Thank you for this nice introduction. So as Bruce announced, I will be talking on the effect of atrial ventricular node ablation on biventricular pacing percentage patients with atrial fibrillation, and this is using some data from an ongoing randomized controlled trial. Now for context, so we know from the MADI-CRT trial and other trials that there is a correlation between the bi-V pacing percentage and the probability of heart failure and death. As the bi-V pacing percentage decreases, we know that the probability of heart failure and death increases. And one of the main reasons on why the bi-V pacing percentage can be reduced is atrial tachycardia or atrial fibrillation, and especially in the patients where we have a very low bi-V pacing percentage, atrial fibrillation is a big issue. And why does this happen in these patients? Because we have intrinsic beats, fusion beats, and pseudofusion beats that lead to non-capture or ineffective resynchronization. And so to solve this issue, it has been suggested to perform an AV node ablation, cutting off the conduction between the atria and the ventricle, rendering the ventricles completely pacemaker dependent to increase the bi-V pacing percentage. And there is indeed some data suggesting that this approach might work. This is from a large retrospective study that showed that patients who had a CRT device and atrial fibrillation, who then subsequently had an AV node ablation, did better compared to patients who were only on red control. So the ones that had an AV node ablation are the ones that are here in green, the ones that are on red control are the ones that are in red. And based on this study and other similar studies, the guidelines now suggest that we should consider AV node ablation in patients who have a CRT device, have atrial fibrillation, where we don't manage to increase the bi-V pacing percentage above 90 to 95 percent. However, I think it's important to highlight that this is all based on non-randomized evidence. And so currently we're conducting a randomized controlled trial where we try to provide evidence for this approach, where we include patients who have a CRTV and have persistent or permanent AF, perform a baseline assessment, and then we randomize them one-to-one, either to pharmacological rate control with a target of 90 beats per minute or lower, or we randomize them to atrial ventricular node ablation, and then we follow up these patients. Now for today, so all these patients also receive a 24-hour, 12-litre Holter monitor at baseline and at six months, and this is the data that I will be showing to you today. So just regarding the trial, the main inclusion criteria for this trial are persistent permanent AF, patients of course need to have a CRTV, exclusion criteria being paroxysmal AF, earlier AV node ablation, and second or third degree AV block. Now the end point for this particular presentation was the bi-V pacing percentage on 24 hours, 12-litre Holter monitor at six months. And we analyzed the Holter data using the Sorensynescope. What we did was we had a single-blinded electrophysiologist look at the Holter data, and he was tasked with labelling template beats that were provided by the software, and then the software would automatically count the number of intrinsic beats, base beats, PVCs, and fusion beats. And here we have an example within one patient, where we can nicely see first an intrinsic beat with an LBB-like conduction, and then followed by a base beat, then something in between, a fused beat, and then a PVC. Patient demographics, we included 79 patients for this analysis, where we have patients who are on average 71 years old, almost exclusively male patients who have predominantly to moderate heart failure. Most of them were also on beta blockers, not all of them were on MRAs, or raw system inhibitors, and the average BIV pacing percentage at baseline was 67 and 69 percent respectively. If we look at the effect of the rate control and the AV node ablation, we can see that the rate control did not significantly increase BIV pacing percentage at six months, while the AV node ablation not surprisingly clearly increased the BIV pacing percentage. And we found that on average that the AV node ablation increased the BIV pacing percentage by 11 percent compared to rate control. Now what we also found was that this effect was mostly driven by the reduction in the proportion of intrinsic beats. As proportion of intrinsic beats reduces, we can see clearly that the BIV pacing percentage increases, unsurprisingly, but what was surprising is that this is almost perfect linear correlation, so the reduction in intrinsic beats seems to be the main driving factor over here. Now this is all pretty straightforward, nothing surprisingly, but I want to take you and take a deeper look into some of the individual data points, and here we had some interesting findings. And the first of all is that, well, performing the AV node ablation does not guarantee us to achieve more than 95 percent BIV pacing percentage. As you can see, there are a couple of patients here marked in black, and those are the patients who did not achieve more than 95 percent BIV pacing percentage at six months. And when we look at their halter data, we see that these patients still had a lot of PVCs present, and I think this is an important message that if the BIV pacing percentage is reduced in these patients, we perform our AV node ablation, we still need to follow up on these patients, and we need to make sure that there's not something else that's reducing the BIV pacing potential, such as the PVCs, because, of course, AV node ablation