about. I think this has a lot of really interesting and hot topics. It's titled The Journey Continues ICD and Athletes and I'm required to read you something here. So it's my pleasure to welcome you to San Diego and Heart Rhythm 2025, the 46th annual meeting. If you have not already done so, please download the mobile app. This is how you can participate in live Q&A, which we do want you to submit questions. I think these are all great talks, so submit us lots of questions and then we'll ask the speakers. When using the mobile app, log in with your HRS credentials. I think that that's probably enough of what I have to say for that. So again, four great speakers. We're gonna go ahead and get going. Our first speaker is Eugene Chung from the MGH. Update on guidelines and consensus statement for athletes with ICDs. Yep. All right. Thank you, Dr. Poole, Dr. Estes, and the program committee for having me. So, my task is to talk about guidelines and consensus statement recommendations for athletes with ICDs. And in general, I'll cover some general concepts regarding athletes with arrhythmias, give some highlights from the 2024 HRS Expert Consensus Statement on Arrhythmias in the Athlete, and give some future directions. If you haven't already had the pleasure to read this document, and we are quite proud of it, but very open to suggestions and recommendations, there's a QR code that'll take you to the latest version, and I'll show it again a little bit later. So, some general concepts. Treatment post-cardiac arrest, or in those who you think may need an ICD and at risk for cardiac arrest, are not a whole lot different from non-athletes, but there are some differences that those involved with athletes have to consider. Choice of medications, which we'll hear about later from Dr. Darden. Choice of device, which we'll hear later from Dr. McIntyre. Confirmation of arrhythmic risk, so particular conditions that I think the science all knows about, ARVC, CPVT in particular, as well as theopathic VF all can be a special risk for arrhythmias related to exercise. And then something that transcends everything that we do is shared decision making in terms of return to play. So, shared decision making, just to kind of go over it, is extremely important, obviously, in the patient-doctor relationship, and well-established as an important part of how we practice, well-documented, how it improves quality of life and patient satisfaction. And decisions about return to play can be challenging, and a particular challenge with an athlete, especially in the context of competitive sports and teams, is that there can be a multitude of stakeholders, and sometimes additional education, review, multiple discussions are required to truly have a shared decision. Oops. Full shared decision discussion, so let's see what happened there. All right, we're back. Good. That was not a shared moment. All right, so before I get to the HRS document, recently the clinical considerations was published in Circulation and Jack, and there's a joint effort from around the world led by the ACC Sports and Exercise Cardiology Council, and there were a couple comments about ICDs, and deeper dives into each of the task forces in this document are forthcoming, but in particular, mirroring some of the things that are in the HRS document, that competitive sports participation is reasonable for a competitive athlete to receive an ICD, that if you get a device, then for, we said four to six weeks, in this document, for eight weeks, of sort of limited activity is important for healing, and that shared decision making is really important as part of the return to play process. In the HRS document, we have a summary algorithm to evaluate those who've had sudden cardiac arrest. Won't go into that too much today, but those who are at risk for sudden cardiac arrest, and we'll go through those in some detail, and so with anyone who you are concerned about risk of sudden cardiac arrest, it's very important to have an expert in the disease in question. It's very important to have a sports cardiology friendly person involved, and shared decision making, as I already mentioned, important in terms of discussing the risk of recurrent sudden cardiac arrest type of sport, wishes of the athlete, and of course, the inclusion of all stakeholders. Before anyone even gets an ICD, it's important to address potential reversible causes, and so reversible causes on the left, commodity of cortis, WPW, need to be carefully discussed. Situational dependent factors in the third column, anomalous coronaries might benefit from surgical repair. If coronary artery disease is at play, that needs to be addressed. Myocarditis also need to be treated before you go down the road of a device. As I mentioned, CPVT, ARVC, sometimes some conditions, some patients with Lung QT type one, you have to carefully consider whether you wanna go the medical route versus an ICD early, and irreversible causes, dilated chromopathies, other inherited chromopathies, unexplained sudden cardiac arrest, you're gonna go down the route of