SAMUEL ASIRVATHAM: We have a topic, just as a starter to kind of get everyone focused on what questions, think about cases that they've had, and things that they would like to have some more discussion about. We'll spend about 10 minutes going over some key features on the topic of the day. And today's topic of the day will be just outflow tract tachycardia.
Please use the chat feature to put in any questions that you have based on patients you're seeing now, cases that you've had before that there was some suboptimal outcome. And we'll be looking through everything in the chat. And topics that are either current or ones that we would like to give our own experience or feedback on, one of us will discuss in more detail.
Similarly, any of the experienced electrophysiologists, any of you who are attending the meeting, if there's a topic that you've seen someone else ask a question that you'd like to chime in on, please do. It'll just take us a minute to move you as a panelist. And you can discuss that topic or question.
Finally, what we would really like to encourage as we proceed in the future with more of these sessions is any of you who have your own cases that have an EKG or you'd like to present in more detail, just mention in the chat box that you have a case that you'd like to go over in more detail. And then we'll move you over and you can present to the whole audience and we can get some discussion from everybody on this group.
So I'll just introduce some of the core faculty who've helped put this together. They will always be on as panelists. All other Mayo faculty and other faculty who'd like to present, we'll have guest panelists for each week. And any of the other faculty who are now attendees, if you would like to present something or speak about something, please just drop a note on the chat. And then we'll get you in as well.
So I'm Sam Asirvatham, one of the electrophysiologist, device, and electrophysiology practice. And then Abhishek, you want to introduce yourself?
ABHISHEK DESSHMUKH: Sure. And I welcome all of you for this wonderful meeting.
SAMUEL ASIRVATHAM: Great. And then, Chris.
CHRISTOPHER DESIMONE: Hi. Chris DeSimone, one of the cardiac electrophysiologists here. Welcome everybody.
SAMUEL ASIRVATHAM: Ammar.
AMMAR KILLU: Hi. Good evening. I'm Ammar Killu, one of the cardiac electrophysiologists also.
SAMUEL ASIRVATHAM: Great. And then Siva.
SIVA MULPURU: Good evening. Silva Malpuru here, one of the practicing electrophysiologists. Welcome to the meeting. And I hope that you have an enjoyable discussion today.
SAMUEL ASIRVATHAM: And Russell.
RUSSELL SLACK: Hello. I'm the media support services tech. I'll be moving anybody who would like to present into as a panelist. And then you'll be able to share your screen and talk and be seen at that point.
SAMUEL ASIRVATHAM: And however, any of you would like to ask a question, it's fine. We are looking at the chat to see if there's a question. We look at the question and answer. If you raise your hand, whatever, any of these would work. We look and see. And if you'd like to ask a question live, we'll bring you over. Otherwise we'll just discuss your question, whatever you have up in there.
So I'll just get things started just to give some commonly asked questions about outflow tract VT to set some groundwork. And then we can move from there to any specific questions any of you have. So 10 minutes, five points outflow tract VT.
So usually when there's a question that comes, a phone call or email, it's about a failed outflow tract VT. So it's an outflow tract VT, typical CG type pattern, typical clinical story, should be someone that has a fairly easy way of mapping and ablating. Earliest activation can be done with a single catheter, reference being the ECG, moving the catheter, finding the earliest site of activation, and ablating.
When it's hard, it's usually some anatomic basis or it's a difficulty for induction. The difficulty for induction most often just winds up being, bring the patient back another day. But the ones that are most frustrating are when there's multiple failures and we're seeing the target over and over again. We see the PVC. We see the VT. We recognize it's an outflow tract morphology, so two, three AVFs, strongly positive AVR AVL negative.
But despite mapping and ablation, there's either acute success and recurrence. Or there's just inability to eliminate the arrhythmia. So I'll just hit on a few points and we'll continue it during the discussion. One point that most experienced APs have learned is pay close attention to R waves in V1.
In V1, what looks like left bundle morphology, if there is a little R wave in V1, little R wave in V1 often means there's room for problems based on the specific site of origin. One example of this is when we have a very high origin where the PVC origin or VT origin is actually so high in the heart that it's originating, perhaps, in the supravalvular extensions of muscle above the pulmonary valve.
The reason this produces a small R wave in V1 is because this is high enough above where we place V1 that even though it's a right ventricular structure, there's a vector towards V1 that produces the R wave. We also know the outflow tract is lying on the left side of the body. So there's also a left-to-right vector going towards V1 and producers that wave in V1.
