SAMUEL J ASIRVATHAM: OK. Thank you, everyone, for joining us. So, this is our second in this question and answer webinars. We have Sam Asirvatham, Siva Mulpuru, Ammar Killu, and Chris De Simone just to work here as panelists to try to answer any questions that you have.

Our point of focus for today's session is AVNRT, but with as any in the series, feel free to ask any questions that you have outside of this, especially if there's been a particular problem, a case, something you'd like to discuss. If, when you would like to ask this question, feel free to use the question-answer format or come on chat and just post your question. If you'd like to come up here as a panelist and present your case, just let us know when you put the question, and we'll bring you up and discuss it.

Last time, we didn't have time to go over everybody's answer, and we reached back to you. Today, whatever questions we don't get to, we will record answers and post it along with the YouTube of the session as well. So, we'll do our best to get everybody's questions answered. We also would encourage you to send in any cases, slides, or questions that you have that you feel should be addressed in a little more detail that you would like to present to us. You can send it to cv webinars-- all one word-- at mayo dot edu to you or email it to any one of us here. All our emails are available in the slide to you.

So, maybe just to get things started and spur some discussion, I'll spend about 5 to 10 minutes, kind of, hitting some high points about AV node re-entry that over the years have been the most common questions that come up when we have a referred case or a trainee asks a question, or we ran into someone in the pre-pandemic days at a meeting and a question came up. It'll usually be about what there's very little-known about the anatomy and circuit of AVNRT when things don't quite work right, some variants like AVNRT with AV block, for example.

Very often, in the last few years, it's been how to approach AVNRT and congenital heart disease. Folks have figured out in practice that the CS plays a role, either anatomically or just as part of the circuit, and when we have to involve the left atrium. I won't cover all of these, but I'll introduce a few things about anatomy and, based on what you feel is the most relevant question, I'll switch and we can come up. The the other doctors on this panel will also jump in to comment. Any of the male faculty who are listening in to this session, please feel free to jump in. Let us know if you'd like to cover some of these as well.

So, just a couple of things-- as a trainee, one of the most perplexing things about this arrhythmia is the simultaneous activation of the atrium and the ventricle. And while the early days it was thought that was because the origin of the arrhythmia was in the node and could go to the atrium or the ventricle, what we know now is AVNRT is largely an atrial circuit that happens to have its turnaround point in some part of the AV node. And, from that turnaround point, we're able to reach the ventricle and atrium at about the same time.

How does this come to be the fixity of the conduction system when we think about sinus node, His bundle, and AV node? The sinus node is fairly fixed external surface and that angle between SVC and right atrial appendage. The His bundle is fixed membranous septum shared space between the aortic valve and the tricuspid valve. The part that has to be approximated is the AV node. And this is fundamental to understanding how to avoid problems with AVNRT ablation.

And we approximate that in this border zone between the septal leaflet of the tricuspid valve, roof of the coronary sinus, and the tendon of Todaro, which, for all intents and purposes, can be visualized as the Eustachian ridge, just extending up to the membranous septum where the His bundle will be available, will be recorded. And another way to think about it mentally, where the AV node is located, is to think about it in a perpendicular plane, like a four chamber plane, cutting through fossa ovalis, the AV node side septal leaflet. And that would look something like this. In here, we see the structure that we cut through is posterior and lower than the membranous septum where the His bundle is located, but in this atrioventricular septum, right atrium on one side, left ventricle on the other side, and this region in this view is where we would visualize this compact AV node.

Note that this site is atrial to the septal leaflet of the tricuspid valve. So, it's an atrial structure on the right side, but, across, its ventricular to the mitral valve leaflets. So, from the left, when we visualize the same region, it's a ventricular structure. On the right, it's an atrial structure.

Autopsy studies in patients who had prior slow pathway or, in the early days, first pathway ablation, the site of the lesion is in the triangle of Koch, where the AV node is located, except lower than the level of the roof of the coronary sinus, whereas the fast battery lesion site is not in the triangle of Koch, but behind the tendon of Todaro-- very important kind of learning experience from that to explain to us the anatomic difference between this slow and this fast pathway site. So, if we think about that, the AV node region versus the slow pathway region, we think about the AV node being atrial to the septal leaflet, but we're visualizing it close to the annulus and above the level of the roof of the coronary sinus.

