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Inside EP: Insights From Clinical Decision-Makers ...
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Panel Discussion
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Of course, catheter ablation of AFib is, of course, one of our favorite ablations. It ranges from fascinating to some procedures where you have to fight to stay awake. So having said this, it has incredible value for patients who are highly symptomatic, and it's truly had a big impact on quality of life. As a general editorial comment, and I'd like to sort of, again, mention this to industry and point out an area where we in academia are still completely puzzled. As Dr. Haynes correctly pointed out, we know catheter ablation of AFib works, but we have no idea why it does so. So that is a huge scientific puzzle, and I think it's one area where all of us should lobby NIH and others to fund even more science so that we can have much better targeted therapies. So with that sort of point is in place, I'd love to start with the panel, and perhaps we'll start from Jack Singh. So let me actually ask some provocative questions, and then we'll need audience participation. We have about 20, 25 minutes. So Jack, could you make a comment, since it's a kind of a nice segue from the previous session with implanted devices. What should be the threshold for symptoms, and what should be the threshold in the absence of symptoms for arrhythmia burden, and would you ever consider taking patients with a certain patient characteristics for catheter ablation irrespective of symptoms? So these are common things that come up. Patients want catheter ablation for stopping coumadin on one end when they're completely asymptomatic, of course, and you have the other extreme where people have a few PACs, and they want a PVI. And everyone now has a wearable device. They have an Apple Watch, and they have a deluge of data they come with. So how do you approach? And it would be nice to get the panel's input. Sure, absolutely. So it's a complicated question, because AF ablation, to a big extent, requires individualization of your approach. And it really needs to cater to whether the patient has symptoms or not. So that's to start off with. If somebody has symptoms, and you've tried antiarrhythmic medications in them, and they continue to have symptom breakthrough, and it's impacting the quality of their life, I have a very low threshold to proceeding with AF ablation. And patients who may not have breakthrough symptoms but don't like their medications and want to get off their medications again seems like enough of an indication for me to go ahead with AF ablation. The ones that are asymptomatic that I will sure shot go for an AF ablation are those that have actually manifested with heart failure. So if they've had AFib with a rapid ventricular rate, and as you know, about 20% or so of patients may never feel their AFib. And if they've had continuous AFib and they've landed up with heart failure, I would have a very low threshold to actually take them for an AF ablation. Because even though I may try antiarrhythmic medications for a while, I would note that their propensity to have a breakthrough is quite high. And if they do have a breakthrough and they don't know that they have a breakthrough, then their propensity for having heart failure is pretty high. So I would have a low threshold to move ahead in that direction. On the flip side. That's why you have to get them to buy an Apple Watch. There you go. Yeah, no, absolutely. And I think there are better monitoring strategies now where asymptomatic patients who've had heart failure presentations can be monitored more safely for longer periods of time. And you may not necessarily need to rush to judgment and do an ablation, but I would still have a lower threshold out there. I think the subset of patients that are symptomatic have had AF for very long durations of time, actually have longstanding persistent or chronic AFib when they first manifested to you with a really large left atrium, which is greater than five and a half or six centimeters with fairly remodeled. The success rate of ablations in them is on the lower side. And then I kind of start weighing the individualized strategy there, depending on how old they are, what is their long-term risk, what their comorbidities are, and then I'd individualize that strategy. I can break it down into more, but I'll give the other panelists a chance to talk. The patient, though, that I'd like the panel's input on is the 50-year-old guy who shows up for his age 50 colonoscopy and is completely asymptomatic, healthy, active, athletic, and they find he's in AFib and they cancel his procedure and he gets referred to me. And you monitor the guy and he's got reasonable heart rate control and you echo him and maybe a little bit of atrial enlargement, but he's completely, completely asymptomatic. Now, what do we do with that patient? So I'll jump in because I've evolved as our technology's gotten better. I've evolved. An evolved man. When we first started doing AFib ablation in 98, 99, it was like a 12-hour horrendous low-yield, just a terrible day, and now it's 90 minutes skin-to-skin. I would argue that we do not know what it means to be in AFib for 30 years, right? Those studies haven't been done, but we do know that people with AFib don't live as long as people without. They have a higher risk of, obviously, heart failure, stroke, and dementia. And I think that if we don't do something now, we will, in that individual, lose the window of opportunity because electrical and structural remodeling will occur, and should we find a decade from now that sinus