Profesionales médicos

Overview

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.

For more information or to refer a patient, visit Mayo Clinic Medical Professionals — Cardiovascular Diseases.

ABHISHEK DESHMUKH: Good evening, everybody. My name is Abhishek Deshmukh, one of the electrophysiologists 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 am joined by my colleagues, Dr. Ammar Killu, Dr. Chris DeSimone, and Dr. Siva Mulpuru, and Dr. Asirvatham. And Dr. Asirvatham will make some introductions, and we'll get the session going. Thank you.

SAMUEL ASIRVATHAM: Thanks Abhishek. So we got some nice questions ahead of time just related centrally to atrial fibrillation. Quite a few of your doubts, questions were either related to complications of AF ablation flutters. The flutters we'll 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 in getting back 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 from you in this, and just as a short introduction. So first of all, all of us got introduced to atrial fibrillation 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, 300 cases under your belt, the questions then become is, what do we do with failures? What to do when there's 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 failure is. Is it an organized arrhythmia? Or is it AFib? Today we'll try to focus where it's AFib. 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 a 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 there? So one of the approaches there is even before rechecking to get an idea if there are spontaneous initiations of arrhythmia, be it monomorphic 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 catheter 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 arrhythmogenic substrates, that is the trigger substrate.

What is causing the initiation of atrial fibrillation? Tends to have these distinct electrograms, and they tend to be contact electrogram, late and sharp. 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 beat? So there, with the catheter in the left upper vein, we saw it's neither early nor is it sharp.

So other thoracic veins that become of interest is the superior vena cava, 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 a chart, but it's not very sharp, meaning probably an ablated, probably has a 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 interelectrode flat lines, interelectrogram flat lines, 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 notice both phenomena, this much more frequent activations compared to the rest of the atrium during fibrillation and the initiator is also early.

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 wall. Similar approach, mapping catheter, late activation, and sinus rhythm or pace 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 ectopic from the posterior wall, maybe catheter-induced, maybe spontaneous, but unable to activate the rest of the atrium. So posterior wall treated very much like you would a pulmonary vein.

I think it's important to just look historically at constructs from the surgical literature, that if we treat the pulmonary veins just as the 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 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 wall.

So question then is, why this posterior wall? Why not this anterior portion? Why not the vestibule? Why not the pectinate muscles, much more complex structures? Why posterior wall similar to the veins that we isolate? And for there, we should appreciate that anatomically, histologically, embryologically, and electrophysiologically, the posterior wall is the pulmonary vein. So the heart, the atrium is made up of myocardium, 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 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 embryological pulmonary vein is isolated.

You could get to that also by connecting the wide-area 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. Now another approach is saying that pulmonary vein substrate is probably best addressed by ablating 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 wall. 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 any of you who are-- been doing this procedure know it's tough because of structures nearby.

And of course, the most feared is the esophagus. Could be simple ulcers, could be a simple erosions, and of course, potentially, fatal fistula that can occur when we do this. So it limits the approach for how much we can ablate 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 an AFib 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 interdigitates with each other and includes the anterior wall. Notice this interdigitation 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. We should also remember every time that we are isolating the whole posterior wall, we are, by definition, setting up an isthmus because we know the mitral annulus 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 macro-reentrant tachycardias.

Now the other issue beyond macro-reentrant tachycardias is myocardial triggers. So this is an example, also, I believe from Abhishek 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 ablate, so as to eliminate the arrhythmia without isolation of the appendage. Presumably, these are types of flutters that include the ostium 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, mapped, 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, 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 intro here was just some of the things about understanding the recurrent syndrome. Is it new? Then think these are flutters, maybe proarrhythmic.

If there's just no change, it may be the pulmonary veins either were not dealt with or simply wasn't the trigger to begin with, and some approaches to consider. So please do send in your questions, and we'll take them as they come. In the interim, I have one question that was sent to me, very specific about our approach to avoiding esophageal trauma. So I believe we have Dr. Munger here as a panelist, or he'll be joining shortly.

