Dr. Div Patel discusses patient selection, mapping strategies and why VT remains a lethal condition even with ICDs and antiarrhythmics.
So thank you guys um for coming grand rounds. Um, hope everyone had a good New Year. The title of my talk is uh Behind ICD Shocks and Drugs, Modern Approaches to VT Ablation. So as we know in the past, ventricular tachycardia or arrhythmias from the bottom chamber were hard to manage, and I'll go over different approaches and how we manage, uh, VT in the modern era. So these are my disclosures. I provide consulting for Johnson and Johnson MedTech. So, to give you an outline of my talk, I'm gonna first talk about why VT remains lethal even with ICDs and anti-arrhythmics. I'll go over a little bit about patient selection, which becomes important and who we bring to the lab, especially the, as these patients are much sicker than our AFib or SVT population. We'll go over mapping strategies and how they've evolved over time. And then we'll go over ablation tools, and I'll talk about some Centera cases that I've participated in with the lab here and talk about the outcomes and what we saw from learning from those cases. And then we'll go over some future directions. So, why does VT matter even with ICDs? So, you can see on the left is the SCUDHE trial, which really defined electrophysiology and ICD therapy as a role, um, over amiodarone and placebo. So, you could see from the left chart that amiodarone and placebo ICDs decrease the rate of death and sudden cardiac death in patients with heart failure, but with an EF less than 35% who are on GDMT. And so ICDs have really improved outcomes. They've saved countless patients. But what we've learned from SCUDH trial is about 15% of those patients will go on to receive shocks. And back in the day when algorithms were not as good, they received shocks for inappropriate SVT, but a lot of patients also received shocks for VT. The average annual rate of ICD shocks that SCUDHP found was 5.1%. So when you advise patients who get ICDs, this is like having an insurance policy, this may save your life. A lot of those patients, 5% per year, if they go on to live 10 to 20 years, they will go on to experience a shock and multiple shocks in some cases. So we know that shocks are not behind. So Jeannie Poole, who was originally, um, she's out of University of Washington, she does a lot of quality of life analysis. From the SCUDHE trial, what we found was patients with both appropriate and inappropriate shocks had a shorter lifespan, so they did worse. So, if you look at the hazard ratios, they, they're well over on the right side of one, indicating those patients with more than one shock, whether it's appropriate or inappropriate, do poorly. They have a high rate of mortality. They have a high rate of worsening outcomes, um, and morbidity as well. And on the left, we program ATP to prevent shots. So ATP is anti-tachycardia pacing, where if a patient has a ventricular tachycardia, the ICD will Try to pace terminate the VT by getting into the circuit. We know that ATP also is not benign. So you can see from the appraised ATP trial that shock only versus ATP plus shock, ATP plus shock increased the episodes of VT storm and VF. And so, the therapies we put in devices are not benign, and we need better therapies to treat VT. And so this is where catheter ablation comes into play. Um, this is a paper that I helped, uh, published when I was a resident at Duke where we looked at meta-analysis comparing VT ablation compared to anti-arrhythmic drugs, and we found the rate of recurrent VT was lower with catheter ablation compared to non-ablative strategies. But there were only 2. Randomized trials at that point vanished one and a smashed VT which showed a benefit of VT ablation over anti-arrhythmics. That has evolved now with the coming out of the trial of vanished 2 trials. So this was just published in 2025 in the New England Journal, where they compared anti-arrhythmic drugs or catheter ablation for VT. And they randomized 416 patients with a median follow-up of 4.3 years. And you can see from the right, their primary endpoint was shocks, uh, mortality, um, and death from other causes. And you could see the combined endpoint catheter ablation did more favorably against drugs. And so the thinking has evolved from Should we save VT ablation for the sickest of sick patients, or should we move it up to more of a first-line therapy just like AFib ablation is? This is a trial called the preventative VT trial. So this comes out of Europe, and what's interesting about this trial is they said, OK, in patients who have scar, looking at MRI and who have a large burden of scar, who need an ICD for primary prevention and they have a CTO on cath, let's randomize those patients after we find out on MRI they have significant scar to either just an ICD on the bottom, 30 patients, or a VT ablation. And then put in an ICD. And what they found from the primary