It's my distinct pleasure to introduce you to this esteemed group that will talk about conduction system pacing, including a smattering of cases that will deal with his bundle pacing. On behalf of my co-chair, Dr. Jianggang Zhu, and myself, Jay Korneru, I'm from Virginia Commonwealth University Medical Center, I'm the fellowship program director there. It's my pleasure to introduce our first speaker, Dr. Bengt Herweg, who will be presenting some interesting cases and difficult implants. And as a general theme, I would suggest that we have a QR code questions. You can send the questions at the end of all three talks, we'll deal with the questions so that we have enough time for all the speakers. Thank you for having me. I'm extremely pleased to be here and honored to present together with the people who have essentially invented this here. So I have three cases. First case is a 64-year-old female with non-ischemic cardiomyopathy, left bundle branch block, that preceded the onset of cardiomyopathy. The EF in 2011 was 50%, and then by 2017 the EF was down to 30%. Heart failure symptoms had occurred. The patient was transferred to our heart failure service and started on guideline-directed medical therapy, normal heart cath, cardiac MRI, EF 30%, no LGE. And the patient then was referred to us for device therapy. And this is the ECG. A notched QRS complex, mid-QRS notching, suggested left bundle branch block. However, in the lateral pericordial leads we have deep S waves, very deep, too deep for a left bundle branch. So this is probably a left bundle coexistent with an IVCD, and there's also left axis deviation. So the question is, is this really a candidate for conduction system pacing? So the patient refused ICD implantation, and she agreed to have a resynchronization pacemaker. So we basically started with a C304 deflectible sheath and tried to put a left bundle lead in. So we first mapped the HISS area here, and high output pacing up to 10 volts did not recruit the left bundle. We then moved on to the left bundle area, screwed the lead in there about two centimeters towards the apex, and got these fixation beads here. Fixation beads quickly progressed in their morphology to a right bundle pattern, and we stopped the screw at that point. And then three volts at 0.5 milliseconds, V6 R wave peak time of 70 milliseconds, and R prime and V1, the limb lead axis had actually normalized, and there was no notching in the lateral pericordial leads, QS less than 130. So likely left bundle capture. So this is a threshold test here. You can see left bundle pacing up down to 0.75 volts, and then when we went down to 0.5, we only had capture of the left posterior fascicle, only selective capture. So there were two QS morphologies we observed during the threshold test. You can see them here. The QS widened at less than 1.25 volts, and it was a right or right bundle morphology, and there was the same V6 R wave peak time. So that was a transition from a non-selective to selective left bundle pacing. So here's the lead position in the septum, and also in the apical four chamber, threshold 0.5 at 0.4, impedance 703, nice R wave. And this is the ECG after implantation. Narrow QS complex, and we basically did a fusion optimization with intact right bundle conduction. Sensed AV delay 60, paced AV delay 1.3, and you can see here these deep memory T waves that we like to see. And this is the ECG six month follow up. At that time, memory T waves had disappeared. The QS was still narrow. Lead parameters were unchanged. The EF had normalized, and the heart failure symptoms disappeared. So the learning points with this case, atypical left bundle branch block, so coexistence of IVCD with left bundle branch block is not a contraindication to conduction system pacing. Left bundle branch block may actually amplify an IVCD, and the correction of left bundle branch block should improve a coexisting IVCD, and I'll show you a cartoon in a minute. The other issue is that left bundle branch block induced cardiomyopathy has recently been looked at in a observational study, and they reported a super response rate in a small number of patients of 100% with left bundle area pacing. That's what Dr. Punasamy, and this is a remarkable observation. Not everybody with a non-ischemic cardiomyopathy may need an ICD, and this patient got a dual chamber pacemaker, and there's currently no indication for freestanding dual chamber pacer as a resynchronization device. So there are different manifestations of IVCD. These are cut letter diagrams. This is normal conduction left on the top, right on the bottom. You see normal hyspokinic conduction. This would be a freestanding IVCD, just slowing of conduction on the myocardial level, a freestanding IVCD. So now IVCD can also manifest itself in conjunction with left bundle branch block like in our patient here, and it would look like something like that, or it could even manifest itself with pacing. None of this has been electrocardiographically defined. So if I show you here a cartoon on the left side, you see intact bundle conduction, a small scar in the lateral wall. Not a big deal. However, once