On the other hand, the fast pathway itself, because it is behind the tendon of Todaro, on the left anterior oblique view, we see that fast pathway site being leftward. Anything in front of the Eustachian region tendon of Todaro is forced relatively rightward because of the structure. But we pull the catheter back-- we wind up being left of that site. Why that's important to understand, that the fast pathway is a distinct site compared to the His bundle, is when we have some variants of AVNRT. So here, for example, we have a situation where a well-placed CS catheter shows eccentric activation, and yet, we have VA timing being exactly at the same time.

The part to try to-- visualize and this is a very, very frequent question-- in a difficult case, is the circuit of AVNRT that's outside the triangle of Koch. So, we know the slow pathway came into the AV node, and then we exited through the fast pathway in typical AVNRT. But what happens to complete the circuit? And, there, we're really left to the vagaries of the atrium-- many possible ways to complete the circuit. It's possible to climb right back across the Eustachian ridge, but when that's not possible-- because this is a line of block when the crista terminalis is acting as a line of block-- those are the cases where we use the left atrium to complete the circuit.

And that could be just along the septum. It could also be around the posterior wall, which is typically devoid of much myocardium, or some fused pattern. And, once we get to the left atrium to make it back to the AV node, we're using the muscle of the CS to get us back to the slow pathway region and up to the AV node. And this is the reason why, even though we're dealing with typical AV node re-entry, with earliest sight at the fast pathway, the CS may show varied activation patterns.

And the way we would sort this out is compare the timing with the true fast pathway site, the lower, behind, and leftward pointing in the LAO view compared to whatever appears to be early in the slow pathway location. I would say once a year, once every other year, would have a case that would be presented or referred by saying what looked like an accessory pathway. When it was ablated, we found AVNRT. And the reason for that is because of this unusual or eccentric activation.

So, I'll just stop there. That was just to get everybody thoughts started. And it would be great to see what questions you have or thoughts you'd like to share. Feel free to put in your questions either in question and answer or in the chat box from everybody else. So, I'm seeing a question about timing of activation and type of AV node re-entry.

And please do let us know if you'd like to come up here and discuss the question specifically. Maybe I'll take a quick shot at this answer and then I'll ask, perhaps, Dr. Killu to, maybe, complete this with any slides that he has. I also see a question about is AVNRT a micro-reentrant atrial tachycardia. And, again, if you would like to come up here and present your thoughts on that, please let me know and I'll move you over. So, let me take a quick shot at both these questions first.

So, first, is the question about timing. So, in other words, we've got the AV node. We've got the His bundle. We've got an input to the AV node. We've got an output from the AV node during this tachycardia. And regardless of what type of AVNRT it is, from wherever that timing turnaround point in the circuit is, if we're going towards the ventricle and we're going back to activate the atrium.

There's really no true VA conduction in AVNRT. There's no true HA conduction in AVNRT. It is a pseudo interval. It's just a race between this turnaround point to when we reach the His and the V to when we reach the A. And because this is a race, depending on conduction characteristics, how proximal the turnaround point in the AV node is, depending on how much decremental tissue remains to be crossed, it's possible to get a complete continuum of VA and HA intervals in any type of AVNRT.

So, in other words, in slow-slow AVNRT, it's possible to have simultaneous V and A activation. In slow-fast AVNRT, it's possible to have a long RP. In that case, it would be the fast pathway exits very early and takes longer to finish going through the remaining AV node and getting to the His and the V.

And just a quick thing-- I believe the question was why don't we consider AVNRT as a reentrant-- I think the question was micro-reentrant-- AVNRT-- atrial tachycardia. And where that question is coming from is all of this is atrial activation. All of this is atrial activation. So why isn't it a reentrant atrial tachycardia? And, in fact, you could consider AVNRT as a reentrant atrial tachycardia that just happens to use a portion of the AV node for the circuit.

But, unlike any other atrial tachycardia, the slow zone for this tachycardia is specifically Av nodal tissue. And that's why we distinguish this and call it AVNRT. Why not micro-reentrant? The reason is the remainder of the circuit does not have to be micro-reentrant. It could be a very large circuit. Some types of AVNRT in some patients we can entrain with concealed entrainment the AVNRT from the left atrium 2 to 3 centimeters away from the location of the AV node. So, I hope that answers your question.

Anything that you'd like to add, Ammar or Siva? So, I see another question. And if you'd like to come up and present these as well, please do. But one question is what should we consider when we haven't performed-- we haven't successfully ablated AVNRT with a very large CS. Specific question is about a persistent left superior vena cava. And maybe I'll just start with that to explain what the issues are in terms of just purely getting the appropriate contact when we have a very large CS.

