Okay. Good morning, everyone. Welcome to this Aura Abstract presentation. My name is Amole Ojo from University of Rochester, Rochester, New York. I will be your moderator this morning. So this session, we explore the role and outcomes of CRT and conduction system pacing among patients in common specific scenarios. This is part five, so we all need the silent disco headset. The color is yellow, so for us to hear us, you need to go to that channel. And for the speakers, I mean for the presenters, please speak into the microphone so that everybody can hear you. If you walk away from the microphone, then people cannot hear you. Each of the presenters, we have ten minutes for their presentation, followed by two minutes of questions. So for the questions, we can go to the app, I mean the HRS 2025 app, and you can ask a question from there, or at the end of the presentation, we can just raise up our hand, and we have about two minutes to answer any questions we may have. So our first presenter is Irene Maria Esteve-Ruiz, who will be presenting on early improvement on cardiac function and desynchrony after physiological upgrading in pacing-induced cardiomyopathy. Well, thank you very much. My name is Irene Esteve-Ruiz. I'm an EP in the south of Spain, in Huelva, and I'm happy to be here presenting our work. As you know, non-physiological pacing is a well-known cause of interventricular desynchrony and cardiomyopathy. Its incidence is variable depending on the study, but it's around 12 to 20 percent of patients with right ventricular non-physiological pacing. This entity, which has been called pacing-induced cardiomyopathy, was first suspected after a subgroup analysis in the DI-VID trial, in which, as you know, in ICD patients, programming in a DDD mode is associated with an increased risk of heart failure hospitalizations and mortality compared with VVI mode, with minimized right ventricular pacing. There are many risk factors associated with this entity, but the more important ones are the presence of pure cardiomyopathy, high right ventricular pacing burden, and the pace cures duration, especially if it's more than 160 milliseconds. This is the reason why, in the latest American and European guidelines, it has been included as a class 2A indication to perform an upgrade to CRT in this scenario. On the other hand, we all know that conduction system pacing has emerged as a novel technique and an alternative to classical ventricular CRT, but the guidelines is only considered as an alternative to CRT, but the evidence concerning both his bundle pacing and left bundle branch area pacing over the years is increasing. And in fact, on the year 2023, we had these guidelines on cardiac physiological pacing for mitigation of heart failure, and many scenarios were considered for both his bundle pacing and left bundle branch area pacing, including the possibility to perform an upgrade in pacing-induced cardiomyopathy instead of with classical ventricular CRT. So we decided to perform a single center perspective study in which we included those patients diagnosed with pacing-induced cardiomyopathy, and they were referred for an upgrade to conduction system pacing, both with his bundle and left bundle branch area pacing, from January 2022 to January 2024. We performed an echocardiogram before the upgrade and at the three to six months of follow-up, and the last eight patients were analyzed using ultra-high frequency ECG. For those of you that are not familiar with this technology, ultra-high frequency ECG analyzed the signals of a 14-lead ECG and transformed them into an activation map of both right and left ventricle. The right ventricle is represented with V1 and V2 leads, the septum with V3 and V4, and from V5 to V8, we have the apex and the lateral wall of the left ventricle. A patient with a normal heart with a narrow QRS will have activation map as the one on the right bottom with a straight and narrow red line, which means that the heart is activating fast via the conduction system, and both ventricles are activating at the same time. On the other hand, when we have a patient with a right bundle branch block, we obviously will have a delay on the leads that represent the right ventricle and the opposite in left bundle branch block. A patient with a normal QRS should have a parameter that is called a ventricular electrical delay of zero milliseconds. This parameter, ventricular electrical delay, represents the maximum time difference between the local activation time of each lead, and it represents this delay that we can see in the activation map. Actually, this value in a normal heart is never zero, but it's normally from five, ten milliseconds more or less, and when we have a left bundle branch block, it has a positive value, and in right bundle branch block, a negative value. And this technique can be used as a right-time guidance for implants. So we included 27 patients. One-third of them were women. 17 of them were upgraded using his bundle pacing, and 10 using left bundle branch area pacing. The median age at implant was 65 years old, and at upgrade, 73 years old. There were no difference in bicep characteristics between the groups of his bundle pacing and left bundle branch area pacing. A left ventricular ejection fraction was normal before the implant of the first device, and decreased to less than 35% before we decided to perform the upgrade. After the upgrade with conduction system pacing, the left ventricular ejection fraction increased to almost 48%, and this increase was similar between his bundle pacing and left bundle branch area pacing groups. The QRS-wide decreased from 163 milliseconds to 150 in the conduction system pacing group, and this decrease was greater with his bundle pacing than with left bundle branch area pacing, as you can see here. This is one of the examples of one of our patients. This is the echocardiogram before the upgrade, and this is the one after we performed the upgrade. Here is one of the examples of the activation map of one of our patients before we performed the upgrade, and as you can see, there is a clear delay on the left ventricle activation. And this is the same patient after we performed the upgrade to his bundle pacing in this case. Here we can see this straight line that means that