that keeps me up at night, that sounds like something we can learn here. I'm Enrique Green, I'm an EP at UCSD, my co-chair is Pamela Mason. I'm going to tell you right away that I'm going to excuse myself a little early because here's the problem with having HRS in your hometown, I'm going to have to go put a pacemaker in. So, I'm leaving you all. All right, welcome. If you've not already downloaded the HRS 2025 mobile app from your preferred app store, please do because this is the best way to answer questions. We're going to have four great talks. We are going to save Q&A for the end in the interest of time, so feel free to send your questions in through the app or there are mics and you will be able to come up at the end as well. And on that note, we will introduce our first speaker who's going to be Dr. Michael Elshammy from Emory University who's going to be telling us about his worst leadless pacemaker case. Thank you, Dr. Mason and Dr. Green. I thought about the case that keeps me up at night, but the only thing that really keeps me up at night is worrying about my kids, but so far, thank goodness, cases haven't kept me up at night. And if you're here to expect a flying leadless device in the RVOT or snaring, sorry, you're going to be disappointed, but I thought I would present something more practical. This is a 75-year-old with history of ischemic cardiomyopathy, EF 25%, prior MI, multiple PCI. I've extracted his ICD in 2021, was a tough extraction, re-implanted him four months later and he was extracted for bacteremia and sepsis and also got infected. So he ended up getting an SICD in 2022. He did really well until late 2024. He started developing sick sinus syndrome, which led to de-escalation of beta blockers and antiarrhythmic drugs. So he came off all his medication. He started having a fib with RVR. This is his EKG. You can see his heart rate is 40 beats per minute. He's not getting any benefits off any beta blockers. So we thought about combining an atrial leadless with an SICD just to minimize the transvenous lead since this guy has had prior device infections. This is the atrial leadless, standard implantation, RAO, LAO, and this is probably the final position. What happened during this case is what we all dread. We started implanting the device, first position, base of the left atrial appendage, lateral right atrial appendage, no capture at 0.4 millisecond. At 1.5, there's some capture. We repeated this multiple times. Second position in the medial aspect, deeper in the appendage, again, no capture at 0.4 millisecond. We end up putting it in the lateral RA, lower lateral RA the same. And if you go back to implantation or what some experts recommend when you implant these atrial devices is they recommend accepting any thresholds three volts or less. So not like your typical transvenous device, but this is probably acknowledging the fact that there's significant current of injury which leads to elevated pacing thresholds. As you are aware, the atrial leadless device has a helix-based fixation mechanism that often causes significant injury during implantation, leading to acutely elevated pacing thresholds. And this helix has a larger surface area than the typical helix of a transvenous lead. Therefore, the expected injury and inflammation is probably higher than what is seen with a traditional transvenous lead. And we've all seen that we rely sometimes on current injury implanting a transvenous device. We look at the current injury. If the threshold is high, you wait a little bit, and the thresholds start to trend down quickly. But what we don't know is what is the extent of pacing threshold elevation with an atrial leadless? And how long does it take before an improvement is seen? Can you wait five minutes intra-procedurally and accept the position if the threshold is trending down? We actually just published this. This got accepted in HeartRhythm. We had 53 atrial leadless device, 70% of those, so 37, 70% had a threshold above three volts. So if we listen to the expert consensus, we would be repositioning all of our atrial leadless devices, or 70% of them. And you can see here, this is the threshold in tether mode, threshold when you release, pre-discharge, half our patients go home the same day, the other half go next morning, so let's say plus or minus 16 or 8 to 24 hours, and then at 30, they discharge. We also rely heavily on current of injury and the relative change in pacing threshold at different pulse widths. And you can see here the delta PT, which is the difference in pacing threshold at 0.4 and 1.5, it's 40%. And this is the pacing threshold distribution over time in the high pacing threshold group. You can see here, some of these, 14 actually, had no capture threshold at 0.4. And if you look at the average, 4.35 at tether mode, 3.91 at release, 1 pre-discharge, 0.72 30 days post-implant. But this is, I think, the most important slide in this talk. In 14 patients, we had no capture at max output at 0.4 millisecond. You can see here the distribution, anything above 6, there was no capture at 0.4. And if you look here at tether mode and after release, there's no capture. And after release, 9 out of 14 had no capture at 0.4. But look at the capture threshold at 1.5, 4.7, and 3.35. And then universally, pre-discharge, the mean is less than 1, and at 30 days, it's 0.68. So back to our patient, we went back to position 1, which is the base of the left atrial appendage. We still had no capture. I don't show it here, but we had great injury current, more than 2 millivolts. And there is capture threshold at 1.5 is 4.5 volts. And after release, there was still no capture, but the threshold at 1.5 was 3.7. The patient was monitored overnight, actually told my fellow keep him NPO, we're probably going to have to revise or snare it from somewhere. And we programmed it 6 volts at 1.5. So by show of hands, who would have aborted? So and to make things more interesting, this is his SICD egrams. And you can see that the patient was programmed at 6 volt. So at least when I looked at it, I was reassured the device is capturing. It's doing what it's supposed to do. But there's a pacing spike over sensing. You see here, sensing the pacing spike and the QRS. So at 24 hours, we checked him in the morning. Pacing threshold was 1 at 0.4. We dropped the output from 6 to 3. That eliminated double counting