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EP Fellows Curriculum: Mapping & Ablation of PVCs
EP Fellows Curriculum: Mapping & Ablation of PVCs
EP Fellows Curriculum: Mapping & Ablation of PVCs
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My fellows, Christian and Nashua, are still getting their beauty slip. Good for them. They'll watch it on YouTube. So it is better than getting on a plane and flying across the East Coast to give a lecture at what ends up being five o'clock. So we'll go from here. See if I can advance. There we go. Breeze passed my disclosures here. I don't think they have any relevance to what we're gonna talk about today. So goals for this talk, mapping and ablation of PBCs. Really common procedure that you're gonna do a lot, really regardless of where you end up practicing. Frequent PBCs are not a rare occurrence. So we'll talk about patient selection for ablation, how to maximize that, pre-procedural evaluation, how much testing a patient needs before they come to the EP lab, a little bit about case setup, and then mapping strategies and principles, as well as ablation strategies, and then some final words of advice. I did want to sort of give a shout out to this series in general, and Nishant certainly in particular, who's arranged this during our unprecedented, challenging times. There are a lot of overlapping lectures that certainly stand on their own as well as this, but I'm not gonna get into as much detail with papillary muscle ventricular arrhythmias, for instance, which ends up being a common PBC ablation strategy. Just this week, Jason Bradfield went over mapping and ablation of athlete-tracked VT, and by necessity, we're gonna have lots of overlap today, but that's fine. I also did not end up including a ton of ice images because we now have a really beautiful repository from Ensor Rosmini and also from Chicago, and you have talks coming up for vesicular VT. A certainly very interesting aspect of PBC ablation is PBC-triggered ventricular fibrillation, but I didn't feel like I needed to compete with Dr. Belhassen, who did go over that earlier in the series here. So you're coming into clinic, maybe it's just telemedicine clinic these days, and the reason for referral is PBC. So how do these patients generally present? So palpitations, I would say, is still one of the most common. We have a very, very active heart failure group like a lot of the bigger academic centers, and so cardiomyopathy with the incidental finding of PBCs is very common. Pseudobradycardia, I still get referrals for folks for pacemakers, and it turns out that their underlying issue is frequent PBCs, and we'll go through that, as well as just the incidental finding of frequent PBCs. Folks who have CRT devices with heart failure, low BIV pacing percentage remains something that we see quite a bit. How frequent are PBCs? I get asked this question a lot. Patients always want to normalize their disease process, and PBCs turn out to be really quite frequent when you do large-scale studies. There have been studies within the VA, studies of medical students over the years who've worn holters, and it's about 1% to 4% of the population that have some degree of PBCs at any given time. 70% of folks greater than 75 years old would have greater than about 0.2% PBCs on a 24-hour holter, so again, relatively low burden. The incidence of, or sorry, the coexistence of cardiovascular disease with PBCs sort of has an inflection point at that 100 to 200 PBCs in a 24-hour period, so not that many PBCs in a particular patient can put them at risk of having some sort of cardiomyopathy, not necessarily causal, but at risk of having that association. So how many PBCs does it require to have a cardiomyopathy? And this is actually a more difficult question to really answer, and it's something that we're called upon frequently to prognosticate for patients. This is the ERIC study, which is the Atherosclerotic Research Study that enrolled 13,000 patients, 13,500 patients, and just followed them longitudinally, and they looked really extensive imaging and EKG and echo. They looked at whether or not patients had PBCs, and the presence of PBCs over time nearly doubled your risk of development of congestive heart failure, and this is very long-term follow-up, over 15 years, blue line here being no PBCs, and red line being really any PBCs on full-term monitor. So we do know that there is an uptick. The question is, if you have an asymptomatic patient sitting in front of you with known frequent PBCs, will they develop cardiomyopathy? And the question's also why. So we know that, say, rapid atrial fibrillation can cause it, but it is a little bit potentially surprising that PBCs can cause a weak heart muscle. And the mechanisms are thought to be multifactorial. So one is dyssynchrony itself, sort of that same mechanism that we talk about with patients with a left bundle branch block, for instance. When you're actually watching on ultrasound, you can see that dyssynchrony during those PBC beats. Tighter coupling, especially of PBC beats, it allows for electrical sort of resetting. The heart is ready electrically for that next beat, but not mechanically. So you don't actually get mechanical contraction with that second, with that PBC in a lot of folks. And so you end up with increased wall stress, essentially. You haven't ejected blood or very much blood, and that next following sinus beat is sort of overfilled. There's actually changes in the expression of sodium and potassium channels, and some changes in the spatial relationship from the endocardium to epicardium in calcium channels, as well as ryanodine receptors. So you actually get molecular remodeling over time as a consequence of this mechanical stress. And there's certainly, I think, sufficient data that in a large group of patients, this can be reversible. Let's see. So this is sort of an interesting study, and this graph gets shown a lot. So many of you have seen it, and if you haven't seen it, you'll see it again. So get familiar with it. It's a little bit funny to look at the first couple of times that you see it. This is a study out of the Michigan group, and it was about 175 patients who were referred for PBC ablation. So pretty select group of folks. They were symptomatic. They'd come to someone's attention. And they basically just plotted PBC burden against ejection fraction, and came up with these quadrants. So the most common quadrant for their PBC ablation cohort was, in fact, those with normal ejection fraction and a relatively low PBC burden. And their cutoff point for predicting the development or association with cardiomyopathy ended up being about 24% burden in a 24-hour period. So there were very few patients who had more than 25% PBCs but did not have a drop in their ejection fraction. And conversely, there are very few patients who had a lower EF but had fewer than 24% PBCs. So that's this orange quadrant here. But you can see it wasn't at all mutually exclusive. So for us to look a patient in the eye and say, oh, you only have 15% PBCs, you shouldn't develop a cardiomyopathy. I'm not sure we can really say that with such certainty. And some of those patients may, in fact, have PBC elimination with either antirheumic drugs or ablation. In this particular study, remember they were being referred for PBC ablation. They went on to have their ablation and they served as their own controls, if you will. So these are folks who had a mean ejection fraction of 35% before ablation. They underwent ablation with our sort of standard success, which I'll show in a second. And at the six-month post-ablation mark, ejection fractions had improved by 20%, absolute improvement in ejection fraction. So really kind of a profound group. Wasn't randomized and wasn't pre-specified sort of what the treatment was gonna be in the sense that these were already folks referred for ablation, however. So then the next questions, and this group has done a lot of work and it's really over 10 years old, but it still forms the basis of a lot of the recommendations that we make in terms of referring folks for ablation. So next question was really, if you have coronary artery disease and presumably have scar due to coronary artery disease, can we also improve your ejection fraction? And this really