Welcome to the 2021 Quality Summit. Thank you for sharing your time with us today. I have the distinct honor to introduce our speaker for Pacing Indications, Guidelines, and Pacing Modes, Dr. Selzman. Kim Selzman is a cardiac electrophysiologist and chief of cardiology at the VA hospital in Salt Lake City. With a faculty appointment at the University of Utah in Salt Lake City as well. Dr. Selzman has been so generous in sharing her clinical expertise and guidance with the ACC. She participated as a member of the EP Device Implant Version 2.3 Workgroup. She is currently a member of the EP Device Implant Registry Research and Publications Committee, and prior to that, she was a member of the AFib Ablation Steering Committee. She is also involved with the Heart Rhythm Society and is currently the chair of the HRS Health Policy Committee. Welcome Dr. Selzman, and thank you for sharing your time with us today. Thanks Christina for that kind introduction. And I just want to thank the program committee for inviting me to speak today at the Quality Summit. As she mentioned, I'm speaking on pacing indications, pacing guidelines, and pacing modes. So before we get into the indications for pacing and the different types of pacemakers that are out there, I just want to do a brief review of some basic electrophysiology. Because when the conduction system of the heart is not functioning, that's when patients are often indicated for the various pacemaker therapies. So the sinus node is this yellow structure here in the high right atrium, and that is depolarizing automatically, and that sets your heart rate. And when the sinus node depolarizes, it goes to the rest of the right atrium and over to the left atrium, and that's what causes the atrial contraction. And that's evidenced by the P wave that you see here on the rhythm strip down below. Once the atria is depolarized, it goes through the AV node to what's called the His-Purkinje system. And this system is really quite remarkable. It's how we electrically depolarize the right and left ventricles in a very coordinated, very rapid fashion. And when the ventricles depolarize and they contract, that's evidenced by this QRS complex, again on the rhythm strip below. So if your sinus node is not functioning, or if you have some type of atrioventricular nodal disease or other types of AV nodal block, it's going to be able to manifest on the EKG. So a lot of times when we're suspicious, if someone has sinus node dysfunction or AV block, we'll get EKGs or halters or some type of event monitor. And as you see here, you have the P wave shown with the blue arrow followed by the QRS. So that's normal conduction from atria to ventricle, and here it repeats and repeats again. But here you see with the black arrow, there's just no P wave and there's no QRS. And so it's in effect kind of a relative pause where there's asystole here and there's nothing going on. Now we don't know if the sinus node just failed to depolarize, or maybe it did depolarize, but it didn't make it out to the atrium due to scar tissue. But either way, there's no P wave. And so there's nothing coming from above for the ventricles to see. And then here you finally have an escape beat because your heart doesn't want it to be in asystole. So then for AV block, if you look at the rhythm strip down here, they're a little smaller to see, but you have P wave followed by QRS. But then this P wave, there's no QRS. So there's some type of AV block that's preventing the conduction from going through the AV node to the His-Purkinje system to allow the ventricles to contract. And that pattern keeps repeating, P-QRS, P with nothing. So this is a two-to-one AV block. So when we see various evidence of sinus node dysfunction or AV block, or even block lower down in the His-Purkinje system, we do have guidelines to guide us in terms of when does that patient warrant a pacemaker or not, or some type of device therapy. So there's three documents I do want to highlight. One is the 2018 ACCHA HRS guideline on bradycardia. So this is relatively recent, just came out a few years ago. And it's really the first guideline that just focused on bradycardia specifically. Now before the 2018 guidelines, there was a pacing guidelines that talked about device therapy. So I want to highlight the 2008 guidelines, which actually was an update from the 2002. And then more recently in 2012, they updated the 2008 guidelines to incorporate CRT or cardiac resynchronization therapy. So when trying to determine does a patient qualify for some type of pacing therapy, I really think these are the three documents that would serve you well to just save on your laptop and have as a reference. So again, just to get into a little bit the different indications. So as I mentioned, bradycardia indications, that can manifest as sinus node dysfunction. And some diagnoses that you may see in the chart that are evidence of sinus node dysfunction