Thank you, Nishan, and thank you, Brad, for the invitation. Good morning, everybody. Essentially, I'm going to be discussing advanced techniques to treat ventricular arrhythmias from the LV summit and the interventricular septum. Essentially, I'm going to give you this presentation. I'm going to talk about why it's important to ablate these PVCs, what's the association between PVCs and cardiomyopathy, sudden cardiac death. I'm going to give you a little bit of physiopathology, and more importantly, I'm going to try to explain a little bit of cardiac anatomy related to the LV summit and how it's so important to be able to ablate these PVCs if you decide to use these advanced techniques. Once I discuss this, I'm going to explain each technique that has been published today. I'm going to be emphasizing on how you can do it at your own institution, the success rate of these techniques, and the problems that you might face when you're doing those approaches. These are my disclosures. I just want to start with this slide. Many people around the world, in many countries, consider that PVCs are a benign entity, and I completely disagree with this. First of all, because we all know that PVCs can cause tachycardia and dyscardia myopathy based on the PVC burden that the patient has. Many PVCs, particularly PVCs from the sinus of Valsalva or from the LV summit, they are being associated with an increase of sudden cardiac death. The mechanisms of PVC-induced cardiomyopathy are very similar to the mechanisms of tachycardia-induced cardiomyopathy. However, the main aggravating factor is every time you have a PVC, you're creating dyssynchrony, ventricular dyssynchrony, and that's going to exacerbate the cardiomyopathy. We know that the natural history and physiopathology of the PVC-induced cardiomyopathy is time-dependent and highly predictable. So as we see here, in the first week, in the first two weeks, we're going to have a remodeling the extracellular matrix, and in more advanced, in two or three weeks of a bigeminy or trigeminy models, you're going to have a cellular dysfunction with severe damage to the calcium ATPase and the L-type calcium channels. However, even though you damage the ventricle and there's extracellular and cellular remodeling, once you remove the insulin, in this case the PVC, you can, most of the PVC cardiomyopathies are reversible. So here, this is an immunohistochemical preparation with polyclonal antibodies, and you can see, this is the control and this is the PVC model, and you can see that the sodium-potassium ATPase activity is completely depleted in this myocardium. This is an electromicrography, and you can see that the collagen here is the control, here is the experimental subject, animal. So you can see that when you have PVC in this cardiomyopathy, all your collagen, struts, and fibers are diminished or even absent in these models. So this was the first paper, the animal model, in which they proved that by causing bigeminy or trigeminy, you time-dependently, you develop PVC-induced cardiomyopathy. So in two weeks of bigeminy, this was a swine model, you're going to have a significant reduction in your left ventricular ejection fraction, and also it's reversible. Once you stop the pacing, your ejection fraction is going to get better. And the good news is like, once we get rid of the PVC, this is a hematoxylin-eosin preparation, you see the mitochondrial content is essentially the same in controls and people who have had PVC-induced cardiomyopathy, and this is mason-trichrome staining, and you're going to, you have the same amount of collagen between PVC and controls, a little bit less, but not dramatically diminished. This is the famous paper that we all know, the famous number to cause PVC-induced cardiomyopathy is 24%. However, you can see here that even with 8%, 10% of PVCs, your ejection fraction can dramatically decrease. Another important factor is the PVC coupling interval dispersion, okay? So if your coupling interval dispersion is more than 99 milliseconds, meaning that the PVC comes at different times, you're, that's a very good predictor that you're going to have LV dysfunction. And this is the paper with, from Jason Bradfield and Chief Kumar at UCLA. They find that also this PVC interval dispersion, if it's more than 60 milliseconds, if it's more than 60 milliseconds, it's going to be a side effect. So most of these pieces with high variability, they're going to be originating from the sinus of valsalva or great cardiac vein. And if it's less, they have other origins, okay? But more importantly, they found this number, okay? So if you have high PVC interval dispersion, more than 60 milliseconds, you're more likely to have a cardiac event. And cardiac event was defined by sustained monomorphic ventricular tachycardia, syncopal episodes or survivals of cardiac events, okay? Cardiac arrest, sorry. This is the paper published by Sam Asilvathan and Michael Ackerman in Mayo Clinic, when they first described this malignant syndrome when you have PVCs from the papillary muscle or outflow tract, and they have also by leaflet mitral valve prolapse syndrome. So you know that these patients have a high risk of sudden cardiac death. They have high level of ventricular bigemini, non-sustainability, and they have multiple forms of PVCs. Also the UPenn group published that even when you think that you have an idiopathic PVC, you should do a cardiac MRI, why? Because if you have delayed enhancement, even in a PVC in this cardiomyopathy, at 12 years, the mortality is 20%. So it's not as benign as we used to think it was the PVC in this cardiomyopathy or just having PVCs. So the UCSF group recently published the ABCBT risk score, and they included these four parameters to risk stratified patients. So they use the superior axis, the PVC burden 10 to 20% or more than 20%, and based on that, you're going to get points for the score, coupling interval more than 500 milliseconds. And of course, if you have ventricular tachycardia, that gives you four points. And based on the score, your likelihood of having a bad outcome is significantly increased. So I think this score is great. Everybody's using it. We have the opportunity with Luigi to write an editorial. However, even though the score is very good, the score is missing very important points