So, if we look here, we get the problems when we have-- here is our coronary sinus. Here is the roof of the CS. Here's the location of the compact AV node. So, the issues that can come up is, one, if we have a very prominent Eustachian ridge, then, when we put a catheter on the ridge and try to torque the catheter towards the slow that way-- and, in fact, this is the same issue when you have trouble with AV nodal ablation-- is this acts as a fulcrum and can move the catheter away from the septum.

So, it just becomes very hard to maintain contact on the low septum. High septum is no problem because we're above the level of the Eustachian ridge. It can be very easy to get a His location, but then you're having struggles with trying to maintain appropriate contact for ablating the slow pathway.

Two issues that happen when the CS is much larger-- so, one is the larger the CS, the more disparity between the floor and the roof of the CS. So, in other words, if we're used to keeping a catheter, say, from below, that is hugging the roof of the CS and we fail to recognize that the CS itself is very large, then what happens is we ablate at the level of the roof. And, in comparison to someone else's roof, which is going to be clearly below the level of the compact AV node, you might underestimate how close you are to the compact AV node, and that could result in inadvertant ablation of the AV node.

Now, the larger the CS, the more likely that we will have a prominent region between the Eustachian ridge and the septum. These are the same patients who may have prominent pouches, who may have very prominent Eustachian ridges, so making it doubly difficult to try to get contact on to the AV node, the slow pathway to the AV node ablation site. I believe Dr. [INAUDIBLE] would like to come in as a panelist. And what is the question that Dr. [INAUDIBLE] has?

ABHISHEK DESHMUKH: So, the question is he saw a patient today, a 45-year-old female with a tachycardia and incessant tachycardia, and this is the ECG he wanted to show.

SAMUEL J ASIRVATHAM: We also have some questions about what are the lower and upper common pathways. Maybe, Chris, if you want to be prepared to discuss that while we look at this ECG. So, do you want to start discussing the ECG, Abhishek?

ABHISHEK DESHMUKH: Yes. Whenever somebody has incessant tachycardia and narrow complex tachycardia, we are obviously worried about the usual three differential diagnosis, AVNRT, AVRT, and junctional tachycardia. This is a very interesting ECG which--

SAMUEL J ASIRVATHAM: Show us the ECG while you're discussing it.

ABHISHEK DESHMUKH: So, this is a narrow complex tachycardia. And the first step would be to identify if we can see any P waves or retrograde P waves. Ideal leads would be to look at the inferior leads, where you can potentially see some of these P waves, if you can see what dots I made, and even here. So, it seems like a narrow complex tachycardia. And a differential, again, based on this could be some form of AVNRT, AVRT, or atrial tachycardia, potentially even junctional tachycardia.

SAMUEL J ASIRVATHAM: Yes. So, Abhishek, I think the history I just saw Dr. [INAUDIBLE] had put in here is 45-year-old-- palpitations throughout her life got worse. I think, here, generally, if you're having paroxysmal palpitations all your life, you know it's not going to be permanent palpitations throughout their life, because there's going to be cardiomyopathy, but paroxysmal palpitations that then become persistent, you know, paroxysmal palpitations that then become persistent. The things we think about-- and maybe I'll just draw a quick picture here to explain that situation. And I'll also ask Dr. Cannon, shortly, to comment, because we run into this more commonly in the younger patient group.

So, one scenario is a patient has a somewhat detrimental retrograde accessory pathway and has normal AV nodal conduction. So the patient is able to get tachycardia, manages OK, once in a while gets symptoms, does OK with the beta blocker. When they get older, AV node conduction gets worse and the pathway characteristics may also slow. There's relatively slow conduction. So, now what was a paroxysmal tachycardia gets induced even with sinus arrhythmia, any old PAC, and becomes incessant. So that's one that we definitely think about.

Another one that when you have one to one conduction, narrow complex, shortish AV conduction times, VA conduction times is AVNRT that has more than one slow pathway. So, what happens here, probably, is they have, say, typical slow-first AVNRT-- paroxysmal, rapid, comes and goes, comes and goes. But then, over time, either there's slowing in the AV node, slowing in the fast pathway, or they develop a second form of AVNRT that may have enough of the AV node as part of its circuit that allows it to become sustained.