And maybe I'll start with asking Dr. DeSimone first to tackle that question. What do you think Chris? Do we have a way to help prevent appendage esophageal trauma? Is it something in evolution? And then maybe I'll ask Ammar to also comment about both surgical and endocardial procedures and appendage trauma. Chris DeSimone?

CHRISTOPHER DESIMONE: 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 posterior wall, even if on the superior, inferior. I always have an esophageal probe, and I move it continuously every time I'm walking down my WACA line. So I'm monitoring for esophageal 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, and 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 big or right where I need to go, I've also been using esophageal 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 too high a voltage or power on the posterior wall. So I never go above 25 watts, and I try to keep my lesions 30 seconds or less.

SAMUEL ASIRVATHAM: So maybe I'll come back a little later to Ammar'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 just a reminder of how this esophageal fistula occurs, this is the 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 esophageal 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 already weakened tissue here that can cause esophageal air and contents to get into the pericardial space.

This is the stage of the pneumopericardium-- chest pain, nonspecific symptoms. And then with continued erosion, it actually becomes a 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 perforation and bleeding at the time of the procedure because it's not a perforation.

It's the inside out. It's coming from the esophagus to then reach the heart. So we have a question that I'd like Dr. Munger to address for us. So first of all, Dr. Munger is our chair of the heart rhythm service, and thanks for joining, Tom.

THOMAS MUNGER: Thank you, Sam.

SAMUEL ASIRVATHAM: So we have a question-- and if I understand it right, what it is it looks like it's a question from someone who's new to the field, I think. But basically what it is from experience, what are the aspects of the AFib ablation procedure that have made it easier and safer today that we have to emphasize for new entrants into our field?

THOMAS MUNGER: Sure. So I think when the intracardiac ultrasound was introduced 20 years ago, that improved the safety of the procedure since you could monitor the pericardium real-time for effusion. And you wouldn't have to wait for hypertension develop before you could identify the presence of effusion, 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, they tend to oftentimes go into the veins just a little bit 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, and valvular structures is quite helpful. So I think that was one big development, Sam, was ultrasound. I think the contact catheters has also reduced, in my practice, perforation just because it gives you feedback about high pressures.

I think steerable sheaths have helped make the procedure easier to do, technically, with the RF. So I think those would be the big things that I've seen come along.

SAMUEL ASIRVATHAM: Thanks a lot, Tom. And I think, also, Tom, fair to say the mapping systems have just created a new visualization approach for trainings.

THOMAS MUNGER: Yes.

SAMUEL ASIRVATHAM: 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 just how well they were doing the venous isolation, 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 feel for here's what we need to kind of go around.

THOMAS MUNGER: Yeah. [INAUDIBLE].

SAMUEL ASIRVATHAM: Yes, Tom.

THOMAS MUNGER: Yeah, I was just going to say, I would agree. It you the anatomy, and much like the CT which makes the understanding of the anatomy and where you put the lesions quite a bit easier.

SAMUEL ASIRVATHAM: Great. So we have a question here from Dr. [INAUDIBLE]. And if I understand, and please feel free to come up and explain if we got this wrong, but can 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 how can they be of value? So we know principle of RF ablation is the RF itself is not heating the tissue.

The radiofrequency 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 in 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.

Now 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 heating this side. 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 is 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. With 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 Bose-type technology, the wireless noise cancellation type technology-- to say if we take the RF wave and put an inverse wave, and just protect from the RF-- so you're canceling out the RF to come there, it 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 benefit.

Now we also had a question prior to the session, and I see that Dr. Madhavan has joined us, that maybe I'll ask her to address. And anyone else, also, if you see questions, please do jump in and bring them out. So is Dr. Madhavan here online?

MALINI MADHAVAN: Yes, Dr. Asirvatham.