endpoint, as you can see from this graph on the right. Is that the patients who underwent VT ablation and ICD implantation did better than those patients who just underwent ICD implantation. The caveat is the major adverse event related to VT ablation was pretty high at 7%. Um, this is mainly because of vascular issues in Europe. They don't use ultrasound and their ways of taking patients to the lab are very different than our methods. And so what you could say is VT ablation has evolved from mostly refractory to amiodarone, sotalol, multiple anti-arrhythmics to more of if we see a large burden of scar and we can make the procedure safer and shorter, can we do it before we even put in an ICD and that's how our thinking has sort of evolved over time. However, patient selection is very important, right? I bring this graph up, uh, because it's a multidisciplinary approach to how do you select patients for VT ablation versus transplant. A lot of these patients are very sick. They have VT storm. They have multiple episodes of VT, um, leading to shocks. They've failed meds. They're failed amiodarone. Some of them are not even on guideline-directed medical therapy. They're on midodrine. A lot of them have low EFs, they have severe heart failure, biventricular failure, they have end-stage cardiomyopathy. So you're basically on a seesaw weighing, should we go for transplant or should we go for VT ablation. Um, it's important to get right heart cath numbers before taking a patient to the lab because with anesthesia, they may get more cardio depressive effects and they may get worse. Um, before they get better from the VT ablation. So, it requires careful communication with our heart failure colleagues, uh, with our other cardiology colleagues, with our surgical colleagues. What is the out? Is an Impella an out, an ECMO an out? Uh, can we crash onto ECMMO and get the patient listed for transplant if they don't do well with VT ablation? Some of them are prohibitive risk for transplant, and if they have no out, VT ablation is the only out, and If they don't do well, there's no big benefit. Uh, the other thing is the high surgical risk and are they a poor candidate for both, both transplant and VT ablation. And then you have to be serious with the patient and say, your better approach for this is a palliative type of approach, um, which is the right thing to do for the patient. So these are some of the difficult decisions that we weigh before they even come into the lab. So what are the current indications, um, for VT ablation? So right now, I would argue ischemic substrate modification of refractory VT on IV therapy. So if you have a patient who comes in with an infarct and they're on amiodarone, lidocaine, or you're trying to wean stuff off, and you can't get them weaned off and. They're a good candidate otherwise for an ablation, I would argue that doing substrate modification before you put in an ICD or if they have an ICD doing a substrate modification could help that patient. Multiple ICD shocks, intolerant or refractory anti-arrhythmics. So, um, it could be two antiarrhythmics. The ones we choose usually are myxillaine and amiodarone. Sotalol can be used. It's not as effective as amiodarone. But a lot of patients are coming in with younger MI's and so we don't want to keep them long term on amiodarone, because we know the amiodarone toxicities of the thyroid, pulmonary toxicity, and the eye stuff, especially in younger patients who builds over time, um, could be adverse. And then VT storm, if stable, if you've tried IV anti-arrhythmics and they're still storming, and you think they're a good candidate for the lab, I, I would argue those patients need VT ablation as well. There's been no studies currently that VT ablation improves mortality. It's more about improving morbidity of ICD shocks and failure of anti-arrhythmics. So, in the planning stages, and this is where advanced imaging comes into play, uh, we usually get MRI's on patients or CT scans, um, and I'm thankful for the service line and the heart hospital for working on getting this in-heart technology, which can basically tell us the coronary anatomy can give us different substrates before we even bring patients to the lab. Because a lot of these procedures we're trying to make safer by making them shorter. So, this in-heart study can quickly localize the scar and image lay with our mapping systems and tell us where coronary arteries are, and they did a randomized trial which showed that using this technology with imaging pre-VT ablation reduced procedure time and cost and improved VT freedom rate because it can quickly identify circuits. Um, in the heart before we even bring him to the lab. So the next part, um, I'm gonna talk about mapping strategies we use in the lab, um, about to try to get rid of BT. So the first strategy we try to use, and this is the gold standard, it's called activation mapping. So in activation mapping, basically