does not affect the burden of PVCs as shown here. But surprisingly, the rate control also did not affect the burden of PVCs. Another thing that I want to highlight, and this is a slightly off topic, but I think it's relevant, is that we compared the BIV pacing percentage on halter and the BIV percentage recorded by the device itself. And what we found was that, on average, the device overestimated the BIV pacing percentage by 16% when you compare it to the BIV pacing percentage on halter. So what we see here is a blunt Altman plot, where on the x-axis, you have the mean of the device and the halter BIV pacing percentage, and on the y-axis, we have the difference between the halter and the device. So on average, more than 16% overestimation by the device compared to halter. And when you look at the individual dots, you can see that they are clearly organized in a certain trend. And indeed, what we see is that the lower the BIV pacing percentage, the higher the discrepancy between the dots. And this is, of course, a problem, because you want to be able to detect the patients where you have a low BIV pacing percentage, but what this tells us is that, when we try to do that, the device tends to overestimate even more. And when we look at it in a binary way, what we can see is that these patients over here, those are the patients where the device tells us that the BIV pacing percentage is above 90%, but according to the halter, it's below 90%, and in some patients, it was as low as just 1%. And so in almost half of the cases, we had false positives, meaning patients had more than 90% according to the device, but less than 90% according to the halter, and this might also influence our decision-making where we want to proceed to the AV notablation. So important for us also to highlight this. So in conclusion, we performed the first randomized control trial wherein we compared AV notablation to rate control, and we found that, for now, AV notablation significantly increased the BIV pacing percentage, and that this effect was primarily driven by the reduction in the proportion of intrinsic beats. It also tells us that we need to be mindful of residual PVCs after AV notablation, and that we should be looking at these patients with halter monitoring. So if we have a patient who does not respond to CRT as we would have expected, and the device tells us that there's more than 90%, well, maybe go and perform a halter because the device, the BIV pacing percentage might be lower than what you actually expect. So important limitations, this is data from an ongoing trial, so this is relatively small sample size, what I'm showing here today. We did not look at outcomes such as the effect of this increased BIV pacing percentage on heart failure hospitalizations or deaths. Almost a third of patients already had a relatively high BIV pacing percentage in both groups, and so the actual effect of the AV notablation might be underestimated when we compare it to the rate control. And the last one is also an important one. So the halters that we used, unfortunately, they're not able to accurately capture the pacing spikes. So we cannot make the distinction between the pseudofusion beats and intrinsic beats. For this particular analysis, the pseudofusion beats were also considered as intrinsic beats. And with this, I would like to thank you for your attention, and also my team, Professor Prash Sanders, who is the lead investigator of this trial, and Jonathan Ariratnam, who was the electrophysiologist who actually analyzed all the halter data, which was a lot of work, of course. Thank you very much. Thank you very much. Are there any questions for our presenter? If anyone, you can enter or you can raise your hand. Here's a question. So the question has to do with management, long-term follow-up of PBC burden and management of PBCs. So can you comment with regard to how these patients may have been approached in the study or what you learned or any sort of interventions that you found worked well? So unfortunately I won't be able to provide you an answer today to that question. So we are collecting that data and how these patients are treated, but we haven't looked at it yet. This was really just looking at the by VPC percentage and I hope we'll be able to report it once the study has completed. We have one more question. So the question is, on the last slide I said that a high number of these patients already had a high Bi-V pacing percentage, and whether this was because the device overestimates the Bi-V pacing percentage. So the Bi-V pacing percentages that I showed you today, they were all based on the halter, so they should be accurate. Okay, thank you very much, that was an excellent presentation, and a really important topic. So we're going to go to our next presenter, Dr. Saga? No, I'm Dr. Liu. Okay, I went the wrong direction. So our next presentation will be by Dr. Liu, and the title of his presentation is Long-Term Outcomes of Left Bundle Branch Pacing and Bi-V Pacing in the Treatment of Chronic Systolic Heart Failure with Left Bundle Branch Block, a Prospective Randomized Controlled Trial. Thank you, Dr. Liu. So good morning, everyone. My name is Liu Xi from Department of Cardiology, Zhongshan Hospital of Fudan University in Shanghai, China. So in this section, I will present our clinical research result, which entitled is Long-Term Outcomes of Left Bundle Branch Pacing and Bi-V Pacing in Chronic Systolic Heart Failure with Left Bundle Branch Block, a Myotest Center Prospective Randomized Controlled Trial on behalf of the HeartSync LBBP trial investigators. So over the past two decades, numerous randomized