SAMUEL ASIRVATHAM: So Dr. Madhavan is one of our electrophysiologists, special interest in congenital heart disease device placement and ablation. So Malini, the question was, how often do we have to manage atrial fibrillation? I think the question was actually structural heart disease, but I'll focus it a little bit more for you in congenital heart disease. Is congenital heart disease, adult congenital heart disease, atrial ablation, is it all about flutter? Or is fibrillation an issue?

And maybe you could share with us some thoughts on which situations is AFib becoming more of an issue.

MALINI MADHAVAN: Sure. So focusing on the congenital heart population, 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 fibrillation. So historically speaking, as the surgical technique started getting better over the course of the past 30 years or so, 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 atrium. But more recently, the last 10 years or so, both in our practice and also in the literature, there is 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 fibrillation. 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 fibrillation, particularly if you think about the moderate to high complexity congenital heart diseases.

The other place where we are likely to see atrial fibrillation is the ASD population. So patients who have isolated ASDs may also present with atrial fibrillation. And there, the question that comes up is, how do you manage the ASD closure in combination with management of the atrial fibrillation do you ablate first? And then think about ASD closure and questions such as that would come up. But for sure the adult congenital population, atrial fibrillation is increasingly recognized.

And in fact, just recently we put together our own experience looking at atrial fibrillation ablation at our center in about 150 patients.

SAMUEL ASIRVATHAM: Thanks, Malini. Thanks. So now we have another question that's specifically about vein of Marshall. So I think it's an anonymous attendee, but asking about vein of Marshall 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. Ammar, 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? Dr. Killu?

AMMAR KILLU: Sure. So thanks for the question. I guess when we're talking about vein of Marshall, sometimes we're also referring empirically to epicardial connections when we're performing pulmonary vein isolation. Sometimes you go around and you do what you think is a perfect WACA lesion, you check the line, no signal. You pace along the line, no capture, yet sometimes you may still have entrance into the vein.

Or it can still demonstrate exit on some occasions is because of these epicardial connections, which I think are becoming increasingly recognized. It's very good to be aware of them. Vein of Marshall, I have not encountered clinically frequently, but I've definitely had other cases where I feel like there has been an epicardial 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 is important, because you don't want to just keep going around, burning along the WACA, getting frustrated, risking complications to the patient and whatnot.

And so being aware of this, you can do certain maneuvers to try and diagnose that problem. In terms of a surgical approach, again, AFib is generally a very anatomical-based ablation. There are different techniques, now surgically, that are adopted, taking the open surgical approach out. Some so-called hybrid techniques have been gaining popularity. One example is the convergent ablation, which is a subxiphoid incision, and then a unidirectional-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 epicardial connections then. If you do concomitant appendage management, you can actually transect the ligament of Marshall at the same time. And if you put a clip on the appendage, you may actually isolate that as well. So those are just some of the nuances I think related to that if that answers the question.

SAMUEL ASIRVATHAM: Yes. I think that's part of the story, for sure. Maybe I'll ask Siva also. Siva, we've been hearing quite a bit now for about three or four years that just empirically trying to target the vein of Marshall, perhaps with alcohol, as part of the AFib ablation paradigm. Your thoughts, your take on this?

SIVA MULPURU: Thanks, Sam. So ligament of Marshall, targeting with alcohol ablation 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 endocardial and through the CS. So those are the patients doing a CS venogram identifying the vein of Marshall, selectively cannulating it, and inflating a balloon, and injecting a little bit of alcohol can take down the myocardium that sometimes cannot be mapped using our current electroanatomic systems.

I think there is certainly a role in a difficult to terminate mitral flutters, patients with hypertrophic cardiomyopathy. And if you have persistent vein connection, and you think that you have a good WACA, and it looks like the connection is through the vein of Marshall, those are the situations where I would consider alcohol ablation, but I haven't been doing it routinely.

