SAMUEL J. ASIRVATHAM: Thanks, everyone, for joining, so interactive question and answer session, just focus topic to get us started today is conduction pathways. And we'll go over this as a series as the months and maybe years go by, with just a brief introduction to the normal conduction system. And then we'll start taking questions from you, cases that you would like to share with us, and some of ours that we'll share with you as well.

Thank you for those who have already sent in some cases and questions. And feel free to send in anyway some of the questions that were emailed to me, we'll talk about. And ones that we can't get to during this hour, like we did last time, the panelists and our guest faculty will just spend an extra 15 - 20 minutes answering those questions. And it will be available on YouTube when you go in after this one-hour session is done.

So those of us here are Dr. Deshmukkh, Dr. Mulpuru, Dr. DeSimone, and myself. And several of you who want to join, we'll bring you on as a panelist along with Mayo faculty as well. We'll start with a brief introduction here. So, overall, the questions that we get for things that come from trainees, practitioners, about the conduction system, will center around, how accurately can we know where the critical parts of the conduction system are? And how do we leverage that information for pacing, including conduction system pacing or avoiding damage during ablation.

So we'll spend just a few minutes to go over. Remember the sinus node, it is an intracardial structure and it's not a structure that's located at one point. It's an area that's at that junction between the superior vena cava, the roof start of the atrial appendage, and the highest point of the sulcus terminalis, between this SVC/IVC axis and the muscular portion of the atrium, important issues that could come up in cases that you've had when you want to avoid damage to the sinus node, or you purposely want to modify the sinus node.

The second spot, which is sometimes hard to understand when we're looking fluoroscopically or moving catheters, but we're saved because of the recording of the His bundle is the membranous septal region of the heart. So on the right side, related to the tricuspid valve apparatus, specifically the anterior and septal leaflets of the tricuspid valve, and when viewed to the right from the left side of the heart, junction between the right and noncoronary sinuses of Valsalva. This is a very reliable location for recording the His bundle electrogram.

Now, in between, to get from the sinus node to this His bundle region, the little furrow between the anterior and septal leaflets is the compact AV node. And, as most of you know, this is the side which is the most variable. And we approximate by drawing a triangle looking at the attachment point of the septal leaflet of the triscuspid valve, the roof of the coronary sinus, and this extension from the Eustachian ridge, and underneath the tendon of Todaro, right up to where the membranous septum would be.

So this triangle helps us to approximate where this compact AV node is located. And then we use fluoroscopic or electrical landmarks to identify these structures, and then say this is where we would like to avoid damage while ablating. Another couple of useful ways to think about this region is in the LAO projection. The LAO projection, you'll notice, the interatrial septum is actually a very small structure, where it's truly a septum. You poke on one side and you're out to the other.

Everywhere up anterior, as we go up towards the head anteriorly and superiorly, you see there is no septum, it's a separation of the right and left atrium with pericardial space and tissue in between. And then, inferiorly, we see a similar kind of an x-shaped deviation, except here on the left side we've got the roof of the coronary sinus, and on the right side we move away the Thebesian valve region, Eustachian ridge, and free wall of right atrium. So septum, when we talk about septal pathway, we talk about conduction system on the septum, so very restricted region of the heart.

One of the things that's also useful to point out, that unlike the infrahisian conduction system, where we have specialized conduction tissue, in the atrium there is no specialized conduction tissue. You'll often see a figure like this. It's from an older concept where it was thought there were internodal tracts. There aren't any. Anything that we look at preferential conduction in the atrium is just the fibrous, the muscular architecture, the way in which the myocardial fibers are arranged.

And just these myocardial fiber arrangements, in the atrium, are based on whether they are all in one direction, vertically, or there are horizontal or slightly oblique variations. The most reliable ones that we see in the atrium are related to this crista terminalis, and, to a lesser extent, this vertical ridge in the left atrium between the pulmonary veins and the atrial appendage, and this horizontal connection between these vertical ridges, which is Bachmann's bundle. So just a kind of early introduction for us to help process some of the questions that you had, and we hope you have to share with us.

And we'll go back when needed to one of these figures or any that you send to us or like to bring up to us, to talk about the conduction system. So maybe we'll start talking about questions. So I know that we'll answer them as they come in real time. Feel free to also send any that you have through the chat messaging, or email any of us for those questions as well. So I'll start with one question that we had, was, what are the locations during ablation, other than maybe node re-entry or septal pathways, where we may injure the conduction system.