Now paroxysmal atrial tachycardia becoming persistent is very rare in the usual areas. Crista terminalis tachycardia-- typically, the syndrome stays the same. Non-coronary sinus of valsalva-- the syndrome, if it started paroxysmal, stays the same. Pulmonary vein tachycardia-- so, it's an atrial tachycardia-- when it starts, it stays the same or transitions to atrial fibrillation over time.

The exception to this may be appendage tachycardias. So, appendage tachycardias in the young tend to start off being paroxysmal, and then, over time, they tend to become a persistent type of tachycardia. Often with what's happening is the appendage itself getting larger over this time. So Bryan, would you like to comment for us about just in the younger age group when you have a shortish RP tachycardia that's incessant. Any thoughts that come to mind?

BRYAN C CANNON: Sure. In young people, the AV node conduction tends to be a lot faster. And, as they get older, sometimes you'll see a slowing of conduction. And, like you said, that may make something more paroxysmal. But, usually, whenever we're seeing tachycardias that are becoming more persistent, I found it to be AV node re-entry tachycardia, which develops in the teenage years. And the typical course is it becomes more frequent or the episodes last longer.

And a lot of times, people actually ignore short episodes of symptoms just because they think that they're palpitations. So, when they start having it more frequently, maybe, when they present to attention. But junctional tachycardia outside of the newborn period and postoperatively is relatively rare. So, you always have to think about it, because if you don't think about it, you'll miss it.

But you also have to realize that that's a pretty rare differential diagnosis. Another thing is if you have atrial tachycardias that are coming very close to the AV node, that will appear to be a short RP tachycardia just because it's so incredibly close to the AV node. So, I think you have to think about all these things as you move forward.

SAMUEL J ASIRVATHAM: Thank. Thanks a lot, Bryan. Chris, would you like to take a early shot? And I see several other questions coming up. If any of the folks, any male faculty would like to answer, that's great. Chris, there's the question about upper common, lower common pathways. And some folks are asking where are they. Others are asking is this even real. Would you like to make a comment? And I'd be happy to share some pictures as well.

CHRIS DE SIMONE: Sure. I'm trying to bring up this one amazing picture you have to try to get that, it's kind of-- the title says AV dissociation in AVRNT. So, really, I've heard of these things, this upper common pathway and this lower common pathway. But, to me, I don't know so much if I'd characterize them as a pathway. I always think of it somewhat as having some tissue that's outside of the AVNRT circuit. Upper common is between that and somewhere in the atrial tissue-- lower common pathway being somewhere between the circuit and the His.

But, again, I don't know. And you'll have much better insight about what you want to call this pathway, per se, or if it's just tissue. I've clearly seen in the lab AVNRT. And you'll see this lower common pathway block. And then you keep watching it, and then all of a sudden it goes one to one. I've seen that plenty of times. But I just don't know if I'm convinced about an actual pathway.

SAMUEL J ASIRVATHAM: Well, I think this is what you were alluding to, Chris.

CHRIS DE SIMONE: Yeah.

SAMUEL J ASIRVATHAM: So, if we look, these are the cases that we wind up asking the question about common pathways. So, sometimes you see this. So, you have atrial activation, which is twice as frequent as ventricular activation, and yet, at other times, the same sequence, the same timing when there is a V and an A, you can prove beyond doubt it is AVNRT.

And you succeed by ablating the slow pathway input to the AV node. So, how does this happen? The second, which is a lot harder to explain, is the exact same scenario. If you take beats where there's equal V and A, and when the tachycardia has equal V and A, it's AVNRT, but sometimes more V than A.

So this has brought in this kind of question about common pathway. So, first of all, when we think about common parts of the circuit with AVNRT, the AV, distall AV node, His bundle are always common parts of the circuit. In other words, you can have the circuit keep going on even if we didn't have those structures. So, here's what I mean by that in a diagrammatic form.

So, if we have, here, AV node, we have one input to the AV, we have a turnaround, and we come out. So, if we think between the circuit and the ventricle, all of this is a common limb. It's all distal to the turnaround point of the tachycardia. But what we mean specifically when we say common pathway is, even before we reach any part of the agreement, we have one input and we have the output that then reaches the AV node through, like, a common stock.

So, if this were to block, for example, the tachycardia would continue, and you'd have no discernible relationship or necessarily relationship with AV nodal activation, so point of decrement can vary, to the His bundle, or to the ventricle. So, this would be what the construct, at least, of a lower common pathway. So, these patients, sometimes-- in the early days, before this entity was thought of-- would be I had a case of typical AVNRT or atypical AVNRT. And then, after oblation, patient comes up with an atrial tachycardia. And guess what? I wound up ablating it very similar to how we ablate the slow pathway.