that I just mentioned. So the score doesn't include the coupling interval, variation of dispersion. If it's more than 99, it's going to predict a left ventricular dysfunction. If it's more than 60, most likely you're going to have cardiac events. The PVC location, as you know, is sinus of valsalva and great cardiac vein PVCs. They have a high PVC coupling interval dispersion, and that's going to also, I mean, it's pretty much the same. If you have a PVC from this location, you're going to have a high PVC coupling interval variation. Also, if the patient, whether or not the patient has bilated mitral valve prolapse, that's going to be a major risk factor to have a cardiac arrest. And of course, if the patient have delayed enhancement in the cardiac MRI. So it's something to keep in mind. So once you decide to go for LV-SOMED PVCs, of course, you need to have some basics of, you know, how to localize PVCs. I know that there have been many lectures about this in this series, but for the fellows or for the early career attendees, you really need to know, once you know that the patient has a, you know, tall airways in the inferior lids and it's an outflow tract PVC, then you look at the transition of the PVC. Most of these PVCs are going to have transition in vitreous. So you don't know if it's, we know that if it's late transition, it's RVOT, if it's early transition, it's LVOT. But most of the time, these patients have transition in vitreous. So what to do? Then you look at the, I mean, there are many criterias, but the criteria that I usually use and is very helpful for me is something that was published essentially two decades ago. You look at the airway in V1 or V2, and if this airway is 50% of the amplitude of the QRS, that suggests LV ventricular origin, or if the RV amplitude, airway amplitude is more than 30%, that's going to suggest also LVOT origin, okay? So once we know that it's LVOT, then we come to this one. So you need to know when a PVC might be epicardial in origin, okay? So we have the maximum deflection in this, if it's more than 55%, that's going to give you almost 90% chance that the PVC is coming from the epicardial or LV somet. However, you have to understand that these criteria only works if you have non-structural heart disease and you're not on antiarrhythmic, particularly amiodarone, okay? So here we have other criteria for epicardial PVC, it's going to give you, it's going to suggest epicardial origin, the maximum deflection in this that we already mentioned, and the intrinsic co-deflection time, if it's more than 85 milliseconds, that's going to suggest epicardial also. So here we have a paper, multi-centers experience, showing the results of different ablation. This is like regular ablation techniques for different locations of PVCs, and as you see, the epicardial or LV somet PVC, the success rate is the worst, 60%, okay? So here we're going to talk about epicardial axis. I understand that one decade or two decades ago, everybody was trying to try to map these PVCs from the epicardium, okay? So we know, we published this with Dr. Dibiase and Dr. Natalia and Chief Kumar from UCLA, showing all the advanced techniques to do epicardial axis, and even though it's much easier than it was 10 or 20 years ago, still doing epicardial axis is kind of complicated. So here, let's talk about the anatomy. So the LV somet is the highest portion of the left ventricle, and is divided by the LAD and the left circumflex. Something really important is like 20 or 30% of the patients have this ramus intermedius branch in the bifurcation of the left main, okay? So imagine if you're going to try to do epicardial ablation or put a catheter in the CS, it's going to be almost impossible to do it, okay? We know we all go through the CS and we do coronary angiograms, but we always expect different results, you know, the definition of insanity, but we know the catheter is always going to be there. Some cases you can get away, but most of the time you're going to have problems with these arteries. Also we have learned from the, these are pictures from the McAlpine collection, courtesy of Dr. Shivkumar and UCLA. We have learned that we can access the LV somet through the first occeptal perforator arteries and also the veins. I couldn't find a picture of the veins here in pathologic specimen, but you can access. So this is a very, and that's how we're going to try to do many of the techniques that I'm going to be describing later, okay? And here also, it's very important that this is the LV somet, so, and you can see that you can attack this area from many different areas, okay? So you have to remember that you can only from the RBOT, from the LCC, LCC-RCC commissure, from the AMC, sometimes from the CS, sometimes from the epicardial, and very importantly from the subaortic region, even though you're not going to be early when you're doing your activation map. So these are 3D reconstruction computed tomography, and you can see how this is the LV somet, the bifurcation of the left main and the great cardiac vein dissect the LV somet into the inaccessible or accessible area, okay? So inaccessible means that even if you get perfect epicardial access and you're on top and you're early, you're not going to be able to already because you're going to be too close to these two arteries, okay? Either the left circumflex or the left anterior descending artery. And if you have PVC coming from the accessible area, so you have more hope, but not great chances to get rid of the PVC, okay? So here we have a fluoroscopic in RAO, LAO, and you see that you need to be, I mean, sometimes you put the catheter and you're away from the LAD and the left circumflex. So this is, to me, it was very important before this paper. So you just have to remember these criteria. I think this is the more accurate criteria to define whether or not the PVC is coming from the accessible or inaccessible area. So you look at the R wave in lead III and lead II, and you calculate the ratio and the ratio of the Q wave in AVL and AVR. So just so you remember, the ratio for the accessible area in III and II, it has to be more than 125, and the ratio of the Q wave in AVL and AVR, it has to be more than 175, okay? If you forget, when you take a look at the EKG, just make sure that lead III is higher than