Chapters Transcript Video Conduction System Pacing Dr Jeff Hedley introduces conduction system pacing as a therapy to achieve cardiac resynchronization in patients with heart failure. I appreciate the opportunity to talk. And so this is gonna be sort of a little bit more of a teaching style presentation so that it's more putting this uh technique on the radar for everybody and we'll go through some data as well. I have no financial disclosure, although I will say that Medtronic did provide a few of the slides just because I liked the graphics. Um And so my goal is, you know, there's gonna be some data, but I am gonna try to not cause death by Kaplan Meyer Curve. Um So hopefully you're thankful of that. Um So when we talk about traditional um pacing, you know, RV, apical pacing, you know, basically, I hate to say it this way, but we're kind of flopping the lead, just any old place down into the, you know, to the right ventricle. And, you know, it turns out after we've learned a lot more about this, that, that there's some negative consequences of that. Here's a echocardiogram of somebody who's being paced um from the RV apex. And you can see it's not a very synchronous contraction, the heart kind of, you know, rocks back and forth instead of everything coming together at the same time and sort of coordinate fashion and it's from this sort of disy chy that uh the large, um you know, the bulk of the issues arise. And so you can see lots and lots of, you know, issues, you know, kind of from a mechanical standpoint when you look at uh echo, don't have time for all those, but also clinical issues such as atrial fibrillation and worsening of mitral regurgitation. Um as well as you know, all the way down to sort of the pathologic level where you can see changes on the tissue um on the tissue level. And so this is what is referred to as pacing, induced cardiomyopathy. Um Traditionally, pacing induced cardiomyopathy has been diagnosed as being 40% pacing the RV or more over time. And in because of that, that results in a at least 10% decrease in the EF to a level that's below 50%. That's kind of the traditional um uh definition. So then the good doctor Kiel here, he did a study when we were at Cleveland Clinic. Um It looked at our experience with patients who were pacing and uh and what he ultimately showed um is that whereas we think of this as probably being a very rare event or at least we did until recently that it is likely present in at least 12% of patients and given the number of people that were putting pacemakers. And that's actually not a very small number at the end of the day. So, um the other thing that he looked at and saw was that, yeah, we use that traditional cut off of 40% of the time pacing in the RV. But in fact, it is likely that it is happening at far lower levels of RV pacing, even as little as 20% of the time, this was then replicated again, um by the Penn group who looked at exactly the same thing. Although in their particular cohort, they saw it go from 12% to as much as 20%. Now, we're saying one in five people who are pacing with a significant portion of the time in the RV are at risk for pacing induced cardiomyopathy. And they too said, you know, the risk of developing pacing induced cardiomyopathy likely begins well below the commonly accepted cut off uh of 40%. So this begs the question, how do we pace the heart in a more friendly physiologic way? And so the idea here is that we're going to leverage the natural conduction system of the heart to pace it in a way that you can't do by just again flopping the lead down in the right ventricle. And so the most physiologic of ways of doing this is by way of his bundle pacing. It's the highest up you can go in the conduction system and pace the heart with any sort of reproducibility. And if you do so successfully, what you're actually doing is just recreating your normal QR S. Uh And so that's ideal. However, it comes with several drawbacks. If you look here, the membranous septum, which is in the middle of this figure is so thin, this is where the hiss bundle runs, it's so thin that if you put a flashlight on the other side of it, you can literally see through the thing. So we're talking about a very, very thin area of tissue. This is it pathologically, that's the inner ventricular septum on the right. And we're talking about a really, really thin area of tissue. So screwing a lead into this area is not only technically difficult, but once you do, so when it then scars, you're scarring up a very small little area. And so now the electrical parameters of the device don't really work all that well. And not to mention, it's not hard for that lead to fall out of that. It doesn't have much purchase in that tissue. So then someone comes up with a clever idea of left bundle area pacing. This was just a few years ago. So it's actually quite new in the world of pacing. Uh And so here's what we do, we sort of use some different tools um then sort of the traditional pacemaker to kind of give us a little bit more specificity. Here's the heart in right anterior oblique view and you can see we kind of, you know, sectioned it off from the base down to the apex and sort of low to high. And you, you create all these different quadrants. This area number two is about where you're gonna find the his bundle. And if you move just a