Oh, good morning. Thanks, Nishant, for doing this. I wish I published more in this area. I really have not done enough. We've been more consumers of imaging in our VT ablation workflows than we have been publishing, although we have a lot of experience with it now. And we'll have some data, hopefully, coming out soon. Let's see if I can advance my slides here. So I love to bring up this slide in any VT talk. We lost, really, two legends of VT in the past couple of years. Dr. Wellens just passed away, I know, recently. And that's been all over Twitter. But his partner in teaching, Dr. Josephson, really led the way in much of our understanding of the substrate for ventricular tachycardia. We want to connect how we use imaging and mapping systems to what was really identified at the macroscopic level in the operating room by Dr. Josephson 40-plus years ago. And it really began with these aneurysm resections for management of VT, but with the interesting finding that just resecting the aneurysm alone was insufficient for controlling VT. And it was from there that they did extensive work to really identify the subendocardial disease with fibrosis, interrupting these sort of bridges of dissociated myocytes that could create the substrate for reentry at the subendocardial level. And this is a microscopic view, but in reality, it's a very complex three-dimensional architecture. And this really had me and certainly many others, and I think in particular the Bordeaux group and Salman Nazarian at Penn, formerly Hopkins, and Frank Bogan, among others, really leading the charge in terms of using imaging to begin to discern those different areas of electrophysiologically vulnerable or rhythmogenically vulnerable areas of STAR. So it's a really complex 3D problem to solve. How do we see these things? There are mapping tools. There's imaging. There's a lot of very nice work that's been done with mapping and some of the difficulties in mapping, particularly by Rod Chung and his group and Shiv and the group at UCLA. How do we hit the target? Are there better anatomic approaches that can be identified? Will imaging be helpful for pre-planning? The classical approach, this is the way I was trained, certainly by my mentors in Boston, to address VT. And this was really before imaging. I was a fellow from 2009 to 2011 for EP, at least. And we identify the scar by the standard definition of less than 1.5 millivolts. And that's a moving target these days with high-density mapping and smaller electrodes. We found an exit region if we had a 12-liter VT either from induction at the time of the procedure or from an ECG, perhaps an emergency department. We would then proceed with pace mapping, initiate VT in the area of interest with the catheter's position strategically in the area of interest, and train briefly if we could, map if we could if they were stable. But that's rare. Only about 20% of VTs are mappable. Most of them fall on the right side of that column, the unstable VTs. And then we would ablate in perhaps just a small line through that circuit. But it turns out the outcomes may not be any better with induction. It's really a probabilistic approach to determining an endpoint. And it doesn't necessarily mean you're going to be any more successful. And so perhaps we'd be better off just identifying substrate and targeting that. This is a nice work from Beruezzo in 48 patients randomized to induction or not, a mix of cardiomyopathies. And basically, if you look at the Kaplan-Meier curves, there's really no difference between substrate ablation first versus induction first. They do about the same. And so it sets up this question that's there we go, of how best to ablate substrate. Do we do precision warfare? Are we kind of like SEAL Team 6, assassinating kind of one little target with limited linear ablation? And that's certainly one approach. That's an approach that I became familiar with as a fellow. Or do we just homogenize star? Either approach is exactly wrong, although I think we've moved to the right of that, certainly. And the five years after I got out of fellowship at Loyola with Dave Wilber really kind of pushed me into the substrate approach. But I was still interested in perhaps being somewhat more precise and using physiology, at least, to guide our decisions about where to ablate. That is, what are the vulnerable areas of star? And I know there's a lot of interest in using various mapping approaches. Can we use imaging, perhaps, to do that? High-density mapping is certainly a powerful approach, but it's confusing. I don't know that there is a single standard. This is a swine and fark model done in a lot of Andrew's lab when he was in Boston. I know he's in Cleveland now with Corey Chavarin, who's now relocated to Canada. They're pretty lucky to have Corey. And this is a dense scar mapped with a linear ablation catheter, basically. This looks like the scar that most of us grew up seeing as we learned as fellows. And then you take the same infarct with this multi-electrode model or a mapping system. You see much more heterogeneity in the star. You see more scar architecture, where you have these little preserved areas of voltage that perhaps may indicate a channel, a conduction channel. And so what, again, is the best approach? And I'm not here to answer that question. The question is whether or not imaging could be helpful. And with high-density mapping and multiple-electrode systems, it gets even more confusing. What's the best way of doing it? There's a list here on the right of multiple high-density electrode catheters. We all have our favorites. I know Rod Tong likes the LiveWire Duodeca. I like the GRID. Some people like the Pentarray. There may be