All right, can everyone hear me okay? Yeah. Good. All right, thanks Nishant. Well, it's nice to be able to talk in this venue to former mentors and current mentors and friends from Northwestern. It's hard to believe that it's been seven and a half years since I completed training there. So I think I'm officially an old man. Today's talk will be, I wanted to try to give something that would be a little bit practical. I know a lot of times there's a lot of beautiful EGMs and 3D electroanatomic maps, but today's will be a little bit more sort of practical. I feel like during fellowship, sometimes the things that you don't do as much are the consultative medicine and the device management. And so today I'll talk a little bit about one aspect of consultative medicine, which is the management of periprocedural AV block. There's gonna be a little bit of a hodgepodge because this can encompass a number of different types of procedures. So for today, we're gonna discuss AV block after catheter ablation, so complications that we cause with our procedures. And then we'll shift gears to talk about AV block after cardiac surgery, sort of talking about some of the management aspects of that. And then I'll spend kind of the last half of the talk, most of the talk talking about AV block after TAVR, just because that's a sort of a procedure that's becoming more and more high volume, more and more centers are doing it. And we have to help deal with the post-operative complications with regard to conduction system damage. All right, I just need to get this. Hey Nishant, do you know how to get the top bar out of the way on this? Kind of like right on top of my slides. We don't see that. Right. As long as it's not obstructing something that you're doing, it should be okay. Gotcha, I might just have to bring up, oh yeah. So it's right on top of my top slide there. Let me see if I can get rid of it. It looks good on our end. It does, okay. Yeah, I just can't read my own slide, but I'll bring it up on a different screen here. So I thought that I would initiate the conversation about AV block after catheter ablation to my very first ablation as an attending. So this is something that's sort of near and dear to my heart. This was the very first case coming out of fellowship. I'd just gotten my credentials. And on Friday afternoon, they transferred a 94 year old patient to our hospital with an incessant arrhythmia. And I think that my co-attendees at that time took great delight in signing me up for the case. So he's 94 years old with a short RP tachycardia that you can see here with P waves here. And we had initiation which showed that it initiated with a PAC long PR interval that then initiated the short RP tachycardia. So consistent with typical AV node re-entry. And he would be in it pretty much all the time, but when he had periods of sinus rhythm, you'll note that his PR interval was somewhere in the vicinity of 350 milliseconds. So what happened was that on a Friday afternoon, this patient was brought to the lab. And I think every single one of my co-attendings came to the control room. And I think there was like popcorn and maybe some beer and they just kind of watched while I sort of tried to tackle this case with a lot of fear. So with that, we started the case. And then as I was sort of mapping the his bundle area and things, my catheter pressure caused complete heart block. And as I came out of that area, conduction resumed, but you can sort of imagine that as you're starting your EP career that you might encounter a situation like this. And so we'll talk a little bit about what happens in terms of risk of AV nodal damage with catheter ablation. And then we'll talk about what happened in that case. And we'll talk about some strategies to try to make things a little bit safer from that perspective. So as we know, the highest risk of during ablation, during catheter ablation is going to be during ablation of parahystian atrial tachycardias, mid-septal accessory pathways and AV node re-entry. Of those entities, AV node re-entry will be by far the most common arrhythmia that you encounter. So in the published literature, the risk of transient AV block during slow pathway modification for AV node re-entry is listed at about 2%. With permanent AV block requiring pacemaker only at about one in 500. So quite uncommon, but not the complication that you want to have. And I think it's important to note that with cryothermy in the published literature, there's a 0% risk of permanent AV block, but there is a three to four times relative risk of arrhythmia recurrence when compared to radiofrequency ablation. So this is the sort of thing that you don't want to see when you're doing a slow pathway modification. Here on the upper left panel, you can see that a patient has an A on B tachycardia. Your maneuvers confirm this typical AV node re-entry. And as you're ablating the slow pathway, you can see that you get fast junctional beats here and that your JA conduction is not one-to-one. And yet the RF application continues. So this is not what you want to see. This is a yikes moment. This RF should have been cut off right here, as you saw that the JA conduction is not one-to-one. Now, if that does happen, and then you're left with this ECG, where you have sinus rhythm with AV wanky block, then you kind of say, okay, well, what are we going to do now? Is the die cast? Is there any management of the postoperative atrial AV block that we can, is there any reversibility to this at all? Or do we just have to hope for the best? And unfortunately, when we look to see whether this is salvageable or not, i.e. is there a way to prevent the normal maturation of the radiofrequency lesions? There's not a lot of published literature. In speaking to people anecdotally, there's a number of operators who say that you can use steroid to try to stunt lesion maturation and limit edema, with the idea that if you can use the steroid to try to make the lesions, the permanent form of the lesions that you've delivered smaller, then perhaps you can limit the damage to presumably the compact AV node if you're doing a slow pathway modification, that perhaps you can get away with this and not have to put a pacemaker in that patient. There's really only one report in the literature that I was able to find. And this was the patient who presented with late AV block after a slow pathway ablation. So presumably there was sort of encroaching edema from the lesion set that was causing the AV block that you see in the left panel here. And they were able to bring the patient in and give methylprednisolone, along with a cocktail of other things that they report, atropine and theophylline and the like, and have resumption of normal AV conduction. Now, I'm not sure whether or not the steroid in this particular case had anything to do with why the patient recovered their conduction, but if you're sort of grasping at straws and you're in a situation where you wanna try something, you can certainly give steroid and monitor the patient in an inpatient setting and see if things get better. But unfortunately, I think that the likelihood is that the dye is already cast and if the patient is having symptomatic AV block, they're gonna need a permanent pacemaker. So I wanted to kind of shift gears and say, well, if it's sort of an irreversible or hard to control thing, if you cause AV conduction system, particularly compact AV node damage with RF ablation, I think it's useful to talk a little bit about, well, what are the ways that we can try to do a slow pathway modification more safely? I'm not gonna talk about perihistane AT or mid-septal accessory pathways in terms of going to the non-coronary cusp or other methods of trying