bundle branch block occurs, like in the second cartoon, you see now that the impulse has to propagate through the scar, and the lateral wall gets activated ultra late. Same is true for pacing. On the right-hand side, the attempts to correct that. So conventional CRT would look like something like this. So with an IVCD, there is slowed impulse propagation. The QAS is wider, so we cannot correct that with conventional CRT. Let's look at the mated CRT data that looked at an ICD arm and a CRTD arm, and left bundle branch block fared much better in terms of heart failure, hospitalization, and death in the CRTD arm. If you look at these now separately, left bundle branch block, the heart failure, hospitalization, and death decreased, but in IVCD, it actually increased in the mated CRT trial. So it remains to be determined how this will pan out with conduction system pacing. Case number two, a 69-year-old male. Aortic stenosis, status post TAVR. Coronary disease, remote cabbage, atrial fibrillation, and tachybradysyndrome. Fatigue palpitations and neosyncope. The Holter monitor showed sinus bradycardia more than 35% of the time, and nocturnal two-to-one AV block. There was also some non-sustainability. The echo showed a normal EF, but mild to moderate LVH. So this patient had a pacemaker indication and got a pacemaker. This is a baseline ECG, sinus bradycardia, first degree AV block, and ARQAS. The PR interval is 220 milliseconds. So the procedure we used, again, a typical C304 sheet. His was located, and you can see here the TAVR cage. It's actually a good landmark. The lower corner of the TAVR cage usually indicates where the his bundle can be recorded. Obviously, it depends on the TAVR prosthesis a little bit. It can be used as an anatomical marker. So then we mapped, basically, the left bundle area, about one and a half centimeters towards the apex from the his recording site. I want to go briefly through the ECG criteria that we observed here. So there's notching in V1, and that notching should be mid to late in the QIS complex. And then there is an AVR-AVL discordance. AVL should be down, and R should be up. That's important. If it's positive concordance, you're to apical, and if it's negative concordance, you're to basal. Then the voltage in lead two was bigger than three, and there's minimal notching in the lateral pericordial lead. So this is a good site to start to drill, okay? So that's what we did. We advanced the lead into the septum, and this is how it looked. There was an RSR prime pattern in V1, but the QIS complex was wide, particularly considering the narrow QIS at baseline. There was also minimal lateral notching. So this was not good enough, considering the narrow baseline QIS, besides that the V6 are at peak time, 85 milliseconds. QIS paced 150. So we moved on. So this site two, we are now about half a centimeter more distal to site one. You can see the RIO and LAO views here. And then you see in the RIO view, we have a two o'clock or 30 degree position there, or angle of the lead. We have some hinging that's being seen with systole, and then you can see the lead is probably about approximately two centimeters in the septum now, and we know that because of marker. It's 101.8 centimeters, the distal marker. And this patient has LVH, has a thick septum, but this is probably well into the septum. There was an impedance drop from 1,000 to 650 ohm, quite brisk, so that concerned me. And the fixation beats now we observed, showed a nice RSR prime pattern, but they were wider than the beats, the baseline conducted beats the patient had. So that concerned us too. Lead parameters looked okay, but the impedance drop worried us. I don't have the local electrogram, but I can tell you what it looked like. It was a QS complex. And if you see a QS complex on that electrogram and your injury is gone, that should concern you. And although our RVF peak time was good, the paced QS was wide and we abandoned because we were afraid this was a microperf. So we moved on to site three. Kind of went counter-clock a little bit, withdrew the lead and then went right back into the septum. And here you can see the difference between site two and site three. It's barely any different for scopically. In the LAO view, identical. And now the lateral notching is gone. The V6 RVF peak time is 60 milliseconds. So we thought that this was a nice result and we took this position. So what are the learning points in AV block, left bundle bench block after TAVR? The AV block frequency is high, particularly with self-expanding valves. New left bundle bench block occurs in 50 to 70% of the patients. So frequently these people need pacemakers. More distal left bundle area pacing is a preferred technique in TAVR patients with proximal mechanical trauma and compression. After TAVR, conduction system pacing has better clinical outcomes than right ventricular pacing. And that's what recent smaller observation studies have shown and left bundle area pacing fares better than his bundle pacing in this scenario. Further, I have reviewed the ECG parameters to find the landing zone where we start to drill and you