SIVA K. MULPURU: Welcome, everyone, to this challenging cases webinar. My name is Siva Mulpuru from Mayo Clinic in Rochester. Today, I am joined by my colleagues Dr. Samuel Asirvatham, Dr. Abhishek Deshmukh, and Dr. Ammar Killu today. The topic today is about atrial flutter. We have received certain questions today and we will post them onto the chat box.

So if you have questions along those lines, we'll try to cover all those questions. And the ones that we don't cover, we will try to post them as an add on video to this session. So to begin the session, Dr. Asirvatham will give us a 10 minute introduction about atrial flutter. And based on the questions that come in, we will take the discussion reviewing those questions.

SAMUEL ASIRVATHAM: Thanks, Siva. So some of the questions that you've sent in already I'll try to cover a bit in this introductory overview mostly related to checking for block difficulties with flutter ablation. And some are very specific. We'll have them written out here and we'll try to discuss as well. And feel free to send in further questions.

Two of you have also sent in an ECG you'd like to discuss from one of your patients. I'll put them up and please do feel free to come up and present what aspect of the ECG was of particular concern. So several issues about atrial flutter. I think I'll just try to go over the frequent concerns that come up, especially for electrophysiologists in training early in their career.

This is the type of ECG that today we call flutter or macroreentrant atrial tachycardia. It's completely unpredictable what the P-wave axis, flutter-wave axis, duration of the flutter wave will be. What is predictable is many of these patients will have structural heart disease, prior surgery, and the vast majority will be in the context of ablating fibrillation or post-AFib ablation flutters.

This is really, today, the flutters that we deal with. Focus initially in this discussion and in our careers is with the flutter that's most studied and we know best how to ablate. And we'll spend a little bit of time about that and why the difficulties we have in the cases of typical flutter help us when we have difficulties in today's flutters.

Things that we have to think about. If a simple atrial flutter, we deduce this from the cavotricuspid isthmus and it's not going away, or it's recurring even after we've done an ablation. Some of the things have to do with local anatomy. We always have to think about wrong diagnosis. It looks like flutter, that's typical, but it's not. And then, issues with incomplete ablation. And this will also address one of the questions that you had.

Most important thing with any type of reentrant tachycardia when we are trying to do anatomic ablation is to not only understand the anatomic obstacles that were connecting with the flutter line, but what's in between. What I mean by that is if we take a simplistic picture in our mind, tricuspid valve, IVC, and it's a line-- literally, a line through flat terrain, it causes a lot of difficulty when we're not quite getting rid of the flutter.

It's important to have a realistic picture whichever place we are doing linear ablation of what the tissue that we believe is an obstacle. That means electrically inert, like valve or IVC. And what is the tissue in between? Is it flat or are there excavations, ridges, things that I need to simply be able to manipulate my catheter through?

Should also be aware of thickness of the tissue in that region. Does it vary? If so, the same type of ablation going from one to another will be difficult to do. And if there are crevices and we get our catheter trapped between those two crevices, it may be difficult with thermal energy to be able to give an effective lesion. We can look at specific examples of this as well.

Just a case-- This is one of my own from a while ago that illustrates approach for when it's not going. Young person, no structural disease, but already on a fourth ablation for typical flutter. This is the index ECG when a patient was seen in the emergency room. Palpitation was the main symptom. Very active person. And definitely looks like cavotricuspid isthmus. What do I mean by that?

When our eye looks at this flutter wave, the terminal portion when we line up, it looks positive and V1. Terminal positive and V1 when we line up with what looks like a sawtooth or continuous flutter way. A lot of the early work with flutter ablation involved right atrial mapping. And we still rely on that to get us an idea when we're not sure what type of flutter it is.

This usually involves multi-electrode catheters. And once we get experience with multi-electrode catheters, using any kind of basket map, quick map of the atrium, we relate back to what we learned from multi-electrode catheters. One important area is the free wall of the right atrium, is that activation counterclockwise or clockwise? Down the free wall or up to free wall?

We rely on closely spaced catheters placed where we are going to do the ablation. So some electrodes on one side of the ablation line, other electrodes on the other side. And it becomes pretty straightforward in that approach when we have ablation done. Pacing from the coronary sinus, closely spaced electrodes, activation goes as expected on one side of the line and exactly the opposite on the other side of the line. Very easy. This is a picture we carry in our mind when we think about [INAUDIBLE] block in any unusual situation.

