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The Beat Webinar Series - Episode 15 from APHRS in ...
APHRS in Sydney
APHRS in Sydney
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Dr. Deepti Varghese, and we're here to cover the late-breaking clinical trial session number two, which will be held later this week at the 17th annual Asia Pacific Heart Rhythm Society meetings being held in Sydney, Australia. Welcome, Deepti. Thank you. So this session is centered on seven presentations all around catheter ablation, and while there's a great deal of interest in pulse field ablation, not all of the sessions or presentations are gonna be related to pulse field ablation. Deepti, what did you pick up on the ones that are not related to PFA? Sure, so there is a session on bipolar radiofrequency ablation, specifically for refractory ventricular tachycardia and premature ventricular complexes. There is another session on cryo versus radiofrequency ablation for persistent atrial fibrillation. Yeah, no, this is great because bipolar ablation obviously is something that's often needed for the management of ventricular arrhythmias, typically areas like the LV summit as well as the septum, so it's really gonna be nice to see this larger study reporting on the efficacy of such an approach as well as the safety of this approach. And essentially, this cryo versus RF is an attempt to replicate the initial FIRE and ICE study, which first dealt with patients with paroxysmal atrial fibrillation, but this so-called FIRE and ICE 2 study will now deal with patients with persistent atrial fibrillation, a population where we've not had such clear evidence on the value of PFA versus cryo. So there are several sessions on pulse-field ablation, Dr. Mittal. Are there any particular ones that stood out for you? Yeah, I thought there were some really novel approaches. Now, there's some new technology being reported, single-shot PFA technologies that have not yet been reported on in the commercial world, and it'd be nice to see what the long-term efficacy of those studies are. Certainly, there's been a lot of interest in being able to do these procedures without fluoroscopy, and at least one presentation is looking at whether this procedure can be done with zero fluoro, and I think that's gonna have a lot of interest to the practicing community. And certainly, a number of sessions looking at the durability of pulmonary vein isolation at six and 12 months after the ablation procedure, and I think a number of these things will inform clinical practice. And finally, I'm pretty intrigued about a session that's assessing coronary anatomy post-PFA. We know that there's the possibility of coronary spasm after these procedures, and so this imaging study is really designed to see if there's long-term deleterious effects on the coronary artery, and I think it's more than likely that that will also be of great interest to the practicing community. Absolutely. Well, I think that we're both excited about this session and look forward to reporting on it once the presentations have been completed. Until then, from APHRS, on behalf of DP, this is Sunit Mittal signing off. Thank you, and welcome to the joint session, HRS-APHRS update on conduction system pacing, 2024 current controversies. I'm joined by co-moderator Martin Stiles from New Zealand and Dr. Xian Chen from China. We have a great faculty. This session is being livestreamed throughout the world, and we will have a series of four talks followed by a question and answer session. There is an ability for anyone over the world listening to submit their questions. And let me go ahead and get this excellent session started. Our first speaker is Dr. C.P. Lau from Hong Kong. He will talk about what does the evidence show us about conduction system pacing, and is it reflected by the current guidelines? C.P. Thank you very much, Chairman and Chair, ladies, and it is my privilege to speak on the evidence that shows about conduction system pacing and how it's reflected in the guideline. I have the privilege to represent the APHRS to join this, the 2023 Heart Rhythm Society, APHRS, ALA-HRS guideline on cardiophysiological pacing. I think we defined cardiophysiological pacing as cardiac pacing intended to restore or preserve synchrony of ventricular contraction. And it can be delivered either in the form of CSP, conduction system pacing, using either his bundle pacing or left bundle branch area pacing, or conventionally with cardiac resynchronization therapy, most often with birentricular pacing. This is one such example with narrowing of the QRS complex with an R wave in V1 and a shortening of the pace to V5, V6 QRS R wave. The evidence, as it's set in the 2023, when we designed this is that there are substantial randomized controlled trial evidence that CRT reduce the symptoms of heart failure and hospitalization and improve LV function and survival. The response to CRT may also include improvement in clinical parameters of heart failure or prevent heart failure progression and LV function stabilization. At that time, we think the majority of data on CSP remain observational, long-term stability of conduction system pacing capture can be a concern. But increasingly, we see long-term cohort data up to about 30 months that suggest durability of left bundle branch area capture. I'll just go through the guideline and some modifications from the published trial. This is an example of a patient with a classic indication of EF 35%, QRS duration 150, the classic indication, and CSP is considered as a 2A indication when CRT cannot be adequately delivered. It is considered a 2B indication for special patient's requirement, for instance, to avoid too many leads in the system and inexperienced centers and operators. In patients who have both intermediate QRS duration, 36 to 50% QRS duration of 150 milliseconds is considered a 2B indication. So at that time, it's a 2B indication, except when there's a failed CRT. This slide shows the details of the indication. I would like to focus on two points. One is the classic indication, QRS duration 150 milliseconds near your heart, two to four, and is a 1A indication for CRT by V. And if it cannot be effectively delivered, then his bundle pacing with left bundle branch correction or the use of left bundle branch area pacing is considered as 2A. The other group would be intermediate LVEF group, and this should be considered 2B indication for either CRT or conduction system pacing. This is one of the largest registry and is an international registry by Dr. Vijay Yaranam and also Dr. Alan Bogan from the chair. And this look at the relatively long-term outcome of CRT versus left bundle branch area pacing in the standard indication group over any international study in North America, Asia, Europe. And you can see that there is a substantial benefit in terms of QRS duration, EF improvement, a reduction in heart failure and death, and echo response. So at least in this observational study, left bundle branch area pacing improved the clinical outcome compared with biventricular pacing. We have now three randomized study that have been published. These are two acute study. This is one from China by Dr. Wang et al. And they looked at in a group of left bundle branch patients, LVEF reduced patients who have dilated non-ischemic cardiomyopathy, left bundle branch pacing caused improvement of LVEF and reduced antipopy NP and promote reverse remodeling at six months. A broader group from Dr. Vijay Yaranam, and this is the HOT CRT, the Hispergine Optimized Trial on CRT. They randomized 100 patients with LVEF at 31%, left bundle branch in 62, and with about 40% ischemic. Again, in this relatively short-term study at six months, there was a significant improvement of ejection fraction and the delivery of the left bundle branch was significantly higher percentage than the CRT. In this meeting yesterday in the late breaking news, Dr. Chen, she is chairing, presented this randomized study from China. And they looked at 200 patients with an LVEF 35% or less and QRS duration 150 milliseconds. And it's a long-term observation of 35.7 months with a baseline EF 28% and a dilated left ventricle, 20% of which were ischemic. And in this study, the combined endpoint of heart failure hospitalization and death was significantly reduced with left bundle branch pacing versus biventricular pacing, but it's largely driven by heart failure hospitalization. There was a better change in EF, better reverse remodeling, and the BNP were also improved in this study. What about the group of 36 to 50%? And it was also again addressed yesterday in this as a late breaking news and is concurrently published in the Heart Rhythm Journal. And this look at the group of 35 about retrospective cohort study, not 