lead II and the AVL is deeper than the AVR, and then you have an idea. Eventually, this is, I mean, to me, at this moment, this is pretty much irrelevant because I never do a picardial access for LV. So the paper that we published with my group, describing step-by-step how to get a picardial access with two-needle micropuncture, needle-by-needle, with needle technique. And even in experienced hands, you're going to have inadvertent RV perforation in 2 to 5% of the cases, okay? We also described the paper that we published with Dr. Natalya and Luigi de Biasi showing the pressure-sensing needle. So it's essentially a two-needle with a pressure sensor at the tip, and once you start advancing the needle, you can see the transition signal between the extracardiac space and the pericardial space, you know? So once you don't have any pressure and you can start seeing the signals that are 5 to minus 5 in millimeters of mercury, and you can also see if you're touching the myocardium because the pressure significantly increased. You can also now, this is very trendy now, you can do CO2 insufflation through the tip of the right atrial appendage or one of the ventricular branches of the CS. However, you have to understand that even with the needle, we have 4% of perforations with significant bleeding, okay? And even with the CO2 insufflation, besides, I mean, just start with the fact that you're violating the anatomy, you're making a hole in the appendage or in one of the veins. So you're already perforating the heart, but of course, lower chambers, pressures. But in this case, they have also 5% of significant bleeding that require intervention. So this is the paper by Dr. Santangel in UPenn, that he did LVSOMED, then he did epicardial axis mapping and ablation of the epicardium using epicardial axis, okay? So as you can see here, in 39% of the patients, the RF couldn't even be delivered because they were close to the LAD or left circumflex. And in 40%, they fell, okay? So they have only 17% success rate. So you have to see if getting axis and getting epicardial axis is not just the risk of perforating the right ventricle, it's the risk of damaging the left hepatic lobe, the fundus of the stomach, the subdiaphragmatic or epigastric arteries, damaging the coronary arteries, coronary veins. So there's a lot of things that can go wrong when you're getting epicardial axis, even if you're an expert, okay? But most electrophysiologists don't get epicardial axis on a daily basis. So it's complicated to be an expert and try to do this once in a while. Then we have, I mean, many people say that, or most people go into the great cardiac vein, anterior interventricular vein junction. And of course, most of the time with LVSOMED PVCs, your earliest activation site in unipolar or bipolar is going to be here, okay? However, as I showed you before, you always have the arteries, or almost always, okay? And this is a very interesting paper. In 2014, they did a systematic evaluation of these PVCs coming from the LVSOMED, and how you can ablate it from the great cardiac vein or anterior interventricular vein. As you see, this is why we use the five millimeter rule, okay? So if your catheter tip, especially in area in this view, is five millimeters away from both arteries, assuming you don't have a intermedius ramus artery, then you're good to go. In only 75% of these patients, they couldn't ablate because they were too close to the arteries as expected, okay? In 25% that they ablated, 4% of these patients, even though you were at seven or eight millimeters, they damaged the coronary artery and they have to stent it, okay? So in my opinion, probably it's a very risky approach, with low efficacy, okay? So how to ablate? So this is, you know, every time we have a PVC, this is our expectation, okay? That we're going to go there, that we're going to find a very early site with perfect unipolar, and that we're going to try to, you know, we're going to do one or two lesions. So the first concept that I want to pass to the fellows of early career attendance is like when you have a LV somen, you know that it's a picardial or intramural, you know that you're going to have to map a lot, that this is not going to be one or two lesion case, okay? More importantly, here with Roderick Tong, when I was his fellow at UCLA a few years ago, we published this paper, and I think it's very important because in 39% of the patients, when we're mapping the left ventricular outflow tract, we notice this aortic valve closure. Okay, so why it happens, because every time the aortic valve closes, it generates an elastic recoil force that is going to, you know, every time it closes, the catheter goes medial, and once the elastic recoil force hits the catheter, that's when you have this closure artifact, okay? It's usually at the end of the T wave and correlates perfectly with hemodynamics, okay? So the dichroic notch, if we are remembering from cardiology, that represents the closure of the aortic valve, and it's always there, okay? So that's how we study the artifact, and clinically, it's very relevant, okay? Because 40% of patients have this, and we always map the LCC, the LCC-RCC commissure, and depending on the PVC coupling interval, you can think, you can misinterpret that this is an early signal, okay? So most of the time, this artifact is 30 milliseconds, 28 to 32 milliseconds in duration, so even if you're on time, you know, zero, not early, you're gonna think that that's an early potential, you're gonna have late, and you're gonna get frustrated because the PVC doesn't disappear, and you can see here that this is a LV-SOMED PVC with early transition and epicardial features, okay? Something very important is, as I mentioned, it follows the T wave, so you don't forget, and when you have the PVC, you don't have the aortic closure artifact. Why? Because most PVCs don't open the aortic valve properly, okay? So these are McAlpine pictures again, so now that we know that we can access the LV-SOMED through the arteries, we're going to start describing the first technique, okay? So the first technique was described by, I mean, Dr. Stevenson, when he was at Brigham, he opened the door for all the, many of the ablations techniques that we do today, okay? So they started doing this, they published this series with 