So not maybe in RT, where we're sort of used to thinking about it, but where else could we injure the conduction system. So maybe I'll ask any of our panelists here, would you like to comment on where in other ablations, where you worry about this phenomenon of inadvertent injury to the conduction system? Siva, do you want to make a comment?

SIVA K. MULPURU: Sure. You know, sometimes when we're doing a PVC ablation or VT ablation, very common to the His-Purkinje axis, like ablating in the cusps, we have to be careful about injury to the infrahisian system. The other situations where you should think about conduction system issue is when you're doing an accessory pathway in the venous system, like in the middle cardiac vein, and then sometimes when you're doing ablation in the mitral isthmus area, where you have arterial supply to the sinus node. Sometimes you can cause sinus arrest with that.

SAMUEL J. ASIRVATHAM: Thanks, Siva. So maybe I can just expand a little bit on that. If we were to look at, Dr. Mulpuru brought up a couple of points. First was the sinuses of Valsalva. So we know that the junction between the right sinus and the noncoronary sinus, this is posterior, this is anterior, sternum will be here. This junction is where we have the His bundle.

And, if you remember, the triangle of Koch, the compact AV node, is posterior to the His bundle, is closer to the spinal column. So the place where it would come as a risk, is if we are ablating, say, in the noncoronary sinus, and we didn't realize that the catheter had slipped in the commissure, or we perforate the noncoronary sinus, then we can have risk to the conduction system there. So that is one area that is important to think about.

Siva also brought up the issue of the accessory pathway in the posteroseptal region. So this is a little counterintuitive. And maybe I'll go back to the slides here to show what the issue is. So, if we think about this region, it should be that when we're in ablating by the posteroseptal space, or in a middle cardiac vein, we're actually extremely far away from the compact AV node. We really are not even in the slow pathway region. We're even more inferior and posterior.

But the issue is the compact AV node's blood supply. The artery to the AV node travels up into the septum and actually is what separates the right and left slow pathway inputs to the AV node. So if we are in the postreceptive space and in the venous system, and our catheter is pointing upward, trying to get myocardial content, it's possible to injure the artery to the AV node.

Now the third scenario that is inadvertent injury because of ventricular tachycardia ablation, the way that can happen is, if we're ablating in the ventricle, the left ventricle, we already have understood that the compact AV node is atrial to the tricuspid valve. And all electrophysiologists, this is kind of bread and butter to us to know, that if you stay ventricular you will not injure the AV node. If we stay ventricular, you won't injure the AV node.

But that's only true on the right side. But because of the separation, where the mitral valve inserts more separate than the tricuspid valve in the normal heart, that region, the AV nodal region, when we look opposite on the left ventricular side, is underneath more ventricular to the mitral valve. So if we were, for example, ablating a mitral isthmus VT, and we tuck the catheter up under the mitral valve, it is possible to injure the AV node.

I think that was some of the main questions that we had related to inadvertent injury during ablation. Now, any other questions that have come up now, or anyone would like to come up, please let me know, as we are answering the questions. Yes.

CHRISTOPHER V. DESIMONE: Professor Asirvatham, I think when some people are putting through a few questions, if I can make a couple of points.

SAMUEL J. ASIRVATHAM: Yes.

CHRISTOPHER V. DESIMONE: So I agree with Siva completely, the PVCs for sure. Especially one thing to be aware of, especially if the patient has a right bundle branch block, is when you're even crossing or prolapsing the valve, you could bump that area between the right and non-coronary cusp, penetrating bundle of His and get complete heart block. I think that's one.

The other thing is some people are doing anterior mitral lengths. With the anterior mitral lengths, if you're too close, maybe you're too close to that left sided inputs into the AV node.

SAMUEL J. ASIRVATHAM: Yeah, and I think that's the key to kind of picture in our mind where the normal AV node is located and work from there. But we should also keep in mind that there are times where the AV node isn't located in that region. So the most important in those areas is that we think about this RAO view. And we have this triangle of Koch, AV node here, His bundle here in the membranous septum. We know that when there's a membranous septal VST, the His bundle just is deflected, either downward or away from the VST. So it's still intact.

Now the VST or the type of defect that takes away this triangle of Koch region is a prime ASV or an AV canal complex. So in those cases, we will never find the compact AV node in this location. And it's typically found in the floor of the coronary sinus. So here also it's important to keep in mind, because intuitively we say the lower we stay, the less likely we'll get AV damage.

One issue we talked about is arterial damage. The second issue that comes up is in congenital disease where we have an unusual location for where the AV node is located.