rhythm actually is good for you, that patient may not have that opportunity. So I would say an ablation or a rhythm control strategy is reasonable, understanding that our time horizon is measured in decades, and if we don't intervene, we're condemning that patient to a lifetime of anticoagulation and perhaps the long-term consequences of untreated AFib. But I'm eager to hear what the others would say. We'll hear from Dr. Crane, who could give a potential counterpoint. So, you know, just the obvious, which is shared decision-making's very important in this kind of situation, and it also helps, I used to do ablation, and then it got too exciting, so I stopped. But realistically, it is interesting as no longer doing it, we get a different perspective. When I go to, I'm in an AF clinic where I see patients all the time and talk about ablation and consent them and so on. So what I would say is, that patient, I always cardiovert them once, even though that's not even indicated by the guidelines. And the reason is, how truly asymptomatic can they be, despite the fact that you beat them up over the presence of symptoms. So that's the key thing, because if they feel better, or if they say, well, I just thought I was getting old, but it actually feels like I'm 40 again, then those are people where I think ablation's back on the table. And the other thing is that, you know, that H4 remodeling process does take time. And Rod, I just think it's just a huge extrapolation of the data for a procedure that still carries a 4% complication rate, 1% of which is really, really life-ending bad, right? So I think if the complication rate was 0.1, I would sort of get that, but not where it is right now, because it's become a bit safer, but not much. So Brad, could you make a comment on that? I was actually gonna make that same point, that if you see a 50-year-old who's in atrial fibrillation, it's pretty uncommon that they're truly asymptomatic. And the notion of cardioverting the patient to try to gauge that is helpful. I've seen a lot of patients who were, once they're diagnosed, once they see Dr. Haynes and you say, you have atrial fibrillation, nothing's changed the next day, but suddenly they are aware of it. They're much more perseverated on it, they feel their palpitations, and again, there's no right or wrong answer, and I don't think we'll ever have randomized data on patients just like that. But I'm kind of in Rod's camp, that I think that my threshold to do an ablation with the current tools we have is lower than it was 10 years ago. Jack? You know, I completely agree. I'm in Rod's camp out here, too. Dr. Haynes, you showed a nice slide, actually, where it was corrected for the CHADS-VASc score, and that atrial fib burden was directly related with a stroke, incidence of stroke. So I would say in a 50-year-old who has 100% atrial fib burden over time, all things being kept equal would have a higher propensity to have a stroke at some point in time, despite anticoagulation. Well, no, we don't know that, okay? There is no data. Association does not prove causality, and we know that the pathophysiology of stroke in AFib people, you know, we've all seen clots in the left atrial appendage. It makes sense, but there are other factors, and I think the ASERT trial, that's one of the most eye-opening trials for me, which is why I showed it, is that there are other factors other than just the AFib event that contribute to the occurrence of the stroke. Totally. I'll respond to both of you. If you saw a 50-year-old in clinic that's that active, he probably has a CHADS-VASc score of zero, and he wouldn't be anticoagulated, and I would ask you, do you really think that that's the right thing to do when a person is gonna be in AFib for the next 30 years? Should they be anticoagulated? Oh, totally. I think if somebody is in, so this is where I think the data on paroxysmal AFib and the data on chronic AFib, we don't have a whole lot of ways of trying to sift out how we treat these patients. If I have a 50-year-old who is now in consistent AFib, and their left atrium is even marginally remodeled or mildly dilated, I would have a very low threshold to put that patient on long-term anticoagulation. Now, granted, we don't have data about that, but intuitively, we don't have data about a lot of things in medicine. So I would err towards anticoagulation. It actually brings up a good question. No, I don't think so. I talked about this at the Western AFib meeting, and I think most of our colleagues felt that if someone has a CHAZ VASc score of one or two, who's permanently in atrial fibrillation, that we shouldn't, I don't know, it's against the guidelines, Andrew. Well, you know what, look here, guidelines is only a suggestion of how you manage, and I can actually, let me jump in to even provoke this a little bit more. All of us have seen paroxysmal AFib patients in whom we find a clot with CHAZ VASc of zero. So the point that Dr. Haynes made, and the point is with all these wearable and implantable devices, is it possible that we can actually truly answer the one question, which when the SPAF trial was published in the New England Journal of Medicine and many of the people from industry who are early or mid-career in your work in industry, you should go read this. It's a citation classic editorial in the New England Journal that Jim Cheesborough wrote. Atrial fibrillation, a risk marker for stroke. So which is the point that Dr. Haynes just made. It's just like the attributable risk that AFib alone, all things say, how much does it contribute to a clot forming? It all intuitively makes sense. So we are still stuck with this big conundrum in our field. So if you look at the