Difficult because one is the valve is moving, opening in real life, makes it difficult to balance the catheter against this location. And we just don't get the contact. And we have to find a workaround to try to get that ablation.
Second big problem when someone fails is when we actually elect not to ablate. And the reason most often when someone elects not to ablate in an outflow tract PVC or VT is either, as in this LAO view you see His bundle catheter just demarcates one of the boundaries for the outflow tract. And mixed in, overlapping with the outflow tract structures, is the coronary vascular system.
Note, for example, very high RVOT PVC catheter, very close to the left main coronary artery. Note also the LAD overlapping with the right ventricular outflow tract. So some locations are going to be close to the LAD. So understanding from the PVC, from the mapping how close we are either to conduction system or the coronary vasculature is important not only to avoid complication but also in explaining why you sometimes choose not to ablate.
So just some key kind of visualization features, especially for those of you early in your career working on mapping in the outflow tracts. Why or how can it be difficult is, remember, the outflow tract that's visible to the eye on the external surface is only the right ventricular outflow tract. So the left ventricular outflow tract is missing from vision because it is a deep structure. It's a central structure in the heart. And we don't have an epicardial surface for the left ventricular outflow tract.
What this also means is the entire RVOT is very close to the chest wall. That's where we're placing all our chest leads, pericardial leads. So the pericardial leads are closest to the RVOT, meaning that when there's origin in the LVOT, there'll be a vector that moves towards all the chest leads. Very difficult to get to QS complexes in any of the chest leads when you have origin in the left ventricular outflow tract.
Other visual to take from this is V1 is placed somewhere here. Lead one is placed somewhere here. As we go higher and higher and higher in the outflow tract, we're getting closer to lead one and we're moving away from lead V1. So the more distal in the outflow tract, the more negative lead one becomes and the more of an initial R wave we start getting in lead V1.
Second visual to kind of keep in your mind, and we can come back to these figures if we have electrograms or any of your cases to share, is because the right ventricular outflow tract is so anterior, the septum of the outflow tract is an anteroposterior structure. So the septum of the RVOT is behind. So a catheter directed posteriorly in the RVOT maps the septum.
Another visual for difficult cases to keep in mind is that septum is only at the level of the aortic valve or below, where it's a true intraventricular septum. Above the level of the aortic valve, the posterior RVOT does not have any myocardium on the LV side. So only place to map or ablate is on the RVOT.
And then this very unique in-between area where you do have muscle of the LVOT, we have muscle of RVOT, and we can have supravalvular extensions of muscle in the sinuses of valsalva. So this appreciation of the outflow tract septum, when and how to get a catheter to balance there, when it's necessary to think about mapping on the opposite side, when it's unnecessary to do so, and that region, that in between region, where we also have to think about mapping specifically within the sinus of valsalva.
So I'll stop there with that kind of brief introduction. And it's something that we can come back to discuss any questions that you have. Feel free, you know, really would like any or all of you to ask us something that you feel has been a difficult case for you, something that we can maybe contribute to with anything from our own experience.
There's a question that we have from Dr. Berra about which coronary artery is closer to the RVOT. The right coronary, the left main, or the LAD? So maybe while I'll take a shot at answering that question, what we'll do is we'll get Dr. Russell Slack-- what we'll get is ask Russell to maybe get Dr. Berra live if possible. And I'll tackle that question.
And if any of our other panelists or faculty-- Dr. Friedman, Dr. Cannon-- anyone would like to make a comment on this, please let us know. And we'll bring you in to this. So let me take a shot at that question.
So we'll actually notice that there's a couple of places where the coronary arteries are close to the outflow tract ablation. Notice that if we're ablating in the anterior part, the free wall part of the RVOT, we really don't have a place where we can ablate the ostia of any of the coronary arteries since the ostia are rising from the aorta and the aorta is posterior to the structure.
But where we can definitely injure a coronary artery is when we're in the RVOT but in the leftward free margin, this left free margin region. This is the region that sort of overhangs the anterior sulcus. And if we have an LAD coursing here, we're doing a deep energy delivery internal to the heart at this region. We'll get the proximal or mid LAD ablated or injured.
Now to injure the coronary arteries from other outflow tract structures, where this can happen is posterior. So this is the free wall of the RVOT. The only place we wind up with the trouble is the LAD. But in the posterior RVOT, in the right posterior RVOT, it's possible to injure the right coronary. Usually separating the posterior RVOT from the right coronary artery, we'll have the branch to the conus. And we'll have a fat pad in that region. So uncommon, I'm aware of one case where there was right coronary artery injury from a RVOT ablation.