on the SICD. And at 30 day follow up, his threshold is 0.7 at 0.4. There was no over sensing on the SICD. And the patient was back on his Sotalol therapy for AFib. And he had no AFib. And he had no AFib. So in conclusion, acute pacing thresholds of AvereAR are commonly elevated. So I think we all knew that. But I think the reason I wanted to present this, and not something where there's a major complication and we're snaring or tapping or sending to the OR is, I think this is very practical. And most of us, when faced with this, at least to me, for the first time, I repositioned the atrial lead less five times. When you're implanting a leadless device and you start repositioning beyond three times, it becomes a bit uncomfortable. Because obviously, you worry about perforation. But I think in the presence of current injury, the thresholds will universally improve. And in our experience, assessing pacing threshold at 1.5 millisecond pulse width might be another tool besides current of injury to predict future improvement in pacing threshold. And the data that I showed you suggests that repositioning the atrial leadless is probably not necessary in the presence with one condition. And I didn't go over the data of the current of injury, even if the thresholds are high. You're probably likely to accept it and have good outcome at the end. And with that, I conclude before my time is done. Thank you. Well, thank you for that excellent presentation, very good learning points. We're going to move on to the next case that keeps you up at night, and this is the extraction case presented by Chris Ellis from Vanderbilt. You guys like doing extractions? You know what MD stands for, right? Makes decisions. So this is a case about making decisions, OK, during an extraction. Very important. When I was in my fellowship, 09, I finished and got my first job. I had implanted a ton of Fidelis and Riata leads from, like, 2006 to 2009. And then I turn around, and I'm taking them all out. And it just became, like, this thing. Like, oh, it's a Riata. It's a Fidelis. We're going to take that out. No problem. We'll swap it out, get a new lead in, at the time of a gen change or other upgrades or such. Of course, leadless pacing and sub-QICD is starting to change our concept about, what's the first device you decide to put in a patient? It makes a difference, because now this is the stuff that we see all the time as extractors, OK? 30 to 50 to 40-year-old patients who have had leads in for 35 to 40 years and dwell times over 100 years. Tons of abandoned stuff. There was even a small period of time where extraction was, like, the easiest part of a case like this. The hardest part was extracting a non-absorbable Tyrex envelope with a bunch of wires stuck to it, OK? Which could be, like, brutal. And if you're dependent, and you end up burning the insulation on all these leads, it's a huge problem. So thank goodness for the plasma blade there. Now, here's the case. I got a 53-year-old guy, coronary disease, MI, EF low, heart block, left bundle, transition to two-to-one heart block, got a Bi-V upgrade in 2010. He's got a RIATA lead and, like, a 1388-old St. Jude RA lead and a LV bipolar lead in a decent branch. He did respond. He was at GenChange. And we were like, well, let's, like, give him an overhaul. Because this RIATA was, like, I don't know, six years old, seven years old. Seemed pretty reasonable to take it out. Unfortunately, we put him on the table, and his left upper extremity venogram is totally occluded. So, OK, well, that adds some complexity. Maybe we'll go to the opposite side and tunnel stuff over it. No, this is not a good idea. So we decide, of course, let's just take that atrial lead out, because it's the easy one to get. We'll get a wire down and retain access. And then we can do one of two things. We can, through that lead, or through that access site, put in a new RA lead and a new RVICD defibrillator lead, cap the RIATA, leave it be. New device, problem solved, right? No, no, no, no. That atrial lead came out so easy. So, of course, we're going to go after the defibrillator lead, too, right? So we get in and start pulling on it. It's really important to control all the components of a RIATA lead. That's the conductor cables, as well as a good locking stylet to the tip. We get in there with a 14 French laser and a VISI. Doesn't quite get it. But I'm getting around the corner. I finally pop that SVC coil off. That's when you kind of have that moment like, oh, good. You're almost home free. Get down to the tricuspid valve, and I'm like, this doesn't feel good. It's kind of a little bit stuck. I'm losing the ability to progress down the coil. Then I started seeing the cables actually falling apart a little bit, as you can see them here. Conductor cables. You'll feel that. You have the bulldog on the conductor cables and a locking stylet. And all of a sudden, you feel something snap. And you're pulling hard, and then, oh, dang. I just lost something. What did I lose? I lost my conductor cables. They start shriveling up into the space between the two coils. This is how you prep that specific lead. So one of those two components I felt pop and kind of lost a little control from above. So what do you do? Go from below, right? I hate un-needleized snares. It's the worst tool ever. But somehow, I managed to actually snare this thing with the needleized snare and an 18 French cook from the leg. And I'm giving it the go, right? I got it. No problem. I am not kidding you. I pulled harder than I've ever seen Roy John pull a lead, which is not a pretty thing. And this would not come out. I'm pulling the heart into the IVC. I kid you not. Little fragments of metal are starting to show up floating around in his hepatic veins, chunks of the lead falling apart. I'm like, no, I can't let it go. It's like 5.30 on a Monday night. I got to get this done. It's the last case of the day, of course. Always put this as the last case of the day. That makes your day easier, right? Instead of like four cases after this that I still had to do. So this is about as far as I could get from the leg. I said, well, all right. We'll just grab a tight rail. And we'll go over the whole thing and just chop, chop, chop. It'll come out, right? That didn't work. Went back up to a 16 laser and a Vizzy. And look at this. How on earth does that not come out? I