clinical trials have demonstrated the benefit of the Bi-V P in patients with heart failure at LBBP. However, several limitations have limited the application of Bi-V P, including the imperfect ventricular activation and suboptimal treatment response. LBBP has been proposed as a novel physiological pacing modality in recent years, and some small randomized trial and large observational study have proved its benefit in treating desynchronized heart failure and its potential to be an alternative to Bi-V P. So, however, until now, no randomized trial evaluated the long-term outcomes of these two pacing modalities. So we conducted this HeartSync LBBP trial, currently the largest RCTs, aimed to compare the clinical outcomes of these two pacing modalities. So this is a pro-certain Myotest Center Randomized Controlled Trial, which enrolled 200 patients with LBBP and severely reduced LVF. And they were randomly assigned to either LBBP or Bi-V P treatment. This study was undertaken at six centers in Shanghai, including the Zhongshan Hospital or the Fudan University, Shanghai Chest Hospital, Shanghai Changhai, Shanghai Changzheng, and Renji Hospital, and also the Shanghai Six People's Hospital. And the study period is from October 2020 to September 2024. In the inclusion criteria, including adult patients with complete LBBP and with a reduced LVF of less than 35%, NYHA function class two to four, and an expected survival time for more than one year, and the exclusion criteria included patients who refused to participate or participate in other studies, or patients with persistent or permanent AF, and also patients with heart transplantation or waiting for heart transplantation, or patients with previous pacemaker implantation, or with mechanical tracheal valve implantation, or with severe runoff, liver dysfunction, or pregnancy. So in this study, the criteria for confirming the LBBP capture include that pacemorphology showed an LBBP pattern with any of the following, including the pacemorphology changes between non-selective LBBP to selective LBBP, or from non-selective LBBP to left ventricular septal pacing, all demonstrated with a selective LBBP pacemorphology. So crossover was allowed when the LBBP failed, and AV delay was optimized to achieve the narrow QRC duration, as we previously described. And BIVP was performed in a standard fashion, and a crossover was allowed when an LVD could not be implanted due to anatomic variations, high pacing stress hold, or unavoidable phrenic nerve stimulation. And AV and VV delay were optimized based on the paced QRC duration. So this slide showed typical LBBP cases performed in this study. In brief, the head spondal potential was first mapped at a reference marker, then the lead was moved towards the right ventricular apex for approximately one to two centimeters, and was deeply screwed into the interventricular septum. And the pacemorphology changes between the selective and non-selective LBBP indicated LBBP capture in this case. And then an AV delay was optimized to achieve the narrow QRC duration. And the study input, including the primary input, was defined as the composite outcome of heart failure hospitalization and all-cause mortality. And the heart failure hospitalization was defined as an anti-invergent failure or hospitalization with heart failure signs or symptoms which require intravenous diuretic therapy. And the secondary input, including the all-cause mortality, heart failure hospitalization, and echocardiographic response and super-response rate. So all the patients were followed up at one month, three months, and six months post-procedure, and then every six months and thereafter. And the echocardiographic measurements were performed by two experienced echocardiographers who was blinded to the study design and the group assignment. And all the effective and safety inputs was independently adjudicated by the committee whose member or winner for the trial group assignment. And all analysis were performed according to the intention to treat principle. And this study was also registered at the Chinese Clinical Trial Registry, which is a WHO certificate prime registry for Chinese clinical trial. So for the result from October 2020 to March 2022, a total of 218 patients were scanned while 18 met the exclusion criteria. Then a total of 200 patients were enrolled and randomly assigned to either LBBP or BiBP group. And there were no significant differences in baseline characteristics with a mean age of 64 years and 68% were male, and 82% had an etiology of non-ischemic cardiomyopathy. And the baseline QRS duration was 168 milliseconds and LVF was 28%. And for the procedure outcomes, the success rate of the initial attempts in the LBBP group was 98%, and the success rate in the BiBP group of 96%. And two patients in the LBBP group cross over to BiBP due to unable to screw the lid into the targeted area, and six patients in the BiBP group feel their first attempts due to four patients had an unfavorable venous anatomy, and one patient had high PCS threshold, and one patient had an unavoidable phrenic nervous stimulation. And all crossover patients performed the opposite arm successfully. And the median follow-up duration was 36 months. So for the QRS duration, both groups have significant improvement than the baseline, while the LBBP group showed a shorter PCS QRS duration than the BiBP group. In addition, both groups have significant improvement in LVEF, LVEDD, LVSD, and baseline, while all improvements favor LBBP compared to BiBP at six months and last time follow-up. So in addition, there were no significant differences in response rate between