100% comparable, but it's a large population. And indeed, the primary outcome of death or heart failure hospitalization is significantly reduced by CSP, and particularly when left bundle branch pacing, background of left bundle branch was observed. While not completely randomized, but these days at least a obvious benefit, but no signal of harm. So there are future trials coming up from all over the world, particularly a very large trial coming up in the States on the left to left. And in the next few years, we are hearing many more of this. So the CRT response can be considered in mortality, heart failure hospitalization, clinical heart failure, prevent progression, and reverse remodeling as the guidelines say. So one area which is to me quite important is upgrades. The pacing-induced cardiomyopathy is happening now 12% in retrospective study. And for this guideline, anything which is more than 10% decrease in EF from pre-pacing from 50%, and RE pacing more than 20%, and no alternative cause. It is considered as a 1B indication when the CRED with LE functioning worsening or heart failure symptom attributable to substantial ventricular pacing. CRT with BI-RE is recommended to improve LE function and improve heart failure symptoms, and not on mortality. And it is a 2A indication when CSP is considered. Now we have a new study which have been published, the Budapest study, which upgrade CRV pacing-induced cardiomyopathy to CRT. This is a fully randomized study and looking at the heart endpoint. And there are 20% pacing, QRS duration 150 milliseconds. They are randomized to CRTD in a three to two ratio versus ICD. The composite endpoint was significantly reduced from ICD to 32%. And the depth, in fact, was significantly reduced. This is a really hard endpoint. And there was a similar procedural complication and also a trend to reduce ventricular tachycardia or fibrillation. So this is taken from the same study and the CRTD upgrade is superior to continuation of a defibrillator therapy. What about the bradycardic indication? Just for another patient, the core not pacing-dependent LVEF more than 35%. These are 2B indications for the use of CSP. For those with a pacing-dependent, it's a 2A indication for either CRT or CSP. And with normal LVEF, the conduction system pacing is considered as a 2B indication. So this is the summary from the guideline. If you anticipate an RV pacing to be substantial, then these patients, if they have chronic left bundle branch block, the ventricular function need to be assessed. The CPP is recommended when there's a 2A indication and may be reasonable if LVEF is normal as a 2B indication, if the pacing is substantial. If the anticipated RV pacing is less than 20%, then patients can go on with the traditional RV lead placement as a 2A indication. For those of intermediate mode, the mid-range ejection fraction, CSP or CRT in those with the left bundle branch block are acceptable as a 2B indication. In patients with normal LV, left bundle branch area pacing may be considered as an alternative as a 2B indication, but by ventricular pacing is not indicated. So the reason behind this is that there are several core studies that show stable pacing parameters and better LVEF preservation in RV pacing than RV apical pacing. And up to recently more than 30 months of follow-up. The meta-analysis in 2018 ACC pacing guideline looked at LVEF group of 35 to 50 and the effect of CRT or his bundle pacing. And indeed his bundle pacing is superior to RV pacing. And after AV junctional ablation, Dr. Huang, the speaker, have shown in this alternative AF, which is a crossover study, to be a beneficial over RV pacing. So this is taken from Dr. Lee and also Dr. Sharma. These are the comparison observational study. They are reduction of heart failure hospitalization and a reduction in upgrade significance in the conduction system pacing arm over RV pacing arm. And there's also a trend to reduce atrial fibrillation. There's now an additional small study which is fully randomized to look at ejection fractions of more than 40% and ventricular pacing of 80%. They were randomized into either the conduction system pacing versus RV apical pacing. And over a very short period of six months, they saw a difference in ejection fraction of 5.8%. And we know that the stability and the ease of delivering left bundle branch area pacing is continuing improving. This is taken from the European multi-center study. Left bundle branch area pacing complications 8.3%, but you have to mind that acute perforation of the LV is what's considered as a complication, but often this can be, is an indication for repositioning at the time of the operation rather than a complication. So these are the indications for bradycardic indication. These are pacing dependent patient. If it's over 50%, then it's a 2B indication. If it's in the mid range, it is a 2A indication. Currently for those who do not need pacing and if the EF is 35% or more on standard RV pacing need, it suffices. If it's normal LVEF, we can consider left bundle branch area pacing as a default for RV pacing need. And if LVEF is low, then it is a 2B indication, particularly in the presence of left bundle branch for CRT. So the additional recommendations from the guideline suggest that LVEF 35% on left bundle branch pacing, this is an indication for CPP may be considered on those with intermediate QRS duration. And if it's more than 150 milliseconds, it's a 2A for CRT based on the older study on the CRT. During implantation and follow-up, this is quite important, documentation of biventricular pacing or conduction system is essential. We do not only check for threshold and you have to confirm the stability of his bundle and left bundle branch area pacing and left bundle branch correction. There are considerations for pediatrics and congenital heart disease. So this is my conclusion here. We need individualized and shared decision making and in heart failure with left bundle branch bulk, CRT remains the cornerstone of treatment, but CSP an increasingly viable alternative. In pericardic pacing, CSP, especially left bundle branch area pacing is a strong alternative to our RV pacing. Targeting the whole conduction system, including right bundle and his Purkinje system will require future research and technological improvement. Thank you very much for your attention. Thank you. Thank you very much. I'd like to introduce our next speaker, Pippin Kojo-Dojo from Singapore, who's talking about stilette driven leads, lumulus or stilette driven. What do we really know, Pippin? Thank you, Martin. I'd like to thank both societies for the very kind invitation for me to speak on this topic. So we're gonna discuss about our choice of leads. If I can have my slide. Great, fantastic. So here's the background. The feasibility and improved clinical outcomes that we see with conduction system pacing, whether it's HISS or left bundle branch area pacing is based on the use and performance of the Medtronic 3830 luminous lead. We all probably in this room have greater clinical experience with probably deployed more stilette driven leads for RA and RV pacing during our careers. And the guidelines that Professor Lau talked about actually gave no clear indications as to which lead to use. So the only description of the lead in this guidelines is that left bundle branch pacing was initially described with a lead with an electrically active exposed screw, other active fixation leads with a retractable screw and dedicated delivery sheets has also been used to achieve left bundle branch pacing. So we don't have any clear recommendations. So in the next sort of 15 minutes or so, I want to discuss whether it makes any difference which type of lead we use. We'll look at some of the lead designs, handling differences between the two groups of leads. We'll look at implantation success, median to long-term survival and performance, as well as the extractability of these leads. So here's the table that summarizes the four FDA approved left bundle branch pacing leads. So we have the Medtronic 3830 in the first column followed by three stilette driven leads from Abbott, Biotronic and Boston Scientific. They share many, many similarities. So you can see that the stilette driven leads are largely coaxial in design. They vary between 5.6 to six French. And if you look at the electrode length across all four of them, they're quite similar. But nonetheless, because the stilette driven leads are actually thicker, they give a much larger tip electrode surface varying from 4.5 to 6.9 square millimeters compared to the 3.6 square millimeters in the 3830. They all elude steroid and the tip to ring spacing is between nine to 10 millimeters. And all of them can be used with fixed sheaths and the Abbott Medtronic system