other catheters emerging. And I know then Rod has done a very nice job. Dr. Tong has done a very nice job with the Orion catheter. So lots of different approaches. But perhaps we could standardize it more with imaging. The approach to mapping, again, is influenced by wavefronts. It's very difficult to identify a rhythmogenic substrate if you just map in one rhythm sometimes. And Rod really drove this point home in this very beautiful paper. This is one of my favorite papers that I encourage all fellows at least to go and look at, where if you look at this QRS and we annotate late potential, which are indicators of slow conduction into a scarred myocardium, you can then measure these yellow lines to indicate timing. And the lateness of that sort of is a surrogate for slow conduction into that area. And you can then create a map, what we call an activation map, indicating timing. And so what Dr. Tong has done in this is show timing. The later signals are purple. The earlier signals are red. And in sinus rhythm, down nearby the apex of the left ventricle, you're earliest. And then there's this migration of a wavefront upwards up the septum to this area where you ablated. And there's this compression or slowing where the colors begin to come together. If you change the wavefront, and instead of sinus rhythm, now lateral LV pacing, it changes the distribution of colors, changes the distribution of late potentials, and conduction into that area. And so this is really confusing again. It's just, I don't know when I do a case what rhythm is best. And we've been, just this week, we've done two large anterior apical MIBTs. We've mapped an LV pacing. We've mapped with sinus rhythm. We've mapped with RB pacing. We've done three different maps before we've ever turned the ablation catheter on just to look at isochrones. So would we be better off with imaging? And we did do pre-procedure imaging. And we're very interested in correlating those things. But perhaps one solution is to use a multi-electrode catheter like this that can then, independent of wavefront, look across splines and between splines. And that may help solve the problem. But that could be even confusing. We look at this grid signal now. This is what we call lavas and late potentials. Lavas are the local and abnormal ventricular activities that were described by the Bordeaux group about 10 years ago. This is your sinus rhythm QRS complex. You see these signals that are well after the sinus rhythm QRS complex. We then pace from that spot. And we see two different QRSs. You see this first one. And then there's a subtle shift. These last two QRS complexes are different than this. And we see variable exit. These signals kind of redistribute. You can see that with a different exit, these signals take on a different morphology. Maybe we can identify SCAR differently with MRI, late enhancement. I know the Northwestern group a long time ago, I think in the early 2000s, really described the utility of late catilinium enhancement to describe SCAR. And there are different SCAR patterns for different disease patterns. In normal myocardium, there's no delayed enhancements. In this instance, with coronary disease and prior myo, there's a subendocardial distribution of SCAR that you can see here. And then in GCMs or sarcoids, you can see this patchy mid-wall stuff, or patchy septal and basal LV. And this is much more challenging to map. Maybe even elude our normal contact-based mapping approach. So can imaging be helpful? This is a patient we took care of at Loyola with Dr. Wilber some years ago when I was still at Loyola, where we did not have imaging. And this is a very elegantly mapped by Dr. Wilber with a non-ischemic cardiomyopathy and had mapped with activation mapping, focal breakthrough on the endocardium and on the epicardium here and here. See this red spot, kind of like X marks the spot? That's the focal breakthrough of a mid-myocardial arrhythmia. There's normal voltage on the endocardium and some scarring present on the epicardium. And with RF, at the earliest sites, it would slow and terminate, but require deblation on the other side. And the question then becomes, and this really made me wonder, and Dr. Wilber certainly kind of pushed us in this direction, begin to consider imaging. In this instance, this was a sarcoid type of patient where you see this scarring that can be mid-myocardial and certainly not visible to an endocardial mapping approach. And it tends to be patchy. And MR certainly can correlate with VT-inducibility and non-ischemic cardiomyopathies. This is now old data from Salman Nazarian, who is an incredibly talented investigator now at Penn, looking at MR-inducibility. And basically, with scar distribution involving just sort of the mid-myocardium, in a sense, you have a higher instance of inducibility at the time of EP study. In infarct models, this is 48 patients with coronary disease referred for EP study. And infarct surface area was more predictive than ejection fraction for inducibility. And in follow-up to that, Andrew Yan and the Brigham Group imaging group, when I was still a fellow, looked at scar heterogeneity as a marker of induction. And what they basically looked at was the grayscale of the late enhancement and divided into a standard distribution with gray zone, which is the area of the standard deviation cutoff of 10 to 28. The core was greater than 28, and the gray plus core is any area greater than 10. So this was dense scar, basically, and kind of less dense scar, if you will. And the question was, if that ratio shifts to less dense scar, are they more arithmogenic? And indeed, they found that with peri-infarct scar greater than or equal to the median