are symptomatic bradycardia. So they're in a normal sinus rhythm per se. So there's a P wave followed by QRS on the EKG. It's just too slow and it's causing the patient's symptoms, which can be very variable, but things like presyncope, dizziness, inability to exert themselves. There's also symptomatic chronotropic competence, incompetence, which means that you can't mount a increased heart rate for your activity. So a patient might be sitting there with a heart rate of 60, but you put them on the treadmill and instead of going to 110, 120, 130, it's just gone to 65 or 70. So they can't increase their heart rate based on their physiologic demands. And that tends to be also fairly symptomatic in terms of inability to exert. Coronary drug therapy can also cause sinus bradycardia. And most commonly, this would be the Betaboxer class of drugs, which we use a lot in our cardiac patients for coronary disease, for heart failure, for reduced ejection fraction. And then symptomatic low heart rates while awake. So these are some of the diagnoses that you might see that are kind of all evidence and fall under what I would call sinus node dysfunction. For AV block, there's different types of AV block. And without going into each one specifically, the more high-grade AV block, so the second-degree type 2 or the 2-to-1 AV block that's considered to be potentially infranodal, so below the level of the AV node, these are considered more concerning for not having a stable ventricular rhythm potentially. There's third-degree heart block, which is essentially the same as complete heart block. So none of those P waves are making its way down to the ventricle to make a QRS. Pauses and then AV node ablation, where we intentionally damage the AV node so that it doesn't conduct from the atria to ventricle. And that's typically done if someone has very difficult to treat refractory atrial fibrillation. And then there's some other kind of less common situations that I put here as special populations. So there's carotid sinus syndrome, where the carotid bulb is very sensitive to neck movement typically. So someone may be driving a car and turn before they turn the car, and that can cause pauses as they're moving their head about. And so you can catch that by reproducing that in clinic or in the ER. There's also infiltrative diseases such as sarcoidosis that can lead to various Brady arrhythmias, both sinus node dysfunction and AV block, as well as tachyarrhythmias. And then heart transplant, this is fairly uncommon, but if the sinus node were to be damaged at the time of transplant, they might have an inappropriately lower heart rate than what would be expected and would warrant pacemaker therapy. And then there are certain neuromuscular diseases where the patients are prone to bradycardia, things like muscular dystrophy and current sears. So in addition to the bradycardia indications where your heart's just going too slow, either from sinus node dysfunction or from AV block or hysperkinegy system disease below the level of the AV node, there's also what I would call hemodynamic indications. So the patient doesn't have a bradycardia issue, but if they have, so what I put up here is kind of a classic left bundle branch block pattern. So if they have a hysperkinegy disease, and as you look at the picture here, so you have the sinus node, the AV node, the right bundle branch block, but let's say the left bundle is blocked. Well, the way for the electrical impulse to get to the left side, to get to the left ventricle, it comes down through the hysperkinegy on the right side. It can't go down the left because it's blocked. And so it has to work its way very slowly over the left side cell to cell without use of this specialized conduction tissue. So that's going to take a much longer time. And that manifests on the EKG by having a QRS that is much greater in duration. So I have here below PQRS, and as you can see, the QRS is quite narrow, but here in the case of the left bundle branch block, you have a very widened QRS. So maybe it's taking twice as long to depolarize the ventricles. In the classic situation where you might want to resynchronize the patient or pace the left side of the heart to resynchronize with the right side of the heart, or actually resynchronize the septum with the LV-free wall, would be with a CRT device. And the kind of classic patient would be a heart failure patient with a reduced ejection fraction less than or equal to 35% with a left bundle branch block that is at least 150 milliseconds wide, which is quite wide. So for definition of left bundle, it's, we typically say a minimum of 120, but the wider you get, the more desynchronous. And so a class one indication, actually the only class one indication for CRT in these heart failure patients is EF less than or equal to 35, left bundle branch block greater than or equal to 150 milliseconds. I also just want to mention briefly, so