SAMUEL ASIRVATHAM: So maybe I'll just expand on this a little bit here. So why this vein of Marshall, I think really Ammar kind of hit the nail on the head. When we say vein of Marshall, we're really meaning four different things 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 a conduit. 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 conduit prevents you from getting isolation of the pulmonary veins. This was a much bigger issue in the early days when we did ablation closer to the vein, but sort of falls away when we ablate in a wide-area manner, and I'll explain why that is the case.

Conduit also means for flutter. So if this is conducting, and we try to do an ablation endocardially, and this is still a way you can get from muscle in CS to muscle in the atrium, we don't quite get rid of the whole connecting fibers for the flutter and wind up failing with ablation at one targeted site, which, otherwise, [INAUDIBLE] might have said is great to ablate.

The third issue is it is an autonomic structure. So just like the SVC, the right SVC sinus node, there's node, there's autonomics in close proximity to the vein, and it's just as true with the left SVC and its remnants. So it becomes an autonomic site. So sometimes [INAUDIBLE] 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 ablate more atrium. So another school of thought is the more tissue you can safely ablate, the less likely atrial fibrillation is going to recur. So in that case, this becomes a method where if you were to inject alcohol, yes, you'd get rid of the trigger, yes, you'd get rid of the conduit, yes, you may modulate the autonomics, but you also have a fairly large area of tissue that you are ablating and maybe that helps us part of it.

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, appendage is here, the forceps is in the pulmonary vein. And this enfolding here, which is really where we do our wide-area lesion, is exactly opposite the vein of Marshall 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 do to some extent in most of our cases. We should also keep in mind that it's this ridge along with the way it connects to the coronary sinus, a beautiful dissection from Dr. Damian Sanchez-Quintana, that may create difficulty with ablation. In other words, we know if we were to try to draw a line here and we have the CS on the other side, that's competitively cooling the tissue that you're trying to heat and ablate.

The same is true if we're doing wide area circumferential ablation around the pulmonary veins, and you have a large vein of Marshall, or left SVC 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 vein. We should also keep in mind that there can be distinct signals from vein of Marshall tissue that we could map from adjacent structures.

So a catheter in the pulmonary vein in addition to picking up left atrial signals, appendage signals, another pulmonary vein signals could also pick up signals from the vein of Marshall itself. So I see there is a question, and I think, Siva, you already answered it a bit, I think, or Abishhek-- is in patients who have an ASD, I'm assuming post-closure and atrial fibrillation, approaches to trying to do the transseptal of puncture. And maybe I'll ask Dr. Munger and Dr. Cha to comment on their approaches, maybe to make it a little more generic the difficult transseptal punctures, specifically to include patients who have a previous patch closure. So maybe I will start with you, Tom, your approaches on this, and then we'll ask Yong-Mei to pipe in as well.

THOMAS MUNGER: So a couple of things about the prior closure with an ASD device, one would be, again, using intracardiac ultrasound, or TEE to-- and then CT even before you plan the procedure to see if there are windows where you can go that's around the device. Many times you can go on the edges of the device, either posterior, inferior, or anteriorly, and avoid adjacent structures. Sometimes you can go through devices, but I would warn if they're old devices--

I had one a few months ago that 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. For either tough symptoms or if you really had to go through the device, I suppose the ballast needle or using RF on a traditional needle would be an approach to get through, and then using either a series of dilators or balloons to balloon or dilate the septum to get the hardware through would be the approach. Ideally, I don't like going through the patches, so I'll go around them if I can.

SAMUEL ASIRVATHAM: Thanks, Tom. Yong-Mei, what about you? Question is on difficult transseptal. The focus of the question is ASD, but do you want to expand on-- if you think of the very first transseptals you did versus now, what are the things that have made it easier and were more confident in even difficult situations?