maybe isn't so surprising to folks in training now, but it was really back then. If you had coronary artery disease and had PBCs, it was felt to be that the ejection fraction decrease had nothing to do with the PBCs. It was because you had a myocardial infarction. But it turns out those folks are also susceptible and can be improved with ablation. So these are folks referred for ICD and they were randomized actually to a PBC ablation and the ICD or just the ICD alone. And you saw that a large number of folks moved into a non-ICD level ejection fraction, if you will. So here we are in the 38% range, mean ejection fraction moving up to 50%. So you can actually potentially decrease someone's sudden death risk as well, though the causation there is difficult. This is true also of non-ischemic cardiomyopathy patients. I tend to see this a lot less than ischemic cardiomyopathy patients in terms of the improvement, but we do see this. In their particular cohort, the PBCs mapped to the scar and you can see this on MRI. This is an unusual scar pattern with sort of an anterior apical pattern. But again, improvement in ejection fraction, modest overall success, however, in the non-ischemic cardiomyopathy group. Can ablation of outflow tract tachycardia or outflow tract PBCs also improve ejection fraction? So if we slice it that way, the answer is also yes. So this is from Stavros Montamanakis when he was a fellow at Penn, a year behind me, a decade ago. Seems like a long time ago now. And so these were folks referred for PBC ablation of outflow tracts and you can see the distribution here of the regions. Epicardial being sort of a smaller number, but maybe larger than a general cohort of outflow tract PBCs because of the referral bias at Penn. RVOT still taking up the chunk of those patients, the cusps, including the right left junction as a unique site and the aortomitral continuity. And ejection fractions were improved from 34% pre to 47. So I think that this is really a common theme and that this should be a tool that's in our armamentarium and can have very important prognostic implications for patients. I love this study from Stavros because I perhaps over-quote it when I'm talking to patients about PBC ablation because he showed that even if we weren't perfect, which we frequently are not with PBC ablation, that there was a similar benefit for patients if you've got their burden down to about less than 5%. So often this means that you didn't get rid of all of the morphologies in someone with coronary heart disease, let's say, or non-ischemic cardiomyopathy. But even folks where you maybe had partial success and are causing intermittent exit block from a region, if you can get the overall burden down, they see that improvement in ejection fraction. And I have to say, we often come back to this with particular patients where we just can't get full success. So if we treat the patients with PBC ablation, or sorry, if we treat the patients with frequent PBCs, how does that go? What are the outcomes that you can expect? And we're gonna be talking mostly about technique here today, but I think the background is really important for setting the expectations for the patient and also setting your expectations during a procedure. Because frankly, nobody ever died of PBCs in and of themselves. And so it's not the same thing as a ventricular tachycardia ablation. And keeping safety in mind with any ablation, but especially with PBC ablation, I think is really important. We're not gonna go hog wild next to a coronary artery to get rid of a PBC that might be able to be treated in another way. So this is a reasonably sort of unique study. This is a study out of the Mayo Clinic database, and they looked at, I think, 5,000 patients who had the diagnosis of PBCs. They cross-referenced it with folks who had more than 1,000 PBCs in their Holter database, and then made sure everybody had echoes to look at. And then they looked retrospectively. There was about half the folks going for ablation and about half the folks, a little over half the folks getting antirhythmics, and they compared the two groups. So again, not a randomized trial. We really haven't had one of those, and I doubt we will. But a pretty large trial, and there didn't seem to be baseline differences in the patients, but decided which treatment arm they went into. This is a little bit busy of a slide here, but I'll walk you through it. So, except for it disappeared. There we go, I'll walk you through it. So this is PBC frequency on the Y-axis, and the gray is baseline for each group, and the black is after treatment. So the first column here is beta blockers, and they go through the gambit of all of the antirhythmic drugs. And you can see that there's a decrease in PBC burden when you use antirhythmic drugs on average. And I don't think that's particularly surprising, but I think it's important to point out sort of the impact here. We have relatively small numbers when we get into sort of the quote-unquote hardcore antirhythmics, like myxilatine and flaconide, but still a really nice effect here. The last column here, which should be outlined here, is ablation. So this is right here if you can see ablation, and they found that to be their most robust effect with a 93% decrease in PBC burden on average, with most patients leading to complete success. So if we look at a large cohort here of PBC ablations, again, how good are we? What is your target in mind, and how are your colleagues doing before you go into this kind of procedure? This is a really nice study that Rakesh from Michigan as well, he collated folks from the original IVTCC cohort, so that's now expanded to about double the number of sites, and PBC ablation is still something that we're recording, so we should have more robust datasets going forward. But this is still 1,100 patients from 10 really world-renowned VT ablation sites. About half the patients, over half the patients were female, and that's kind of rare in ablation cohorts at all. So somewhat notable. They had a reasonably high PBC burden of 20%, and fairly preserved ejection fraction, I found this interesting. I thought the number would be lower. You can see the site of origin here, and this is in percentages here. So Rb-out clotract is 45%, cusps end up being 15, and epicardial, 11%. I thought that was actually a relatively high number for an epicardial procedure, and then sort of a mixed bag on the others. Pat muscle is 5%, and again, we'll get a separate lecture on that. So what did they see? And this was divided by those regions. So overall, it's sort of this light purple that ends up right in the middle here, the fourth one down. But you can see for any site, our acute procedural success is reasonable, and it's best for Rb-out clotract. And that becomes obvious when you look at the anatomy, and we'll go through that. So cusp comes in second, and then we start to sort of drop off. Pat muscle is a little bit more modest at 80% acute procedural success, and epicardial is somewhere down here in the 65. Long-term success, totally off drugs. There's an attrition rate here, and that's really important to recognize as well. So about 25% of patients who had acute success initially will then have recurrence and follow-up. So it's something that you need to be prepared for emotionally if you decide to be a PVC ablationist. So it looked good, and it looked good in the procedural holding area, and they come back at three months and it's back. And this is something that I hope that further ablation research can help us figure out why that might happen. But you can bounce that back up to that original success by reinitiating the antiarrhythmics. And I think this is something to keep sort of eyes wide open with the patient when you're going into that procedural discussion. But also recognizing that it's all site-specific. So these are the common areas like we talked about in his slide here. So RV and LV outflow tract, and that includes the cusps. The papillary muscles, both in the RV, meaning the RV papillary muscles themselves as well as the moderator band, which seems to be more common. The Purkinje network itself. And then I put AV valvular, so this would be mitral and tricuspid valve. For whatever reason, the mitral valve ends up being far more common. And then the LV