an ICD earlier in the management process. So in terms of the, once you're down the road of considering an implant ICD, then in yellow we have class two indications, and green in general, class one indications. So as mentioned, return to play is gonna involve shared decision making, and then you need to consider what type of device, consider the form factor and the sport when you place the device, and then the waiting period. So we're gonna hear about this, about the different type of devices shortly, and so I'm not gonna go over this figure in detail, but in the HRS document we do have a figure inspired by other figures out there, but does cover the main form factors available. And I'm just gonna highlight that for the adult master athlete population that I see the most of, that there is a role for dual chambered transvenous devices. Now an athlete, if they need a transvenous device, and they don't need atrial sensing or pacing, maybe try to put in a single lead device, but a lot of the patients that we see, the masters athletes that they fit, it's helpful to have atrial sensing, so there is a role for that. Sub-Q ICDs have some advantages, of course, of not being in the venous system, but of course don't currently have a setup where you can do pacing or sensing. If there is in the near future a system where you have a leadless pacing device that can communicate smoothly with your sub-Q ICD, that might be an interesting combo form factor. The recommendations we have in the HRS document are built on data that Dr. Lampert provided to us through her registry starting back in the, well, about eight years ago now. So 440 participants, and just to highlight, there were no sudden cardiac death or external shocks needed during or after sports, and that in the initial study and in a follow-up study by Dr. Link that definite or possible lead malfunction was quite rare. A sub-study, subgroup analysis of just the European data led by Dr. Heidbuchel looked at competitive versus recreational athletes, and competitive athletes did have more total shocks, but there was a high proportion of those related to AFib or inappropriate sensing of sinus rhythm. Shocks, importantly, whether you were recreational or competitive was not associated with death or bodily harm and that ARVC, corroborating other data, particularly from the Hopkins group, ARVC was particularly associated with the highest odds risk of having a shock. Another analysis by Dr. Slansky of Dr. Lampert's registry showed that, and it makes sense, that those with a high conventional rate cutoff, so over 200 or higher, and those programmed with greater than nominal detection zones, both categories had reduced all shocks. One point of emphasis in the HRS document was that exercise testing is really important. It's important for psychological reassurance. It's important for reassurance that the medical therapies, if you've applied one, that are suppressing the arrhythmia, and important for those who have, particularly with transvenous leads for sinus node dysfunction programming, and also for T-wave sensing and ruling out over-sensing, particularly those who have subcutaneous devices. In terms of device follow-up, the recommendations we put here are not that different from the non-athlete population. Of course, if someone has an event or an episode or maybe ATP-treated events, then you're gonna have to reevaluate your medical therapy and potentially repeat the stress test. We also made sure to have a couple other things that in the recommendations, they're outside the algorithm, but they're, and we didn't have a dedicated ICD section, per se, because the role of the ICD transcended different areas of the document, but one of the recommendations we had there is that those with inherited arrhythmic syndromes who have a clinically indicated ICD that sports participation is reasonable, and so this mirrors what was, ended up being in the clinical considerations document, and then athletes with inherited arrhythmic syndromes as well as inherited chromopathies and ICD for the sole purpose of return to play is potentially harmful in class three. So in terms of future directions and things that maybe aren't quite in the document, so one of the devices you're gonna hear about is the epicardial ICD that is right now just implanted at the Mayo, and I just happened to bump into Mike at registration, and he's about to submit some follow-up data on his device, so that's gonna be very welcome data. The EVICD is an attractive option, but it's still relatively new, so we're still learning about its role, but it is an attractive option for some of the younger patients who may need to use their arms quite a bit for whatever they choose to do. As I mentioned, a combined device with a leadless pacemaker and a sub-QICD may be an interesting future form factor. Protocols for exercise testing, and so we have the benefit at my institution of having a CPET lab dedicated to the sports cardiology practice, and so we're taking quite a bit of time doing programming post-implant for the sinus node dysfunction