we induce VT and we're trying to map where the VT is coming from. And so you can see here, this is the central common, um, this is the cartoon image that Josephson and uh Stevenson used, which shows that a VT circuit starts because you have scar in the middle. And so it spins around that scar. And what we're trying to localize is this central isthmus and exit site because terminating here will get rid of this VT because it's going spinning around and around. And so you can see here on the right with beautiful colors, we can see where the common isthmus is and we're going to try to burn there. The problem with activation mapping is we know from being in the lab that when we induce VT, all of a sudden the blood pressure is a map of 30, a map of 20. So you'll get two signals and the patient's hypotensive and they're not perfusing. Um, so the workarounds to that are either you need an Impella or you need some kind of high-risk support, or you try to come up with other strategies on how to localize VT without actually inducing VT. The other difficulty in activation mapping besides the hemodynamics is you may induce other VTs that may not be the clinical VT. So, By burst pacing the ventricle, you may induce another VT, you may induce a third VT, and all of a sudden, you're 4 VT circuits in, and you don't know how, where the common circuit is. So activation mapping, while good, poses a lot of challenges in the lab, and I'd say about 1 out of 20 VTs I do, I'm able to activation map the whole VT before the patient. Uh, and then I can burn it and get rid of the VT, but it's the rare case where we can do activation mapping. The other type of mapping we sometimes did in the past was entrainment mapping. So, what we do in entrainment mapping is basically pace the ventricle at a faster rate and see by how far, first we see if we have concealed or manifest fusion, which is basically, does the pace. Um, circuit looks similar to the VT circuit, and we see how close we are by measuring the return cycle length away from it. Uh, we used to do this a lot in the past, but now with hemodynamically unstable VTs, we don't do it as much as well. Um, but it's another strategy before mapping systems existed to find the central isthmus. Now we do more of island mapping. Um, and this uses the, what I IA mapping basically is isochronal late activation mapping. So what we do here is we don't know where the VT circuit is, we're not inducing VT, but we can pace the heart either with different pacing strategies using extra stimuli, and what we're trying to find is areas of slow conduction or deceleration using the latest activation. So usually in VT we're looking for the earliest activation, but in ILAM mapping, we're looking for late activation mapping, and you can see here we're looking for the latest signals after the QRS deflections to see where the central isthmus potentially could be. So here's a VT circuit where you could see the ILAN basically tried. It's a similar type of circuit compared to actually activation mapping. And you can see on the right, large dense area of scar, red means scar, purple means healthy voltage. You can see that this scar on the left, if we just did. Now, if we just did. Voltage mapping, we wouldn't know where the circuit is, but once we do isochronylate activation mapping and lower our threshold, we can see there's a circuit right in that scar in the purple there, and you could basically burn that area to prevent further VT through that channel. Another strategy we use is pace mapping, and this helps with more PVCs than VT, but pace mapping is someone in the ICU printed a 12 lead of the VT or you have a 12 lead of the VT and you pace different areas of the heart and you say, OK, how does this compare to the VT that I found? The problem with pace mapping is it suggests more of a focal mechanism, but VT we know mostly is re-entry, especially around scar, and so this works much better for PVCs. Doesn't work as well for VT. So you can see here uh in B is the VT EKG and you, you pace on C and you could see that it closely matches the exit site. So somewhere in that vicinity is your VT probably localization. The most other common mapping technique we use is scar mapping. So we do a voltage map in sinus rhythm or with RV pacing or CS pacing, and what we're trying to find is areas of border zone. So purple again is healthy scar or no scar, purple is healthy voltage, red is scar, and we're trying to ablate around the border zones of the scar. And healthy tissue because around those areas is likely where VT circuits are are starting from. And so we used to do this back in the day, we used to call it painting the heart because it's a tedious process, this can take hours, two bags of fluid. Um, you get tired, your hands hurt at the end because you're just, there's large areas of scar and our catheters are 4 millimeters. So in a large anterior infarct, this could take 2 to 3 hours just ablating point