So, good morning, everybody, and welcome to this first session of the day on atrial resynchronization. My name is Haren Buri from the University Hospital of Geneva in Switzerland, and I'm very happy to co-chair this session with Dr. Vettigay from MassGen. We have an expert panel of speakers today who are going to be covering this really interesting topic, I think, of atrial resynchronization. Just before we kick off with the first speaker, please pick up these nice sunglasses. You won't need them very much outside today, I think, but you'll need them for this session because our first speaker, who's Dr. Mori Shumpei, will be presenting anatomy and EP of the atria. So, please, Dr. Shumpei. Please, Dr. Shumpei. There we go. There you go. Thank you very much. If you just come in and grab the 3D glasses, please. Thank you very much for your kind introduction, and good morning, ladies and gentlemen. It's too early to wear the glasses I am going to announce. So my topic will be the anatomy, and mainly I'm going to talk about the anatomy related to the Bachmann's law of pacing. So there's three inter-atrial-epicoidal connection. One is the Bachmann's bundle connecting between the medial right and left atria. The second one is the inter-cable bundles connecting the sinus benarum with the antrum of the right pulmonary vein. And the last one is the coronary sinus musculature connecting to the posterior wall of the left atrium. The physiological contribution of these three fibers to the inter-atrial conduction is not identical. I mean, the Bachmann's bundle plays a major role for the inter-atrial conduction, as you can see here, as the anterior breakthrough to the endocardium. In other words, it is also deemed as physiological to see this kind of a slight delay. I mean, like a 40 millisecond of inter-atrial conduction delay can be the physiological. The left atrium exhibits multilayered and multidirectional myocardial orientations, as you can see here. The Bachmann's bundle between the right and left atrial appendage is located in the most epicardial side, facing to the transverse sinus. This is the human sample showing the micro-CT. The Bachmann's bundle viewed from the epicardial direction, and here you can see the sinus node artery running in oblique fashion on the Bachmann's bundle. The multilayered myocardial orientation can be appreciated like this. We are going from the epicardial side. The horizontal myocardial fiber of the Bachmann's bundle suddenly changes to the vertical orientation, also referred to as septatrial bundle. When viewed from the superior direction, the Bachmann's bundle is like an epicardial-myocardial bridge over the anterior inter-atrial groove. When viewed from the LAO cranial direction, the Bachmann's bundle is located here between the right and left atrial appendage. With trans-illumination, you can see the beautiful three-dimensional course of the Bachmann's bundle, which is continuing from the crystal terminalis, carrying the sinus node, continuing to the pre-cable bundle here, and connecting to the Bachmann's bundle here, and it separates into posterior and anterior myocardial fibers surrounding the left atrial appendage. Like this. Therefore, from the viewpoint of anatomy, the optimal target region for the Bachmann's bundle pacing is here, on the inframedial side of the superior vena cava. With this image, I also would like you to see two more things. One thing is here. What is this? This is the left sinus node artery running on the epicardial surface of the Bachmann's bundle. You can expect in 50% of cases. Another thing. This is my dissection. Before this dissection, I need to remove the entire ascending aorta, because it blocks the view. That means this region is facing adjacent to the ascending aorta, or it is facing to the transverse sinus. What is a pre-cable bundle? When viewed from the frontal direction, pre-cable bundle is like an arch-shaped continuity of the crystal terminalis. Before merging to the Bachmann's bundle, here you can see the right sinus node artery. Viewed from the posterior direction, the pre-cable bundle can be observed as the inferior anterior wall of the SVC extending from the lateral sinus node region to the medial region before merging to the Bachmann's bundle. With this image, you can also appreciate the three-dimensionality of the pre-cable bundle to the Bachmann's bundle. That kind of three-dimensionality can be readily observed when you observe the heart from the inferior diaphragmatic direction. This is the virtual dissection of the human heart. When you view the heart from the inferior direction, you can see the SVC orifice, crystal terminalis, and pre-cable bundle running toward the left anterior direction towards the ascending aorta. Here is the pre-cable bundle. There are multiple components related to this pre-cable bundle. One is the sagittal bundle, running towards the free wall of the right atrial appendage. The major component is directing toward the ascending aorta. Finally, this component is continuing to the Bachmann's bundle, which is running towards the left posterior direction. This is the endoscopic view of the human heart. This is not a 3D image. It's too early to wear the glasses. Please. This is the pre-cable bundle. It suddenly changes direction. This is not a 3D image. It changes direction towards the Bachmann's bundle. These two bundles are located near the orthogonal. That kind of anatomy can be readily appreciated using the regular cardiac CT. You can see here the pre-cable bundle, like the anterior wall of the SVC, and continue to the Bachmann's bundle by changing its direction, like this. In the LAO reconstruction, you can see the Bachmann's bundle here as the bridge over the anterior inter-atrial groove. In the previous study by Professor Salermi in USC, the size of the Bachmann's bundle is measured 6.1 by 4.6 in width and thickness on average. Of course, this is thicker than the average left atrium wall, but still be such a small region of target. If you can see the Bachmann's bundle with CT, you can potentially reconstruct this kind of image. This case shows an 11 by 4.8 millimeter Bachmann's bundle. I mean the right side insertion of the Bachmann's bundle. Why is this important? Because the procedure should be performed under fluoroscopic support. So this kind of reconstruction also gives you the information about, first, the relative location of the target area within the cardiac silhouette. It can tell you the unfussed view and the tangential view of the target region. Getting such kind of information is fundamental for any intervention procedure. under the fluoroscopy. And also it can tell you the relationship with the surrounding structures, including the sinus node artery, as well as the ascending aorta. You can see how it is close between the target region and the ascending aorta. And if you use only LAO, the ascending aorta and target region is not separated because of the significant fluoroscopic overlap. The potential collateral injury, therefore, includes sinus node artery injury. Then you may think, it doesn't matter anyway, you are going to place the atrial lead. But as I said, this region is facing to the transverse sinus, so you can potentially create cardiac tamponade if you perforate this artery. Right sinus node