But far more worrisome, I'm personally aware of several cases where this has happened is when we have a high focus pulmonary valve region focus [INAUDIBLE] posterior where we can get spasm or actual permanent injury to the left main coronary artery. So for Dr. Berra's question, all arteries can be damaged. But which one depends on the location that we're going.
The most frequent, just from the literature and anecdotes, is the LAD. And it's the right free wall that was being ablated more leftward. The next and most catastrophic, potentially catastrophic, is posterior near the pulmonary valve and then ablating or injuring the left main coronary artery. So Dr. Berra, do you have any other specific questions you wanted to ask from that?
DR. BERRA: No, sir. Thank you so much, sir.
SAMUEL ASIRVATHAM: OK. Perfect. Thank you. Thank you for joining. So, Russell, let's get Dr. Friedman live. He has a question and a comment about the role of fat when there's epicardial mapping that we need to do to get to that. And then, Paul, do you want to make a comment about that? And I can pull up some slides as well.
PAUL FRIEDMAN: I was actually going ask you to comment while you were showing the images of epicardial fat, especially towards the base of the heart and the impact that has on electrograms in terms of their amplitude, the importance of fractionation versus amplitude size for mapping there, and the ability to deliver energy.
SAMUEL ASIRVATHAM: Sounds good. So for the epicardial fat distribution, so the big areas are just wherever there are arteries. So we've got this thick fat that runs along both the annulus and then around the LAD, and on the posterior wall as well. Now the places, first of all, the times we want to ablate on the anterior sulcus or posterior sulcus are fairly uncommon. And we usually have the ability to ablate or map along the vein, the anterior intraventricular vein.
But sometimes the annulus is really where we have to ablate. And the reason for that is because of this shelf-like structure in the ventricle. So for example, if we have an epicardial accessory pathway in this region, it's extremely difficult to ablate across this entire shelf of ventricular myocardium to get the ventricular insertion.
And let's say the epicardial insertion is related to the vein. Then when ablating in the vein, we may have trouble because there's an artery nearby and we want to deliver energy over this fat. And fat with RF is a problem. Because the impedance increases so much that we'll get ohmic heating almost all entirely on the fat. And it's hard to get in beyond that.
Now some solutions that have been tried anecdotally is cryoablation instead of RF ablation. Potentially electoporation may be more agnostic to fat that's in that region. Or making a case that we're just not going to ablate the pathway itself but we will try to map and ablate the atrial insertion.
And if there are any comments or questions on how we would map to ablate that, we could do then. Does that sort of cover it, Paul?
PAUL FRIEDMAN: I think it does. Just as you were looking at those images, I thought in terms of knowing where the fat is. And the second issue, of course, is that fat causes small amplitude electrograms, so not to be mistaken by your map, for example, showing low voltage in those areas, thinking it's a potential arrhythmogenic focus and rather looking for pre-potentials or fractionated signals or other markers of disease. And I noticed that Ammar has a video that might be of interest that highlights this point in terms of the distribution.
SAMUEL ASIRVATHAM: Perfect. So, Ammar, why don't you show that to us?
AMMAR KILLU: Sure. I'll just share my screen. Let me know, can you see the video?
SAMUEL ASIRVATHAM: Yes.
AMMAR KILLU: Perfect. So this was during a surgical case. It was a median sternotomy. And I'm just going to play it but just to orientate everyone so that the video is coming from the patient's head looking down. You can see the cryoprobe in place here with the icicles on it.
This contraption with the two kind of fingers is called the starfish. It's basically a cardiac stabilizer. But the thing to highlight is just look at how much epicardial fat there really is. And you can see the surgeons are actually pointing out where they've dissected some of the fat out. And you can see the LAD in the diagonal. And the ablation was performed in that vicinity.
PAUL FRIEDMAN: And, Ammar, maybe point to the pulmonary artery to highlight that as well.
AMMAR KILLU: So can you see my arrow?
PAUL FRIEDMAN: Yes.
AMMAR KILLU: OK. So I'll just replay that. So you can see this is kind of coming in the RVOT and pulmonary artery here. And then the aorta will be coming up behind them. And so the cryoprobe is really very close. I mean, it's essentially juxtaposed to the coronary arteries to the diagonal and the LAD.
SAMUEL ASIRVATHAM: Great. Very nice. So thanks, Ammar. So we have a question from Dr. Kulkerni asking about late termination of PVCs. So in other words, if you do a PVC ablation and it's not successful right now, is there room for this ablation to be successful later?
