In this Heart Rhythm Webinar Series challenging case discussion, Mayo Clinic cardiology experts Samuel J. Asirvatham, M.D., Abhishek J. Deshmukh, M.B.B.S., Siva K. Mulpuru, M.D., M.P.H., Ammar M. Killu, M.B.B.S., and Christopher V. DeSimone, M.D., Ph.D., discuss atrial fibrillation.
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Mayo Clinic Medical Professionals — Cardiovascular Diseases. mm hmm, wow, Good evening everybody. My name is Abhishek Deshmukh, one of the electro physiologists at Mayo Clinic, first of all, we really appreciate all the amazing cases we have been getting and really a lot of excitement and interest in this program. Today, I'm joined by my colleagues Dr amar kilo dr chris de simone dr siva Marlboro and dr acid bottom and dr Watson will you know, make some introductions and we'll get the session going. Thank you. Thanks Abhishek. So we got some uh nice questions ahead of time, just related centrally to atrial fibrillation. Quite a few of your doubts. Questions were either related to complications or post af ablation flutters. The flutters will handle in a different session in a few weeks. We'll cover some of the questions about complications here as well. I also want to tell you those of you who sent in cases for discussion or comments. We're a little bit behind and gotten back to some of you. We've got about another 10 to get back to. We will do that for sure in the next week or so and feel free to come back and present some updates on those patients as we go along. So I'll cover some of the essential questions that we got uh from you and this and just as a short introduction. So, first of all, you know, all of us got introduced to atrial fibrillation uh and in at different levels in the evolution of this procedure. But one thing that has stuck through the whole time has been pulmonary vein isolation. And I think really the questions that start arising early in training for someone is what's the best and safest way to do pulmonary vein isolation? And then a little later it becomes durability of pulmonary vein isolation. And then after any of us of you have 200, cases under your belt. The questions then become, is what do we do with failures? What to do When there is back to Square one with symptoms. And we're having to deal with atrial fibrillation. And that's really reflective of some of the questions that came back. So, I'll try to cover a few of these. one of the things that come up is trying to understand what the failures. Is it an organized arrhythmia or is it today? We'll try to focus where it's it's really the same syndrome the patient had initially, the character has not changed and we're back to it after we've done our pulmonary vein isolation and we may have some good evidence at index procedure and after the procedure that the pulmonary vein isolation is actually complete. That could be the scenario, one scenario where we all get questions and some of you have sent in questions, what are some of the things to look at their. So one of the approaches there is even before rechecking to get an idea if there are spontaneous initiations of arrhythmia, be it manu more fick or atrial fibrillation. What is that initial beat? What is the initiating beat. This is the concept of recurrent atrial fibrillation mapping. And to illustrate some basic points in this, we're going to keep the catheter our mapping catheter somewhere or ablation catheters somewhere. Multi electrode catheters in some key locations like the coronary sinus. And what we look for is sharp signals at a site where we feel the initiation is and early signals. Both of these are important concepts. The reason they're important concepts is that we know the classic rhythm, a genic si substrates that is the trigger substrate. What is causing the initiation of the tra fibrillation tends to have these distinct electra grams and they tend to be contact electra graham late and shocked. If this reverses, then the initiating beat is from there. So two things we're looking at is is it early and is it sharp and early? Whereas it's not sharp for the initiating. So there with the catheter in the left upper vein, we saw it neither early nor is it sharp. So other thoracic means that become of interest. It's like the superior Munakata concept is straightforward. We're placing the catheter in that site. And if we are fortunate to see these recurrent syndrome of atrial fibrillation. We look again here we see it's sharp but it's not early sharp meaning probably uninsulated? Probably has myocardial sleeve but that's not the trigger here we see a situation where we see a semi organized rhythm in some parts of the heart with long inter electrode flatlines, inter electra graham flatlines, suggesting that it's fairly organized but some other site which is highly disorganized and rapid. Now, what we won't know from looking at a tracing like this, is this an isolated portion, maybe a pulmonary vein that is just fibrillating but has nothing to do with what's going on elsewhere in the atrium? Or is this the primary driver that's then passively activating the rest of the atrium with variable degrees of organization. So one of the ways to address this and this is a case from dr Deshmukh, I believe, where the multi electrode catheter was in the posterior wall of the left atrium so you can keep the catheter there and then see with the subsequent initiation, is this early, is this sharp? Is it early? Then we noticed both phenomena. There's much more frequent activations compared to the rest of the atrium during fibrillation and the initiators also worried. So if that's recognized, then it is possible if this isn't already part of your construct for initial ablation, To isolate the posterior one similar approach, mapping catheter late activation and sinus rhythm or a paced rhythm and then attempt to isolate and similar endpoints. After isolation, we're losing the signals, no passive activation to that site and we may have this exit block activity from the posterior world. Maybe catheter induced, maybe spontaneous but unable to activate the rest of the atrium. So posterior world treated very much like you would a pulmonary vein, I think it's important to just look historically at like constructs from the surgical literature that if we treat the pulmonary veins just as these cylindrical veins here it was in the evolution of the animal studies, mitral regurgitation model for atrial fibrillation, not anywhere nearly as effective as when more sites multiple sites with an isolation type approach were used. So here multi electrode catheter. One way to do this isolation of the posterior wall is to connect where the pulmonary veins were previously isolated so that there is no conduction that's possible into this world. So the question then is like why this posterior wall? Why not this anterior portion? Why not the vestibule? Why not the Impact in eight muscles, much more complex structures? Why posterior wall similar to the veins that we isolate and for their we should appreciate that anatomically histological E. M. Bria logically and electro physiologically the posterior wall is the pulmonary vein. So the heart the atrium is made up of my cardi um from the primordial atrium which is the