to not cause conduction system damage. But when we're talking about slow pathway modification, I think there are a few sort of simple steps that we can take to try to make it as safe as possible. Number one, the thing that I like to do is I rearrange my electrograms when I'm doing this low pathway modification to make sure that the Vs and the As are easy to see and very digestible. So as you can see here, I moved the CS electrogram prox or whatever electrogram you have where you have all A and no V, you put that between your ablation and your surface. So here you have a clear V that you can look at on the surface and the clear A that you can look at on the CS electrogram. And as you start your slow pathway modification, you will have a clear view of when you're having a V, when you're having an A, and that relationship will tell you whether or not you're having junctional beats or conducted sinus beats or what have you. And you will clearly see if you have JA block that all you have to do is look just in this area. And I think that that's helpful. If the slide is not busy, if your review screen is not busy, then you're gonna have a better chance of being able to appreciate when you have JA block and be able to immediately come off. Because if you're able to come off within a second of seeing JA block, your risk of causing permanent AV block is very, very low. So I think that that's really important. The other thing that you can do to make things a little bit simpler for yourself is to change the sweep speed on the review screen so that you are able to see things in a more digestible manner. If you like to look at things at 100 or 200 sweep speed, perhaps moving to 50 sweep speed during the slow pathway modification will allow you to see things. And sometimes when things are going off the screen, coming from right to left, that's when you miss things. So 50 sweep speed can help you in that sense. And it's just easier to process. One of my attendings at Northwestern, Al Lin looks at everything in 200 sweep speed and that for me is just too fast. I can't process it. So you got to sort of set everything up so it's very comfortable to look at for yourself. The next thing you want to do when you're doing the slow pathway modification is have a threshold in your mind for how fast is too fast for junctional beats during RF application. If the J's are coming too fast for you to in real time, be able to assess JA conduction, then those J's are too fast. Now there is some literature to suggest that if the J's are over maybe 150 beats a minute, something like that, then maybe those are too fast. But in real time, it's hard to tell, oh, is that a 400 millisecond coupling interval between the J's or what is it? You just have to have a sense of, this is going too fast for me to assess JA conduction. I need to come off. And in this case, that didn't happen. You can see that the RF continues well beyond JA block. The other thing I like to do is I like to really make sure that I define the coronary sinus well. So when I'm making the electroanatomic map, I like to define where the ostium of the coronary sinus is. And you can do that by just feel to see how the catheter flips in and out of the coronary sinus os, so you can nicely define the anterior lip of the coronary sinus, which is gonna be a region of interest. And you can look at impedances because when you fall into the CS, your impedances are gonna rise. And you can look at the relationship of the atrial and ventricular electrograms. So when you flip into the CS, your A is gonna suddenly get a lot bigger. So your A to B ratio is going to rise. If you can define your CS os, you're gonna make your slow pathway modification safer. So what I did here is on this blue dot, that's sort of inside the CS. And then this darker blue dot is outside the CS. So I've defined here the anterior lip of the coronary sinus. And so you know that you're gonna be just, you wanna be just atrial to that. And then you're gonna be safer. In general, with slow pathway modification, I think you wanna stay out of the coronary sinus during ablation, unless you're really out of options. Because when you start dipping into the coronary sinus, that's when you start risking AV block. Because if your catheter gets up toward the roof of the coronary sinus, you can very easily damage the compact AV node. And perhaps more important than anything else, when you're doing a slow pathway modification, I think it's important to make sure that everyone in the room has a job and they're paying attention. So this isn't like when you're doing a PBI that you have some loud music going and someone's telling a joke or whatever. When there's a slow pathway modification, I think everyone in the room needs to be paying attention to what's happening. I always ask that the fellow holding the catheter is watching for catheter stability. The mapping rep is looking for catheter stability. And then I'm gonna be looking at the electrograms to make sure that we're having Js with JA conduction. And I kind of give everyone in the room carte blanche to yell off. So if anyone sees anything that they don't like, they can yell off and we'll come off and nobody will get mad at them. So if you kind of get all on the same page, you can make this process a lot safer because multiple eyes are better than one. So if someone sees something that they don't think is good, they should feel comfortable in saying off and that they're not gonna be reprimanded for that. And lastly, if you do get into a high risk situation, you can always reach for cryothermy. So cryothermy, as I mentioned earlier, really safe in terms of permanent conduction system damage, but there is a significantly higher risk of recurrence of AV node re-entropy or any other arrhythmia that you're ablating focal arrhythmia with cryothermy. But it's a good option in high risk situations. And those could be patients with extremely long PR intervals at baseline or in children where you'd much rather have the patient have a recurrence of arrhythmia than cause AV block, particularly in a child. And children will have a smaller triangle of coke, so less room for error. So I think that that's a good option in that particular patient population. So back to my 94 year old guy, he again was having incessant AV node re-entry and catheter pressure caused AV block in the area of interest. And so I was pretty worried, but I called the family and I talked to my colleagues in the control room who are watching me do this. And basically said, I called the family and said, look, there's a high chance that we're gonna cause AV block, but this arrhythmia is incessant. So I think we should proceed. And so we did. And we did a slow pathway ablation at 15 Watts, which is considerably below the 50 Watts of what we would normally do with short duration applications. And we're able to render the tachycardia non-inducible with no appreciable change in the PR interval. But I was prepared to put a pacemaker in that patient if need be. And sometimes it's better lucky than good. And so that was my true life first ablation procedure as an attending. So, just my sort of takeaways in terms of the AV block as a result of RF delivery. So there's a high risk of it being permanent. You can wait on pacemaker implant provided that the underlying rhythm is stable and try steroids. Although I'm not very confident that that's gonna have a significant impact on the natural course of that. And again, I think prevention is the key. So systematic vigilance of conduction system damage during your procedure, do it the same way every time, make sure that it's a team effort and make sure your finger's always on the button and come off RF quickly when you see something