artery, if it's taking the retro-cable course, or left sinus node artery, if it takes the pre-cable course. That can be appreciated where the CT data sits. Also, this is a virtual facing lead. The sky blue is a virtual lead facing regular right atrial appendage. The yellow green is a virtual pre-cable bundle facing lead. Yellow is a virtual Backman's bundle facing lead, and red between them. What I would like to say here is because the pre-cable bundle and Backman bundle is nearly orthogonal, so virtual lead could be nearly orthogonal. And because the right atrial appendage is in the same direction with the pre-cable bundle, this virtual lead between yellow, green, and sky blue is almost parallel. Anything between yellow, green, and yellow is facing to the ascending aorta. It is this red region. It indicates potential risk for scratching the ascending aorta. I'm saying this not to discourage this procedure, but one of the main purpose of this kind of session is to expand the procedure. We also have the responsibility to prevent some nightmare thing from happening. So please wear your glasses. Red for your left eye, please. Otherwise, you will not see any 3D. You can pause in bidirectional, but please place red one. Give me a few minutes. Yeah, every time I see this view from this stage, I think what I'm doing right now. Okay. So I hope you can see, feel the 3D, and feel the 3D. So I hope you can see, feel the 3D. The angulation matters. Maybe you scoot to the left side. And if you shake your body or head like this, maybe you can feel 3D much easier. So this is my personal B-section. And here, right atrial appendage, left atrial appendage, SBC, and left sinus node artery running on the Backman's bundle. With translimination, you can see the crystal terminalis pre-cable bundle. It transitions to the Backman's bundle, and it's separating to the posterior and anterior bundles surrounding the left atrial appendage. This is a frontal view of the pre-cable bundle. Again, the red for your left eye. Red for your left eye. This is the crystal terminalis continuing to the arch-shaped pre-cable bundle directing towards the ascending aorta. Therefore, this pre-cable bundle is also referred to as arcuate ridge. When viewed from the arial direction, you can see the direction of the pre-cable bundle directing to the ascending aorta. Arial quarter direction, you can finally see some component is directing to the Backman's bundle. This region. This is the exact target when you approach from the SBC. This is the crystal terminalis and this is the pre-cable bundle separating the SBC from the right atrial appendage. This component is Sagittal bundle and this component is Backman's bundle. As you can see here, like a three-dimensional continuation to the Backman's bundle. In this dissected heart, the ascending aorta separated by the transverse sinus here. In the living situation, it is almost directly adjacent. This is my acknowledgement. I would like to thank you for the individual who has donated their body and feel free to visit my 3D Anatomy Theater at the Sales Pavilion. Thank you very much for this great presentation, beautiful images and the added experience of a 3D visualization of the heart. We're a little bit running short of time so I just have a very short question for you. You mentioned that the thickness of the Backman's bundle is four millimeters on average, is that correct? Yes, by CT. Most of the pacing leads that we have are screw lengths of helix lengths of 1.8 to 2 millimeters maximum. Do you think there's a risk of touching the aorta with this screw length bearing in mind the thickness of the Backman's bundle? Thank you for the beautiful question. If you pace the Backman's bundle, there is no risk but if you go outside of the target area, there is a risk of ascending aorta injury. The electrophysiological properties of these fibers in the healthy heart, not with intellectual conduction delay, are those fibers conducting with the same velocity as the atrium or is it faster? At least in my limited knowledge, I know the Backman's bundle has a different component for the intercalated disc where the predominant expression of the connexin 40 or 43 that is different from the regular atrium myocardium that will allow the Backman's bundle is a little faster conduction compared to the regular atrium myocardium. Thank you very much. Thank you so much. Next, I have the pleasure of introducing Dr. Steven Balin from University of Iowa. We all are familiar with traditional right atrial appendage pacing so hopefully he's going to give us some insights into why we should be thinking about the benefits versus the risks of the Backman's bundle pacing. Thank you very much for the introduction. I don't have any 3D images. I wish I did because they're kind of cool. Feel free to wear the glasses. It might make this talk better. Not really much for disclosures. I want to take you back to the 1990s where things were a little bit different. I was younger and I had a full head of hair and some excitement about electrophysiology. And probably many of you are in grade school. But we have to remember there was no atrial fibrillation ablations. And so pretty much atrial fibrillation treatment was antiarrhythmic medication or you did an AV node ablation and paste. We did know that atrial fibrillation involved prolongation of activation within the atrium. And that was primarily due to, you know, the progressive fibrosis and loss of connexin intercellular connection. And sometimes that was manifested by a prolonged P-wave duration that you could see even on a standard EKG. And around this time, of course, people were looking at signal average EKGs. And it was applied actually to atrial tissue. And it did find that there were significant delays and low voltage extensions beyond the main body of the P-wave. And so there was a lot of interest in maybe modulating atrial activation as a way to influence atrial fibrillation. And there were a few different ways to do that. There was what was called dual site atrial pacing in the right atrium in the CS. And there was CS pacing. And then, of course, we looked at Bachman's bundle. And this kind of was a summary of the signal average ECG. The point of which was that, again, there was evidence that there was sort of a heterogenic activation that was disparate and may contribute, in fact, to atrial fibrillation. And as sort of brilliantly discussed earlier, Bachman's bundle offered a way to intercept the activation or pacing from the right atrium. And as was described, its sort of location was anterior and septal in the right atrium. And we did a bunch of studies acutely with ablation catheters sort of mapping around within the right atrium. And like other centers, described sort of the impact of various activation on, or pacing sites on atrial activation. And as you can see, your worst choice was the right atrial appendage. And as you can see, there was fairly significant delays to the left atrium when you look at right atrial appendage pacing. That was a little bit better when you did CS pacing. But the problem was is that it really sort of pre-excited the left atrium more than it excited the right atrium. So at the, what we sort of described as the anterior septum, you can see that the activation throughout both atrial