two groups, while the super response rate was significantly higher in the BiBP group. And for the primary endpoint, the intention to treat analysts showed that the incidence of the primary endpoints in the LBBP group was significantly lower in the BiBP group, and the treatment effect for the primary endpoint was constant across most of the specified subgroups. And no significant differences was observed in all cost motility between the two groups, while the LBBP group showed a significantly lower risk of heart failure and hospitalization than the BiBP group. And some limitations should be emphasized in this study. So firstly, the patient enrolled in this study had a high percentage of non-ischaemic cardiomyopathy, so our finding may not be generous to a patient with an etiology of ischaemic cardiomyopathy. So secondly, the intervention were all performed in Chinese patients, and it needs to be determined if the treatment effect is similar to populations with a different ethic background. So thirdly, this study was performed in experienced centers with a high success rate and low cost severity, which may differ from other studies without similar technique expertise. So finally, to make a conclusion, in this randomized trial involving the patients with LBBP and severely reduced LVEF, LBBP was superior to BiBP, reducing the risk of heart failure and hospitalization and the risk of all cost motility, and should be considered a first choice in this patient population. So thank you. Thank you, Dr. Lu. That was a very, very interesting presentation. Any questions from the audience? I would sort of repeat the question and then answer it. The question is, we said that the success rate in the LBB group was about 98 percent. Is this all real LBP? Actually in this study, all the success rate indicated that it's a true LBP, not included the LVSP, and we also performed the procedure even with long time, even until the LBP capture was confirmed. So the success rate is just a real LBP, not included the LVSP. Another question. Do you want to just get up and ask it to the mic? Hi, what was the amount of ventricular pacing in each group? The amount of ventricular pacing in between the two groups, was it similar? And how much was it? Like was it 95 percent pacing, 99, how much? Actually the ventricular pacing rate was not commonly collected at our study, however we think that it's more than 95 percent as we follow up, we say. Okay. Oh, we got one more, you can come up and. I'm sorry, what was the study called again? What was the study called again? What's its name? The name of the study? The study is called the Hatsink LBB trial. Thank you. That was an easy question. Any other questions from the audience? I have one question. In terms of the, from the CRT group, the left ventric, not the LVB group, was there any sort of quality control, because sometimes with CS pacing for CRT, you know, you can get a good spot, you can get like not such a good spot, and this would probably be something hard to do. I don't know if you did this in the study, but in people who got a good location for their, and I don't know how you'd measure that with a QRS narrowing or things like that. Was there any, is there any interest in looking at that part of it, because, you know, is it that we're just putting in, we're accepting less quality CRT lead location, and is it something where you should say, well, if you get it in a good spot, it's equivalent, but if you don't, it's worse. Anything like that? The answer can be no. That's fine. Oh. I had a hard time. Well, then, I'll leave that as a comment, not a question. How's that? Because I think it might be hard in your study, but it's a really interesting study, and thank you for delivering it today. So we'll do our next presenter, it was great. Thanks a lot. So, Dr. Saga, and where are you, what institution are you from? Temple University. Temple, okay. So our next presentation is from Dr. Anash Saga, and the title of Dr. Saga's presentation is Bachman's Bundle, Pacing is Associated with Increased LV Synchronized Pacing Delivery in Patients Undergoing Cardiac Resynchronization. Let's see if I can, oh, start, here we go, okay. Dr. Saga? Good morning, everyone. My name is Anusha Saga. I'm a second-year resident at Temple University, and today I'm here to talk to you about Bachman's Bundle, Pacing and its association with increased synchronized pacing delivery in patients undergoing cardiac resynchronization therapy. And these are our author block disclosures. A little bit of background, cardiac resynchronization therapy, or CRT, is a standard of care to improve ventricular synchrony in patients with heart failure and left bundle branch block. Typical lead placement in CRT cases includes an RA, RV, and LV lead, and the RA lead is typically placed in the right atrial appendage. The RV lead is typically placed in the apical septum, and the LV lead typically in the coronary sinus. However, this placement of leads can ignore intact right bundle branch conduction and could possibly lead to negative side effects from pacing the RV when it might not be necessary. This is a diagram demonstrating synchronized LV pacing using the adaptive CRT algorithm versus biventricular pacing. Conventional biventricular pacing is on the right, and you can see that the AV node is conducting down the bundle of HISS, and you can see the intact right bundle branch. However, you can see the two pacing leads that are still producing electrical currents and stimulation, producing some sort of disorganized electrical activity that ignores the intact right bundle. On the left is the adaptive CRT algorithm, which