patients, as well as looking at the T waves and T wave oversensing the sub-Q patients, so a space where I think needs some more formal protocols, and fortunately we have the space to start looking at that actively. So we know in non-athletes as well as athletes that AFib is a major cause of inappropriate or unnecessary shocks, and so in our document and in other documents, AFib ablation is now considered first-line. I think we can get rid of the term early ablation, but first-line ablation, and that maybe it needs to be even more first-line in the athlete to help prevent unnecessary shocks, and hopefully at the end of this month we're gonna get approval of a patch wearable defibrillator that's gonna be waterproof, and that's gonna be an interesting option for patients who are bridging between not having a device and getting a device as you're doing your sudden cardiac risk assessment. So I've gone over some general concepts, some broad strokes of the HRS document, and a little bit, a little taste of some future directions I think are forthcoming. Please encourage you to read this document and feel free to reach out if you have any suggestions or recommendations. Thank you for your time. That was really a wonderful summary of the document. Please, audience, feel free to come up to the microphone and if you have questions or comments, or you can submit some, which right now we don't have any. So I just have one comment for you, and that is the discussions around PTSD and inappropriate shocks, did you look into that any further? That is a fantastic topic. We did not specifically look in that other than we did provide some extra text that psychological readiness is an important part of the return to play plan. Yeah, I mean that is a huge issue for all patients, but particularly the younger the patient, the worse that experience is going to be for them. It certainly has to be factored into all of your shared decision making. Any other questions, comments? What protocol, exercise protocol after placement of the defibrillator do you recommend? You showed ERG, but usually it's an accelerated BRUCE, is that correct? So we rarely use the BRUCE protocol in our lab. We basically tailor it to the patient, and because we have the benefit of being able to take a little bit of time, because we have our own dedicated CPET lab, we might take up to an hour and do multiple runs. We may even do thrusts sometimes. We have an ERG treadmill and a stationary bike, so we try to pick and choose as close as we can, and sometimes we may just do straight hill workouts, so we tailor it to the patient. So, yeah, BRUCE is usually not mentioned, yeah. The shared decision making includes the governing body, be it a college, sports. I know that the MBA has gotten much more liberal. We now have a separate committee that evaluates on an individual basis. Are you running into shared decision making in which everyone agrees it's reasonable, looking at the risk and benefits, but the organization or institution says no? The latter case that you mentioned, unfortunately, had been infrequent. I think one has to be ready to have multiple conversations and involve everyone early in the process, and with my experience, with that kind of open-mindedness, that usually we can come to a joint agreement. Yeah, and just historically, this is a sea change, because previously, ICDs were sort of a paternalistic prohibition against athletic participation, and there's been a lot of progress with the shared decision making and institutional willingness to do it, going back to a famous Nick Knapp case in which he was cleared by everyone, but Northwestern said no, he sued, and Northwestern actually prevailed. So there's been a lot of progress. Hi, Ziggy Whitman from Temple. I have a specific question about, with ICDs, obviously, these are very sophisticated devices, but you could answer this about SVT or any other of the arrhythmia syndromes that we see in athletes. What specific education have you done for trainers at these institutions who haven't gone to medical school, aren't electrophysiologists, but have to have some understanding about SVT, AFib, and ICDs? That's another really good question. Part of the return to play should be emergency action planning, and while maybe AFib, not necessarily an emergency, can lead to shocks and can lead to symptoms. So case-by-case basis, I would say. I don't have a formal protocol, but depending on the condition, certainly would involve, is there an athletic team setting discussion with both the supervisor and the athletic trainer, and as we all know, athletic trainers are first line. I don't have a specific protocol, but we would definitely reach out to anyone involved with that player and then have a discussion. Okay, we'll move on to the next session. We do have time allocated at the end of this session to questions and comments, which we'll use after each of the presentations, but the next session is by Mitchell Cohen, who's gonna talk about channelopathies, cardiomyopathies, coronary artery anomalies, congenital heart disease. Are