both right and left ventricle are activating fastly, and at the same time, obviously using the conduction system. Here is an example of another patient in whom we performed the upgrade using left bundle branch area pacing, and here we can see a slight delay on the right ventricle activation, but still both ventricle activating almost at the same time. So here we can see the difference before the upgrade and after the upgrade in both his bundle pacing and left bundle branch area pacing groups. We can see that there was a significant improvement in the QRS-wide in left ventricular ejection fraction, left ventricular end-diastolic diameter, and functional class in both groups. Concerning the synchrony parameters, the ventricular electrical delay parameter I was talking before, before the upgrade in both groups it was 40 to 50 milliseconds, which is quite a delay in the left ventricle, and after the upgrade we were able to achieve a delay of 16-17 milliseconds in his bundle pacing group, and 17-22 milliseconds in the left bundle branch area pacing. And finally, concerning electrical parameters, the air wave amplitude was a little bit lower in the his bundle pacing, but not clinically relevant, and the thresholds of both groups were similar without any increase in the follow-up. As a conclusion, physiological pacing can be performed safely and successfully in pacing induced cardiomyopathy. Chondrocystin pacing upgrade may induce reverse left ventricular remodeling and early improvement on QRS-wide left ventricular ejection fraction and functional class. Ultra-high frequency ECG provides useful new information of ventricular activation, and with this software we know that ventricular desynchrony can be measured and improved after physiological pacing upgrade, and it is our belief that conduction system pacing should be considered as an alternative to classic CRT via coronary sinus and as a first-line approach in some cases. Thank you very much. Thank you for that wonderful presentation. Do we have any questions from the audience? So as we are waiting for the audience, one of the questions that we have for you is, the decision to implant his bundle pacing lead versus left bundle, was that operator dependent, or it was just early on his bundle, then later left bundle? In our center we always perform his bundle pacing as a first-line approach, and if that's not possible, then we go for the bundle branch area pacing, but normally we always perform his bundle pacing as the first approach. Any questions from the audience? I guess one of the other questions is, what do you need to be able to perform the ultra-high frequency ECG in addition to your ECG machine? Well, not much. It's only like 14 lead ECG, normal ECG that you have to, obviously, before starting the procedure, and it actually doesn't interfere a lot in the procedure, and it's quite a useful technique, because it gives you immediate, the activation map, it appears in like 10 seconds, you just press the record button, and in 10 seconds you have the activation map, so it's quite useful, especially in CRT cases like this. Thank you. Any questions from the audience? Okay. Actually, if you don't mind so that people can hear you, use the microphone. Hi, that was a great talk. Are there scenarios where you can use this ultra-high frequency analysis during the case to help you determine when you've achieved left bundle capture conduction system capture? Yep. When we performed this study, we didn't use it for guiding the implant at that time, because it was the first case that we had this system, but right now we use it in our daily practice, in every case, because in our center we perform 100% conduction system pacing, so it's really, really useful when we are doing any case, especially in CRT cases, but also when we perform left bundle branch area pacing, it's quite useful to know, not only with the signal, but it also gives you more information if you are actually achieving actual left bundle branch area pacing or just deep septum, it really makes a difference. Thank you. Okay, our next presenter is Hiro Kawata, who will be presenting on the long-term clinical and echocardiographic outcomes of left bundle area pacing in pacemaker-dependent patients. Thank you very much, Chairman, and audience. Thank you for coming to this session. I'm pleased to present here. So the title is long-term clinical and echocardiographic outcome of left bundle area pacing in pacemaker-dependent patient. So background, long-term outcome of left bundle area pacing, including lead, related complication, EF, have not been well studied. So objective is this study aim to evaluate the echocardiographic and clinical outcomes of left bundle area pacing in pacemaker-dependent patient. Our cohort is almost, most patient is 99% pacing, and pacing-dependent patient. Left bundle area pacing was performed using the secure melatonin 3-acetyl lead with fixed-curve C, C315. Left bundle area pacing was considered successful according to current accepted criteria. Definition of QRS morphology, because QRS morphology can change. We use morphology three months after, because I see many times immediately after implantation, three months later, it's different. I think three months later is more reliable, because after three months, maybe stabilized. Using a 12-lead KZ, recorded at 15 micrometer-second, QRS relation was measured from the patient spike to the last QRS reflection observed. Stimulus to peak LV activation time was defined as the interval from the pacing stimulus to the peak of the R wave in V5 to V6. So I use this guideline, but this is very busy, so I just, this you can find in the Europe phase, but this is a little bit too busy, so simplified. So basically, if you see the V6 R wave peak time, less than 85 millisecond in narrow QRS baseline, or right bundle, or less than 100 millisecond in wide QRS, we think this is like left bundle branch pacing. If not, we check the unipolar pacing morphology in V1, so right bundle branch block pattern, QR, then we think this is like left ventricular septal pacing. Otherwise, we consider those EKGs as RV septal pacing. Let me show you the example. So here are representative EKG examples. Using the simplified algorithm, each case can be categorized as left bundle area pacing, septal