Now, this, of course, does not explain how you can get more V than A. And for that, we'll have to go back to the figure that we had looked at in terms of the circuit of AVNRT. So, here, if this is where we have the compact AV node, we have the inputs to the AV node here, say, slow pathway, say, left side slow pathway, any input to the AV node and output behind the tendon of Todaro.

If that output wasn't behind the tendon of Todaro, and rather could complete the circuit in this region itself, then the way you are getting to the rest of the heart is through the usual exit of the fast pathway. But that exit itself is not essential for the tachycardia circuit. So, if we were to get block at that site, the tachycardia can continue, go down the His and to the V, but doesn't get to the rest of the atrium.

So, how do we know if such things actually exist? I mean, one of the questioners asked is this even real. Part of it is. It's just difficult to come up with any kind of explanation for those phenomena. The other is just spacing maneuvers that try to pick up for us how much of this circuit could be potentially outside of the AV conduction system axis.

And if we use that kind of constant, then comparing the time it takes from when you record the His to A anywhere when we paste the ventricle versus tachycardia, how much difference would exist between these two intervals gives us an idea of how early is the turnaround back to the atrium. And if the difference is huge, that turnaround is very proximal, making you think that it turned back to the atrium even before you reached the AV. In other words, there is some kind of common stock or common pathway that's a part of the circuit.

Now, there's a question I see from Dr. [INAUDIBLE] about what are the signs during early RF energy that could be harmful and that we're not actually targeting the slow pathway. And I see, also, another question about what is the potential downsides or harm with empiric-- I think what is meant is empiric-- slow pathway ablation. So, maybe I'll ask Dr. Killu to just give us a construct of what do you use to monitor ablation when you're doing a, sort of, classic slow pathway site ablation.

AMMAR KILLU: So, with slow pathway ablation, obviously, one of the concerns with AVNRT is we want to avoid AV block. Right? So the approach, I think, is important. I favor using a CS from the neck. That's the change in practice that I had earlier on in my career. Part of the reason is twofold-- one, is stability and two, it hugs the floor of the CS. And with the ablation catheter, when I'm doing the slow pathway, I like to get that underneath the CS catheter. And I find that that actually provides some protection in case the catheter slips and it saves it from going superior right into the AV node His bundle region.

The other thing once I'm doing the slow pathway is I usually start very low and I'll go slow. So, the approach I take is I'll use a lower power and I'll gradually uptitrate it. And I'll be watching for any prolongation in the AH interval. So, I actually will set the calipers on the AH and sure I have a very stable reference. And I'm having the nurse in the room, the fellow, all of us, basically looking at that while we're ablating, making sure we're stable, making sure it's not getting longer and then gradually uptitrate the power incrementally. So, for example, I may start at 15 or 20 watts depending on the catheter I'm using and then go up very gradually, up to the target.

SAMUEL J ASIRVATHAM: So, Ammar, you've told us the approach for catheter stability. But in terms of when will you know, in terms of the junctionals that you are seeing or not seeing-- so I think the question that a couple of people have had is a, if you don't see junctionals at all, can you still be successful with ablating the slow pathway and what are the early clues that we're running into trouble, that we might be having potential for AV block.

AMMAR KILLU: So, yes. To answer your first question, yes you can be successful without seeing junctionals. And if you do a very low line, you may not see any junctionals. But I've certainly had cases where we've eliminated AVNRT ability by doing that. And I favor a linear line from the leaflet, tricuspid leaflet, back to the anterior lip of the CS. But yes, you can be successful without necessarily seeing junctions.

SAMUEL J ASIRVATHAM: So I guess one way-- I guess I could use this picture to demonstrate this. If we have the AV node as a septal structure, and then we've got the inputs to the AV node, as it approaches the AV node, we're getting narrower and narrower. I sometimes like to picture it as like two hands making a handshake. The AV node puts its hand out through an inferior extension. The atrium is tunneling all together, putting its hand to, kind of, meet at some point.

The atrium is much bigger than where this connection to the AV node is, so it's essentially like a fan. And if we're very close, we're going to be close enough to the AV node where we'll see automaticity in the junctionals and not many ablation lesions to transect that slow pathway. If we're further away, we're not going to be able to heat up automatic tissue to cause these junctional beats. But if we are in a protected area where we can transect all of the atrial fibers that are going to reach that slow pathway input, we could still be successful.