SIVA K. MULPURU: We have now a question from the panel, Sam, asking how likely is it to see sinus node injury while we are ablating an upper loop flutter. We are mapping an upper loop flutter. And we create a lesion set to interrupt that flutter. What are the precautions that we can take to prevent a sinus node injury?

SAMUEL J. ASIRVATHAM: Sure, yes. So now, does the doctor who has that question want to come up to talk about it? OK, so first of all, just a little bit about what is upper loop re-entry or upper loop flutter. So lower loop we know, IVC, cavo-triscuspid isthmus, tricuspid valve. And a type of flutter that will use the myocardium posterior to the IVC, and anterior. That is, the cavo-triscuspid isthmus.

This is our lower loop re-entry. Lower loop re-entry, if we ablate a standard flutter line, cavo-triscuspid isthmus, it transects this critical tissue for this type of re-entry. And that's why we rarely think about mapping or ablating lower loop re-entry separately. Cavo-triscuspid isthmus will take care of lower loop re-entry. Now, upper loop re-entry is a type of circuit that does not occur in the normal heart.

The reason for that is we don't have an inferior boundary for upper loop re-entry. So we have muscle behind in the posterior part of the SVC-RA junction. And then we have the sinus node region and the right atrial appendage junction region in front. And this whole cylinder is called myocardium. So theoretically we could get re-entry that just goes around the SVC.

But the reason it does not happen in the normal heart is we have the crista terminalis and myocardium that's completely posterior and inferior to the SVC. So it's impossible to restrict the circuit. So to answer that question about how do we avoid AV nodal, sinus node damage, we'll have to bring up the issue of why that particular person actually got re-entry related to the upper loop.

So if I just bring this up here, so how do we do that. How do we get re-entry around this site, because very important question, and almost certainly would worry about damage to the sinus node. But the only way this happens is if there is scar inferiorly. So upper loop re-entry, we run into this arrhythmia in people who've had cannulation or a right atriotomy. So if we have here an inferior scar that can restrict this circuit, then we get upper loop re-entry.

It's possible to get upper loop re-entry. But the same scar now gives us a way. The same scar now gives us a method of trying to anchor to the scar and avoiding the sinus node altogether. So we would then go from the SVC to wherever that scar is, and anatomically remembering where the sinus node is located, we skirt around it and ablate. And we would be able to anchor the lesion and get rid of upper loop re-entry with really zero risk of damaging the sinus node.

So does that does that get to the doctor's question, Siva?

SIVA K. MULPURU: Yes. I think so.

ABISHEK J. DESHMUKH: To make a point here that sometimes we talk about the right atrial flutters. But even while ablating left atrial flutters we can get profound sinus, we can probably damage the sinus node artery when we are ablating on the roof of the left atrium for permanent roof fllutters, because sometimes the sinus nodal artery can traverse around the roof of the left atrium and certainly that can be damaged during that. I can show you a picture if you want.

SAMUEL J. ASIRVATHAM: Yes, that would be great. Why don't you bring that up for us?

ABISHEK J. DESHMUKH: Can you see this. Can you see my picture on the screen.

SAMUEL J. ASIRVATHAM: Yes.

ABISHEK J. DESHMUKH: So say, for example, we have done our VACCARS and then the roofline is being done. But you can see this sinus nodal artery goes around the roof of the left atrium. And as we are ablating here, we could certainly obviously terminate the flutter but sometimes can also damage this artery and cause profound sinus bradycardia, or even junctional bradycardia and sinus arrest. So this is the artery, and post-ablation you can see this artery completely going away, or getting ablated.

SAMUEL J. ASIRVATHAM: Great. So we have another question about understanding this conduction system anatomy and where it is located from a pacemaker standpoint. Where exactly do we pace to capture the conduction system, His bundle facing, left bundle facing, conduction system facing. Siva, do you have some comments on that? And then I can show some slides as well.

SIVA K. MULPURU: Sure, you know conduction system pacing these days is being popular and many people are doing it to restore synchrony, and even using it instead of biventricular pacing. So initial pacing the conduction system was mainly the proximal His bundle or the distal part of the AV node. But there, because the lead is in the membranous septum, the thresholds tend to go up with time. And the field has evolved to do the deep septal pacing, trying to target the conduction system on the left side of the septum.

SAMUEL J. ASIRVATHAM: And do you have a-- so maybe we can like just--

SIVA K. MULPURU: I'm happy to share a slide, too.

SAMUEL J. ASIRVATHAM: OK, why don't you do that.

SIVA K. MULPURU: OK, so here, this is an RAO view. This is a patient--

SAMUEL J. ASIRVATHAM: We're not sharing your screen right now. Are we?