But it's important to remember that this should be closely spaced electrodes. If we have electrodes that are widely spaced, it becomes very difficult to know whether there is slow conduction or there's actually block. So also very important to remember that some electrodes have to be on one side of the line and on the other side.

If we have electrodes further away or they're not closely spaced, then we get fused wavefronts even before we ablate. And once we start ablating and there's delay on one wavefront, it will look like we have block when we actually just have a different degree of fusion as a result of slow conduction from our ablation line.

We should also remember that cavotricuspid isthmus flutter is not the same as peritricuspid valve flutter. In other words, the posterior boundaries that keep a circuit near the tricuspid valve are not complete all along the tricuspid valve. So we may have a tricuspid isthmus dependent flutter, but parts of the circuit may be away from the tricuspid valve.

This is important to keep in mind because we may and train tricuspid isthmus dependent flutter at some unusual sites when we're not certain of the etiology of the flutter. And then, focus our attention in that region when we could have had a much simpler solution with our own usual cavotricuspid isthmus flutter.

And one of the questions that came up-- and I'll just address it since it has to do with difficulties in flutter ablation-- is this concept of lower loop. And if the doctor who asked-- sent in this question wants to discuss it in more detail, please do. But the issue of this lower loop is there is myocardium behind the IVC and in front of the IVC. So it's possible to get a flutter that goes around like this.

Now, if you ablate a cavotricuspid isthmus, this flutter also goes away. That's why we don't really make a distinction between this and cavotricuspid isthmus peritricuspid valve flutter. But where this becomes an issue is the lower loop can be a limb for conduction to the free wall and to the isthmus even after we have started ablating.

What I mean by that is if we have only catheters on the free wall, even though we have a complete line of block on the cavotricuspid isthmus, conduction through this part of the lower loop will cause activation upward on the free wall from CS spacing making us think that we have conduction, so-called pseudo conduction. No need for further ablation. Solution is just bring the electrodes down here and you'll see this part is showing a reversal of activation.

Perhaps more important is the opposite phenomenon, and that is when we have very slow conduction. When we pace the coronary sinus, we might shunt around through this lower loop and give an appearance of reversal of activation on the distal side of block. On this side of our ablation. Making us think we have block, the clue will be flutter continues and we're confused whether we made a wrong diagnosis. It's some other flutter, misinterpreted entrainment, et cetera.

Solution is closely spaced catheters straddling where we ablated. However slow the conduction is, there will be some activation that's going and showing us that there still is conduction if there's dense enough electrodes, closely spaced electrodes, or an actual map that's done at that time.

Now, this question came up in one of our early sessions about how to use double potentials as a way of knowing we have block. Widely spaced double potential suggests that conduction from one side cannot get to the other. Now, if we have a complete line of block, the widely-spaced double potentials will be uniform across that line.

On the other hand, if it narrows, it suggests there is still conduction. And at that point where there is conduction, the electrogram might be single or it will be fragmented. We can use the same principle also for free wall flutters just taking a multi-electrode catheter and sweeping it anterior to posterior.

Anterior, you have wave one wavefront. Posterior, to some scar, you have another wavefront. At the site where there's a turnaround for the flutter, you can see this double potentials pointing to where the gap is. And if an electrode placed at that gap shows fragmented signals, a very good bet that ablation at that site will complete that line of block.

We discussed this last week, but very important to remember technique. Wherever the flutter line is done, it's possible for us to check for block anywhere. As long as we can pace on one side and we can map on the other side. Dense points of mapping should show complete reversal. If it doesn't and there's even a slight activation going through, that suggests we only have slow conduction and not complete block.

So just a quick recap. If we have trouble ablating flutter, we first think about issues that are making it difficult for us to know if we've blocked across the line. We remember this concept of lower loop conduction. And the real difficulty is defining whether slow conduction or block is present. Normal conduction versus block, usually easy to tell. But slow conduction means closely spaced electrodes that are straddling the line of block. If we're unable to put an electrode there, we can do a dense map in that location.

Just a few words about wrong diagnosis. Remember, a pattern of activation does not define a circuit. We can have just bystander patterns of activation. This is a patient of mine where I've already attempted cavotricuspid isthmus ablation because the pattern of activation suggested it. Patient did not have structural disease. Patient did not have atrial fibrillation.