mean, I'm almost to the tip of the lead with a Vizzy sheath. And I've been pulling on this thing for two hours. What to do? So that's basically what it looked like on Floro at the end of my procedure. I was not particularly proud of this. But the LV lead, remarkably, you actually could watch it up here, up in the SVC region and axillary vein. It was getting moved around all over the place while I was extracting the other leads. But fortunately, the tip didn't dislodge. So I was still able to LV pace off that lead. So I hooked it up back to his ICD generator. And I stopped what I was doing. So I started with a perfectly good Bi-VICD system in a responder who was at ERI with a recall lead that was actually functioning fine. I opted that I said, well, I want a new ICD lead. And I had it. I had the atrial lead out. I had access. I could have been A lead, RV lead, home. You know, perfect. Instead, we kept going because it seemed like it was right there. The other lead came out easy. This one, no problem. That's a class 2B indication, right? Deciding to take out a retained or superfluous lead that was functional. The next day, he went to the operating room. Cardiac surgery did an open removal of the remaining part of the lead. And I'm going to show that to you. It's graphic. Additionally, his tricuspid valve pretty well came out during the surgery, of course. But they didn't bother to give him a tricuspid valve replacement. That's what the lead looked like. Now, the distal centimeter and a half of this thing was in just a block of calcium. That was like a shark tooth, literally. You can see where I got to with the VZ and the 16 French sheath because it just hit a dead end. I was about 2 thirds of the way down that RV coil. Could not believe that that didn't come out. Couple years later, actually about a year later, he starts having GI bleeding issues, ends up getting a Watchman. The TEE we do on the table, he's got pretty wide open severe TR. He's got moderate to severe MR. So he ends up actually getting worse. His heart failure gets worse. He ends up getting an LVAD, ultimately gets a heart transplant because we transplant everybody in Nashville. So he's doing great now without a bivy ICD, no problem. I kind of wonder, did he need all that? And it was really because of a decision that I made to go after that RIATA when I could have left that alone. Now, he was in his 50s, so there's a lot of decision making for the future that you make. You don't usually think it's heading towards transplant. You think it's more like, what is the risk of leaving the lead behind? So about 15% or so of leads that are extracted are taken out because they are superfluous, but they are functional, so 15%. A decent number, 40% of extractions are for a non-functional lead. That's a fractured lead or noise, some kind of conductor abnormality, insulation break. And about 35%, 40% of cases are for infection. So just remember, when you're taking out a superfluous lead, that is a minority of cases, and it's what we call a class 2B indication, means you could do it, but you probably want to have a good risk-benefit analysis of that and discuss carefully, I think, with the patient and family before you enter into that. Sometimes, as you're going through an extraction, take that little baby step, and you can't go back. And that's what happens. You just have to keep going. The long-term outcomes from abandoned leads do increase risks of thrombus, CID infection, all-cause death, and they make future extractions more complex. So it is not a bad idea to try to take out superfluous leads when you can, but you have to be willing to accept that that may not go well. And that could be a great learning experience for you in terms of how to become a better extractor, because you'll encounter cases like this inevitably, where I was trying to do gen change, take out a fine line, give the patient conduction system pacing, his bundle pacing, because that's what we're supposed to do now for heart block, right? And I ended up with a, like, literally, I kid you not, I tried to grab the thing for like four hours. Could not get the tip of that. Another case where you're like, once you get the atrial lead out, OK, you can abandon the lead. You can abandon one lead. That's OK. Don't end up with five leads in the SVC, but one extra lead is probably not the end of the world. So my extraction case, you suffer the consequence when you're aggressive about class 2B indication, but at the same time, that is how you grow and evolve as an extractor, so it's a delicate thing. You can't be shy to do it on every case, but there will be times when you'll regret the decision. Always have a backup plan. Femoral extraction is like structural heart. It overlaps with a lot of stuff we do with appendages and having to remove embolized devices and other things, so that skill set actually can help you in other ways in your practice. But having a cardiac surgeon is essential to any program, of course, for extractions, and sometimes that ends up being really the path that you might want to take. So I just had a case, total occlusion in an SVC in a patient who had an upgrade several years ago, and she's a singer, and her voice is messed up because of the SVC syndrome. And she was sent to me for an extraction, and I did a whole lot of CT scans and thinking about it. I consulted with thoracic surgery. We were going to remove it and do a SVC stent and all this thing, and eventually, I called my cardiac surgeon, who, once I call him, the patient's on the way to the OR. So I was like, I knew that was going to happen, so I called him. He's like, absolutely, we're going to do an SVC bypass. So sometimes, surgeons are a little bit more aggressive than we are. But learning from these mistakes is really a positive thing in the long run, and making sure, of course, any step along the way in a case like this, keep good communication with the family. Always make sure that they understand that you're looking out for their loved one's best interest. Thank you. Thank you so much. That was excellent. So our next speaker is going to be Dr. Gaurav Appadhyay from the University of Chicago, and he's going to be presenting on that left bundle lead case. Thank you so much, respected chairpersons, panelists, ladies and gentlemen. It's so great to be here. I'm so excited to be here. It's so nice to be here