does come with the option of using deflectible sheaths. So when we first started doing stilette driven leads after doing sort of more than 250 cases of luminous leads, we noticed that there were some differences. And one of the differences was that we needed more leads to complete the case. So again, this was a very early experience and this is probably from a clinic experience four to five years ago, whereby 10 out of 34 patients that we started doing this, we needed about 2.5 leads per patient to complete the case, as opposed to 250 leads for 246 patients. And what we saw was that there was a higher incidence of sort of lead deformation, which you can see in the photograph there. and there were also instances whereby the helix actually extended as we tried to retract the lead from a site where we could not capture the left bundle. And in fact, sometimes when we tried to take these leads out, we left part of the helix behind. But nonetheless, the acute success rate and procedural time were all similar. We had actually excellent threshold and sensing in both groups, and we explained these observations by thinking that this is due to the learning curve, which we'll talk about a little bit more. We also had evolving handling instructions, because at the time, I recall having different handling instructions for every successive case. We were told helix out, helix in, turn the helix, not the lead, and so that was actually something that we were grasping with. And there were certainly no dedicated tools, such as the helix locking tool, to help these leads perform in the left bundle position. So it is great that now we actually have some robust bench data to better understand how these leads actually perform, and I want to share with you the platform that Dr. Ganesan's team at Flinders have done to understand this concept of torque transfer during left bundle pacing. So essentially, the platform is a lead over a sheath, and it's mounted onto this experimental gig, and what they do is that they will rotate the lead in 90-degree turns. And there's a high-speed camera at the other end that looks at how much of this turn is transmitted to the tip of the catheter, and that's what you see there. And they measure this by putting a flag at the tip, so that when you turn the lead, if it turns 90 degrees, you can see the flag turn 90 degrees. And so that was the experimental setup, and what they saw was that the mean rotational response for the four common leads are actually very, very different. So you can see the ideal one-to-one rotation response, which means that when you turn the lead by 90 degrees, the tip also turns by 90 degrees. But that doesn't happen with any of the leads. You can see that the Boston Scientific Ingevity and the Biotronic Soliar Dust has a better rotational response, and the 380 and the Tendril lead from Abbott has a smaller rotational response. Now, again, so even among the stylet-driven lead group, they are not the same. They don't behave the exact same way. The other thing that we noticed from this observation from this experiment is that when you look at each of these rotational response curves, the curve is not smooth. So if you look on the top left there, basically you transmit the talk to the lead, and at some point in time, the talk transmission decreases. And what actually happens when you photograph the interface between the lead and the endocardium is that you start to get entanglement of the endocardium. And when you store up enough rotational energy in the lead, the endocardium will either tear or the muscle will give way, and that allows an abrupt change in the talk transfer. And so what we can only see in our hands is that sometimes if you look at the picture on the bottom left, that is where we start to see a little bit of the crinkling in the lead insulation. Now, when you do this for a group of leads, you can see clearly, first of all, the gradient of the curves are slightly different, and that relates to the talk transfer, which I showed you in the first slide. But there are also these abrupt points where there is a sudden release of stored energy, and that makes the lead have these talk breakpoints. And if you look at the talk breakpoints for four of the leads, they tend to occur at different points of lead transmission, and the stylet-driven leads tend to have more of these talk breakpoints compared to lupinous leads. So the experiment actually tells us that all the leads behave differently. Now, what the experiment doesn't have looked at is whether or not if you have less than perfectly 90 degrees coaxiality to the septum, or if you change the speed at which you drill the lead, whether that makes any difference. Now, this is another set of experiments that was done by Dr. Okubo, and they used the longevity plus lead with the Boston sheath, and they did some bench testing in porcine hearts. And so for 40 leads, they deployed the helix perpendicular to the RV septum, and in the other half, the sheath and the lead was not coaxial. And what they found was that when you do not place the lead coaxially and you retract the lead, there's a much higher incidence of lead tip deformation, which you can see on the picture on the right. Similarly, the other testing condition that they looked at was how you remove the lead from the septum if, for example, you didn't get to a position where you had good conduction system capture. And so in half the group, they rotated the lead body, which is what we are now recommended to do, and the other half, they took the helix back. And again, if you try to take the helix back without rotating the lead, you have a much higher incidence of lead tip deformation. The other thing that is being studied and of some concern is that there's the potential of high mechanical stress at the site between the distal and proximal electrodes. So this is looking at a Belgium experience from 325 patients who had lap underbranch pacing, 149 RV pacing patients, all using the same solia lead. The lap underbranch pacing success rate was high, but there was a 0.6 percent difference in early conduction failure during a follow-up of 18 months versus none of it at all over more than nine years of follow-up in patients who had the lead placed in the RV apex. And what you can see there are examples of this stress fracture between the proximal and distal electrode. And the authors figured out that basically if you have an angulation of more than 12 degrees, which is seen in 1.3 percent of patients, that makes it more likely for this to occur, and that if you were to then rotate an excessively angled lead, it also increases the risk of conduction fracture. So there are things that we should do to try and avoid this. We must try and achieve coaxility. And for some of the leads that are coming through now, such as the out-of-pace lead by Abbott, they have actually strengthened the distal housing so that the lead is a little bit stiffer at the end. And what we often don't see is that a lot of our industry partners have actually subjected their leads to quite a lot of bench testing, where they apply quite aggressive bending conditions to them, and they try and stimulate almost the stress that's on the lead if they were in a patient for more than 10 years. So here are some considerations about the difference between the luminous leads and the stylet-driven leads. So the luminous lead is of a smaller caliber, so in the event of a septal perforation, perhaps less collateral damage. The isodimetric helix and body allows for easier penetration and removal. There's no risk of helix retraction. These leads have higher tensile strength on bench testing. On the other hand, the stylet-driven leads are stiffer and have better transfer of torque. The stylet changes allow you to vary the support and maneuverability. There's continuous monitoring of impedance and pacing, morphology, as well as the injury current. And the larger sheets that come with them allow for better support. Now, we're reaching a consensus where the stylet-driven leads are largely used pretty much in the same way, and this is sort of something that all three manufacturers would agree with. So it consists of mapping with the helix withdrawn to prevent entanglement, inserting the stylet maximally to the tip of the lead to provide support, deploying the helix with or without overextension, and this depends on which brand you're using, to prevent lead retraction using the locking stylet. You can clip the crocodile clip to the stylet to monitor for the injury current and impedance, which you see in the picture here. You should turn the whole body clockwise to drill into the septum, and compared to the luminous lead, we have to turn these leads more slowly and with less rotations. And in order to withdraw the lead, as I