should take note of those and try to achieve those as extremely helpful. And if you have a high level of suspicion for a perforation, even a low one, just reposition. The perforation acutely is not a big deal, but on the long run, it's not a good thing to have. So my third case, a 58-year-old female on ischemic cardiomyopathy. EF is 24 and the patients are milrinone, inotrope dependent. Atrial fibrillation, status post ablation times three. Increasing AFib burden, recently persistent atrial fibrillation. The patient has a CRTD already and recurrent admissions for heart failure. So we're really in the corner here. This is a baseline ECG, AFib with RVR. The QIS, the conducted QIS, 130 milliseconds. And then the patient has a CRT and when he's pacing, actually QIS doesn't look bad. There's a dominant RV in V1, the negative complex is in one. QS duration is 140, so not too bad. But these patients in AFib will not have fused CRT. Adaptive CRT is not an option. So we put a left bundle area pacing lead in and we try to achieve lot CRT in this patient and our plan was to ablate the AV node. This is a lead position and the left bundle lead was inserted into the atrial port. That's free in a patient with atrial fibrillation. And the left ventricular lead into the LV port. Here are the recorded electrocardiographic morphologies for bivy pacing, RV and LV on the left side and for left bundle pacing on the right side. And you can see here the QS duration with left bundle unipolar pacing is 109. And then with lot CRT, once we had optimized this, advancing the atrium where the left bundle lead is to the LV by 30 milliseconds and then the LV to the RV by another 30 milliseconds, we got this down below 100 milliseconds. So this is the ECG. I think that's a fantastic result. After AV junction ablation, this looks like a normal ECG already, right? Left bundle lead, non-selective capture in the atrial port, AV delay 30 milliseconds, left ventricular lead, LV port, VV delay 30 milliseconds. And this is follow-up. At one month, EF approved, volumes down, left ventricular end diastolic volume down. And also the milrinone was discontinued. No recurrent hospitalizations, class two of milrinone. So we were very pleased with this. So the learning points here. Hot and lot CRT is a good option in patients with complete heart block, which precludes fused biventricular pacing. That includes after AV junction ablation. So those people are not candidates for adaptive CRT. In CRT non-responders with preexistent left ventricular lead, even if the left ventricular lead may be in a suboptimal position, it could be in the apex, you can still include it. In patients with AFib, the atrial port is available. Remember that. And in patients who have coexistent left bundle branch block and IVCD. These patients may have a long V6 RVF peak time during non-selective left bundle area pacing. Remember that left bundle area pacing is most of the time non-selective. So if your conduction system or your myocardium is diseased distally and you can't get the activation time down, consider to add a conduction system lead. And you can maybe combine it with a left ventricular pacing and we may be able to further narrow the QIS complex. Thank you so much. Thank you. Yeah, we have we have looked at this and this pattern in multiple patients and you know when I see cubes particular QS Complex and a lateral pericordium I get really I don't think it's a clean left bundle anymore But I agree with you that lead position can definitely make a difference, but this was present on multiple ECGs Thank you for the presentation just on the last case Just to clarify could you talk us through? When you put the left bundle, did you put it in the atrial port? Did you exchange? What did you do exactly in the last case? I? Put the left bundle lead into the atrial port in an ICD device. It can only program into bipolar That's important Sometimes that doesn't work because you've been bipolar, you know may have a different QS morphology, but the atrial port is available So if you have given up on AFib, you can utilize the atrial port for the left bundle lead So, how did you program the device? We programmed the AV delay to 30 milliseconds and the interventricular delayed also to 30 milliseconds advancing LV So that advanced left bundle in front of LV by 30 milliseconds and then LV in front of RV by 30 milliseconds Yeah, the story then becomes very complicated Then we have to resort to put one of the leads into the Port of the device that's only possible if you have a trifocated lead right with three adapters We have gone so far in some patients to remove leads If they were not that old and put a trifocated lead in that then allowed us to do that Remember that you don't have any MRI compatibility with this Okay, because you're capping a port of the lead so you're losing MRI compatibility That's all less than optimal. So we can only hope we will have devices Okay Next we have dr. Zanno from Italy to present the second case Dr. Zanno is a very Famous exporter he's a distinguished So, these are my disclosures. So, just a small introduction. His bundle pacing is