So I think that's a very important question. Because patients ask us that. And we have to have an approach for how we think about them. So, Abhishek, do you want to take a shot at that? And I'll provide some comments also.
ABHISHEK DESSHMUKH: I think it's kind of wishful thinking that we hope that if we are unable to ablate the PVC for a reason and then spontaneously the PVCs go away, whether there's a particular mechanism behind it.
SAMUEL ASIRVATHAM: So I'll just-- the issue is, first of all, is there such a thing as late success with ablation. So we ablate. We know with RF ablation our maximum heating is going to be at the tissue surface. And then from there, we have this heating that goes deeper into the tissue.
So if we have a focus that is within where we get tissue cell death, we get acute success and there's no reasonable way that we're going to get recovery later from that spot. But two kind of allied questions, I think clinical scenarios, is after ablation, we find that there are PVCs still there, even though we felt we were in a great spot to ablate. Is there a realistic option that this PVC will then eventually die away or go away?
And second is, we never had success acutely but felt we were in the vicinity. Is it possible for the PVCs to become less and go away later? So I'll just kind of go over maybe my own approach. If someone has what we thought was a great ablation but then they go to their room and we see a bunch of PVCs, then I look very carefully at the morphology of these PVCs and where we ablated.
If our ablation, if the PVCs look in any way different from the index PVC we ablated, then I look and see, did we do an insurance lesions, extra burns. That could explain this morphology. So we ablated this part PVC went and then for good measure, we ablated around it. And if these PVCs match those sites, this could be some automaticity, some irritation from the ablation. And it'll go away.
If the PVCs look exactly like the index PVC, then I look to see, are they changed their behavior. Are they much more frequent now? Are they occurring in little bursts compared to what the patient had before? Then it's possible this is from that ablation.
What's more worrisome is if they look exactly the same and their behavior is exactly the same, we probably just never got it. Or if it looks different but we never ablate at a site that explains this difference, then it's possible that we ablated one of the exits for the PVC. Very common phenomena with supravalvular PVCs or papillary muscle PVCs.
Because of the interconnectivity of the tissue at that level, it's quite possible that what we had was a primary exit. And now we have a different exit. Those are unlikely to go away. But beyond that, the question is a biophysics question.
Is it even possible to get late ablation? So we'll hear talk about maturation of the lesion. Another one is penumbra effect of the lesion. It's actually unclear if these phenomena are real. But if they're real, the common explanations have been you get tissue edema following the ablation that eventually causes ischemia of intramural vessels. And that produces a distance of lesion. And that can give you a late. In other words, you didn't map the right side. You didn't ablate the right side. But patients still does well.
Another is contraction ischemia. So it's not the edema but you get fibrosis. The fibrosis is myocardial cells have died but there were preserved, small, intramural vessels. And as this fibrosis tightens or contracts, then you get this ischemia at a distance and can get a success that's somewhat late.
Both of these are hypothetical. There's some work, some that I'm aware of, from Dr. Nakagawa and also from Denver some years ago that said that it is possible to have sparing of vessels and later involvement of these intramural vessels when you get a lesion. But any other comments [INAUDIBLE] and then we have a response, also, from Dr. [INAUDIBLE] saying about automaticity.
And yes, post-RFA automaticity, definitely a real thing. And it's probably from the heating, the edema. And it's where the membrane potentials have been changed enough not to kill the cell but making it easier to have this automaticity. And that's where if we're actually looking at the automaticity to compare it with what was the index arrhythmia and what we're seeing now after the ablation. Then we can try to come to an answer about that.
I see, maybe while I look at some of the other questions, Siva, any comments about this issue of when we can tell patients that they're going to have a better lesion, a better result later than what they have now?
SIVA MULPURU: So when I think about this, if you have a really good electrogram, very early timing, most likely what we are seeing in the post-procedure is some sort of irritation. And we have a good outcome.
One of the things that I think about is if you have some lymphatic obstruction or microvascular damage from an ablation lesion, lesion expansion that has been hypothesized, those patients, if you ablated high energy, down the line, those patients, there may be improvement in the burden of PVCs. But I agree with you. There are several reasons on why we see these PVCs go away even though you have far field looking grams down the line, a day or two down the line.
SAMUEL ASIRVATHAM: Sounds good. So we have a question from Dr. Gopi about where do we worry about perforation. Where is the places with outflow ablation that were most at risk for perforation? So maybe Chris, just from what you've seen, your experience, any comments about that? And then I can try and pull up some images to help explain that as well.