But the real flutter was related to a scar in the left atrium for unknown reason. Small circuit. That was the cause, but it just activated the cavotricuspid isthmus region and tricuspid valve like that was a flutter. So it's this region of activation, whether it's actually the circuit or whether it's a wrong diagnosis, something else stimulating it, we can usually sort out by seeing where we have the cycle length of the flutter and by employing entrainment.

If any of you have specific questions on entrainment, we can use an opportunity to describe some of the difficulties when we have these multiple arrhythmias or multiple circuits how we would employ entrainment.

Just finishing up with this particular patient. For ablations flutter, clue was that flutter lines that were done at each procedure did appear to be complete. Why does a young person get multiple flutters? In this patient, the issue was a trigger, much like we think about paroxysmal atrial fibrillation. This patient, when mapping a variety of activation sequences, had very high frequency activation in the right upper pulmonary vein.

So patient, just like paroxysmal AFib but presents as stable flutters. What really needed ablation and what was done in this patient was isolation of the pulmonary vein and that takes care of these flutters. Now, we'll come back later after we look through some of the questions about how we transfer our understanding of cavotricuspid isthmus flutter difficulties and use that knowledge when we're dealing with other obstacles and other portions of the atrium, especially post-ablation flutters.

Siva, anything you'd like to add here or questions that you've come across that you would like to address now? Otherwise, we can go through some of the questions that were already sent in.

SIVA K. MULPURU: Yeah, thank you, Sam. I think there are a couple of questions there talking about epicardial connections in difficult to ablate flutter. So the ECG looks like typical flutter. And we do an ablation, but we're still not able to terminate the flutter. Dr. Lowell says, is it possible that there are these epicardial connections that we are not really getting into during that ablation?

SAMUEL ASIRVATHAM: OK, fair enough. So maybe we'll use that as a segue way for left atrial flutter as well. But here's the issue. When we have peritricuspid valve, IVC, and we're ablating flutter here.

Now, the epicardial fibers, endocardial fibers in the vestibule of the right atrium--

SIVA K. MULPURU: Sam, we're not seeing your marker well on the screen.

SAMUEL ASIRVATHAM: OK, let me try another one. How about this one?

SIVA K. MULPURU: No.

SAMUEL ASIRVATHAM: No? OK, let me do it this way. So when we think about the peritricuspid valve, this region where we ablate, the vestibule has fibers that are all parallel to each other. Now, there's really not much of separation in the vestibule between endocardial and epicardial.

However, when we start going out laterally, we sort of get this separation because we start getting pectinates that form like a layer or plane that's more endocardial. And then, the fibers of the vestibule that are on the floor become like they're epicardial. So there, usually the solution is trying to ablate more medially.

Now, this is very different from the left atrium where we truly can have it epicardial connections. But in the case of the right atrium-- and let me share an image that might be able to address this. Can you see my slides?

SIVA K. MULPURU: Yes. Not now.

SAMUEL ASIRVATHAM: OK, I'll try again. Able to see them?

SIVA K. MULPURU: Yes.

SAMUEL ASIRVATHAM: OK, so here's an example of a cut section that might be-- that might help to illustrate this. So if we look here, this is a vestibule. And you notice how there's really just parallel fibers. And the thickness there is not that different from the floor of the coronary sinus.

But as we go out more laterally, then we get these pectinates that are encroaching. So we get one layer like this at the plane of the pectinates. And we get another layer that is the plane of the vestibule. And gives this kind of impression of endocardium versus epicardium. Fiber orientation of the vestibule is different from the fiber orientation of the pectinate.

So if we do a high density map, it looks like conduction from one side is coming to another, also giving this appearance like we have some kind of connection. But in reality, in the region of the cavotricuspid isthmus, that's not an issue.

Now, contrast that with a couple of other scenarios. When we have free wall flutters and we're trying to anchor to the tricuspid valve, we do have an epicardial layer. And this epicardial layer can actually be seen to be continuous with the plane of the CS and the vestibule. So that becomes epicardial. And then, we have thick muscle that you can trace into the appendage and you have the pectinates that have come out of the appendage here.

So this layer-- this area for trying to draw a line, for example, some electrophysiologists, if you have a right free wall flutter will ablate that flutter and anchor it to the tricuspid valve with the idea that simultaneously I'll get blocked that will prevent cavotricuspid isthmus flutter.