SIVA K. MULPURU: OK.

SAMUEL J. ASIRVATHAM: I don't see. Or I have a slide here, Siva.

SIVA K. MULPURU: OK.

SAMUEL J. ASIRVATHAM: And then you can help me look through this. So this is, I think, the key kind of image for all of us to keep in our mind when we're thinking about pacing for the conduction system. So, first of all, there's lots of terms in terms of this region, membranous septum, His bundle region, atrioventricular septum, pacing conduction system without crossing the tricuspid valve. And I think this simple image is a nice one to kind of think through.

So if we remember this tricuspid valve has got like a free portion, moves back and forth, systole and diastole, and this kind of pasted down portion, this line of attachment near the annulus and partly into the atrioventricular septum. So everything that's proximal to this line of attachment is not going to be the His bundle. It's either compact AV node, or it's going to be the transitional zone or trigger zone, as the AV node moves forward to become the His bundle.

But once we cross this, we're in the membranous septum part of the ventricle. And there we could get, we get the actual His bundle. And we also get the separation to the right and left bundles.

Now, if we take a section through here and look at it, what we'll notice is that the His bundle, because the membranous septum is a fairly thin structure, when it lands on muscle, this His bundle when it comes and hits the ventricular septum, that's when it's going to separate into the right and left bundles. One thing that's worth noting here is the separation actually occurs relatively leftward.

The left bundle is the natural continuation. And then we have the right bundle, that will partly traverse through muscle and then come out on the endocardial surface. So when someone says His bundle pacing, Siva, what's your guess, most commonly, like cases you've done or you've reviewed? What's your guess, what it is that we're most likely to stimulate or capture?

SIVA K. MULPURU: Most likely the distal AV node is where it kind of transitions into the His bundle, because it's hard on the membranous septum to exactly capture the His, you know, it's such a thin structure. I think most people are getting the distal AV node or maybe, more distally, the proximal part of the right bundle.

SAMUEL J. ASIRVATHAM: Yeah. So if we're not right on the membranous septum, it's going to be either the end of the His, or, as you said, possibly the beginning of the His. If we're really proximal, we're getting some sensed atrial electrograms there. It could be something close to here. The only difference between actually screwing the lead in this apex of the ventricular septum, the crest of the ventricular septum, and left bundle is really just distance.

If that screw reaches right up to here, that's still His. If that screw reaches up to here, the distal part of the helix, the cathode reaches up to here, that's going to be enough bundle of His. So another useful image to try to keep in mind. I know the questioner had some follow up questions about examples, and we will devote some of these sessions just focused on special aspects of pacing. And we'll come back and ask those as well.

And I have another question. I believe it's Dr. Lewis. Sort of related to this topic, but feel free to ask questions about any topic, during this time as well.

SIVA K. MULPURU: So while we are on this topic, you know, Dr. Rutland is asking a question, when we are pacing for His bundle or conduction system pacing, is it better to do it more on the atrial side or do we cross the valve to do it?

SAMUEL J. ASIRVATHAM: So, Siva, maybe I'll just take a shot at that. So let me bring this back up here. So it's kind of one of those six of one, half a dozen of the other. So if we target this region, the nice thing is we're not messing with the tricuspid valve regardless. So that's a plus. The other nice thing is that we don't have to go through a thin part of the septum, like the membranous septum. So it's probably a plus.

We have probably a little bit broader target. But the downsides would be that the more proximal you come, the more likely you're going to sense atrial electrograms. And if those are large, they're going to mess with the timing cycles. So, certainly, all of these have been observed both ways. And if we come really proximal, it's definitely possible to capture and get a very narrow QRS.

But we might now start having some decrement of tissue between our pacing site and the ventricle, because we're now not really in the transitional zone, but more actually in the compact AV node. On the other hand, if we pick a site like here, crest of the interventricular septum, this area has got a nice broad landing zone. And if we miss, in other words, we're not exactly capturing one tissue, it's generally all good in this region.

If we've gone all the way to the left bundle, not bad, because left bundle is getting stimulated, and we can have a retrograde wavefront coming down to the right bundle in most patients. If we miss that and we're getting the distal part of the His bundle, we're probably OK. If we're getting the right bundle and there's no left bundle branch block, we're probably OK. It's a narrow-ish QRS.

And if we only get myocardial tissue, it is septum myocardium. And you'll remember that the septum in this region, the fiber orientation, like if we look at these fibers here, they're all parallel and very similar to the left and right bundle orientations. So even though that's technically muscle, the muscle is oriented in a way to mimic the way in which the conduction system leaves this region of the heart.