appendage, the vestibule which has a multifaceted origin close to the mitral valve and everything else is the developing pulmonary vein that comes in and merges with the heart? So when thinking about pulmonary vein, there really isn't that much difference when we think about pulmonary vein Just as one vein as a set of veins or as the true entire pulmonary vein. Several ways to kind of think about doing this technically, probably the most difficult but so called true pulmonary vein isolation, that is where a lesion set is made, where that whole embry logical pulmonary vein is isolated. You could get to that also by connecting the wide areas circumferential circles, but you have portions of the pulmonary vein that would still be left unaddressed. That's even more true. If you just make really wide circles with a common limb, there would be this as well, but all still getting towards the same thing. Another approach is saying that pulmonary vein substrate is probably best addressed by obliterating in the pulmonary vein. Kill the tissue. That's the culprit but we cannot do that in the pulmonary vein at least with present technology because of pulmonary vein stenosis. But we don't worry about that stenosis of the posterior world. So one approach is just direct ablation of the true pulmonary vein portions which you don't have to worry about stenosis. But the issues here is the posterior wall. As we any of you are. I've been doing this procedure no, is tough because of structures nearby and of course the most feared is the esophagus. Could be simple ulcers. Could be simple erosions and of course potentially fatal fistula that can occur when we do this. So limits the approach for how much we can oblate there. Sometimes though the esophagus isn't really adjacent to the posterior wall, it's a little bit to one side or the other, but even then getting portions of the anterior part of the esophagus can be a problem. This is an example of a very large stomach shadow here with food contents from days staying inside the stomach. In a patient who had any faith ablation procedure. And the issue there is the vagus nerve. So the vagus nerve, although it runs to the side of the esophagus, has got this rich type of plexus that interdigital dates with each other and includes the anterior world. Notice this inter digitization has got these looping type filaments so they go more lateral to where the esophagus is. So even if we're not directly in front of the esophagus, the posterior wall, that could be a problem. Should also remember every time that we are isolating the whole posterior world. We are by definition setting up an Islamist because we know the mitral analysts cannot conduct. And now if we have a perfect posterior boundary that's created we have to for sure, then think about the propensity for micro macro re entrant tech courteous. Now, the other issue beyond micro reentering tech guardia's is myocardial triggers. So this is a example also I believe from bishkek where a patient with same syndrome of recurrent arrhythmia. But here with the mapping catheter placed in the myocardial appendage can cause these triggers and in that situation it is possible to oblate. So as to eliminate the arrhythmia without isolation of the appendage, presumably these are types of flutters that include the Ost e um of the appendage for part of its slow zone for others where it is truly a trigger from inside the appendage, then we have the left atrial appendage treated like a vein matt, late activation, making sure that the signals that are being seen aren't actually the pulmonary vein very important. Especially if you see signals that you have interest only in one part of the appendage and then isolation in a circumferential manner. Some issues when you do this, isolation is the mechanical function and technical difficulty with doing it as well. So if we kind of summarize like maybe tackling a few of the questions that you had brought up issues is learning about technique of pulmonary vein isolation. But beyond that it's about durability and it's about how do you handle it when it doesn't work. And this brief kind of intro here was just some of the things about understanding the recurrent syndrome. Is it new then? Think these are flutters maybe pro arrhythmic. If there is just no change it. Maybe the pulmonary veins either were not dealt with or simply wasn't um the trigger to begin with And some approaches to consider. So please do send in your questions and we'll take take them, take them as they come in the interim. I have one question that was sent to me very specific about our approach to um avoiding uh is a facial trauma. So I believe we have uh uh dr munger here on as a Panelist. Sorry, he will be joining shortly. And maybe I'll start with asking dr de Simone first to kind of tackle that question. What do you think chris do we have a way to help prevent appendage? S a vigil trauma? Is it something in evolution? And then maybe Alaska um are to also comment about both surgical and endo Cardell procedures and appendage from chris Christie simone. So I don't think there's a 100% foolproof way. So, I think we've got to be very, very vigilant, especially when I'm on the post here wall, even if it's on the superior inferior, I always have esophageal probe and I move it continuously every time I'm walking down my back online. So I'm monitoring for sufficient temperatures and if I need to stop, let the esophagus cool down so I don't stack the lesion. That's one approach. If I need to go to the anterior wall and come back, that's my second approach. Third approach. If I can't do it and usually it's not the first time. But if I know I ran into it and it's a redo procedure or if I get clues from the ct that the esophagus is really bigger, right, where I need to go I've also been using a salvageable deviation approach to just get it out of the way. So that then I feel much more confident I still have the temperature probe down there, regardless. I think the fourth thing is I don't use to higher voltage power on the post here wall. So I never go above 25 watts And I try to keep my lesions 30 seconds or less. So maybe, maybe. Well, I'll come back a little later to Amar's comments. There's a question about why we don't have bleeding at the time of the procedure. When we get esophageal fistula, and maybe I'll just address that here and then we'll take a couple of the other questions. So, you know, if we just a reminder of the how this, it's a federal fistula occurs, This is the left atrial of left atrial posterior wall. And to just remind everyone, we have this little sleeve of pericardium here, which is the recess behind the atrium, the oblique sinus. So one of the things that made it difficult in the early days to know what was going on is this temporal sequence of fistula. It doesn't happen at the time of the procedure and what appears to be the case. It's heat related trauma that produces some s official erosion, That's all that's happened at the time of the procedure. The fistula doesn't exist at the time of the procedure. This then becomes an ulcer, The ulcer, then has erosion. And this is already weakened tissue here that can cause is a fragile air and contents to get into the