chambers was relatively uniform. And that's what we were looking for. So we did the Bachman trial to look at the effect of pacing on subsequent development of atrial fib. And remember, these were significantly, seriously impacted patients with atrial fibrillation. In the study, 50% of the patients underwent an AV node ablation with pacemaker implantation. So we had 120 patients that were randomized to either the right atrium, right atrial appendage, or Bachman's bundle, which I'll describe in a few minutes. And then the important thing was we took everybody off antiarrhythmics because we just wanted to look at the effect of the pacing. And we followed patients for two years. And basically, we were looking for progression to what we called chronic atrial fib at that time, which was basically atrial fib that persisted for more than two months. So people would come in once they were in atrial fib. We had them come back and confirm that they were in atrial fib a month later. And at that point, if they were symptomatic, they could put back on their antiarrhythmics. So as was described in the slides, in part, my approach to this was to try to make it as easy as possible because you have to remember people were still using passive J leads in the right atrium. So I didn't want to make it that complicated. And based on sort of the acute studies, this is what we found. So the important thing to remember is in the RAO view, the lead needs to be anterior. But as stated, you can be in the right atrial appendage or other places and still not be at Bachman's. So sort of the key was sort of the LAO view where, as you can see, the septum sort of lined up with the right ventricular septum. This was a sweet tip, which is a fixed helix. The advantage of that was you could overtorque it a little bit and change your lead vectors, which is also kind of an important thing relative to, say, right atrial appendage pacing because you can change the vector of sensing by either adding lead or pulling lead back, or in this case, we actually made a little loop. So unlike the appendage where you're sort of stuck with whatever you get, you can't move the lead to necessarily adjust the sensing. The other thing was that we used kind of a modified J tip. So if you have your regular J tip, you'll notice that the curve kind of faces inward a little bit. So what we did was we just opened that up. And in fact, we did have a lead design, or a stylet design for that, which was shown in this. It's actually still available in, I think, an accessory kit. It's the orange stylet. But the point was is you brought the stylet down, you put the lead down, you went over to LAO, and then you pulled up. And most patients have kind of a little bit of a bridge between the SVC and the septum. There are some that don't. That makes it a little bit more challenging. But most patients, you can actually get to that junction between the septum and the right roof, and you'll see the lead deflect at that point. So that's how we defined it. And we're going to hear some other, probably more scientific approaches to the application of the lead. But what we did find, I think, has been fairly consistent in most of the studies. And that is that you can impact the P-wave duration. And as you can see, compared to sinus rhythm, Bachmann's is shorter. And as you can also appreciate, right atrial appendage pacing is awful. I mean, that's a horrible P-wave. You wouldn't want to leave the lab with that. The one thing I would say relative to the morphology, even though we're only talking 10 to 20 milliseconds of difference, it's even at 25 sweep, you can appreciate that it appears shorter. And the other thing is that the upstroke of the P-wave is very abrupt, much more sharp in the inferior leads. So that's what I use to kind of eyeball it. But that's important, because I think that kind of confirms that you're actually in the right area. So the proof was sort of in the pudding, which was that if you got the lead in the right atrial appendage, you'd not do as well as if you got it in Bachmann's bundle. And as you can see, there was like 72% at the end of the study versus 40%. And it is sort of interesting that they sort of come down and then sort of taper off. Now, that was a bit controversial at that time. And things never came to fisticuffs, but there was a lot of emotion about what all this meant and other studies. And again, subsequent speakers, I think we'll deal with some of that. So I copped some of their data, which is a bit more recent, which basically now has more modern pacemakers so they can look at burden and things that we commonly do now, that pacemakers when we were implanting in the study, basically had limited capability for that. But this study did show that atrial arrhythmias were decreased relative to right atrial appendage pacing and also right septal pacing, which I think they will probably go into a little bit more detail. And the burdens were also decreased. So there are other benefits, which we really didn't recognize upfront, because you also have to remember this was the 90s. So we didn't have CRT until really the latter part of that decade and beginning of the 2000s. So there are some hemodynamic effects, one of which is that it does affect the PR interval relative to right atrial appendage pacing. This was taking the sinus PR interval and then subtracted what you were left with. So point of the study was that Bachman's bundle was not significantly different than what the PR prolongation in sinus. And then other people have looked at Doppler effects. For example, when you're setting your AV intervals in CRT, you may be limited by your intrinsic conduction. So you might actually truncate the AV interval. And that has consequences in terms of how the atrium is able to mechanically contribute. And as you can see on right atrial appendage pacing, there is truncation of the atrial contribution to filling where it's not present in Bachman's bundle. And that's because on average, it only takes, sorry, it only takes 60 milliseconds to activate the lateral atrium as opposed to 120 to 140. So in conclusion, I think pacing at Bachman's bundle results in symmetric and greater homogeneity of atrial activation. And this is reflected in shortened P wave duration and overall atrial activation times. And compared to right atrial appendage pacing, Bachman bundle reduces atrial dysrhythmia and the subsequent development of atrial fibrillation. In addition, pacing at Bachman's bundle has advantages over the right atrial appendage pacing in patients needing CRT, both in terms of the incidence of atrial fib, as we mentioned, but also improving atrial activation and timing of atrial mechanical function. And therefore, I would argue that Bachman's bundle should be the default position of pacing for the atrium. And with that, I will say thank you. Thank you so much, Dr. Bailyn, that was great. One question that I have is, what do we confer the reduced risk of stroke to? Is there any evidence that there's reverse remodeling of the atria, or is it attributed to potentially restoration of atrial synchrony? Yeah, so I think that's an interesting question. We didn't really look at measurements of atrial function or dimension. Now we do know after atrial fibrillation, there's remodeling. In part, I've