10 or 12 patients using a trans-coronary alcohol infusion, okay? So here you can see that, I mean, they do the angiogram, they localize the artery base, they try to localize always the earliest site with an ablation catheter that is not here, but that's how you're gonna localize the artery, I'm gonna show you later, but once you localize the artery that you wanna target, then you do intra-coronary mapping with a vision wire or BMW wire, any insulated wire that you can do unipolar mapping. And how do we do unipolar? You usually connect one of the alligator clips to the proximal portion of the vision wire or BMW wire, and the other alligator clamp is gonna be connected to a needle in the groin of the patient to create the circuit. So here, so they localize it, they put the wire, they put the balloon, and then they inject the alcohol, okay? Very important, if you ever do alcohol infusion, then you inflate the balloon. Before you inject alcohol, they use ethanol 96% or 98%, depending what's available at your institution. Before you do this, you need to inject a coal or ice saline, okay? Because you don't wanna damage a huge area of myocardium. If you're not 100% sure, you're gonna terminate or eliminate the arrhythmia. And also you need to make sure whether or not you're gonna cause complete heart block, okay? So you do it, if you don't cause heart block, then you can inject, you inject, you leave the balloon inflated for 10 minutes, and then you check if there's complete obliteration. So if you still see flow, then you have to do two, three, four, up to five injections, okay? So that's important. Also they have, in this area, they have 38% risk, no, they damage the AV node in 38% of the patients. However, when I was at Brigham, also sometimes you think that's a crime against humanity, but most of these patients that they used to do alcohol infusion, they had really advanced ischemic or non-ischemic cardiomyopathy, and they already have CRTD devices. So even though you cause complete heart block and you make the patient pacemaker-dependent, I mean, they're already using the CRTD, so it's not the end of the world. Here, you can see also with echocardiographic contrast, where the piece of muscle that you're gonna damage, this is using cold saline, and you can demonstrate suppression before you infuse the alcohol, and that's how you're gonna see it with echo. This is Miguel Valderrabano, after they tried it with the arteries, Miguel tried to to use the venous system, okay, with the aim of trying to decrease the amount of complete heart block, and he has succeeded, okay? So it's the same concept, they use a vision wire, they localize the first septum. The problem with the veins is like, they're like very tiny veins, sometimes they're very difficult to define, but I mean, it's much more difficult than cannulating an artery, I would say in my experience, but it works, okay? So here you can see the pre- and post-ethanol, and here I'm going to show you a better example here, they localize the first septal perforator here, and they advance the vision wire, and you can see that they do perfect, and you can do pace map, and it's 12 out of 12 based on the EKG, and you can have unipolar very early, minus 40. When you do venous or coronary mapping, you're gonna be sometimes minus 50, minus 60, minus 70 early before the PVC, and this is beautiful, you know how you have trigeminal, one injection, one cc of alcohol is gone, okay? And you have pre-procedure and post-procedure, and you see what you did essentially, okay? That's why it's very important, not only for recess stratification, but only to know that the patient didn't have anything in the basal septum, and now you have your lesion there, okay? This is just a polish a few months ago, and this is again Miguel Pater-Rabano with a multi-center experience, they included 60 patients, and the success rate of this technique was 78%, good in my opinion, for LV summit PVCs at one year, and something really interesting is that they instead, I mean you usually use the first septal or the second septal perforator for this ablation, but they found that you can also use the first diagonal and second diagonal veins, and this vein that is called the left ventricular annular vein, so all of them related to the LV summit area or interventricular septum, and zero, zero percent of a complete heart block, okay? The only issue when you do alcohol ablation is you also have to inflate the volume to get contrast, and if you have a lot of collateral flow, probably it's not indicated because you can cause a massive damage in the myocardium, okay? And then Chief Kumar, a Polish in 2013, intra-coil embolization using the same technique, they put the vision wire in first septal perforation, you can see how early you are using the vision wire, minus 90 milliseconds, they inject the neurovascular coils, and you can see the lesions that are done with this technique. Also, this technique is a very good technique, but it's same like a coronary alcohol ablation, you're damaging the first septal and the second septal perforator are big arteries, big branches, so you're going to damage a big piece of myocardium. We published this with Roderick Dunn, also a patient with LV summit, when it's close to the coronary arteries in the epicardium, we can do high power, long duration using 50 watts for three minutes and a half, and we get, I mean, it's a little bit risky because you can have a steam puffs and myocardial perforation, but I mean, we have good experience with that. You get late termination of the VT, but it's something that I do, essentially, every time I do LV summit with ablation of other sites that I'm going to explain a little bit later. This is the technique that I had the opportunity to do with Dr. Chief Kumar. This was the first case in the world in 2016, when I was a fellow at UCLA. What we did was to do the same thing, do intracoronary mapping, but instead of mapping the artery, we map the myocardium and we ablate inside the myocardium, okay? So what we use was CTO balloon system. It's a balloon used for a complete total occlusion, revascularization, interventional cardiology. Once we inflate the balloon, we perforate the arterial wall with the steam gray wire, and we transmit the radio frequency energy from the tip of the ablation catheter. You