little bit, you know, um further down, you're gonna find the left bundle. And this is sort of if you overlay the conduction system on an X ray, this is what we're targeting. We're targeting the, the the left bundle. So bear with me here, there's going to be a little bit of EP but I promise my, my goal is to make it sort of interesting. OK? If you pace along the right side of the inner ventricular septum, OK, you're going to capture the right side of the inner ventricular septum. However, if you pace in such a way that you can kind of use a big antenna, then you can sort of reach from afar, the left conduction system. And so just by pacing along, you can sort of map out and say, aha, I think I'm in a pretty darn good place. It's worth going after this area. And so that's what's called unipolar high. I'll put unipolar pacing and we use pretty low tech stuff. We actually use just our knowledge of the EKG to say, are we in a pretty good area? Are we too high? Are we too low? And we can tell all this just off a 12 lead EKG. And so then here's one, this is just a nice physiologic point. One of the things that guides us is what's called the LV activation time. And so I'm going to try to explain this but the shorter the better. So if you pace along the right side of the inner ventricular septum, then that impulse has to travel down across the septum and up to the LV. Right. And so if you pace from, if you actually capture the left side conduction system, then that impulse has really rapid and sort of, you know, um immediate access to the left ventricle. So one thing that's of particular interest is the time just to cross the inner ventricular septum alone is 60 milliseconds. So why is that important? Because if from the time you deliver your impulse to the time that the great majority of the left ventricle has already fired, it takes only 70 some odd milliseconds or the cut off is like around 80. But if it's only taken something to 70 80 milliseconds, and it takes on, you know, 60 milliseconds just across the septum, you know, for sure that you have gotten into the left conduction system, it just cannot possibly happen any other way. So this is where math is fun. It kind of proves things. So uh can I go back? Yeah. So here's another interesting little pattern that we see. So this little hump in the middle of what we call the w pattern, that's actually the right side of the heart firing. Ok. So when you first start, it's kind of happening in the middle of things and as I move more and more and more to the left kind of, but, you know, it makes sense that the right side should, should fire later and later and later. And that's exactly what we see. So it moves a little bit later and then a little bit later proving that we are getting into the left sided conduction system. And you can actually see this as you screw in the lead because it's irritating to the heart to, you know, to have a metal, you know, drilled into it. And so it causes PV CS and as you watch that lead, go across the septum, you'll actually see that exact same pattern play out. And so you can just tell by the, you know, the irritability that you're causing that a ham in a nice, uh pretty place. So left bundle area pacing has a lot of, you know, benefits and, and then some theoretical risks. We don't have time for all of this. I will say that one, you know, point that I always make to patients is that you're getting a new technology, but you're getting it in such a way that it really comes at hardly any additional, if not demonstrably lower risk to you. So it's sort of a win win. One of the benefits is quote, quote unquote, bypassing a site of block. And I wanted to explain this because one question I get a lot is you're gonna tie into the left bundle. Well, what about patients with a left bundle branch block? It sort of doesn't make any sense. You're saying, why should I use that faulty wire? So this is kind of my simple diagram of the conduction system. And um, and so I think the common misconception is that when you have a left bundle branch block, that the whole thing is out, it's not, you actually have just a site of block and everything past that sort of works just fine. So it's kind of like coming up to a road closure and all you have to do is sort of take a detour. So if you can just get around the site of block, you're using a perfectly functional wire. And so that's in large part what we're doing. So now we got to do a little bit of data so that you don't think that I'm just, you know, telling you lies that there's actually some science behind this. So what what this is, this study is really useful is this is patients with, you know, kind of uh in stage a FB that we've given up on, we ablate the A V node. And now we've got to put a pacemaker in. And so how are we going to do this? In the most friendly way. Well, again, in theory, the best way to do it is by way of the hiss. But how does it stack up against the left bundle? So it is true though. If you pace the hiss, you're gonna get a narrower QR s than you are with left bundle. However, again, it takes a long time. It's hard. The leads don't work that way and left bundle area pacing is certainly faster. Um The other thing is I mentioned that sometimes with his bundle pacing, the leads fall out or they stop working well, if you've just made somebody utterly dependent