with you on an afternoon on a Friday. In a city white, would anyone ever leave this city? I mean, it's just so beautiful here, except to do a pacemaker case. Looks like I chose the wrong case. Let me choose one of my own. What we're going to be talking about is a left bundle case. And I hope that you get a piece of information out of this. This is the case that kept on giving for us. There was no one particular piece of it that was impossible, but it was a case that kept on giving for us. Summed together, we learned a lot. So this is the left bundle case, challenges in extraction, assessment, and follow-up. For those of you who have the app, scan it. There's one audience response question. And let's dive into the case. So this is a 66-year-old male with a past medical history, notable for unheralded syncope, who underwent a His bundle pacemaker placement four years prior to presentation, who presented for a generator change due to early battery depletion. His cardiovascular history is notable for syncope with left bundle branch block and transient two-to-one block noted at the time of initial presentation. He had non-obstructive coronary disease, a mildly diminished LV dysfunction with no definite late catilinium enhancement, and no lymphadenopathy suggestive of sarcoidosis. His bundle pacing with a corrective threshold of 1.25 volts at one millisecond was noted at implant. His next echo showed LVF declines. I'll just give you some EKGs here. So this is the EKG prior to pacemaker implant. It's a left bundle branch block, meets all of Strauss's criteria. And we had an echo about three months after. And this is after a His bundle pacer implant. And what type of capture is present? Well, here, of course, we have a His bundle pacing capture with no correction. That's because the corrective threshold had risen. It had risen by one volt. So the simple thing to do here is to simply dial up on the output, and that's what we did. And here was the ECG after readjustment. So what type of capture is present here? Well, this is non-selective corrective His bundle pacing. So we've corrected that left bundle branch block. So the EF had initially reduced, and it subsequently improved. But because of the increased battery drainage, we hit ERI early. So here's the audience response question. What do we offer this patient now? It's a 66-year-old male with a left bundle branch block and heart failure recovered ejection fraction. Could do a generator change only and just change vendors, try to get a better battery. Add a left bundle lead and retain the His bundle pacing lead, extract the His bundle lead, add a left bundle branch area pacing lead, extract the His bundle lead and perform a traditional IV CRT or something else. So here, if some of you want to take the app out, and you can vote on the poll, doing the gen change, of course, would be the easiest. Maybe for a much older patient, we'd consider that. But we thought that we should take some steps, and we should have the results here. Good. OK, so the majority of you chose extract the His bundle pacing lead and add a left bundle branch area pacing lead. So we're in agreement. That's what we did too. And we really wanted to make sure that we were capturing the conduction system, so we also performed left septal mapping. So we'll return to that. So device extraction for His bundle pacing leads traditionally has been reported to be quite simple. The vein was patent. We start the extraction process. Things are going OK. Then the lead gets caught up. And then it's just kind of stuck. And you can actually see here on the Sine our fatal error, which is we've broken the insulation, and we can begin to see the conductor cables that are inside the lead beginning to unravel. So that's OK. So we decide to snare from below. And now we're pulling it. And if you notice, I'm panning down a very long distance. This is longer than that length of that lead. So we're like, uh-oh. So this is not ideal. So probably working on a technique that Dr. Alaset or Dr. Alchami or Dr. Green had already reported, we went up with an agilis, up that lead from below and then from above. And we had kissing sheets and were able to snap the lead. And it came out nicely. OK, so this is the simplest part of our procedure. So now we place the left bundle branch area pacing lead. And here is our final paced QRS. Those of you who are keeping score might say, well, why didn't you leave the His bundle lead in? You would know if you had conduction system capture. But after this process, you can tell why. Actually, extraction was the tricky part. But now we have this left bundle branch area pacing lead. We really wanted to make sure we capture the conduction system. So you see the left bundle. Here's the paced QRS. It's 134 milliseconds. The V6 V1 interval is 35 milliseconds. The left ventricular activation time, or the V6 R-wave peak time, is 73 milliseconds. So have we achieved left bundle branch pacing? And I'd submit to you that most of the criteria that we use use measurements that haven't been validated. But we could actually validate this. We could do septal mapping. So we're like, aha, we'll just figure this out. We'll do the map. So here's our setup. So we have a tridecopolar catheter placed via retrograde aortic access and a right-sided quadrupolar catheter. And what we're doing here, and this is from another case just to show you the catheters, we have a catheter placed on the right side, a catheter placed on the left side. And what we're really interested in is what's happening at the conduction system, so the left side of the septum. And if you go back to Tawara's original figures, we're really trying to see what's happening right there. And for this patient, this patient had left intrahissian conduction block, so a block in the conduction system that was super high. So that was at the start of the procedure. With his bundle pacing, because we had mapped beforehand, we had non-selective corrections. So here, we can tell that we're engaging the conduction system. We see the hisperkinesis being activated, anterograde with his bundle pacing. And if you reduce the output more, all you get is septal capture, so no Purkinje signals beforehand. So that was before the case. Now, at the time of this mapping, we've got the left bundle branch area pacing lead in position. We've positioned a catheter where we see left