can use an eight millimeter catheter or the regular STSF biosense catheter, thermocool catheter. And you have to do it in saline, otherwise you're not gonna be able to transmit the energy. So you put a saline bath and you use 30 to 40 watts for two or three minutes. And that's how you deliver the energy intramyocardially. So very important for this technique is like you really need, or for anything, anytime you're gonna cannulate the coronary vasculature, you need to have an interventional cardiologist with you. I know some of you may think that you have very good skills also in interventional cardiology, but ideally start building your relationship with someone that you trust, that's someone that you feel comfortable working with because, I mean, it's better if someone has a lot of experience, especially handling the CTO balloon, okay? So as you can see here, this balloon has two opposite, it's like 180 degrees opposite and offsetting exit ports. When you inflate the balloon to give stability and then you perforate with the stingray wire, it's like a very stiff wire. And that's it. So here, I'm gonna show you the case that we did at UCLA. So this, just briefly, a patient, 48 year old, a lot of PVCs with a PVC burden of 35%, normal MRI and normal PET CT without any evidence of cardiac sarcoidosis. Here, we can see the PVC, classic LV summit PVC, ablated before from the JCV AIV, high impedance, but they, I mean, they ablated, but they didn't do anything. Then epicardial ablation. They delivered, by their report, they delivered 25 minutes of RF in the LV summit, unsuccessful, of course. We did a quick map earliest in the JCV AIV junction. We were minus 20 milliseconds early in the JCV AIV. And then we decided to do angiograms, okay? So as you can see, this catheter is on top of the LAV. So not a good place to ablate. And that's why probably they didn't ablate it before. And this is the arrow view. You can see that, I mean, the first septal perforator is not close to that side, okay? So we decided to try to advance the ablation catheter a little bit more distant into the anterior interventricular vein. And now we're very close to the first septal perforator. Why it's important? Because then you can try to do what we did, okay? So at that time, we were with, we called CT surgery people to see if we can do a limited thoracotomy. But Dr. Stevenson also published that even if you do a lateral thoracotomy, a limited thoracotomy, using cryoablation, you have damage of the LAD in 25% of the patients. So not even if you open the chest and you ablate looking at the spot, you're too close to the arteries. That's the take-home message, okay? So we use this guide wire and we advance into the first septal perforator. We map with the catheter at that level. It was 24 milliseconds, a little bit earlier than before. We did pace map and it was a perfect match. This is what we published. Then since this first septal perforator was kind of big, we decided to go to a more proximal branch, a septal branch, and we decided to do coil embolization with the neurointerventional people at UCLA. And you can see the coils here. So, but this was not a good branch because it was too basal, okay? As you can see, unsuccessful. We continue having the PVCs. So then we decided to go to the first septal perforator. And here you can see the CTO balloon being advanced. This is the balloon and this is the stingray wire. And look, this is a very tiny wire, 0.01.4 inches. So we exchanged the guide wire and now we're gonna go with the stingray wire, okay? So once we inflate the balloon, we advance the stingray wire to perforate the myocardium. And here we can see the injury, you know, current of injury, meaning that we're inside the myocardium. We were minus 28, so we were not that happy. We repositioned the balloon a little bit deeper and we perforated the artery again. And now we were minus 59 milliseconds early. Then we decide to go for it. And we use, I think, 30 or 40 watts. And this is the PVC burden free ablation. One lesion, we decrease it to half. Seven lesion, we eliminated all the PVCs. And this is the post after ablation, just to make sure that the arteries is patent, okay? That we haven't damaged the whole or occluded the whole artery. This is the post-procedural cardiac MRI. And here we can see it in different planes. Before and after, you can see the massive lesion that we caused. This one is from the coils and this one is from the wire. And the follow-up at three years, or maybe now at three years and a half is a patient. I mean, as I said before, you're never gonna make this patient zero PVC, okay? So if it was 35%, 2%, that's like 95% reduction, which is very good. And the left ventricle ejection fraction improved from 35 to 60%, which also is what we want. So I wanna show you this video because there's a lot of people are very skeptical about two issues, okay? One is how you can transmit the energy from the ablation catheter through this wire and really create a lesion here, okay? And also the second point is like the wire is so tiny that people say that, how are you gonna create a big lesion to create, I mean, to do some myocardial damage and to get rid of this PVC, okay? So this is an ex vivo in the animal lab and you can see how the lesion is being created here. And this is a two minute lesion, okay? And you can see, you know, we're showing how you do it with the proximal tip of the stingray wire and the tip of the ablation catheter. And you see that you create a big lesion and we also demonstrated by cardiac MRI, okay? And these are the images at 45 seconds, 60 seconds, 90 and two minutes. So that's the intramarocardial ablation. Now let's talk about a bipolar ablation, okay? So this was initially described by Dr. Viver Ferreria and Hurd in Mount Sinai here in New York. So for bipolar ablation, what do you need? You need only one RF generator and two catheters, okay? So one catheter is gonna be your active catheter and the second catheter is gonna be your electrode catheter, okay, or your receiving catheter, okay? So the problem with bipolar is like, you need a special connector to connect both catheters to the generator, okay? So BioSense has that connector, but only five or six institutions in the U.S. are part of this prospective registry for bipolar ablation. So if