coronary venous system. So we tend to see this a lot, but whether or not they're truly coming from the venous system and the muscular sheaths around the venous system really is of debate. Most of the time what we're doing is ablating from within that region, but still ablating the actual myocardium underneath it. Again, I find that true epicardial PBCs are rare. And then RV and LV apex itself is sort of an idiopathic region we do see from time to time. So switching gears to the actual PBCs and localization with EKG. I didn't get enough time to get all of my diet Dr. Pepper drinking in in the morning, so I'm trying to stay awake. Nishant has my telephone number, so if I fall asleep, he'll nudge me. So I know you guys went through this with Dr. Bradfield earlier in the week, and it really does bear repeating though. The outflow tracts of the heart until you start trying to ablate arrhythmias from them and putting catheters there are honestly a complete mystery. I think that it's really helped in cardiology and in cardiology training that the structural heart teams are doing so many more interventions and so many more complex interventions and that they are using somewhat disparate tools that seem to affect the anatomy and interact with the anatomy in such different ways. When I was a fellow, we were just starting to do TAVRs, we were just starting to do mitral clips and things. And the anatomy wasn't something that had been so critically important in this area. But for us, I really think electrophysiologists know the anatomy sort of as well as any group within cardiology, even the imagers, because we're forced to recognize the physiology of the physical interactions between these regions. This is sort of a famous cartoon. I think Sam showed it when he did his anatomy lectures earlier in the COVID pandemic breakout here. But I think it bears repeating again. Basically, looking from anterior to posterior and from rightward extension to leftward extension from the perspective of the EKG lead of V1. So what's gonna happen, and we'll get into more detailed EKG criteria, but V1 ends up really being what I call the lead that will embarrass you, basically. So if you don't pay attention to lead V1, if you don't pay attention to disparities in your pacemaps, or disparities in the morphologies in V1 in the lab, you will end up with a long day. So it tells us a lot. If you're in the anterior RVOT, you are essentially right under lead V1. You are between the substrenal space and the actual physical lead V1. So there's not gonna be any deflection towards yourself. My cat. So there's no R-wave here at the beginning of the QRS. Even moving into the posterior RVOT, you should get some R-wave, and it tends to be very narrow. As you move more posterior into the cusps, and then certainly into the summit area, which we'll talk about, you start to get a broad R-wave here. And then into the aorta mitral continuity, a much more broad R-wave. And along the mitral annulus here, you get full positivity. There isn't really very much muscle posterior to the mitral annulus itself underneath V1 that's gonna cause depolarization to be moving away from that lead. So why do we get PVCs from the outflow tracts? And most of the time when I ask this question, I just get a shrug. But there's actually a reasonable amount of interesting embryology studies that have come from this. And I think also speak to why some complex congenital heart disease patients have more XTP and sometimes even VT from this area. And it really is that the right ventricular outflow tract and a small component of the LV outflow tract actually come from different tissue. So these are mouse embryos, and you can see that the right ventricle and outflow tracts, and in this case, the PA being the pharyngeal arch, not the pulmonary artery itself. But when these are stained for unique proteins that really are only expressed in this region, and then followed through to further development, you can see that these areas of muscle really uniquely contribute to these particular areas. When we get into more detail and stain with things like Connexin 43, we again see differences in tissue characterization right around this pulmonic valve. So especially evident here in a fetal heart in the middle panel, you're seeing an absence of Connexin 43 right around the valve and sort of the anterior RVOT that seems to diminish as we get older. And clearly this isn't the entire story here because we don't have a lot of kids where we're ablating outflow tract tachycardias. So there's clearly some maturing of the cardiac myocytes themselves, maturing of the autonomic system, maybe some acquiring of fibrosis in the area as well. So still some question marks there, but this is actually different tissue. And when you start to think about it that way, and then also think about the anatomic relationships, these aren't molds, right? They're not solid sheets of muscle uniformly lined up in the outflow tracts. These are very complicated areas where heterogeneous tissue is coming together. And it helps you understand why you can get some funny results or maybe not have completely straightforward mapping in terms of activation. So this is sort of the summary slide from that article. And you can also see there's differential expression in that region for even sodium channels as well, the SCNA5A gene. And probably this leads to some of the other phenotypes that we see more severe than PVCs like Brugada and the more severe arrhythmias that we see with ARVC. Speaking of those, when should you be concerned about ARVC in particular when someone presents with frequent outflow tract tachycardias? And I would say really always when you're seeing these kinds of patients, it should cross your mind. Certainly folks that have multiple RV morphologies, so not just the outflow tract, but the body complex ectopy. So that's a non-sustained VT, especially shorter coupling intervals, couplets or triplets, and really any RV echo abnormality. I think that most of these folks with any of these risk factors or certainly any abnormality on the resting 12-80 kg, the sinus rhythm ECG, should undergo a cardiac MRI. And it's really debatable everybody with outflow tract tachycardia deserves a cardiac MRI. And I have to say, I don't do a full RV voltage map in everybody, but I do if there's been any suggestion of abnormality. And I get an MRI in most folks unless there's really a challenge in doing that for that individual patient. So here's an example of a patient who had frequent what turned out to be RVOT septal PVCs, but had some T-wave inversions that extended across the pericordium. And so I did a full voltage map during that study, and it was actually really surprising. This is a patient who had never had syncope, did not have any dilation yet on the echo, and at that time had an MRI. And although we had normal bipolar voltage, we had wildly abnormal unipolar voltage. And this patient ended up developing VT. This is why it's beneficial to be at the same center for a while. You get these kind of longer term stories. Was a patient of Jeannie's. And when I looked back at her endocardial voltage from that original procedure, really did foreshadow this epicardial abnormality. So I rarely put these full abstracts here, but I think this is really kind of one of those ones that deserves a look. So if you haven't spent time reading this article, came out last year in Heart Rhythm Society, on how to use a 12 lead EKG to predict the site of origin of idiopathic VTs. In all honesty, if you follow me on Twitter, sometimes I get into Twitter wars about this, like the EKG is really important in mapping arrhythmias. It's really important in identifying potentially exits of ventricular tachycardias, but it's not the end all be all. And you really do have to put it together with the patient's unique anatomy and their unique conduction in the area. I do find that sometimes the trainees especially, get really rigid about these things. And I'll show you some examples from even this paper itself that don't always fit with the quote unquote rules that we're talking about. So I would say learn these, and you'd be expected to have this verbiage sort of as currency when you're talking with other electrophysiologists. But recognize that there's as many exceptions to the