you know, it's less precise. You feel less great about just kind of carpet bombing an area. The substrate is not always straightforward, and endpoints to date have been suboptimal. This is another example. So this is a patient with monomorphic VT, a history of prior infarction. Just for the sake of exercise, I'd like you all to try to determine where the VT exit is here. So let me go back one. Oh, sorry. So the options are the, oops. Oh, I just wanted to mention that you should never forget the surface ECG. In all the kind of high detailed mapping that we do, we always go back to the surface ECG to sort of ground ourselves. Sorry, the options didn't show up there, but I'll put this back here so you can pontificate. So is this coming from the RVOT, LVOT, basal infralateral LV, or apical infralateral LV? Okay. Okay, great. So going back to this cartoon, to try to use ECG vectors and knowledge about vectors. Importantly, I really emphasize, just as Mark Josephson and the people who taught me did, that you should really use the baseline information about understanding of vectors in order to arrive at a decision. That is true for identifying the potential exit site for a VT, the site of origin for a PVC, as well as, you know, kind of localizing where a bypass track would be. You kind of use your understanding of how the ECG vectors are, and then you don't have to memorize things based on an algorithm, because I'm not actually very good at that either. So this is the cartoon. So the limb leads and the heart, relatively speaking, have this sort of relationship. So you're looking at the heart and cross-section. The precordial leads are just unipolar leads that kind of represent activation to or away from that lead at various locations along the chest. So the first thing I look at is lead V1, because that actually gives you information about if it's more likely to be coming or exiting from the left ventricle or the right ventricle. If it is predominantly positive, we call it a right bundle morphology, much more likely to be exiting from the left ventricle. If it is the, if it is a left bundle morphology, which is not strictly speaking a left bundle branch block, it just means that it's predominantly negative in lead V1, it tells you that it's more likely to be exiting from somewhere in the midline. So that could either be midline or more rightward. So that could either be the septum in the LV, or it could be from the right ventricle. So that's the first step. The next thing I look at are the limb leads. And so in lead I, if it is a left axis, that means it's going with the vector of lead I, it should be positive. So if you're talking about a right bundle VT and it has a left axis, it is most likely coming from somewhere in the middle here. The opposite is true if it is negative in lead I, because that implies or tells you that the activation is against this vector. So it must be coming somewhere from here on the LV free wall. So septal versus lateral. And then the front, the rest of the frontal plane axis with the inferior leads, if it's superiorly directed, what that means is the activation is against the leads that are going, the inferior leads. And so the side of exit is most likely to be coming from the inferior portion of the LV. The opposite is true if it is positive and it's inferiorly directed. That means it is going with the direction the vector is much more likely to be coming from the top. And then the pericordial transition gives you an idea of whether or not it's coming from the base. If there is a, it's a right bundle and it's a very early transition or positive throughout the pericordium, much more likely to be coming from the base. If it's a right bundle and transitions very early, much more likely to come from the apex. And if it's somewhere in between, then it's probably somewhere in between. So that gives you a rough estimation and knowing that at the time of a real-time ablation is important because it tells you where you need to focus your efforts if you decide to induce, where you should plan to have your catheter parked because you know that you won't have a whole lot of time to map and you want to optimize the amount of time that you have without it being futile. So in this case here, we're looking at lead one or lead V1. It is a right axis and in varying leads, this one and this one, so it looks more superiorly directed here. So that kind of puts it in this this rough region here because then in like slight positivity in three on this beat, it is much more positive in three on this beat, which kind of puts it maybe even a little bit higher up. So this is an interesting case in which there are actually alternating exits ongoing during VT, suggesting that there are just different routes of circuits that are being taken through an area of large scar. And we call it an indeterminate axis. And the pericordial transition here when you're just looking at this beat that I've highlighted is, you know, somewhere in the middle. So in that infralateral region in the mid-LV. In this one here, the transition is earlier, and so it's actually more towards the apex. And so both of these answers are actually correct. This is an example. In selected cases, we will perform dual LV access, both retrograde