you don't have access to that registry, then you have to create this, I mean, you have to make it at home, okay? So it's gonna be less reliable. But it has very good technology. You can see that you can, I mean, if you do bipolar, you do almost two centimeters, 20 millimeter thickness lesions, you know? So this is amazing if we have the technology available for everybody. The good thing about bipolar is that you can use, for one PVC, you can ablate from the coronary sinus and the subaortic region, coronary sinus and RCC. So, and it has very good results, okay? So this is a recent paper published by this group. Pascual is part of this group with the UPenn attendings. This is bipolar ablating from the left pulmonic valve to the subaortic region, okay? So you can see that here, even, I mean, this is anatomical. You know that the earliest, not that earliest, minus 20 in the GCV, but in the pulmonic valve cause, and in the LVOT, in the subaortic region, you're late. Okay, zero on time, at least, but you don't have anything early, okay? So they do, they did bipolar in only seven patients. So very small sample size, and they got a success rate. They didn't give you success rate, yes or no PVC, but they give you 88% total reduction in PVC burden, which I think is amazing. Something that you have to keep in mind with when you do, every time you go to the pulmonic valve is, I mean, they go with, I mean, I also do it with the inverse U shape of the catheter. Try to go through the septum and try to loop the catheter so you don't perforate the LVOT. But more important, once you're gonna deliver a sequential unipolar or bipolar ablation, you have to make sure that your LAD is not close to your catheter, okay? So here, you can see that the proximal ring are very close to the LAD, but not to the tip of the catheter, okay? And you can see here, patient by Gemini, the moment that you start bipolar, the PVCs disappear. An 80% success rate is amazing, in my opinion. Here, you can see the PVC burden, how it goes to essentially 5% from 30%. So if you don't have the connector for bipolar, you can do simultaneous unipolar RF, okay? The problem with this is like, it's not as good as bipolar by any means. And you need two RF generators, two ground patches, and two catheters, okay? What we use here, we use the Smart Ablate and the Stoker from Biosense. And the key to do this, I mean, effectively, because sometimes you have a lot, you have to troubleshoot the system, is to ask the catheter specialist. We ask here, Vito, who's like another electrophysiologist. So he set up the pre-RF lag time to zero and zero in both generators. So the moment that it's zero, zero, then you coordinate with your partner and everybody step at the same time, and you can start deliver energy, okay? If you don't do it simultaneously, then it's gonna create a problem and you're not gonna be able to do it. Some generators, they have two or three seconds pre-RF lag time. So if it's two or three seconds, you have to know these things. So you have to start, press the pedal three seconds before the thermocool catheter, okay? Pasquale also published this, success rate of simultaneous unipolar, 50%. But these were patients, all redo patients. So if you can do 50% of the patients, it's better than zero. And now half normal saline. So I was very excited about this. And you can see that the whole point of doing half normal saline is like, when you use normal saline, you have a high ion concentration. And when you have high ion concentration, you have a very low impedance environment. And every time you have a low impedance environment, the energy is gonna dissipate in many directions and the tissue is gonna get just a fraction of that energy and the temperature is not gonna be as high. On the opposite, if you use a low ionic concentration or non-ionic, like dextrose 5%, you're gonna get a high impedance environment and then more energy to the tissue and higher temperature to the tissue, okay? Here, you can see that this is sequential unipolar, small lesions. Sequential unipolar with half normal is essentially as, or it was essentially as good as bipolar with normal saline, okay? This is the clinical experience, 89% success rate for very difficult PVCs. And especially, this is amazing because if you were successful acutely, you were essentially successful a long time, one year, okay? You have a lot of steampups with half normal saline, but only one or 2% of these steampups translating through myocardial perforations. However, also very recently, UPenn and Dr. Sauer, they published this paper. This is an animal model, in vivo animal model, okay? And they use, they compare half normal saline with versus normal saline using the same power, the same duration, the same contact force. And as you can see, the lesion depth, the lesion width and the cross-sectional area are essentially identical. You can see it here. So the future of half normal is to be determined at this moment, even though I use it for all my PVCs, papillary PVCs, LV summit PVCs, I use it for everything. But based on this data, it doesn't add much. So here we come with the latest paper that we published with Dr. Natali, Luigi and the UPenn group. And it's like to, you know, instead of doing these crazy techniques, we can just map very carefully. And if you find many early sites, especially when that's very common, when you're mapping a trans LV summit or interventricular PVCs, you're gonna find many early points that are not too early, 25, 26 milliseconds. And you start out late and creating edema and getting desperate. So we said, okay, for all the PVCs, we're gonna try to map it carefully. If we find a very early PVC, 30 or more or 35, then we're gonna have late. If you don't find any PVC, we're gonna finish the map everywhere. And then we're gonna target all these early sites, regardless of if you're targeting it for the VT, okay? Why we decided to do this is because, you know, we have this misconception that the 27 or 30 millisecond, that's the perfect site and you're gonna be successful. So I try to find why everybody talks about 27 or 30 millisecond. And it's from this abstract in circulation in 2015, never in a paper, but this paper shows that if you have minus 20 millisecond before the PVC pre-QRS, then you have a 80% sensitivity and 85 