rhythm itself, all of us, our gut instinct says that we have to correct this rhythm, but we still, it's very hard to quantify and to make especially a case to a funding agency or elsewhere. And even how to study this is a big, big area of contention. So I think Dave, you should comment on that. So when your only tool is a hammer, everything looks like a nail, right? And so we as AFib ablationists, it's kind of a default move to treat the AFib. And it's a necessary psychological mechanism to believe what you're doing is helping patients. But if you really take a half a step back and critically examine the data supporting what you're doing, it's not all there. And yes, it's limited by the fact that this is a decades-long problem and the longest follow-up we ever get is five years. And we will never, not in the near term, have the real answer to this. And just to go on the record, I'm totally on board. I would totally ablate this guy, personally. But I'm, again, honest with my patients. And I put that in the category of religious decision-making rather than scientific. I believe it, but I can't prove it. And I think- And what would you say if it didn't turn out well? Well, I am very upfront with people in terms of stating the risk. And I don't breeze by it. I spend as much time talking about the risks of the procedure as I do about the anticipated benefits. And yes, it is shared decision-making, and it's got to be. Because even if it's a one-in-a-thousand risk, if you're that one patient, it's 100%, okay? And we've all had to have those talks post-complication with our patients. So, I don't want them to be surprised if something bad happens. I have two comments. Well, first of all, Andrew, you should send your patients to Northwestern for their ablation, because our complication rate is way lower than 4%. So, I'm just kidding. He's at 1% serious complications. Right, serious. So, I would add this. I think that we make a mistake in electrophysiology talking about stroke as one mechanism. It's like the stroke neurologists or the medicine community talking about arrhythmias, and we are seeing all arrhythmias as one entity. The fundamental question is, is it the rhythm that causes the stroke, or do these patients have an atrial myopathy, and the rhythm is simply a marker? And therefore, eliminating the rhythm doesn't necessarily treat the myopathy. So, in studies like a search, you see a temporal dissociation. But because all these patients had devices, they didn't have brain scans to adjudicate stroke mechanism. When they retrospectively adjudicated stroke mechanism, first of all, in that study, the mean age of those that had a stroke was 78. The mean chance of that score was five. And when they retrospectively adjudicated stroke mechanism, there were only five cardiomobolic strokes, four of which occurred within 30 days of an AF episode. So I think we need to focus in on those strokes that we think are cardiomobolic in nature and amenable to anticoagulation, and otherwise we're gonna get lost in the noise. Jack, do you wanna make a comment and then? Absolutely. You know, if I can just stress that our existing risk scoring system, that's the CHADS-VAS scoring system, is highly ineffective and inadequate. It is a risk scoring system that is trying to quantitate the metabolic milieu that puts people at risk for having a stroke. It does not take into consideration left atrial size, dilatation, left atrial contractility, it does not take into size or consideration what the anatomical phenotype of the left atrial appendage is. We know that certain left atrial appendages are highly predisposed for having clots even with paroxysmal AFib, whether it's a chicken wing versus the other kinds. So I think our phenotyping really needs to be, you know, elevated to a different level before we can really put all our eggs in one basket on a risk scoring system. So there are many inadequacies out here, and I think that's where clinical judgment really comes into a play, and we may not have one fixed answer to these questions. Andrew? So let's do a little math together. So first of all, there's something called a C-statistic. Can you press the button? Yeah, yeah, the C-index. And that, when you do a model that develops risk factors, that tells you how much of the risk you predict by using your score. So CHADS-VAS or CHADS, the C-statistic is about two-thirds. So it means a third of the bad things have nothing to do with the risk factors that you're calculating. So that speaks to the severe limitations of our simplistic scoring systems to predict risk. But the other math goes like this, for the people who like history. So the original paper of the association between AFib and stroke was Philip Wolf Framingham, 1979, Neurology. And that says that your risk of stroke is increased five-fold by having AFib. Okay, good. Five more epidemiology studies have come out since then, and they have adjusted for more and more things that are also associated with stroke. And now the odds of having a stroke contribute to AFib, AFib increases your risk by about two-fold. Okay, we're pretty good with simple math so far, right? Okay, how much do anticoagulants reduce the risk of stroke? Let's make it up, 80%-ish, right? They work too well, right? If they took away all the AFib risk, they should reduce stroke by 50%, right? That's one over two, right? So they're preventing stroke from other mechanisms, because AFib is so enriched by people who have other reasons to be worried about stroke. So when we think that it's the rhythm, this is part of that, it's association and not causality. Even if it's causality, it's not causality for all the strokes, because of the other things that AFib