So those would be all plus points. But the minus points that we would have in this region would be, we definitely have to cross the tricuspid valve. So if that's one of the main reasons we're doing this, that wouldn't work so well. And if someone has a high septal infarct, then we would have a narrow zone where we would be able to get this capture. Anything else you'd like to add to that, Abishek?

ABISHEK J. DESHMUKH: No, I think this is fantastic. Even your panel B, actually kind of off topic, but you know why people get complete heart block after TAVR, you know, one of the things is if you have a low-seated valve in the LVOT. One of the reasons why they have complete heart block, again, would be you are compressing on that structure, from the lower side of the valve, and which can cause complete heart block, which you can see from panel B.

SAMUEL J. ASIRVATHAM: Very nice.

CHRISTOPHER V. DESIMONE: I think panel B also, too, shows you, not only is it really hard to get to that His, like when people are seeing true His, but if you're at that membranous septum and you screw in, you'll end up in the LV.

SAMUEL J. ASIRVATHAM: It could be. Interesting that that hasn't been reported, which also makes me think we're probably putting it into muscle. Otherwise I would have guessed we would have seen quite a bit of that.

Now, there's another question here, that the question is from Dr. Lewis about premature atrial beats. Premature atrial beats, anything about locations that tell us there's a predisposition to atrial fibrillation? What do we know about natural history of PACs and likelihood of getting atrial fibrillation? Abishek, do you want to take a shot at that one?

ABISHEK J. DESHMUKH: Sure, so we know that the majority of the triggers for atrial fibrillation start from the pulmonary veins. And, if you look at how AFib gets initiated, a lot of times it is the PACs or non-sustained attack which could potentially set off atrial fibrillation. Now the question is, is that an absolute PAC burden which we should be aware about for setting off atrial fibrillation?

I'm not clear about an exact number, but there have been epidemiological studies which have been performed, which have looked at various PACs burden, but generally if it is about more than 5% or 10% based on some studies, then there is a risk of having atrial fib, or at least those patients may have atrial fibrillation. But again, atrial fibrillation, as we all know, is so complex, way beyond the trigger it is also a vascular disease. It is a substrate-based disease. So there is a lot which will go into it for genesis of atrial fibrillation.

SAMUEL J. ASIRVATHAM: Great. Thanks, Abishek. So another question here about, we've shown the AV node, but the question is, left side input to the AV node. Where do we look at for ablating the left side input to the AV node?

Maybe I'll take a quick shot at that. And we'll use this figure that we saw a little while ago. So just to understand the concept of these inputs to the AV node, AV node is going to be a septal structure. But notice if any myocardium wants to reach the AV node, whether it's anterior inputs or posterior inputs to the AV node, they have to start off the septum, and then eventually encroach onto the septum, to reach the AV node.

And this Is the anatomic basis of discrete inputs to the AV node. AV node's on the septum, but not much else is. So any other way we get in there, we're going to have to have an input rather than just any known part getting to the AV node. So a specific question here is about the left inferior input. So if this is where we are imagining the AV node, we see right myocardium can encroach up here, region of the coronary sinus ostium, and come on.

The left myocardium, left atrial myocardium, can also come up to that region. But because this septum separates out at the pyramidal space and because the AV node artery is coming right in the middle here, we don't have a single posterior input to the AV node. We've got a right inferior input and we've got a left inferior input. Now how do we ablate that left inferior input?

Well, one option is to get into the coronary sinus, go towards the roof of the coronary sinus, staying away from the septum, which means staying away from the ostium of the coronary sinus, and pointing atrial. That would give us ablation of this extension of the AV node to receive the left inputs towards the AV node. Another option is to get to that same location, but transseptal, and then getting a catheter down to this region.

Some folks, my own preference in cases where it's clearly that's what needs to be ablated, and by that I mean that's the retrograde limb that was mapped, or the anterograde limb that was mapped, what with entrainment, to show that that's where we need to ablate, is to do both, both the CS approach as well as the approach down. Hopefully that answers that question.

Any other questions that any of you have seen that you'd like to highlight or if someone would like to come up here to ask?

SIVA K. MULPURU: One of the attendees was interested in if you could explain the AV conduction system access in CCTGA.

SAMUEL J. ASIRVATHAM: OK, sure, I can do that. And then, let's see, maybe, I see another question here, about damage, that I believe what the question being asked is damaging the left bundle easier than the right bundle. I think asking like bundle branches, if we were to ablate, is it possible to ablate, is one easier than the other. So maybe while I'm pulling up a figure about conduction system in CCTGA, maybe, Siva, do you want to take a shot at that question about damage to the infrahisian conduction system?