aortic as well as transseptal. And that is in this particular circumstance. If we think that, you know, this patient in particular had relatively hemodynamically tolerated VT. So we think that the concept here is that we can acquire relatively quick information with a multipolar ablation or mapping catheter to know or confirm the site where we should focus on with ablation. And then if we are lucky, we can kind of hold the pentarray or the multipolar catheter in that position and then advance the ablation catheter to that site of interest. Many times the signals that appear on the multipolar catheter are slightly different and characteristic and certainly more voluminous than the signals that you get from just a single bipole catheter on the ablation catheter. And so it's often useful to have both, because at this point in time we can't ablate from a multipolar catheter that maps. And then you can kind of go to that area, do some limited entrainment, and do some ablation real time. It's just a way to sort of optimize the efficiency of kind of looking at the electrograms. And you can see here, this is the difference if you just look at one spline of this multipolar catheter in a single location. These are the splines that are directly adjacent to it. You see here, this doesn't look of interest at all because it's kind of within the timing of the QRS. But these other splines are right next to it. And so you see you can relatively rapidly see how quickly and more efficiently you can acquire relevant information when you have a lot of poles kind of mapping at the same time compared to just one pole with the ablation catheter. More relevant when mapping during VT, of course. And with that, you can get information about activation as well as do some entrainment. Now things to mention about activation, and this is particularly important for fellows who are kind of starting out understanding what mapping is. These areas of red and all the red colors of the rainbow during activation are really kind of big. You can change them around based on the window of interest within which the timing is referenced. So many times the mappers will set, when they think it's a re-entry, a fairly equal window of interest that roughly approximates the tachycardia cycle length. Half of it is in the front part of that window, and the other half is in the latter half of that window. And they're hoping to get, when they say it's early here, what they mean is if they've timed the window in the middle of diastole here in the VT, that means that it's potentially an isthmus site, potentially an isthmus component. That's what it means. But early and late can be altered depending on how they set the window. So this is a representative example of an early signal that is acquired from this location. The same location, all I did was alter the window of interest and then re-annotated all those points through this mapping system. And now that same area is late. So it doesn't make a whole lot of difference when you're talking about re-entry. It certainly can make a difference when you're talking about focal arrhythmias. And in general, the concept here is that you shouldn't just trust the colors that are displayed by the mapping system and the mapper, even if they're really good. You still have to kind of periodically look at the data yourself to make sure it makes sense for you. And then it's also important too, with all these fancy tools that we have, that we can still do the baseline things that we've understood that we've been doing for decades to try to understand re-entry and re-entrant circuits. And in this case we can perform entrainment or try to perform entrainment. So this is an example of ventricular overdrive pacing here. What does the ventricular overdrive maneuver suggest in this case? So this is another polling question. Is it an exit site, isthmus site, entrance site, or none of the above? I'm going to move this out of the way. And I'll start. So this tachycardia is 380 milliseconds. And this is the pacing interval. Okay, great. Okay, so let's walk through this. So we have accelerated the tachycardia. We've reset the tachycardia, which we've confirmed by, sometimes it's hard to tell from the surface, especially if it's concealed fusion. But what you do is reference, use the measurement of another reference ventricular catheter. And the RV quad is a good choice in many cases. So you can see you've accelerated it, and you can see that it's a little bit less in many cases. So you can see you've accelerated it compared to the tachycardia cycle length. So the tachycardia has been reset because it continues. This is the pole from which we're pacing. So this is the probable signal that we're interested in. And when you look at that signal, to confirm that that's the signal that you've actually captured, because there could be potentially low amplitude signals in here that you've captured, that you can get fooled in thinking that this is the signal that you want to measure to. But in fact it's not. In this case, you measure from here to some reference on the surface QRS. And in this case, I think I took the little divot here in lead 3. So that's an EGM to QRS time of 80 milliseconds. And here, the stim then to that same relative reference