showed you earlier, you should counterclockwise torque the lead body without retracting the helix into the housing. When we take the leads out, we should check for trap tissue, inspect the helix for deformation, and then we should withdraw the helix before we reinsert it for the next attempt into the delivery catheter. And the red ones are the ones that are unique to stylet-driven leads, and we don't have to do those for luminous leads. So in the interest of time, I'm going to go through some of these slides quite quickly. So this is the registry data for the stylet. You can see for all of these sort of registry datas, the implant success is quite high. The thresholds that you achieve are quite good, but the follow-ups are also very short—nine months in the Belgium registry and only three months in the BioConduct IDE study. There was a 2.2 percent reported risk of perforation in the Belgium registry and about a 0.8 percent rates of helix deformation. But nonetheless, at two years, even looking at the threshold and the sensing, the parameters were excellent compared to historical leads left in the RV apical position. But nonetheless, as Professor Lau said earlier, good capture threshold does not represent persisting CSP capture. Similarly, for the tendril registry, this was a prospective registry of 200 over cases, 91.4 percent acute success for left bundle, no helix disruption. There were satisfactory thresholds at six months. There was one case of lead dislodgement and no lead fractures. This is data from the inside left bundle branch pacing registry for the Ingevity lead. Again, retrospective single arm up to 15 U.S. sites. The follow-up was about three months, and you can see that 99.2 percent of patients had a threshold of less than two volts at 0.4 milliseconds at three months. Sensing was excellent. There was about 1.1 percent risk of dislodgement with elevated threshold, and one case of myocardial perforation with temponade. And if we look at data on the left bundle lead with the Ingevity plus lead, comparing left bundle versus RV pacing data from the latitude registry, you can see that up to three months, the pacing thresholds were actually very good compared to leads that were historically left in the RV apex. So this is data from the Geneva registry, so 153 patients with left bundle lead and 153 with a mixture of stylet-driven leads. Again, success rate equally high. The authors noted in the top right that there is a learning curve of about 50 cases with stylet-driven leads, and they certainly saw more helix damage with the stylet-driven lead at 6.1 percent. So in the interest of time, I'm going to skip this slide. And so yesterday at the late-breaking session, there was actually a randomized trial of left bundle versus stylet-driven leads. This is the Compare Left Bundle Branch pacing study, and 100 patients were randomized by Dr. Pathak's team to 1-1-3-3-0 luminous lead versus a stylet-driven lead, which is a tendril. And essentially, in both groups, there was no difference in success rate, implant times, implant duration, the post-pacing QRS duration. There was a slightly higher R wave amplitude and slightly higher impedance in the luminous lead group, but both groups, the numbers were excellent. Pacing thresholds were equivalent. There were more septal perforations in the stylet-driven lead, seven versus one, and there was a 6 percent loss of left bundle capture at three months, three in each group. And this will be important for patients who rely on these leads for CRT. Dr. Vijayaraman has shown us some data about the extraction of CSP lead. The important thing to remember with all these is that the dwell time is relatively short, 29 months for his bundle pacing, about nine months for left bundle pacing. Procedural success was 99 percent, and 95 percent of patients could undergo CSP re-implantation. So at least in the short term, this is very good. However, extraction of CSP ICD, which some of us are starting to think about doing, may be a little bit more challenging. So in conclusion, the stylet-driven lead handles better than the—different to the luminous lead. Each stylet-driven lead actually handles differently, so you can't even lump them as a group. Talk transfer is not uniform. There is a higher risk of helix deformation and septal perforation with stylet-driven leads. The acute procedural success and short-term electrical performances are comparable, but longer-term data on lead survival and persisting CSP capture is needed, and removing CSP leads with short dwell times are highly successful. With that, I thank you very much for your attention. Thank you, Dr. Conrad Jodlow from Thinkable, and let's welcome the next speaker, Wei-Jian Huang, who is from Wenzhou Medical—First Medical Hospital from China. As we all know, Dr. Huang is a pioneer of LBB pacing, and which—this technique was considered as Huang technique at the first of time when it get published. So let's welcome Dr. Huang. Does conduction system capture match term? Does—what about the septal pacing versus conduction system pacing? It's welcome. Good morning. It's my honor to be here to talk about some conduction system pacing. My topic is does conduction system capture matter, deep septal pacing versus conduction system pacing. First, let's review the first paper reported Wenzhou septal pacing. We use special lead with long helix, and in patients with sick sinus syndrome, and yes, the sick sinus is less than 10 millimeter. Here is ECG. We found that the left ventricle pacing produce a narrow cascading, but we—also because only local mechanical capacitor is so different from true LB capacitor, but at that time, it's not clear how to differentiate. So we found LV septal pacing produced a better hemodynamic compared RV pacing, right ventricle septal pacing. And here is a first case with left bundle pacing. Yes, we should know whether it's true LB capacitor. In this patient, we have selective LB pacing. It's very clear there is a selective sign, a stimulation that are discrete between stimulation and ventricle activation. So it's true LB capacitor. So the patient have a very excellent clinical outcome. In 80 years follow-up, his ejection fraction improved to more than 90 percent and remained. And ejection stable—threshold is stable. So after battery depletion, we downgraded to only DDD device, no ICD. So it's very economic. And now we should know what's the definition and classification of left bundle branch pacing. It's in our center, and we usually think left bundle area pacing is anatomic idea. We just place the lead at the left bundle area, usually very close to the left ventricular endome. So left bundle branch area pacing include true LB capacitor. And left ventricular septal pacing, just local myocardial capacitor. And also we know sometimes we tested to confirm whether there is a bundle capacitor, but we are unable to confirm it. So some patients are clear. Usually more than 90 percent is clear, definite LB pacing or left ventricular septal pacing. Sometimes especially in patient with IVCD is unclear, or sometimes we don't have tested to confirm it. So include clear and unclear. And this is a definition and a classification of left bundle by different heart association. So how to differentiate? I think it's very important according to the electro-characteristic of cell. For conduction system, there is a very rapid propagation. So from conduction system to non-local myocardia or from local myocardia activation to conduction system, there is a transition resulting changes in morphology of paced ECG. For example, new onset of R wave in lead wave one, and or still as a change in still LVAT. We use EP study to confirm it, this phenomenon. We using retrograde potential, conduction system potential or anterior potential to confirm it where the very conduction capture. So I think now for most of the patients, it's clear for us we can make diagnosis whether there is a conduction capture. Why we should have conduction capture? This data showed if left conduction capture, there will be shorter left ventricle activation because at same patient site, we think it's comparable. So someone will ask, his bundle pacing produce prolonged still LVAT compared to left ventricle. So we should know using LVAT should be comparable. So in this paper, we pacing at same patient site. So this study showed LVAT pacing produce better left ventricle synchrony, but better interventricular activation. How to explain it? This is our data. From left ventricular septal pacing to non-cellular LV pacing, we know. We found we will have a shorter still RV peak time. That means left ventural, left conduction system capture will improve right ventural activation because red grade conduction system to activate right ventural activation. So that's why we