SIVA K. MULPURU: Yes, so in books when we look at the pictures, the left bundle is commonly depicted as just two branches downstream. Usually it's a very simplified explanation of that. And it's the infrahisian system on the left side is far more complex. And you have multiple branches. In general the right bundle structure, after it traverses away from the membranous septum, is a little bit more superficial structure, thinner structure. And once it is sub-endocardial, that area we could potentially even cause transient block by pressure in the right bundle region.

Compared to the left bundle region, left bundle at least a proximal left bundle is a thicker structure, bigger structure, and is sub-endocardial. Potentially you could ablate the proximal left bundle. A part of the proximal right bundle can be intramuscular and could be difficult to ablate.

SAMUEL J. ASIRVATHAM: Sounds good. So let me use just a diagram up here to talk about CCTGA. And we do have a special session that we'll give you the dates for shortly, where we will have one of our cardiac pathologist, Dr. Melanie Boyce, will be a guest panelist and will have actual key congenital heart disease specimens, to look at the common issues for electrophysiologists. And Dr. Boyce will have a CCTGA heart, will also have a post-Mustard heart and post-Fontan heart, for session one.

Later in the year, we'll focus on tetralogy of Fallot and some of the VT congenital heart disease. But to give a quick answer to the question that was asked, so, first of all, a couple of things. So when we think about the normal heart conduction system, we had our AV node here. We had the His bundle here. So single His, single AV node, connection, one axis to get down.

Now in CCTGA, we can get a second AV node, with its own His bundle, and potentially linking up with this to produce, like a sling or a monkey bird sling. Now one of the things, the clues in CCTGA, to anticipate a second conduction system axis, is if the right ventricular outflow, the infundibulum, is small. The smaller the infundibulum of the right ventricular inflow, the more likely you are going to find this situation. And this can make SVT ablation in CCTGA quite confusing, because it's possible to get AVNRT related to either of these AV nodes, or possibly both, with slow pathway input to one and exit through the fast pathway to the other.

Rules of thumb once you've recognized it, is first try to define which AV node is conducting really well. So we identify a His, we identify another His, we face the atrium, and see which tends to block first. The idea is to understand in our own mind if we ablate one of these AV nodes, are we leaving the better conducting AV node alone? So that's one. Second is, with induction of tachycardia, to have multi-electrode catheters on both His bundles. So if we have, say, four-fold, for one, proximal, distal.

And if we see conduction that's going proximal to distal in one of the His's and distal to proximal in the other one, then we do have a sling type tachycardia. But if, on the other hand, it's proximal to distal in both, then that's not it. It's not enough to just ablate one of the AV nodes. We've got a supraventricular tachycardia, possibly AV node re-entry, that's just using this tissue as a bystander, like in all AV node re-entries, going from proximal to distal.

So we'll have to ablate the AV node re-entry, either with our standard approach or mapping, entrainment mapping, to find out the key part of the circuit and ablate it. The other difference to keep in mind with CCTGA, and for that I'll just do a share here, is to understand that the noncoronary sinus, so if we look up at this figure here. So if we notice here, this is a very beautiful dissection from Dr. Damian Sanchez-Quintana, and it shows this central location of the aortic valve.

So we use this aortic valve as our landmark, noncoronary sinus versus right coronary sinus, His bundle. And we know sometimes anterior inputs to the AV node can be ablated, say, from the noncoronary sinus, several reports now, and something recognized some years ago with anecdotal cases. In CCTGA, we should remember that this valve, the central valve, in the heart, is not the aortic valve, but the pulmonic valve.

So the central valve is the pulmonic valve. And that's why, in tough AVNRT and CCTGA, some of the ablation that's successful is in the posterior RVOT, because the posterior RVOT and pulmonic valve is the equivalent of noncoronary sinus of Valsalva ablation in CCTGA. So I don't know if you're chatting with the person who asked the question, Siva, but does that kind of give a brief answer to that question? And then we will have a special session, for sure, and maybe if we could bring up Dr. Cannon to just comment also about unique issues of CCTGA ablation, particularly in the context of avoiding conduction system damage. Would you be able to do that for us, Russell?

MODERATOR: Yes. He said no.

SAMUEL J. ASIRVATHAM: Hey, Bryan.

MODERATOR: Yeah.

SAMUEL J. ASIRVATHAM: Any bits to add to-- so it was just we will definitely do a focus session later. But just this specifically for CCTGA, stuff that you keep in mind when thinking about conduction system location, pulmonary valve, pulmonary outflow.