CHRISTOPHER DESIMONE: I think one of these came through the Q&A as well. And I think that's a good worry to have about perforating. You could essentially perforate anywhere, less likely in other places, like if you're along the septum. And what we had mentioned to who was in the Q&A is kind of one thing to kind of try to help you with that is use your eyes to guide you.
Someone had asked about the anterior RVOT and the free wall of the RVOT. So what I mentioned was one thing I like to do is kind of watch my catheter go in through the RV and up through the outflow tract, but stay septal and go above the valve and then make my mapping start high and go down, rather than go against the contraction of the heart and have forces go against the anterior outflow tract.
SAMUEL ASIRVATHAM: Sounds good. So we have Dr. Cannon here with us, Brian Cannon, one of our senior pediatric-focused electrophysiologists. And I'll ask Brian to comment also with younger patients doing outflow tract, are there some regions where you're particularly worried about?
BRIAN CANNON: Sure. I mean, certainly in very anterior portion of the RVOT, it's a very thin area. And you can actually see through it on anatomical specimens. So you have to be very careful when you push or put any pressure against that, especially when you're doing ablation lesions. Because you can certainly perforate through. Because you worry about coronaries because the distance is less large. And also, you worry about the thinness of the RVOT, particularly in the anterior portion, whenever you push there.
SAMUEL ASIRVATHAM: Great. And maybe I'll just share this, just to explain what we mean by the free wall and what we mean by the septum in the RVOT. So notice that the part that's free, in other words, if you poke a needle through, you're in the pericardium, is this anterior wall of the RVOT.
So good rule of thumb is your distance to the sternum. So whatever fluoroscopic view, if we look at where the sternum is and you look at where your catheter is while you're ablating, if you're pointing towards the sternum or your catheter tip is near the sternum, there's a good chance that you're on the free wall. And that's a place you can perforate.
On the other hand, if your catheter is pointed away from the sternum, for example in the RAO view, even with a [INAUDIBLE], even with an impedance drop, you still have the septal sign that's kind of protecting you from ever going into the free wall. So kind of this using this idea of anterior is dangerous. Things closer to the sternum is where it's more dangerous.
A couple of exceptions to that, though, is in the RVOT, if sternum is over here, when we're pointing rightward versus pointing leftward. So posterior, no problem. Anterior, always a problem. But what about right-left? When you go left, the free wall is restricted because it's like a triangle here with a large base coming down to an apex.
But when on the right side, the free world is extensive. So the right free wall, even though you may not be directly near the sternum, but you're pointing rightward, is a danger site for perforation. Add to that right free wall comes in our triangle of dysplasia. So dysplasia, when it affects the RVOT, it's usually this region as well.
So it's free wall, risk already. And then dysplasia on top of that, that becomes an issue for when we are thinking about where we can perforate. Only other place where perforation also we have to think about is this little rim of tissue. This is actually an overhang.
So if we put a catheter in the RVOT on this tissue, we can perforate to the free wall. We can abut against the coronary artery. Or we can abut on to the LV inflow. It's the so-called RV outflow, LV inflow septum. So it is a septum, but it's a septum not between the outflow tracts but between the LV inflow and the RV outflow.
So there's a question I see and please feel free to come live to answer this as well. But a question that asks about which catheter tip or which size of the catheter is more likely to produce a perforation or a large lesion with late success or maturation. So really, a question about the biophysics of ablation which gives us the biggest lesion.
And maybe I'll ask Russell to bring Dr. Friedman back to help us with this question. And Siva, do you want to give some comments related to that? So kind of like lesion size with the irrigation, non-irrigation, depth with an 8 millimeter tip. You've done some original work about putting two electrodes and ablating, bipolar ablation. Maybe you can share briefly some of your Insights on that. And I'll ask Dr. Friedman to comment also.
SIVA MULPURU: Yeah. Thank you, Sam. So in general with left-sided mapping and ablation, mostly we use an irrigated catheter to reduce the risk of thrombus formation and possibility of a stroke. Right side, if you want precise mapping, a smaller tipped catheter, a 5-millimeter catheter for a non-integrated, would be better to get a good precision of the electrograms. And as far as the energy is concerned, find the best electrogram, early gram, near field morphology. Start it at a reasonable output [INAUDIBLE] looking at your impedance drops.
SAMUEL ASIRVATHAM: Great. Paul, do you have some comments? Or if you want to do a quick diagram for us, that's fine too.
PAUL FRIEDMAN: Sure. I had a brief audio glitch. So if I just want to make sure I understood the question, it was size of lesion with irrigated versus non-irrigated in catheter tip size?