And it's true, if it's done and it's perfect, that's true. But it's much harder than if you were drawing the line here. So many times, in recurrence of those cases, that'll be the problem. And rather than over-- going over it again, we might be better off to just do it here like we would with a normal flutter. Does that answer the question, Siva?

SIVA K. MULPURU: Yes, I think so. In the same line, Dr. Marco is asking us a question. How about we use just the electrodes from an ablation catheter to check for a block instead of using a multi-electrode catheter?

SAMUEL ASIRVATHAM: OK, so maybe I'll draw a picture here for that as well. And if any of you have a case you'd like to share that illustrates that, that'd be fine, too. So here's the problem is if this is where we've drawn the line, whatever this is, mitral isthmus, tricuspid isthmus, roof, and we want to know does conduction go from here to here.

The problem is if there is very slow conduction that we're trying to look to see does it come out there. So if we just put two electrodes here and they're slow conduction and say we go around IVC or pulmonary vein in the case of the left atrium through another scar in the right atrium free wall, we will very readily see that this could look like it's blocked. The proximal electrode will be earlier than the distal electrode if this is how we've kept the catheter.

Now, we get a little better when we have a multi-electrode catheter. We get even better if we span that multi-electrode catheter moving it from all sides of that distance to see any place, do we see distal is earlier than proximal activation. Still can be difficult in some cases. Multiple ablation, longitudinal lines, then we do have to do a high density map to try and clarify if activation is going through.

Now, I know we had some question about the left side flutter ablation difficulties. Should we try to answer some of those? Are there some others that any of you have come across from the audience today?

SIVA K. MULPURU: So we have a question about, while doing a CTI flutter and we are using a electron atomic mapping system and we are using a high density mapping catheter, are there any specific pitfalls that we have to consider if you are not using a multipolar catheter?

SAMUEL ASIRVATHAM: Do you want to take a shot at that, Siva?

SIVA K. MULPURU: Sure, definitely. If it is a difficult to ablate atrial-- typical atrial flutter, so using a high density mapping catheter like a grid or a PentaRay, it gives you an idea. The problem with most electron atomic mapping systems is automatic annotation. You'll have to go back, clearly look at how the system is annotating the signals, and try to make sense of all the points you have created.

And one of the things that I find difficult is if it is endocardial, you have these projections, or if you have a prominent Eustachian ridge, you may not annotate it well if you just rely on a high density map. Having an understanding of the anatomy using intracardiac echo sometimes helps you to localize those points better.

SAMUEL ASIRVATHAM: So maybe I'll just add to that. When we do a quick map, fast map, multiple electrodes map, and if we're pacing from this side. While we're doing that map with whatever we're using, if some of the electrodes picked up a signal on this side of the line, then the whole map becomes very difficult to interpret. Because then, you'll have something here that will get interpolated to being something earlier than this site and it will look like it's conduction where it may not be.

So it's a tough thing. I think if we wanted to, we could do a multi-electrode map, grid, PentaRay, any of those, even a non-contact map on one side of the line. But then, when we get close to the line, it's probably better to do point-to-point mapping so we don't have those crossover guide points.

Now, so we had-- we have several very specific questions about ablation difficulties along the mitral isthmus. And I think we can address those. Maybe I'll just do a quick overview of what the source of those difficulties might be. The three big points, at least, from my experience. Maybe add some-- anything that any of you would like to. And then, we can take a look at some of the specific questions.

Now, I think this slide and the next one illustrate-- are we able to see this?

SIVA K. MULPURU: Yes.

SAMUEL ASIRVATHAM: So unlike the right atrium, the veins of the left atrium all have muscle. So the biggest difference is when we draw a line to a vein, it's just half the isthmus is ablate. So we have to create a boundary by going around the vein. So that's why we have to pair atypical flutter ablation in the left atrium with pulmonary vein isolation.

So it turns out that many times it's iatrogenic flutters after an ablation that we've done in the left atrium. So we have to or have already isolated the vein. But that's a very important concept, especially for those who are new to EP to understand that a line has to be anchored. And that anchor is an artificial anchor in the case of the left atrium.

Second thing to remember about this mitral isthmus region is, unlike the cavotricuspid isthmus, the mitral isthmus region has a definite epicardial surface. And that epicardial surface is the muscle of the coronary sinus. So the coronary sinus is something that we don't have an equivalent in the cavotricuspid isthmus.