the risks the same? He comes from Inova Children's Cardiology. Do not think we have a mouse that's working. There we go, got it. You got it? Yep, okay. Because I think I can start. Nope, you're good. All right, I'm just about getting over a cold, so for those of you who know me, this is probably not what I normally sound like. Exactly. All right, so anyway, Dr. Estes and Dr. Poole and everybody else, thanks for the organizing committee for having me here. So this is sort of like a very broad topic, right? Talk about like everything we do in pediatrics and sort of sum it up, like are the risks really the same? I have no disclosures. And I would say that decision making is difficult. I think it's not so simple, and I'm gonna kind of go through why that is. Let's sort of see if this is going. So when it comes to recommendations for sports participation, it's really not all conditions are the same. And so when you sort of like go, you can't really sort of start thinking about congenital heart disease and think, we all know that every congenital heart disease is different. We know that, whoops, this is not. Sort of all the cardiomyopathies, whether you're gene positive, gene negative, which type of cardiomyopathy you have, and whether you have which type of channelopathy. So to sort of say that every one of these is really the same and you're gonna treat them all the same is probably not practical. So with that being said, I think it's important to kind of go that not all running shoes are the same. So this is, when I lived in Arizona, this was my running route. And I would say that I ran into that guy in my backyard. I definitely ran into this guy in my front yard. And the last one I ran into once, that's not a picture of the one I ran into, but a mountain lion will definitely cause sudden cardiac death, but probably in a completely, totally different way. Sorry, the advanced one's not working. Okay, and I think that's very different than high school track, where they're all set up and they're all there and you've got teammates and you've got people who can sort of have emergency action plans and you've got an AED. And it's very different, I think, along those ways. And I think if you sort of look at the same thing we'll hold true for, this was my kids' high school swimming pool with Camelback Mountain in the back. And that's a very different sort of look than where you are if you're sort of in a swimming pool, outside, sort of in a outdoor open ocean kind of thing. So we can't sort of look at every single sport and say it's all the same, the conditions are all the same. It's certainly very multifactorial. Sorry, Jeannie, this is just not advancing. Yeah, I think, so when you look at the genesis of arrhythmias and ICD shocks, for a lot of reasons I think it's multifactorial, and I'm not going to go into all these, because all these are really contributors of all of that. Sorry, guys. So what are we really worried about? And I think that what we're really worried about, what about failure to defibrillate during a sporting event, lead failure, lead fracture, injury related from a syncopal event during exercise-induced arrhythmia or shock, lead damage, needing another operation, the risk of extractions, generator damage during high-contact sports, heightened incidence of inappropriate shocks, which we've already sort of talked about a little bit, psychological effects by withholding sports on kids, which is a real issue, certain conditions may advance disease progression and cause more shocks. And lawyers, well, I would say that I'm married to one, so I always worry about a lot of things in that regard. All right. This is definitely not advancing. So I also never understood why these things were really at zero risk for class one conditions because they're sort of not all the same also. I think it's going to take me 12 minutes just to get to advance my slides. So we have to sort of rethink kind of where things are. And so if we look at the safety of sports, we're going to go back about 10 years and kind of look at the entire cohort. So this was the original study that looked at safety of sports, which is a prospective registry, and there were 24 pediatric patients out of the, 24% of the pediatric patients were the entire cohort. So about a quarter of the kids in this entire study were those that were 10 to 19 years of age. And if you looked at the primary endpoint, there was no recurrence of the primary endpoint, which was tachyarrhythmia, death, externally resuscitated VT. So this sort of started the question of, is sports safe for our pediatric patients who have devices? And so if you looked at that entire study group, so not just the PEDS patients, 10% had experienced shocks during competition or practice, 8% experienced shocks during other physical activities, so there was really no difference, 6% experienced shocks during rest. So there were more individuals who received shocks during either competition or practice or physical activity than during rest. However, there was really no difference between the proportion receiving