allows for fusion of the right bundle branch conduction with the pacing from the CS lead to lead to a more physiologic contraction response. Adaptive CRT was studied in the adaptive CRT trial as well as the adaptive response trial. Compared to conventional biventricular pacing, the adaptive CRT trial found that there was a significant reduction in AFib incidence, heart failure, all-cause admissions, and overall improvement in those with a higher percentage of synchronized LV pacing. The adapt response trial was a larger trial that followed patients over a long time period. However, it didn't find that the adapt CRT algorithm didn't significantly reduce death and heart failure events. However, looking back, this could be due to a low event rate in both groups overall. And on post-hack analysis, patients with greater than 85% synchronized LV pacing actually had a significantly lower incidence of the primary endpoint, which is all-cause mortality or heart failure interventions. This is demonstrated in the figure to the right. The y-axis is all-cause mortality, and the x-axis demonstrates this over time. And the bottom light blue line is the group with adaptive CRT and synchronized LV pacing greater than 85%. So you can see there's a significant difference between this group and the other groups, which were conventional CRT and adaptive CRT with LV pacing less than 85% of the time. This overall suggests that measures to increase the delivery of synchronized LV pacing might overall be beneficial. However, synchronized LV pacing is often limited due to AV delays. Bachman's bundle is a potentially more physiologic atrial pacing site compared to the right atrial appendage. In this study, we compared the PR intervals between sinus pacing, right atrial appendage pacing, and Bachman's bundle pacing. In the figure to the right, you can see there's a significant reduction in PR interval when comparing sinus rhythm to Bachman's bundle pacing, as well as right atrial appendage pacing to Bachman's bundle pacing. And the figure to the left shows the tracings of sinus node pacing versus right atrial appendage pacing versus Bachman's bundle pacing. And the PR interval is a little more difficult to see from this figure. But if you compare the P wave tracings in A and C, you can see that the P wave looks a little bit more like sinus node P wave. The morphology is a little more similar when compared to the RAA pacing. So this suggests that Bachman bundle pacing might improve delivery of synchronized LV pacing. So this brings us to our objective, to investigate whether patients with atrial leads implanted at Bachman's bundle have a higher percentage of synchronized LV pacing delivery when compared to those with atrial leads implanted in the right atrial appendage. So this study was conducted at Temple University. It was a retrospective single center study. Patients included underwent CRTd implant with a synchronized LV pacing algorithm programmed with adaptive CRT. And we compared patients with right atrial appendage lead placement versus Bachman's bundle lead positioning. And the outcome we studied was the percent synchronized LV pacing at 3, 6, and 12 months. This was our demographic data. Overall at baseline, the two groups were very similar. And I will point out that the groups were relatively small. We had an N of 30 in the right atrial appendage group and an N of about 7 in the Bachman's bundle group. But overall, the groups were very similar at baseline. Again, the groups were similar at baseline in terms of amplitude, impedance, and threshold as is demonstrated in this chart. And just a quick term definition. Often in reports, biventricular pacing often refers to total ventricular pacing, which can be a bit of a vague term in this study where I'm trying to distinguish biventricular pacing from synchronized LV pacing. So here we're referring to total ventricular pacing as CRT pacing. And then CRT pacing is further subdivided into synchronized LV pacing, which takes advantage of the intact right bundle branch versus biventricular pacing. So these are our results at a three-month follow-up. You can see that there is a significantly increased amount of synchronized LV pacing in the Bachman's bundle group of about 95% when compared to the right atrial appendage group, which clocks in at about 73%. And consequently, the percentage of biventricular pacing is also significantly lower in the Bachman's bundle group when compared to the RAA group. Interestingly, the CRT pacing percent was significantly different as well. However, when actually looking at the data, comparing 97% to 94% in such small groups doesn't seem too remarkable. And looking back in the Bachman's bundle group, there were two patients with frequent ectopy that influenced the amount of CRT pacing and V-sensed events. These are the results in graphic form, just for a little more clarity on how significant the difference in synchronized LV pacing was between the Bachman's bundle group and the right atrial appendage group. So we continued this analysis at 6 and 12 months, and you can see that this difference was preserved out to 12 months with an increased percent of synchronized LV pacing of almost 95%, 94% in Bachman's bundle group when compared to the right atrial appendage group, which was at about 70%. Significance was preserved at 6 months, not so much at 12 months, most likely due to the small number of patients in the study. And you can see the CRT pacing percent was not significantly different at 6 and 12 months. So overall, this indicates that atrial lead positioning at Bachman's bundle is associated with significantly higher percentage