of concern. So with that, we'll switch gears then to our second topic, which will be AV block after cardiac surgery. So as you know, everyone having been on the consultative side of things, there's significant risk of AV block after cardiac surgery, particularly with aortic valve surgery and with septal myomectomy procedures. We're not gonna talk as much about septal myomectomy procedures just because those are sort of specialized procedures that are only done at high volume at a few centers in the country. But I just wanted to kind of call your attention to the anatomy that governs this because this will be important for this portion of the talk as well as for the TAVR part of the talk. As you can see here, that here's a sort of a top-down view, look at the aortic valve and where the right and non-coronary cusps beat is gonna be the region of the membranous septum. Just below that is gonna be the membranous septum. And that's near where the bundle of HISS, the penetrating bundle of HISS goes from the compact AV node through this fibrous annulus and then separates into the right bundle branch and the left bundle branch. And so this area here is going to be potentially affected when the aortic valve gets replaced in a surgical or a transcatheter manner. And this part of the conduction system can get compressed. And I think it's important to remember that there's a number of variants in terms of where the left bundle branch comes out, where exactly the HISS bundle is. Those of you that do HISS bundle pacing know that you're not gonna find the HISS bundle in the same location in everybody all the time. There are three kind of main variants of where the HISS bundle lies in terms of the superficiality of it, leftwardness versus rightwardness. And that same anatomical variation will govern the likelihood that a patient is going to have problems with their conduction system after they've had valve surgery. Unfortunately, you're not gonna know that ahead of time. You just have to deal with the ramifications post-surgery. So I think that this is just important to remember that the anatomy that governs the risk for AV block and knowing that that anatomy is variable from patient to patient. The one thing I'll say about septal myomectomy procedures, I won't mention this anymore, is that the risk of AV block with that particular procedure where the surgeon scoops out part of the septum to treat hypertrophic cardiomyopathy, that risk is somewhere in the region of five to 20%. So it's a wide range depending on patient population and center expertise, but it's relatively high. So when we talk about mechanisms of how AV block occurs during cardiac surgery, we think about a few sort of ways that this can happen. The first is that calcium can be displaced from the valve and compress the conduction system. The second is that you can get edema and hemorrhage into the tissues around where the surgeon has done his or her work. And then thirdly, in valves that require sutures, the suture material itself can cause damage to the conduction system as the valve is being implanted by the operating surgeon. So all of those sort of factors are at play. And this is an interesting study that I showed here. The slides are a little bit hard to tell in black and white, but you can see some, you can see some suture material here from where the surgeon has done their work. This is a study from 1976 of pathology from patients who had aortic valve replacement and then subsequently died. And so they had their valves pathologically examined. And so these are some of the findings that you can see hemorrhage into there and the suture material in key areas that could explain AV block. So with that, we have to think about, well, what are the expectations for recovery when patients have AV block after cardiac surgery? A big part of this is hemorrhage and edema in the areas of interest. And so I think that you can expect that hemorrhage and edema as a causative etiology may resolve over time. And that's part of the reason why we do see resolution of perioperative AV block in this population because the edema will get better over time. And if the edema is the main reason why the conduction system is not behaving, then you can expect that over the course of time as the edema resolves that this will get better. And you can't underestimate how much edema is created when the surgeon goes in there and replaces a valve. There's a fair amount. With regard to compression from displaced calcium, that may resolve. There's going to be a prosthesis in place that may be continuing to push the calcium into an area of the conduction system. And that eventually could resolve or it could cause necrosis from long-term pressure. So compression from displaced calcium might resolve. In valves that are placed with sutures, if there's a suture injury to the conduction system, that would not be expected to resolve. That's going to continue to damage the conduction system and will cause permanent injury almost in all cases. So when you're sort of waiting out a post-cardiac surgery AV block, you're hoping that hemorrhage or edema or the causative etiology is that you can sort of with tincture of time that things will get better. So there are some pretty good large studies that we're able to look at of patients undergoing cardiac surgery who are examined for AV block. So in this particular study from AJC in 2017, at this center, they looked at 1,200 patients who had cardiac surgery and about 6% developed postoperative AV block. The predictors of AV block in that particular cohort were advancing age, which almost always in anything you're looking at is going to be a predictive of a complication. So sure enough, advancing age in this particular cohort, female gender, active endocarditis, which makes sense because a lot of times those will involve aortic root abscesses, ring abscesses, which will be eating away at the conduction system even before the surgeon gets in there, and then aortic valve replacement. So those are the main predictors of a potential AV block or problems with AV conduction system post-op. And interestingly, suture-less AVR comes with a 3x higher risk than conventional AVR, suggesting perhaps that the pressure from a suture-less prosthesis, which is going to exert some radial force, that that is higher risk than the surgeon actually putting a suture through the conduction system. That's relatively less likely than having a problem with the compression from a valve that relies on some radial forces to stay in place. So how long should you wait after cardiac surgery when you're seeing this patient, the surgical team is getting antsy, they want you to do what you were going to do so that the patient can go home as soon as possible. And I think that this is an instructive slide from that same study that I showed you in the last slide. Of the 72 patients or the 6% who had AV block, 30 of the 72 acutely recovered AV conduction. And I'll kind of bring you over to this cumulative incidence, this Kaplan-Meier over here, which kind of shows that 90% of the recovery that is seen happens within seven days of surgery. So when you're in the position of being an EP consultant, seeing that post-AVR SAVR patient, waiting anywhere from five to seven days after the procedure I think is quite reasonable to give the patient some time to have their AV conduction recover if it happens that their AV conduction problem is due to hemorrhage or edema around the surgical site, because that will get better, but you have to give it five to seven days. And then of those that are going to recover, 90% of that recovery occurs at seven days. So I think that, you know, trying to be patient in that situation, although it's not easy, is