in addition to heart failure patients that have dyssynchrony manifested on EKG by kind of the classic is a left bundle branch block. There's also dyssynchrony that can be induced from RV pacing. So what I'm showing here is the same picture of the left bundle branch block, which is really wide and negative in V1. And if you look here on the pacing, you see the pacing stimulus artifact in V1 and V4, and then it's followed by a fairly wide negative deflection that is fairly similar to what you see in the intrinsic left bundle. And what I'm trying to show here is that pacing in the RV apex is almost like a pacing induced left bundle branch block. So they don't have intrinsic left bundle branch block, but they have it due to the RV pacing. It's the same similar physiologic phenomena. And the reason why we care about this is because RV pacing can have, not always, but can have deleterious effects. So there is an entity called RV pacing induced cardiomyopathy, and this tends to happen in patients who require a lot of ventricular pacing and just have a lead in the RV apex. And so in some of those instances, if they develop an RV pacing induced cardiomyopathy, one option would be to upgrade them to our CRT device. And then they would be CRT pacing instead of RV only pacing, and hopefully recover from this RV pacing cardiomyopathy. One thing I just also want to mention about CRT, because you might see it mentioned in the medical records, is multisite pacing. And multisite pacing is just CRT pacing, but what it means is that you're pacing from two different locations from the left ventricle. So in classic CRT, you have a lead that's down in the RV apex. And so this kind of bullseye is where the pacing is coming from, the tip of the RV lead. And then it's a little hard to see, but there's an LV lead that goes through the coronary sinus and kind of wraps around to the left side, the epicardial surface of the left side. And hopefully you can get that lead in an epicardial vein on the lateral free wall or posterolateral spot. And so this would be classic CRT, where you're pacing from the left side, from the LV lead, and you're pacing from the RV lead to give you a synchronized kind of paced contraction. And multisite pacing is using, again, the RV lead and the LV lead, you're just pacing from two different spots from the LV lead, trying to increase your chances that the patient will be a CRT responder. And again, this is the same kind of classic wide left bundle branch block pattern that we see. This is pre-pacing, and then after pacing, it is still somewhat wide. You see the pacing stimulus artifact, but now it has a very different morphology. It's upright in V1, meaning that you're pre-exciting the left side, which is what you want. So just to change gears and talk a little bit about the different types of pacemakers. So the simplest is the single chamber pacemakers, and that just means that you're pacing just one chamber of the heart. So the classic is a pacemaker generator that's put under the skin, typically on the left side. The lead plugs into the pacemaker, it goes through the subclavian vein to the SVC, through the right atrium, through the tricuspid valve, and down to the RV apex. So this would be kind of your classic standard RV apical single chamber pacemaker. Now in the last several years, there's also been available to us the use of leadless pacemakers. So as you can see, there is no pacemaker under the skin, there's no generator. Everything is contained in the pacemaker here. It's actually implanted from below, from the groin, and it's released, and you can see these little tines kind of help it stay put. So through the groin, use a sheath, and you put it in the RV apex, and it's doing the same thing. It's pacing the ventricle, but there's no leads needed and no pacemaker generator. So there are different types of dual chamber. The standard over here is you have the pacemaker generator, there's two leads. One goes into the right atrium, it typically will have this kind of J shape, and it goes typically into the right atrial appendage, and then the ventricular lead, like I showed you on the single chamber, would go down into the RV apex. Now there's newer pacing modalities that will get into some of the benefits that they may have over standard dual chamber pacing with a lead in the RV apex, but they're his bundle pacing as well as left bundle branch area pacing. So it's still a dual chamber system with two leads, one in the atrium, one in the ventricle. Here you see the lead going up into the atrium, but instead of going down to the RV apex, this one is very high on the septum. And the idea is that you're going to pace right below the AV node, right where the bundle of his is, and if you can successfully capture, then you can use a patient's own intrinsic conduction system, that his Purkinje system going into the right bundle and the left anterior fascicular, left posterior