always been a little bit hesitant in terms of claims about Bachman's bundle, because I can't really say, is it right atrial appendage proarrhythmia versus whatever benefit that Bachman's bundle? I suspect it's probably both. In terms of its effect on stroke and remodeling, I guess I don't have personally any information. And then one other quick follow-up question. It seems like there's good data for patients that already have some evidence of remodeling, have AFib. Is there any data to support implanting these in patients that, let's say, have a normal PR interval, no evidence of interatrial conduction to them? Yes. We didn't, in the original study, we didn't make any qualifications in terms of the underlying atrial conduction. We did find that patients in these groups had longer P-wave durations, but we didn't make any distinction in terms of the implantation. My current practice is basically, I put it in everybody. I think there's probably a good reason to look at, say, the patients with sinus node dysfunction and how they develop over time with different pacing strategies. And then we have one virtual question from the audience. So the question is, is it expected that if you combine ATP pacing in the atria with Bachman's bundle, how that would potentially compare to ATP with radiatory appendage pacing? Well, again, I don't have any data. My guess would be that because radiatory appendage pacing causes so much disparity in terms of activation that that's probably rife with sort of micro-reentry and other issues. In general, when we were doing studies on atrial pacing for maintaining sinus rhythm, the response rate was pretty small, maybe 15% of patients. So it's not clear that ATP offers an advantage. I will say, electrophysiologically, as noted, the Bachman's bundle is different. The ERPs are different, and in atrial fibrillation, the fibrillatory waves typically are more organized compared to other areas. Great. Thank you so much. Yep. So thank you very much. We'll move on now to the next talk, given by Dan Loosgaarden from Vermont. Very important topic, which are the criteria for Bachman's bundle capture. Please, Dan. Thank you very much. Got it. Right. I have no control yet. I still have no control. Great. So I'm honored and really gratified to see the attendants here this morning. It's really astounding to me, and deeply appreciative of both Dr. Mori and Dr. Bailyn's discussions, which I think are going to be commensurate with a lot of what I have to say. So a careful review of alternate site atrial pacing that Steve referred to in the past. Very few of them looked at Bachman bundle pacing specifically. In fact, Steve's was one of the only studies that really focused on the Bachman bundle as a target site. And even in this study, which showed a strongly positive signal that Steve already showed with respect to decreased AF incidents head-to-head. In their study, as Steve mentioned, they didn't explicitly develop criteria for Bachman bundle capture to define their site. They were relying strictly on fluoroscopic perspectives for practical purposes. And essentially, in the paper, they go on to explain that using this fluoroscopic approach, generally speaking, the P-wave normalized in morphology and narrowed in duration. So picking up on the example of Steve's study, I started using a lead delivery system, a site-selective system, in order to start doing His bundle pacing back in 2006. And became aware of Steve's study around that time and figured, well, I may as well use the same system to put it in Bachman bundle because here's a clinical signal, a unique clinical signal that suggests that there may be a benefit. And it seemed to me a reasonable alternative to the appendage, which is imminently perforatable, accounts for more than 50% of lead perforations. If you trans-illuminate a right atrial appendage, it's a see-through structure between the pectinate muscles, very easy to perforate that area. And as Steve pointed out, grossly abnormal to pace from it. So it made sense to me to start doing this. The consequence of which is that by 2019, we had about 1,000 patients in whom we put these leads. And retrospectively, under the steady and determined hand of our then fellow, Maggie Infeld, who's now at Tufts Medical Center, we retrospectively analyzed our patient population. And we decided to look at the P-wave morphology so everybody had the lead placed in the same fluoroscopic approach. And then we looked at the P-waves of patients who were pacing at least 20% of the time. And the ones that looked what we expected Bachman bundle to look like, namely, normal morphology and narrow, we called Bachman bundle. And anything else, again, reminding you, everything was placed technically the same way. But all the other patients that the P-waves didn't look quite right, as in this example, sort of completely flat in lead three versus positive in lead three, we would say, okay, this was not Bachman bundle. And for want of a better term, we just called those right atrial septal. And then we wanted to ask, well, what were the differences in outcomes with respect to AF in these two patient populations over time? And we also added a matched right atrial appendage cohort from our clinic. And Steve showed this curve demonstrating that we kind of reproduced what he found. Again, this is a retrospective single-center analysis as opposed to his six-center prospective randomized controlled trial. But the septal group, the ones that were placed fluoroscopically using the same technique, looked like right atrial appendage in terms of incidence of AF over time. The other thing that's notable is look how quickly these folks develop AFib after their pacemaker implant. So there's clearly a profibrillatory component of appendage pacing. The question is how much of this delay is antiarrhythmic effect versus just preventing this, as Steve also questioned. And the other thing about this study is we showed that in each of these cohorts, the P waves at baseline were the same. So we weren't looking at differences of atrial myopathy. The best explanation is that this is different pacing sites that are giving different morphologies that have clinical implications, therefore raising the importance that using fluoroscopic assessment alone is not adequate. Because we've looked at the percentage of pacing that actually met Bachmann bundle capture using fluoroscopy alone, and it was only 50 percent. So you needed something better to do this more predictably. So criteria are critical. And what we've come up with, essentially, is the lead needs to be in a specific anatomic location, and you need to have a really good working knowledge of the anatomy that Dr. Mori shared so beautifully with us. The sensed electrograms in the Bachmann bundle area are characteristic, hence they are mappable, so you can get information from them. The response to screwing into that tissue shows a very specific response, confirming that you're actually in Bachmann bundle, which I'll show you in a second. And then the final arbiter of success is once you've used that information to guide you, you look at the P-wave morphology. And morphology, if you are in Bachmann bundle, compared to sinus rhythm, the morphology must normalize in all 12 lead axes, more or less, V1 being an