good thing. And the things that might push you otherwise, or if the epicardial temporary pacing wires are not working properly, or if the surgeon tells you that whatever they did is almost certain to cause permanent AV block, then you have to listen to that and heed their counsel. So if you, and I want to stress that as well, that talking to the surgeon before you put the pacemaker in, is essential because the surgeon is going to know what they did in the operating room, and they will be able to tell you whether or not they think that there's a good chance of recovery. And I think that taking that into your decision-making is important, especially having a good relationship with your surgeon in that sense. So in patients that do get pacemakers, you know, the question becomes, well, how many of these patients would have eventually recovered if we had waited two, three weeks, which obviously is not practical in the hospital setting. So at the Cleveland Clinic, they studied 301 patients who had a heart block after cardiac surgery, and subsequently had a pacemaker placed. Interestingly, about, you know, 10, 12% of those patients, 37 out of 301, recovered AV conduction at six months. But I think what's important is that none of the patients who had a preoperative PR greater than 200 milliseconds and a QRS duration greater than 120 milliseconds recovered their AV conduction. And I think that that's the main sort of instructiveness of this study is to say that, well, if you're seeing a patient who has post-cardiac surgery AV block, post-SAVR AV block, and their pre-op ECG was markedly abnormal in this way, long PR, wide QRS, then it may not be worth waiting. You might go ahead and just go ahead and put that pacemaker in on post-op day three or post-op day four, rather than waiting the full seven days for recovery. So I think in that sense, it's helpful. We decided we were going to take a look at that because we we'd seen some, you know, a handful of patients in our clinic who had had cardiac surgery, who had AV block after their surgery, who then required a post-operative pacemaker implant. And so we did a systematic review of the evidence. And what was interesting was that at follow-up, the pacemaker dependency of these patients was not super high, right? Any ranging anywhere between 30 and 90%, 30 and 90%, but a lot of these cohorts, only about 50% of the patients were pacemaker dependent. So we thought, oh, okay, well, that's interesting. Maybe most of this perioperative AV block is edema or hemorrhage that just take, can take a really long time to recover. But when we dug into some of the details of this, we were less impressed because the definitions of pacemaker dependency in these studies were pretty stringent. So you had to have no intrinsic activity in this study when you were set VBI 30. I don't think that's necessarily a good surrogate of whether or not you need a pacemaker. If your heart rate is 32 in this study, you would have been a non-dependent, which I don't think is quite fair. So I think that what we saw was that the basic take-home of our study was that there's just a tremendous amount of heterogeneity in defining pacemaker dependency in this particular population. And it was very difficult for us to arrive at any conclusions in terms of, you know, what patients, you know, could you put a temporary pacing wire in and send them home for a couple of weeks and then bring them back and see how they do. We just weren't able to draw any great conclusions from that. All right, so takeaways from cardiac surgery is that it's important to know that AV block is fairly common after valve surgery and really quite common after surgical myomectomy. After valve surgery, AV block, waiting for five to seven days after the surgery is quite reasonable before moving to a pacemaker implant, particularly if the pre-op PR and cure-as duration were relatively normal. And again, I'll just reemphasize this. It's always worth talking directly to your surgeon because they're gonna have a good idea of what they did and they're gonna be able to tell you what degree of forbearance, what degree of patience is warranted. If they tell you that they obliterated the conduction system doing their ABR, TBR, MBR, maybe you don't wait quite so long. All right, so moving now to the talk that I think is the most vexing consultative question or one of the more vexing consultative questions that we deal with, which is getting more and more common, which is AV block after a transcatheter aortic valve replacement. So as you recall from the cardiac literature that the highest risk of AV block with surgical ABR is with a suture-less aortic valve prosthesis. So we know that prostheses that put more radial strain on the annulus are more likely to cause problems with the conduction system. And the whole principle of TAVR is that these prostheses are pushing against the annulus and that's what keeps them in place. So there's going to be a lot of radial strain in those areas. Therefore, it's not terribly surprising that AV block is a major consideration with TAVR. So when we look at the mechanisms of AV block after TAVR, it's not terribly dissimilar from what we described with cardiac surgery, except that there's no sutures to worry about. So we know that TAVR can cause displacement of calcium into the conduction system. You're going to have direct prosthesis compression of conduction tissue and much like cardiac surgery, but maybe to a lesser extent, there's certainly going to be periprosthetic hemorrhage and inflammation. And the degree of that maybe is likely determined by what type of prosthesis you use and whether a balloon dilation of the valve is performed prior to the implant of the TAVR prosthesis. So we need to ask ourselves, hang on one second, I'm just going to try to, I can't see the top of my slides. Give me one second. So just ask ourselves why there's such a variation on the effect of the conduction system from a TAVR prosthesis. And again, going back to our experience with his bundle pacing, you know that the his bundle is going to course in different places in different patients. So the fact that the AV his bundle course is quite variable as to its left, right displacement in the interventricular septum affects which patients have severe conduction system disturbances with the TAVR and those that don't. We know that the depth of the TAVR prosthesis implant varies depending on the patient's anatomy, as well as the type of prosthesis that is put in and the depth of that implant matters because the level at which the septum is being compressed matters. And then that leads us to a discussion of why different TAVR valve types will compress the interventricular septum in different ways and thus confer different risk of AV block. So the two kind of main valve types that we use right now, I won't talk about the Lotus valve or other sort of valves that are less commonly used, but the core valve is this here. So this is a self-expanding TAVR prosthesis, and then this is the sapien valve. So this is a balloon expanded TAVR prosthesis. I just wanted to show you guys this because we all did sort of cath lab experience when we were general fellows, but as we get further and further away from those experiences, we maybe are less facile with the techniques used for these various implants and what the ramifications of those techniques are in our world of the conduction system. So here's what the valve deployment looks like for the core valve. So you can see here, it's a self-expanding prosthesis. So the way that it starts is it's an unsheathing process. So you have your pigtail and the aortic root here, And then here's the delivery system for the core valve. And so you basically