distribution, these people tend to have more inducibility. They have more arithmogenesis. So the idea that getting back to that heterogeneity, that very first slide I showed, showing a scar that was heterogeneous with collagen and myocytes distributed, when there's enough heterogeneity in that scar that we can image, they have a higher propensity for developing BT. They're more prone to BT. This is a patient that drives home this point, where ejection and the limitations of ejection fraction for predicting inducibility. This is a 64-year-old man with inferior MI, lots of non-sustained BT. Normal ejection fraction had this inferior MI visible on an MR, had peri-infarct scar volume of 27%, and died a sudden death outside a hospital 11 months before it's infarct. Did not have a defibrillator. So in follow-up to that, an EP group then looked at MR heterogeneity, tissue heterogeneity in scar, and wondered about predicting scar channels. This is a patient with an entry of septal MI and BT. And this is a patient with an entry of septal MI without BT. And the blue represents areas of some heterogeneity. And there's basically more of it in the patient with BT. And they then went on to look at, and this is difficult. I think one of the questions is the applicability of these approaches with MR in the general population. And I think the overarching goal of all of us who ablate BT in centers like MUSC, in Northwestern, in Chicago, is to make these procedures more accessible, not less accessible. And with MR, though this is very beautiful work, it's pretty difficult to do. And so it opens the question of whether or not CT imaging could be more helpful. We'll talk about that in a minute. But I want to drive home this point. This is a mitral annulus, dense scar here. And you see this little bridge here. And could this be a site for BT erythrogenesis? Can it predict a medicine site? This is a patient without BT. And you see basically more confluent red areas than these interrupted red areas that may indicate a lack of a channel. And indeed, this is a little area of scar. They've taken the voltage calipers way down from 0.2 to 0.21. And there's this little area of preserved voltage. And it correlates fairly nicely with a little bridge area. And they showed that, indeed, that area was consistent with an area of slow conduction, what looks like an entrance area, or not quite an entrance, but early area for activation. Why do we fail? This is a slide. I think most trainees who've come out of the Brigham have. This is a patient that Dr. Stevenson took care of when he was there, who underwent ablation and then ultimately transplantation. The heart was explanted. And this was a patient who continued to have BT. And these are the ablation lesions here. And there was presumably an area of reentry involving this sort of mid-myopartial scar here. So can imaging be helpful? This is a patient that was sent to me with recurrent slow BT after two prior ablations, had a remote inferior wall MI, a remote bypass operation, so couldn't go up a cardiole, at least not easily. And the backside of the heart is very difficult to use surgically. There is no inclusion of the right corner in a vein graft to a right TDA. This is, oops, oops, there it is. This is our BT. It's very, very slow, right around 600 milliseconds with this kind of left bundle, unusual axis that we presumed was inferior, coming from some area near the septum. We saw with our CS activation, you had this AV dissociation here. And here's our RV catheter. The RV catheter was sitting kind of mid-septum and isn't exactly early. But then you see this signal kind of along the mitral annulus, which was intriguing to us. And the proximal CS almost looked like it was mid-diastolic. And the question was, could imaging be helpful here? We didn't have imaging at this point. We ablated like everybody else had done from the inferior wall in this dense scar area, and slowed and terminated BT almost immediately. We felt great about ourselves, but we wondered what the big deal was. The prior group had ablated and terminated BT there. So we didn't feel too good about it because we induced BT again. And we went then down to the coronary sinus, into the coronary sinus, because we'd seen those very intriguing signals on this decant catheter. We went down here to the MCV and found this wonderful signal that was about 114 milliseconds pre-QRS and trained, sorry, this is a lousy entrainment. It's a good entrainment, but a lousy slide because it's hard to project the best I could do. But basically, we had a concealed entrainment with a stim to QRS that equaled the electrogram to QRS, and it was spot on. And we came on RF and slowed and terminated it almost immediately from that location. But I would have loved to have seen this anatomy sooner. And the question for me was whether or not imaging could have guided us to this position before messing around over here in the left ventricle, which had been tried and failed twice before. So this brings us to this InHART. And I know there's some other emerging technologies, but InHART is a group out of Bordeaux. This is Pierre Chez and Hubert Cochet and the music consortium of which we and I know Lucia Tedra and several other groups in the US are a part. And it provides some scar imaging beforehand, including all the chambers, the epicardium, the coronary sinus, which would have been relevant in the last case, the location of the phrenic nerve, which I'll show in a few slides in another case and how that was helpful to us. The music consortium includes many centers. We actually started at my first exposure to this was at the very tail end of my time at Loyola, thanks to Dr. Wilber. I know the Penn Group is