a challenging procedure. Why? Because it's a small target area, it's in fibrous tissue. So, everybody know that could be challenging in locating, could be challenging for electrical parameter. That for many years there was just one tool with the flexible delivery system. Then after a year, many companies introduced different tools, making the procedure much more popular. Then on the other side, thanks to Dr. Wang from China, he discovered the possibility of pace, also the left bundle. And so, another approach has been available. And making the conduction system, so changing also the name from his bundle to conduction system. But, of course, also to have a good pacing modality is also essential to know the electrophysiology, also the different change. So, just to go to our case report, is a man of 70 years old. He was discharged for internal medicine in Howard Hospital with diagnosis of syncope in patients hypertensive cardiomyopathy and permanent AF. Was implanted a loop recorder. And when we analyze loop recorder, we see a very rapid arterial fibrillation and a significant pause, more than five seconds. So, there was a clear indication for pace and ablation, subsequent AV nodal ablation. The patient, with the other things, was obese, smoking hypertension, normal ejection fraction, and a mild, a little bit more than mild arterial dilatation. So, implant procedure, and then I describe with a movie. So, I think it's better just to go to the movie. So, it's six minute movie in which I will show you. So, our technique is mainly based, you can see here the loop recorder, is mainly based on when we look for his bundle on fluoro, minimal or even no fluoro. In this case, you use just a little bit of fluoro. And why, what we look for in the, in red is the filtrate and in white is unfiltered electrogram. So, it's clearly, you can clearly understand that because it's on QRS, we are in the ventricle. And the mapping, these are my hand and you can see that my movement is very, very gentle movement with the left hand that move the delivery system and the left hand that just pull and push. In this case, we use not the standard 3830, we use the 3D, the selector 3D with the solia. And we just push and pull the lead just to understand if you are in contact with the myocardial tissue. And we move on. And here, you can clearly see that, look, here what happened here is clear. You are on the, on the tricuspid lift because you have a ventricle and atrium. Okay. So, move, move again. And here, we observe an adhesive deflection with an HV interval of 42. So, after that, we screw and, and paste, we start screw and paste. And at this moment, we have this nice indicator of, which is the interval between the hiss and the LVAT or peak wave in, in V6, which is equivalent to the stimulus air wave. So, we did the, we performed the testing. And we see two different capture. And I will show you here better. Okay. So, if you look, those are pacing. This is non-selective because, why non-selective? Well, if you remember, from the H to the peak of the air was approximately 90 milliseconds. And now, it's the same. And now, in this case, it's more than 100. What does that mean? It means that we lose the hiss capture. This is just only myocardial capture because there is more than 20 milliseconds. Okay. And this is what is the changing from non-selective to just myocardial capture. After that, we, we did more turns. You can see. And then look here, this is a China loop. So move to a slow velocity on the AP system, just to understand what we are doing. And here we observe that we are now in from this, this one is the native one, and this is the pace in selective wave. So approximately the distance is the same, 84, and before it was 88, so more or less we are on the same. And we observe from 3 to 2, here is clearly capture also of the myocardium and here is isoelectric, so is selective. The interval between stimulus and air wave is approximately the same, means that we are capturing. And also, if you go, we observe another interesting thing that is the injury current on the filtered and unfiltered. We can see better now on this one. Look here, this is the unfiltered and very big lesion on unfiltered. So we were really satisfied, good parameter. Good parameter, so we just usually wait a little bit for lead stabilization, not so many minutes. And after that, there was a reduction in the small reduction after a few minutes. the after removal, we did not observe, look here, we did not observe any macro dislodgement, okay? But surprise, we have to wait for a, not for a coffee, nor for the cappuccino. You know that Italian are very fond of coffee. So look here. After that, we taste again, and surprise, a very wide QRS complex due to micro dislodgement. And also, if you see the electrograms, which will appear now, look. Also, you can see the difference between the electrograms. If you remember, before there was a big ventricular electrograms, and now is completely different. So we have just capture of the cell, of the septal. So what we did is, move on, look here. We started, and this is an important message, to know the different