position it with the distal part of the sheath kind of where you want the bottom of the prosthesis to sit. And then the device is unsheathed and flares out as you pull back. So here's kind of the gradual unsheathing process. And then here's the final product with a significant portion of the prosthesis below the valve. Okay, that's the important part about the core valve. And then for the valve deployment for the sapien device, which is a balloon expanded device, you can see it's a completely different method here. First off, you can see the exuberant mitral annular calcification in this patient. But there's a balloon that expands and that's what expands the prosthesis. So here's first, they do a balloon dilation of the aortic valve and then they bring the prosthesis up and then the prosthesis is balloon dilated. And that's the mechanism by which it stays in place is that the balloon is crushing the device up against the opposing tissues. And that's what's making it stay there as opposed to the core valve, where the device itself has a self-expanding properties which create radial strain, which anchor the device in place. So it's important, I think, to think about for the self-expanding valve, the core valve, that the radial strain is purely a function of prosthesis size in relation to the LVOT dimension. So prosthesis dimension versus LVOT dimension is what determines how much force the device is placing against the tissues that it's opposed to. In contrast, the balloon expanded valve, the sapien, the radial strain is a function of both the ratio of the prosthesis size to the LVOT as well as the host tissue stiffness. So the patient's own intrinsic tissue properties play more of a role in how much radial strain is expressed to the tissue with that sapien valve. I tried to get a, I looked at this paper in medical engineering and physics here to try to get a better sense of understanding. It was not helpful to me, unfortunately. You can see here that they did a lot of sophisticated experiments that looked at something called hoop forces and really the takeaway here is exactly what I told you before is that the ratio of the sizes of the patient and the prosthesis are really important with the core valve. They're also important with the sapien valve, but also the tissue parameters of the patient in the sapien valve are important to determine the so-called hoop forces or radial strain that is pushing on the patient's tissues and is potentially compromising their conduction system. So again, I just wanted to kind of show you why this is important. So in this histological view here, you have the non-coronary cusp, right coronary cusp, and where the commissure of those leaflets is is in direct relationship to the membranous septum. And the membranous septum is where the penetrating bundle of his will course through and then ramify into the left bundle branch here. And so you can imagine that any of these prostheses are going to be sitting in this area and compressing this part of the upper septum and this commissure, and potentially compromising the AV conduction system. So we kind of look at this cartoon and we imagine that the prosthesis is sitting here and then we look at the real histology here and you can see where that's gonna be compressing. So if you look at the core valve, it's gonna kind of look like this. You can see that there's gonna be a component that's supravalvular and then there's gonna be a significant part of the prosthesis, the skirt that sits underneath the valve that compresses against the upper part of the intraventricular septum, including the membranous septum, which can cause AV block if the conduction system is compromised. If we compare that to the sapien valve, you can sort of, this is my own version of pasting one thing onto another, but you can see that the prosthesis doesn't extend as far down into the left ventricle outflow track. And so it's potential for disrupting AV conduction is less. And then this is just a comparison between the two, just to give you a sense of why the core valve is going to be more associated with AV block, both because it's self-expanding and because the skirt goes further down into the left ventricle outflow track and compresses more of the intraventricular septum. So let's talk a little bit about AV block after TAVR. So we know that conduction system abnormalities are the most common complication from TAVR. And in early work, the pacemaker implant was really quite common. So 17% in the balloon expandable group and 38% in the self-expandable group. So 17% in the sapien, 38% in the core valve. Now, those for initial experience was for high-risk patients. And so with operator experience and with the patient population becoming gradually more healthy, contemporary publications, about 10 to 15% of TAVR procedures lead to pacemaker implant. So I just wanted to kind of talk through a few cases or start a few cases to sort of frame our discussion for what we do with patients that develop conduction system abnormalities after TAVR. So this was a 94-year-old patient that we had who had a severe native valve, aortic stenosis, permanent atrial fibrillation, progressive dyspnea referred for TAVR. And this is his preoperative ECG. So you can see he has atrial fibrillation, sort of a borderline left axis deviation and a right bundle branch block. So I think it's important to note that he has baseline conduction system abnormalities and he's pretty old. So he's gonna be at relatively high risk for having an issue. When the TAVR prosthesis was deployed, he developed a complete heart block. So a complete heart block with a fairly stable escape rhythm here. And then he had his AV conduction recover about four hours after the procedure. And so that's our first case. So a 94-year-old man, atrial fibrillation, baseline right bundle branch block, it's a sapien valve, had heart block during valve deployment and the valve AV conduction recovered four hours post-procedure. So we'll talk through the literature and we'll talk through what we should do with him at the end. Here's our second case is a 67-year-old male with severe prosthetic valve aortic stenosis. So he had a prior SAVR and then developed a severe aortic stenosis of that SAVR, class II NYHA, referred for valve and valve TAVR. This is his preoperative ECG. You can see that he's got sinus rhythm here with a fairly prolonged PR interval, but a narrow QRS complex. And he gets a core valve put in. And you can see here that perhaps right after the procedure, the PR interval may be a little bit longer than what it was before, but the QRS remains narrow. And then post-op day one, he develops a left bundle branch block with still a fairly long PR interval, perhaps slightly longer than what it was before. And so we're gonna take those two cases and think about them as we go through the literature surrounding how we manage patients with TAVR. So let's look first at the preoperative risk factors for AV block with TAVR. So preexisting conduction system abnormalities are a key risk factor. So right bundle branch block confers a very high relative risk. So you can imagine that that makes sense. If you have a baseline right bundle branch block and you're putting in something that's going to compress the left part of the upper septum, particularly in relation to where the left bundle branch comes, then you can imagine that you're at increased risk for having complete heart block in that situation. It turns out that left anterior fascicular block, PR prolongation, and any other conduction system abnormality are also risk factors for developing post TAVR AV block. But right bundle branch block is the big one. Age greater than 80. So this is a consistent theme amongst pretty