working on it. And Dr. Santansali and I are talking about one project with that. And there is a lot of collaboration here. These slides are compliments of Pierre Chez and Hubert Cochet. So I've left the lyric stamp up there. But what they basically asked is, what do we need to do these procedures safely? Can imaging be helpful? I know there's some debate about this. I had a really nice discussion with one of my heroes, Dr. Callens at Penn, who was sort of less, he's much more of a skeptic given issues of registration. But I think we can learn something, maybe. So accurate anatomy of the cardiac chambers is, of course, necessary. We need anatomical landmarks for optimal registration. So can we take the CT image and can we merge it with our 3D mapping system and perform an ablation where there's high spatial fidelity between the data on the CT and the data from the mapping system in real time? Can we identify structures at risk during epicardial ablation, primarily the coronary arteries and the phrenic nerve? Can we then localize the structural substrate? So we know where the scar is, but can we find the target-rich areas of scar? Can we become more like SEAL Team 6 rather than white infantry invading a scar and just pounding everything to oblivion and shock and awe? Can we identify structural substrate heterogeneity? And the software is pretty sophisticated. It builds all this entire model. They do it very quickly. Sometimes we have sent cases in the morning or an afternoon case, and they'll have the model back in two to three hours. And it's really rather remarkable. The anatomy always comes back with the left atrium and the aorta, the LV endocardium, the LV epicardium, the RV endocardium, coronary sinus. They identify thrombus on multiple occasions. I've actually gotten notification from the group in Bordeaux that my patient, heading for VT ablation later in the day, has a thrombus that was missed on an echo. And it's before even I get a read from our radiology group here. And we've, on numerous occasions, probably once a month, we'll pull a patient off or cancel the procedure based on the identification of that thrombus. So this is the model that is built. And you get this anatomy that you can then integrate with the mapping system. It's helpful to place catheters and venous structures. That's often our workflow, is to use coronary veins. And we can create a pretty dense map. You get more branches, all the better, because it makes for easier registrations. And that's relevant for avoiding coronary injury, particularly in epicardial procedures in the front nerve. And so here's your great cardiac vein extending out to the EID. And a catheter there can certainly help guide our registration and avoid injuring large diagonal vessels or obtuse marginal vessels in particular, or the front nerve you see there. In RV ventricular disease, we did an ARVD just last week. And the CT was actually not available, which was frustrating. It had been done, but was not available just due to some informatics issues on our end. We did it the traditional way. But I sure missed it, because it's nice to be able to see the RV marginal branches coming off this right coronary artery here, which runs along the AV groove and the tricuspid valve and sends those branches out. Visualizing fat can be helpful. Here's some scar there. And then visualizing the substrate. And what I like about CT compared to MR, and we're lucky here at MUSC, the radiology group here actually came from Brigham and had a lot to do with developing late iodine enhancements. And it's really given nice images. And what I like about it is it's more easily reproducible and more accessible than MR is, at least in our center and probably in most centers. And gives us thinner cuts. So we have more spatial resolution with a CT compared to an MR, where you get more of a stair casing artifact, as you begin to stack thicker cuts of myocardium. And so from the CT, you get wall thinning and hypotenuation and calcification that can be indicative of arythmogenic substrates. From MRI, you get just the late gadolinium enhancement with the orange and yellow areas indicating dense and less dense scar. And the MRI with the late enhancements, again, looking at the signal intensity, gives us that sense of scarring. But this is not easily done. And certainly, in a research protocol, it looks great. But in the real world, it's much more challenging. And so I think the multi-parametric imaging available from CT is particularly helpful. You can see the wall thinning. You can see fat and calcification. And it correlates very nicely with late iodine enhancement that is similar to what we use as late gadolinium enhancement in MRI. And we're now at a point where we don't just get late iodine enhancement. We get dense scar and less dense scar. The same concept of late gadolinium enhancement, we see this distribution of signal intensity. The group in Bordeaux is now able to provide the same information to us. And so from this, we get the late iodine. We get the arterial phase with the wall thinning. And the wall thinning is, again, a surrogate for scar density. And it's very similar to what we would see on an MR. So this is the same part, SCAR-CT, MRI. And the scar looks very similar. And then you can look at the late iodine enhancement with dense and less dense scar and again the distribution looks very similar. So I have a lot of confidence in this and this is moving on to a case with substrate registration. This is a post-MIBT inferior wall MI. We're going to be doing a patient almost identical to this later today with this backside scar. Here's your wall thickness. Dark brown areas are less than one millimeter thick. See this little