pacing, RV septal pacing. So as you can see, the left bundle pacing, left ventricular activation time is short. Then LV septal pacing, QRS is wider, then LV activation time is longer. However, compared to RV septal pacing, QRS is still shorter, then activation time is also shorter. Also, you can see the difference morphology in V1. So the RV septal pacing, you don't see any RWEB, so those are using current guideline algorithm. So this is example of the activation mapping during the RV pacing. This is RV apex pacing, not septal pacing. So left bundle area pacing, usually you can activate lateral very quickly, even like left anterior fascicular capture or left posterior fascicular capture. That's creating shorter left ventricular activation time or shorter QRS. So we're almost like 100% within left bundle pacing right now. So we included 282 patients from 2020 to 2024 using 3ACZ-LEAD. We eliminated 30 patients, a short follow-up, transferred back to the original hospital. Also, we eliminated 73 patients who doesn't have much pacing. So the definition of the high burden is that we set V pacing more than 80%. So after that, we included 179 patients to our analysis. Median follow-up is 664 days, average is almost two years. So we analyzed clinical outcomes by dividing cohort into three groups based on the EKG, three months. So this is the baseline patient characteristic of entire cohort. We have, again, like 179 patients. Average age is 77 years old. Then, as you can see, hypertension, diabetes, I think similar to other studies. Then echocardiography, like, you know, the characteristic. EF is average, most patients are normal. But we have 48 patients who have low ejection fraction at the baseline. We also look into TR because I was really concerned TR might get worse after the left bundle pacing. So baseline ECG characteristics. Average QRS is 136 milliseconds. Then 53 patients, no QRS. Then, as you can see, right bundle, including bifascular block, maybe 63 patients. Also left bundle branch block patients, 36 patients. We include also the patient with pacemaker. So this is the result. 3S3, 3ZML20 was implanted successfully in all patients. Successful left bundle pacing was achieved 163 out of 179 patients. Left bundle pacing 152, LV septal pacing 11, RV septal pacing 16, according to the algorithm that I showed you. Ventricular pacing ratio was 96.7, so almost all patients have a very high pacing ratio. Median follow-up within two years. So among 179 patients, 172 patients underwent echocardiography. So we missed seven patients who refused or who doesn't want to have echo. Otherwise, almost all patients get echo. Then echo was done three months or later. Complication, device-related complication, two-pocket division due to pain, atrial lead dislocement. But those are not associated with the left bundle lead. So left bundle-related complication, we have one patient left bound or dislodged later. So this is the result of the QRS. So as you can see, we have three groups, left bound area pacing, LV receptor pacing, RB receptor pacing. So we compare. So as you can see, left bound area pacing of patient QRS is shorter compared to LV receptor pacing or RB receptor pacing. But there's no difference, significant difference between RB receptor pacing and LV receptor pacing. Also, LV activation time, obviously left bound area pacing patient have a shorter LV activation time compared to LV receptor or RB receptor pacing. But again, LV activation time doesn't have a significant difference between LV receptor pacing and RB receptor pacing. Even the QRS MoFoG is different. This is a planned post-pacemaker ejection fraction. So the baseline left bound area pacing patient have a higher ejection fraction compared to LV receptor or RB receptor pacing patient. However, there's no significant difference. I think this is probably a patient we can achieve if the bound area pacing is healthier. Someone who has a very sick heart, it's hard to get a little LV left bound area pacing. So therefore, I think baseline difference, even this is no significant difference, I see some difference because of that. But it's harder to get left bound area pacing if you have very sick heart. Then this after pacemaker ejection fraction, basically it doesn't much change overall. So no significant difference between before and after the pacemaker implantation. So planned post-pacemaker tricuspid regurgitation, basically there's no significant difference in any groups. So this is LV diameter. So also LV diameter looks smaller, but not significant difference. But in some like patients have a smaller left ventricle size after the pacemaker. Therefore, I see some difference. So instance of pacing in this cardiomyopathy after the left bound lead replacement, among 131 patients with normal baseline ejection fraction, so only five patients developed LV systolic dysfunction. For example, the LV bound area pacing among six patients, four patients developed pacing in this cardiomyopathy. So basically those patients potentially left bound or in conduction, they might not be the reason for the low ejection fraction. So therefore, they might have another cardiomyopathy, the etiology, or these patients may need colonized sinus pacing. LV septal pacing, only one patient developed pacing in this cardiomyopathy, but probably we need more number. We can't say much about from the data from 11 patients. Also, we know that LV apex patient, after three, four years, 15% patient developed pacing in this cardiomyopathy. I think probably LV septal pacing less than the LV apex pacing patient because there's data from micro lead spacemaker showing less pacing in this cardiomyopathy compared to LV apex pacing. Probably LV septal pacing may be worse than LV septal or left bound area pacing, but not very bad, like apex pacing. If changing patient with a leadless ejection fraction, this is a cohort of patients who had a low ejection fraction at the baseline. So among 48 patients, so the QRS baseline 157, then after the left bound area pacing, the QRS much shorter. Also, ejection fraction was improved from 37 to 47%. So conclusions, left bound area pacing demonstrate a high implantation success rate, low complication rate, and effectively preserved ejection fraction patient with normal ejection