YONG-MEI CHA: I think Dr. Munger has given his experience. I think the key here is because we use the intracardic ultrasound guidance so that visualization really helps us to know the septal anatomy. And then [INAUDIBLE] from there, how much, of course, you want to use, the more anterior, or more posterior, or superior, inferiorly. But regardless, sometimes we do have challenging septals, especially if a patient has had multiple [INAUDIBLE]. It really makes a scar around the [INAUDIBLE] area.

In that case, sometimes we use [INAUDIBLE]. I think that's a very nice set of tools to help us to cut into the left atrium. And once we get into that atrium, sometimes decide later, and the sheaths have a difficult time to go in. So it's better to use either [INAUDIBLE] or using that long wire to cut into the left atrium and guided to the pulmonary vein. So in this way, the [INAUDIBLE] you can use a bigger [INAUDIBLE], but avoid the dilator of a sheath. It really perforates the left atrial myocardium.

SAMUEL ASIRVATHAM: Thanks, Yong-Mei. Maybe what I'll do is use a figure to get to work both you and Tom brought up here. So just a few things. So just a reminder about the interatrial septum, this actually is an important tissue for mapping and for ablations in a variety of areas. So a couple of things. So first is 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'll appreciate that the interatrial septum is actually a very limited structure, just this little box here. And posteriorly will be the fossa ovalis. 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 then 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 limbus approach. But the thing to remember about the superior limbus is the superior limbus is not part of the symptom. It's an invagination. It's separated the right and the left atrium with various amounts of soft tissue and fat. So if you do do superior limbus puncture, you can certainly get into the left atrium. The risk would be that if you don't have enough tissue here, extracardiac 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 limbus, when you push contrast, you'll get some staining. It's not a free effusion, but some staining in the epicardium, and that's because there's tissue there that's kind of containing that structure. So one thing, at 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 limbus puncture, like in a patient with a device, I will leave a wire and have one of our colleagues who is very comfortable with blood devices, or putting in another closure device, pull the sheath out, and then watch for about 30 to 45 minutes on ultrasound to see if there is an effusion that's building up. You should remember that if we do it more anteriorly, we have a small rim. But the minute you come in front of the eustachian ridge-- so that is the inferior limbus-- then we are risking some damage to conduction tissue.

So if patient already has AV block, has a pacemaker, it 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 right atrium to left atrium, but we're actually crossing to the pulmonary vein, and from the pulmonary vein to the atrium. So this is certainly doable. It's sometimes done inadvertently and patients have done OK, 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 vein 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, inferiorly, also, there's 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 answering that question.

AMMAR KILLU: Sam, I don't know if you want to have a fluoro image just showing the puncture and then the [INAUDIBLE] wire. Is that helpful to demonstrate just--

SAMUEL ASIRVATHAM: Wonderful. Why don't you talk us through it?

AMMAR KILLU: OK. Let me just share my screen. So this was a patient who had a prior ASD closure device, and it was coming from atrial fibrillation ablation. And the concern was, could we get across as just questioned. And so I'm just going to show you the ICE image--

SAMUEL ASIRVATHAM: For those not familiar with ICE, do you want to identify the structures for us.

AMMAR KILLU: Absolutely. Thank you. So the ICE catheter is in the right atrium, and you see this triangular sector. So the immediate chamber is the right atrium. And then you can see this big echo density, and that's the ASD closure device. A [INAUDIBLE] is just coming in at the 2, 3 o'clock position, slightly off-axis, and then you can see the left atrium. And often 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 inferiorly that we could safely go across, or at least attempt. Sometimes people do try to go through the device. In this particular device, 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 fluoro-- can you see the PowerPoint now or has it stopped sharing?

SAMUEL ASIRVATHAM: It stopped.

AMMAR KILLU: How about now?

SAMUEL ASIRVATHAM: Yeah, I think-- Yup, there it is.

AMMAR KILLU: OK. Sorry, two screens is throwing it off. So again, in that case, we were able to go inferior to the device successfully, and then what we use is this [INAUDIBLE] wire. And it's basically a wire that as it comes out of the sheath, or the dilator, it 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, and also when we're doing transeptals 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.