Purkinje potentials. We know that because of a PVC that was fortuitous near the conduction system. So we placed the catheter there. And we were hoping to see conduction Purkinje connections before ventricular activation. And at high output, we don't see that. So we're a little crestfallen. But then interestingly, as we decreased output, we see those his Purkinje signals emerge. And they're before the ventricular activation noted on the same recording site, but they're after the onset of the QRS. So you might be wondering, why am I showing this to you? And it's to point out that our nomenclature is insufficient. When we talk about left bundle branch area pacing, we make a presumption that it's capturing the conduction system. Sometimes the truth may be a little different. It could be that we're capturing this ramification of a complex, trifurcating, quadrifacicular system, which is not the simple tripartite system that we learn about in medical school. We go retrograde, anterior grade. It could be that we're actually just capturing the septum next to the conduction system, and then we just run in. So that's left ventricular septal capture adjacent to the conduction system. Or it could be that a linear recording catheter is just the wrong way to go, that we got into the conduction system in the first place, and it's our catheter setup that's the problem. I say all that to say this, which is that for patients who are vulnerable, who need to have conduction system capture, we have to think about ways to describe what we're capturing better than simply by saying, oh, it was less than 85 milliseconds of a V6R wave peak time. So here is the final paced ECG with optimized delays. Looked OK. ECG at post-op check. Uh-oh. So this is the two-week visit. What happened? Did the lead move? Do we have a problem? So this is at the programmed output and delays that were set. We did decremental testing in unipolar configuration, and we still have the same morphology. In fact, you can see here a transition between non-selective and then selective just before loss. So what was interesting here, and where we learned even more, was that it was the sensed AV delays here that mattered. So this is 30 milliseconds. This is 40, sorry, 50, 60, 70, 80, 90, 110, and 150. Now, I don't know how many of you program your left bundle patients with a sensed AV delay of 60 when you leave the lab. We programmed them at 110. But it turned out for this patient, 60 was a better delay. And that's what allowed us to be certain that we were beating the intact Purkinje activation. Same thing goes for the paced AV delays, where we found a longer paced AV delay, 150, which was appropriate. And I put this out for you, for those of you who are doing left bundle branch area pacing for CRT, if you program the out-of-box delays or anywhere close to it, you might not be getting any CRT. And it's looking at the ECG which will make the difference. So here is the final paced configuration. Here's the lead position on CT scan. He had come in. EF over time, that EF went from 40% to 49%. He was banging away when he was admitted with that pneumonia. Subsequent EF after that was right around 49% as well. So CSP is not as easy as it looks. It's here to stay. The data's growing to support left bundle branch area pacing and heart failure with mildly reduced ejection fraction. Extraction of the left bundle branch area pacing leads are straightforward until they aren't. Be prepared with ephemeral system. Assessing conduction system capture is not clear. Beware of limitations of absolute number cutoffs. And as important as implant is post-implant care, check all 12 leads and follow-up. Thank you so much. I really look forward to the discussion. Thank you. That was another example of just absolutely great teaching points. The last case of the day is going to be that CRT case. And that would be presented by Judy Mackel from University Hospitals of Cleveland Clinic. Well, good afternoon, and thank you, Drs. Green and Mason and colleagues. It's a pleasure to be here as the last talk of the afternoon. I'm going to talk about a CRT case, and these are my disclosures. So I'll start the case with giving you some background of the consultation for the case. So this was an 81-year-old woman with a history of hypertension, hyperlipidemia, heart failure preserved EF, and hypothyroidism, who, in January of 2021, had presented with dyspnea on exertion, chest pain, and was found to be in complete heart block. An echo showed a mildly reduced LVEF at 40 to 45 percent with apical hypokinesis. They felt it was consistent with takotsubo cardiomyopathy. They did a cardiac catheterization, which showed non-obstructive CAD, and she underwent a permanent dual-chamber pacemaker implantation in the traditional locations. Following that implant and during that admission, she was noted to have a typical atrial flutter, so they initiated flecainide, and she was discharged in sinus rhythm with ventricular pacing, ASENS V-PACE, on flecainide 100 twice a day and Eliquis. And then she followed in the heart failure clinic, and within eight weeks, her ejection fraction had normalized, and it appeared that the takotsubo cardiomyopathy had resolved. In May the following year, she was seen in clinic. They added the SGLT2 to get her on to guideline-directed medical therapy for heart failure. Her diuretic dose was actually decreased. They felt she was euvolemic. She had no symptoms. And then she wasn't seen again for a couple of years, and at that next visit, which was the summer of 2024, she was short of breath. She was found to have an elevated BNP at 266, and they performed an echocardiogram, which now showed heart failure reduced EF of more severity, 25 to 30%, and it was globally decreased. And so the patient was sent to me specifically with two questions. Hey, she's now HFREF. What do you think we should do about her antiarrhythmic therapy? And what about this dual-chamber pacemaker? Is it time to think about upgrading or changing to a different device? So this was her ECG when she presented in 2021, just so we can all agree that it was a complete heart block with a narrow QRS escape, and this was the typical flutter that was documented after the implant when the flecainide was initiated. And this was her ECG before she came in to see me, AV pacing with a QRS duration of 164 milliseconds and a left bundle