pericardial space. This is the stage of the new mo pericardium chest pain, non specific symptoms and then with continued erosion it actually becomes the fistula. And there we have the endocarditis. We have air in the circulation every time you swallow something is going to the brain and an extremely emergent situation to try to get rid of. So that's why you don't see like perforation and bleeding at the time of the procedure. Because that's not it's not a perforation, it's the inside out. It's coming from the esophagus to then reach reach the heart. So we have a question that I'd like dr munger to address for us. So tom First of all dr mongers are chair of the heart rhythm service and thanks for joining tom. Thank you Sam. So we have a question and if I understand it right. What it is is it looks like it's a question from someone who's new to the field I think. But basically what it is is from experience, what are the aspects of the ablation procedure that have made it easier and safer today That we have to emphasis for new entrants into our field. So I think when intra cardiac ultrasound was introduced 20 years ago that um improved the safety of the procedure. Since you could monitor the pericardium real time for confusion and you wouldn't have to wait for hypertension developed before you could identify the presence of infusion and then treat it similarly. You can locate the catheter in relationship to the pulmonary vein cuffs. Now that's a little less I think an issue now with the new mapping systems as far as giving you detailed anatomy. But I think for new operators it's still they tend to oftentimes go into the veins just a little bit when when you're doing mapping. And so I think having ultrasound to identify where the catheter is in relationship to the veins and the esophagus ah and valvular structures is quite helpful. So I think that was one Big Development Sam was ultrasound. Um I think the contact catheters has also reduced in my practice perforation just because it gives you feedback about high pressures. I think steerable sheets have helped make the procedure easier to do technically with the R. F. Um So I think those would be the big things that I've seen come along. Mhm. Thanks. Thanks. Thanks a lot tom. Um You know and I think also tom fair to say the mapping systems have just created a new visualization approach for trainings. Yes. You know I was doing a case last week with one of our new trainees and I kind of know the person very well their strengths, weaknesses but I was shocked at how well they were doing the venus isolation Like probably skill level as me five years out of training. So I think it's because of that visualization and then maybe not getting the whole picture but can field for here's what we need to kind of go around now we have a yes ma'am. Yeah I was just gonna say I would agree. It gives you the anatomy much like the C. T. Which makes the understanding of the anatomy and where you put the lesions quite a bit easier. Great. So you know we have a question here um from dr Vass ready if I understand right and please feel free to come up and explain if we got this wrong. But can you put can you use something in the esophagus as a heat sink? So I can just maybe briefly review that issue. It's worthwhile understanding. Especially for new folks for what do we mean by heat sinks and like how can they be of how can they be of value? So we know like principle of ablation, arif ablation is the R. F. Itself is not heating the tissue. The radio frequency waves do not cause ablation. They do not cause a lesion or collateral damage. But there's heat that's being generated because of sudden change and impedance at the tissue interface. So this impedance heating occurs here and is going to spread on all sides here. We have cooling. So it's not much chance to spread into the blood pool. So it's spreading this way and could hit the esophagus. Very interesting ideas have been explored to try to minimize this. One of them is to use a cooling device in the esophagus so we can actually keep the esophagus side cool while we're hitting the site. And some of the early ones were literally cooling devices. Others have been like porous balloons or porous catheters to kind of create some cooling, much like irrigation on this side. Now, at least in preliminary studies the early days studies, these weren't of much value. And probably the reason for that is two things happen when we create a heat sink, as you may actually promote the heat transfer and the second is the instrumentation and the cooling and irrigation. All of them may add to any damage. You didn't see that produces the erosions that start the whole process. So they never really became mainstream. It's a bit better material design. Maybe something worth thinking about. The other interesting idea that was also tried, but I think may have been a misunderstanding of the nature of lesion formation is using a both type technology, the wireless noise cancelation type technology to say if we take the R. F. Wave and put an inverse wave and just protect from the R. F. So you're canceling out the R. F. To come there and actually works really great in terms of canceling the wave. But the problem is, it's not the wave, it was the heat that was coming there and it was not possible to show benefits. Now, we also had a question uh from prior to the session. And I see that Dr Mahadevan has joined us that maybe I ask her to address and anyone else. Also, if you see questions, please do jump in and bring them out. So um is dr madeleine here online? Yes, doctor. So dr Madeleine is one of our electro physiologists, special interest in congenital heart disease device placement and ablation. So martin lee, the question was, how often do we have to manage a tre fibrillation? I think the question was actually structural heart disease. But focus it a little bit more for you on in congenital heart disease, His congenital heart disease, adult congenital heart disease atrial ablation. Is it all about flutter? R is fibrillation an issue. And maybe you could share with us some thoughts on which situations is fib becoming more of an issue. Sure. So focusing on the congenital heart population. Okay, um in a traditionally atrial flutter has definitely been a bigger concern and we see more of the atrial flutter rhythms that are related to surgical scars than atrial population. So historically speaking, as the surgical techniques started getting better Over the course of the past 30 years or so, the the initial patients were repaired when they were younger, we were seeing more of the atrial flutter rhythms And that is mostly related to surgical scar. Mostly in the right daydream. But more recently, the last 10 years or so, both in our practice and also in the literature, there's an increasing recognition that as these patients age due to the success of the initial surgery and also the success of managing these patients very closely in the congenital clinics we are seeing more of atrial population. So at least in the population that we are seeing by the time patients reach 40 and 50 years of age we are seeing more atrial population of particularly if you think about the moderate to high complexity, congenital