fraction. Then also the ratio of pacemaker in this cardiomyopathy is usually low. So thank you very much. Thank you. Thank you. Great presentation. We have a minute for questions from the audience. Yeah, come and use the microphone. Thank you. Thank you very much for the presentation. Thank you. Very nice. My question is in relation to those five patients that developed AVB pacing cardiomyopathy. Did you try to look why these patients developed that cardiomyopathy? Was anything like where was the lead position? Because sometimes you capture like the left posterior fascicle instead of capturing the actual left bundle branch as such. Potentially that can cause cardiomyopathy. We have seen patients having DVC induced cardiomyopathy coming from the left posterior fascicle. And if you put a lead that's fixed in the left posterior fascicle, even though you get a narrow PRS, potentially that could lead to cardiomyopathy. Did you look into those details? So we didn't look into details of all patients, but I see some patients, for example, I have one patient, sarcoidosis. So even like, you know, that we put left bundle because heart block. Initially we did MRI, for example. There's no significant change in septum. But two, three years later, ejection fraction going down. Then we saw she's not responding to the left bundle pacing, but we did MRI again, actually. It starts showing the sarcoidosis. So some patients probably will be missing the diagnosis. Also, maybe your theory might be correct. Even we capture, even we create a narrow QRS in the EKG. So like some other patients with significant ischemic cardiomyopathy, even like, you know, the EKGs, electronically we fix the problem, but mechanically, if the lateral is dead, so basically even you shorten the QRS, probably I don't think we can improve ejection fraction. Was there any difference in the LBAT time in this case in relation to the other cases? Did it have a longer LBAT? You mean the elective activation time? The elective activation time in those cases. I don't think so, but we have only five patients, so it's very difficult to show the significant difference, but we have to look into it. Thank you very much. Thank you. Because of time, we'll move on. Okay, our next presenter is Michael Guerin, he will be talking about left bondu area-pacing patients with cardiac sarcoidosis. Good morning, everyone. My name is Michael Gurin. I'm an EP fellow at the University of Pennsylvania, and I'll be discussing left bundle area pacing in patients with cardiac sarcoidosis. So we know that left bundle area pacing has emerged as an important physiologic pacing modality that mitigates the risk of pacing-induced cardiomyopathy and provides an alternative to biventricular pacing. Implementation of the left bundle lead in the muscular septum facilitates rapid depolarization of the basolateral left ventricle without the high capture thresholds associated with his bundle pacing and has shown efficacy across multiple patient populations irrespective of cardiomyopathy type or severity of conduction disease. However, there are some limited studies that show that patients who have septal scar in non ischemic cardiomyopathy have less improvement with left bundle area pacing compared to biventricular pacing, particularly with respect to improvement in ejection fraction. And we know that patients with cardiac sarcoidosis have a proclivity for basal septal involvement with granulomatous disease leading to AV block. And the success rate and long-term outcomes of this particular patient population are not really well defined. So in our study, we sought to characterize the procedural and clinical short as well as long-term outcomes in patients with cardiac sarcoidosis undergoing left bundle area placement, lead placement. So this is a single center study with a retrospective identification of patients using the electronic medical record and any patients with cardiac sarcoidosis undergoing left bundle lead placement were included. And we used the 2014 HRS consensus criteria to identify patients with the diagnosis of cardiac sarcoidosis. The implant strategy was a traditional implant strategy using either deflectible or non-deflectible sheath using commercially available pacing leads. A region one to two centimeters anterior and inferior to the HISS bundle was targeted with a W pattern in lead V1 prior to screwing in the lead and a resultant terminal R wave in lead V1. During the lead screw process, we monitored for fixation beats and used contemporary left bundle capture criteria in order to at least aim for a selective left bundle capture. We collected device parameters both at implant and at follow-up which included the paste and sense QRS duration, the left ventricular activation time or LVAT, and we collected other parameters such as the threshold, impedances, and R wave sensing. We looked at procedural time, complications, electrocardiographic, and echocardiographic parameters and performed a statistical analysis using the Wilcoxon signed rank test to compare baseline to follow-up. We had a total of 19 patients in this study. The average age was 59 years, a fifth of them were female, and we looked at the indications for pacing. One patient had sinus node dysfunction. The majority of patients had atrioventricular block. That was 11 out of 19 patients. Three patients had left bundle branch block with a QRS greater than 130 or right bundle branch block with QRS greater than 150 milliseconds. Two patients who had AV junction ablation for permanent atrial fibrillation and the QRS prior to pacing was, the average width was 137 milliseconds and the average ejection fraction at baseline was about 44%. We also looked at septal involvement as defined by scar on cardiac MRI or inflammation on PET scan. Ten out of 19 patients had septal involvement with late gadolinium enhancement in the septum. Eleven out of 18 had inflammation. One of them did not have a PET scan available. That's why it's only 18. And there were four out of 18 patients who had no involvement, septal involvement, either on MRI or on PET scan. These are the baseline device parameters at the time of implant. You can see the pace QRS duration was 139 milliseconds. The average LVAT was 84 milliseconds, threshold 0.75, impedance as you can see