Now, the other aspect of that doctor's question was what can we harm other than the AV node. And maybe I'll take a quick stab at this. If you see any other questions you'd like to answer, any of you, please let me know. But if we are thinking about where can we ablate-- so one thing is definitely AV nodal damage.

The other is if we're ablating proximate to the coronary sinus, we might inadvertently get into the CS, and it's possible you could fall into a middle cardiac vein. And if that happens, you could have coronary injury. This is much more common when we're doing posterior accessory pathways. We worry about it. But if we're not watching that catheter, that is a possibility.

Another is the story of a patient where it's hard to induce AVNRT, you don't know if you have good end points, patient is extremely symptomatic to begin with, not too much documented tachycardia. So, these times we might overablate in this posterior region. We're overablating because we don't have good end points. We're staying posterior because we're not even sure we want to do this, and we want to stay far away from the AV node.

In that case, we must remember one of the occupants of this pyramidal space, the outside part of the heart. Here is the autonomic nervous system, part of the fat pad and ganglia in this region. And if they are overablated, we can have higher sinus node rates. So these patients could develop, if they didn't already have, a syndrome like inappropriate sinus tachycardia.

Now, any of you have seen any other question that we'd like to look at? [INTERRPOSING VOICES] Yes? Yes, Siva?

SIVA MULPURU: Dr. Singh has a question on how to approach slow pathway ablation when the patient has one for two response during the diagnostic part of the procedure.

SAMUEL J ASIRVATHAM: Fantastic. Fantastic question. Do you want to take a shot at that, Siva, or should I go through it?

SIVA MULPURU: I can start and maybe you could add on. So, first of all, during AVNRT procedures, we try not to ablate during tachycardia. It's very difficult to separate junctional beats compared to tachycardia when the patient is going fast. So, if the diagnosis is confirmed to be AV node reentry, try to do the ablation when the patient is at sinus rhythm so you can observe the slow junctional beats with one to one response to the atrium.

SAMUEL J ASIRVATHAM: Yeah. I think this is just a great question. And it's a very, very common issue. And I'll just generically try to answer. So, one is when you have these weird types of AVNRT, not weird because the slow pathway is in some unusual location, but the physiology behavior of the AVNRT is unusual, how do we monitor. So one of the issues is if you have more A then V or more V than A, then our classic maneuvers to diagnose AVNRT are not helpful.

Our classic maneuver to diagnose AVNRT is you put in a PVC and only by advancing the retrograde His, you're able to advance the retrograde A without a change in activation sequence and reset the tachycardia. But you can't do that when the numbers of As and Vs have no good relationship with each other. So, the simplest and most practical way to answer this question is just sit tight and wait. Nobody always has VA dissociation or interval changes during AVNRT.

You will see, with some change in autonomic tone, putting in a PVC, putting in a PAC where they'll have one to one conduction. And when they have one to one conduction, you can make the diagnosis on familiar grounds. Your usual ways to establish the diagnosis will still be operative.

But if there is a case where it stays with more A than V, for example, then we can still define this arrhythmia as AVNRT by using the construct that whatever it is-- the circuit of AVNRT. The inputs to the AV node near the AV node are necessary for this tachycardia. Even when we have more V than A, the A in front of the tendon of Todaro close to the AV node are still required for this tachycardia. It is a tachycardia that uses some, but not necessarily all, atrial myocardium.

So, it is possible to entrain the tachycardia from this site to show that we have atrium really close to the AV node that necessary for the tachycardia. The rest of the atrium is not essential. The AV node and His are there for every beat of this tachycardia. So then we put that all together and say it's AVNRT.

Now, in real life, though, you'll always see that you'll have some two for-- in all of these variants, you'll see some one to one conduction. Now, the other part of that question was if you start out with the weird VA relationships at baseline, how do you monitor the slow pathway oblation. So, in other words, Dr. Singh is giving us a scenario where at baseline, there is no VA conduction.

We know that even if there's no VA connection, there's no HA conduction at baseline, you can still get AVNRT because the place where the V to A, the pathway that's being taken is not entirely shared by the turnaround site from AVNRT. So, all of us have observed this at some time or the other.

The problem is when we're monitoring for slow pathway ablation, the junctionals that are seen may not show a retrograde A. Now, this is usually something that gives us a minor heart attack, when we see a junctional without A. But yet, the junctionals without A may be exactly what we'll see in patients like this, when they have adequate good sites slow pathway ablation. So a good way to try to address this is to be ready to pace the A.