heart diseases, the other place where we are likely to see atrial population as the SD population. Um So patients who have isolated A. S. D. S. May also present with atrial fibrillation and there the question that comes up is how do you manage the asd closure in combination um in combination with the management of the of the atrial population, do you? A blade first and then think about asd closure and and questions such as that would come up. But for sure in the adult congenital population aged population is increasingly recognized and in fact just recently we put together our own experience Looking at a total population population at our center in about 150 patients. Yeah thanks. Thanks man. Thanks. So now we have another question that's specifically about the vein of Marcia. So you know I think it's an anonymous attendee but asking about the vein of martial related to atrial fibrillation ablation. So maybe I'll take some opinions here and then we can feel free anybody else who has questions in that area. We can look at Omar do you want to take a shot at that, Is that a thing? This vein of marshall, Is it something we address and your take also from the surgical perspective where we have direct visualization of the site. Is that something that's part of the paradigm for surgical ablation? So thanks for the question. I guess when we're talking about vein of marshall's, sometimes we're also referring empirically to um epic coddle connections. When we're performing pulmonary vein isolation, Sometimes you go around and you do what you think is a perfect waka lesion. You check the line, no signal, you pace along the line. Know capture Yet sometimes you may still have entrance into the vein or it can still demonstrate exit. And on some occasions is because of these epic coddle connections which I think are becoming increasingly recognized. It's very good to be aware of them. Um vein of marshall I have not encountered clinically frequently, but I've definitely had other cases where I feel like there has been an epic coddle connection either into the carina region, for example, on the right veins or sometimes actually into the vein itself. And being aware of that. I think it's important because you don't want to just keep going around burning along the waka getting frustrated. Risking complications to the patient and whatnot. And so being aware of this, you can do certain maneuvers to try and uh you know, diagnose that problem in terms of a surgical approach. Um Again, if it is generally a very anatomical based ablation, there are different techniques now surgically that are adopted. Um taking the open surgical approach out. Some so called hybrid techniques have been gaining popularity. Um one example is the convergent ablation which is a subsidy foid incision and then a uni directional three centimeter probe is put into the oblique sinus and complete posterior wall ablation is performed from one vein side to the other and that can electrically isolate the posterior wall and usually takes care of some of the epic ideal connections. Then if you do a concomitant appendage management, you can actually transect the ligament of marshall um at the same time. Um and if you put a clip on the appendage, you may actually isolate that as well. So those are just some of the uh nuances I think related to that. If that answers the question. Yes, I think that's uh that's part of the story for sure. Uh maybe Alaska several also in Asaba. We've been hearing quite a bit now for about three or four years, just empirically trying to target the vein of marshall perhaps with alcohol as part of the eifel ablation paradigm, Your thoughts, your take on this. Thanks sam So ligament of martial targeting with alcohol ablation. Um in my clinical practice I've done a few cases in patients with hypertrophic cardiomyopathy. They have a mitral flutter could never get block both endo cardio and through the CS So those are the patients doing a CS venogram identifying the leg, identifying the vein of Martial selectively. Kanye waiting it and inflating a balloon and injecting a little bit of alcohol can take down the maya kardian that sometimes cannot be mapped using our current electoral and atomic systems. I think there is certainly a role difficult to terminate mitral flutters patients with hypertrophic cardiomyopathy. And if you have persistent vein connection and you think that you have a good vaca and it looks like the connection is through the vein of martial. Those are the situations where I would consider alcohol ablation. But I haven't been doing it routinely. So maybe I'll maybe I'll just x expand on this a little bit here. So you know just you know why this vein of marshall I think really um are kind of hit the nail on the head. When we say vein of marshall were really Meaning four different things. We're meaning trigger because this vein is a remnant of the left superior vena cava running in this fold between the pulmonary veins and the appendage. And like the right superior vena cava. Like the pulmonary vein this tissue can be a trigger, it's a thoracic vein. Just like anything else. We also say vein of Marshall. When we're thinking about he can't do it by conduit. I mean muscular conduction from the vein to connect the pulmonary veins to the rest of the atrium via the coronary sinus. So this can't do, it prevents you from getting isolation of the pulmonary veins. This was a much bigger issue in the early days uh when we did ablation closer to the vein, but sort of falls away when we have played in a wide area manner and I'll explain why I think why that is the case can't do it also means for flutter. So this is conducting and we try to do an ablation endo card really. And this is still a way you can get from muscle in the CS to muscle in the atrium. We don't quite get rid of the whole connecting fibers for the core for the flutter and wind up failing with ablation at one targeted site, which otherwise entrainment might have said is great to a blade. The third issue is, it is an autonomic structure. So just like the spc, the right as we say sinus node, there's no, there's autonomic six in close proximity to this to the vein and it's just as true with the left as we see and its remnants. So it becomes an autonomic site. So sometimes try to target when you're trying to do an autonomic and autonomic modulation approach for atrial fibrillation. Just make the action potential duration fundamentally longer for the atrium. So it's much more difficult to get a rapid arrhythmia. And finally it's just a vantage point to a blade Marie trip. So another school of thought is the more tissue you can safely a blade, the less likely as atrial fibrillation is going to recur. So in that case this becomes a method where if you were to inject alcohol. Yes, you get rid of the trigger. Yes. You get rid of the conduit. Yes. You may modulate the aerodynamics but you also have a fairly large area of tissue that you are bleeding and maybe that helps us part of. So just some background to when we think about what this the reason that wide area circumferential ablation. So this is an inside the heart perspective appendages here, The forceps is in the pulmonary vein and this unfolding here, which is