sensing. Average procedure time was 159 minutes. There was a lot of variability in that depending on the type of device that was being implanted. And 15 out of the 19 patients had a CRTD implantation. Notably there were zero complications which included pneumothorax, pericardial tamponade, dislodgement, periprocedural device infection or stroke. These were our outcomes at the time of follow-up. So the average follow-up was about a year and a half, 437 days. Pace QRS duration was 138 milliseconds, threshold impedance and sensing as you can see. Ejection fraction was about 47%. We looked at end ventricular diastolic diameter and your functional class. Most of the patients had pacing burden more than 40% and in fact here you can see better our baseline versus our follow-up. There were no significant differences with respect to the QRS duration. The thresholds, sensing, impedances did go down over about a year and a half period. And importantly ejection fraction did not go down. In fact it stayed about the same at follow-up. Functional class did not change. Sixteen out of our 19 patients actually had more than 90% ventricular pacing. We were also particularly interested to look at patients who had cardiomyopathy due to ventricular dyssynchrony. There were a total of four out of the 19 patients who had this and we looked basically at the ejection fraction implant and follow-up. All four of these had septal involvement with scar and all of them had improvement in their ejection fraction. So we think this is an important study because it's a very understudied population. Patients with cardiac sarcoid previously, patients with hypertrophic cardiomyopathy undergoing left bundle area replacement have been looked at and there have been some challenges there with device parameters due to presumably septal fibrosis or thickened myocardium. But none of our 10 patients here had any significant changes in their pacing parameter at a year and a half follow-up. It appears that it's safe, effective, and feasible with stable lead parameters. And as mentioned, the inflammation or scar did not seem to impact parameters at our follow-up. Some limitations are that this is an observational study retrospective in nature and it's a single center. We only had a limited number of patients with dyssynchrony-induced cardiomyopathy. And we did not quantify the degree of inflammation or scar. So those are additional factors that may be important to look at. In conclusion, we think this is feasible to implant left bundle leads in patients with cardiac sarcoidosis with favorable lead parameters. There are no obvious barriers to implantation of these leads and we'll need further research to look at the stability of left bundle area pacing with longer-term follow-up. Thank you very much. Thank you for that presentation. As you're waiting for questions from the audience, I have a couple of questions for you. The first question is, I know this was a retrospective study, do you know whether there were patients with cardiac sarcoidosis in whom CSP lead placement was attempted but you could not achieve evidence of left bundle capture? We're not included in this study. Oh, I see. So no, because it's really a rare disease, we try to include every patient that we could identify in our electronic medical record over the last five years and we included everybody that we could identify. Of course, diagnosis of cardiac sarcoidosis can be challenging and so there could be patients that we in fact missed or did not capture based on that. Okay, yeah, you can step forward to ask your questions. Did the presence of the scar and the septum have any implications in the technique to implant the lead that is making it more difficult to penetrate the lead in the septum in your cases? And number two, is all the 19 patients with two left bundle branch capture or there were some of them with just septal pacing? Yeah, great question. So to my knowledge, your first question, I don't know the answer because whatever is basically in our procedure logs and the medical record is what we can go off of. So if the lead was multiple attempts were made to find a suitable location, we may not know all that information. And remind me again, I'm sorry, your second question. Yeah, so I can tell you about at least half the patients had selective left bundle area capture based on at the time of implantation, about half were selective and presumably the other half were deep septal pacing. Okay, yeah, you can step. As you step forward, just one question for you. I noticed that the duration of the baseline QRS was 137 before implant and it was like 138 after implant. Most of the time with CSP lead implants, you narrow the QRS up to a certain degree. Do you know why that is? Also, great question. You know, there is a lot of sort of heterogeneity also in our population. So, you know, there were three patients with dyssynchrony, cardiomyopathy due to dyssynchrony, and those patients had nice narrowing of their QRS, but, you know, right bundle branch block, IBCD, we didn't always see that same degree of narrowing. So I think that heterogeneity is why we didn't see any significant changes. That would be my hypothesis. So I think the current standard is to put ICDs in these patients, so that they can up front, all these patients were just conduct, you said four got an ICD, four were CRTD, and how did you manage the ICD lead? Where did you place it? Yeah, so I don't remember off the top of my head, but most of the patients did also have an ICD in addition to the left bundle lead. There were, I'd have to go back and check, but most of them did have an ICD. And consistent with the guidelines to implant primary prevention ICDs in this patient population. Okay, thank you. Because of our time, we have to move on. Okay, our next presenter is Kevin Lee. He will be presenting on tricuspid regurgitation after CRTD using biventricular pacing versus left bundle branch area pacing. Hello, everyone. Good morning. Thank you all for coming here. I have no disclosures. Today, I'm going to talk about tricuspid regurgitation after CRTD. So, we're going to explore that using biventricular pacing versus left bundle branch area pacing. So, just a little bit of background. For this talk, when I talk about biventricular pacing, I'm going