tool, different tools could help. So at the beginning, we choose the selector 3D. There are three different curves. We choose the so-called small one, which is 40, 42. And now we change for the medium one, which is 50, 50, 42. And now we are going down, and try also to go for. approximately near, just a little bit down, in a more distant position. And we observe also, in this case, a small, here, a small lesion, quite heavy. This is the second attempt. Perfectly, again, the distance between the hiss and the air wave is 90. In this case, the stimulus is approximately the same. So we were very happy. and 5 volts, 4 volts, 3 volts, and lose or capture. So that's selective, 3 volts, no capture. So the strategy at that time was a changing approach. So we commonly say we go down. And here, we go down. We move. We don't use the RIO projection. I know that many also expert use the RIO. We just use the LAO projection. So look here. And why? Because we always do contrast. And you can see the syringe in my hand. I just perform a sort of an angiography here. You can clearly see the tricuspid valve. Here is under the cuspid. Here is clearly seen the triangle of caulk, approximately here. To the apex, there is the previous hiss. There is the left bundle lead that we're going to try. So we try to screw. Look at my hand now. What we do is a rapid turn with two hands. But look, the lead goes a little too high and we did not observe any fixation bead. So probably we were a little bit too high. So we move. You have to know that you have to be maybe more perpendicular. And now look here. Now we are going a little bit down and flush again with contrast. This is the syringe and this is the second angiography. And you can see that we are a little bit down a few millimeters. Always remember to flush with saline solution just to clean the contrast. And then now, again, rapid turns. Look at my hand here. It's very, very rapid and immediately appear here a run, I would say, a run of 1, 2, 3, 4, 5, 6, 7, and the end, look at this one. And so now when I see this one, airwave in V1, I stop. That means that we are on, and this is, you can better appreciate. So starting here, you look for a left bundle morphology means that you are solicitating the right part of the septum. So approximately, we imagine that here we have a small, I don't know if it's. and the inter-pick. So in terms of what was published, index is less than 75. Again, there is also, when we move from five to one, we observe a small jump of, in this case, 12 millisecond. And we always do also an angiography to confirm. In this case, probably is a little bit point to the higher part, it's not so perpendicular as we would like, but the result was quite satisfactory. And yeah, it's removal. So, final points. I think that the main message is that we have to have knowledge of what, of different approach, so there is not only left bundle which seem to be the most popular from cardiologists. So if there is still this bundle, so there are two approaches as to know, you have to know different tools because there is no, as in this case, we couldn't have a proper position with one delivery system, so we move to the other. And also, you have to understand the electrical signal and the HEG criteria. Thank you very much for your attention. Well, to be honest, we had some problem. We use both, stylet and non-stylet. To be honest, at that time, we didn't have any non-stylet. So I was forced to use what we have, of course. But particularly, what you mean is difficult to penetrate. But I find that I use all the three different companies that are stylet-driven. And it appeared to me that the stylet is more stiff, so you have much more support. And also the stylet and the body, which is a little bit big, is more easy to do rapid turns, like in this case. You have seen that in two seconds I penetrate. Because it's much more easy compared to 3830. But, you know, I think that you need to know all the different tools and apply them. Next up is Dr. Weizhuang Wang. He's an electrophysiologist at the First Affiliated Hospitals. Please take a chance at the end of the talk to ask questions. These are legends in the field, some of the first people who have ever done this procedure and refined the procedure for all of us. So please take a chance to engage actively and ask questions. It's a very rare opportunity that you'll have such experience on conduction system pacing here. Good afternoon, Chairman, and it's my pleasure to be here to present a case. I'm Weizhuang Wang, First Affiliated Hospital of Wenzhou Medical University, China. And today I will share a demo-level case. No disclosure. And she's male, 77 years old, previously myocardial infarction with coronary stenting 80 years ago. He complained dyspnea for five days. The diagnosis is ischemia, cardiomyopathy, and heart failure. And his ECG, we know this is a typical left bundle branch block. There is a notch at mid. So I believe this can be corrected by conduction system pacing. This is a coronary angiogroup showed no severe stenosis. And this is echo, showed ejection flushing is 34, and MRI showed scar in the septum. So