of LV synchronized pacing than in patients with right atrial appendage leads. And this suggests that pacing at this Bachman's bundle site may have significant benefits in patients undergoing CRT implant. And that's all I have for you today. Thank you. Do we have any questions from the audience? So I'll ask one question. Any differences in programming of baseline rates or AV delay rates in the two arms? Honestly, device programming is not something I'm too familiar with. But I have Dr. Cronin here, who was involved in placing a lot of the Bachmann's bundle leads and RAA leads, who might be able to answer the question. Thanks, Tricia. I'm Ed Cronin. I'm the senior author of the paper. These were only in patients with adaptive CRT turned on. So the AV delays were determined by the device algorithmically. So there was no difference in programming. Thank you. Nice presentation. So I noticed the HOPC rate is higher in the Bachmann bundle group, although there's no significance. So does that have something to do with the AV synchronization rate? Yeah, like I mentioned, two of the patients in the Bachmann's bundle group, which is pretty notable as the population was only seven patients, had frequent atrial ectopy and one had frequent PVCs. So I'm sure this led to a difference in the amount of atrial pacing percentage in the Bachmann's bundle group compared to the RAA. Thanks. Thank you so much. Thank you. Very interesting presentation. Good job. And we'll go on to our next. So let's see. OK. Our next presentation is by Dr. Deschamps from Grenoble. And the title of her talk will be Leadless Left Bundle Branch Area Pacing with WISE CRT. Thank you for this introduction. So good morning, everyone. My name is Elodie Deschamps. I'm very pleased to present our experience of leadless left bundle branch area pacing using the WISE CRT system. This work is part of a collaborative effort from the University Hospital of Grenoble. And I thank my mentor for their help for this work. As you know, conventional CRT is a class one accommodation in heart failure patients with left bundle branch block. Despite its proven benefits, implantation can be technically challenging due to anatomy. And there is a certain percentage of non-responders estimated up to 30 percent depending on the criteria used. Over the past few years, conduction system pacing, particularly left bundle branch area pacing, has emerged as a promising alternative and may offer better electrical synchrony and possibly a superior outcome compared to bi-way pacing. In fact, a growing number of studies, largely observational, have compared LBBAP with conventional CRT, showing for most of them improved outcomes in terms of ejection friction, curious narrowing, LV remodeling, and clinical response. That's why a recent consensus presented at ERAS this year recommends CSP as a first-line therapy along with bi-way pacing for CRT indication. However, LBBAP still requires transvenous lead with the onset of long-term risk. This brings us to the YCRT system, which enables totally leadless pacing of the left ventricle. It involves a two-stage procedure. First, the implantation of a spectral transmitter and the battery, and then in the second step, the implantation of a heavy electrode for the femoral approach. The effectiveness of the system was demonstrated in the self-CRT trial. A case study conducted in CRT candidates considered non-responder or at high risk for upgrade. They found a significant reduction in LV volume and an improvement in ejection friction, all while meeting safety criteria. This supports the leadless LV endocardial pacing as a viable alternative to conventional CRT. The traditional use of the YCRT system focuses on lateral LV wall pacing, but recent authors have explored the septal positioning to target the left bundle branch area. So our objective was to share our center experience using the YCRT system for LBBAP for three different cases. Case 1 is a 61-year-old man with non-ischemic cardiomyopathy and reduced ejection friction. He had a prior CRT-D for primary prevention. Unfortunately, LV threshold was high and the patient reported phrenic nerve stimulation. So we opted for YCRT in this case. So we used a triceptal approach and first assessed the pacing site using an EP catheter. Then we implanted the LV electrode in the mid-septal region. At that site, the airwave peak time in V6 was 64 ms, which was subjective of left bundle branch area pacing. We will just advance the quick video to see the deployment. I will show you at the end. As you can see on this panel, the curve direction with LV-only pacing and even more when synchronized with the LV lead of the CRT-D was clearly narrower compared to LV pacing alone and BV pacing alone. At 6 months for LV, the patient reported a better functional status and echocardiography revealed an increase in ejection friction to 42%. The second case is an 81-year-old man known for mitral valvuloplasty who had a prior micro-ARV implanted for AV block. He then developed a pacemaker-induced cardiomyopathy where his ejection friction decreased to 35%. A YCRT system upgrade was preferred to preserve the lead-less pacemaker. The implantation of the YCRT was performed following the standard step we described earlier. The electrode was finally deployed in the middle of the septum, as you can see with the blue arrow. The airwave peak time at this location was 58 ms. LV-only pacing showed greater electrical and synchronization compared to BV pacing and baseline ARV pacing. At 6 months for LV, the YCRT system achieved 99% of BV pacing and the patient reported an improvement in quality of life and ejection