SAMUEL ASIRVATHAM: Yeah. The specific question was is there a particular catheter that we're using where two things we've talked about-- deep lesions with late maturation effects or risk of perforation that you're more worried about?
PAUL FRIEDMAN: So first, from a practical standpoint, frequently we'll use actually a smaller catheter tip but with saline irrigation. And before saline irrigation was an option, one way to get a bigger lesion was to use a larger electrode tip, which would have more cooling, which would let you get a deeper lesion. And I'm not sure how I can draw. Do I hit--
SAMUEL ASIRVATHAM: I can draw.
PAUL FRIEDMAN: Why don't you draw it [INAUDIBLE]
SAMUEL ASIRVATHAM: Sure. Sounds good.
PAUL FRIEDMAN: [INAUDIBLE] if we take for any given size, if you have a non-irrigated lesion and you think about the way RF works, you have a very small electrode in contact with tissue, and then a remote or distant back patch. So you have a high density of current where the electrode is. And then you want the diffusing back patch, or usually more than one grounding pad, so that you have low impedance and no injury at the return site.
And the electron motion is disrupting cell membranes just at a tiny rim, really. And almost all of the energy is caused by heat. And so you're getting direct potentially electroporation at a tiny distance.
SAMUEL ASIRVATHAM: So I just want to interject there, just to emphasize what Dr. Friedman said here, is the way that radio frequency energy ablates is heat, not radio frequency waves. So it's not somehow the radio frequency waves are traveling through and killing the cells. That is a negligible effect.
So the real effect is heat. And the radio frequency is a way of generating heat at the surface. Go ahead, Paul.
PAUL FRIEDMAN: No. No. I mean, that's a really important point. And in contradistinction to electoporation that maybe we discuss later where a high energy for a very short interval is given and you're actually directly causing disruption of cell membranes by the electromagnetic energy. It's a point source of heat. And that point source of heat dissipates very quickly as you get farther from the tip.
And a typical RF catheter may make a lesion depending on where it is and the amount of energy that's roughly 75 millimeters deep. And what happens is that the maximum heat is often right where the tip of the catheter and the tissue meet, which is also where the blood pool is, which can lead to denaturation of proteins and forming clots on the electrode, which then make the electrode even smaller. And you get an amplified effect. And you can get very high energy and then actually [INAUDIBLE] from overheating.
So the concept behind irrigation is that the saline is cooling the electrode. And that means the hottest point, rather than being at the surface of the tissue where it's touching the electrode, is now a few millimeters into the tissue. So you get a deeper and wider lesion, maybe 7 or 8 millimeters deep.
The other issue is, if you don't have a saline irrigated catheter, then the cooling really depends on blood flow. And if you get the catheter tip tucked into between [INAUDIBLE], for example, there's very little flow or when you're ablating in a vein, the absence of flow means it gets very, very hot. There's not much heat dissipation, not much energy delivery, and not much of a lesion.
So maybe to answer the question more specifically, I think most of us typically are using a 3.5 millimeter tip. And we're varying the flow depending on where we are. Sometimes, I know we're talking about outflow tract tachycardia, but to use this tool, if you're in a thin walled atrial area and you want a shallow lesion because there's some delicate structure behind you like the esophagus, then you may actually lower the amount of irrigation which will give you a shallow lesion. Whereas you would increase the irrigation in areas when you understand the anatomy and want a deeper lesion. And that's where intracardiac echo, understanding of the anatomy, clear visualization of potential neighboring structures can be very helpful.
SAMUEL ASIRVATHAM: Right. So we have Dr. Evan Marto. Thanks for joining us, and had a question based on how protract cases inducibility. Evan, do you want to explain the situations that you came into this and we'll share our experience?
EVAN MARTO: Sure. So I'm just an EP fellow in Canada. So I don't have a lot of experience.
SAMUEL ASIRVATHAM: Just an EP fellow, come on. Prized, prized place in the hierarchy of all.
EVAN MARTO: Just to say, I don't have a lot of experience as yet. But I have seen a couple of cases where there's been some difficulty in eliciting PVCs. And there's been some differences in terms of approaches that people have taken to try to bring out PVCs that are shy. So I was curious to know some approaches that you guys have taken.
SAMUEL ASIRVATHAM: Great. So let's go through this. It's probably the most frustrating thing is you have a patient who has 30,000 PVCs, runs of VT. And then you bring them to the lab and we can't induce any PVCs or VT. Sometimes all you can do is really say, we'll come back another day. But let's just share some of our things. And anyone in the audience would like to share their approaches, you're welcome to, as well. Abhishek, you've got your audio fixed?