need to make sure that the right ventural activation is activated at the peak time. So that's why we need to make sure that the right ventural activation is activated at the peak time. Here is the tool case. Let's look at the comparison. Left bundle pacing and left bundle pacing. The right bundle pacing is And here is case, patient with heart failure and left bundle block. We tried first, first left bundle branch pacing is successful. Unluckily, threshold is increased to more than nine votes. After so, the patient after seven days only left the central pacing. We found ejection flushing don't improve. So, at six months, we redo. Then we have a true conduction capture and ejection flushing improved. And also, we found echo have a better electrical synchrony during true LBB capture. And here is some study in animal. There is a three group. The results showed true LBB capture have a better hemodynamic effects compared left to central pacing. And this is also left bundle pacing has a better movement of left ventricular ejection flexion. And here is another study showed binary pacing and his bundle pacing have a similar electrical synchrony. But only left bundle pacing have a better hemodynamic effects. And then this is a study about a clinical outcome between left bundle pacing and left ventricular pacing. And the result showed. LBP patient resulting better political outcome, improved ejection fleshing better. And this is another, this is a study showed LBP patient produced low incidence, improved clinical outcome, reduced all-cause mortality and all-fault failure. And also, this is a study showed same results with narrow class comparison and improved ejection, a greater improvement in ejection fleshing compared to LBP patient. And also, reduced composite outcome. And this is another study showed LBP patient resulting narrower class comparison, a greater improvement in ejection fleshing. And this is our data. Non-patients lost capture of left bundle. So we redo. Non-patient with CRT indication or heart failure. This is a result. And upgraded to true LBP capture, left ventilation improved. So how to get true LBP capture? We should know criteria for true LBP capture. We should simplify the criteria for LBP capture. This is technique to get a true LBP capture and avoid septal perforation. Because we know if we want a true LBP capture, we should screw the patient deeper enough just beneath of left ventricular abdomen. So we should know how to avoid septal perforation. The current injury of local myocardium is very important. So we should toe channel one for LB potential, one for current of injury. And continuous monitoring. This is case. There is a potential with higher LBP potential. So we screw the patient a little deeper. Then LBP potential become bigger, bigger. And finally, with current of injury, that's final target. This is a real change of left bundle potential. In our center, we have more than 95% of patients with LB potential and current of injury in neurocures complex. So what we concerned is complication. Only one patient with septal perforation at subacute phase. And one patient with lead flex. We have finished more than 300, 200 cases with left bundle branch pacing. So let me make a summary. Left bundle pacing includes left bundle pacing. Left bundle pacing delivers better left ventricular electrical synchrony. And have a better clinical outcome. Yes. Data is limited. We need a more prospective clinical trial to confirm it. Thank you for your attention. Thank you, Dr. Wong. I want to remind everyone that this is being live streamed. In addition, you can go on to your tablet or phone and submit a question. We'll have a question and answer session. We've already gotten several questions from folks all over the world. So remember, go to your app on your phone or tablet. Go to this session and submit a question, and we'll read your questions at the end of the session. Our next speaker, Dr. Pugal Vijayraman, will discuss how can I be sure I'm pacing the conduction system. His take on the algorithms and techniques for conduction system pacing, what his experience has taught him. Good morning, Ken, chairpersons, colleagues, and friends. A great opportunity to present my observations here. And Dr. Wong talked to us about how important it is to achieve a left frontal branch capture. While in many bradycardia patients and in patients with narrow complex and non ischemic cardiomyopathy, it may be fairly straightforward to confirm left frontal branch capture. It may be challenging in many other situations. And the conduction system pacing as such has evolved into multiple different terminologies, but the most important thing is still ensuring that you have conduction system capture. While in his bundle pacing, I would say more than 90, 95% of the time, it's fairly straightforward to confirm his bundle capture. So not too much of a challenge there historically, at least when you do it with a 12 ADCG. And the procedural end points were often very clear, although we had technical challenges, threshold challenges, and that's what led to the left frontal branch pacing. And in the left frontal branch pacing, even for left frontal branch area pacing, the right bundle branch conduction delay in lead V1 was considered to be a quite important criteria, almost 100% sensitivity for that in many studies. However, I want to present you some challenges and give you information on how this may not happen all the time. So here is a situation where you have leaders advance deep into the conduction system area and during left frontal branch pacing, and V1, which is our traditional lead, we look for R prime, although we've seen nice R primes in V2 to V3, and short peak R wave times in V5 and V6. So it's something we don't know if we have left frontal branch capture or not, even left frontal branch area pacing yet, but when we do threshold testing, so we do high output and low output pacing, now you have evidence for transition from non-selective to selective here. And why? Because in this patient with underlying left frontal branch block, you can see there is during selective left frontal branch capture, there's no retrograde conduction, anterograde conduction down the left frontal, but maybe engagement into the right frontal retrogradely. But RV septum in the proximal left frontal branch area, so LV septum in the proximal left frontal branch area, there's rapid conduction transeptally, and there's not enough right ventricular delay, so it can be masked. So even when you have clear left frontal branch capture. So here's another scenario where, again, leaders advance into the conduction system, base QRS morphology is fairly narrow, and the question is, should we advance it further or not? Always check at high and low output, because here at the lower output, we transition into LV septum pacing, opposite of what we just saw. So here, if you're on the proximal left bundle, there is rapid conduction retrogradely into the his bundle, and anterograde conduction down the right bundle, so you have pretty narrow QRS. And as you can see, the same patient, there's transition from non-selective to selective, and you don't have the right bundle, right ventricular conduction delay. So that can be masked on the opposite direction. So both scenarios can cause masked right frontal branch block pattern. So not look at just one criteria to confirm left frontal branch area or even left frontal branch capture. So these are critical to know this happens in about 5% to 6% of patients. And there are additional scenarios where you can have anatomical variation, and in literature it's reported about 5% of patients, the right bundle originates from the left septum. So you may be in the distal his bundle on the LV septal side, and not have RV delay because you have distal his bundle pacing. And sometimes a scar in the septal area can completely confuse you the whole way, because the scar and differential conduction and delay can make it very hard. And also important to understand that many of the criteria, especially with numbers of peak RV times, are all developed from bradycardia population of predominantly narrow QRS patients. And so these criteria may not always work well in patients with LV dilatation, conduction disease, or scar in the septum. So just want to go through some of the criteria quickly. And when you have transition from non-selective to selective or septal during threshold testing is considered to be one of the gold standards if we can do LV septal mapping to confirm conduction system capture. So this is what we rely on for the most part, especially in left bundle branch block where you can't even see left bundle potential as very nicely Dr. Wong demonstrated to us. So how important is transition? The transition is important, but