really where we do our wide area lesion is exactly opposite the vein of martial tissue. So ablation here just by default is a vein of marshall modification. So even though we may not willfully target the structure, we probably due to some extent in most of our cases. Should also keep in mind that it's this ridge along with the way it connects to the coronary sinus. A beautiful dissection from doctors. Damian Sanchez Quintana, that me create difficulty with emulation. In other words, we know if we were to try to draw a line here and we have the C. S. On the other side that's competitively cooling the tissue that you're trying to heat and a blade, the same is true. If we're doing wide area circumferential ablation around the pulmonary veins. And you have a large the vein of marshall or left as we see in that site that will produce competitive cooling. So it may be the cause of difficulty with ablation that forces you to go in some cases closer to the main should also keep in mind that there can be distinct signals from vein of Martial tissue that we could map from adjacent structures. So capita in the pulmonary vein. In addition to being picking up lefty, true signals, upended signals and other pulmonary vein signals could also pick up signals from the vein of martial itself now. Um So maybe so I say there is a question and I think siva you already. Uh huh, answered it a bit I think or the A. V. Shape is in patients who have uh and S. D. I am assuming post closure and atrial fibrillation approaches. Uh to trying to do the transept of puncture. And maybe I'll ask dr munger and dr cha to comment on their approach is maybe to make it a little more generic. The difficult trance septal puncture specifically to include patients who have a previous patch closure. So maybe we'll start with you tom you're approaches and this and then we'll ask young mate too my pain as well. So a couple of things about the um prior closure with an ASd device. One would be again using inter cardiac ultrasound or t. two. And then seti even before you plan the procedure to see if there are windows or you can go. That's around the device. Many times you can go on the edges of the device either posterior inferior or interior lee and avoid adjacent structures. Sometimes you can go through devices but I would warn if their old devices, I had one A few months ago that was had been in for 22 years and I could not go through that device. I think it had been so thick that you just couldn't get through it. Um For either tough septum zor if you really had to go through the device, I suppose the Bayliss needle or using our F on a traditional needle will be an approach to get through. And then using either a series of dilator zor balloons too balloon or dilate the septum to get the hardware through would be the approach ideally. I don't like going through the the the patches so I'll go around them if I can. Thanks john young man. What about you? Just question is on difficult trans septal The focus of the question is A. S. D. But do you want to expand on like if you think of the very first transept als you did versus now, what are the things that have made it easier and we are more confident than even difficult situations? I think dr munger has given his experience. I think the key is here is because we use the intra critic out with sound guidance. So that visualization really helpless, you know, to know the septal anatomy and then to charge from there. You know how much force you want to use the more anterior or more posterior or superior interior. But regardless, sometimes we do have a challenging septal, especially a patient outside the multiple have issues really made this car around the focal provided area. So in that case sometimes uh we use, you know, sometimes we use the same except I think that's a very nice set of tools to help us to get into the left items and the one we care about agent. Sometimes the violator and the sheets had had a difficult time to go in. So it's better to use either six steps or using the long wire to get into the left atrium and guide it to the prom intervene. So in this way the force, you can use a, you know, bigger force but avoid the dilator or the shoes. Really appropriate the mild cardio. Thanks. Thanks. Yeah, maybe what I'll do is use a figure to kind of get to what both you and tom have brought up here. So just a few things. So just a reminder about the interracial septum. This actually is an important issue for mapping and for abrasions in a variety of areas. So a couple of things. So first, as you'll notice from this dissection if we think about septum is a way to go from right side circulation to left side circulation And there's a curtain separating the two. You will appreciate that the inter atrial septum is actually a very limited structure. Just this little box here and posterior lee will be the faster of Alice. That's it. So if we have a large asd patch or we have an angel wing device, older device that's closing that fossa and encroaching on this when we look at approaches, how can we cross? It's kind of pick your poison. What's the problem that you could run into? If we want to avoid this, the largest surface area will be above the device, the superior nimbus approach. But the thing to remember about the superior nimbus is the superior nimbus is not part of the septum. It's an imagination. It separated the right and the left atrium with various amounts of soft tissue and fat. So if you do do superior limb bas function, you can certainly get into the left atrium. The risk would be that if you don't have enough tissue here, extra cardiac tissue, that when you pull back you can get bleeding into the pericardial space. Many of you would have noticed that if you are inadvertently trying to cross and you're thinking, why is it hard? And you're in the superior limb bas. When you push contrast, you'll get some staining, it's not a free of fusion, but some staining in the upper cardi and that's because there's tissue there that's kind of containing that that structure. So one thing that least in my practice that I do so far it hasn't been necessary. But I always do. It is if we are doing superior nimbus puncture. Like in a patient with a device I will leave a wire and have one of our colleagues who is very comfortable with plug devices or putting in another closure device, Pull the sheet out and then watch for about 30-45 minutes on ultrasound to see if there is an infusion that's building up. Should remember that if we do it more interior lee we have a small room but the minute you come in front of the U. S. Station rich so that is the inferior nimbus then we are risking some damage to conduction tissues. So if the patient already has a block as a pacemaker may not be an issue. But that's a risk. When we think of an anterior approach, When we think of a posterior approach, then the risk is you may not actually puncture in a way that we're crossing directly from the right atrium to left atrium. What we're actually crossing to the pulmonary vein and from the pulmonary vein to the aircraft. So this is certainly doable. It's sometimes done in inadvertently and patients have done okay anecdotally. But the problem that you might wind up with is