configuration and an RV apical location. So we looked at her device interrogation, and she actually has been pacing 100% of the time since 2024. She was short of breath just walking into the office despite guideline-directed medical therapy and additional diuretic. But on physical examination, okay, this is an EP physical examination, didn't really appear very volume overloaded, clear lung fields. When I looked at her pacemaker site, I did appreciate prominent collateral veins. So the first easy decision was stop the flecainide. She'd had no atrial arrhythmias in four years. My suspicion was that this might have been a little pericarditis after implant. And then I talked with her about what we could do for her with regard to device therapy. So we essentially did shared decision-making where we talked about every option, including lead extraction, upgrade to CRT, upgrade to ICD. And she was somewhat toward the frail side of 80, 81. And she would be willing to undergo an upgrade to biventricular pacing, but she really was not interested in a defibrillator. And she did not want to undertake risk, any risk, such as would come with lead extraction and the potential for surgery. And so we planned the case as an upgrade to a biventricular pacemaker. And the plan was to add in a CS lead. And so we start the case with a venogram from the left side. And we appreciate that there doesn't appear to be filling of the subclavian, although very distally it does fill. And we actually do an injection of the vein just to make sure that, gosh, couldn't we just get something through? And no, we could not get anything through to add the CS lead from the left side. And so we go to the right side. And of course it's wide open. So we cannulate the right subclavian. We place a 10 French lead. And then we use an Abbott 115 CRT delivery sheath over a guide wire. From the right side, we pop like right into the CS and we're congratulating ourselves on our skill. And then we do the injection. And she has one very large posterolateral branch, somewhat tortuous. And yet we are able to cannulate it. And I'm thinking two steps ahead. And I'm thinking, boy, I'm worried about the lead stability here. This is a big vein. We should think about what we're going to use. We ultimately used a large S. And we advanced it over a whisper. And then we couldn't capture distally. So the entire apical segment to the mid-segment was not paceable. And then when we got more basal at higher outputs, we could capture. But we also had diaphragm capture. And that was in every possible configuration. And so we had to abandon this branch. And yet we were determined that we could try to get this LV lead in. And so we started to explore all the other little tatty branches, I call them, that we could cannulate, get a wire in, kind of get a lead in, and never really be able to advance the lead. We did have this little anterolateral branch. We got the first two poles in. We could only capture unipolar. And we also had diaphragm stem without a good safety margin. So we then decided that we would change to a bailout and pursue LBBAP pacing. So we pulled the LV lead out. We pulled the sheath out. We now added the Abbott large sheath and the L2 pace lead. And we spent some time mapping the septum. And we were looking for a mid-septal location. Although we did look low, we looked high. We were able to get a nice location with regard to, you know, narrowing of the QRS and being mid-septal. But we never saw an R prime in any location. And so this is why this kept me up all night. Because now we've been in this case, which has now turned into like two cases, and we still have to tunnel the lead over to the right side to hook it up to her other leads. But this is where we ended up. And this is what we ended up with. And while this is okay, I think, for an 81-year-old, it always should give you a little cause for concern when you're using both sides. Because if you get an infection, you're pretty much done. So here we are. We end up in this great location. We tell her, you know, this is a great result. You're going to feel good. Because we've gone from this QRS of 164 to 130. Our LVAD is less than 80. We're feeling pretty good. And when I see her back at four months, she is feeling well. Her sites are healed. The thresholds look good. She hasn't had any atrial arrhythmias off of the flecainide. And we get the echo expecting that we're going to see a great improvement in ejection fraction. And in fact, the reader who I think knew that we were looking for improvement was able to give us 3%. So we went from 29 to 32. And her RVSP came down, you know, for what that's worth. And we declared victory. But I'm not really sure that we have victory. Because I think she was probably already feeling better before she came in. And so I think, you know, as you've heard our previous speaker say, I think when you pursue conduction system pacing for a heart failure indication, I think the data are not out there that you can achieve that 100% of the time. And even when it looks good, I'm not sure what we're pacing. This is LV septal pacing. Somehow we're getting into the conduction system. But I'm not sure that we've actually made a significant improvement. But she feels better. So I think that that's good. Thank you. Thank you so much. Those were all outstanding cases with a lot of good teaching points. And so we appreciate you guys all sharing your experience. We're open for questions now. So if folks would like to come up to the microphones, you're welcome to. We do have a couple questions online from the audience. So Dr. El-Shami, we'll start with you. You had presented a case of adding an atrial vein in a patient who had a subcutaneous ICD. And so an audience member had a very specific question. How do you follow these patients? Do they need DFT testing, right? If they go into ventricular fibrillation, are they going to pace their atrium? Is that going to interfere with things? That's a good question. We did not do DFT testing. I guess the concern is if you have pacing spikes that will interfere with sensing VF. But there's, I think, enough data. And we've done a lot of SICDs with ventricular leadless or patients with pre-existing devices that based on prior data, I have not seen VF under sensing despite intermittent pacing. So for this patient, we did not. And I don't think it will