to be talking about pacing where we have a lead in the right ventricle and then a lead in the coronary sinus. Now, as we've seen from all the presentations before us, left bundle branch area pacing has really been emerging as an alternative to biventricular pacing. We wanted to explore, especially for CRTD, for instance, patients with sarcoidosis, like the presenter before me mentioned, a lot of these patients have indications for ICD. So, at least for now, currently CRTD requires two leads when you do left bundle branch area pacing. You require the left bundle branch, the 3830 lead, as well as a separate ICD lead. So our question was, does CRTD with left bundle branch area pacing increase the risk of worsening TR or tricuspid regurgitation when compared to biventricular pacing? So we had consecutive patients at our institution that received CRTD either with a left bundle branch area pacing or with biventricular pacing between January 2022, which is around when we started implementing left bundle branch area pacing up to November 2024. TR severity was classified as either, I don't know if you guys can see them, you cannot, okay, it's classified as either zero, which is none or trivial, one mild, which you see on the left, moderate, which you see in the middle, or three as severe, which you see on the right side, both 12 months before and 12 months after CRTD implantation. The primary endpoint was a change in TR defined as a difference between the pre and post. So for instance, if someone started off with mild TR, which would be a score of one and ended with severe TR, a score of three, that would have been a score of two that they would have ended up with. So these are our baseline patients. We had 262 patients, consecutive patients, which received CRTD between 2022 and 2024. About 20% of them received left bundle branch area pacing and about the rest of the 80% received biventricular pacing. We had to exclude about half the patients in each group because they did not receive an echocardiogram or because the TR was unable to be graded in those patients. And so our final patient population was 29 in the left bundle branch area pacing group and 90 patients in the biventricular pacing group. These are the baseline characteristics of our group. There were no significant differences between the two groups. The average age was about 73. About 30 to 40% of our patients were female in both categories and 60 to 70% of our patients had a low EF. The baseline left bundle branch pattern was present in about 55 and 60% of our patients. Here you see our results. And so on the graph, you see the left bundle branch area pacing patients had a worsening of their TR on average about 0.7 points, which on average would mean in about four patients, three of them went from, let's say, mild to moderate or moderate to severe TR. In the biventricular pacing group, there was basically no significant change in TR with a change of 0.1. The P value was 0.002 in this case. Interestingly, 34%, just to be clinically relevant, 34% of the patients that got left bundle branch area pacing went from no or mild TR to moderate or severe TR, whereas only 13% of the patients that were in the biventricular pacing group had the same change. This is an, I'm an advanced cardiac imaging fellow, so I had to show some TTE pictures. But this is an example of one of our patients. So this patient has pretty much trivial TR at baseline. And then after the biventricular pacer was put in, I believe this was graded, you know, probably moderate to, if not severe. You can see that there are the two leads going, crossing the tricuspid valve here. So potential causes of the worsening TR. So first of all, of course, currently there are two leads crossing the tricuspid valve. This could be altering the tricuspid annulus and things like that. The other possibility is that the left bundle branch area, the lead often has to make quite an acute angle to get to the septum. Here on the right side, you'll see a transesophageal echo. This is a transgastric view of the TEE. And you see that actually the left bundle branch area pacemaker on the right side of the image is the septal leaflet, is actually impinging on the septal leaflet and not letting it open, causing this person's TR. Limitations, of course, this is a retrospective study. Overall small patient population. We did not really try to see which is a better overall pacing modality. We were very focused on just the tricuspid regurgitation and we'll need randomized control trials for further determination of clinical outcomes. We had to exclude some patients because not all patients receive echocardiograms at our institution both 12 months before and 12 months after CRTD implantation, leading to an inherent selection bias. And of course, as we're all aware, conduction system defibrillator leads are likely coming to market soon. These defibrillation leads that are based off the 3830. However, I still believe that this is important. There are many patients that have, let's say, an ICD and may require an upgrade in which this would still be something to think about. In conclusion, we show that patients who receive CRTD with a left bundle branch area pacemaker develop worsening of their tricuspid regurgitation when compared to patients who receive biventricular pacemakers. And of course, further study will be required to determine if this results in any changes in clinical outcomes. Thank you everyone for coming. Thank you for the great presentation. As we are waiting for questions from the audience, one question for you. I know that in regards to the clinical outcomes of the TR, you said you are still working on that. But do you know if any of these patients who develop severe TR require intervention? That's a great question. I'm actually on the intervention side. And so of the patients that we studied, about two of them have been referred to interventional cardiology for discussion on what to do about the tricuspid regurgitation. Now if the tricuspid regurgitation is due to impingement, these transcatheter edged edged repair devices don't work. And so there's always discussion about are we taking out the 3830 lead and doing coronary sinus pacing for CRT or some other. But these are kind of ongoing discussions. Of the patients that I