that it's very tough to isolate this vein then to do the wide area lesion and you may get a small fistula between the pulmonary main and this when you go more inferior, then it becomes really like you're entering the CS and then getting it. So just like this is not a true septum inferior lee. Also the separation, but instead of tissue that takes the gap, it's the CS that's taking the gap here. So I hope that kind of gets a little closer to uh answering, answering that question. So um I don't know if you want to have floral images showing the puncture and then the in we wire. Is that helpful to demonstrate just wonderful. Why don't you talk us through it? Let me just share my screen. Mm hmm. So this was a patient who had a prior asd closure device and was coming from atrial fibrillation ablation. And the concern was, could we get across as as you had just questioned. And so I'm just going to show you the ice image. I'm not familiar with ice. Do you want to identify the structures for us? Thank you. So the ice catheter is in the right atrium and you see this triangular sector. So the immediate chamber is in the right atrium is the right atrium. And then you can see this big echo density and that's the asd closure device Aorta is just coming in at the 2:30 position, slightly off access and then you can see the left atrium. And often if if we look very carefully we may find a small rim of tissue that we can puncture. And in this case I thought there was enough in fear really that we could safely go across or at least attempt. Sometimes people do try to go through the device in this particular device. I I didn't think it was possible. It was a very old device. And the other thing to consider is if you are successful in puncturing through it when you come out there's a hole that you often will need to close, assuming the indication was solid enough for closure in the first place. So that's the video just to demonstrate that. And then if you can see my floral, can you see the power point now or is it stop sharing? It's still how about now? Yeah, I think it's coming, yep. There it is. Sorry to, screens is throwing it off. So again in that case we were able to go inferior to the device uh successfully. And then what we use is this in we wire and it's basically a wire that as it comes out of the sheath or the dilator, it would just basically loops in on itself. And so that gives you some protection as you're advancing the dilator and sheath into the left atrium. And so we use this not uncommonly in these cases or at least I like to um And also when we're doing transept als for left atrial appendage occlusion procedures just because it gives you that added safety to advance the sheath without worrying as much about going through the back wall. Fantastic. Uh And um are do you want to add any comments about like the issue of pericardial patch, closure, patient's surgical closure. What is our approach for cross crossing there? You still avoid the patch. Go through the patch. Yeah it again if I can find a remnant of the true septum, I will always try to go through that first um pericardial patch I have gone through before if it was big um closure closing it haven't done acutely. Um If there's concerns during follow up we can always consider. I always counsel the patient of that possibility but I haven't had to do it acutely but puncturing hasn't been um as challenging for the most part. But some of them can be very calcified and so they're the ones that may be more difficult. I don't know what other panelists or colleagues may think maybe I'll just add a little bit too too. That I think the the key is what you said is you know when we have a closure device, it's always a good idea to see is there a rim that we can try to go through. But surgical closure for an sde, they're going to suture to muscle on all sides. So we are not going to get a rim in that case unless it was just suture for api fo in which case it's not a difficult cross. But the point you brought up about calcium is extremely important. So the pericardial patch, especially bovine pericardium over years. One of the risk is it can become like boom. The issue is I don't think as much that we can't cross it because I think you know sometimes we just brute force with electro Kateri, all kinds of things that we do, we're able to cross but we have to remember the risk of calcium embolization. So example of a patient who hypertrophic cardiomyopathy, atrial fibrillation. Asd closed early in life calcified and actually when we retrospectively look at the sinese you can see calcium there and then had a multiple symbolic episode. The toes, the hands, the liver, the kidneys, acute renal failure, fortunately no stroke and fortunately a lot of it that improved. But another thing to keep in mind is when we cross and it's hard. Is it just fibrosis. Is it just because we have less of landing room or is there something that like calcium that's formed that we have to be careful about in closing. So I think we're getting close to finishing up sam. There is a there is while we're talking about this asd trans septal there's a question about how do we differentiate septal staining versus superior limbo staining when you were in the middle of a procedure. Okay sure. So maybe I'll go back to this and we'll just do a very quick one on that. So the key difference this location and movement of the stain. So when we have the fossa itself sustaining, you have a sheet that you're using to inject the contrast. So the pressure of that sheet in the lao view will make the stain move leftward versus rightward. So if you push the catheters, just like tenting, that tenting is best observed in the L. A. Overview and you see it going left back to right as you relax the tension or with breathing or cardiac movement. On the other hand, superior limb bas and epic arterial tissue straining. It tends to be more widespread and there will be no movement in the lao view. It will be fixed because there's no scope for painting. It's actually this tissue here that's come up to the site and then comes in another clue you may get when you have a superior staining of the tissue, even though there's no free pericardial, you may see the indentation of the aorta uh in that in that area and that indentation of the aorta with the staining is actually better observed in the view. And the reason for that. Maybe I'll show with the different view on the dissection. You can see what's actually filling that area and what that is is when we in a superior plane anterior early we have this non coronary sinus of val salva pushing into that separated area from the limb bas. So you can imagine left side of the limb Baseer, right side of the limb Baseer and this in turn. So if you have staining here, you'll see this outlining of the aorta. That's something you'll never see when you're in the faucet because the fossa is a more superior posterior plane to the limbless. Does that answer the question to some extent? Civil, yep, yep. Great, well thank everyone. And it's really once again the questions and cases that you put together, we'd love to have you come back and put to present to the rest of this and we'll do this through the rest of the year. We will also make