goes with, like hypertension and age, that contribute to risk of stroke. So the whole notion that we're going to get rid of stroke risk by fixing AFib, even if we can cure the rhythm, is unrealistic and not supported by the data. What you will do is you will debulk the risk by treating AFib, and that's a conundrum. If you're on the neuroscience of stroke side of things, there's a whole bunch of clinical trials and registries that have looked at sort of blindly anticoagulating people, and that doesn't work either. You either increase risk or it's relatively ineffective. So the solutions are going to be complex, but the rhythm itself is not going to be the entire solution. Yeah, but at the same time, sorry for just, you know, if you don't sort the rhythm issue out, you're allowing that, and you know, all of us know the adage, AFib begets AFib, and AFib leads to more AFib, and AFib then leads to worse remodeling of the atrium. The atrium gets more dilated, more ineffective in its contractility, and what do you get then? I mean, that is again a potentiator of abnormal rheological factors within the left atrium that can cause a stroke. So it's all interconnected. I don't think we can sift one apart and say this is responsible and this is not. You make a phenomenal point. So in spirit of full disclosure, in any given week, I schedule three or four patients for AFib ablation, and I actually schedule it even for my colleagues because I personally like to do more VTs, but having said this, it again goes back to the whole finding that taking care of patient symptoms is actually a very important goal for us, and what gets to be somewhat challenging is other than patients like Dr. Singh said, ones who have actually heart failure or an evidence of tachy-induced myopathy, even if they're asymptomatic, we are very aggressive about trying to reestablish sinus rhythm in them, and we can actually do MRIs, prove that they have no other reason to have a depressed EF and so forth. So there is a lot to be said for searching and finding a good rationale for ablating, and the point that Dr. Andrew Crane made is also a very important one because people start adjusting their lifestyle, and they slow down or they stop playing tennis or doing something because they're correcting to a preexisting problem. So giving a period of people of sinus rhythm may be the only way in which you can get subjective symptoms out, and it's very sad that we don't have an objective test where, like a CPX, where you can put someone on because nobody gets a CPX at baseline to compare to. So the only way we can do that is to get them back into sinus rhythm and compare life, and it'll be interesting to see those types of studies or some other way in which you can objectively quantify how patients feel. So, because I think this, many of the payers are asking for these questions, and many years ago I was once asked on a panel, in a general cardiology panel, and I remember one of our good friends, our mentors, Fred Moradi's response. People said, oh, the affirmed study, as many of you know, people did very well in the rate control arm, but then if your patient comes to you in clinic with highly symptomatic AFib, something like Dr. Knight showed, what do you tell them? Go read the affirmed study and go sit at home? We can't quite do that either. So which is why the industry here, and one of the points that we perhaps nicely can segue into is, is there more that industry and we as academia and sort of centers that do this procedure, what could we do this so that we reduce, we make the risk of complications asymptotic at a very, very low level? And would that be, this is a goal for this particular conference, and perhaps we should get some quick comments from the panel, and then open it up for audience questions. Dave? Yeah, so again, I think PFA is going to be disruptive in the field in terms of lowering complication rate, shortening procedure time, and hopefully improving success rate. So I think that that is at hand, and I think within a couple of years we'll have a good idea what the new kind of baseline is. But then, my personal bias is it's all gonna be about mapping. Quick comments from rest of the panel about how much technology can make the risk of complications as low as possible. Mapping is Dr. Haynes' answer, and the new energy source for ablation. What about, make a comment, forward-looking. I totally agree. I think mapping certainly has made ablative strategies much more directed, focused, easy to do. I think balloon-based strategies have also created, it's kind of what I call the great equalizer, where a second-year fellow can do an ablation as good as an attending who's been practicing for 10 years. So balloon-based strategies are also, I would say, certainly strategies that have made the procedure much safer. Pulse-field ablation obviously is gonna change field. Ron, Brad, Andrew, quick comments. Yeah, obviously our goal is to make the complication rate as low as possible. I'll tell the fellows, a lot of people can do what we all do, but the key is to do it without any complications. And what are the risk factors for complications? Technology will, I think, as it gets better, lower those risk factors, but the other risk factors are largely beyond our control. Patient comorbidities, we see increasingly older patients in the community being offered AF ablation that probably aren't good candidates. Extremely obese patients that are not gonna tolerate a complication are probably not good candidates. And then there's a whole issue, particularly in the United States, of procedural volume and experience and how we handle that. Should low-volume centers be permitted to continue to do