know of, two have been referred for kind of TR management. Any questions from the audience? Okay. Thank you. So we'll move on to our last presenter. So our last presenter is Motea Sobranmenia, who will be talking about the effect of septal scar on clinical outcomes of left bundle branch area pacing in non-ischemic cardiomyopathy. So good morning and thank you all for coming. So the topic is effects of septal scar on clinical outcomes of left bundle branch pacing in patients with non-ischemic cardiomyopathy. So we know that left bundle area pacing is now a safe and feasible alternative for CRT compared to biventricular pacing. And there are certain subsets, like non-ischemic patients, where in a head-to-head comparison, left bundle pacing has done slightly better in terms of VF improvement even compared to biventricular pacing. But even if you use the standard CRT selection criteria, the non-responder rate to left bundle based CRT still remains 15 to 30%. And one of the traditional reasons why we had a poor response to biventricular pacing CRT was the presence of scar in the lead position. So in a patient who had a lateral or an infralateral wall scar, and you had a coronary sinus lead in this position, oftentimes these patients would be poor responders to biventricular CRT. Now, similarly, a septal scar would probably affect the outcomes in patients who undergo a left bundle based CRT. And that's what we're going to investigate in this study. So to determine the effects of septal scar on clinical outcomes in patients with non-ischemic cardiomyopathy undergoing left bundle branch area pacing for patients for CRT. So these are consecutive patients with a non-ischemic cardiomyopathy undergoing left bundle branch area pacing for CRT over the last three years. So patients were excluded if they didn't have a pre-implant cardiac MRI, and if patients did not achieve a suitable left bundle branch capture during the implantation. And I'll explain what those criteria were. The patients who underwent a non-ischemic patient who underwent left bundle branch pacing for CRT, and who we achieved a good left bundle branch capture, and who also had a pre-implant cardiac MRI, were finally included in these 96 patients. And in here, we divided these patients based on the presence or absence of a septal scar. The primary endpoint was a hard endpoint of composite of heart failure hospitalizations and major ventricular arrhythmias. And secondary endpoints were an echocardiographic response, loss of conduction system capture, or complete loss of ventricular capture during follow-up. So I won't go into this too much, but standard criteria for left bundle branch capture, including a terminal R, a short LVAT, left bundle potential, or transition from a non-selective to selective capture, echocardiographic response as 10% improvement in EF at six months, and loss of conduction system capture as a complete loss of R wave in V1, or a lack of transition if the patient showed a transition during implant. The baseline characteristics of these 96 patients, you can see the group one with the septal scar and group two without the septal scar. So the EF of the entire group was roughly around 35%. You can see that after pacing, the QRS was quite narrow at implant in both of these groups, with a QRS roughly around 112 to 116 milliseconds, a short and acceptable LV activation time. And regarding the type of devices that were implanted, so it was a dual chamber pacemaker with a left bundle pacing, so only two leads, and this was roughly in 60% of the patients, and a left bundle branch optimized ICD, or a dual chamber ICD with a left bundle branch lead in roughly 40% of patients. So this is an example of a 60-year-old male, non-ischemic, EF 30% at implant, left bundle branch block. At implant, good left bundle branch capture characteristics. You have a distal R, deep S, and V1. The EF improved from 30% to 42% after 2.5 months. After 3.5 months, during follow-up, there was a loss of conduction system capture, and you can see that's shown by a widening of the QRS, there's a fractionation in V1. And when we went back and looked at the pre-implant cardiac MRI, you can see that this patient has a patchy mid-myocardial scar within multiple segments of the LV septum. This is a 72-year-old female, similarly, good implant characteristics after the implant in terms of QRS duration and improvement in injection fraction. After just 1.8 months, we found that the patient had a loss of conduction system capture. And you can see the widening of the QRS, the notching, and the loss of the S wave in LEAD1. Again, the pre-implant MRI, when we went back and looked at it, had a transmural scar within the septum. And we've also measured the total LG, that is just beyond the septum, within the entire LV, how much was the late gadolinium enhancement. So the primary endpoint was heart failure hospitalizations and major ventricular arrhythmias, which were a higher number in the group 1 compared to group 2. And the secondary endpoints, the echocardiographic response was less in patients with a septal scar. Loss of conduction system capture and complete loss of capture were more in patients who had a septal scar at baseline. Now regarding the scar distribution, we labeled these patients as either a mid-myocardial, endocardial scar, or patients who had a transmural scar. And as we probably expected, patients who had a more transmural scar, the eight out of the 22 patients who had a transmural scar, had more heart failure hospitalizations and an increased loss of conduction system capture. So it's not only that the scar makes a difference, maybe the distribution of scar also has an effect on the long-term outcomes of these patients. And so we didn't quantify in terms of the exact location of the scar and septum lateral wall, but we did look at the entire scar burden. So patients who had a higher scar burden, or we said more than 10% of LGE, these patients again had poor outcomes with regarding to the heart failure hospitalizations, conduction system capture loss, and a poor echocardiographic response. Now 20 or 22 of these patients, we wanted to actually try to understand what was the reason for the septal scar. So these patients underwent 18 FDG PET CT and a clinical exome genetic testing. And