upon their pacemaker, if it stops working, they stopped working. Um And so, you know, you don't have to have a backup lead when you put a left bundle pacing uh in and then from kind of an electrical standpoint, there are some parameters that may mean a lot to us, the sensing and the um pacing thresholds are a whole heck of a lot better in left bundle pacing than they are in his bundle pacing. Um And that's kind of shown here. So, but what, all right, what about outcomes? So if you get a better result with the his bundle, maybe, you know, patients do better. Well, that, that actually didn't turn out to be the case. So in both his bundle pacing and left bundle uh pacing, the ef after you do an A V note ablation with someone with uh with a FB, the EF goes up in both and without any significant difference, their heart failure, symptoms go down in both without any significant difference. And then your mitral regurgitation and your tricuspid regurgitation all get better. And this was true at both one year, two year and three year follow up. So, although the EKG looks slightly prettier with his bundle pacing, the device works better and you get the same outcomes as basically the take home point, no difference in mortality. Although the complications are higher in his bundle pacing, as I just said. And so those are primarily lead dislodgement changes in the thresholds um and uh and issues of that sort. So OK, well, what about our sort of gold standard nowadays, C RT? So we are in the infancy of this sort of comparison and the trials are small and somewhat limited. But when you compare them head to head, for example, this small clinical trial with non ischemic patients in the left bundle branch block, then if you look head to head, those who get left bundle area pacing have narrower QR S than do their C RT counterparts and they actually do better. Their uh their LV ejection fractions improve more in left bundle pacing. And this was true in both the intention to treat and per protocol analysis as well as the heart begins to shrink back down to normal size more with left bundle pacing. Uh and your B MP levels go down more with left bundle pacing and then one that's actually literally hot off the press so much so that I didn't have access at home to be able to dig through the, the, the, you know, kind of nitty gritty showed exactly the same, exactly the same findings and so much larger trials are absolutely necessary here. But it is looking exceedingly promising for uh left bundle pacing. So I wanted to show a few quick cases. Um And uh I didn't pick the ones that are sort of like, you know, uh chip shot cases, the ones that you put on your refrigerator and show to mom, you know, these were like the hard ones, right? And so the first case is a patient who had a TVER earlier this year and at baseline had uh you know, b fascicular block. Um and after TVER had an exceedingly long um first degree A V block in addition to their B fascicular um disease. And so this patient is ultra high risk for, you know, developing complete heart block amongst other complications. And so you might look at this and say, OK, well, if that's what they've got, you know, at baseline, that is their intrinsic conduction. How are you going to pretty that up at all? Um And the fact is is that we absolutely can. So here is left bundle pacing. If you compare them directly, then we literally chop 38 milliseconds off the QR S and paste them in a more physiologic manner. This one is even more striking. So there are many patients in which, you know, for various reasons, be it tricuspid valve replacement or other, you know, regurgitation. We don't want to cross the the tricuspid valve. And so we put a CS lead in. Well, CS leads are supposed to be excellent, right. We're pacing from the LV, not cause any trouble. However, this patient undergoes CS lead pacing and gets this exceedingly wide, nasty looking QR S and uh and really in that setting, their EF goes even further down despite their recalcitrant heart failure prior to this. And so they, you know, we decide, OK, let's see what we can get when we do a left bundle pacer and this is the result. So if you compare the two, we went from 258 milliseconds down to 100 and 19 milliseconds, which is, I mean, just an astonishingly um you know, better uh way to pace the heart. So th this is sort of what's what's possible and and when you have somebody who comes in and their baseline QR S is is ultra narrow, you know, you're going to get a good result by and large. Um but it's actually more challenging when you got folks like this. So in summary, pacing induced cardiomyopathy is much more common than we previously believed. It may be as high as one in five it is occurring at a lower pacing burden than we used to believe was 40%. Now, maybe it's just as little as 20% of the time physiologic pacing is a very promising solution. Logistically left bundle area pacing is preferred to his bundle pacing with simple an atomic and EKG guided approach. We can get high success rates with our implants. Um And that left bundle pacing may be superior to C RT and select patients. That's a whole other nuanced discussion and much more research is required. Thank you. Published October 13, 2023 Created by Related Presenters Jeffery Hedley, M.D. Sentara Cardiology Specialists View full profile
BROADCASTMED