I think this challenge for us to advance lead deeper into left endocardium. How we should do. Yes, the patient need ICD for primary prevention and cardiac resynchronization therapy. Yes, it's no problem. But what pacing mode we should we select? In the center, we always try his bundle or left bundle pacing first for this patient with typical left bundle block. Because we have more than 95% of success. So we usually perform his mapping, not to find his potential, just his mapping. It's very easy for us. Usually 10 seconds, okay. And then to see where the left bundle branch can be corrected with his bundle pacing. It's very important to see whether there is a distal conduction disease. If there is anterior, fascicle, or posterior, we should place the lead not at the diseased conduction system area. That's very important. So we found left bundle can be corrected by his bundle pacing. And also with nearly normal electrical access. And also, because this is a live demo case, we performed tricuspid valve angiography to see where the details of tricuspid. That will help us, especially if you are new practitioner. And first slide for his bundle pacing. Here, very proximal. With current injury, that's very important. That means the pacing lead at right ventricle. And not at tricuspid valve. If we place the lead at the valve, no obvious current of injury. And in the center, usually, if potential is recorded, we don't start screwing the lead. Because we believe potential is right bundle branch potential. If you perform it, there is a high percentage, high incidence of right bundle branch block. And this is second slide for left bundle branch pacing. And then we paste to see whether the electrical access is nearly normal. Because except besides left bundle branch block correct, we also try to get QRS complex with nearly normal electrical access. And then we failed. Because SCAR. And then we try to add, deliver sheath support. So we use sheath-in-sheath technique. But it's no help. Still failed to achieve left bundle branch pacing. And then we map many area for left bundle pacing. No current of injury myocardium in loss of ventricle septum. So that means SCAR. Why no current of injury? If you try to screw lead deeper in area with no current of myocardium, that means you will fail. We can see. Turn the pacing lead. Then release. Turn back fast. The pacing lead is stuck in the fibers. Fibers. So we should give up. We have to give up. At one point, we screw the pacing lead deeper. But we know at right ventricle site. Because failed, we tried his bundle pacing. Deliver sheath is Biotronic 3D 50 file. But we get high threshold, 3 to 5. This is selective. His bundle pacing. Because maybe right bundle branch injury. I don't know. But we increased output. Right bundle branch block can be correctable. Then I screwed the pacing lead deeper. We get lower threshold, about 2 volt at 0.5 milliseconds. Then we withdraw the deliver sheath at right HM to see whether the threshold can be decreased. the pacing leader is fixed better. It's very that the picture told us we have a good fixation and then we have a threshold 1.3 to 4. It's acceptable. But in the center, then we can use dual technique, dual lead technique. His pacing leader guided LV pacing implantation. That will increase success rate. So we mapping at this area to find whether there is a high amplitude of current of injury to see whether we can screw it deep in. So we find here there is an obvious current of injury. Then we try to screw lead deep. We found we have a left bundle capture with a typical right bundle block pattern and have a shortening L stimulation LVAT. It's true left bundle capture, but with high threshold. The threshold is 2.5 millimeters. The depth of the pacing lead is about 4 or 5 millimeters. Sorry, 9 millimeters. Then I tried to turn the pacing to get reach deeper. Then there is a premature ventricular couplers like right bundle right block pattern and there is a potential before ventricular activation. That will indicate we success. We will have a low threshold and stable. That's very important. Important than instant threshold of low instant low threshold because we know why we have a low threshold. We have a right position. What is the right position? Potential with current of injury. It's very clear there is a potential when there is a premature with narrow cuirass complex, but in wide cuirass complex, no potential can be observed. Then we withdraw the deliver sheets to right atrium. Then threshold test showed 1.8. At last his bundle pacing threshold is 1.3. Left bundle pacing threshold is 0.7 volt and other amplitude 8. So what we do next. Bose pacing lead is keep kept. Yes. His bundle pacing connected to LV port and the left bundle branch pacing connected to right ventula port. How to determine lead stability? Pacing parameter yes, but if you get potential that's important mark for lead stability. And how to determine initial site for left bundle pacing? Yes, we have performed his bundle pacing according fluoroscopy and but just for fluorescence is not suitable for abnormal anatomy. For example large and or vertical