BRYAN C. CANNON: Sure, I mean, it's an excellent question, and I think before you do any ablation on a congenital heart disease patient, you should try to figure out where the AV node is. And a couple things is, typically, the AV node will run posterior, but in CCTGA, it tends to run more anterior. In addition, the node, because of its position around the VST and around the valves, tends to be not quite as stable. So the actual incidence of AV block is about 2% per year.

So you have to be very careful when ablating, because these AV nodes are not strong and, a lot of times, they don't function well, as you mentioned. The other thing is that the septum, instead of being activated from left to right, is now activated from right to left. So actually one of the clues that you may have congenitally corrected TGA is you'll see a Q wave in lead V1 rather than V6, just because of that opposite activation of the septum.

But these are patients who are at risk for accessory pathways. It's one of the higher incidence. But sometimes you have to make sure, before you ablate the accessory pathway, that the AV node is actually there, because they can have AV block underneath, and some conduction is better than no conduction. So that's my couple of comments. Thanks, Sam.

SAMUEL J. ASIRVATHAM: Great, thank you. So maybe I can just draw a little sketch about the ACG issue that Bryan brought up. So this is our normal septum, without ventricular inversion, just the normal right ventricle, left ventricle. We have right bundle here, we've got left bundle here. A few of the things we remember about right and left bundle that's slightly different, is the right bundle, in addition to taking that little intramyocardial course we talked about, is also slightly longer in terms of its insulated portion, before it breaks out to ventricular muscle.

So because the left bundle is the natural continuation of the His bundle, because it's slightly shorter, the segment that it has insulation, and you wind up exiting on the left bundle earlier than the right bundle. So as a result, your normal conduction across the interventricular septum is left to right. This is the normal heart. And as a result, we have these so-called physiological or septal Q waves in V5-V6, activation moving away from V5-V6.

It should also be noted that, from the exit of the left bundle, the usual exit of the left bundle on the posterior fascicle, fiber orientation is slightly angled from inferior to superior. So not only do you go left to right, but you go from posterior to anterior, go higher. And that gives the small Q waves that we see sometimes in the inferior leads, especially in EVF and in sometimes all the inferior routes, small septal cues. So Bryan's point is when to suspect ventricular inversion, just from the electrocardiogram, is when, in CCTGA, the ventricles are inverted. And when the ventricles are inverted, we also have inversion of the conduction system.

So right bundle is now on this side. Left bundle being on this side, now this is shorter. This is winning the race and we're moving this way. So now we lose our septal Q waves in V5-V6. In fact, if we had right sided leads, you will see the septal Q wave there, in those leads, for this. So just ECG variation in CCTGA conduction system. So AV node, we talked about sling, multiple AV node potential for pathways, and then this natural difference in the infrahisian conduction system.

Now I see one more question here in the chat. Any others that any of you would like to bring up, Abishek, Chris?

ABISHEK J. DESHMUKH: I was just pulling up a BIV I had done in a patient with CCTGA to show the small acute marginal veins. But I'll just bring it up and then show you, in a minute here.

SAMUEL J. ASIRVATHAM: Sounds good. That'll be great. So that's another question that comes up sometimes, when we think about CCTGA, is not only the conduction system itself, but the veins, the ventricular veins. So it's right ventricle, which is on the left side of the body. And we know the coronary sinus keeps time with the atrium, the annulus, the valve. So coronary sinus is normally located, but what about the ventricular veins. What do they do?

The ventricular veins go with the coronary sinus. So will they be left ventricular veins? Or, because they're draining the right ventricle, will they be right ventricular veins? Very small, small margin vessels, and the answer, as Abishek is going to show us, is, even though the CS is normally located, the veins keep time. They go with the ventricle.

So it's right ventricular veins, very small, tend to be very small. On the other hand, the septal veins are still like normal. So the anterior intraventricular vein, and the middle cardiac vein, are like the normal heart. So if we just have to get a lead in a vein, we tend to target one of the septal veins, because it can be tough to get a lead out in one of the smaller veins. Abishek, you wanted to share an example with us?

ABISHEK J. DESHMUKH: One second. I will pull it up. I just have to put it on a slide. Give me like one more minute. I'll do it.

SAMUEL J. ASIRVATHAM: OK, so maybe while you're pulling that up, I'll just make a little sketch on what we're going to see here. So if we see a coronary angiogram, if coronary venous angiogram or a lead position, the proximal part of the CS would look normal. And then we'll see abrupt tapering, and then small marginal vessels, and then coming back, more towards the septum, sometimes an anterior intraventricular vein that's fairly normal sized.