rules as there are rules basically. So this article does this really nice job. There's sort of this beautiful diagram, which a hidden part of here, I apologize. It's a posterior sort of tilted up view of the heart, and they're dividing it axially down between the right and left side of the heart. And we've cut away the atrium, so you're looking through the AV valves here. We've got the outflow tracts up front, and they've done these cutaway views so you can see inside to the papillary muscles. So it's an ambitious paper really trying to cover all of these areas. Main sort of big heading discussions, or maybe main headings to get you going in one way or the other is looking at whether or not these are superiorly directed PBCs or inferiorly directed. So it turns out there's not a lot of middle ground, statistically speaking on this. You're either outflow tract or non-outflow tract, and those tend to be obviously very positive waves in lead two and three. So taking that group first, the inferiorly directed PBCs, we're then gonna look at lead one. So not necessarily AVL, but lead one itself. And that really delineates, are you gonna be on the left side or the right side of midline? That doesn't mean you're gonna be in a left-sided or right-sided structure. So it's really important to recognize that that right ventricular outflow tract crosses over midline, right? Your arms are crossing over when you're mimicking those outflow tracts. And the RVOT is actually markedly leftward of the LVOT of the aortic cusp, but not the entire thing. There is some overlap there. So as you move through, if you're positive in lead one, these are structures that are rightward of midline, you can have some positivity in lead one from the posterior RVOT, sort of posterior free wall. The right cusp itself is fairly lateral there. Perihistion, and then some tricuspid valve PBCs, which are fairly rare. Those will have a much more, a much later transition in the pericordial leads. And then the negative ones here, anterior RVOT, left cusp, and AMC. And they have little hints here. And it's worth going through and sort of memorizing these to some extent, but you should be doing that with this picture in mind and trying to work out in your head, why would that give you that transition? I think V1 can be a bit of a funny lead when you get back to the mitral annulus, but otherwise the findings that you're seeing on EKG should make sense anatomically when you overlap that EKG axis onto it. Similarly, you can walk through this article and I'll leave this for you guys for reference, the superior directed PBCs. They came up with this algorithm again. I find it to be a bit daunting, but it's a good reference for starting this conversation in your own head and working this through. One of the regions of the heart, or regions of the EKG that we really focus on is the transition in the pericordial leads. And what's meant by that is where does a left bundle of PBC move from negative or predominantly negative in V1 to predominantly positive, right? So again, remembering, thinking back in your mind to how those leads are placed on someone's chest. And I find this to be really important and something that as electrophysiologists we often have to get our hands dirty. So I'll go into the pre-procedural area and I'll see that someone's getting a nice EKG and V1 and V2 are in the mid-clavicular line for some reason in that patient, completely wide spaced. Or V1 and V2 more commonly are placed too high, let's say in the second intercostal space and not the fourth intercostal space. This can also happen in your lab. Most of us have travelers coming in and out and most of us make mistakes, it turns out. And that's true of your lab staff as well. So really taking a peek at that, scrutinizing that, especially if you have patterns that don't make sense. You can get big changes and all of those criteria will be irrelevant if your pericordial leads are moved around. This is also really important in obese patients and in female patients where folks sometimes get squeamish about the female breast and don't put the EKGs in the correct place. So making sure that we're really lining them up with our usual landmarks. So with all of the EKG findings in mind, this is the table example that Furman and colleagues have in their paper. And I thought I would just go through a couple of them to highlight sort of how we're thinking. And again, something that you'll practice on the EKGs that you see coming from the lab. So if we look just at panel A and B here, column A and B here, these are clearly inferiorly directed PVCs. So we're somewhere in the outflow tracts. And my next move is to really focus on B1 and B2. So you can see the difference between EKG A and EKG B is honestly fairly subtle, right? But they're hoping that we'll see PVC A as a posterior RBOT PVC. So that's gonna be slight positivity in lead one, sorry, a slight positivity in lead one. And really very little to no R wave, sorry, slight positivity in lead one, limb lead one, and some very little R wave in V1, the pericardial lead V1. Whereas when we move more posterior to the right coronary cusp, you start to get more positivity here. And it's actually fairly wide in V2. And if you draw a line up to V1, you'll see that there is actually a fairly broad R wave there. It's just low amplitude. That's another thing to say. So just like your Delta wave algorithms, we really should be drawing those vertical lines, trying to look at these EKGs. These are rhythm strip EKGs, right? Not just the standard 12 lead EKGs, so that we can really compare where the onset is in neighboring leads. So here's another example. This is C here. We've got another left bundle inferiorly directed. But if you notice, we have a very early transition here, sort of like what we were seeing in V2. But lead three is not very positive. So we're not as high up in the heart as we were before. And there's some sort of disparity in the amplitude between lead two and lead three in the limb leads, really is unique to the parahysian region and worth pointing out. Again, an inferiorly directed left bundle PVC, but this one has a very late transition. We can compare that to that RVOT PVC that we saw in the earlier panel. We're seeing much more negativity up here. It's probably hidden underneath that thing for the zoom controls, but much more negativity in lead one at a very late transition. And that's gonna be your anterior RVOT. So we've moved over to left side when we're more anterior and they tend to be broader because they're not engaging that interventricular septum as easily. so there are more examples on there and the other region that really bears some unique discussion, and I know it's a standalone lecture, but I couldn't possibly discuss PVC ablation since this is where the bulk of my ablations end up being. I end up doing a lot of redo and sometimes three-do procedures from other electrophysiologists and it tends to be the LV summit that's giving people trouble. So it's either giving them pause because of the proximity of the coronary arteries or just an inability to ablate because you aren't able to get down onto that muscle. So we define the LV summit as the region of tissue, sort of the LV tissue that's above the plane of the aortic valve itself and bounded by the region crossing over of the great cardiac vein into the anterior interventricular vein and bounded again by the bifurcation of the left main into the circumflex and LAD. So we've got some important neighbors when we're in this area. It's an area that you can see would be covered with epicardial fat were we to be in the epicardial space. So this really is an area that essentially is nearly inaccessible for ablation from standard percutaneous epicardial access. You guys have access to a lecture on epicardial anatomy that I think goes through this really nicely as well. One unique area in the septum, I'm sorry, in the LV summit is the anterior interventricular sulcus itself. So words that maybe we haven't really used very often in common conversation in general cardiology but become really important when we're trying to ablate here. So this is sort of the divot, if you will, when you remove the epicardial fat between the RV and the LV. And these are those beautiful models from the UCLA group but being