by point, um, and it's frustrating because you don't know actually where the circuit's originating from. So you've not identified the critical isthmus, you're just dehomogenizing the scar. And so this is where I'll go through techniques and how it's changed and how it's gotten faster and safer for patients. So, from mapping, we go into ablation because ablation is how we prevent further shocks. It's how we reduce morbidity. It's how we try to prevent mortality. You can see on the left is the current ablation catheter called an RF catheter. Um, there's two types, there's irrigated, non-irrigated, and you can see we, in the past, we basically used heat energy to cause a lesion, and that lesion develops over time. The problem with our RF catheters are their small surface area, and heat energy takes a while to heat up the tissue to cause edema and cause cell death. So it can take anywhere from 120 to 180 seconds of lesion time. And it's frustrating because we may not even penetrate transmural lesion, uh, that's required in VT. So in VT we look at the heart either using fluoroscopy or looking at mapping. We think of the heart as more of a 2D structure, but it's a 3D structure. And so the central isthmus might actually be more transmural, might be located under the endocardial surface. So, this is an RF catheter. Um, sometimes we use strategies like D5, which is changing our ionic current. So, the normal fluid we use is. Normal saline at 0.9, we can lower the current to 0.45 or half normal or use D5, which gets us a deeper lesion. We could use impedance modulation, change the impedance or change the power to get a deeper lesion. Needle-tipped electrode, um, they do this at, mostly at Vanderbilt and Penn, and at the Brigham, Usha Tidro does this where they use a needle-tipped electrode to get deeper into that transmural lesion. We've done this simultaneous unipolar ablation, and I'll go over a case, uh, where I've done that to get a deeper lesion because the circuit was probably originating in between the epicardium and the endocardium. Bipolar ablation, um, is when you change current from one side of the heart to the other and that gets a very deep lesion. We've done that with our structural heart colleagues. I'll talk about a cryoablation case where you freeze the tissue to get a deeper lesion. Uh, we haven't done any chemical ablations, but it's something to think about, um, with summit, um, type of PVCs or intramural septal substrate where you can get a coronary sinus branch and get deep into the septum, um, to cause an effective lesion. I'll go over some pulse field ablation cases. The advantage of pulse field ablation is it can get deeper. Um, tissue, less edema, and it can get a wider surface area. And then radiation therapy, uh, with all the rage and excitement in the past. And there's some centers, especially WSU doing that stuff, um, but that, the data is sort of mixed, and not many places except Penn and WashU are doing that. So here's a patient case. Uh, this is a 40 year old patient with a history of myocarditis who presented VT storm. He underwent ICD for secondary prevention, uh, and because he was younger, he was only 40, he was only put on Mxillatine and propranolol. And you can see from this VT circuit, it's an outflow VT 23 AVF or upright. And this is classic for what we call a summit VT. You see a right bundle branch pattern in V1, and then you get a pattern break in V2, meaning instead of positivity in the precordial leads, you get a negative V2 and then upright in V3, and it's negative in lead one. The problem with summit VT is it's deep inside the heart and it's hard to access epicardially. So you need a strategy for this patient because he's felt 6 ICD shocks. He's on Xanax now, he's failing 2 therapies. You could put him on amiodarone long term, but given he's only 40 years old, what's your exit strategy? And his ES 50%, so he's not a great candidate for transplant if you can avoid it. So we got an MRI which showed mid-myocardial and subepicardial scar in the basal anterior septum consistent at the anterior septal location right under the coronary cusp where we would expect a summit VT from, or to originate from. So for this patient, I think Doctor Hedley was on consults and we recommended Adagio to get deeper. It's a cryo catheter. I'll go over the results. Uh, Doctor Woolletz, the PI and I was a sub-investigator on the trial. So, we use the Adagio catheter to get a deeper lesion into that region. And you could see we dropped it retroaortically. And we were able to map in VT where the circuit was coming from, and you could see their scar, that red area on the right image is the scar, and you could see that in that scar is probably where his VT is originating from. And so we did a freeze there, and we were able to terminate his VT on the bottom. You could see he's an incessant VT and we come on and we freeze it and we terminate his VT. So successful case as part of the