So proximal CS, middle cardiac vein, will be OK. But lateral veins we'll anticipate being significantly smaller than normal. You have that figure, Abishek? OK. So talk us through what we're seeing here.

ABISHEK J. DESHMUKH: This is an RAO view. We are trying to do an angiogram, a CS venogram, to put in a CS lead. And here, you can see, as we engage the coronary sinus, these veins are quite small, very, very small branches. So sometimes lead deployment is difficult. Sometimes thresholds are very high, impedance is very high, because of the smaller tributaries and smaller branches.

Sometimes the question also becomes, can we completely resynchronize this ventricle, which again, is going to be very difficult to do this. Certainly what I try to do is try to find an opposite factor, maybe get the lead somewhere higher up, and then see if we can pace that way.

SAMUEL J. ASIRVATHAM: Great. Thanks a lot. Other questions that anyone has there? Otherwise I have one more here to address. Let me know if there's someone who wants to come up and ask a question. So the question here is a bit of a difficult question. But specific areas in the infrahisian conduction system prone for arrhythmia. The word Purkinje or infrahisian conduction systems, so maybe I'll start with just a slide of what it is we mean by infrahisian conduction system. And I'll ask maybe Dr. DeSimone to--

CHRISTOPHER V. DESIMONE: Have a nice slide to show if you want to take a peek.

SAMUEL J. ASIRVATHAM: Yeah. No, well, first let me just show this.

CHRISTOPHER V. DESIMONE: Sure, sure.

SAMUEL J. ASIRVATHAM: And so just first of all, it's important for somebody to remember that the infrahisian conduction system is far more complex than we normally consider. It's not like, here's the left bundle, and here's the left posterior fascicle, here's the left inferior septal fascicle. It's really a network.

And that network is relatively discrete towards the annulus, towards the His bundle region, but gets very, very intricate in the mid-septal region at the level of the papillary muscles, and then gets a little bit more discrete as we get towards the apex. So, in other words, the chance of getting very complicated circuits, circuits nonetheless, re-entering, but highly complicated circuits is possible in this mid-portion of the ventricle, whereas more distinct vesicular-type tachycardias, more proximal, or occasionally when much more distal.

I think also important to kind of remember here, the hole is the region of the membranous septum, is that there's a difference when we just say infrahisian conduction system. There is distal filigree-like Purkinje network, which, at any point, can connect to the ventricle. Any point, there's no insulation. The only reason we see distinct signals in that level of the conduction system is the orientation of these specialized fibers, whereas more proximally, we're seeing this kind of insulated portions where distinct circuits, relatively larger circuits, are possible, whereas here, almost impossible to define what are the components of the circuit there.

Chris, you had some questions, some comments you wanted to make.

CHRISTOPHER V. DESIMONE: Yes, I just wanted to share the screen. It's exactly actually the figure you showed.

SAMUEL J. ASIRVATHAM: OK, and then any comments that you have on that, please go ahead. And then I see there's a couple of more questions that came, including one by Emil. We'll definitely address it. We'll kind of go over it and add it to YouTube, or bring it up when we start our discussion next week. So, Chris, go ahead and we can finish up with that.

CHRISTOPHER V. DESIMONE: So everyone can see what I'm showing?

SAMUEL J. ASIRVATHAM: Yes.

CHRISTOPHER V. DESIMONE: OK, so I guess, lower down that you said, one thing to mention is the false tendons, where a conduction system could be running through these actually. So I really like this picture, shows that it's not really an easy system as we go from proximal down to more distal. And specifically things like fascicular VT, or this Purkinje PVC-triggered VF could be around these areas.

SAMUEL J. ASIRVATHAM: But I think the question that was asked is a tough one, and maybe we can even devote longer, nice discussion to this. Any area in this conduction system is more arrhythmogenic, I think what's being meant is more likely to give malignant arrhythmias like VF. Maybe we'll keep that as a thought. We'll try to discuss that a little more fully, and add that to the YouTube along with one other question that I see just from up there.

But thanks. Thanks, everyone, for joining, and please keep the questions. Feel free to ask, any manner that's good. Send an email to any of us. If it's something you need urgently addressed before the next webinar, we'll address it to you directly through email or give you a call. If not, please submit them online, more cases that you have or questions from your own practices, the nicer that it will be. Dr. Majumdar, your question, as well, we'll make sure that we get addressed in the add-on which we'll post on YouTube. Thanks a lot.