is roughly the same, so 75 milliseconds. So that is in fact the valid EGM to measure to. And therefore, when you look at the PPI there, it's really pretty good. So the PPI basically approximates the tachycardia cycle length. You can already see, and it's inferred from the way that you took the stim to QRS and EGM to QRS measurements, that it's a concealed complex that we're talking about. And the timing of it is relatively close to the surface QRS timing. So it is more consistent with an exit site, as most of you have said. So nice job. Okay, how about this one? Same question, same options. And I will give you those measurements there. I was criticized once for not showing measurements when holding a fellow responsible for making sure that the measurements presented were accurate. All right. Very nice. So walking through this, we've reset the tachycardia. All right. This is the stem to QRS. And you can tell that this is the QRS that's captured because of what? It's manifest fusion, right? So it looks distinctly different than the QRS complex that's going on during BT. Although I have to say that the morphology is not terrible. The overall vectors sort of match this. You're probably not too, too far away. But anyway, the stem to QRS here, if you look and work backwards, because sometimes this is an example of how multiple electrogram signals, and it's hard to tell what you've captured. So this is one way to figure it out. You have to determine what the last captured beat is. In this case, it's obvious. In some cases, it's actually this beat. So you have to actually verify that the measurements work out, that this is truly a longer time, which visually it's obvious in this case, than this pacing interval here. And then if you're not sure which electrogram it is, you can kind of work backwards from that same reference on the QRS back about the same time. And it's maybe some electrogram in there that's captured. And actually, you know, it works out to be much longer, relatively speaking, than the tachycardia cycle length. So it's none of those. But I have to say, it's not too, too far. The timing is off, but it's somewhere close, because you're at least producing a similar sort of exit as what the VT is doing. And as mentioned, it's manifest fusion. Okay, so final example here. All right, great. You guys, you already know this stuff. That's great. So I'm walking through this We've confirmed because we've advanced the tachycardia to the paste cycling. This is the last captured beat. It's a little bit hard to tell in this case because the surface looks concealed right So this is the stem to QRS reference timing. So 80 milliseconds there. And if you work back from that same reference. About that same timing. This is what we're pacing from. So this is the electrogram actually that we're interested in and So that is what we measure to to get the PPI, which is again identical to the tachycardia cycle length And it's right in the middle here mid diastolic activity low amplitude But it's important and this it was indeed an isthmus site Okay, so same patients. This is the voltage map acquired fairly large area of scar and sinus rhythm compared to, you know, the activation map, which in this case showed the earliest or isthmus activity in this region here, which you would have anticipated based on the surface QRS So it's, it's really nice when you have multiple modalities of information that reinforce one another are inconsistent. So what would be the ablation strategy of choice. Do we target the VT termination site. Once we achieve termination and reinforce it target the isthmus and associated components or do comprehensive substrate modification or something else. When if there's a question about tools that you use. How often do you use him a dynamic support and then the other one is, do you use a multipolar catheter for every VT case. Those are good questions human dynamic support prophylactically used is relatively rare. You know, there's data from Penn use with use of the pains D kind of score to assess what their baseline risk might be of acute human dynamic decompensation. But even in people who score relatively high with that I don't necessarily prophylactically do it. Because of the logistics involved and the fact that many times we haven't needed needed that support, especially if the approach is mostly to reduce the risk of acute hemodynamic decompensation. So, because of the logistics involved and the fact that many times we haven't needed needed that support, especially if the approach is mostly to do most of the work and sinus rhythm, which You know, it has has emerged to do that in cases that are not ischemic or in whom I think that we might have to do more activation mapping and I'm worried about the human dynamic stability throughout it, then yes, then I will institute prophylactic human dynamic support. But we always do use an a multipolar mapping catheter to a bleed, especially substrate based BT. All right, target the isthmus and associated components. Okay, so. Alright, so then along those lines, because those are the acute options. This I don't think is a survey question, but when, how, for how long do we have late is it till we get non inducibility of the clinical BT non inducibility of