Fulcrum BT trial. And he's done well. Um, he's now getting PET imaging at Duke to figure out why he's having this stuff, um, and they're considering him workup for sarcoid, but he hasn't presented back in VT storm since the, since the trial. So, the acute results, uh, let me just go through what the Adagio catheter is. So, this is the Adagio catheter. It's a freeze thaw type of cryo catheter. And so, it uses a similar type of catheter to our 4 millimeter, but it's a bigger tip. So, instead of just a pen tip type of 4 millimeter lesion, you could burn or freeze in this case all along. Uh, the, the distal end of the catheter and it's about 15 millimeters, so you get a much. Much bigger lesion and it's a thicker lesion. So it's a deep titraritable lesion, and there's no apparent attenuation of lesion depth in areas of scar. So sometimes when we try to burn those areas, We worry that it won't get deep enough because the scar prevents the, the heat from transferring transmurally deeper. Uh, but in this freeze catheter, we've seen no issues. There's no irrigation, so you don't have to worry about fluid for our heart failure patients, and it seems to be safe. And so we, we've done 7 cases here between Doctor Wollet and myself, and this was presented as a late breaker at the VT symposium in Philadelphia, which is the big VT meeting. And using that catheter, they showed that it had a high acute procedural success. 97% of VTs were non-inducible at the end. Uh, the complication rates were two groin bleeds, um, in the case. So there will be more data in the follow-up as the trial finishes. Uh, but it's an exciting catheter with a new tool that we have available thanks to our research coordinators and staff at Centera. So this is another case. Um, It's a 7-year-old male with a history of non-ischemic LVEF of 30% CRTD who has undergone two endocardial VT ablations by my, uh, two of my partners in 2024. And because those non-ischemic, sometimes these patients are referred for sympathectomy. So a patient who had sympathectomy, had two VT ablations, who presents for further management. He's having more ICD shocks on amiodarone maxillatine. He's not a transplant candidate for Doctor Tusak because of his age and comorbidities. So, these are the options I talked about in my clinic um with this patient. I'm like, you've had 22 VT ablations. We could do a redo endocardial ablation. Um, but you've had two of them. We could do an epicardial ablation where we go outside on the heart, or we can decide on palliative or hospice type of options because you're failing our two strongest anti-arrhythmics, and you're getting too many shocks from your device and you're getting VT and he was not able to drive his car. He was getting dizzy. And so we came to a joint conclusion that I thought he was pretty healthy enough to undergo epicardial VT ablation. So, we decided jointly to try because non-ischemic, a lot of times the scars on the outside of the heart. So we like to think of it as mostly on the inside. In his case, it was on the outside, so we decided to go for epicardial VT ablation. So you could see this is the case of the epicardial VT ablation. You could see on the left is the fluoro image. Uh, the ablation catheter is epicardially, the octaray or mapping catheter is endocardially through a transeptal approach. You could see his CRTD device. Doctor Robertson was kind enough to do the cath, uh, to make sure we weren't in close proximity, and you could see on the right, we induced VT and you could see from that right image all the way on the right that most of the scar was located on the outside of the heart. Anteriorly, and so we saw areas of light activation. We were able to burn in VT. And terminate his VT and then we did some endocardial ablation as well just to shore it up. And so these are the follow-up results that the lab never gets to see on these patients. So this is a 3rd time VT ablation, now this time going epicardially. This patient in March, um, I did his case in April. In, in March when he presented multiple ICD shocks, you could see on the left ATP sequences, um, he was not doing well. And on the right, you could see his most recent follow-up in December, I just read his CRTD device, you could see ventricular high rate events, none on the right. So you've gone from. Treated VTs to now none because we offered him a third time ablation because he was not a candidate for transplant. I've lowered his amiodarone given he's in his mid-70s to 100 mg daily and put him on propranolol, which we think as EPs that propranolol is a better beta blocker because of its non-selective properties, and we have good data for that. So we've we've treated this patient, he's done well, and some of the stuff we do here, including epicardial VT ablation, is very favorable for patients. This is another guy. This is my own redo, so he's in his late 80s. Um, he has mixed cardiomyopathy. He has an LVF of 30%. He previously underwent