pulse-field ablation once a year? And how do we manage that? How does HRS help us address that? How do other countries handle that? So I think procedural volume's another important one. Andrew and Ron, quick comments. Well, a quick comment. It was alluded to earlier. I think that we've derailed ourselves by having the definition of failure of a 31-second episode of AFib. So you take someone with, it's been an AFib consistently for two years, you ablate them, and on their device, they have a single one-minute episode, and we call that a failure. I guess the patient calls that a success. So I think that we need to leverage advances in sort of monitoring and talk about more AF burden and the AF density and how we impact those because studies like the used ILRs show a 98, 99% reduction. So I think that we're making advances not only in how we treat these patients, but how we define success I think is important because people get a misconception by reading the literature with that very hard, unachievable end point. Andrew, any quick closing comments for this part of the discussion? I think historically, there's this concept that the more you do, the more effective you are, but that's a trade-off with more complications. And I think if we do it better, it'll both improve efficacy and reduce complications. That's a good challenge for the engineers, and I'm sure they're up for it. So we need some questions from the audience before we close this part of the discussion. Please. One question, sorry. I'm gonna use the salt before he passes it. That's right. Cut off at the pass, I love that. Going back to this 50-year-old with asymptomatic AFib, where did lifestyle modification, behavior modification, we know there's a dose dependency for weight loss on AF burden and severity. There's great data out there to support this. Where does that come into play, either pre or post procedure? And do you think we'll see AF added to the cardiac rehab indication list soon? So lifestyle modification is critical, and I am the biggest cheerleader for all of my patients for it. Unfortunately, it is one of the toughest things to achieve. There was a great study published very recently in New England Journal about alcohol abstinence showing a dramatic effect in terms of AF reduction. Out of a study cohort in Australia, they were only able to enroll about a quarter of the patients who qualified for the trial because they had to convince them to quit drinking for six months, and that was not accepted by the majority of patients. Especially Australians. And even the non-drinking group was reduced to .4 drinks per day, so it was not entirely non-drinking. So things like that, and we all know the challenges with weight loss with our patients, and we all know the challenges with getting third-party payers to pay for patients to exercise, which has a huge positive benefit. And we've got a great cardiac rehab program, and patients love it, but it's out of pocket, and they don't do it, as a rule, for more than a short duration. So that's a frustration, because that is really our upstream therapy option right now, is to improve those factors. Yes? I just have a very quick question. So do you expect IRE ablation will completely replace tradition RF ablation for PVI in the next decade? Well, personally, and full disclosure here, is that I'm working closely with one of the companies that is developing that technology. So I do have a bias, but I've seen the preclinical data, and I think for pulmonary vein isolation, it will be a superior technology to everything else that is either available today or in the pipeline for development. Now, I will say, beyond the pulmonary veins, the jury is still out. The attractive thing about Pulse Field is that there's no collateral injury to critical structures like phrenic nerve, pulmonary vein, coronary arteries, and esophagus. And so if you are able to find the right place to ablate in the atria, I think PFA is going to be the preferred energy source. But the delivery, the catheter that you use to do that, I think we don't know which catheter that will be, and I think a lot of the catheters that we're using or that are in testing for RF right now will be very adaptable for Pulse Field as well. So the balloon-based electrode catheters, I think would be great tools to deliver Pulse Field ablation. Thank you.
Video Summary
Catheter ablation of atrial fibrillation (AFib) is highly effective in improving patient symptoms and quality of life. However, there is still much to be understood about why it works. The panel discusses the thresholds for performing ablation in patients, particularly those who are asymptomatic but have risk factors for stroke. They also emphasize the need for individualized treatment approaches, considering factors such as symptoms, medication preferences, and comorbidities. The use of wearable devices for monitoring and improved mapping technologies are mentioned as ways to better determine the impact of AFib and guide treatment decisions. The panel also highlights the importance of lifestyle modifications and behavior changes, such as weight loss and alcohol abstinence, in managing AFib. The discussion concludes with the suggestion that newer technologies, such as pulse field ablation, have the potential to improve the safety and efficacy of AFib ablation procedures.
Asset Caption
Topics discussed:
The Patient Journey to Ablation: Medical vs Ablation Therapy
Challenges in Ablation
Emerging Tools for Ablation
Preventing that Catastrophic Complication
Keywords
Catheter ablation
atrial fibrillation
patient symptoms
individualized treatment
wearable devices
lifestyle modifications
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