SAMUEL ASIRVATHAM: And Ammar, do you want to add any comments about the issue of pericardial patch closure patients, surgical closure, what is our approach for crossing there? Do you still avoid the patch, go through the patch?

AMMAR KILLU: Yeah. Again, if I can find a remnant of the true septum, I will always try to go through that first. Pericardial patch, I have gone through before if it was a big closure. Closing it, I haven't done acutely. 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 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.

SAMUEL ASIRVATHAM: And maybe I'll just add a little bit to that. I think the key is what you said. 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 ASD, 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 a PFO, 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 the years, one of the risk is it can become like bone. The issue is I don't think as much that we can't cross it, because I think sometimes we just brute force with electrocautery, all kinds of things that we, we're able to cross, but we have to remember the risk of calcium embolization. So example of a patient, hypertrophic cardiomyopathy, atrial fibrillation, ASD closed early in life, calcified.

And, actually, when we retrospectively look at the [INAUDIBLE], you can see calcium there, and then had a multiple embolic episode, that 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.

SIVA MULPURU: Sam, while we are talking about this ASD transseptal, there's a question about, how do we differentiate septal staining versus superior limbus staining when you're in the middle of a procedure?

SAMUEL ASIRVATHAM: OK, sure. So maybe I'll go back to this, and we'll just do a very quick one on that. So the key difference is location and movement of the stain. So when we have the fossa, it's [INAUDIBLE]. You have a sheet that you're using to inject the contrast. So the pressure of that sheath 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 LAO view, 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 limbus and epicardial tissue straining, it tends to be more widespread and there will be no movement in the LAO view. It'll be fixed because there's no scope for tenting. 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 superior staining of the tissue, even though there's no free pericardial, you may see the indentation of the aorta in that area.

And that indentation of the aorta with the staining is actually better observed in the RAO view, and the reason for that maybe I'll show with a different view on the dissection. You can see what's actually filling that area. And what that is in a superior plane, anteriorly we have this non-coronary sinus of valsalva pushing in to that separated area from the limbus. So you can imagine left side of the limbus here, right side of the limbus here, and this [INAUDIBLE].

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 fossa because the fossa is a more posterior plane to the limbus. Does that answer the question to some extent, Siva?

SIVA MULPURU: Yup, yup.

SAMUEL ASIRVATHAM: Great. Well, we'll thank everyone. And once again, the questions and cases that you put together, we'd love to have you come back 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.

ABHISHEK DESHMUKH: 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 phrenic nerve? And what would be the potential locations or lesion sets by which we can injure the phrenic nerve? Dr. Asirvatham, would you like to answer that?

SAMUEL ASIRVATHAM: Sure. So I think unfortunately, the physician who asked us this question did have a phrenic injury, and maybe I'll just hit a few high points here. So a couple of things is naturally, we have this right hemidiaphragm a little bit higher than the left because of the liver, and it's something that can be fairly subtle in just the resting state when we have phrenic nerve injury. So 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 pulmonary vein stenosis.

So there it's like cough, shortness of breath, effort intolerance, some hemostasis. This one is just dyspnea, uncomfortable breathing, and it's worse when they lie down compared to sitting or standing. Worse when they lie down, but it's not the air hunger of orthopnea. 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 phrenic injury.

I think this is a case of yours, I believe, Abhishek, to kind of illustrate how the sniff test can bring this up very obviously-- or it might be Siva. Just a few things about that phrenic nerve where it gets injured. When you look at the high parts of the phrenic nerve, it's an SVC relationship. So it's SVC ablation. When we think of the lower parts, then it's an equal relation of the right upper pulmonary vein and the SVC. So it can be injured, especially balloon where the balloon is seated literally into the pulmonary vein versus ablating in the SVC-RA junction.