fascicular, kind of the left bundle branch block system, left bundle system. Left bundle branch block area pacing is similar, but you'll see here the ventricular lead is still fairly high on the system, on the septum, but it's really burrowed into the septum deeper to get to the left bundle. And again, if you can get to the left bundle, you're going to use the patient's intrinsic conduction system rather than the RV apical pacing, which doesn't use the his Purkinje system at all. And then just to talk a little bit about CRT, I mentioned it a few slides ago, but CRT, you're going to have typically three leads, one in the atrium, one down here in the RV apex, and then one that goes through the coronary sinus to an epicardial vein on the left side. So it's a three lead system typically. If a patient has chronic AFib, they won't put in the atrial lead, so you would just have the RV lead and the LV lead. And so CRT is kind of synonymous with biventricular pacing because you're pacing the left side and the right side, trying to get that dyssynchronous heart to resynchronize. If for some reason you can't get the LV lead in, the vein is too tortuous or too small, or they just don't have any good branches on this left free wall, a lead can be placed on the epicardial surface. So that's just a picture of that here. And typically you consult CT surgery. The patient is in the hospital for a couple of days, probably with a chest tube. So it is a little bit more, certainly it's more invasive than a standard CRT implant in the EP lab. So when we talk about the different types of pacemakers, they also have different pacing modalities. So again, the kind of standard, kind of typical single chamber pacemaker would be VVI. There's also such a thing as AAI pacemakers. And again, just to focus on the first two letters here, the first letter is talking about what part of the heart is the device going to pace? And the second letter is what is it going to sense? So a VVI pacemaker is going to pace the ventricle and sense the ventricle. AAI, we don't see those very much, particularly in the United States. So it's pretty rare that you would see something programmed AAI, but again, it just is speaking to the fact that it's going to pace only the atrium and sense only the atrium. So it can't see what the ventricle is doing and it cannot pace the ventricle. And then more commonly, we see the DDD, which just means it's gonna pace and sense in both the atrium and the ventricle and the dual chamber devices, whether it's with an RV apical lead or his bundle pacing or left bundle branch area pacing, you're gonna wanna sense and pace both the atrium and the ventricle. Similarly for CRT, you're typically gonna program them to DDD because you want to see the atrium, pace the atrium, and then for sure, you wanna sense and pace the ventricles to get that, you wanna pace virtually 100% to maximize your chances of resynchronizing that ventricle. And then the R just stands for rate response. So I should have had it throughout here. So there's a VVIR option and AAIR option and a DDDR option, and all these devices have sensors built into them. And so not only do you program the pacemaker to say, look, I don't want you to let the pacemaker go below, let the heart rate go below whatever number I program it to, whether it be 50 or 60, 70 beats per minute, but also you can program the sensor. And so if it detects activity, the patient walks up a flight of stairs or carry something inside the house, the sensor will detect that motion and the increased work of breathing potentially, depending on the type of sensor they have, and will increase to whatever you set the sensor rate to. And you can set that to, you know, whatever you feel is appropriate for the patient, 110, 130, and so that's, so it's DDD. And if with the rate response on, it would be DDDR. I just want to spend a couple minutes talking about the EP device implant registry. It was a lot of fun. I was very grateful to be part of the team that was invited to kind of work on this and kind of revamp it from the ICD registry with the idea that, you know, we should incorporate these newer pacing technologies that are not defibrillators, but really gonna be used more and more and would be worthwhile to catch in the registry. So just to go through the registry a little bit, go through some of the questions. I'm sure this is all familiar to you, but one of the questions, is it ventricular, is there ventricular pacing present? So if some of the complexes are paced, you would say yes. If they're paced throughout, either because they have complete heart block and so they need pacing 100% of the time, then, you know, you would only see paced QRS complexes. If it's intermittent, some are paced, some are not, then you would put no. So here's section G, I think is where a lot of the changes were made. So I just wanna focus on this section for a few minutes. So it just asks whether a