much anything. You'll see age as a risk factor, male gender in this particular case, and mitral annular calcification. And that may be because mitral annular calcification in and of itself is a risk for AV block in all comers, but that may also be a sign that there's a lot of aortic annular calcification that may get displaced during the placement of the TAVR prosthesis that might cause damage to the conduction system that may not reverse itself. So those are the pre-op risk factors. The intra-op risk factors are whether or not a balloon predilation of the valve is performed. That is a risk factor probably because of the amount of displacement of calcium that occurs with a high pressure balloon predilation of the valve. It turns out that a transapical approach is higher risk. And quite intuitively, a higher prosthesis size to sinuses of valsalva diameter ratio is a risk factor. You can imagine that the larger the size of the prosthesis relative to the patient's own anatomy, the more radial forces are being exerted on the tissue. The more radial forces that are being exerted on the tissue, the more chances there are for inducing ischemia, displacing calcium and causing perioperative edema, inflammation, hemorrhage that can damage the conduction system. The depth of the TAVR prosthesis is important for the same reasons that I showed you the cartoon where the core valve skirt goes further down the septum. Any of these TAVR prosthesis, there's a variation in how deep they can be implanted. The deeper they're implanted, the higher the chance that you're gonna cause a problem with the conduction system. Another important intra-op risk factor is if you see AV block when the valve is being deployed, then you're gonna be at higher risk for having AV block down the line, even if the AV block acutely recovers in that situation. And then lastly, but very important, the type of valve that you use for the anatomic reasons that I illustrated, the core valve is going to confer a much higher risk of AV block than will the sapien valve. So the self-expanding valve will give a higher risk. And then the post-op risk factors are fairly straightforward. Did the ECG change from baseline? So is there a new bundle branch block? Is there a widening of the QRS? Is there a prolongation of the PR interval? Those are gonna be your sort of main easy-to-read metrics of the risk of AV block based on post-operative findings. So with that, this is obviously a significant clinical problem. And so there are a set of guidelines that are designed to help us. And so this is the sort of the, I think the best set of guidelines to say, okay, well, what are we supposed to do with these patients who have TAVR, who have conduction system abnormalities? And they've broken the patients down. And I hate to, I'm gonna show you a lot of slides from the guidelines because I think it's important and then talk about some of the literature that underpins those guidelines. So when we break down these post-TAVR patients, they break them down into five groups. So group one, we don't need to talk too much about because it's fairly straightforward. There are no ECG changes and the patient did not have any right bundle branch block pre-procedure. So those patients are fairly straightforward. They can be kind of fast-tracked for discharge from an EP standpoint. The group two, we'll talk about next. So no ECG changes in patients with a pre-existing right bundle branch block. We talked about how a pre-existing right bundle branch block is a significant risk factor for post-procedure AB block. And so they break those patients down and it's fairly straightforward. If what they suggest is that if there's, if they're not having any issues and you can send them home and if they develop high-grade AB block, the high-grade AB blocks, then you should put a pacemaker in them. And then if they develop ECG changes so their QRS gets wider or their PR prolongs, then you need to go to the management strategy for group three. So we don't need to worry too much about that because we'll talk about group three next. Group three is the group where we look at ECG changes in patients with pre-existing conduction disturbances. So if they have a right bundle, left bundle, IVCV, first grade AB block, and there is a ECG change. So the QRS changes gets wider or the PR gets longer. Then they make some recommendations in terms of how long the temporary pacemaker needs to stay in. But really the main thing here is that when we look at whether the changes are dynamic or whether they regress. So if the changes are not dynamic, so either they regress or stay stable and they're within these parameters, the QRS is relatively narrow and the PR is not over 240 milliseconds, then they provide you with a pathway to get the patient out of the hospital without any further intervention. However, if the PR continues to prolong or the QRS continues to widen, or they've reached these thresholds of a QRS width of 150 or a PR greater than 240, then they make suggestions in terms of they're being at higher risk for high-grade AB block or complete heart block. But that's where the guidelines kind of leave you with a sort of a choose your own adventure where this higher risk of high-grade AB block or complete heart block leaves you with the recommendations for EP study or ambulatory monitoring or a pacemaker. So in my mind, that's not super helpful because you kind of would want to know with a better granularity, whether to send someone home with a monitor or put a pacemaker in. So we'll talk a little bit more about that. So here are our group four patients. So with a new left bundle branch block. So their recommendations here is that if the left bundle resolves, then you can go ahead and send them out. If the left bundle is still there, but not with a terribly long PR interval and not terribly wide QRS, then hospital discharge at day two with some ECG monitoring is okay. And if the left bundle is wide or with a very long PR interval, then you have to think about your options of EP study versus send them out with a monitor versus put a pacemaker in. So we'll talk a little bit more about that. And then lastly is the group that had intra-op AB block. And I think that this is fairly straightforward in terms of if it recurs, you got to put a pacemaker in. But if there's any sort of ECG conduction system abnormalities without recurrence of AB block, then they refer you back to the other groups. And then if not, then they say you can send them home, perhaps with a monitor. So let's talk about where these guidelines come from. So first off, who is it that we should be monitoring after a TAVR? And so this is, I think, a good study looking at about 150 patients who had TAVR done. And then they basically took patients who didn't have a pacemaker put in and who didn't refuse the monitor and put a 30-day monitor on them. So they had about 120 patients who they put a 30-day monitor on and they saw what happened. And as it turned out, about 10% of those patients, so about 12 of those 120 wound up having a presentation with delayed heart block requiring a pacemaker. So within 30 days, they had about a 10% hit rate on these patients. And you can see that all but one of those patients had some conduction system abnormality after the TAVR. And as we break down what were the major risk factors, right bundle branch block was kind of the main thing and left bundle branch block was also fairly prevalent among the patients who had developed AD block. So these patients had right bundle branch block, left bundle branch block, and some of them had a combination of that, including PR prolongation. So I think that the take home from this study is that if you have no conduction system