a shock during competition practice and those receiving a shock during other physical activity. And if you break down those that are in the sort of high school, JV, varsity, traveling subgroup, the percentage of individuals in the competitive subgroup receiving appropriate shocks during competition was not any different than those that were not in the competitive subgroup. If you flash forward five years and we get to one of the first papers that really started to break down the pediatric groups, this was 129 athletes under 21 years of age that the majority participated in some sort of competitive sports, the vast majority being adolescents, about half having long QT, and about a third having HCM. And if you looked at the, again, no patient reached the primary endpoint of tachyarrhythmia deaths or externally resuscitated events. The secondary endpoint, which was number of shocks, lead damage, about a quarter of the athletes received at least one shock. Only four athletes received appropriate shocks during sports, though, and 4% had inappropriate shocks. So the rate of appropriate shocks was actually quite low, and less than 25% occurred during sports, but 35% of the shocks were actually inappropriate. And I think along those lines of the psychological impact, we see that a lot. This was also sort of at a time where the RIATA leads and the Fidelis leads were quite active in the pediatric population, and that had a whole different thing. But as we've learned a lot about programming at high rates and T-wave over-sensing and all those things, so I think we've made a lot of headway in trying to reduce inappropriate shocks. There was really acceptable freedom from lead malfunction, but I think there is a reality in what we do as pediatrics. And for those of us who've had kids, sports end for the vast majority at some point. 82% stopped playing competitive sports upon graduation from high school. Only 6% stopped because of an ICD shock, and of the seven athletes who stopped because of shocks, only one, many continued other sports and switched sports that they were playing. But there's a limited timeframe generally for the majority of the patients we're going to see as adolescents. This was the 2021 PACES consensus paper that basically sort of said, and I think we all would agree with this, that primarily should be based on the consideration of the diagnosis and the physiology, not just the fact that they have an ICD. And I think this gets to the point that you have to be a splitter. You cannot sort of lump all these patients together. So if we look at HCM and vigorous exercise with or without ICD, you can sort of see that in this registry study, there was really no difference between those that are performing vigorous exercise versus non-vigorous exercise for the composite endpoint of experiencing a life-threatening event. And if you actually break down this study and you sort of tease out all the pediatric patients, so there's 203 HCM patients that are between 14 and 22 years of age. About a quarter are participating in varsity sports, another participating in other vigorous exercise, not necessarily varsity sports, and about half sort of moderate sedentary activity. And what you can see is that there's very few patients who actually have an event with an ICD in the middle sports with HCM. And in fact, one here had it during sitting in assembly, and one was just running around outside with his friends. And if we go to the same thing with the long QT population, the results are not too dissimilar. There's the breakdown. I would say that most of these studies are significantly white Caucasian, and I think it's sometimes very hard for us to give recommendation on African Americans and Hispanic patients because we just really don't know if they're the same risk criteria or they have additional risk factors. And I think when we look at these studies, we have to keep that in mind then when we're counseling patients from different backgrounds. But again, about 10% of these had ICDs, and there really was no difference in the incidence of appropriate and inappropriate shocks, and certainly very few occurred during sports. Now, there are huge differences between American football and European football. Not only do the players and the coaches look different than the players in Europe and from those that are in North America, especially since it's draft day here. But if you look at this study, so this is a study that looked at competitive athletes versus those that were intense recreational. To use the term intense recreational, basically these were people that were doing intense physical activity on a regular basis, two days a week for at least two hours to improve their physical performance. Now, there were differences in the two groups. One had more CPVT. Recreational athletes were more likely to be on beta blockers. But there was no tachyarrhythmia events during resuscitated VT events. Nobody met the primary endpoint. There was no difference in lead or generator malfunction. They were pretty comparable between the two. But what