device was implanted, yes or no, and then what type of device. So if a defibrillator was implanted, is it single chamber, dual chamber, or a CRT by ventricular device? It also asks if they got a sub-Q device. I didn't really talk about those in this talk since sub-Q defibrillators cannot provide chronic pain pacing support. In terms of the pacemakers that are available for this, in terms of what patients would be enrolled, it would be a CRT pacemaker. So they get the resynchronization therapy, but without the defibrillator component. The leadless single chamber pacemaker. And I suspect over next several years, this, you know, we may see dual chamber leadless devices, but right now we just have the one single chamber device available to us. And then the dual chamber devices that I mentioned with using a HISS bundle pacing or left bundle branch area pacing. And it also asks if a CS lead was implanted. For example, if you were putting in a CRTD device. And then it asks if you implanted a HISS lead or lead in the left bundle branch area. It asks you if it was just attempted, successful or not. And then down here on primary tachycardia indication present. So what that's trying to get at is, what is the primary reason that this person is getting this device? It does the patient have a tachycardia indication, or in other words, is the main reason why they're getting the device because they need a defibrillator. And if that is the case, if they have a ICD indication, and that's the kind of the number one reason why they're getting the device, then the question follows. Well, if they're getting a defibrillator, and that's the main reason for the device, do they also have a bradycardia indication? So an example would be a primary prevention, low ejection fraction patient that needs a defibrillator, but maybe they also have sinus node dysfunction. So there is a bradycardia component to it. And that might have the implant or put in the dual chamber defibrillator instead of a single chamber defibrillator so that you could pace the atrium. Primary bradycardia indication present. Again, so the primary reason for the device is bradycardia and not tachycardia. So these patients would not be getting a defibrillator. And then the reason pacing indicated, again, a lot of these kind of fall into those buckets that I showed you earlier of the sinus node dysfunction or the AV block or block lower down the His-Purkinje system. I just wanna point out a couple here, the heart failure, unresponsive to guideline directed medical therapy. So kind of a classic patient there would be that low ejection fraction patient with a wide left bundle branch block, who you put them on all guideline directed medical therapy and they're still symptomatic, still with an advanced NeuroCard association class, their ejection fraction hasn't really improved. So this would be a good indication for a CRT device to try and resynchronize that patient that has that left bundle and that to synchronize secondary to that. And then the anticipated requirement of greater than 40% RV pacing. So as I mentioned earlier, one of the things that we worry about when we do put in these devices is RV pacing induced cardiomyopathy. So if they need to pace a ventricle, obviously we wanna give them a pacemaker so they have greater cardiac support. But if they're gonna pace a frequent amount of the time, let's say someone with complete heart block and they're gonna pace virtually 100% of the time, they are at risk for developing possibly this cardiomyopathy. So if you're anticipating that they're gonna pace a lot in the ventricle, that may affect the choice of device that you implant in that patient. So that's the purpose of that question. And then the primary pacing mode as we talked about DDD versus VBI. I just wanna highlight these two on the right side. The DDD slash AAI is a pacing algorithm that's really designed to try and minimize RV pacing. So if they do have an RV apical lead in their device and they're pacing the ventricle with that, you might wanna use an algorithm like this to try and minimize RV pacing and minimize your risk of causing an RV pacing induced cardiomyopathy. I've also seen it written the other way, AAI slash DDD, but again, it's just an algorithm to minimize RV pacing. And then there's this RVPP, which is an RV pacing prevention algorithm. And it's really just a grab bag for all the other pacing modalities that you may see that different manufacturers employ trying to reduce the amount of RV pacing. So just to finish up, I just have a couple of clinical scenarios where we could talk through the type of arrhythmia issue they have and what kind of device you may wanna implant and how you would program that device. So scenario number one is an 82 year old gentleman with chronic atrial fibrillation and a heart rate in the 30s, normal ejection fraction. And he's complaining of dizziness that you think is due to his bradycardia. So