bridge here? This is in cell trouble and you can imagine there's perhaps a conduction channel through here. CT fat. This is often a predictor of a difficult ablation. I think Frank Bogan and Hubert Cochet had a nice paper describing this just very recently. CT iodine imaging showing dense scar in gray zone and often there's some discordance between wall thinning and late iodine and that can also be concerning and it's almost identical to MR. But the topology of the scar perhaps you get a better sense of at least an ischemic from this wall thickness. This is an index case substrate registration and ischemic with high density mapping. This is somebody who had an inferior wall MI, prior CABG, ejection fraction in the 40% range and certainly somebody that we think would benefit from ablation compared to amiodarone when the ejection fraction tends to be better. They had a VT arrest with secondary prevention ICD implants and then managed the SODA wall and after some discussion the perception was that amiodarone would not would not be a better option than an ablation. So we went forward with that. Again use this multipolar mapping approach with the grid catheter seeing these different potentials. Here's our inferior scar. I have a CS catheter up here. There's an atrial signal. ECG leads up on top. Barfield ventricular signals. Here's all of our grid signals and you see these very nice late signals and our setup in our lab is to look between and across every spline. So that's why you see all that data there and we're annotating the latest late. The way the system works is you can look you can set it up to look just down the splines or you can look between and across splines. This is what the scar looked like with what was called the non-wave. So we're looking just down the splines and we have some some dense scar here in this area of preserved voltage and we fuse it with the in-heart CT and we see this kind of this is three and five millimeter wall thickness. We see this little channel here and it makes us wonder is this an area of interest but we don't really see a bridge that easily. Maybe it's registration error. Certainly the map may not be complete and there are there's always issues. I'll be the first to say that contact is incredibly important and often very difficult with multipolar catheters. It's a point that I've had discussions with Dr. Callens and others at one point. If we look at the wave then where we're now looking at the highest voltage potential recorded between or across splines we see a bit of a different scar distribution now and it's this island of preserved voltage is perhaps a little bit bigger and maybe we're seeing a little bridge form there. We register more. We've actually taken now a larger map of that better contact and it's kind of taking points that are interpolated and pushing them out a little bit. So look it's a model. It's a simulated reality but we're beginning to see this channel perhaps emerge with the wave approach versus the non-wave approach. You can see our ablation lesions were fairly extensive. I don't love this as early days of our group using isochronal late activation mapping or ILAMP for short. It doesn't look as well annotated as Rod's very beautiful maps but I think it makes a point that the colors are just different. So late potentials are mapped in blue and green and where we see the colors begin to come together we think that's a slow conduction zone. Late is just late as Rod says. I love that phrase but the distribution of these lakes is somewhat different. I think there's more blue and purple certainly on the right than there is on the left and so the mapping software you know depending on how we annotate those signals will give us two very different maps. So again it leads me to this question of how can we use imaging to better identify areas of interest because it's really challenging. There's so many variables to consider with how we map it. The capitors we use, the density of mapping, how many points we take, which wave fronts. It's really challenging. There's only so many hours in the day and there's cases to do. So we need to make it easier and we're not there yet. I think I hope we generate a lot of discussion from this talk and certainly stimulate more research. So can we use imaging to discriminate substrates? And this is a patient from Florida, had lots of kids, had no familial history of Park disease, had cardiac arrest, went to the hospital with palpitations and was found in the EDT, had the normal workup for anybody with a wide complex tachycardia in any hospital where they get the calf and don't find coronary disease. They have an echo and it shows a big enlarged right ventricle but the LV looks fine. Has a dilated right ventricle on the MR with some wall motion abnormality. The LV is a little bit big but otherwise normal. Has this ECG. They got an ICD for secondary prevention. You see this very nice epsilon wave, these T wave inversions and certainly with the imaging and that ECG we think of ARBD. Not hard. Has this VT which is really an unusual left bundle morphology VT. So we think slam dunk. Why are we even talking about this guy in imaging? We know the diagnosis on clinical grounds. That's what the task force criteria exists for. So who cares? But you got this funny VT and we're always worried. I mean I always worry about RV VTs. I just don't always know and this was a point driven home to me by really my mentors, Dr. Tedrow and Dr. Stevenson, who really kind of struggled with this and published this really nice paper in 06 with Bruce Copeland showing scar-mediated RV origin tachycardias and look similar. This is an idiopathic VT. Those aren't hard. The RV is normal and you