it's also critical to understand some challenges in QRS transition. So here is a patient with cardiomyopathy failed IV pacing comes for conduction system pacing. So here during thresholds, I've already gone to the left septum, I have right bundle pattern, but peak RV times are fairly long. And doing threshold testing, I see the transition from the inter-peak interval changing significantly from 24 to 45 milliseconds, but with a change in peak RV time also prolonging. So I'm confused what this is. But when I pace at a much higher output, I see significant shortening of peak RV time to closer to 90, 95 milliseconds. And so this is resulting from transition in different septal myocardial bundles in the presence of scar. And only when I pace at a high output, I could get conduction system capture. So I needed to advance the lead a few more millimeters further, but few more rotations. And it's important to evaluate all these criteria in context of what you're dealing with, whether you have septal scar or conduction disease. So I would have missed an opportunity to get conduction system capture if I hadn't advanced the lead further, otherwise this patient would have been left with septal pacing in the setting of a scar, not able to overcome capture in the conduction system. Here's another example, wide left bundle branch block. This is a similar scenario, but a long HV interval, significant conduction delay. And I'm pacing also with history of anterior myocardial infarction. And I have pacing from 5 volt to 1.5 volt. I have this QRS morphology with what looks like not a real good right bundle branch delay pattern. But then at a lower output, it makes some changes in V2 suggestive of R prime. And then even lower output, I now can see the R prime, but the peak activation times are longer. Only when I pace at really high output, I get short peak R wave times, but no R prime in V1. So the amount of septal scar and transeptal conduction delays so much, and conduction down the left bundle and RV actuation is faster than transeptal conduction here. So I don't see the R prime, but I still have conduction system capture at a high output. So I had to advance the lead even further in this patient and then get the final morphology, achieve certain degree of LV synchronization in this patient. Here's another patient with the right bundle branch block. And you have with his bundle pacing, there is a shortening of peak R wave times in this patient. And then at a lower output, there is some prolongation. So even in the setting of right bundle branch block, you can achieve certain degree of LV synchronization as demonstrated by the short peak R wave times compared to even his two R wave peak times in V6. And then at a lower output, you have only myocardial capture. There is varying degrees of bundle branch block correction and some masquerading left bundle conduction delay in this patient. For the same patient with left bundle branch pacing, you can see multiple transitions here. In the first two transitions, you have his bundle capture. It means left bundle capture with rapid conduction to the retrograde his bundle. And then at a lower output, you have only myocardial capture. So what was the first transition in the setting of his bundle capture? Again, differential myocardial capture can give you different patterns. So you got to explore all of this in the context of underlying disease and scar. And we have seen that there are many criterias of peak R wave times of less than 75 being good enough for 100% specificity for capture. It's often in the setting of a narrow cure as normal at left ventricle. But if you look at the numbers on the distribution code, there's significant overlap on either side. You can have left bundle capture with long peak R wave time, and you can have short peak R wave times without left bundle branch capture. This is without considering distal or apical position of the leads. And same thing with left bundle branch block, similar wide spread on what your conduction time should be. And this was obtained from only a handful of patients, about 16 patients, not a lot of them had LV myocardial dysfunction. So we have to apply these criteria in the context of when and where and what type of conduction disease, and not just use them as pure numbers to satisfy that we have conduction system capture. Because all these criteria can fall apart. So here's a patient with cardiomyopathy, left bundle branch block, 145 millisecond, not a very wide left bundle. So I was pacing left bundle here, and I have what I thought was great results, was one of my early experiences, peak LV activation time of 75 milliseconds. We had biotronic vision wire in the LV to assess how well we are shortening. There was significant shortening of peak activation on the lateral wall. However, when I did his bundle pacing, you can see the peak LV activation time is only 70 milliseconds. How could left bundle branch pacing get you only 76 milliseconds? But you can see how much we can shorten the LV activation time with his bundle pacing. If only I had advanced the lead a little further to get left bundle capture, I would have gotten this amount of resynchronization. So I left something on the table for this patient, this is one of our early experience. So you got to understand what should be your ideal peak activation time. We always use his corrective pacing to help us decide what should we get. We should get at least 10 milliseconds shorter than what we would get with his bundle pacing. Again, in a patient with mixed conduction disease, very hard to decide when we have left bundle branch capture. Similar criteria falls apart. Peak LV activation time is very long. There is no R prime in V1. And then when we do selective capture, lower threshold, you can clearly see the right bundle branch block pattern. And there is significant LV shortening. But this is still not good enough in this patient. So you have to do combined conduction system pacing plus coronary sinus pacing. And this was very effective in this patient with a very poor LV function. And higher LV dilatation. So you have a lot of myocardial disease, a lot of conduction delay. So the more we encounter in patients left bundle pacing for cardiac resynchronization therapy, especially these advanced heart disease patients, you may see these scenarios. And you have to provide the best possible resynchronization for these patients in order to achieve the best results for this patient. Within six months, this patient's EF went from 10% to 50%. So the power of adequate LV resynchronization, both electrical leading to mechanical resynchronization is important. And so conforming left bundle branch capture is very nuanced. And we have to understand all of the situation and the criteria, how to apply them. And the criteria is just a guide, not absolute. There are going to be quite a few variations in this. And so we need to apply them carefully. And lastly, I want to emphasize a few things. So left bundle branch potential matters. Here's a patient, just as Dr. Wong was demonstrating. This was a patient with left frontal, sorry, L, left frontal branch pacing for AV node ablation. And I'm pacing at 5 volt, I get 78 milliseconds. But pacing, that would have been adequate, but pacing at 8 volts, I see that I have much more shortening of peak LV activation time. So I had to advance the lead a little further. Now you have great left frontal potential, which was already looking very good, but now with injury current. So now I have transition from non-selective to selective with a shorter peak activation time. So you have to assess, even if you have potential, do I really have left frontal branch capture? So that is important. And we often use his frontal pacing as our guide because of the peak activation time with his frontal pacing is 75 milliseconds. The left frontal pacing has to be much shorter. And the opposite is also true. Here's a patient with post tower AV block. I'm trying to get left frontal branch pacing and I see very small or no potential. And pacing at 10 volts, I get a very short peak LV activation time. At 2 volts, I have similar in left frontal activation times. And so threshold testing, you can see transition from non-selective to selective. Even though the potential is very tiny, what we couldn't see was that there was injury current on the potential and that was important to pay attention. You have to have adequate gain. Sometimes the potential is not very big and may be masked because of injury current and may emerge into the ventricular myocardial signal and may not see it. So even smallest of potential, presence is helpful, but more importantly, other criteria for left frontal branch capture is important. So there are limitations to left frontal branch capture. How we assess