used in a Penn Group publication from JCE talking about this unique finding. In these patients, V2 in the same way we talked about V1 but V2 will be right over this area. So if you were to take a needle and stab someone in the chest right underneath V2 or do a CT scan while they were wearing EKG leads, you'd see that this lead has a perfect view of this outflow tract right up at the sulcus. And because of that, you have what is termed a pattern break in V2 here. So overall left bundle morphology meaning overall negativity in V1 but we transition to more negative in V2 and then become positive again in V3. And so here's a couple examples of this. They tend to be very high up and somewhat leftward of midline. So we're gonna have that negativity in lead one. This is an important group to look at because we tend to have difficulty ablating this. We're limited by proximity to the LAD when we're in the coronary venous tree or epicardially and our success is lower in this region. So important to counsel your patients on going in and understand your limitations going in. Okay, let's get to some ablations in our remaining 20 minutes here. So how are you gonna get the patients to the lab? First off, you have to have that 12 lead for all the reasons that we've just talked about. And I really encourage you to run a rhythm strip. So get to know your EKG text. They should know that you want a 12 lead EKG and you want a rhythm strip. It's okay to waste paper, trust me. This is really important. If you're doing this for device patient, you may also run intracardiacs and kind of match that up, see which one is which. Certainly this is very important in the PVC-triggered VF patients. You need a Holter monitor. You need to know what you're starting with and some sort of substrate evaluation. So at a minimum, these folks should have some sort of echocardiogram. We should know what their ejection fraction is. And I would argue that most patients should go on to have a cardiac MRI, looking for sort of occult LGE and the risk of sudden death there. In terms of Holter, I think it's important to do longer term monitoring. So this was an interesting study. I think it was about 500 patients. And they saw that folks who ultimately went on to have at least 10% PVCs in the red or even 20% in the green, they didn't necessarily manifest that high number in the first 24 hours. So there is benefit here to moving past. We tend to do seven day monitors, patch monitors, or at least 48 hours at the minimum. You can see there is that uptick as you continue to go forward. So some variation there. So you've decided to take the patient to the lab and oops, they left their PVCs at home. So I tell the patients when I'm talking about the procedure that this is one of the ways in which we end up not being successful. So you're sitting there at the pre-procedure area with them and or you've already brought them into the lab and they happen to disappear. So what went wrong? What I find most frequently is that there was some failure in the medications. So either the patient didn't understand their instructions or they decided to continue taking their medications because of symptoms. You really do need at least two or three days in sort of your standard BID medicines like beta blockers and class 1Cs to let that wear off. Underestimating the menstrual cycle components. And again, if you've done longer term monitoring, that may help you get a hint of that or done a more careful history. Illicit and non-illicit drug use. I practice in Washington State and I have to say, it's not infrequent that my patients use marijuana before their procedures because they are nervous. And that tends to make PVCs go away. We don't know if it's a therapy for PVCs long-term because we're really not privy to very much investigational data on this. But it does happen more than I would like. And some patients will have a sleep cycle change. So your patients that work a swing shift or a night shift, maybe they didn't go to work that day and they actually got a better night's sleep. So on that end, what can you do? You can rebook them and tell them to get a terrible night's sleep. Really making sure that your anesthesiologist or your nurses aren't sneaking any of those for sed and fentanyl. So I'm surprised that often I say no over sed and fentanyl and they've gotten just 25 mikes or just 50 mikes and two milligrams. Really important to not give these longer-term acting drugs. You can use isopryl, IV, calcium. We have some success with phenylephrine. Another thing to remember once you're in the case is ventricular pacing may bring out PVCs and even physical mapping in the area may sort of wake the area up, if you will. But some patients atrial pacing can bring it on. And then pace mapping as a final sort of last resort. If you really are unable to get the PVCs going and unable to do any activation mapping at all, if you have a PVC-12 lead with the leads in the identical position, and you sometimes can put a patient on a treadmill and do that, have them actually wear the EKG labs, sorry, EKG leads from the EP lab and go from that. Okay. So we finally got a patient to the lab in our final 15 minutes here. So 27-year-old woman. She's got peripartum cardiomyopathy, which was diagnosed five years ago, actually. And she was referred to me, this was in my first job in Chicago, for an ICD. And I was looking through and everyone kept saying she was on optimal medical therapy, but really she was only on Carbadol six and a quarter. And she was limited by bradycardia, interestingly. She was actually pretty symptomatic still. New York Heart Association class three. And her EF was less than 30%. They were even thinking that she was gonna need to go on for advanced therapies. And this was her EKG. And when I looked through her records, this had been her EKG for five years. So we have, again, a very inferiorly directed PBC. We're very positive in lead one. And we have a relatively early transition in V3, although the sinus also transitions early, with a noticeable, although not overwhelmingly prominent, R wave in V2 for the PBC. So I was already thinking that this was coming somewhere from the left side. So how do I go about this for this patient? So I did an MRI for her and there was no delayed enhancement, just dilation, which was pretty significant and corroborated on her echo. And the Holter monitor showed 38% monomorphic PBCs matching the one we saw in clinic. So I decided that it really wasn't appropriate to sort of mess around with antiarrhythmics necessarily in this patient, that we really needed to try and go after this because I felt like it was coming from an accessible area. I don't think it would be at all appropriate to put an ICD in this patient. We haven't done everything to improve her ejection fraction. The other question became, was this a chicken or egg problem? I get asked this a lot. And it depends on how you look at it. But alpha-tracked PBCs do not tend to be a effect, if you will, of cardiomyopathy. To say it another way, folks with cardiomyopathy do not tend to have PBCs because they have cardiomyopathy, but rather the other way around. So morphology is really important. So whenever somebody tells me they're sending me somebody with PBCs, I'm always wanting to know the morphology. And the answer is often, well, I don't know, that's for you to do, but it is for us to do. And those alpha-tracked tachycardias or alpha-tracked PBCs should really catch your eye. So I brought her to the lab and the anesthesiologist got really nervous because they had their pulse thing set to the arterial line, or actually the pulse ox. And what you saw was her bradycardia, her sort of pseudo bradycardia, if you will, where we would see no perceivable pulse amplitude after the PBC beat. So really she was sort of running on half speed there. I didn't hold the Carvedilol for days in advance because she had this very high burden and I was worried about precipitating heart failure in her actually. I used Probofol for access and really important, we should all be doing ultrasound guidance for growing access anyway, but it helps you avoid infiltration of lidocaine inadvertently. So this was sort of a standard ablation. I had the MRI, I brought it into the NSIGHT system. I don't tend to use a multipolar catheter for