exception, which I'll discuss in a moment. And the duration has to be shorter, by definition. So this is a gross dissection from Girard-Girodon showing the epicardial extent of the Bachmann bundle, which is the vast majority of the tissue. The left-sided inputs extend and start to activate in front of the right superior pulmonary vein in the roof of the left atrium on the left side. And on the right side, this insertion predictably, as Dr. Mori pointed out, inserts in the inferior most portion of the septal aspect of the SVC. This is where your target is when you're implanting a lead. Histologically, what this looks like is a beautiful slide that Damien Sanchez-Quintana shared with us in a paper we recently published demonstrating the Bachmann bundle connecting to these extensions. This is the pre-caval bundle that Dr. Mori mentioned. There are also, to varying extents, posterior extensions that come around the back of the SVC, such that when the sinus node activates, there are two potential routes into the Bachmann bundle. And again, as Dr. Mori pointed out, these attach into the Bachmann bundle at oblique angles. In addition, if you look carefully at the histology of this region, there's a paucity of sarcomeric tissue, a fair amount of fibrous and adipose tissue. So the safety factor of activation here is low. As all of us age, our SVC dilates. That stresses this tissue. That probably explains why, as all of us age, our P waves prolong, which is strongly correlated with our ever-increasing incidence of AF. All of that, and this is the normal activation pattern of the Bachmann bundle. The result of that is that you wind up potentially with marked delay between right atrial and left atrial activation, this being an example of what's referred to in the literature as interatrial conduction delay. When you pace the Bachmann bundle, you're at the same time advancing activation of the Bachmann bundle, while going through the initial antegrade portion of what activates the Bachmann via the sinus, to get back to where the sinus node then activates the right atrium. So you have a brief period of time that's retrograde. This is where the disease is that you're going to be correcting, so you're downstream of that disease, which is why it would be pointless to try to correct this disease anywhere along or close to the sinus node, which is why that's not where you want to pace if you're trying to resynchronize the atria in an adult, even modestly diseased, atrial chamber. The consequence of this form of pacing, this is the same patient I just showed you. This is what their P wave looks like when you pace the Bachmann bundle. It's a dramatic difference. And when you see this, I think that when you do this practically, at least from my perspective, there was no turning back to going back to the right atrial appendage, because we know that the likelihood of this patient developing AF is higher. The likelihood that you're getting a clinically meaningful effect from this, I think, is very, very good. We need data still to prove that, but I think the probability is, from a logical standpoint, it's more logical to conclude that this will be important than that it won't be important. Using CARDO, electroanatomical mapping, you can see in this example that during sinus rhythm, the major activation route to the Bachmann bundle is indeed this anterior branch. In this instance, what we're doing is we're pacing the left atrial breakout of Bachmann bundle and mapping the right atrial, so you can actually see Bachmann bundle where exactly it is in the right atrium. So your target is this broad area. The easiest place to access technically is in the infraroceptal aspect of the SVC. When you pace there, the result is the initial portion of the antegrade activation is retrograde, but the right atrium largely is being activated almost identically to what the sinus node does, because eventually you're just getting back to where the sinus node goes antegrade down the crista, going down the posterior wall, the RA, the free wall, and down to the annulus. So you're essentially normalizing both LA and RA, but you're advancing the LA timing and slightly delaying the RA timing, which is what causes full atrial resynchronization. So we just published a paper that should be out any day now. I was hoping it would be out in HeartRhythm this week so people would get really excited, but it hasn't quite made it. It will be available in the electronic version in a couple of days, I suspect. But what we did is we did these retrograde maps in 15 patients, and what we found is that in the superior-inferior direction, everybody consistently has inputs at the infraroceptal SVC. There is some variation in the anterior-posterior plane, which means practically when you're doing an implant, you need to be able to scan a little bit along the anterior and posterior aspects of the inferior septal SVC. So specifically, the way this looks during an implant, here's an REO view with the lead intentionally, a lead delivery system and a lead inside it, intentionally high up in the SVC using a little bit of contrast injection for didactic purposes to show the length of the SVC and the junction where it starts to fan out into the RA. It's right in that nexus that you're going to be looking and FOS in the REO view at the Bachman bundle. When you then go to the LAO view, you confirm that you're septally placed, so you're not going to be going towards the aorta in this plane, and the Bachman bundle now is going to be looked at in its length, and the target's going to be down here, right at the junction where the SVC, just before the SVC starts going into the RA. In order to screen the anterior-posterior aspect of the septum, you can then go to a caudal view, so you're now looking in FOS up at the SVC from bottom-up view, and it's along this arc, along the septum, that you're going to be looking for desirable electrogram targets. A little bit of clockwise torque on a sheet delivery system delivered from the left side will drive the tip of the catheter anteriorly and counterclockwise torque posteriorly. You don't want to over-torque this, because then you can start getting into the planes where you could be adjacent to the aorta. The other thing is if you're using a pre-shaped sheath and you over-torque it, the shape can actually get you more superiorly than you're aware when you're looking in the LAO view, or more posteriorly in the RA, in the other direction. So the electrograms are very characteristic. Typically when you see a Bachman electrogram, what you're going to see is evidence of far-field CRISTA being activated at or near the beginning of the P-wave, and a little bit after that, this complex fractionated signal. Typically multi-component, high-frequency, usually within the first third to the first half of the P-wave, depending on how much conduction disease there is. That's that CRISTA potential. This is an example of an implant case where I'm exploding the unipolar filtered signal, which shows this far-field component in this example of the CRISTA, and this fractionated stuff. You can see even far-field stuff extending out quite late when there's a lot of disease, as is the case in this patient with this abnormal P-wave. When you press the delivery sheath up against that tissue, you can