abnormalities, again, this was all comers after TAVR who did not get a pacemaker while they were inpatient, that there was a very low yield for putting a monitor on patients with no conduction system abnormalities. You can see here that this is the outlier. One patient who had a normal ECG before and after wound up with a delayed presentation with AD block. And in medicine, there's only so much you can do. This one's gonna fall through the cracks with any sort of normal rational monitoring scheme and you have to accept that. But in general, if someone has a right bundle branch block, even if that right bundle branch block is unperturbed after the TAVR, they're at pretty high risk for developing AD block and may benefit from monitoring when they leave the hospital. The next study looked at patients with a new left bundle branch block after TAVR and went with a more aggressive approach of putting a loop recorder in them. So this was fairly interesting that they got a fair number of patients that they put loop recorders in that had a new left bundle branch block after their TAVR. And what they found was that there was a decent hit rate, about 10% hit rate in terms of having an indication for a pacemaker or a defibrillator within a year of the loop recorder implant, which was put in before they left the hospital after their TAVR. What I think is interesting here is that a lot of these patients were diagnosed with their high-grade AV block or their indication for their pacemaker within 30 days of when they left the hospital. And of the ones that had symptoms, syncope, presyncope, syncope, presyncope, only one of those fell outside of the 30-day event horizon. And so, I think in the new left bundle branch block patient population, putting in a loop recorder may not be the best use of healthcare resources. However, putting a 30-day monitor on them might be quite reasonable because even a hit rate of 5%, I think it warrants the use of that sort of technology to be able to make sure that you're sending a patient home and have eyes on them to see if they develop any sort of significant AV block-related bradycardia. So there are other techniques that we can also use for risk stratification before patients leave the hospital. Now, some of these are preemptive. There's been some decent literature to suggest that we should maybe put ambulatory monitors on all patients prior to their TAVR because a significant percentage of those patients are diagnosed with AV block or atrial arrhythmias or sinus node dysfunction even before their TAVR is placed. And it may give us a better idea of what we should be doing. It may inform future management post-TAVR if we have that pre-TAVR ambulatory monitoring. So this paper by Urena here, I think it's a fairly good paper and I don't think it's something that we do on a regular basis, but I think it's something to consider. There are other papers that look at atrial pacing during the TAVR to try to figure out whether or not the Wenkebox cycle length is excessively long to suggest that the AV conduction system is compromised and that a pacemaker is indicated. I think it's a nice idea, but practically speaking, trying to do this in the cath lab and having atrial pacing occurring and assessing Wenkebox cycle length after the TAVR, I think is, while in concept it's nice, I think practically speaking, it's very difficult to implement. And then the last technique that we have for risk stratification is an EP study. So what about the EP study? Unfortunately, though it shows up in the guidelines for what to do with those patients that we're worried about but don't have a slam-dunk indication for a pacemaker, there's no really good large high-quality studies to look at. The best thing I could find was a study of 75 patients where they performed pre- and post-TAVR hispundal studies in all of those patients. So they're very consistent. They took all comers and they did the hispundal study before and after, which is quite a task actually. And 14 of those 75 developed AV block. And their conclusion was that, what they saw was that a delta HV of 13 milliseconds, and then in post, delta HV of 13 milliseconds or more was predictive of AV block. And then an HV interval greater than 65 milliseconds in patients with a left bundle branch block were associated with AV block. And so their conclusion was that these sort of EP studies may be useful. Now, the issue is that of the 14 patients in that study that developed AV block, 11 of those were diagnosed with AV block during their inpatient stay. And so they were able to do a little bit of telemetry or what have you, diagnose their AV block. And probably the EP study didn't really inform any decision-making at all. It was just part of the study and they did it. And so, the utility of the EP study may be just in those patients who don't develop AV block during their hospital stay, but have a left bundle branch block and you're concerned about them. In that case, doing a hispundal study and seeing if the HV exceeds 65 milliseconds may be helpful in decision-making and push you toward or against putting a pacemaker in before they leave the hospital. So let's get back to our cases here and kind of think about what we do as we wrap up the talk. So our 94-year-old male with permanent AF pre-existing right bundle branch block who developed heart block during the TAVR deployment, but conduction recovered about four hours later. So what happened in this particular case was that the temp wire got pulled out, unfortunately, which is I think not the right thing to do because in a 94-year-old with a pre-existing right bundle, if they develop heart block during their TAVR deployment, they're gonna need a pacemaker. And when they don't get a pacemaker, this is what's likely to happen. So this patient had a big long pause and then got brought down to the EP lab and got their single chamber pacemaker put in and ultimately did okay. But when you see this sort of situation, pre-existing right bundle and any perturbation during the TAVR process, I would advocate for putting in a pacemaker. What about our second patient? Decision-making not so easy. This 67-year-old valve-in-valve TAVR who had baseline PR prolongation and then developed a new left bundle branch block where the PR interval is maybe a little bit longer, but fairly similar to what it was before. And here, the decision-making is not so easy. And what do we do? We put an ambulatory monitor on the patient. And this particular was a ZIO monitor, which is not a real-time telemetry type of monitor. So what you can see here is that the patient had a 12-second episode of asystole. So we wish we did place an MCOT, or maybe this would have been a good patient to do an EP study and see if their HV interval exceeded 65 milliseconds. And maybe they would have wound up with a pacemaker before going home, rather than winding up with this sort of finding, which is all the more alarming because when you get a ZIO report of this, this is something that happened a while ago. And so having mobile telemetry in this particular situation, I think is preferable to having something like a ZIO monitor. So in response to cases like this, we sort of modified our approach to the new left bundle branch block to something like this. And it's not terribly dissimilar from the guidelines, but when we have a new left bundle branch block with a stable ECG for 48 hours and no AV block, we discharge them with a mobile cardiac telemetry. So basically, I have a live monitor for 30 days. So if they develop heart block, we're gonna know about it right away. The only way we send them home without a monitor is if the left bundle branch block resolves. If the PR is showing that it's dynamic in any