endocardial VT ablation with me, uh, because there's a lot of non-ischemic myopathy, but he's frail. He's wheelchair-bound, he's CKD stage 3. He presents for options. He got shocked 4 times by his device. He's not doing well. So his options are hospice, take him to the lab for a redo, do an epicardial, same options as the last patient, and he's like, I really enjoy life. So he's a guy, he's with it, his brain's sharp, he enjoys going on walks, uh, with his caretaker. His caretaker wheels him around. He just, he's like, I want another shot even though my risk of death is high. I said, OK. But epicardial VT ablation in you is too high risk. I don't want to stick something outside if we perf a coronary, the surgeons are not going to be excited as we're getting epicardial access to come down to the lab and open him up and fix it. I said, we have this new technology called PFA. I think it gets deeper lesions, especially if we stack 4 lesions on top. I think this is the right choice in technology for you, and he was game for it. So we brought him down for redo VT ablation with me, and we did PFA in him to try to get a deeper lesion through his non-ischemic scar, which is usually located at the base of the heart. So you could see I induced VT. On the left, and you could see as I stack on that lesion, his VT terminates uh with ablation. And you could see on the right that these ablation lesions with PFA are much bigger, much deeper, and able to get through into the substrate of the heart. And this procedure only took me 2 hours because I knew where I was going, I knew how deep I had to get. We induced VT and we terminated with VT ablation. And this is his follow-up. So you can see on the left is his device before we did all this ablation. His VT was treated with 441 joule shocks. He's had multiple shocks, VT1, VT2, VT3, and you can see on the right, his most recent remote just two weeks ago in December, he's BV pacing 99% of the time. He has some PVCs but no ventricular high events. I've maintained him on 200 daily of amiodarone, just given he's in his late 80s, he's on mealitine, propranolol, he's doing well. He's not getting any morbidity from his ICD shock. So more of a non-ischemic substrate patient who I thought was too high risk for epicardial VT ablation, who I took for PF VT ablation, who's done well afterwards. So what is the data on PFA in the ventricle? This is a nice Atul Verma paper, um, where they looked at. Basically meat tissue, and they looked at how deep of lesions does PF get RF, which is our heat radiofrequency energy, which is what we classically use RF then PF or PF then RF. And you could see that PF alone doesn't get deep lesions, RF alone doesn't. But if you use the combination of two PFRF, you get a much deeper lesion. And that if you use RF and then PF, you also get a deep lesion. So you get a central zone of coagulopathy, you get a thermal necrosis and hemorrhagic zone, and you could see the biggest lesion on this. Is the PF than RF. It gets a wide lesion, it gets deep into that tissue, and so that might be the strategy that wins, um, for these deep transmural VTs that are deep inside the heart. And data, more and more data is coming out for VT and PFA. So this comes from Europe where they've now done hundreds of cases using Efera, which is our PFAN catheter in the ventricle. And you can see that the majority of patients do well. You could see on the right, acute success was anywhere from 80 to 90% depending on whether it was a redo, PVC or de novo. Um, and their complication rates were low, uh, but not insignificant of 5 to 6%, and mostly from groin complications. And sometimes with the affer catheter, people were using high wattage, 90 watts in the ventricle without uh titrating their temperatures, and so they were getting a lot of steam pops. Mostly, what we've used the affir catheter for is pulse field ablation in the ventricle, and we've seen good acute and long-term results. Were they stacking in that, or are they, uh, stacking they were stacking, yeah. So this is another case. It's a 50-year-old female um who presents to Centeria Harbor Hospital with VTSTORM with previous non-ischemic cardiomyopathy. And these are hard cases because they're non-ischemic, they're not substrate cases, myocarditis, LVF of 50%, multiple ICD therapies. She had two previous ablations, one in 2014 and another in Chesapeake in early 202025. And she was referred for a third VT ablation at Centerra Heart Hospital. Uh, the operator who referred her here wanted an Impella, uh, but the difficulty with Impela, as the EPs know, is the vasoplegia caused by the Impella and the morbidity caused by the Impella is not great. And with her EF being 50%, we thought she could tolerate a third VT ablation, um, without. Uh, without issue. So we decided to take to the lab, uh, we decided more on an endocardial and epicardial approach given it was a redo and non-ischemic substrate. And you could see, uh, my