So it brings in a whole new vantage point for ablation. It brings in a whole new source of difficulties. So you can be perfect with cavotricuspid isthmus ablation, know every trick in the book to ablate it, but you have a few new things with left atrial ablation. One is the posterior boundary isolation of the vein.

The second is the issues with the coronary sinus. So if we look closely at this, you'll notice we have the vestibular fibers from the mitral isthmus plus we have muscle, potentially, in the coronary sinus, depending on where this lesion is done. So because of that, the muscle here and here might be related to each other.

And if it is, if they connect with each other, it's possible to shunt around ablation lines. That's one source of difficulty. The second source was probably more common is we have competitive cooling. So we're trying to ablate on the endocardial surface, but were cooling because of the blood flow in the coronary sinus. And if that happens, we'll have a rim of tissue that we're not able to get adequate temperature increase and complete that line.

This is probably the most common reason why we wind up ablating in the coronary sinus in some patients. It's not so much the muscle acting as a shunt, although that is possible, it's more likely that that's the place where it's cooling. So that's where we have the gap. That's where we need to put the catheter and ablate.

There are other ways to get around that issue, and that is like occluding the coronary sinus, for example, can temporarily cause cessation of that flow and we're able to ablate in that location.

Now, last point of difficulty I'll just share in general. And then, let's look at some of the specifics is we have to appreciate, just like with the cavotricuspid, peritricuspid valve flutter is not the same as cavotricuspid isthmus flutter. Perimitral flutter is not the same as mitral isthmus-dependent flutter.

When we say mitral isthmus-dependent, all we mean is part of that circuit is using the strip of tissue between the pulmonary veins. But usually, the left lower pulmonary vein and the mitral valve. When does that disjoint come to play is if we imagine a circuit that's only hugging the mitral valve. And then, we entrain that this yellow spot here-- we should eliminate the flutter with this ablation. But, that circuit, instead of going-- only hugging around the mitral valve may be going in and out of the pulmonary vein and then completing the circuit.

Now, even if we isolate the pulmonary vein, it's still possible through gaps in our isolation sequence or even going through slow areas of conduction in the posterior wall, in the roof, between a roofline, we can complete the complex circuit of flutter even though we can entrain near the mitral valve in one location.

That's why we have to pair entrainment with a map of the floor. Are we able to also entrain at other sites along the mitral isthmus-- mitral valve. If not, it could be one site that's using near the mitral valve. Others are complex going through gaps in a roofline, posterior line, or in the pulmonary vein circles.

In a way, even though this is a complex flutter, it does gives us multiple ways to solve the problem. For example, we entrain here. But entraining here is way up. That should suggest some posterior part of the circuit. And a simple solution could be completing an isolation of the right upper vein in some patients, depending on what the rest of the map is, what you're going to have to ablate and isolate anyway, and what the entrainment at multiple sites is.

Conversely, we may have a complete isolation of the vein. But entrain a flutter here and find either the sinus node artery or esophagus is nearby making it difficult to complete. But part of the circuit is the mitral isthmus. And perhaps a line there will solve the problem, even though we don't have to-- taking away the need to ablate near a difficult structure.

So that's just kind of a setting the table for issues related to difficulties when we transfer our knowledge from cavotricuspid isthmus ablation over to the left atrium. Now, some of these specific questions here are with difficulties with this line. But maybe I'll ask each of you as we tackle those questions. Ammar, anything that you'd like to add or solutions that you found in difficult cases or cases to share?

AMMAR M. KILLU: Sure, thank you. So for mitral flutter, I think you mentioned the main points in terms of difficulty blocking it sometimes. If we're ablating endocardially and sometimes epicardial via the CS, sometimes you have to resort to using other techniques such as alcohol, which someone specifically asked about. And I know that's gaining increasing traction and popularity in the literature.

And if you'd like, we can show an example of that.

SIVA K. MULPURU: Why don't you show that.

AMMAR M. KILLU: OK, Siva, do you want to show your mitral or should I show just my alcohol?

SIVA K. MULPURU: don't you go.

AMMAR M. KILLU: Yeah.

SIVA K. MULPURU: Why don't you go ahead.

AMMAR M. KILLU: So I'm just going to show an example of alcohol ablation. And then, we can show it relative to perimitral flutter. All right, can you see the fluoroscopy?

SIVA K. MULPURU: Yes, we can.

AMMAR M. KILLU: Perfect. So this was a somewhat unique case. It wasn't perimitral flutter, but it was a case where they had undergone pulmonary vein isolation on two separate occasions elsewhere and they couldn't isolate the left pulmonary veins.