was different was that in those who are performing competitive athletics, they had a higher incidence of both appropriate and inappropriate shocks, but it's a generalization. So you can't look at this and say, oh, this was all CPVT patients or this was all HCM patients and about a third stopped playing sports. So we have to sort of really become splitters and break down the data of who we're talking about so we can give really good recommendations to patients. And again, not all roads or conditions are the same. So if we look at ARVC, we know that patients who have PKP2 mutations are very different than other ARVC patients. So if you are an endurance athlete, even if you are a family member who is positive for DSP, and you're more likely to meet task force criteria, and you're more likely to develop VTVF. And if you look at the pediatric data, the same holds true. So in maroon are those with meeting task force criteria and sustained VTVF. And you can see that the adolescent and young adult patient population who are more active doing higher physical activity are more likely to meet task force criteria and develop VTVF. So I think athletes with PKP2-mediated arrhythmogenic cardiomyopathy should be advised that competitive endurance sports are likely going to increase the risk of ventricular arrhythmias regardless of whether they have an ICD. The ICD doesn't really matter. And the same probably does not hold true for DSP mutations. And just to use the last one, CPVT, if you look at CPVT athletes and non-athletes, this is a much older study, but sort of similar events. There was really no difference in athletes and non-athletes with CPVT regardless of whether they had an ICD. And in fact, if you looked at the athletes, I think this is an important point for a pediatric population, they have events that are not necessarily occurring during sports. Wrestling at home is just a typical, I had two brothers, we wrestled probably every single day and drove my mother crazy. And the other thing I think is an important point is that non-compliance of beta blockers is a real issue. And it's a big trigger. And so you have to be counseling them about are they adequately compliant with their beta blockers. So CPVT in sports, we don't have all the answers. Athletics is not a uniformly stressful endeavor. Training makes exercise safer with fewer cardiovascular outcomes than those who regularly prepare for physical exertion. But is the weakened warrior at higher risk because the stress of exertion is greater for the infrequent participant? Is it possible that the regularly exercising patient with CPVT is a lower risk than the deconditioned burst exercise athlete? And could regular intermediate intensity exercise actually be protective? Is there really much difference between the toddler having a temper tantrum, the high school kids getting super worked up at a video place after work, or girls playing varsity competitive soccer? There's no way you could get into congenital heart disease. The difference of what we do within heterogeneous population is too much to even get into. I would only argue that we definitely know for those of us that take care of single ventricle Fontan patients that Fontan patients who exercise regularly, even if they have an ICD, are going to do better in the long run. And I'm going to end with one other comment about shared risk decision making. And that's different for us than probably our adult colleagues. We have to make sure that both parents are involved. And so sometimes if you have one parent that comes to the office, you cannot finalize the decision about shared risk decision making till both parents are present. And there's a lot of other stuff goes into it. And as already pointed out, there has to be an emergency action plan. I'm sorry, my clicker wasn't working, but thank you very much. Thank you very much, Dr. Cohen. The presentation is open for comments or questions. You can send them in electronically. I don't have any. Or come to the mic, identify yourself. And perhaps, Mitch, as people are formulating their questions, in a PKP2 genotype positive, genotype negative child or adolescent, do you restrict them, or do you go through shared decision making? I think you go through shared decision making, but you really have to emphasize that this is going to be a progressive disease. And I think that it's easy when they're in elementary school, because you can gear them towards different sports. You can get them really involved in golf and other things. I think it's a little harder when they're coming to you when they're in 10th and 11th grade. But maybe they only have a year left of high school sports, and they're not going to play in college. And you can kind of balance out the psychological risk of them all of a sudden having to walk off a team. But I think you tailor it towards the age of the individual. Just to point out is that in the erythrogenic cardiomyopathy consensus statement, it was a class one indication for restricting them. So one needs to be mindful of that. And if you make exceptions to