ABHISHEK DESSHMUKH: Yes. Can you hear me? This is certainly extremely frustrating when this happens, that there are PVCs the day before and then they disappear. I can share a recent case. I had a similar story, 30% PVC [INAUDIBLE] and RVOT, very symptomatic. So her a week back, had PVCs. Came to the lab and no PVCs.
So if that happens, generally, you know, isopropyl, maybe phenylephrine, maybe caffeine, maybe some exercise can help. But one trigger at least I have learned in female patients is that also try to time maybe the halter or even the procedure with the hormonal changes what they go through in their life. Sometimes PVCs appear to be more during ovulation or just before menstruation. So maybe time the procedure that way for females.
But generally, again, [INAUDIBLE] spacing, if none of those things are happening, I think before we start the procedure, if we are meeting them in the morning, we need to have a very honest discussion with them that if there are absolutely no PVCs, then maybe best not to ablate and bring them back some other day when they are having more PVCs, than see how things go.
SAMUEL ASIRVATHAM: Great. Ammar, any tips that you have?
AMMAR KILLU: Sure. Can you hear me?
SAMUEL ASIRVATHAM: Yes.
AMMAR KILLU: OK. So I agree with everything Abhishek said. I think one thing I like to do when patients get into the EP lab is before we give them any medications, as soon as the ECG is hooked up, get a good template of the PVC that we're going to be targeting. Sometimes they come into the lab with the PVCs and then they get medication from anesthesia. And unfortunately, they become much less frequent or disappear altogether.
I haven't had too much issues with lidocaine for local anesthetic. But I have seen reports that if you give too much analgesia, then that can also eliminate some of the PVCs. One thing I try to do is minimize sedation. Obviously sometimes, it takes a discussion with the patient, really getting them mentally prepared for what may be a long, tough procedure, I think is very helpful. Whereas if they're not aware of that, they can sometimes struggle. And with a 3D mapping system, if they move, it just makes it frustrating for everyone. So really, a good communication with the patient beforehand is helpful.
I have had some success with serial seven subtraction. So getting them to count down from 100 and subtracting seven, sometimes the mental stress brings out PVCs. But honestly, I think it's trying everything and anything to try and bring it up to maximize the likelihood of success.
SAMUEL ASIRVATHAM: Great. So just to kind of summarize, I think one thing is pay close attention to the patient history in terms of what brings on their symptoms. There may be a clue there. It could be caffeine. It could be a drug. It could be a position, a particular type of activity. And try to mimic it in the lab.
I had one patient, three ablutions. Each time, couldn't see any PVCs. But she swore it peaks at a particular number of days in her cycle. So we actually monitored and showed this is true. And then you make the ablation to time with those days in the cycle. Saw it, got rid of it.
Some patients, it's a very specific position. Another useful thing is look in their Holter. Are you seeing more PVCs when they're active or when they're sleeping? If they're sleeping, it could just be that the sinus rates need to be slow for you to get these PVCs. It may not be vagal tone. It just could be the sinus is fast enough, it's gone.
So there, isopropyl may make the PVCs come up. But what's happening is sinus is even higher. So sometimes in that situation, you want to suppress the sinus. One drug you can use for that is phenylephrine. So phenylephrine brings up the pressure peripheral resistance a bit. There's like a reflux vagal that'll bring your sinus rate down. So it's not that it's eliciting the PVCs. But you can see them.
Another tips, sometimes it's just very rapid stimulation. Not even all the beats are being able to be captured, but very rapid stimulation in the outflow tract or distal outflow tract. And it's so rapid you won't be able to capture enough to really induce VF. But sometimes that will bring out the PVCs.
Then, at other times, like everyone has said, sometimes the best thing to do is to kind of try another day. We have a question from William Cho here. William, would you like to ask that question live? And we'll try to answer that. And everyone else who had questions that we didn't get to, we'll do some short answers back to you. But please do join next time. Bring them up and we'll talk about them as well. William.
WILLIAM CHO: Thank you. I don't know if you can hear me.
SAMUEL ASIRVATHAM: Yes, we can.
WILLIAM CHO: This is an impromptu question. But the conduction system, we had a difficult case of RVOT ablation where we didn't think we were anywhere near the conduction system since we were high up. We ended up with a right bundle branch block at the end of the case.
And even though we did not-- we recorded the His recording, marked it well, and we were nowhere near it. So just curious as to anatomically how we could have been near the conduction system.