left frontal branch capture depends on the conduction disease, underlying conduction blocks, underlying myocardial disease, the amount of LV dilatation. So in order to provide the best benefit for our patients, we need to make sure we understand all of these criteria, how well these apply in each of the situation. So use them appropriately. But most importantly, confirm that you have left frontal branch capture beyond doubt so that you can provide best resynchronization, especially in those who are undergoing cardiac resynchronization therapy. Thank you very much. Thank you, Pugal. We're going to go ahead and start off with some of the questions that have come in through the chat session. I'm going to start off with a question for Dr. C.P. Lau. The question is, why don't we implant left frontal leads in everyone and just abandon RV apical pacing? It becomes a problem when patients come back with pacing-induced cardiomyopathy. They need to be upgraded, and the vein is occluded. Let's do CSP first go. What do you think about that, Dr. Lau? That might be a strategy in the future if we prove it. Currently, in my center, we are more or less doing for Brady pacing, left frontal branch area pacing in most of our patients. But we have heard, and there are also some issues on the long-term stability of the left frontal branch area lead, for instance. There are situations of fracture in some of the, because this is not particularly in the stylet-driven lead, there may be an issue. And we also see long-term complications of left frontal branch area lead, such as failure and repositioning. And we need a good randomized study to show that this is the case. C.P., can I put that question another way? You showed a lot of data where the conduction system pacing was better than bi-V pacing. Are you aware of any studies where the opposite is true? Having presented, there are lots of enthusiastic report, mostly observational, that suggest the CS pacing better than the bi-ventricular pacing. And the randomized study, as we have seen, there are only limited numbers. The largest probably is Dr. Chen's group with 200 patients, and most of them are non-ischemic. So we don't know. I think at the present moment, we have very strong data from the CRT, and that improve also survival. Now all these studies do not look at survival, and the survival group are all driven by heart failure hospitalization rather than survival. And we do not know the quality of follow-up of the left frontal branch area pacing, for instance, because while we know the thresholds are very good, we do not know whether they are quality left frontal branch area pacing. We have good data from some excellent center, but I dare say there are lots of the follow-up do not use a 12-week ECG for documentation, just to quote one example. And that put the doubt on a very severe disease of heart failure and not an effective treatment on the table. That's my opinion. Let's move on. Another question, I think it's related to Dr. Huang or Dr. Viji. So accepting left frontal branch capture is better, but if LVSP is equivalent or not inferior to CRT, which was in heart failure patients, so how can we choose in the clinical practice? So the question is, to just be specific, it is we know there's a lot of evidence that left frontal branch block pacing is the best, but how do you choose between LV septal pacing and CRT when there's lots of randomized data in heart failure patients that show CRT decreases mortality? How do you choose between LV septal pacing and Bi-V? Yeah, so that was the reason you asked me to present the topic on left frontal branch capture. So it is challenging, and that's why it's quite important to confirm left frontal branch capture. In our center, if I'm not able to prove left frontal branch capture and I only have LV septal pacing, I don't stop there. I go on to put a CS lead and probably accept as a bi-ventricular pacing as a first choice, and then add CS, the conduction system pacing lead if it makes any sense or benefit in that particular patient. But most often, if I only have septal pacing, I would not accept it, and I would advise people not to accept LV septal pacing and choose left frontal branch area pacing as a first line, because you should choose bi-ventricular pacing in those patients and cannot provide patients with less than optimal outcome. Dr. Wang, do you have a comment? In our center, we do our best to have a true airway capture except for IVC patients, IVCD. So for example, while we failed to have a true airway, we feel that those screw lead deeper enough. So we can use some new technique, for example, using electrical cut. Yes, that will help us if we know how to avoid septal perforation, damage to tricuspid valve, and or conduction system. So I use electrical cut before. We should know to increase very high output to see where there is a bundle capture. If there is, we shouldn't use electric cut. That may help us to screw the lead deeper for some patients with much scar. And in IVCD, I would try CS pacing lead when there is a necessary, if it is necessary. So it's my opinion. The next question is, what are some of the common errors in programming CSP patients? We'll start with Dr. Lau, and maybe everyone can give two or three very quick errors people make when they program conduction system pacing devices. I think when we program, there are first the threshold, for instance. And we should, it is in the guideline that we recommend careful look at the EKG to look at the capture. I think there are also the issue about the R-wave at back of the V1 or V2. This depends also in some instance on unipolar pacing versus bipolar pacing, because sometimes if you bipolar pacing capture the right septum, then you may lose the R-wave as well, in addition to what Vijay has spoken. I think there are also, remember to note that on remote monitoring, the thresholds are not reliable. So again, we sometimes get these scares whereby it looks like the lead is not capturing on the remote monitor, but actually it's just because of the algorithm of looking for injury current. Dr. Wang, any errors people make when they're programming their conduction system pacing devices that you can recommend they avoid? One of the things that we've learned in the last year or so is that when we were doing bipolar pacing and we're concerned about the R-wave conduction delay from unipolar pacing, we would often program bipolar to offset R-wave actuation. Maybe okay in patients with bradycardia, but in the CRT population with cardiomyopathy, R-wave pre-excitation from anodal capture may not be as good. And so we have nice acute invasive hemodynamics studies showing that anodal capture does not add value, even in the setting of R-wave delay, and anodal capture actually may make hemodynamics worse because we are causing R-wave pre-excitation, which we don't need. We need to maintain LV synchrony. So I've changed my practice to almost program every CRT patient into a unipolar pacing for LV pacing and avoid anodal capture. Thank you. There's a question here asking, is left posterior fascicle pacing acceptable for cardiac physiological pacing? Vijay? Sure. So it depends on where you're talking about. So often, proximal left bundle pacing can be challenging. In some of the studies, it's only about 10%. While we strive for it, the current trend is people don't use his bundle as a guide. And when you go just anatomically, more often, you're on fascicular pacing. And for CRT, we believe that proximal left bundle pacing is important. But left posterior fascicular pacing in the proximal location is quite acceptable. But as long as you don't go too distal and apical. That's my thought. And so it sort of leads to the question, how good is good enough? Because the enemy of good is perfect. And we've all been in a situation where we've given up something that was adequate, striving for something better. And when you first start doing this, you think it's you. Because you haven't done many. But once you've done a number of these, you realize it's the patient, it's the equipment, there's other factors. Yes? No, no, absolutely. You're right. It's not like we can be 100% perfect. But we start with proximal left bundle branch area. Can't get it. You can go to the left fascicular pacing. Posterior fascicular pacing is pretty good. And Ken and we have discussed on this paper that's previously published in Heart Rhythm, looking at how is the connections between the fascicular system. There's acute muscle block studies showing that even pacing slightly more distally gets into the conduction system extensively. But if you go too distal, then that doesn't happen as well. So staying proximally is good. Proximal left posterior fascicular pacing is pretty good. Dr. Wang, please. In a center, we