So what we're really interested is antegrade conduction. Is it getting destroyed or not? So we have someone with their thumb ready to pace the A just a little faster than the junctional rhythm that's being seen without an A. And if the antegrade conduction is intact, we can continue to ablate.

An even more difficult scenario is when we're ablating in the vicinity of the coronary sinus. In some patients, the pyramidal space is very deep, the ganglia is right opposite a traditional slow pathway ablation site, and when we ablate, we get a prominent response like a vagal response that gives you even complete AV block. Now, you need a lot of courage to continue doing that ablation in that situation.

So, what to do in that circumstance-- because here, even if you pace the A, you're going to get AV block. You will see this as AV block. Now, in such cases, it's good to just regroup, look at your fluoroscopy, see where the catheter position is, look and see when the patient got their every block. If the sinus rate also showed, did the sinus rate also slow? And if the sinus rate also slowed, suspect a vagal mechanism.

And once you've got all the anatomy in line, you can either pretreat with atropine, or glycopyrrolate if the patient is on an LMA or a ventilator, to reduce this vagal tone. And then you can continue with the ablation the same way. I hope that answers Dr. Singh's question.

Any others that any of you have seen that you feel we should address in this last 10 minutes? And we will definitely get to all the other questions in a separate session that will be part of this YouTube link when we go through this as well.

SIVA MULPURU: I have one question from the audience.

AMMAR KILLU: Oh, go ahead. I'm sorry.

SAMUEL J ASIRVATHAM: I can't hear you well, Siva.

SIVA MULPURU: Can you hear me now?

SAMUEL J ASIRVATHAM: Yes.

SIVA MULPURU: OK. So one theme that people are asking--

SAMUEL J ASIRVATHAM: Oh, it's difficult to hear you, Siva. Maybe I will to just go to Ammar for this one.

AMMAR KILLU: So, I was just going to say in some circumstances when you're abrading in the slow pathway, you can get permanent junction of that and then keep reinducing tachycardia. And that's something in an interesting scenario can be challenging, because you don't want-- at least, I don't like doing ablation during AVNRT in the slow pathway. There are some patients where as soon as you come on and you're low down, you know you're safe, but the junctional beat then starts triggering AVNRT. So, I think--

SAMUEL J ASIRVATHAM: Yeah. That's a fantastic point, Ammar. So, you just brought in two issues together, and that is ablating during AVNRT and the second is junctionals in the role of inducing AVNRT, including during ablation. So just a couple of things-- I think it's useful, especially, for trainees in the audience.

One is because the Eustachian ridge naturally guards the septum-- job of the Eustachian ridge in fetal life is to direct stuff to the PFO rather than towards the ventricle. It's never easy to get good contact on this region. And because we struggle with good contact in this region, if their heart is beating at 180 beats a minute, it's that much harder. And while we get pretty good at making sure we don't ride high enough even when contact is not good, we just won't get a good ablation.

And what do we wind up doing? We wind up torquing the catheter for contact. And when you torque the catheter on the Eustachian ridge, two things will happen. The catheter will move towards the septum, the tip. It will also ride up because it's a diagonal ridge. So, when it rides up, you're going to maximize your contact exactly where we don't want to maximize contact. So we really try to avoid ablating during AVNRT.

Now, on the other hand, if we have a situation where junctionals are inducing AVNRT-- in fact, in some ways, when we think about it, junctionals are the best way to induce AVNRT because from the junction you have absolutely coming out through the exit, the fast pathway. The slow pathway may be completely unoccupied or recovered because your origin was close to the slow pathway. And you can start AVNRT.

Unlike a PAC that has to tease out the differences between refractoriness of the fast and the slow pathway, junctionals are a good way to start tachycardia. And, in fact, a good little trick is trouble inducing, you can very gently-- catheter-induced junctional beats may be a way to start AVNRT in some patient. Gentle because you don't want to bump the fast pathway, making it super hard to proceed with the case in those patients.

But your point that you brought up is while you are ablating the slow pathway, you're getting junctionals cells that are now it's off to the races. So one little tip that I like to share when that's happening is stay away from automaticity, but still stay close to the slow pathway-- so go for a lower line. The lower line may give you PACs like from the CS myocardium, for example, but you're less likely to get junctionals and may or may not have been able to complete the circuit. But now, if you go back to your usual site where you tried to ablate, the tachycardia itself may be no longer inducible or much harder to induce.