And so coming into the case we were thinking, could this be something unusual, such as an epicardial connection, vein of Marshall, something like that? Now, we were able to isolate the vein just with catheter ablation on the left [INAUDIBLE] both on the vein side of the left lateral ridge, the Coumadin ridge, as well as from the appendage side.

But given that this was what-- was her third ablation procedure, we wanted to be as thorough as possible. And with adenosine testing, we continued to have dormant conduction into the vein. And we noticed what we thought was a very thick left lateral ridge as well as potentially a vessel through it. So we did an angiogram in the coronary sinus.

And we could actually see that there was this structure going right through that ridge. So you can see both the RAO and the LAO, the vessel, which is the vein of Marshall. And so after we occluded that and injected alcohol into it, we were able to eliminate dormant conduction in that way. And sometimes this kind of technique is used for perimitral flutter.

SAMUEL ASIRVATHAM: Thanks, Ammar. Now, maybe I'll just show a quick anatomy section of that same site.

So this is the region that Ammar is mentioning, this ridge here. And if you notice this ridge, unlike the crista terminalis, it's not really a thick tissue ridge. But it's an invagination. And this invagination is from the left superior vena cava. So sometimes, if we have a significantly large vein of Marshall or there's good flow through that vein, the same issue as mitral isthmus and CS, we get problems with competitive cooling and this epicardial fiber is different from the fibers that are on the ridge itself.

So if you do a cross section here at the ridge, your fibers on the appendage side, fibers on the vein side, longitudinal fibers of the ridge itself. And then, deep to this would be fibers left behind by the left SVC. So if we want to ablate that epicardial tissue either because there's a trigger there or we need isolation of the vein or we have flutter that could go through there, then that becomes a vantage point for us to use.

Now Abhishek, you do some careful intracardiac echo when doing your Afib ablation-- flutter ablation. Any thoughts to share on how you estimate this relationship or any examples to share of the relationship between the CS and the mitral isthmus in real time?

ABHISHEK DESHMUKH: Yes, absolutely. Let me share an ICE image here shortly. Can everybody see this?

SIVA K. MULPURU: Yes.

ABHISHEK DESHMUKH: OK, so this is the left atrium trans-septal puncture. Now, we are doing a mitral isthmus line connecting the left inferior pulmonary vein to the mitral annulus. At least, in this case, we went over it a couple of times and still it was not blocking. But looking at-- so we wanted to make sure A, we are in good contact. Our signal is changing. And whether you are making a good lesion based on intracardiac echo.

So as you are looking at it, behind this you will see there is this a vessel which is the coronary sinus. And that sometimes acts as a heat sink area. Now, the unique thing about this case is whenever you're ablating here, one could see a far-field atrial signal in addition to the near-field left atrial signal. So that was a clue that while ablating, we were just not changing that far field signal.

So at least, in these cases, it's sometimes worthwhile going into the coronary sinus and adjacent-- ablating it adjacent to this site from the CS. A couple of things to remember here, we can certainly endure a lot of things in the coronary sinus-- coronary arteries become the major rule. But as long as your catheter in RAO view is looking more atrially and you have a big atrial electrogram, I think that could be somewhat of a safety net. If any-- there is any concern, we should certainly do a coronary angiogram.

If you are looking to atrial, again, the chance of damaging the phrenic is going to be low. But again, if you are seeing more and more ventricular electrogram which is much bigger, then we should not ablate. And if that is the only way we are able to ablate this, then check for phrenic becomes important.

Some of the other challenges would be impedance. How to titrate the power based on that. Certainly, the catheter sometimes can get wedged in that location. And then, some of the other tricks you can [AUDIO OUT]

SAMUEL ASIRVATHAM: I think we lost you there, Abhishek. But thanks for sharing that.

ABHISHEK DESHMUKH: [INAUDIBLE] while ablating from the left atrium.

SAMUEL ASIRVATHAM: Thanks a lot, Abhishek. Now, there's a comment from, I believe, Dr. Strauss about accessing the epicardium. We actually covered this at the end of one session a few weeks ago. That should be available on YouTube as an addendum. And if, after that, there's still some questions about epicardial access, we'll cover it in one of our weekly sessions for sure.