sure that we catch up and respond to your questions and cases. Thank you everyone. I think we had some fantastic questions and really timely questions what we encounter in our ablation for atrial fibrillation. One common theme was how do we account for the frantic nerve and what would be the potential locations or legion sets by which we can injure the frantic nerve dr axelrod. Um would you like to answer that? Sure. So I think unfortunately the physician who asked us this question did have a chronic injury and maybe I'll just hit a few high points here. So a couple of things is, you know, naturally we have this right hemi diaphragm a little bit higher then the left because of the liver. And it's something that can be fairly subtle in just the resting state when we have Franek nerve injury. So a few things to keep in mind is it's usually work up of shortness of breath. But it's very different from the shortness of breath with primary main stenosis. So there it's like cough shortness of breath, effort intolerance. Some hypothesis. This one is just Disney uncomfortable breathing and it's worse when they lie down compared to sitting up or standing worse when they lie down. But it's not the air hunger of our talk and when you have this weird kind of conscious difficulty uncomfortable breathing when the chest x ray is done we should ask for a sniff test. So this kind of Mueller type maneuver and then it's very obvious that we're dealing with this frantic injury. You know a couple of I think this is a case of yours I believe I'll be chic to kind of illustrate that how you the sniff test kind of can bring this up very obviously it might be civil. Just a few things about that frantic nerve where it gets injured. When you look at the high parts of the forensic nerve it's an sbc relationship. So it's spc inflation when we think of the lower parts then it's an equal relation of the right upper pulmonary vein and the spc so can be injured especially balloon where the balloon is seated little into the pulmonary vein versus a bleeding in the S. V. C. S. V. C. R. A junction. Now obese patients are most at risk for being symptomatic. Most reported cases recover if you give it enough time when it absolutely doesn't recover. Then occasional patients you can do diaphragmatic application, an occasional reports of frantic injury from other reasons where stimulators, coherent stimulators to try to improve the situation. So that'll be kind of just maybe getting to why it happens where it happens and where we need to be particularly careful I would say balloon because balloons seating little inside the vein. You have to be careful host of patients surgical patients because the strictures from the pericardium, the pericardial fibrosis may move the frantic nerve which is a pericardial structure. It's an intra parietal pericardium structure. Might move it to a site. You're not used to thinking of frantic nerve. Be careful in those situations there. Does that get to the question of? Yes I think that's fantastic. We always talk about the right frantic nerve. But we also need to remember that even though sometimes the left Franek nerves can get, you know a plated. Unfortunately the case you showed about the appendage isolation, we are very careful. Especially if you go deeper inside the appendage you might be getting approximately close to the left sided, frantic nerve. Yes. So I think maybe I'll just do a little sketchy out of the shape. So this is appendage. This is the preliminary outflow tract. Usually it's one third two third distance on the appendage from the tip is where the frantic nerve runs. So this is also very close to the anterior lateral coronary vein. That's why basil positions in the intra lateral coronary vein for pacing. We get sometimes frantic stimulation whereas its distal postal lateral gain that we can get the stimulation. Just a couple of things about the course of the frantic nerve as it runs over here is when we're isolating the appendage, that is an issue, but it's also an issue. It's also an advantage in some ways as we're learning more about frantic stimulation for central sleep, apnea, linda, cardinal approaches venus approaches to try to do the stimulation rather than the present venus or a pericardial approaches also come into play for this left friend? Great. Any other questions we didn't get to today? Oh yes, there was another question. So if you're mapping of flutter and say cycle length is 400 milliseconds or so and you're not able to account for the entire cycle length, both in the right atrium and in the left atrium. So when should we start to think whether the epic are ideal. Atrial surface is part of the circuit. Yeah. So would you want to try that to take a shot at that? Yeah, definitely. So first step would be to confirm that the diagnosis is macro reentry if entrainment shows that it is possibly a large macro reentry circuit and you're missing. Certain parts of the cycling. So one thing is to make sure that you have annotated all the points appropriately. Um Some of the operators don't really annotate it annotate fractionated signals. So that may result in not having the full map on your activation map. The second step would be, where are the other areas? Um The remaining cycle length could be hiding, it could be septum ridge between the appendage and the veins and in some cases Epic are ideal substrate. And if it is truly a macro re entrant circuit, you can sometimes get away by designing lesion sets to try to interrupt the path and in, in patients who you suspected Epic are ideal circuit then maybe a pericardial access and mapping that area is a reasonable option in my practice in somebody has a history of prior high power short duration or high power low flow ablation. It can create a substrate where end accordion may be very different compared to the Epic Ardian in those patients you can consider upfront. Epic are real mapping. Does that make sense? Abhishek Yes, absolutely. Maybe I'll just add a few things here. Abhishek um so just using the screen here. So you know, one of the points that silver made is we want to be sure that we have mapped both a tree in because some tech cardio as large circuit tech guardia's involved both atria so called by atrial tachycardia, especially post mais patients for example, this is something you could happen but this is easier said than done because we may have part of the circuit here and then the other part of the circuit could be going away from the septum and bank. So if that happens some parts of the septum actually are not in the circuit. So it makes you think this cannot be by atrial. So just that thorough mapping of both, atria sometimes may be needed. And silver made a very important point about fractionated signals. So this is a very important issue and it's a little different the issue if you do multi electrode mapping with minimal annotation, what point to point mapping with your own annotation? It's a different problem in these two situations. So Silva pointed out that if you're in the habit of doing point to point mapping and you found fragmented signals that take up maybe 80 milliseconds, 100 milliseconds of our taco cardio circuit. And if we take that as a location only