any BT or some other endpoint. And I think just to move this along. I will. Can I end the poll. Thanks. Okay, so I'm looking at this patient. Okay, so we saw what the easily spontaneously occurring clinical BT was and many times. That's what we call the clinical BT And if you look at all the events in this person's event long there's there are many they all roughly have that same cycle length. So it's probably just cycling oscillations. But if you actually look at representative examples of the stored EGM, you can get a very different picture of what clinical actually means It may not be the most frequently spontaneously occurring BT. In fact, and it could be actually that there are spontaneously occurring BT that have happened that just haven't been captured on a 12 lead. Those are still clinical and certainly clinically relevant. And it gets. It's an important point to make. In this case, because again, this was the spontaneous BT that the patient presented with frequently Relatively stable tachycardia cycling. In sinus rhythm when we're pacing at the edges of various components of this very large much larger area of scar. We get the we get these pace morphologies. I'm sorry, we get these exits. Sorry. These were induced BT at the time of the BT ablation easily induced, you know, with singles or doubles, but they weren't what we're clinically observed Are you going to say that you're going to if you if you look at each of these exits, you can see. So this is probably where the clinical BT exits from If you look at closely how each of these morphologies look You could guess that they are all are just exiting differentially, just like this guy had alternating exit from this site. Why couldn't he alternate alternatively exit from other sites other utilize other channels differently within the same substrate and to me, I would not feel satisfied with only getting A Form at this site and still easily be able to induce all of these others to me. Those are still going to be trouble and probably in the near future, given how incessantly the patient presented with BT in the first place. And so the strategy here that we use at our center is this concept called core isolation. It's a name. It's actually not that different than any of the other substrate based approaches that are out there that are named slightly differently. The only difference is that we evaluate the employee, a little bit differently. And so we've identified scar here. In this case, we have a multipolar catheter in the middle. The other advantage to having both catheters like this in position is that you can kind of get real time information about the progress that you're making. So we go around and around and around this region which we've identified this whole region to be important. And, you know, we've gone around multiple times actually at this point, we still have apparent entrance conduction into this region. So do we have core isolation. Okay, so we already it's already suggested that we don't because we still have this residual near field sharp signal and when we actually pace and capture that signal. In fact, We still activate the rest of the global myocardium. So we have not achieved entrance or exit block in this region core isolation has not been achieved. So what are potential reasons for lack of apparent isolation, depending on where you are in the case, you can come up with all sorts of explanations. If you're late in the case and you're just really tired of ablating you might use this sort of reason far field EGM anodal capture There could be continued entrance or exit along the lesion set you've already kind of constructed and it's just a matter of finding where that tiny little breakthrough is Or a probably a more common reason. And the reason why more comprehensive oblation works. In many cases, is that there can be this three dimensional component to these scars and circuits and you can have endocardial to epicardial breakthrough. So, This is a one way if you're trying to if you're imagining a relatively two dimensional substrate. One way to figure out If it's just a gap that's left in the line somewhere that you have to find and seal up. This is one way to do it. So this is an example of a gap that was intentionally left around this large scar. And if that's the concept and you only have one exit. If you pace and you pace as you get closer to the exit the stem to QRS time should shorten accordingly until you're basically at the exit point. In this case, it's a really nice example of this And then when you seal it up and you pace within the middle, you get exit block and you know that it was, you know, that was it. It was just a residual gap that was along the line that wasn't contiguous enough And and then the other proof of concept that we use with this approach is is to achieve VT non inducibility. In this case, so we're pacing around Look at the timing here. So this is the concept of proving or trying to see whether or not there could be endocardial to epicardial breakthrough. So this is the positioning of the ablation catheter as we're pacing and this is the Penta Ray position within here. And so we are pacing from Penta Ray one to It is immediate. It's not immediately opposite is pretty close to that. And so the