these. I find that the multipolar catheters, even the HD grid, which is fairly gentle, although you get gorgeous signals, you still have to get your ablation catheter there and figure out if you're in the same exact spot or not, which isn't always straightforward. And that those multipolar catheters tend to cause more ectopy. And I have difficulty adjudicating whether or not I've caused catheter ectopy with a multipolar catheter than with a single ablation catheter. Other people do use those and I think they're interesting research tools to be looking at arithmogenesis and questions that way. But from a practical standpoint, it's pretty stripped down for me. I'm gonna use an ultrasound catheter and an ablation catheter. And for a case like this, I will get arterial access upfront and not gonna waste my time on it. So we were thinking, because we were so positive in lead one and had that early transition that we were gonna be ending up in the cusp and sure enough, we were. So this was for clinical PVC in the lab. This was pace mapping from the right cusp. And in the more modern verbiage, I would have gotten a 97% match or something. But in our sort of qualitative verbiage, you can see that all the nooks and crannies are the correct direction. And even the sort of more isoelectric leads are matching up. I tend to find that those isoelectric leads get switched very easily if you're not in the right spot. And my distal ablation signal, kind of funny, nice and low amplitude here was 30 milliseconds out in front. So when I look at the anatomy here and use the MRI, I had the overlapping RV here. If I strip that away, I also mapped the great cardiac vein here, as you can see. And we were reasonably early in the great cardiac vein, but earlier in that right cusp, even though they're pretty far away, there's some preferential activation, it seems towards that left, as also shown in the 12 ADKG. And ablation here in the cusp eliminated the PVC and her LV remodeled and our ejection fraction got back up to 55% over the few years that I was there. So this is a really important case. So when you're ablating in the cusps, and Dr. Asavatham went through this in his lectures, you're not truly ablating cusp tissue, right? I think this sort of cutaway view really says it the best. You are ablating at the top of the septum, the top of the LV, the most basal portion of the left ventricle, where it abuts the leaflets. So here's a sort of curled up coronary cusp, or sorry, aortic leaflet here. And remembering that your coronary arteries are gonna be coming off in the middle of the sinus where the sinuses are the deepest, where your catheter really should be sort of at the bottom of the sinus anyway. So you're generally not really close to the coronary ostea. So I often get asked, when do you do an angiogram during a PVC ablation? And my sort of obvious answer is when you're close to the arteries. And from that anatomical description here, I don't feel like we're generally very close in the coronary arteries. And if you go back and you look at all your angiograms that you did as a fellow, you'll see that when you're shooting those coronaries and there's reflux into the cusps, there's quite a bit of distance, usually greater than a centimeter there. So I don't routinely do that. I visualize especially the left coronary osteum on ice before I'm ablating and making sure I'm lower. You generally don't record an electrogram when you're too high. So there's no reason to be in there. However, that's very different in the LV summit, right? And if you're in the great cardiac vein, especially if you come around to the AIV, you're by necessity probably crossing over some arteries. And so it's important that you look here. This is a nice example of this. This is a 42 year old man with a dilated cardiomyopathy, low EF, very high frequency PVCs. You can see again, we've got that inferiorly directed PVC quite wide. We're negative in lead one. So we're somewhere over on the leftward side of the heart. And when we look at the pericordial leads, we see something that should make you say, well, this might be a long day. I already knew it would be a long day because I was the third electrophysiologist to try this, but we have a very broad R wave here, right? So more than 50% of the QRS is positively deflected in V1. I mapped both the right cusp, the left cusp, the LVOT itself and the RVOT. I was very late in all of those except for the right cusp, but I was essentially right on time with the QRS. And what does that mean? It means you're not sitting on the tissue that's firing off and creating that QRS. You're somewhere remote from it. You may be at the most accessible site from your catheter standpoint, but you're not sitting right on that orienting muscle. And the pacemaps in that whole region were poor. So I went ahead and I mapped the coronary sinus and I included this image here showing an agilis catheter kinked at the ostium of the coronary sinus, which happens more than I would like. But I've delivered this into the coronary sinus and I'm injecting contrast through it. You can also inject contrast through the ablation catheter itself. I generally mix it a little bit. It's hard to push through very much through those irrigated catheter holes, which are pretty small. But I like to do this kind of image before I go sort of aggressively mapping in the more proximal corner or sort of distal coronary sinus here, so that I'm not over aggressive with how far back over to the right-hand side that I push. So it helps me delineate sort of the margins there. It's not always clear from your 3D electro-atomic mapping how far you can go. So when I got out, sorry, this is from the right cusp, just illustrating that on-timeness, if you will. So I've included the unipolar electrogram here, and this is a very key component for mapping these PVCs. If you're right at the site of origin, your unipolar electrogram should be a relatively brisk downstroke with no positivity, right? Makes sense. Like you're at the site, all the action should be away from you if you're sitting there as a unipole. So even though all the action, if you will, was away from the right coronary cusp, I was not very early on the initiation of the PVC. And it turned out we really didn't end up being very early anywhere for this particular patient. I had my best pace maps, which we ended up using a lot in this case. So I had my best pace maps in the proximal anterior interventricular vein. So when I was in the distal coronary sinus without sort of making that turn, I had too much positivity in lead V1, and maybe even some sort of unusual findings with the capture in lead one. But if I got out that proximal AIV, I got that positivity in V1 that I was looking for, but also that negativity. So sometimes I'll use this sort of comparison. The system will give you percentage matches, but that's not really what you're after. It's not that this was 87 and this one was 92. It's the quality of it. So you need to train your eyes. And I'll actually, on the live screen in PRUCA, have these be different colors. So because I was at that transition point, I did do an angiogram. And I also don't like it when they move the table with my cardo magnet underneath. So I ended up with these standard REO and LAO views. And it's a little bit hard to see, but it takes really scrutinizing these. You can see in the REO that you've got the LED coming anteriorly and that there's a large bifurcation here of a diagonal. And my tip of my catheter, at least in REO, is right at it. And when we come over to the LAO, we've got the CERC sort of ghosting in behind. And then that large branch, you can see I'm sitting right on it. So if I'm out further where I had that better pacemap, I'm sitting right on the artery. So obviously we can't ablate there. So we pull back and we surround it. So we pull back there, we ablate endocardially, and we ablate more proximally. And that's really as good as we can get. And this was using half normal saline at that more proximal site, distinctly being back. So I had a worse pacemap, but using that half normal saline, trying to get a deeper lesion, which is an argument in and of itself, knowing that I was ablating on the myocardium and not up against that artery. How can you set yourself back here in the final moments