already see in the unfiltered signal evidence of injury in the latter portion of this fractionated complex. That means you're pressing right up against Bachman tissue, because that's going to be the latest local signal that you're sitting at at that point in the anatomy. When you screw in there, that injury current can be quite massive. It's important because this resolves very quickly, and often thresholds start, when you do this immediately, the threshold's going to be somewhere like 3 or 3.5. In minutes, you'll start to see that going down by tenths, going down into the twos. When you see that, you can rest assured that by the next day, the capture threshold is going to be somewhere around 1 volt on average in these patients. Then, again, the final arbiters, the normalization of the P-wave, look at what this was and what it now is. This is an impressive change in morphology. This is speaking to interatrial conduction time that we know correlates with an increased risk of AF. Oh, good lord. I have to conclude. Very quickly, if you're too high up in the SVC, we've identified that there are myocardial extensions that extend right into the Bachman bundle. If you're too high, you'll know you're too high because you have a really, really late electrogram. When you pace at that electrogram, no matter what your output, you're going to wind up with a really long isoelectric segment. Now, you're unnecessarily adding time to the AV interval, which is undesirable. Alternatively, if you encounter a lot of local disease at the target site, and here evidenced by the fact that you have two high frequency but very separate potentials, as you decrement your output, you can also see the onset of an isoelectric segment. You want to maintain your output so that you're always capturing that tissue immediately. To conclude, the final arbiter of Bachman bundle capture is the paced P-wave morphology and duration. Solid anatomical understanding gets you in the neighborhood using fluoroscopic landmarks and lead delivery system interplay, and electrograms confirm location to help select sites providing predictably good capture and sensing thresholds, and I'll conclude with that. Thank you. Thank you. Thank you very much, Dan. Very good tips and tricks there. Which sheath do you use for the luminous lead? So I do use the 3830 system Medtronic's lead is incredibly well suited to this for a couple of reasons. The flexibility of the lead makes it such that you can create a J-loop that the local sensing at your tip is going to be low amplitude. You need the ring to sit down in the crista below the SVC to give you your sensing. So you need a flexible lead that doesn't have high tension at the tip when you create that arc, which this lead achieves very well. There are pre-shaped sheaths. There's one called the S4 and the S5 that have slightly different lengths. For a more distended or larger anatomy, the larger length sometimes is helpful. Sometimes neither of those sheaths work very well depending on how elastic the SVC is and how arced it is. So not, I mean, in my case, most of the time I use a deflectible sheath that's called the C30459 centimeter. That's a single-plane deflectible sheath and it's a little bit simpler from the perspective of when you're scanning anterior and posteriorly, you get less height change because there's no orthogonal deflection built into it. I use a combination of any of these three sheaths depending on the anatomy. What do you think of the C315 hiss? Do you think that will get you to the right spot? Actually recently because I was endeavoring to put in a hiss that failed just once and had an additional lead already in the left bundle branch area, I ended up using that lead and the sheath to deliver and it worked great. Just one very last question, very quick answer because from the audience there, how do you distinguish between high septal and Backman's bundle pacing? So that last slide where I showed the electrogram, the key is in the electrogram. If you're, oh, high septal. So high septal you're going to see large typical atrial electrograms. The electrogram is much, you don't get the fractionated appearance. It is going to be a little bit later because it's later in time after you've gone over the pre-caval bundle, but the morphology of the electrogram is clearly local and easy to distinguish. Thank you. All right. We're going to introduce our final speaker. So it's my pleasure to introduce Dr. Nicole Habel from the University of Vermont. I think we're getting a lot of questions from the audience on how do you practically do this? How do you start this in your practice? So we're looking forward to learning from your experience. Thank you very much. Thanks to HRS for inviting me to speak to you today. I'm really honored to be here and super excited that this room is filled. Just a year or two ago, Bachman-Spandau pacing was relegated to this little corner pocket of hodgepodge lectures and now it gets its own lecture, which is fantastic. So I'll speak to you about how to incorporate Bachman-Spandau pacing into clinical practice. And we can simplify that to the question of who should get Bachman-Spandau pacing and why. And I would answer that quite simply by saying, everyone. This comes with an asterisk. So I would strongly argue that if you're planning an atrial lead placement, you should think about Bachman-Spandau pacing. But I would also throw in there that if you're planning a pace and a blade approach, some of these patients may actually benefit from adding an atrial lead when you otherwise wouldn't have thought about adding an atrial lead. And then it should definitely be a Bachman-Spandau lead. And we'll dive into the details about that. So we have a beautiful lecture about the anatomy of the heart. From a safety consideration alone, I'm a strong proponent of Bachman-Spandau pacing. The risk of atrial lead perforation and the right atrial appendage was alluded to earlier. And even though clinical perforation risk is estimated relatively low, if you, on the account of one study that did chest CTs for about 100 patients, the rate of asymptomatic right atrial appendage lead perforations was actually surprisingly high at 15%. In the same cohort, the perforation seen by CT scan for ventricular leads was around 6%. The other piece I want to point out here is that in this cohort of, yes, just 100 patients, but it was a mix of active and passive fixation leads. So your passive fixation leads aren't necessarily your saving grace. Then in contrast, if you look at Bachman-Spandau area, I'm showing you here kind of a different perspective of the heart than we have seen in the previous talks. This is a formalin-fixed heart opened up from the lateral aspect of the right atrium. So we're looking right at the SVCRE junction. We've taken a 3830 lead here right to the area where we would clinically implant the Bachman-Spandau lead. And then the same view kind of positioned on the right side here advanced, she's over the 3830 lead to give you kind of an anterior and slightly cranial view on the same area just to highlight how thick this area is and much safer in terms of risk for perforation. This is a slightly, another view of the, to highlight the same point of the thickness of Bachman's bundle and the intersection with the terminal