interfere. I'm not sure if the rest of the panel have had experience with this, but not to my knowledge and based on my prior experience. Okay. All right. Thank you. And for Dr. Apatia, an audience member was asking about when you're following these patients up and you're looking at the delays and trying to find the optimal capture, what are you looking at? Are you looking at the R prime and V1? Are you looking at the QRS duration? Because as we've all experienced, those things don't necessarily correlate. So what are you specifically following? Yeah, no, that's an excellent, excellent point. I think that if you are doing this for correction of a left bundle, and if you look at the EKG and it looks like a left bundle, that's probably not good. And the first thing that we will do is to ensure that the lead is where we thought it was at the time of implant. So looking unipolar to just see if you have the R prime. And then when it comes to programming the delays for that particular patient, it behaved a lot like a Hisp bundle lead. Hisp bundle leads, we would often say that you need to program the AV delays up to 50 or 60 milliseconds shorter because of the time that it takes to break out of the conduction system when pacing high in the Hisp. I think that we are probably closer to the higher part of the septum here, proximal portion of the conduction system. I actually think that of the three little descriptions that I showed, I think this was LV septal pacing adjacent to the conduction system. So it took a couple milliseconds to get in. And so in order to make sure that we were pre-exciting and beating the conduction system natively, we programmed it so that we continued to see that R prime. Now, you'll see a huge delta. The sense AV delay and the pace AV delay was 60 versus 150. And that's not uncommon. And that probably has to do with the time that it takes to get from the right atrial appendage to the septum and then atrial activation. So I'd look at both. Yeah. I mean, I guess for the whole panel, could you guys comment about how you do follow these conduction system pacemakers? I know some clinics are fortunate and actually have conduction system clinics where they're actually getting ECGs. Other people are basically not following. So can you guys comment about how you're following these patients? Yeah, unfortunately, we don't have a dedicated conduction system pacing clinic. Usually, when we see them in the clinic once or twice a year, we do the EKG. And if we see any major changes, we send for check and we do an X-ray. But I have to say, we have not moved to replacing CRT with conduction system pacing in our practice. So most of our conduction system pacing are for people with bradycardia indication. Half of them don't use RV pacing most of the time. So maybe that's why we don't have a dedicated conduction system. Yeah, similar, I'd say a lot of the times when we're doing that, it's CRT, LLT, LV lead plus septal LV lead. And usually, the clinical status of the patient will determine if we're going to investigate. But I try to get a 12-week EKG on those patients when I see them in the clinic every year. So I'm always looking for that. But we don't have a formal clinic for that either, no. So we allow additional time for our conduction system pacing patients when they're coming back for their first follow-up and their chronic settings follow-up. And we get 12 EDCGs. If we can do unipolar pacing, we do unipolar pacing. And we do the differential capture all the way down. So that gets reviewed. I don't know really how often it ends up in programming changes. But we're at least doing that to assess whether or not we've been successful. I would actually advocate two things. One is if you are doing conduction system pacing for a CRT indication. I agree, by the way, that the guidelines have not changed. And Bi-V pacing is still the first line. But say you do it. For those patients, I think it's mandatory to do a 12-week EKG if it's for a CRT indication. Because unlike Bi-V pacing, Bi-V pacing, the fundamental premise is that you're fusing an epicardial wavefront with an RV1. The QRS will never be narrower. And it kind of doesn't matter. I mean, people have looked at this. And people talk about ECGs to narrow the QRS. But it makes less difference. There's a totally different assumption here. The assumption now with conduction system pacing is that your benefit is driven by how pretty that QRS looks. And so I think that if we don't look, then we might be missing some changes. So we try to do it to make it practical. We do it at the first post-op check, three months, and then at least once a year. And are you guys sending your patients out to program bipolar or unipolar? Bipolar first. Same. OK. I mean, I think all of this, I mean, what both of your cases highlighted is there's a whole lot we don't know about left bundle branch area pacing, right? I mean, we all sort of accept that it's certainly better than standard RV pacing. But exactly how to program these patients and how to follow them, there's a lot we don't really know. So sort of changing tact here, Dr. Ellis, when do you go straight for snaring at first? And do you think that that would have been helpful in this case to have started with snaring? Yeah, actually, a lot of times now with a S, there's a dual coil lead. And I had a case that I had put in there, but I took it out for time, where someone had three dual coil leads. And she was like 30 years old, a long QT patient. I ended up taking them all out, putting the SICD in. But before I lasered at all, I went to the leg. And just breaking up adhesions from the leg can be really helpful. In addition, it also straightens out the curve of the lead. So if you lock it, go in from the leg, and pull down, you'll end up with a much straighter band to laser over. So many times, I go to the leg intentionally before going laser for that reason. Removing something just straight up, completely femoral, I don't do it that often, honestly. But it can be done, I mean, for sure. Some places go IJ, right? Specifically in Europe, they have some pretty good experience with that. But I typically use it as an adjunct to laser. And then, or mechanical, I do use tight rail a fair amount. It's pretty helpful, I think. But oftentimes, it ends up being something that is going to occur to me in the middle of a case that this is