of the talk here with mapping during PVC ablation? And I think Ed Gerstenfeld gave a nice mapping lecture on how to use the system, but ways in which in PVC ablation, in particular, things can go awry. If you choose a bad reference, or if your mapper chooses a bad reference, it's going to be a long day. And so an example of that would be choosing V5 here, where you have sort of a double notch. As they go past, is the system updating at the same point in the PVC? Technology is really helping us move past these limitations, but there's still some manual sort of decision-making behind the scenes that can affect the course of your case. In the ESI system, we use a 12-lead match. So you really have to match all those 12 leads in terms of morphology, but there's still a timing reference, right? So V2 in this instance, it was the negative portion of V2. So learn your systems and what they're actually doing. And I think PVC ablation in particular can point out some of the problems here. That was a RV floor. Mapping catheter ectopy, and this is sort of getting used to it. This is a patient who had single PVCs, and then suddenly we're in the region of interest getting nice morphologies here, and this is on a papillary muscle. But we've got a very, very early signal. And you have to think to yourself that this is probably too early. Varying annotation, this is a big one for me. So automatic mapping systems still need some manual adjudication. So where in the unipolar, where in the bipolar signal is it being annotated? You don't need a million points, right? For PVC ablation, you need a couple of dozen really good ones in the area of interest. So here's an example where we were in the RVOT here, and with one particular annotation, it looked like we were pretty early here, whereas in the coronary sinus, we looked like we were pretty late. But you can see the coronary sinus is being sort of preferentially annotated a little bit later. If we moved that coronary sinus annotation forward, now the CS was the place to be. And PaceMaps had looked pretty good in both sites in that particular instance. Inventing early signals, here's an example on a PAP muscle where I'm like, oh, cool, I've got a fascicular potential here before the QRS. But turns out if I'm really looking at the whole strip, that potential isn't there with every PVC beat, and it's sort of here, there, and everywhere. We all have noisy labs, and there's lots of structures that you're intervening, especially if you're in the papillary muscle, if you're through the mitral leaflets, you're through chordae, and you're potentially through the aortic valve as well. And those mechanical events can create pseudo-electrical signals. So training your eye to see those, I think, is really important. If it seems too good to be true, it probably is. So there's the example. Another way to say this is hope is for fools, or as my friend Jen Silva says, there are no hope burns. So she's a pediatric electrophysiologist, and that's really important when you're talking about pathways. Under-appreciation of map dislocation with ectopy, and Ashant, I've got about five more minutes, if that's okay, you let me know. Sorry. I said that's fine. Perfect. I know that San Astrobathum went for like five hours, one of the early ones for anatomy. This last point is really important, and this is a really cool study out of the Barcelona group, where they mapped both in sinus rhythm and the PVCs, and they're mapping both the anatomy as well as the activation, and this is point-by-point mappings. You're not doing FAM or geometry collection where it's wherever the catheter goes. I'm only going to make geometry when I'm there during this beat. Oops. And you can see that when we look at the shells of, sorry, in the right-hand column here, when we look at the shells in sinus in purple and the PVC map in green, they don't overlap perfectly. There's a reasonable amount of displacement, especially in the free wall of the right ventricle, but really importantly, the earliest activation sites get annotated completely differently. So this ended up being the successful ablation site, and if you're on an activation map that's populated only in sinus rhythm on geometry that's populated only, sorry, during PVCs and populated only on geometry during PVCs, you're sort of right where you'd expect at that earliest activation point. But in sinus rhythm, that point was translocated about a full centimeter. This is really important and something that I underappreciated for many years when I was ablating, and I really pay attention to now. So the mapping system is really just a notepad for you, right, and if you're taking notes on things that aren't the right thing, you will end up with confusing maps. I liked this other image from that paper, I'm ghosting in here, you can really see that translocation in sinus rhythm. And another aspect of that to think about is if you're doing peso mapping correlation maps, so you're not having frequent ectopy, those will be different than the site of activation during the PVC, so you sort of have to reconcile that in your head. I don't generally do two separate maps, but I will watch the catheter translocate during pace mapping or translocate during the PVCs and think to myself, okay, I'm going to this site in PVCs, but in sinus, I always ended up over here, a centimeter over, let's say. And so when you ablate and you're successful and you get rid of the PVCs, it means you can never get back to that exact site unless you also knew where it was in sinus rhythm, right? Can't do your insurance burns if you didn't keep track of that. Lastly, another sort of big concept, and this is the last sort of point here, just a really beautiful article out of the UAB group now over a decade old as well. And they were looking at preferential conduction across this outflow tract. This is such a unique area of the heart and it is really confusing, honestly, for the beginning mapper because we tend to think about conduction as uniform when you first start learning about it. But they were looking at right ventricular as well as left ventricular outflow tract sort of breakthroughs. And what they found were different patterns. So this is a left coronary cusp PVC, successfully ablated from the left coronary cusp. And there's apparent insulation around these myocardial fibers. So the origin may be right at the cusp, but the breakout site where you would have early activation may be in the RVOT. If you pacemapped in the RVOT, it would look terrible, right? Because it wouldn't at all, I'm sorry, it would look wonderful in this example because that is the breakout. We're not getting out towards the left side in this particular example. If you pacemap from the left coronary cusp itself where activation should be a lot earlier, you get a great pacemap. You may have some latency on that pacemap because of this insulation here. And if you have to pace at higher output, you may get some preferential conduction more leftward where we don't get that with the spontaneous ectopy. You may be capturing some muscle cells just a little bit beyond that. So you're having to integrate the anatomy as a really big component here, activation as well as pacemapping and recognizing that it's not as simple as best pacemap, best timing. There's some overlap here because of these insulating fibers. And they go through some other examples of more complex arrangements. This is even worse in this area if you're doing redo procedures. And that also means redo mapping during your own procedure. So lots of mapping before you come on RF the first time is important. The saving grace is that we may do very fine-tuned mapping and we still honestly with good force and irrigated tip catheters are able to do a lot of destruction in the area. Also a humbling thing when you think about the salmon colored arteries that were right next to. But we're often able to overcome sort of this confusion by essentially doing our nice big lesion. It's not very sophisticated. So I'm gonna skip that last example and go on to my summary slide here. So really prep yourself for success. Rule out structural heart disease are my sort of final tips. Catalog your morphologies. Have a mapping plan. Know how you're gonna set up your map. And then test your work when you're done with