way, then we get involved and we're fairly aggressive to recommend permanent pacing in that situation. So this is sort of, there's a lot of data there, but this is sort of my proposed approach to post-TAVR. And it may be more aggressive than what you do at your institution, but having seen patients coming in with bradycardia-mediated seizures and things like that, I tend to be fairly aggressive. So if I see a PR interval greater than 240, regardless of what they were pre, I would recommend a 30-day mobile telemetry. A new right bundle branch block, which is rare, should be strongly considered for pacemaker implant. Because if you have a new right bundle branch block and you have a prosthesis pushing against the left bundle branch, I think that you're a high-risk situation. Pre-operative bundle branch block with no change post-TAVR, I think deserves a 30-day mobile telemetry. That may be a little bit controversial and some people may say it's excessively aggressive, but I do think that they're a high, fairly target-rich patient population for people that are gonna develop late AV block. New left bundle branch block with a stable PR interval, I do think deserves 30-day MCOT monitoring, particularly if the QRS is wider than 150 milliseconds. New left bundle branch block with PR prolongation, I think should be considered for a pacemaker implant before they leave the hospital. And then lastly, when you do have intraprocedural AV block, I think the default should be to implant the pacemaker, really with the exception of if the pre-op ECG was normal and the post-op ECG returns to baseline, or if you can sort of look at the tracing from the AV block and make it for a bigotonia or something like that. But otherwise, we tend to be fairly aggressive because we've just seen too many patients where their conduction recovers, we feel better about it, we send them home and they come back with heart block. It happens all too often. So that's kind of my take on the proposed approach for post-TAVR. Open questions that I think are interesting to think about. Now, is there a subset of patients who should be offered a permanent pacemaker before their TAVR? If they have a bifascicular block with PR prolongation, is that someone that you just bite the bullet, put a pacemaker in so they don't have to deal with this whole rigmarole post-TAVR? And I'm curious about what people do at other institutions, but what's the role of placing a temp perm system immediately pre-procedure in those moderate to high-risk patients? At our place, our cath lab and EP labs are in geographically different areas, so it makes it very difficult for us to make decisions like that. And then lastly, food for thought is what should be the organized process in choosing TAVR prosthesis based on AV block risk? That is to say, if someone's at moderate to high risk for AV block based on their pre-op parameters, should they get a sapien balloon expanded valve rather than a core valve self-expanding valve to try to mitigate their AV block risk? So with that, I think I'm at the end of my time, and I'm happy to take any questions, and thank you for your attention. It's been a pleasure. No, Prashant, that was great. Super practical and very useful. Thanks so much for that. Maybe I can just ask a couple of questions, and other people can chime in as well. With regards to the first part of your talk about difficult AVNRTs, do you have any advice for the fellows on redo procedures, particularly if you didn't do the first one? Yes, so in that situation, first and foremost is make sure that you have the right diagnosis, right? Because I think that of those redo AVNRTs, there's gonna be a significant number that are something that's different, a parahystine AT or something like that. And the tricky thing about parahystine ATs is that they oftentimes initiate with a critical age prolongation. And so you kind of get into that mindset of this must be AV node reentry, but make sure that you're dealing with AV node reentry before you start hammering at the pre-hammered slow pathway. The second thing is that I think that really creating a good anatomy is important because in those patients who are failed, who are truly typically AVNRT, I think the main pitfalls are a really big CS where it's difficult to get good contact and understanding exactly where you are. Sometimes a persistent SVC can be at play. And then the other thing is that rather than going into the coronary sinus as your first approach on a redo AVNRT that you're having trouble with, I would go transeptal and go to the mitral annulus and wrap around to the left-sided slow pathway. Because especially in someone who tried to do a slow pathway, didn't have success, I think that a leftward extension that you can get, I think is a good approach in that situation. At a referral center, you'll see these not infrequently. So that'd be my advice. Read the op report, confirm your diagnosis, make sure you understand the coronary sinus, make sure also you're not dealing with a node of ventricular or some node of vesicular or other sort of funny pathway where you might want to use an alternate mapping strategy. And then don't be afraid to go transeptal. I think that you might be surprised that it's not technically that challenging. I think there's just an activation energy towards getting out your ice catheter and doing it, but I think it's worthwhile. Great. And then in your schema that you put up as to your practice pattern, I actually didn't see EP study on there. So you moved away from doing them and just kind of deciding that the person needs a pacemaker? Oh, on the post-TAVR patient? Yeah. I can't even think of the last time we did it because I think that, like I said, the studies that are there really suggest that the majority of the cases that they identify as needing a pacemaker by EP study, the majority of those are already identified as needing a pacemaker because they're going to have AV block on their telemetry and things like that. And as we look at those studies, they took a series of consecutive patients and signed them up. So they're going to get an EP study regardless of whether or not they've already decided to put a pacemaker in. So I find that that subset of, you know, we're not sure, but we're kind of not feeling good about a mobile telemetry, the patient that you might do it in would be that sort of left bundle branch block that's new with a PR interval right around 240, where you're just not sure putting up a catheter and seeing, you know, what your AV block cycle length and if you have in for a HISS block and what your HV interval is. And that situation can be useful. Are you guys doing that a fair amount, Nishant? Yeah, we are still doing EP studies in some of those borderline cases and we use the HV interval. And I think most of us are doing atrial pacing to look at the block cycle length as well. And what do you use for your cutoff for that? I think it's like a 500 milliseconds, 120. Okay, so 120, okay, gotcha. Yeah, and I think that, you know, and then you gotta make sure that your sedation situation is consistent and things like that. But I think that really the key is that you just have a sort of consistent institutional policy about what you're gonna do. So, and it's easier said than done because every operator has different preferences and among our group, we have different preferences for how we deal with these things. And so getting everybody to agree on a protocol is challenging. I don't know if you guys have the same. I would agree, I think there's some variation.

AV block

management

medical procedures

catheter ablation

cardiac surgery

aortic valve surgery

septal myomectomy

conduction system damage

pacemaker implant

TAVR