Now, we have two questions relating to post-MAZE flutter. So maybe we can spend about 10 minutes on that. And then, we can tackle a few other questions. Maybe we'll start with a case. And then, we'll get comments from everybody about this. Abhishek, I'm going to share the screen now.

So a typical scenario. The key things about post-MAZE flutters is there's so many kinds of MAZEs. So you have to understand which MAZE it is. So best way I think about it is there's the cut and sew MAZE, and then, there's everything else.

Everything else is more like scar-related flutters. How do you tackle that? The thing that's unique about the surgical MAZEs is that you really do have pulmonary vein isolation in most cases. You have a very clean set of lines in most cases. And then, we really start thinking of large circuit flutters. Most other MAZEs, limited MAZEs, thoracoscopic MAZE, combined hybrid MAZE, have to treat them more like scar-related flutters. And I'll ask Ammar to comment after just looking through this case quickly.

Most of the time, the pulmonary veins will be isolated. So the patient with the flutter. But you can see here, I believe this was one of the veins-- maybe right sided vein that clearly there's exit blood coming through this vein. Look at another vein. You'll see it's still fibrillating after all this time, but can't get out to the rest of the atrium.

Many times, with a cut and sew MAZE, especially for large circle around all veins was done, you'll see that the posterior wall is also isolated. So really solid line of block posterior. So some things to keep in mind is it's not usually going to be an issue where there's some porosity of your posterior anchor point in flutters that are post-cut and sew MAZE.

What are some of the things to think about is here, we're putting a multi-electrode catheter across the cavotricuspid isthmus. I'm sorry, across the mitral isthmus at the level of the left lower pulmonary vein. And you get the sense that there is a reversal of activation. So kind of block.

Now, the thing to remember here is this is a situation where endocardial and epicardial separation is real. So second principle of post-MAZE flutters. First is, in cut and sew MAZE, posterior part is usually really an anchor. The second is you cannot trust endocardial activation to be the same as a epicardial activation and vise versa.

In other words, the CS ceases to be a surrogate for endocardial activation. And an endocardial map does not tell you whether there is the same activation of epicardial. In an extreme case, you could have had the surgeon using a cryo pen or a incision endocardially that gives you a nice block, but didn't do anything in the coronary sinus.

So this is an important, unique feature of post-MAZE flutter. What you'll notice and usually will be an easy early clue is despite this weird activation endocardially, you can entrain and get good evidence that you're in the circuit with approximation of the post-spacing interval with the tachycardia cycle length from the CS.

And usually, you need only little output. You don't need a big output from that pacing to do it. Because all you need to do is capture the CS muscle. Now, the activation sequence and entrainments in post-- entrainment mapping in post-MAZE flutter can be very confusing. What do I mean by this?

When you look at the map, it will actually look like you can trace most of the circuit visually endocardially, but the cycle length will be not even close what you have met. And that's because the slow areas and complete circuit can be far more complex.

Why is it that entrainment mapping can be confusing is it will look to you like there's just too many things in the circuit. You do the cavotricuspid isthmus, it looks like it's in a circuit. If you look at the CS, it looks like it's in a circuit. You do the roof, it looks like circuit. Septum looks like in a circuit. These are truly very large circuits. And they could even involve right atrium and left atrial myocardium.

But these circuits to complete. Let's say, the classic interatrial flutter, right atrium and left atrium. You connect from right atrium to left atrium through Bachmann's bundle. But how if you have block endocardially can you connect back to the right atrium? There, we have connections epicardially to the coronary sinus. And the coronary sinus is used to bring you back here.

And that's why if the cavotricuspid isthmus hasn't been ablated you might entrain it from the cavotricuspid isthmus. But ablating there alone will take this limb out of the circuit. But you could still usually, not always, but you could still usually use the septal myocardium to finish the circuit. The key is finding a common limb. And that could be the roof by Bachmann's bundle, but could be the muscle of the coronary sinus.

And if the ablation report doesn't mention cryo in the CS muscle, that's a good bet to think about where you could ablate. So that's the one that we took as an approach. In this case, ablating within the coronary sinus and that terminated the flutter. This is just an adjunct toward the Marshall-- vein of Marshall. This is a human heart autopsy. And flip it around-- sorry.

And when we flip it around and we do a section through here, that's exactly the ridge between the pulmonary veins and appendage. So just some points that distinguish MAZE flutters-- post-MAZE flutters assuming this is a cut-and-sew MAZE.