we found underlying diagnosis of tuberculosis was made in five patients, a cardiac sarcoid in seven, and underlying genetic cardiomyopathy in another five patients. So on follow-up, this loss of conduction system capture was identified roughly with a mean duration of 3.4 months and 8.2 months in group one and group two respectively. In the patients in which there was a loss of conduction system capture, we revised the leads with the additional coronary sinus leads. There were three other patients other than the ones that were in the endpoints who had an increase in thresholds from 0.5 to 1.9. But since they maintained a good conduction system capture, no lead revisions were done for these three patients. So to conclude, among patients with a non-ischemic cardiomyopathy who underwent left bundle branch area pacing, the presence of a septal scar led to worse clinical outcomes during follow-up. So a pre-procedural cardiac MRI would probably give us useful information to identify responders, especially patients who are undergoing left bundle branch pacing for CRT indications. And obviously, a larger prospect of studies will be needed to validate these findings. So thank you. Thank you for that presentation. As we're waiting for questions from the audience, I have a question for you. So earlier today, one of the presenters, Michael Gorin, shared with us their experience of left bundle area pacing in patients with cardiac sarcoidosis with septal scar. And their results seem to be good in the long term. 35% of the population in your study had cardiac sarcoidosis. Can you tell us about their results? If you look at just those with cardiac sarcoidosis and septal scar, did they also experience like loss of left bundle area capture in the follow-up and the clinical outcomes? So thank you for this question. I think even cardiac sarcoidosis, it's probably a heterogeneous cohort because you see patients with different amounts of scar based on their time of presentation. So what we did was in those seven patients, two patients did have a loss of conduction system capture during follow-up. And there was, in those two patients, there was a poor echocardiographic response. So it's not that all patients with cardiac sarcoid, that left bundle pacing cannot be used. But I think another idea from this study is probably we need to have these patients on closer follow-up and also look for loss of conduction system capture when these patients come to clinic on a regular basis. Thank you. Any questions from the audience? I guess another question in the same way, whenever, you know, we listen to findings from studies, as clinicians, the questions that comes to our mind is, would this change my practice? How do I apply this? So from your standpoint, your findings, how will it change your practice if you have somebody with septal scar who needs CLT? So I think how this may affect your practice is, one, we consider all non-ischemic cardiomyopathies as one group of patients and who traditionally do very well with left bundle branch pacing. So the idea here is pre-procedural evaluation, especially with a cardiac MRI, would definitely allow you to understand patients who may not respond as well. And I would tend to, if patients have a large amount of septal scar or transmural scar or a large amount of LGE, we should be careful in just using only a left bundle branch lead to achieve CRT pacing in some of these patients. Okay, thank you. Two questions came up through the app. One question says, follow up, are the device patients in EP annually? That's what somebody is asking. Oh, okay, oh, it's the follow up to the first, okay. So I will just read the first. So the first is, how is this implemented in device clinic where there may not be regular EKGs being taken? And then the follow up is, are the device patients in EP annually? Yes, so I think each institution is different, but whenever we see patients with our conduction system pacing, along with the device interrogation, we make sure we do a 12-lead ECG whenever the patients come in. So oftentimes, we cannot pick up a loss of conduction system capture unless there is an abrupt change in the patient's symptoms or a drop in ejection fraction. So we've made it a point to do a 12-lead ECG whenever these patients come for a routine follow-up. Okay, yeah, please step forward. You, speak into the microphone so that everybody can hear you. It seems like you have the CMR before the implants. Why didn't you use the CMR scar location to guide your lead implant location to avoid a loss of capture in the end? So this was a, thank you for the question, but this was a retrospective analysis. So these are patients where we already did the left bundle pacing, and we went back and looked at the cardiac MRI after the procedure was done. But prospectively, yes, that would be a useful tool in sort of understanding where the scar is and where we may be able to enter with the lead. A follow-up question. So if you were able to do this preoperatively, like seeing the scar with an MRI, would you say like if you see scar, you wouldn't choose conduction system pacing at all, just do conventional by V? Or would you actually use the CMR scar location or size to kind of choose to implant the lead in a different location? What would you handle? Like how would you handle the scar information? So I think the goal of when you use left bundle pacing for CRT, I think the goal is to get a good left bundle branch capture. And oftentimes the location of the scar cannot really help us in terms of where we're going to try to screw this lead for left bundle branch capture. So I think the idea here with this retrospective data is just a word of caution that if you see a non-ischemic patient with an extensive septal scar, you should be careful when you're just implanting only a left bundle pacing lead, especially when it's only for a resynchronization therapy. Thank you. Okay. And thanks to all our presenters. This concludes this oral abstract presentation. And thank you everyone for attending.

cardiac resynchronization therapy

conduction system pacing

pacing-induced cardiomyopathy

physiological pacing

left bundle branch area pacing

cardiac sarcoidosis

non-ischemic cardiomyopathy

septal scarring

tricuspid regurgitation

advanced imaging