because of the chronic atrial fibrillation, he doesn't need a lead in the atrium. So you just need to pace and sense the ventricle. So kind of the tried and true option would be a pacemaker under the skin with a transvenous lead down in the RV apex. That's again, like I said, tried and true. We have a lot of data over many decades and this is kind of a good potential option for this 82 year old gentleman. Another option would be a leadless pacing, which would also allow VVI pacing just like the transvenous device. The advantages would be that there's no pocket, there's no lead. And maybe you think the patient is a good candidate for this because he's at high risk for infections or maybe it's a dialysis patient and you don't want things and leads in their veins trying to kind of minimize the hardware there. So a leadless pacemaker would be a good option in certain scenarios. And then the third potential option would be instead of an RV apical lead, you would place it in either the his bundle position or the left bundle branch area pacing. And again, his heart rate's only in the 30s. So he probably will pace a lot. And if you were concerned about a pacing induced cardiomyopathy, this would be another thing to consider. And regardless of which of these three options you choose, you would program it VVI and you'd put the sensor on if you felt like you needed the additional kind of Brady support. The second scenario is a 75 year old female with symptomatic sinus bradycardia, heart rate in the 30s, normal ejection fraction and complaining of presyncope when walking. So unlike the first scenario, that patient had atrial fibrillation, this patient has sinus bradycardia. So you definitely want a lead in the atrium. You're gonna wanna pace the atrium to allow her to increase her heart rate when she's walking and doing activities. There's a good chance you're probably gonna put the sensor on as well. And so one option would be just kind of a nice dual chamber standard positioning in the right atrium and the RV apex. But again, you could consider a dual chamber system with a right atrial lead and either a HISS bundle or a left bundle branch area pacing. Because maybe you're concerned that she'll develop AV block down the road and you don't, again, you're worried about RV pacing. Either way, either device, you're gonna program it to DDD. And like I said, you're probably gonna turn rate response on. The last scenario is a 68 year old gentleman who does not have bradycardia, but he does have a low ejection fraction and a wide left bundle branch block on EKG. And he's telling you after a shared decision-making conversation that he really, he wants to see if he can improve his heart function with resynchronization, but is not interested in a defibrillator. So he would be a good candidate for a CRTP. And he would get the resynchronization benefit. And again, unlike RV apical pacing, where you're trying to minimize how much you pace the ventricle, in a CRTD device or a CRTP device, you want them to pace 100% of the time or as close to 100 as possible, because that's gonna maximize your chances of resynchronizing the ventricles. So just to close up with a few takeaway points. First, you know, most post pacing indications will be for bradycardia or symptomatic pauses due to either sinus node dysfunction or AV block. Pacing can also be indicated for resynchronization. Again, the kind of a classic patient would be the left bundle branch block patient with a low ejection fraction. His bundle pacing and left bundle branch area pacing are newer pacing modalities that are dual chamber pacing, but they're more physiologic than RV apical pacing because they're using the patient's intrinsic conduction system. And so it's gonna be more physiologic with a narrower QRS than what you would get with RV apical pacing. The pacing parameters really depend on the chamber that you need to be paced and sense, whether it's the A or V or both. And the EP device implant registry was updated to include these novel pacing technologies such as leadless pacemaker, his bundle pacing and left bundle branch area pacing. And I think the registry, you know, will continue to be updated as the technologies evolve. And please feel free to put any questions you have in the chat or feel free to email me as well. Thank you so much, Dr. Selzman, for that very informative presentation. I know I learned very much and I'm sure our audience did as well. And I know this will be a big help for our participants who are using the registry for collecting their pacemaker procedures. So thank you. We do have a few questions that I'd like to tackle. So we'll dive right into those. During your presentation, you talked about dual chamber pacemakers. Can you explain a little bit about the use case for when the physician might elect to use his bundle pacing, the dual chamber versus a scenario where they would use the left bundle branch area pacing? And