SAMUEL ASIRVATHAM: Sounds good. While I start talking about that, I'll ask Dr. Desshmukh to pull up a slide of the inflow of the RV with the conus papillary muscle. I'll just start with this first object.
ABHISHEK DESSHMUKH: Yes. Can you see the slide?
SAMUEL ASIRVATHAM: No. I'll just do this one and then come back. So this is a key view that I kind of like to keep in my mind when we think about where do we have conduction tissue for VT ablation. And then we'll look at the slide from Abhishek in just a minute.
So one of the things, one of the ways to think about it is if we follow the inflow septum up, straight up, so if I were to just draw a line straight up from the inflow septum, this axis, this line as we go from ventricle to annulus to atrium is often the troublesome spots that we get conduction signals or conduction damage.
So notice there's a gap between the ventricular septum and the rest of the heart. And this gap is bridged by this membranous structure, the membranous septum. And that's where you have the bundle of His traveling through and then landing on the ventricular septum. Notice how the ventricular septal muscle reaches out to reach the His.
And this is the crest of the interventricular septum. So the crest of the interventricular septum is like a hand that the interventricular septum reaches out to get to the His. And then from there, we have the right bundle and left bundle going out.
Interestingly, the left bundle is the more superficial of the structures with the right bundle having a slight intramyocardial course until it reaches the surface. So the very proximal right bundle is difficult to damage inadvertently. But the very proximal left bundle, it's possible to damage inadvertently.
But when we go a little lower, the left bundle goes deeper and very tough to ablate even when we want to. And the right bundle becomes more superficial. So if we picture in our mind that interventricular septum and then think up from there, so for ablating outflow tract of atrial tachycardias, inflow tachycardias, anything that axis going up, that can be a problem.
For your question, very specifically on how do we ablate the right bundle, for that we'll just pull up a slide that Abhishek has for us. And maybe Abhishek, I'll get the remote option from you.
So this is a kind of unique thing about the right bundle. And that is if we take the course of the His bundle-- this is the tricuspid valve septal leaflet-- the His bundle is at this site, junction of the septal leaflet and the anterior leaflet. But then it goes deep to meet the interventricular septum crest. Where the right bundle reemerges is right by this papillary muscle of the outflow tract.
Now there's two issues here. The very first branch of the right bundle is to this conus papillary muscle. In some hearts, that's the only branch that still-- oops. Can we go back one slide, Abhishek?
In some hearts, that's the only place where the right bundle is exiting. And some of the [INAUDIBLE] in this patient, if you ever get left bundle branch block, they get a strong inferior axis. This main exit to the right bundle is very anterior. And those folks, if you're ablating an outflow tract PVC around the papillary muscle of the conus, you can get right bundle branch block.
The second issue is it's you have all the branches. And I'll just take this again. You have all the branches of the bundle. It's not only this branch of the bundle that's present, but the trunk that emerges, the trunk that emerges-- and maybe Abhishek, you can point to that-- the trunk that emerges from right underneath, right here, right underneath the papillary muscle is the one that eventually goes to the rest of the right ventricle along the septomarginal trabeculation and on the moderator band.
So it may be all three branches of the right bundle are present. But because this is the emergent trunk, you can ablate there and get it. How do you know or to be aware of this possibility? It's really this papillary muscle of the conus, which is your marker. You can visualize it within intracardiac echo. Or what you'll notice is when you want it to map and get your catheter into the outflow tract, you need it to go fairly close to the free wall before you could turn into the outflow tract.
And the reason is you're bumping into this conus papillary muscle. And by chance, if that's the sites that you mapped and you're getting ready to ablate, you should think about this possibility that you can get right bundle branch block.
So I know we're out of time for today. But that was awesome. And maybe if you could stop share there, Abhishek. This is great that we got so much of not only tips but questions or things from cases that you've had a problem for. Abhishek, can you stop share?
ABHISHEK DESSHMUKH: Yeah. I'm doing [INAUDIBLE].
SAMUEL ASIRVATHAM: It's OK. So it'll be great in the future for all of you who are joining us. We'll do our best to get as many questions as possible. And what we can't do a more detailed or deep dive, we'll try to give a very short answer just in the chat or Q&A. But we'll keep tabs of these questions. And when we re-discuss the topic, we'll come back and focus more on that.
Feel free to let us know ahead of time if you have a case you'd like to present. Just come on and we'll bring you on as a panelist. And then we can have that discussion in real time. Thanks, everybody, for joining. And thanks, Russell, for your help organizing this as well.