morphology that we're getting, even though we're pacing from the top of the ventricle is a superiorly directed morphology. And this is the time, you know, from the local activation to the time the activation time of captured on the ventricle. It's pretty long. It almost looks like CTI like long And when you do the opposite, as we did in this case. So I showed you the positioning of the ablation catheter. It's just outside of the lesion set This is, again, positioned outside of the lesion set anteriorly. This is that local signal from where we were pacing earlier. It's the same timing almost looks like bidirectional block across the line. And look at this. It's very interesting. This is, again, positioned outside of the lesion set anteriorly. This is that local signal from where we were pacing earlier. It's the same timing. Almost looks like bidirectional block across the line. It's not proof. In this case, the patient had a cabin. So we couldn't prove this by going to the epicardium easily. But going to that spot basically that that spot where we still had residual electrograms and ablating there was enough to then eliminate that that entrance of conduction and in fact enough to achieve exit block as well. So this is just to reinforce the concept that, you know, there are a lot of substrate based approaches that have evolved, be it evaluation for an elimination of all late potentials. Focusing on a variant of late potentials, which are called local abnormal ventricular activities. Basically the same thing because, you know, late potentials are an example, but sometimes Sometimes they're only produced when you do things to change the way from an activation or uncouple, you know, that local near field low amplitude signal from the larger amplitude signal representative of activation of tissue that's more normal that's near it. There are there's this concept of identifying the entrance conduction channels into scar. And normal potentials. In the end, this approach, although it looks, you know, a lot is very, very commonly the approach that is that is taken when we go to kind of do more effective ablation. This is the only randomized trial that is kind of looked at this comparison of more limited ablation compared to substrate based ablation, you can see That those in whom more extensive ablation is performed targeting all potential channels of conduction do better in in follow up in terms of VT free survival compared to those in whom only limited ablation is performed. This is a meta analysis that sort of confirms that same point of all of those substrate based studies of single center that are accumulating together. So a couple of closing points just other scenarios that can be encountered in the setting of post infarction VT. So this is a patient who's older has coronary disease, a remote obtuse marginal stents dual chamber ICD for secondary prevention recurrent VT despite antiarrhythmic drug therapy on the nuclear scan that's done for ischemia evaluation no infarctor ischemia. The TTE shows an inferior wall motion abnormality, which, um, you know, it's probably not too far off from where the stent distribution might have provided And this, though, this, though, is the the representative ice image from that patient. So this is of the left ventricle. This is the inferior wall. What do you see here. You see this stripe that goes from the mid myocardium out to the epicardium maybe at the base here. You can convince me that there's one more. To the epicardium maybe at the base here. You can convince me that there's more transmute representation of an of a post infarct kind of sequelae. But this here this mid to epi substrate that you see on ice is not consistent with infarction. This is in case this is this is what I refer to as the schemic VT fake out So you get this history. And I think we're seeing this more and more as patients are taken for earlier revascularization that they actually don't develop If they develop a cardiomyopathy. It's not related to the prior infarction. This is the distribution of scar that you would expect because The coronary vasculature goes from the epicardium to the endocardium. So when you have an occlusion, the area that is compromised. The most is the endocardium. And so that's why this concept of following infarction. You can just do endocardial ablation and many of these patients and get away with it. That's why that works. That's why the surgical approach of the Pennsylvania peel peeling away just a sub millimeter Depth of scarred endocardium worked in terms of controlling VT in the early VT treatment days. And this is kind of just to illustrate the difference in the scar distribution. That can be seen in these post infarction substrate substrates compared to non ischemic substrates of which those ischemic VT fake outs are apart. And you can get into the situation where you think, oh, it's going to be a great case, we're going to be able to map and in actuality, what you have is a mixed substrate that is much more predominantly non ischemic This is a nice illustration of what that might look like. So the endocardial voltage map looks normal in this person who's had VT But the epicardium is abnormal. That's where we had to go to ablate to get rid of this. Clues can be that