heart. So Tri-Cosmography Angiography is relatively precise position for us and eyes or 3D mapping is not practical now. And but I think characteristic of a paced morphology and e.g. is the most important step because for example if there is a potential then you screw that will cause right bundle branch broke. And no current of injury that means scar or Tri-Cosmography. And also if you want nearly normal cost complex you should try to pace then to compare paced morphology of cause complex to native cause complex. Or to to see whether conduction block can be corrected. So how to avoid it Tri-Cosmography damage is very important. So let me make a summary. Advantage of proximal left bundle pacing especially in heart with scar. Yes because this toe with scar but proximal maybe we have a central fibers body, but you can try to avoid central body. Please advance the pacing leader to the left. Yes, we can do. If you try you will have an experience. Dual leader technique will help us to precise position. And I also for this patient his bundle pacing plus left bundle pacing I think there is no absolute right or wrong decision. I'm not sure but his bundle pacing with left bundle pacing is a choice to improve interventional synchrony. We should know site for left bundle pacing no potential high amplitude myocardium pacing is very close to normal ECG. Thank you for your attention. On behalf of my co-chair Dr. Xianggang Zhu we thank you all. It's open for questions. Any questions that you have? A question about staying proximal on the left bundle. Clearly there are advantages to pacing proximally in terms of achieving better synchrony. But there may be at least some theoretical concerns about pacing very proximally. You are more likely to tether the septal leaflet of the tricuspid valve and if God forbid you hit the septal perforator it's likely to be a bigger perforator more basally than more distally. So there may be some theoretical reasons why you may not want to be very basal maybe a little bit more towards the mid septum. Does the panel have any preference or concerns about being very basal very close to the common bundle? I just told because this patient with septal scar we failed in distal area. So we try proximal area. But in our center we always try left bundle pacing at the proximal area. You can see our paper. Our paper showed the left bundle pacing showed normal electrical access compared reported by other center. I just told you should need experience because proximal left bundle pacing need precise position. Not wide left bundle pacing. Not wide area conduction at distal. So we need his bundle area to guide us how we can success. Dr. Wang, thank you very much for this case because I'm always embarrassed if it happens to me I perform his bundle pacing and then I have a right bundle branch block. Okay, if it's always there during pacing and without pacing then I just damage the right bundle. That's easy. But sometimes you can have with pacing a right bundle branch block and if you stop pacing there is a narrow QS complex and I implanted a lead at his. So my only explanation but it's I have no idea what's happening then is either there's a very high division between right bundle and left bundle and by chance I think I got the distal his but I was stuck into the left bundle directly that can happen and you could show see on your slides also that you when you don't have a current of injury then you screw a little more and you get a little bit deeper. So sometimes I think if you have a more or less naked left bundle that perforates only later to the left side then you can also target the left bundle inadvertently when you think you do his bundle pacing. What do you think? Difficult. Yeah. Very difficult to answer because maybe language but we know if you would if you wanted to let damage right bundle branch lastly we should place the pacing later posterior because we know right bundle is located relatively anteriorly. So this is the first and the second I never tried to screw the deeper lead deeper with potential at right ventricle. This is very important. For example, if you have a clear with current of injury of local myocardium, I believe this is right bundle not his bundle because we know his bundle at the ventricular side usually located left So cannot be recorded a potential potential recorded at right ventricle I think this is right bundle not left bundle. So in a sense now there are less and less incidents of right bundle branch damage. So one other thing potentially one can do is high voltage and low voltage pacing unipolar and if your QRS morphology changes with high voltage pacing versus low voltage pacing but your LVAT remains constant so you could potentially go deeper to get more selective because you're removing that virtual electrode effect. I mean it's a nuanced question, but I think it's great. Thank you very much to all of you. Thank you all

conduction system pacing

left bundle pacing

resynchronization pacemaker

non-ischemic cardiomyopathy

aortic stenosis

transcatheter aortic valve replacement

AV block

His bundle pacing

ischemic cardiomyopathy

cardiac function