So, while completing the slow pathway line, you're actually doing, like, a perfect EP study by inducing your junctionals. And now you see you don't have that problem anymore. So, it's kind of downshifting to a lower line. But because you're not used to doing the lower line and you want to be sure, after that, you come back to the same mid-CS level where you're used to doing that line. Does that seem fair, Ammar?

AMMAR KILLU: Yeah, it does. The only other thing, I think, some people like to do is use cryo in that situation as well-- I don't know your thoughts on that-- because less likely to get junctionals. And I think it's a valid approach.

SAMUEL J ASIRVATHAM: It's a fantastic idea. And, in fact, pediatric colleagues, or when we do pediatric cases, we prefer that. It's often said that cryo gives us better contact. That's true. But it doesn't give you contact, necessarily, where you want to have the contact. In other words, the same Eustachian ridge that's making it tough to get there will make it tough to get there for any catheter. But once we're there, we're there. And because the junctionals are far less common, you won't have this issue coming up.

The other way is occasionally the best way to get contact, is to come from above. And, here, you remember that the natural way the catheter goes, it's tough to go into the fossa ovalis behind the Eustachian ridge. Maybe Abhishek can share some examples of where he's tried to do transseptals from above, of how difficult it is to get contact in that site, but naturally gets you this angle catheter with the Eustachian ridge this angle to get your contact on that site. So cryo, doing this double line, getting to that location from above may all be ways to try to solve this problem.

I see some other fantastic questions about the left inferior extension and then should you come off when you have fast junctional beats. Since we're out of time, what we'll do is our panelists will answer these questions, and we'll put it as an addendum to the discussion place for when we post this recording on YouTube. Anything you'd like to add, Russell? And thanks a lot for your help with putting this all together. And--

RUSSELL SLACK: I think-- I think we're good.

SAMUEL J ASIRVATHAM: Great. Great. Thank you everyone for joining us. I think there were three very nice about questions we could not answer during the live session we'll try to address now. One is the left slow pathway. There were a couple of questions. One is about its existence and where is it, when do you ablate, how do where it is.

Another outstanding question was about in atypical AVNRT, in other words, retrograde slow pathway, do we ablate anatomically or do we map the earliest site for the A and ablate at that site. And another very nice question about the slow pathway potential, what is it, and can we use this to guide ablation in cases where there's unusual physiology or unusual anatomy. So, Abhishek, if you'd like to start on this left side slow pathway, and I'll find us some slides that we can potentially use as an adjunct to your discussion as well.

ABHISHEK DESHMUKH: Great. So, certainly the left-sided slow pathway, it becomes an important entity when we start to look at tachycardia and the retrograde activation is earliest in somewhere in the coronary sinus and not on the fast pathway location. So, at least, we know based on that, that the retrograde limb is the slow pathway left sided inferior extension. Generally, they exist about 2 to 4 centimeter into the CS on the roof of the coronary sinus.

So, when you get into the coronary sinus, not immediately at the roof of the coronary sinus, very proximally, you will also go to ablate the AV node. So you don't want to ablate there. But as you advance the catheter more in, about 2 to 4 centimeters in, and confirm it on the LAO view that you are more distal here, those would be the targets where-- those would be the A location where you would potentially ablate the left-sided slow pathway, or the left inferior extension, what we call. And there's another inferior left-sided extension which is even further in that is extremely rare and that also can be ablated from the coronary sinus.

There was another question whether to ablate it through the coronary sinus or to do a transseptal and ablated. I think both approaches are reasonable. I think, sometimes, if you're unable to ablate from the coronary sinus or if you feel that the local electrogram is not changing or the impedance is starting to get too high in this location, then certainly a transseptal approach can be performed so that you can target the same area-- same location from the left atrium. But the key thing is that you have to ablate 2 to 4 centimeters inside the CS and not ablate very, very proximally, because there's going to be a very high risk of ablating the AV node and complete heart block if you ablate too proximally.

SAMUEL J ASIRVATHAM: Great. And maybe I'll add to that here, Abhishek. I'll share my screen now. If we go to-- So, in a way, I like to tell myself about left slow pathway ablation. First of all, numerically, there's so many different variants of inputs to the AV node, but outside of our usual slow pathway, this left inferior extension is the most common, because anatomically, the AV node-- the extensions are the right inferior, left inferior, and right in the middle. Separating these two incision-- these two extensions is the artery to the AV node. So the artery to the AV node, sort of, is what's causing the symmetrical inferior extensions on both sides.