the VT morphology is either inconsistent with the CAD distribution. Or you have an imaging abnormality inconsistent with or out of proportion to the CAD distribution. This is a nice example that same patient that we brought activation during VT. This was very limited activation because the patient didn't tolerate it well. They'll be with the use of a multipolar catheter placed in exactly the right position, we could get the information that that's where That's big. So we've acquired a scar base map prior to that. And we placed the Penta ray catheter or sorry the HD grid catheter in this case. Immediately opposite those sites of abnormality on the epicardium induced got activation and then from the endocardium And what I think you can see here is that it's transmural conduction here. So you have breakout here, it goes through and activates the inside and comes back and activates the outside again. This is an example of kind of transmural involvement of a VT circuit. With alternating exits, by the way. So varying exits there. So to summarize, VT in the setting of structural heart disease, including non ischemic heart disease. Centers around substrate. It does make a difference. Even if you get a history that this person has had a prior infarction, you should make sure that you know what you're dealing with before you bring the patient to the lab. Clinical VT in my mind is semantic different VTs can result as a result of alternating exits from the same substrate. And more and more, we're finding that more comprehensive ablation is necessary to more effectively control VT durably And this is assisted greatly with the use of high density mapping tools as well as other contemporary ablation tools, but we still have a lot of progress to make, especially And many of the concepts that are applied here can be applied there too. I will end here. I want to highlight How much I enjoy these people that I work with, as well as the beautiful place in which I live. Any questions. I know we're running a little bit long. Sorry about that. Oh, that's fine. That was a fantastic lecture. Thank you so much. There is a question here. If you have a case where you have multiple VTs in the same substrate. And if you have a case where you have multiple VTs and everything's non inducible in the lab. What is your strategy and do you have any tips to try and induce in that situation. That those are really good questions that are not unfortunately relatively commonly encountered, especially when when patients have gotten a ton of anti arrhythmic drugs to control VT prior to coming to the lab. So, Fundamentals would be if you can't induce even you've at least got a substrate based map. And so you can if there's a fair amount of substrate. If you've had the opportunity to get a 12 lead ECG or even telemetry leads to approximate where you think the VT exit might be And it's consistent with what you're seeing on the substrate based map, then that's helpful. And then you can what I often will do in that case is just move forward with modifying the substrate. In the, in that case, you know, the endpoint of inducibility is flawed right it's flawed in general too, but it's what we have that's best. When they're non inducible at baseline and they're non inducible after you've ablated. I'm not sure that you've gained that much more information about what you did. So that's where this concept of pacing to demonstrate electrical and excitability comes into play. So if you've rendered that area that you think is involved in these VTs that the patient has had Electrically and excitable, then you can feel a little bit better that you've made some strides and potentially help the patient. Tips for induction include, you know, some people will go out to quadruple extra stimuli pacing from multiple sites. We don't do that, but Pacing from multiple sites can be helpful because sometimes it's just kind of sort of introduction of The way from from a different angle that will sort of allow reentry to occur if it's a very specific kind of cycle length or Coupling interval that's required to induce VT. In some cases, Many cases, these patients are already on some form of presser during the case. So if we augment with like additional epi or Rarely, but can be done in some cases use of isoproteranol to try to kind of rev the system up. Sometimes that's helpful, but many times, you know, human dynamics don't Allow the latter. And it's really just if you can identify substrate and you're pretty convinced that the substrate is involved in the clinical presentation, then you just modify it. The tricky thing is if you get in there. They've had a lot of VT and you see nothing that looks good on the inside and the decision is, okay, do we go to the epicardium And sometimes I have, especially if they've clearly presented with ICV storm. There's no substrate that can be identified on on the inside in either chamber. So that's right ventricle and left ventricle, then sometimes it will go to the epicardium to look to look there.

ventricular tachycardia

substrate-based ablation

structural heart disease

scar tissue distribution

comprehensive ablation

high-density mapping tools

inducing VT

modifying substrate

electrical inexcitability

non-ischemic heart disease