what would be the use case or the patient presentation in each of those cases? Sure, no, that's a great question. So I do wanna start by saying that, you know, RV apical pacing is still a good option. It's tried and true. We have so many years of data and lots of experience. We know the safety profile of RV apical pacing. So it's really, we know it's safe, it's reliable. And again, great long-term data. But if a patient has AV block and is needing a pacemaker, the pros of his bundle pacing versus left bundle branch area pacing is really that both those pacing modalities are gonna use the patient's intrinsic his protingy system. So the QRS is narrower. There's not the dyssynchrony issue that you can have with RV apical pacing. And you don't have to worry really about RV pacing induced cardiomyopathy. There's some other deleterious effects of RV apical pacing, such as may increase AFib burden and structural adverse remodeling of the heart. In terms of his bundle versus left bundle branch area pacing I'd say that his bundle has been around longer. And although it has all those benefits I just mentioned there are some issues with it as well. It has higher pacing capture thresholds compared to RV apical pacing. It has issues with the pacing threshold increasing over time, and it also has a higher dislodgement rate. And so left bundle branch area pacing is a lot newer. We don't have as much data, but so far the data is showing that it's probably a little bit more stable. And so I think the current thinking is leaning more towards left bundle than his bundle for those reasons. Very interesting. Thank you. We have another case here. So there's an interesting case. There's a physician. He implanted a CRTP with atrial, a deep septal RV and CSLV leads. The deep septal lead was found to have better QRS results than with biventricular pacing. So the physician turned off the LV pacing. Although a CRTP device was implanted, it's functioning as a left bundle dual chamber pacemaker. Please explain the physiology behind that clinician's decision to use left bundle pacing instead of the biventricular pacing. Sure. So when you say better results with the left bundle branch area pacing, I'm surmising that what they're talking about is what the EKG looks like. So, you know, CRT, resynchronization therapy with a left LV lead, you know, it's certainly better than RV apical pacing. And you are resynchronizing, as I mentioned, the LV septum and the LV free wall. However, that QRS could still be wide. And so if you are using the patient's intrinsic conduction system, you might have less dyssynchrony evidenced by a narrower QRS. So what I'm guessing is that they saw the QRS from the left bundle branch area pacing, and it looked pretty much like a normal QRS, nice and narrow. And then when they were using both the LV lead and the left bundle branch lead, it gave kind of a wider, less synchronized kind of looking QRS. And so, you know, the thinking is, again, if you can successfully pace using the patient's intrinsic conduction system, narrower in general might be better and less dyssynchrony, more physiologic, I would say. Makes very good clinical sense. Thank you. You explained that very well. It makes perfect sense. I think we have another question here. We have time for one more question. In our hospital, we've seen the implant of an RA lead, a HISS lead, and a backup RV apical lead. Would we consider that a dual chamber or a by V device? Yeah, that's a good question. Yeah, that's a good question, and that comes up a lot. It's a little confusing. With HISS bundle branch lead placement, as I mentioned, the thresholds can increase over time, and they also have a higher dislodgement rate. So if you have someone with, let's say, complete heart block, they may put in this kind of backup lead. So if the threshold exceeds, if the pacing capture threshold exceeds what the output is, you're going to have loss of pacing therapy. So this backup is kind of a safety, but I would still consider it a dual chamber device because you're not resynchronizing the septum and the LV free wall or the RV and the LV. So you have kind of a, it's a dual chamber device with a safety, extra safety lead built in. Thank you. Well, I want to thank you very much again, Dr. Selzman, for your time today. And again, this very informative presentation that really, I think, dug deep into understanding the data capture and the registry related to pacing indications and pacing modes and guidelines. We really appreciate your time. So thank you again, and thank you to our audience as well for taking the time to be with us today. Thank you for all your support and working so hard to optimize patient care. We appreciate all that you do, and I hope you have a great rest of your day. Thank you. Thank you.

pacing indications

guidelines

pacing modes

electrophysiology

pacemakers

resynchronization

EP Device Implant Registry

clinical scenarios