point because we don't know which one to annotate, then it becomes a part of the circuit that necessarily will be missed by the man. So you have to go back and see what did you take location only without annotation. And if that happens to fill the gap when we look at the width of the fragmented signals then not only will you get your complete circuit but you'll have a high degree of suspicion that this is necessary not only to finish your map but to finish the tachycardia circuit and would be a good place for doing the ablation. Some operators will take appoint an activation point arbitrarily as one of these and note there are fragmented signals. So even then when you look back at the fragmented signals, if they were not location only points, you still would need to go back and see what could I take here for automated systems where there is minimal annotation. This produces a different type of a problem because several beats are being mapped each time you could have taken a difference signal and it will give you a map that's difficult to visualize the circuit, but you'll see crowding of signals at one particular site. Multiple timing's very, very, very close to each other. This doesn't mean the circuit is there. What it means is the equivalent of a fragmented signal site that you need to go back to explore and see if I did take all of these. Would I get the whole tech cardio cycling? I think the question of the sheikhs you asked is about epic. Are deol, could it be a Picardy ile? And the answer is yes, but what is epic cardia? What is the Picardy alone? Could be the epic cardinal Myocardial in but it could also be an epic arterial structure that forms a bridge between the chambers or parts of the chamber, notably we have non coronary sinus of val salva interior lee and the muscle of the coronary sinus, the true coronary sinus inferior early so there we may need to make a separate map of these structures and add them to the map and a cardio to get the full tech cardio circuit. I'm sure we'll tackle some of these issues even more as we move towards macro reentering tech guardia's at a future session. Great. Where are there other questions as well? Yes, there was one more question that it is always difficult to oblate attack or packs with the earliest site, Say at CS 78. You know, near the Middle Angeles or near the coronary sinus. How to explain it in anatomy. So at least maybe I'll give one example why sometimes it can be difficult as you're getting close to the coronary sinus, there can certainly be a heat sink effect and you may not be able to give a good lesion at that point. Second, it could potentially be a breakthrough point for another flutter which is going on. It is just that you potentially map the early side which is there and a bleating. There may not result in termination of the tachycardia. These are some of the things I would think of but maybe some of the other, you know, you are other panelists could answer that more. Yeah, maybe chris do you have some thoughts on this? So I think the doctor is saying that by experience they've noticed that I think they're talking about like post day of ablation scenario, there's a atrial tackle cardio or That's in the vicinity of CS 78. And by that I think what what's meant is like posterior, posterior lateral um uh mitral annular region map with the coronary sinus catheter. And it's been really hard to oblate to get rid of it in that situation. So Abhishek pointed out a few things, you know, the cooling issue, uh your experience or your thoughts on why it could be difficult in that region. I think if I'm understanding the question correctly, what they're trying to get it, I think that region specifically, it's just really hard to get catheter stability and maybe that's the reason why they're thinking that it's kind of difficult. So at that region it's you know, I rely on ice as much as I can but it's hard at that vestibule area. Sometimes there's that step off, hard to keep your catheter stable I think. Um I'm not sure how that relates into after the ablation of atrial fibrillation though, I'm not sure if they're catheters just keeps falling off and going into the ventricle but that that that would be something I would I think of. Yes, great thoughts, maybe I'll just add a few a few things here. Um So you know, I think this is the region that we're talking about. So CS 78, something around here, so few kind of things to think about here first of all is that a re entrant tachycardia that we mistook to be a automatic tachycardia that we're failing to inflate. In other words, the reason we may have thought this is an automatic tachycardia is because we have a focal breakthrough here bracketing best as we can see and it looks like a pebble in the pond should be easy ablation, get a catheter there and a belated. And you pointed out, you know, because of the mitral analyst nearby, this could be tough for stability and I think Abhishek pointed out, it could be, it's the CS that's cooling and making it tough to get a trance mural lesion there. I think another thing to be very cautious about is the CS and the left atrium are not always telling us the same story. So we may have the large atrial electra grams showing us that there is indeed a focal type of breakthrough. But this may be the exit site for attacking cardia that's using the CS as a way of completing the circuit. So it's kind of like a mitral is thomas type tachycardia. But the mitral list must may look blocked and this may look like it's bracketed but that's just the CS to L A connection in that location. I can draw an analogy to an epic are ideal accessory pathway that uses the CS, but the way it gets to the left atrium might be at this site and we could have played all day and you never get rid of it. So if we have really a re entering tech cardio nian blade here, then it's just going to maybe still complete the loop through here and you just never get to it. So one step there is to define is it automatic or reentry? This gets even harder when it's ph when if these packs are just single beats of reentry so there I kind of fall back on the clinical story. Is this like an automatic automatic tech cardio patient scenario or is this a re entrant patient scenario meaning post af ablation scarred in the atrium, joe grand syndrome, post bypass surgery lupus. All of the things that tell us car and if it's card then we think could this be exit. And you have to think about linear revelation to sell if it's automatic in this lesion, it's exactly all the scenarios that you've brought out. You know, is it a stability issue? Is the schooling from the coronary sinus? Is the issue? Is this an epic are ideal structure like the vein of marshall? That's the real issue and we need to get in there to try and and bleed. Does that sort of get to the question you think? Yes, I think so. Great. So I think some of the remaining questions are more thematic and will try to address that future sessions in more detail. Anything else would be chic or do you want to close. I think this was great And thank you everybody for attending. And please keep us keep sending us your questions and suggestions, and we'll try to address them as much as possible. Thank you very much.