see all this pink normal voltage stuff but then you have ARBD and sarcoid and there's a lot of scar there and to me at least I can't look at one and say that's ARBD and that's sarcoid. I would say it's an arrhythmogenic right ventricle and it could be genetic. It could be inflammatory. I just don't know. And then there's a repair test. That's easy because although I guess they could have sarcoid, they certainly have a surgical history that we're going to know about. But there's certainly a lot of different ways to slice and dice the right ventricle and can we use imaging to better discern the arrhythmogenic potentials or the arrhythmogenic areas. And so this is the ablation. This is very similar to where we ablated the gentleman with ARBD last week. Kind of here on this lateral tricuspid valve. Some dense scar here. This is always a difficult area to get contact in. This is the back side of the tricuspid valve ablated there. Went great. Feels good. Everybody high fives and says okay we're done. Not inducible. So what next? Do we discharge on antiarrhythmics? Is there any further evaluation of the cardiomyopathy? And again I think there's these lingering questions. Do we genetically test? We looked at the family history and there's nobody with arrhythmogenic cardiomyopathy. However, a family member who has sarcoid and there are down here in South Carolina here in the sarcoid belt we have not identified a genetic susceptibility gene or locus. But gosh there can be familial clusters. And so maybe and certainly there is a prior description again by Bill Stevenson and Bruce Copeland of sarcoid mimics of ARBD. This is work done at the Brigham when I was a first year cardiology fellow. A 33 year old guy who had ARBD and intractable arrhythmias ultimately underwent transplant. And it wasn't until after the heart was transplanted that they said oh my gosh there's granulomas here. This isn't ARBD at all. But that map sure looks you know pretty impressive. And sarcoid VTs certainly can look like any other VT from an arrhythmogenic right ventricle. These weird left bundle VTs. And I think most of the EP crowd understands this. And so you know we got a more advanced imaging here. Not a CTRNMR this time. This is a PET scan. But I'll show you in a minute a CT that was useful to detect sarcoid. This is PET imaging and it shows perfusion imaging up on top and FDG uptake on the bottom. You see this perfusion defect here on the septum and then you see this dark area down here on the mid to basal inferior septum with FDG uptake. And that's consistent with or suggested certainly a sarcoid. And in this case biopsy and voila here are these nice granulomatous findings consistent with sarcoid. And so we got lucky. But can we use better imaging to identify these people? I mean it's really hard. Sarcoid is really challenging. It can look like whatever it wants at least on MR. These are all patients with sarcoid and it can look transmural. There's this funny star here. There's this mid myocardial stuff. Here's some RV stuff and some basal inferior subepicardial stuff and then this sort of patchy stuff in the LV. But it can certainly mimic at least up here in patient A an ischemic patient. So what about CT imaging? This is a patient that was sent to me. He was post-CABG labeled an ischemic. His EF was in the 35 to 40 percent range. Had a known CERT territory infarct. Had been bypassed. It was kind of a weird bypass. It was a single vessel bypass with a main graft to an OM. But that's what they did. And had VT and we said okay. It's worrisome a little bit because sometimes those VTs along the mitral valve can be epicardial and could be challenging. We're going to image this guy beforehand. Get the board OCT and we do see some wall thinning here in the basal lateral LV. But what we also found was some late iodine enhancement here in the basal septum. I said oh that's interesting. That's very strange. But we had not seen the actual VT. We take him to the lab and we induce VT from the LV summit area. Right in this area up here of the LV ostium. I thought that's very strange. But not so strange because there's late enhancement there. So maybe this isn't ischemic at all. The guy has coronary disease has been bypassed. So that has nothing to do with the disease. And so we petted him in the hospital after the VT ablation. Sent it off to the Bordeaux guys. They said yeah look at this. There's this here's the FDG uptake that correlates very nicely with the wall thinning the late iodine. We thought wow that's really that's pretty cool. We put him on medical therapies. He's pulsed with steroids and started on methotrexate. He's come back now once. We had to ablate him again from up here and actually had to ablate via the epicardial coronary vein and with high power half normal staining. Thanks Will Sauer for the half normal trick. We ablated there and that took care of the problem. So here's another sarcoid patient now. The multi-parametric modality is interesting. This is the same patient but seemingly distinct substrates. This is somebody who had a biopsy confirmed sarcoid based on a endobronchial biopsy and had a positive PET scan. At this arterial phase imaging we had this kind of patchy wall thinning here and the anterior and lateral wall. Here's your front nerve portion down here. You always see this wall thinning up by the mitral valve. It doesn't always mean anything. You just see wall thinning there for a variety of reasons. I think there's a twitter thread that Will Sauer posted I don't know like two years ago about why that may happen. Then you see this delayed iodine enhancement here that is certainly showing a more dense scar than what you're seeing just from the wall thinning