image on the left shows my ablation catheter epicardially outside the heart. Uh, the endocardial lesions are on the inside of the heart, and we ablated both from the outside and inside of the heart. And on top of the RF energy, on the inside of the heart, I applied pulse field energy, um, to prevent further VT. So we ablate it RF outside, RF inside, which are the red lesions, the blue lesions are the PF energy to get a deep transmural VT localization. And her follow-up is, she's not on amiodarone. He referring to talk to me cause she's 50. She's maintained only on monotherapy, myxillatine. She had some post-procedural pericarditis from our epicardial ablation. No further VT recording on device 4 month follow-up, and then I've referred back to Chesapeake for her follow-up to the EP that referred to us. So these patients seem to be doing better um after these kinds of approaches of attacking VT with PFA RF and even going epicardially. This is another patient, um. And now it gets into ischemic cardiomyopathy, so you'll see a lot of voltage being red, which is a lot of scar from coronary artery disease. She's a 70-year-old female who had an ischemic cardiomyopathy, LVF of 14%, so pretty sick. CT of RCA, previous VT ablation two weeks ago, who presents with recurrent VT. So, um, this was a patient who underwent a RFVT ablation, who comes to me with recurrent VT and I saw her at the CarePlex ER and I was like, listen, you're pretty stable in your VT. So you could see her VT's, um, coming from an inferior substrate. And she was, her hemodynamics were fine, even though her LVEF was 14%. It was a slow VT. So I thought, and she was already on amioxylatine. I said, I know your VT ablation was 2 weeks ago, but you need to go back to the lab. We need to ablate you again. So we took her back, um, after having her VT ablation done elsewhere, and we did extensive scar modification with RF being the red and blue being um the PF energy applied on top of the RF and you could see we did a ILA map where you could see areas of slow conduction through on the left, through that scar substrate. We knocked it all out. And she's, she's done well. We just did her three weeks ago and she's had no recurrent VT. So this is the last case. This is one we just did yesterday, uh, with the lab. It's an ischemic cardiomyopathy. It's a 70 year old male with late presenting anterior infarc to underwent implantation of impella and RVD. Um, and the surgeons were able to get the RVD out, who presents for VT ablation as they were having VT while on amiodarone and lidocaine, and they repositioned, Doctor Unger did the Impella multiple times and we were still inducing VT. And you could see more of it, it's an apical anterior septal substrate. And we decided, uh, because it was ischemic cardiomyopathy and the scar might have been fresh to just use PF energy to get done quickly with the case because the worst thing you could do in this case is introduce tons of fluid, introduce tons of anesthesia time because of the vasoplasia. So, here on the left, you could see the scar was extensive throughout that anterior wall. Um, we went through the apex, uh, found areas of fractionation and late activation just like an island map. The green dots are how big our catheter, uh, with the afferre catheter system applied PF energy to. And then you could see on the this image, you could see we're in VT and we come on with PF energy and the VT terminates nicely. So, again, VT you could see the rate's fast. The Impella kept it stable, so we didn't have to shock it. We did a quick activation map and grenade launched it away with PF energy. The nice part was this took, even with the Impella, even with the anesthesia, this took just as long as one of my partner's Afib ablation, and we were done probably in 2 hours. Um, so we were able to do a VT safely with an impella, not introduce tons of fluid, um, and terminate the VT and the patient's done well, not on any drips, and they just extubated him to BiPAP this morning. So conclusions, VT management is multidisciplinary endeavor. VT ablation can reduce ICD shocks and long-term effects of anti-arrhythmics. Uh, but it does require pre-procedure imaging, and that's where we need help from advanced imaging, um, and may require endocardial and epicardial approaches. Newer technologies will only increase the demand and efficacy of VT ablation going forward. And so I think we'll see more of these cases in the lab. We'll see more of these patients referred for VT ablation early on rather than when they're on death's door. So thanks to EP lab team, the anesthesia team, the heart failure cardiology and surgical teams, the ICU teams, referring physicians, all the lab staff, um, and the companies for developing better tools, but most of all for our patients for trusting us, for doing stuff that I think is cutting edge and. And moving forward, um, in the field of VT.
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