high-dose isopryl. And a reasonable waiting period. Those of us who feel constantly rushed, this is a hard one to rush, especially if your PVC went away after your fifth ablation lesion, you need to wait. And sometimes you need to wait an hour. You don't want it to come back while they've pulled sheaths. It's really not a great day. Scrutinize your map setup. Avoid that map bloat and wander that can happen with taking points in both sinus and with PVCs. And be tenacious with safety, especially in that outflow tract area and with the coronary arteries. No hope burns, as I just said. And really important, I said it earlier in the slide, but live to fight another day on these. Nobody dies of PVCs in and of themselves. So this isn't ventricular tachycardia. And I think our burden for safety should be higher in these cases. And I would leave you with that. It's okay to not be successful. So thank you. And thank you so much, Nishant, for letting me do this, even though it's very early. That was an incredible lecture. Thank you for that. Maybe I'll ask a couple questions here because people are clearly trying to work through their management of these. This was asked the other night, but what burden, PVC burden, are you comfortable taking to the lab? When do you think it's just a waste of time to bring the person in? Yeah, and I had included a slide and took it out at the beginning. I have taken people with a burden as low as 1% if there is some proof that it's adrenaline driven. So either treadmill or when you're looking on their Holter monitor or that it's with activity. And those tend to be, you're really highly symptomatic patients and you're going in eyes wide open. If you don't see a PVC with isopryl, you're not opening the mapping system, patches, you're not opening the ablator. You may give the isopryl in the holding area before you actually bring them back. But we have to have something. So I think the burden can be low. Those patients should be highly symptomatic and probably unresponsive to medications because the chance that you're gonna have not just difficulty having something to pacemap or certainly activation map, but also not having a great endpoint, right? So if their PVCs come and go anyway during the day and have that, it's not usually a uniform 1%. Every hundredth beat is a PVC. It's that they come and go for sometimes hours at a time and that may encompass the time they're in the lab and you may pat yourself on the back and they come right back. So that's a non-answer. Yeah. I like it when it's more like at least 10%. Right. And the chicken or the egg question here, multifocal PVCs with LV dysfunction, do you ever medically manage rather than take them to the lab to make sure that the PVCs are the cause? Yeah, absolutely. And I think in that context, the medical management is amiodarone, right? So most of those patients really aren't candidates for class 1C agents. I don't find that Sotalol is as safe as we'd like it to be in cardiomyopathy patients, especially ones with scar. They don't tolerate it as well. So it's usually amiodarone. So if your patient's willing to do a trial of amiodarone, that may give you sort of that push to bring them to the lab. If their PVCs are from idiopathic regions, I still may primarily go in for ablation and see what we're left with. So if it's outflow tract and pat muscle, that seems to be a combo that goes together a lot. In those patients, I will bring them. If it's consistent with their scar in a ischemic cardiomyopathy patient, I will bring them. I'm less excited about that in the non-ischemic, the sarcoids, the lamins, et cetera. The efficacy really does start to decrease. But that's a good strategy for sure. And then along those lines, there was a question about using class 1Cs for presumed PVC-induced cardiomyopathy in idiopathic patients. What's your comfort level with that? I saw that our lecture series is sorely lacking in non-ablative talks, right? So I think the antiarrhythmic talks are good. I did a session at the ACC two years ago and Yang Mei Cha from Mayo was tasked with discussing antiarrhythmics. And she was like, there's not very much data because we just started ablating these folks. And PVC treatment with antiarrhythmics got such a bad rap with the CAST trial that it was really difficult to imagine treating those patients. But I think the pendulum has swung again. If you have an MRI with no or minimal delayed enhancement, the Penn Group has shown in a small series, I think it's about 70 patients, it's not very many, that it is safe to get flecainide. I'm not really sure that that safety signal is strong enough in such a small group of patients. That being said, with full disclosure to my referring cardiologist and full discussion with the patient, if they do not have delayed enhancement, I will use class ICs. And I do have patients on chronic therapy that way as well. So it's not just as a litmus test to see if they're gonna get better and then bring them to the lab. Some of those patients opt to just remain on the medication. So I think it is a place to be, you're out on a limb. I don't think there's a great supporting data, but I think in the MRI era, I feel more comfortable with that, but it's not gonna be pro-arrhythmic. Okay, great. And then there was one question about adjusting power time and impedance when you're using half normal saline. What settings do you adjust when you're in the CS or even in the cardioly? Yeah, we definitely need a lecture on ablation physics. So I need one of the guys who do those talks all the time. The coronary sinus, and I didn't go through all this. I think Jason went through some of it. The coronary sinus can be a very difficult place to ablate itself. So the impedance is often very, very high and you have to sort of override all the controls in the system to even come on. I tend to come on very low power. So 10 Watts, even without half normal saline, just even normal saline. Because if you come on too high, 20 or 30 Watts, you immediately get an impedance rise often and that'll cut you off. So I'll start very slow and after 20 or 30 seconds, titrate up and I tend to do very long lesions in this area if I'm not right at the optimal site. So two and three minutes and sometimes up to five minutes. With half normal, I would definitely start with that lower power, but you need to ramp up still relatively early in the lesion. Otherwise you're going to limit your ability to penetrate tissue from sort of our current understanding of energy delivery. So you're gonna get edema and swelling at sort of a superficial level. So if you're trying to get deep, you need to start giving those higher powers. I end up using half normal on the endocardium sort of site opposite those coronary sinus activation points a lot in redo procedures where we've just given as much as we can. Remember, we're not actually, you know, abutting the muscle or abutting the vein and there's interstitium and then there's muscle below us. We've got a lot of reasons why, especially in a redo procedure, that you might have impedance barriers to energy delivery. And so you have to use neighboring structures to kind of help you. And that's where half normal can be helpful.
Video Summary
The speaker in the video talks about the mapping and ablation of premature ventricular contractions (PVCs). They discuss the importance of patient selection and pre-procedural evaluation. The speaker also covers mapping strategies for PVCs originating from different sites in the heart, such as the right ventricular outflow tract, left ventricular outflow tract, papillary muscles, and aorta mitral continuity. They emphasize the use of EKG findings to determine the site of origin for PVCs. Advanced imaging techniques like cardiac MRI are highlighted for evaluating patients with frequent PVCs. The benefits of PVC ablation for patients with cardiomyopathy and the challenges and outcomes of the procedure are also discussed. The video provides a comprehensive overview of PVC mapping and ablation, emphasizing key considerations and strategies for successful treatment.
Keywords
mapping
ablation
PVCs
patient selection
EKG findings
cardiac MRI
ventricular outflow tract
papillary muscles
aorta mitral continuity
cardiomyopathy
outcomes
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