alone. We took the patient to the lab. The patient had been ablated elsewhere. We find this endocardial scar or I'm sorry complete lack of endocardial. Here's our endocardial voltage map. Those orange we draw our scar on ice. That orange line represents what I thought represented the scar area on the endocardium on cardosound. We drew that area just to mark it for ourselves because we knew we were going to go up the cardio. We did and we found this VT. I don't love this what do they call this map from Cardo. I don't use it very often but it's you sort of see this area of slow conduction through here and you see this right here right on top of that patchy area that kind of correlates with the wall thinning we saw on the arterial phase. We were concerned though because the phrenic of course this is our decanav sitting right underneath that. The registration by our Cardo cast it was fantastic. We have a very talented Cardo team here. The fusion was excellent and I could not ablate here without damaging the phrenic. We did insufflate the area. This is our patchy scar here. Here's our activation. It's sort of focal through there. We insufflated the epicardium with about 300 cc of half normal saline. We did not have a balloon available. Unfortunately it worked. It doesn't always work to do it that way. The balloon is actually probably better at least in our experience. In this case we used a fluid. We pushed the phrenic out of the way. We ablated there and terminated the VT. The Bordeaux imaging really was relevant. Here you see the coronary vessels. We were right in this little gap here. We felt that we were safe. Imaging really can be helpful we think. I know these arrhythmogenic cardiomyopathies are challenging. There can be a lot of overlap at the histological level, at the clinical level, at the genetic level. We really hopefully can perhaps refine our use of imaging. I know Dr. Tedra and I have talked about looking at some of the genetic myopathies with our imaging databases. In conclusion, using imaging, can we use it to define substrates beforehand? Can we assess scar locations? I like it more and more to plan our attack. I think there will be more data emerging about this. Can we use it for risk stratification for VT, for predicting arrhythmogenesis? Certainly, the heterogeneity of scar by CT or MR can be a compelling way to at least predict arrhythmogenicity. Can we use it during ablation to enhance our definition of scar and anatomy and to navigate and avoid the coronaries and the phrenic? That's all I have. Thanks very much for your attention. It's really been an honor and a chance. Really, the whole group in Chicago really got this going as a local set of discussions amongst the really amazing EP groups in Chicago and making it now, I think, a global phenomenon. Thanks to you, especially a special shout out to Michant for really making this happen and coordinating all of this. Thank you very much. This is close to my home. You're welcome to visit anytime. Fellows who want to come down and work with us, please come. Thanks so much. All right. Thanks, Jeff. A few questions that have come through. It looks like you're, are you routinely using the music software or is that just part of a research protocol? Is that your standard workflow at this point? We do have an IRB for it. We have a research database, both a retrospective and now prospective database. We use it in most instances. We don't use it all the time. We are using our own independent funding to cover it because it's not commercially available right now, though I think they're exploring that. I know the centers that are participating in this are independently funded to participate. It had been covered, I know, for a while by a grant from the French government to the Bordeaux team at Lyric, but now we're using our own funding. I'm not actually sure where the status. I know I've been hearing some rumors of getting FDA approval for this, but I want to be very clear. It's completely off-label. There's no service available yet, but we certainly hope. I have no financial interest to state that, by the way. I want to be very clear about that, too, so thanks. Yeah, Paul's eye just chatted or texted me saying that music is going to go commercial for whatever that's worth. I guess the other questions are related to, you know, if you don't have access to that software at this point, what would you consider your essential pre and interprocedural imaging tests that should be had in every case? Well, echo first, right? You know, an echo is easily available. Almost every patient has one, and it's also a safety issue. Patients that are sent to us for BT ablation, particularly ischemics or those with really very severe TCM, I'm always concerned about thrombus, and so a contrast echo is certainly helpful, and it also allows you to see wall motion abnormalities that, you know, at least points you in the direction of where you might want to go to target your mapping. I know when we create these three-dimensional electroanatomic maps with whatever mapping system we use, it doesn't really matter. You know, we want to create, I mean, at least me, I like to see the whole chamber just because it's really hard for me to navigate unless I see the whole chamber, and it's just easier for me to get a three-dimensional sense from that. It doesn't mean you map it with the same intensity in all areas. It just means that you can refine, you know, with some better assessment of scar location, then you can really target your fine mapping, if you will, to those areas, and so echo first. If you can get a CT, you know, the late iodine enhancement is really a special protocol. I'm happy to put people in touch with our