friction increased to 46%. Finally, in case 3, we present a 60-year-old man with non-ischemic cardiomyopathy and prior CRTD who had lead extrication due to infective endocarditis. Because of multi-complicated diabetes and left subclavian thrombosis, totally lead-less CRT was considered the best option for him. Implantation was more challenging in this case with a high threshold in the first position. The device was finally positioned in a basal antheroceptal location. Unfortunately, the system could not be programmed in LV-only pacing mode. Then we were not able to obtain a 12-lead ECG under this configuration. Based on the anatomical position and carotid narrowing during BV pacing, at least LV-septal pacing was assumed. Unfortunately, despite successful implantation, he developed terminal heart failure and died one month later. This slide provides a quick summary of the key outcomes at baseline and at 6 months for the first two patients. It is a buzzy slide, but it highlights the improvement in QRS duration, ejection friction and clinical status, confirming the electrical and clinical effectiveness of the YCRT approach in this selected case. In our experience, left bundle branch area pacing using YCRT was technically feasible. We observed pacing patterns consistent with conduction system pacing in two cases. However, we did not visualize LBB potential and transition was not systematically observed. Also, this is the strongest criteria described. In addition, also LBB criteria seemed to be met during LV-only pacing. The YCRT system is synchronized with LV pacing, so the QRS morphology corresponds to a fusion between LBB and LV pacing. This result should be interpreted with caution. The second important point is that, to our knowledge, this might be the first reported series of totally lead-less CRT with permanent conduction system pacing, combining the YCRT system with a micro device. This approach is particularly attractive for patients with high-risk comorbidities, infectious or vascular issues, while avoiding lead-related complications. The cost of the YCRT system and the requirement for a staged procedure might present a substantial barrier to broader adoption of this technology. Lastly, also the reported complication rate is comparable to conventional CRT methods. Specific risks associated with a completely lead-less approach require careful monitoring. In conclusion, YCRT is a feasible technique for lead-less left bundle branch area pacing. Furthermore, totally lead-less CRT using LBB-P for the YCRT system may represent an effective solution for patients with high-risk comorbidities. It is an effective alternative to conventional CRT in selected heart failure patients. Thank you for your attention, and I thank my mentor, especially Professor DeFay, who implanted all the LV electrodes in this case. Thank you. Thank you very much. Excellent presentation. Any questions from the audience? I guess I'll ask one. Any issues related to anticoagulation? Thank you for this question. The device is supposed to be endothelial in a couple of weeks. The system says 45 days, so the patient doesn't need anticoagulation for long term. They recommend three months anticoagulation or antiplatelet therapy. And then after three months you stop, even though there's a lead-less device in the LV? Yes, we can stop it because the preclinical study in Goethe particularly showed that all the devices are completely endothelial. This is 6 millimeters in length and 2.8 millimeters in diameter, so it's completely endothelial. Great. Any other questions from the audience? It seems like the standard CRT device is on its way to becoming something you'll see in museums or something. We'll see. So our last presenter is Dr. Emmanuel Offey. His presentation is Capture of the Left Ventricular Conduction System Leads to Improved Success Rate of Anti-Tachycardia Pacing Delivered to Left Bundle Branch Area vs. Right Ventricular Pacing. Hi, good morning. I'm Emmanuel Faye and I'm representing our group to present this work on the capture of the 11 tricolor conduction system. So, the efficacy of anti-cardiac placing for VTs are well-proven, but then this efficacy reduces once we have fast VTs. And then, when ATP to the heart fails, in terminating VTs, we would normally apply high energy shocks to the heart. The problem with this is, however, there's an increased risk of mortality. And from this study, it was shown that between inappropriate shocks to the heart and then appropriate shocks to the heart, there were some low trend of survival rates. And this was actually highly significant between that for inappropriate shocks and then no-shock groups of patients. So, LBB pacing is actually being applied widely in clinical routines. And that this group will show that for lead implantations to the head bundle and then the right ventricular apex and then the left bundle branch area, the LBBA site actually saw an increase in the number of newly implanted leads, the percentage of mentally implanted leads. Now, for the lead R trial group study, this group is actually looking at defibrillation leads in the LBB area. And it's quite interesting. So, this points to the fact that there's an increase in clinical application of left bundle branch area pacing. A couple of years ago at Louisiana, we presented this to the community, the HRS community. And then we did this work in the canine VT model we developed in our lab. And from this study, we realized that about 70% of ATP attempts in the LBB area were successful in terminating VT, whereas only 47% of ATP attempts to the RV were successful in terminating VT. So, for the reports we're