going to turn into a femoral extraction. Now, at the beginning, if you prep every case the same, and you have large bore sheets, and you're pretty much ready just to upsize and go. And so you always want to have a groin ready. And can you guys comment? I know several of us up here extract. We sort of have the intersection of conduction system pacing, particularly 3830s and extraction. And I think a lot of us have experience with the HISS bundle leads. But none of them were very old, right? And so can you guys comment about your experience in extracting them? My experience is they hold up really well until they don't. And then they just go. Most of the one I've extracted actually have been easy extraction, relatively. So when I saw this one today, I was like, wow. But yeah, they are robust. Unlike some other lead, like the Ingevity leads, these leads hold pretty well. And you can advance your laser sheath or mechanical sheath over. I have never had one where I had to snare it from the leg. But I think it's always a good tool for bailout. I don't love that that doesn't have a lumen, to be honest with you. Because as we get down the road further, it's going to be a problem, I think. Like a 25-year-old left-sided lead with a, you know, we've seen ones where patients, they've had a kink in it. And then they lose capture. And especially if they have heart block, you're going to have to do something with that. But you're not going to laser through the septum. But when you start pulling on something really hard, you may just take all that meat out anyway and leave them with a VSD. So hopefully that's not something we're prone to be seeing. But my guess is, eventually, we probably will. Yeah, I think that one little tip at this location. Honestly, we have not extracted many of these from the septum. So we'll have to wait and see. But we've noticed at the Hisp bundle location that the weld between the helix and the tip is actually pretty good. And sometimes it'll even just straighten completely. And that usually gets the lead out. But once you lose the conductor cables, if that pin gets disrupted, then the lead just falls apart. Yes. Hello, my name is Reinhard Knops from Amsterdam. I'd like to compliment everyone on their excellent talks on their nightmare cases. I have a question for Dr. El Chami. You postulate that the high thresholds are due to the injury of the helix. So what I missed in your data was the mapping that you can do where you passively engage the myocardium without making the injury and also use the thresholds that you can measure there and the P waves to find your sweet spot. Can you comment on that? Yes, thank you for the questions. We do map. Obviously, we do the same described technique, actually, in the paper that you're an author on. We check. We make sure we have injury. So before we even fixate, if we don't have injury, we push the device. And for this paper, actually, we submitted all the data and it was asked to be submitted as a research letter. So a lot of the current of injury data was pulled out. But we measured injury current as relative injury current. First, we measured the ST elevation. We never accepted anything less than 1 millivolt. And we also measured the relative current of injury because some of these patients have very small, even intracardiac P waves. And it's important to account for the injury current based on the egram that you have, so the width and the ST elevation, the amount of ST elevation. So a simple answer to your question is when you're mapping, never fixate the device until you see adequate injury current. So if we don't have injury current, we basically push the device forward or try to change location. And then we fixate. But I think assessing injury current is crucial to atrial leadless sensing, ensuring adequate sensing and capture down the road. And the advised location to implant the device is in the area of the right atrial appendage. What's the strangest position you've tried and were successful in placing a leadless pacemaker in the right atrium? Yes. Most of my implants are, luckily, standard base of the right atrial appendage. But I've had implants deeper, even though the original data suggests the dislodgement is higher if you implant deeper. And I've implanted on the lateral RA wall. I haven't gone septal or anything. I don't know if you can fixate there. But I would be interested to see where was the strangest location you've implanted. Also, the lateral wall. Yeah. So the lateral wall was basically the. But the thing that I learned from the data is most of us will never accept with a transvenous lead threshold that no capture at 0.4. But with this particular device, I think if you have good injury current and significant difference in pacing threshold at different pulse width, then likely your threshold will be great within 24 hours. And if you spend time moving that device like I did on my first one, you probably odds are going to end up with some kind of either small or big perforation. So injury current, differential, and pacing threshold are your friends when you're trying to implant an atrial leadless. That doesn't make me sleep well. To be like, oh, I'm just going to put. I'm like, how many atrial AVRs would you have to put in to find one where the threshold doesn't come down? I'm sure. I mean, I'm sure we've all had even transvenous devices where we have threshold very high the second day or dislodgement. And that's the more you put, you're going to have some of these cases But I think the reassuring thing is, and we have data in this paper on 14 patients. I think that's pretty good where there was no threshold at all, no capture at all at 0.4. So I know it's hard to accept, but I think once you gain more experience, it become. Do you ever pull out ice to guide implant? No, never pull ice. I'm minimalistic plus my hospital administrator would probably say, well, you're going to have to pull out ice. My hospital administrator would probably kill me if I pull ice in this context of atrial AVR. But it's a good idea, I think, if you have a tough case. All right. I think that brings us up to the hour. Thanks, you guys, so much for wonderful presentations.

Heart Rhythm Society

conduction system pacing

lead extractions

atrial leadless pacemakers

RIATA lead

left bundle branch area pacing

12-lead ECGs

CRT

LBBAP

patient-specific approaches