seldom place the patient in the distal or posterior. Because at first, at early stage, yes, it's challenging to place the patient at the proximal. For example, his bundle pacing is challenging, challenging, challenging. All challenging. But now some problem have solved. So if you want to place a better pacing site, you can achieve it if you want. I think we shouldn't know. We shouldn't place the pacing leader at the diseased conduction system area. That will result in bad electrical signaling. Distal, okay. Posterior, okay. But shouldn't place the pacing leader at diseased conduction system area. We have a couple of minutes. We have about less than six minutes left. I'm going to read some questions. We'll get some quick answers from the faculty. One question, when do you pace or not pace? What sort of peer interval makes you nervous in patients with structural heart disease or without structural heart disease? When is the peer interval too long, probably maladaptive? Any answers? I would have thought the left‑sided AV interval is one of the most important to look at. You have a very early left‑sided activation, but you may have a very long AV delay. I think that could be appropriately adjusted with echocardiogram determination. Give us a number that you like when you're programming a patient or when you're thinking about where to put the ‑‑ Yes, I think, of course, depending on whether the patient requires pacing or no pacing. If he does not require pacing, perhaps we should use some form of AV pacing reduction algorithm to do that. Then it would be less critical. I would have thought normally my ‑‑ the time would be about 100 to 120 milliseconds for me. Dr. Wang, is there any benefit in checking injury current in the ring electrode? Yeah. If the septal is thick enough and pacing is deep enough, yes, we have a current of injury of myocardium from the ring. Yes, it can be. So, if there is a current of injury, there will be low threshold for right septal pacing capture. But we seldom use bipolar pacing because we don't know whether there is a better. But I will use bipolar sensation to get better AV amplitude. Sometimes for ‑‑ we'll back up pacing for safety. Thank you. Pippin, is there any data on risk of worsening TR and how proximal and distal you go in the conduction system on the septum? And is there any difference between stylet‑driven leads versus non‑stylet‑driven leads? The simple answer is no. There is a lack of data for this. There is some data for his bundle versus left bundle because one is almost an atrial lead. But for the different leads in the left bundle position, there isn't. Okay. There's a question about septal scar came up multiple times. Is there any advice you can give us for how to approach those patients other than taking the lead out and trying somewhere slightly different, different angle? Yeah, there are a couple of MRI‑based studies that have shown septal patchy scar is not something that can prevent you from doing it. But if you have dense scar that you know already, I wouldn't start as conduction system pacing in those patients because the failure rate is almost 50%, especially if you're going to do CRT in that patient. So patchy scar doesn't matter. We can still get fairly high success rates. So the last question, I think maybe what about left anterior fascicle pacing? Or maybe the different side of pacing, like posterior or more anterior? What's the difference or what do you recommend on this issue? Yeah, so our experience is that very few we get left anterior fascicle or separate pacing because it's quite anterior. It's a thin bundle and often people label anterior fascicle pacing because they have normal axis or more of a rightward axis. But that's often a situation where the lead is quite anterior, not actually getting into the septum. I tend to avoid that location. It's challenging to really define as anterior fascicle pacing. I have one more very practical question. So you're doing a patient with cardiomyopathy and an IVCD and you try, but you can't get left bundle capture. Do you think it's okay? You're going to put a CS lead in. Do you think it's okay to accept an LV septal lead? Since you tried a couple of times, you can't get the septum, you've got the CS lead. So it wouldn't be lot CRT, it would be LV septal CRT. So an LV septal lead plus CRT. Let's go down the list and see what you think. Google start us off. Yeah. So that's what we did in our original description of lot CRT study is that when you have IVCD or when you cannot get left bundle branch capture, we got long peak LV activation time. We had empirically 90 milliseconds and we didn't want to short change that patient. So we would add a CS lead and those patients did do well. So I don't think we can do harm by having LV septal and a CS lead in those patients. Dr. Wang? Yeah. I have a recommendation, suggestion. We should know whether septal pacing have a partial or complete correction of block. If not, so I think the pacing sector is more important. So I will try, in this case, I will try, I will place a CS lead first, then according the anatomy, then we decide where we should place the septal pacing site. So I would do the same. I think the only problem is that there is an additional lead and it does officially make a system MRI incompatible. So that's the only consideration. And so if it doesn't add to it, I may remove the septal lead if I get a very nice CRT ECG morphology. I think there are two options because the current arrangement is for IVCD and the RV septal pacing versus a CS lead is guideline indicated for CRT. It's actually a form of biventricular CRT, so it's acceptable. The other option, if you want to do it better, is it possible to try a Hispano pacing for better correction of the, at least of the proximal part? Thanks, everybody. We're out of time. I'd like to thank you for coming to this joint session. It's the strength, the collaborations between Heart Rhythm Society and Asia Pacific Heart Rhythm Society. It's been great to have a combined faculty, combined chairs, and I wish you well for the rest of the meeting. Thank you. Thank you for joining this live session from Sydney, Australia. Please log into HRS 365 for a recorded webinar.
Video Summary
The session at the 17th annual Asia Pacific Heart Rhythm Society meetings in Sydney focused on advancements in catheter and conduction system pacing technologies. Discussions included various ablation techniques like bipolar radiofrequency ablation and comparisons of cryo versus radiofrequency ablation for atrial fibrillation. The presentations also explored pulse field ablation (PFA) innovations, including zero-fluoroscopy procedures and the study of coronary impacts post-PFA.<br /><br />The session on conduction system pacing, a joint effort by HRS-APHRS, addressed current controversies and explored evidence from new guidelines. Dr. C.P. Lau highlighted how randomized trials show that cardiac resynchronization therapy (CRT) reduces heart failure symptoms, hospitilizations, and improves outcomes, though challenges like pacing-induced cardiomyopathy remain critical considerations.<br /><br />Another significant point was the evaluation of lead technologies, especially comparing stylet-driven leads with luminous leads in conduction system pacing. Discussions assessed implantation techniques, the durability of pacing leads, and potential complications, noting the need for improved handling instructions.<br /><br />Additionally, the importance of true left bundle branch pacing was emphasized, showing superior outcomes in terms of ventricular synchrony and patient prognosis. Various strategies for optimizing pacing conditions, such as AV delay adjustments and innovative lead placement techniques, were highlighted as critical to improving patient outcomes. Practical programming considerations and nuanced decision-making based on individual patient conditions were advised to ensure effective therapy delivery. <br /><br />Overall, the sessions underscored the necessity of continued innovation and rigorous data to refine practices in cardiac rhythm management.
Keywords
APHRS
HRS
2024 Scientific Session
catheter ablation
conduction system pacing
bipolar radiofrequency ablation
cryo ablation
pulse field ablation
His bundle pacing
left bundle branch area pacing
cardiac resynchronization therapy
heart failure
electrical synchrony
arrhythmia management
ventricular tachycardia
atrial fibrillation
procedural efficacy
lead stability
guidelines
patient outcomes
Asia Pacific Heart Rhythm Society
catheter pacing technologies
cryo versus radiofrequency ablation
zero-fluoroscopy procedures
pacing-induced cardiomyopathy
stylet-driven leads
luminous leads
left bundle branch pacing
cardiac rhythm management
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