giving here, we want to look at the unraveled mechanistic underpinnings for this efficacy rate. So, we completed this study using canines. In six of them, we completed the study on two days. So, on the baseline day, we implanted leads in the RV apex, and then one at the left bundle branch area. And then following the thoracotomy procedure, we ligated the proximal and distal parts of the left anterior descending artery. And then following that, we actually sent the animals back to the animal facility after we closed the thoracotomy site. And then when we brought them back after four days, and anesthesia, we deployed a femur basket catheter within the RV to record the LV endocardial electrical activity. So, on that same day, we induced 79 VT episodes using programmed electrical stimulation. And once the stem VT was detected, we tested ATP delivery at two regions of interest. And then that was at 88 percent of the VT cycle length. So, we delivered a set of ATP pulses. Now, testing ATP at two sites either restored the sinus rhythm or ATP failed in terminating VT. So, from the endocardial electrical recordings we did with the basket catheter, we created activation maps. And then this actually corresponds to the geometry of the basket catheter. That is the activation map I'm showing. So, the center is actually corresponds to the apex of the LV, and then the periphery of the plots corresponds to the LV base. And while you're looking at this set of activation sequence within the LV when we induce VT. So, we also created maps for when we have the capture of the LBB area or the RV. So, this is showing a capture of the LBB area. Then, for the set of ATP pulses we delivered, we created activation maps for those as well. So, we proceeded to perform this Spearman's round correlation test. And what we did was for the activation sequence for the LBB base beat or the RV base beat, we found the Spearman's correlation coefficient between that and then the first ATP beat. So, while you're looking at the Spearman's coefficient for the first ATP beat. And then we did the same analysis for the remaining seven beats. So, afterwards we fitted a regression line to the ATP coefficients. And then we did the same for the VT beats and then the set of ATP beats. So, that's what you're looking at. And then we came up with this index we call the crossover point, where we see that from that crossover point we start to see a transition of the ATP beats to look more like our captured beat pattern for the LBB area. And this crossover point for this particular example was 2.6. So, we realized that for the successful group, the crossover point was well advanced in time, about 2.4 beats earlier for the successful group compared to the failed group. And that ATP to the LBB area learned about this crossover point one beat earlier than when we delivered ATP to the RV apex. So, for the successful ATP attempts, for the last ATP pulse, we determined to look at the stimulus to a Purkinje interval, right? That interval from when we delivered the ATP pulse to when we have a Purkinje activation. So, this is the time I'm talking about. And we realized that ATP delivered to the LBB area, right? What about an ATP time interval, right? To the Purkinje time interval, that was about two times earlier than when we have ATP delivered to the RV apex. And then, we did a similar analysis for when we delivered ATP, right? And then we looked at the myocardial activation, the time interval from the ATP pulse to the myocardial activation. And realized that for this analysis as well, the time interval was shorter for the LBB group, and it was about 1.5 times earlier than when we delivered ATP to the RV apex. So, we determined the earliest Purkinje, the earliest pulse activation to be emerged after we delivered ATP, right? So, we created a set of 56 bipolar channels, and then we looked at what's emerged first from all those 56 channels. And for this example, what you're looking at is a Purkinje emerged first, okay? In other examples, the myocardial activation would emerge first. So, we realized that 85% of the time, right? Purkinje activations led myocardial activations when we delivered ATP to the LBB area, right? So, RV ATP led Purkinje activations, led myocardial activations. Purkinje activations led myocardial activation more frequently when we delivered ATP to the LBB area than when we delivered ATP to the RV. And then in less than 40, less than 50% of the time, Purkinje activations led myocardial activation when we delivered ATP to the RV. So, overall, we concluded that we have this effective and direct capture of the Purkinje system when we deliver ATP to the LBB, and that this explains why we have this increased efficacy rate for the ATP to the LBB area, and that this calls on the implementation of this in human populations clinically. So, this is a group I work with, and thank you. Thank you very much. That's our last presentation. Any questions for our presenter? So, one question I have is, any of the patients have, or any of the canines have bundle branch re-entry as their mode of VT, and did you notice any differences there? Okay, no. We didn't look at the analysis. So, the ischemia area, right, was the LAD, and we didn't look at the analysis whether we have bundle branch re-entry. Yeah. Any other questions? Well, we thank our speakers, all of our speakers today. We had a very nice session, and hope you all enjoy the rest of the meeting.

cardiac resynchronization therapy

heart failure

left bundle branch block

atrial ventricular node ablation

biventricular pacing

leadless pacing

anti-tachycardia pacing

heart disease

patient outcomes