crest. You've seen this example of a histological slide provided by Dr. Sanchez-Quintana. Of the extent of Bachman's bundle, right where the SVC kind of starts entering the right atrium in a cross section and you see the extensions of Bachman's bundle here in the area being quite thick in which you implant Bachman's bundle lead. So generally speaking, Bachman's bundle pacing leads have a very low risk of perforation from the anatomic considerations. But what about electrical considerations to placing Bachman's bundle leads? So atrial resynchronization certainly has the potential to correct intraatrial conduction delay and it is really important to recognize just how strongly associated intraatrial conduction delay is with new onset atrial fibrillation. And that is an exponential relationship and directly grows with P wave duration exceeding 120 milliseconds. But you even get in slide increase even before that 120 millisecond cutoff that folks in the literature often refer to as intraatrial block or complete intraatrial block. But it's important to recognize that intraatrial conduction delay is not only an electrical problem. This is a retrospective analysis of almost a half million people across five centers published in Jackie P in 2023. And it shows a strong association between intraatrial conduction delay highlighted here each in yellow both with heart failure, thromboembolism and MACE. So combined endpoints of death, myocardial infarction, heart failure events, stroke and thromboembolism. We've seen some good examples throughout these talks about comparing what sinus rhythm looks like in a patient to right atrial appendage pacing. And as Dr. Balin nicely said, it just looks awful. So to some extent you can point out that right atrial appendage pacing actually introduces intraatrial conduction delay. We know it's associated with prolonged P wave duration, increased intraatrial activation time and the delay in atrial kick as you've seen by the previous speakers. You've also seen portion of this graph here before that I wanna re-highlight in this context. This is an aspect from our retrospective analysis, Maggie Infeld being the first author on this paper where we looked back at our cohort of patients that received atrial leads over a long period of time only included those that were pacing 20% of the time or greater from their atrial lead in this cohort and then looked at their AF burden over time. And in the right atrial appendage cohort, you're looking here in this graph at freedom from atrial arrhythmias. So you have a sudden drop off right after implant time and pretty much everybody two and a half years out has AFib. When you contrast this with electrogram-guided Bachman-Spandau pacing or the Bachman-Spandau pacing that achieves a narrow P wave as highlighted in this example here on the left, you have a dramatically lower incidence of atrial arrhythmias and the size of the cohort in each of these was just above 100 patients. But then most importantly I would point out that the high right atrial septum when you target Bachman-Spandau fluoroscopically alone don't achieve P wave narrowing with a normalization of P wave axis follows much closer the trajectory of the right atrial appendage cohort in terms of arrhythmia incidence. So even if we don't know yet what the big benefit of Bachman-Spandau pacing is, at a minimum it can avoid if not correct intraatrial conduction delay and that certainly can impact AF burden as we've seen in some limited data sets but may actually have impacts on heart failure and MACE. So what about our patients with systolic heart failure? Right now the approach is whenever you have a CRT device to minimize right atrial appendage pacing. In this study right atrial appendage pacing with a high burden defined as greater than 50% pacing was associated with worse left atrial morphology and function that also impacted just how much reverse remodeling can you achieve with your CRT device. And they followed, they had an imaging core to the study and a big cohort in whom they analyzed clinical outcomes. They saw in the high pacing burden right atrial appendage group high incidence of AFib. If you had a lesser burden of right atrial appendage pacing your AFib burden was significantly lower your incidence of AFib was significantly lower. And I just wanna plug in here data from the CASLA-AF trial that looked at the relationship between AF burden and all cause mortality. And in the dotted lines here both in blue and in red you see a cohort that had either received in red antiarrhythmic drugs or in blue initially ablation. But if they ended up after initial treatment still with a high pacing burden their mortality rate was significantly higher. So AF burden in your systolic heart failure patients is actually a big red flag in terms of overall survival. The same study that looked at LA morphology lack of reverse remodeling also found not surprisingly a higher rate of heart failure admissions with high burden right atrial appendage pacing. Now if we minimize right atrial appendage pacing in the HFRIF cohort should we maximize Bachman-Spandau pacing in those patients with systolic heart failure? We really don't know yet. Because their data on really electrogram guided Bachman-Spandau pacing hasn't accumulated much. But I'm hoping that all of you who are interested in learning this technique will contribute to moving the field forward. But there's certainly a potential benefit of atrial resynchronization via electrogram guided Bachman-Spandau pacing not only to reduce AFib burden but also to optimize AV delays and optimize the hemodynamic aspect of treating our heart failure patients. And that might in turn affect heart failure outcomes in MACE. Lastly, what about our HFPEF cohort? I would say Bachman-Spandau pacing is essential in those folks. There is kind of new recognition that accelerated resting heart rate pacing can be beneficial in HFPEF. Two of the trials that speak to the benefit of that come from our group, the MyPace trial, the first author Maggie Infeld and the PACE HFPEF trial, which both showed an improved health status for patients who received accelerated resting heart rate pacing as well as higher activity levels either by pacemaker detected activity or six minute walk test. And it went in hand with lower antiprobian P levels and in the MyPace trial, lower AF burden. So the mechanism of that is higher resting heart rate pacing lowers LV filling pressures. And this example here is from a computational model from our colleagues in Maastricht where Bachman-Spandau pacing lowers left atrial filling pressures across the spectrum of heart rates whereas if you do the same simulation with higher rate pacing but do it from the right atrial septum or the right atrial appendage, you get less of a benefit in terms of lowering filling pressures and you get it over a narrower spectrum of heart rates. So on the pace and ablate strategy, I would urge you to think about maybe the potential of a pace and wait strategy because if you are able to treat your heart failure and or dyssynchrony, you can be able to restore sinus rhythm with a pacing strategy. And when that is the case, having an atrial lead in place that can achieve atrial resynchronization will be beneficial for AFib. This is just an example of