specificity. So let's say 87, okay, success rate. And by every millisecond that you're earlier than the PVC, that gives you another percent of success. So we're talking for you to be a hundred percent successful, nothing is a hundred percent, but to be a hundred percent or close, you need at least minus 40 milliseconds to start up later, okay? So that was one of the reasons. And the other reason, this is a paper with Marmar Vaseghi and Shiv Kumar. They tried to measure the distance between the RVOT and the RCC, four millimeters. But more importantly, look, this is a patient without LVH, without the ventricular hypertrophin. And the LV summit or the basal portion of the septum is almost two centimeters from the RVOT to the aortomitral continuity and two centimeters from the LCC to the JCV, okay? So this is a massive muscle, so thick that is inconceivable to think that you're going to have late intramural PVCs with one lesion from any of these sites, okay? And also we demonstrate with CT, you see 18, almost two centimeters of distance using a cardiac computed tomography. So these are the results. If you have a single site, of course we got very good acute success and long-term success, but for the intramural LV summit PVC with multiple early sites, but nothing too early, acute success and long-term success was 93. Remarkable, in my opinion. This is an example. I want to thank Vito again for making this picture for us. It's for example, this page, this PVC from the LV summit. You see a picardial features, we met minus 27, minus 34, minus 21. And that's how we do it, okay? We are late from all early sites, regardless if we suppress it from one site or another. And the most important point is like, when you have a single activation site, again, it's 37 milliseconds, they mean when you have one early site. So that's why from now on, probably try to find 35, 40 milliseconds to be sure that you're going to be successful. On the other hand, if you have 25 millisecond sites, nothing is too early, then immediately think that you're going to have to ablate from multiple sites. And this is from my friend and colleague, David Reseno with Fermin Garcia, when he was a fellow at UPenn with Fermin. You know, he does also mapping from the venous system here. I've been showing you a lot of PVC cases, but look at this image. He can also map and do entrainment from these septal veins, okay? And you can see the patient is in VT and the PPI minus tachycardia cycle then is two milliseconds. So it's concealing treatment. So you demonstrate that that portion of the myocardium is part of the circuit. Of course, he ablated here, but then the VT changes. It has two or three different exits, but if you ablate from the left ventricle and right ventricle using this technique, also you get very good results. And he mapped in the veins, but he uses that wire as a fluoroscopic reference to go with the ablation catheter endocardially and try to hit that wire from many sites. Also very good PVC burden reduction from 22 to four. And I see the therapies also from five to one. This is another picture, pretty much the same. We decided to do this study. Recently, we presented an AHA with Luigi. So for LV summit, so I've been doing floral cases for the last five years, but the only case that I need to do floral was LV summit PVC. So I decided that I didn't want to do it because the only thing that you need floral for is epicardial axis or just to do a coronary angiogram. And I don't believe in ablating in the LV summit area, okay, for the reasons that I just gave you. So we compare floral versus fluoroscopy. Same thing, the only difference that you don't ablate in the CS, okay. Not too many patients, 32 and 43 in each group. When you use fluoroscopy, you're increasing probably half an hour, 30 minutes, because you need to wait for the interventional cardiology and do the coronary angiogram. But otherwise, pretty much the same. Success rate, acute success, and long-term root success is pretty much the same, 81 and 84, decent, and no complications. This is an interesting case that we did that Luigi was kind enough to let me do it out of fellowship. So this is, again, intramyocardia. This was one of the patients that we failed doing a multi-site mapping and ablation. So this is the case. So you have this PVC, a transition in V3, V4, early in the RVOT. This patient already failed two ablations in another center, my ablation, and now it's coming for the fourth time to the lab. So early 31, but we already ablated here, but we just map, and you can see here, he has another morphology, more LV summit PVC with transition in V1 and a lot of epicardial features, and we are minus 20, not that early. But I want you to understand that when you have these two PVCs coming from RVOT or the coronary sinus muscle, I mean, I would say this is the same PVC with two different exits, alternating exits, you know? So this is the baseline PVC burden. The patient had like 40,000 PVCs in one day. Of course, in the lab has less, but still a lot. So we decided to do the coronary angiogram. You can see some top, again, of the LAD. In area, you can see, again, similar to the case that I did with Chief Kumar in 2016, it's like every time we do these cases, the catheter is here on top of the first septal perforator, which is good. So we went with the vision wire. We advanced the CTO balloon into the first septal perforator. We exchanged that guide wire for the stingray wire is a stiffer wire to be able to perforate. And here we have perforated. And this is very interesting. Probably, I don't know if you can see it, but here we have the PVC coming from the JCV anterior interventricular vein and the PVC coming from the RVOT. And you can see that we're early for both PVCs at that. Here is the catheter that Vito was able to put for me. So you can see it with the electronatomic mapping, your wire in the interventricular septum, the first septal perforator. So we're minus 75 and minus 90 milliseconds early. Here is ablation on and how we terminate the PVC with one lesion of two minutes. I know people don't believe it. So I made a video yesterday. So, you know, ablation on and you see how they, how, I mean, it takes a while, but eventually they're gonna disappear here. Okay. And we do coronary angiogram just to look for patency of the artery. And