group here. I know that Brigham does it extremely well, too. Amongst, at least as of last year, I was visiting Bordeaux, and I was told by Hubert Cochet that only about three centers in the world, at least at that time, were really doing high-quality late iodine enhancement. Our group was one of them, and that's really radiology-driven. That's not something that an EP can drive, but there's ways of doing that, and again, I'm happy to facilitate discussions. I suspect Dr. Tedrow would do that, and I know the Michigan group does it well, in addition. MRI, you know, look, I mean, it's hard to get MRIs, you know, in patients that are sick VT patients transferred in, you know, in a timely fashion before VT ablation. It's generally a challenge, and our MR quality is so-so. We have not done a great job with the lead and can artifacts that can alter your ability to perform fine imaging of scar, and, you know, the other issue is just one of staircaseing. You have thicker slices of myocardium with MR compared to CT, so when you try to integrate an image that's already somewhat adulterated by the artifacts from the can and the lead, it just becomes a more difficult registration. That's just our experience, though. And then, I guess, along those lines, there's a question about using ice routinely in every VT case, and do you use the images that you get from ice to help guide your mapping? We do, so we do, and actually Mike Field and I just wrote a paper about ice imaging and VT ablation, and we use ice for every VT for a variety of reasons. We use it for transeptal. If we go transeptal, we use it to visualize catheter location. We use it to visualize ablation, lesion formation. We use it to visualize endocavitary structures like the papillary muscles, and we use it to identify scar, and you can see, you know, areas of increased echogenicity. I sent a picture of a difficult VT using this an inferior schemic with a pap muscle. The Penn Group published a very nice paper showing the sort of pap concealment, if you will, of critical elements of VT and those interior scars recently, and I sent a picture of one to Dave Callens, who wrote that paper, and it's really, I mean, you can sometimes see these little areas. It's just where you just can't go, and so ice, I think, is indispensable for visualizing those scars. Absolutely. Sorry, so there's one that just came through here. So a patient with a normal EF with VT. I guess, would you recommend performing cardiac MR or some other advanced imaging, as opposed to just labeling it idiopathic VT? I'm always suspicious. I mean, I think, yeah, there was a paper a few years back by, I think it was Antonio Corrado, is from one of the biggest science centers, looking at patients with ostensibly normal hearts and finding, I think these were an elite athletes in Italy, that there was actually a surprising, very small, but subset of folks that had these inflammatory myocarditis, these sort of lymphocytic myocarditis that affected the RV, and I do like to, if they're young enough, I'm always suspicious. One patient comes to mind. It was a woman sent to me, who was actually a former professional tennis player in her early 30s, but a professional tennis player, who was at that point, I think, a professional at a club somewhere down here in the Southeast, and developed a rapid tachycardia, didn't faint. She was an incredibly fit woman, and her heart rate was about 220 beats per minute. EMS came, they got a wonderful 12-lead ECG of it in the field, transported her, they shot her en route. I'm not sure why. She was stable, but it looked like just a classic RVO TBT. They took her to the lab at this other center, and they failed in ablation. They sent her to us for possibly an epicardial dull. We took her for imaging, and she had low immunity. She actually had ARVD. She had been undiagnosed, and there's no family history. We did pat her too. I showed that overlap, so we did pat that patient as well. I do utilize MR in many instances, probably more than I don't. Probably, I would say, 70-80% of the time. The guidelines for that are, if the ARVD is enlarged on an echo, I'll do it. If the ECG shows any abnormalities, repolarization abnormalities in particular, I'll do it. If there's any evidence of a conduction delay, I'll do it. Those are the usual guidelines I use for ARVD. Okay, great. If there are any other questions or comments, people can unmute themselves. Otherwise, as Jeff said, there's only limited hours and lots of cases to do. I have a real quick question, Jeff. This is Brad. Hey, Brad. You've talked a lot about MR and CT, and I saw a case report the other day of a patient getting an ablation of an accessory pathway, and they merged the 3D echo with the cardo map. Have you ever seen 3D echo used as imaging for BT or others? I haven't. I've wondered about it, but I have not seen it done. That sounds really interesting. One of the questions is, what kind of software is out there? I'm sure there are people working on this, but using IAC, you can imagine a sweep of a chamber. It's difficult and eventual, but sweeping the chamber and creating through some AI algorithm, you get the endocardial surface, the epicardial surface, and then everything in between. The software can identify based on signal intensity areas of scar. That would be really an interesting approach. I have not seen it, but I can imagine it coming in the next few years. I'm not sure who's really leading the charge in ice research. I don't know. Berman, maybe? I don't know. That's really cool.

imaging

ventricular tachycardia

ablation procedures

substrate for VT

mapping VT

electrophysiological vulnerability

high-density mapping

scar detection

inheart software