But other MAZEs, my own personal approach, is to think of it like scar-related flutters. Try to understand what procedure was done. Don't anticipate very thin lines like you do with the cut and sew. And then, map out the scars. Use entrainment and mapping and try to figure out what that flutter might be. Ammar, any additional comments to go along with that?

AMMAR M. KILLU: No, I think that was very helpful. One thing I like to do and I'd be interested to hear what the others think is for post-MAZE or postsurgical AF ablation, I think it helps to try and consolidate everything that was done by the surgeon if it's not intact as well. Sometimes that simplifies the approach, I think.

Because even though it may not be necessarily key for the flutter at hand there and then, it may be in the future, especially if you can induce it. So that's something that I try and do in these cases.

SAMUEL ASIRVATHAM: Great. And I see a question from Dr. Marco here about effective anterior mitral lines collateral damage. So just a quick thing about what we mean. And I'll ask Ammar to comment on this as well.

What do we mean by an anterior mitral line? So mitral valve, CS, vertebral bodies coming in the backs of posterior part of the annulus, anterior part of the annulus. Usually, what's meant by a anterior line is a line that's connecting the pulmonary vein circles to the mitral valve. So it's kind of going anteriorly from the pulmonary veins to this mitral valve.

You'll hear the same term also for lines that are parallel to Bachmann's bundle on the roof, but placed relatively anteriorly. For example, if the appendage has been isolated connecting to the appendage. So specific question here is about collateral damage. Collateral damage to the mitral valve. I mean, for an anterior mitral line.

Ammar, do you want to tackle that? We have about four or five minutes left. And then, maybe we can handle other questions offline.

AMMAR M. KILLU: Sure, so I think that's a great question. Some people, I think, like to do an anterior line rather than a true mitral isthmus line. The thought is that it may be easier to get block. It's maybe thinner tissue. I think in the literature the risk of perforation may be a bit higher for that reason.

But the other thing is you can actually delay transatrial conduction time. So you may get issues that way. Sometimes, I think you have to be careful as well if you're going to do that is to really try and analyze the CT scan as well and see if you can determine the anatomy based on the sinoatrial nodal artery as well.

Because there are some cases where it may come up from the left sided system. And the way it traverses, it may actually get inadvertently injured. And so I'm not sure if that's one of the main points you wanted to bring out, Dr. Asirvatham, but I think that's--

SAMUEL ASIRVATHAM: Yes, so it's just going back to this figure. It's really kind of [INAUDIBLE] structures if you're ablating here you need to worry about. So this is the crevice where the aortic valve sits. So non-coronary sinus of valsalva will be right here. That's why perimitral tachycardias sometimes we ablate from the non-coronary sinus.

That's not so much collateral damage, but a collateral structure. We have to think about and remind ourselves is located in that region. The sinus node artery, when it comes from the circumflex, will traverse right over here. And as you pointed out, 45% of patients it's exists and may be an important supplier for the sinus node. So if we do a line there and we don't realize that artery is there, we might block-- ablate that artery and get sinus node dysfunction.

Best ways to avoid it is just avoid the line, if you can. Solve the problem somewhere else. If not, look at imaging and see if you can see there is a major artery there. At the very least, don't ablate during flutter. So you're in sinus while ablating. Maybe you'll be able to pick up that something's happening to the sinus node and you can stop ablating in that location.

Sometimes folks will ask the worst place to ablate. You have in the middle the non-coronary sinus. You have anteriorly the mitral valve. That little triangle between these two here, that's the thinnest part of the roof myocardium. Behind you get thicker with the thicker portions of Bachmann's bundle. In front, you get the valve. To the side, you get the non-coronary sinus thinner there.

That's the part where you're most likely to perforate. It's not a common sight for perforation because we don't do much ablation there. But simple thing is to remind yourself if there's no electrogram there or very little electrogram there, you don't need much ablation.

Maybe I'll just take a minute to ask one question that Dr. Majumdar is asking. If the veins are silent, do you still need to encircle the veins to create a posterior boundary? The answer is no. But veins, if they're silent, it usually means they're isolated.

In most adult human hearts, there will be some myocardium that's viable going into the pulmonary veins. Not true in young children. But most adult hearts that's true.

SIVA K. MULPURU: Yeah, I think we are coming to the end of the session today. And thank you all for attending and sending your questions. We have a couple of questions that are answered about the alcohol injections into the vein of Marshall. We'll try to answer those questions and post on to the YouTube video.