it's open. And this is post ablation, 30 seconds just to show you that no one PVC. Okay. I wanna stay a little bit so you can believe me. And just to finish the presentation, I just wanna talk a little bit about the catheter needle that Dr. Stevenson has been developing with Biosense. This is a similar catheter to the one that we use, but you can extend a needle up to 10 millimeters in depth. You can map unipolar or bipolar. It has a proximal ring here. And usually you find your every site of activation or wherever you wanna ablate and you put the catheter perpendicular, you extend the needle and you apply contra just to make sure that you're not in the epicardial space. And you can do bipolar or unipolar mapping with this catheter. They just published the results last year, complete elimination of the artery network 50%, but significant improvement in 19% of the patients or 70% success in my opinion. Good. The needle is still under investigation and it's not being approved by the FDA yet. With this slide, I'm gonna finish. So this is an algorithm that we created. One of the reviewers from HeartRhythm made me do it. So every time you think you have a PVC coming from the LV summit, at this moment I would say, knowing if it's accessible or inaccessible area is irrelevant because I mean, you shouldn't be doing epicardial access for LV summit PVCs. But this is important. If you have a PVC very early, more than 30, but in my opinion, 35, 40, ablate. If it's less than 30, map every single place, find the early points and then ablate all the points and you're gonna be very successful. And if you fail, then you have to pick, I mean, there are no head-to-head comparisons between these techniques, but I would say if you have the connector for bipolar, it's a very good option. Coil embolization and alcohol ablation using the arteries, not great because you're causing a lot of damage to the myocardium with high risk of complete heart block. The intramural needle in the future maybe, probably these techniques, I mean, you need someone with expertise in interventional cardiology, but all of them, it depends what is their resources or the availability that you have on your institution. Thank you so much. That was great. Fantastic lecture. I'm gonna include that paper that you guys just wrote that's in heart rhythm so people can look at it. And I like that workflow because it kind of shows that you don't write away off the first procedure, think that you're gonna use these techniques. It might be the second procedure or even the third procedure before you decide to do that. So along those lines, in terms of patient selection, when you're deciding which patients you actually wanna do this stuff, because it's always a risk benefit, which ones are you thinking of using this for? Is it for PVC-induced cardiomyopathy, symptomatic PVCs that's only 5% or how do you decide that? I mean, first of all, I mean, in my own experience, we have laid all our PVCs with multi-site ablation. We do careful mapping, ablate from all the early sites. We never ablate from the CS. If it's too early in the CS, we go endocardially, so aortic region, high power, long duration. If we fail dramatically, meaning that we didn't, I mean, if we have 80, 85% PVC reduction, we think that's success. If we can make it 4,000 PVCs a day from 40,000, we don't do anything else, okay? We don't wanna bring a patient for another, even for a regular procedure for that. But if we really, really fail, like the case that I just showed you, that I think this patient had more PVCs than before the ablation, then we, I mean, we discuss with the patient and we tell them that we can try the standard ablation or we can go a little bit more aggressive, but it's up to him. And it's very patient dependent. Some people don't wanna try any new things. Some people are more open to the new technologies or strategies, but I would say, just to answer your question, if someone is not really that symptomatic and the PVC burden is no more than 10,000, I wouldn't really do any of these techniques, okay? But if you have 20, 30,000 PVCs, even before you go into cardiomyopathy, I will try to get rid of the PVC. And of course, if you have sustained VT, I mean, that's not a question. You need to get it. And then a couple other questions here that came through the chat. So one was about ablating through the coronary wire. Any other special precautions? Is there something special about the wire that you choose? Do you have a preference on which wire you use to ablate? For mapping, you can use any wire. Everybody uses the vision wire of Biotronic because the last, the distal tip, the 1.5 centimeter distal tip is, that's the only portion that is not insulated, okay? So you can, it's better to have an open wire. But even if you don't have the wire, you can put a balloon catheter and make it insulate that tip of the catheter, okay? For the CT or for the intramarocular, you need to use the CTO balloon system, okay? So the CTO comes with the balloon with the side ports that you're gonna, and the stingray wire that is a very stiff wire because believe it or not, to perforate an artery, you need something really stiff. Otherwise, it's very difficult. Yeah, but for mapping any wire, but for delivering the energy, you need to use the CTO. It's expensive, like $2,000 or $3,000, I mean. And is your standard ablation time two minutes for each of those lesions? Yeah. Okay. And then there was another question which frequently comes through on talks like this, is just what settings you're comfortable with with standard RF ablation in these various sites. You already kind of mentioned that you don't like to ablate in the vein, but if you're gonna ablate, what type of settings are you comfortable with? 50 watts for how many minutes? So I usually, if when I, I mean, I mean, I do CS ablation for other arrhythmias and I usually use 30 watts for 10 seconds. That's what I use with the results band. Luigi uses 43 for 10 seconds. I mean, I don't really know if there's solid data to give you a specific answer, but I use 30 watts, 10 seconds.

ventricular arrhythmias

left ventricular summit

interventricular septum

premature ventricular contractions

PVCs

cardiomyopathy

sudden cardiac death

transcoronary alcohol infusion

bipolar ablation

RF ablation settings