one of my patients who underwent dual chamber pacemaker implant for persistent atrial fibrillation. They got a higher resting heart rate approach to treating their half-path, spontaneously converted after 18 days of pacing to sinus rhythm after previously being in AFib for over six months and then maintained sinus rhythm with a Bachman-Spandau pacing. Thank you very much for your attention. Thank you. Thank you so much, Dr. Habel. That was great. One question that I have is if you can speak to the programming of these devices. So typically we're thinking about sort of a rate threshold to pace. So in patients that have some evidence of interatrial conduction delay, are you programming those patients to be Bachman-Spandau pacing 100% of the time? Yeah, if I achieve adequate Bachman-Spandau pacing, then I will certainly maximize it. I will turn on atrial preference pacing to mandate atrial pacing. And then often for the folks that have features of heart failure with preserved infection or diastolic dysfunction, I will often also raise their lower rate limit. Thank you. And I think probably a lot of us in the audience are wondering if we're at an institution that is currently not implanting these leads, what's the first step to incorporate this into your practice? Yeah. So I would say Dr. Lesgarden is the first author on a paper where we describe sort of the how-to, which is a good summary of what you're looking for, what the moves you're going to do. And it might be daunting to learn a new technique on your own at first, but I assure you it's actually a lot easier than Hespandau pacing, left spinal branch area pacing. You will have the, if you do any of those, you will have the skillset to implement Bachman-Spandau pacing. From a stepwise approach, it's in the right atrium, you pull up to the SVC-RA junction, and you don't manipulate the sheath until you're in that area, and it's very subtle movements to look at your electrograms. That's sort of the biggest kind of pin I can put up. Maybe just two very quick questions and two quick answers. Yeah. So the question was whether there's any interest in leadless for Bachman-Spandau. I think that's an interesting opportunity. I think the technology needs to improve in order to get it electrogram guided and not just fluoroscopically. But yeah, can I see the field moving there? Absolutely. Yesterday, there was a session devoted to Dr. Parsonnette, and there was a discussion about the Bachman bundle, kind of concluding that the Bachman bundle does not exist. So the question is, does it really exist? Because anatomically, does it have a fibrous sheath that insulated from the surrounding tissue? Because from the activation map, I see that the activation starts from the Bachman bundle core, so it looks like it's not isolated. So maybe this is just anisotropic properties of the tissue of the right atrium rather than a functional bundle like his bundle or left bundle. This is pretty important. How do you define Bachman bundle? Is it a histological definition or is it functional physiological definition? Because this translates what to expect during pacing. This is why I ask. Yeah, I think everybody has probably a good answer to this along the way. I would say it's a combination of the two. It's certainly, Bachman's bundle is certainly not like the his bundle, but it has morphologic differences that distinguish it from the atrial myocardium with including fibrosepti, including longitudinal arrangement. So from my perspective, the anatomy or the design of the heart is kind of a means to an end. It gets the rapid activation to the left atrium, left atrium to left ventricle organized quickly, but I'll pass it on to the other panelists. I think that, is this on? Testing, testing, can you guys, okay. I think it's been problematic historically that people have been hung up on this notion that we're not in the atrium meeting the Ashoff criteria of what a conduction system is. And the Ashoff criteria is a tautological definition because what they had back in the 1890s and 1900s was a strict, they had one conduction system to look at, and that was not present in the atrium. And the consequence of that is how that translated into the history of pacing is that people are like, oh, well, there's not a conduction system in the atrium, so it doesn't matter. The fact is there is a conduction system irrespective of how specialized it is compared with the His bundle or the surrounding atrial myocytes. The sinus node is where it is for functional reasons, and the tissues that it activates serve functional purposes, and we're leveraging those tissues to correct for an abnormality that develops in time. Irrespective of whether their specialization is beyond anisotropic conduction, from my perspective, it doesn't matter. What matters is that you're normalizing the conduction time with a P-wave morphology that reproduces what your sinus node looked like back when you were 14 years old rather than 56. That, I think, is the critical issue and the psychological shift that needs to occur for people to sort of say, oh, yeah, there is an atrial conduction system pacing, and we've been ignoring it. I think the other thing to remember is, I mean, the original description, which was 19-something, he not only described the fibers, which were longitudinal, as you say, promoting conduction, but he also disrupted them and was able to note the delay in terms of activation. So how you, as you were saying, how you define what is a conduction system, I think, is irrelevant. Because it's from a functional standpoint. You have activation of the bundle and then the breakthrough far away if this is selective capture. But we don't see that with the Bachman bundle pacing. You pace the Bachman, and you have activation all around. You don't have a single breakthrough far away in the left atrium. Yeah, so it remains unclear to me exactly how distinct the Bachman is from the adjacent crista. What's clear is that the inputs from the crista, whether they're posterior or anterior, are oblique. So there's going to be lower safety factor as that angles into the Bachman bundle. And I think that's the critical issue that elicits the disease that's relying on millivolt-level activation. You come in with 1,000-fold higher energy, and you are resynchronizing that activation. What is non-physiological is the retrograde conduction across the pre-cable bundle. So you're starting, the reason you see the P wave immediately start when you immediately capture that adjacent crista is you see the immediate onset of the P wave because you're going down the face of the right atrial appendage. But after that, everything is exactly as what the sinus node does, the posterior wall, the lateral, and the approaches to the AV groove. So that's sort of how I think of it. All right, thank you guys. I know we ran over here, but just want to thank all of our presenters. I think the audience turnout today really speaks to the movement of this atrial physiologic pacing. So thank you for your attention, and thank you to our speakers.

atrial resynchronization

Bachman bundle pacing

atrial synchronization

atrial fibrillation

electrophysiology

cardiac resynchronization therapy

anatomy

pacing lead placement

heart failure

atrial arrhythmias

clinical practice integration