it, you need to be mindful. Questions, please. Great talk, Mitch, as always. Just a question. I think I'm just trying to see where the pendulum really falls. I think one end of the spectrum was all patients with hypertrophic cardiomyopathy or CPVT, restrict them. Don't let them play. And I think the data from Dr. Lambert and everybody else says, hey, you know what? They can safely do a lot of things, so don't be so restricted. Message gotten. The other end of the spectrum, which I want to make sure we're not getting, is that all patients with hypertrophic cardiomyopathy and CPVT are OK to let them go and play and do whatever they want to do. Because clearly there is at least a theoretical risk. The more you play, the more your adrenaline, the greater you are at risk for having a cardiac event. Yeah. I mean, I think that's the whole. I think CPVT and HCM are two different conditions, for starters. I think you have to also have, and we're talking about patients with ICDs, right? And I think you have to, one, have exercise tests in your office that you feel very comfortable that they're fine and they're not going to get appropriately or inappropriately shocked. I think you have to hear what they want, and I think you have to balance it all out. I think an obstructive hypertrophic cardiomyopathy with a low EF, with a mid-myocardial LGE burden of 20% is not the same thing as somebody who's genotype positive HCM with no LGE, clean halters, that kid's obviously probably not going to have an ICD though, right? So we're sort of talking like something got them to getting an ICD in the first place, so they're already a little bit of a higher risk candidate. But I think that if the question is, are they safe to play, are they going to get shocked appropriately or inappropriately, I think you have an honest discussion with them about that. I think the CPVT patient who you put on the treadmill and they're still having runs of arrhythmias and you don't have them adequately controlled with beta blockers and flecainide and you're talking about a sympathetic, you're not going to let that kid play regardless of what they want to do until you get it under control. So I think at the end of the day, every decision is different for every single patient. I agree, and there are always extremes, but if you take the patient who's, let's say, controlled, but he does have hypertrophic cardiomyopathy, I think you still have to be careful. The risk does go up with activity, even though if they have a defibrillator, their risk is still going to be substantially higher than a patient who doesn't have hypertrophic cardiomyopathy. Yeah. I mean, I had a kid in Arizona and he wanted to play baseball and I let him play baseball, but I moved him out of playing catcher and I put him at first base. And I think you can tailor the situation accordingly if that's really what the family wants. But yeah, I think we can't go to the point that we're so cavalier about it, and I hope I didn't come off along those lines. Yeah. Thank you. I just wanted to kind of convey that. All right. Two quick, quick questions, perhaps, with a quick answer. Specifically, is there a sport that you say no? Is it the long QT syndrome type 1 or HCMICD patients? I think I tailor, it's not a specific sport. I think I want to make sure they're in a safe place. So I will let kids do track, but I might not let them do cross country. And that seems crazy, but I can tell you where I ran doing cross country in Arizona, you wouldn't want to be found. There's no way you can have an AED there. So you literally have to go through every single sport. And the same with skydiving, scuba diving, all those things have to go out of the question. So that's a definite maybe, okay, is what you're saying, all right. Which factors do you consider to decide and what type of device do you decide in the pediatric population? And perhaps a summary statement, I know there's a very nice image that you showed that was showed by Eugene actually as well. So maybe just give us a summary statement on that. On what type of device? The type of device in the individual patient, pediatric patient. Yeah, I mean, I think we're all trying to get away from putting transvenous ICDs in. We know the long-term issues with somatic growth, right? Many of us are congenital heart patients, don't even have access to get transvenous ICDs in. I think there's a real interest in what the EVICD is gonna look like in pediatric patients moving forward. So I try to do everything I can not to put a transvenous ICD if I can. Yeah, I would agree with that completely. Me too. Young patients, those leads are gonna not perform well. We'll move on to Dr. Poole. Yeah, great talk again and great questions. So more about what type of device to place. We're gonna hear from Kirsten McIntyre from Queen Elizabeth II Health Sciences Center in Nova Scotia. And the title of the talk is Subcutaneous versus Transvenous ICDs, Pros and Cons. Thank you so much to the organizers and to the panel for having me here today. Hopefully the clicker works better for me. The timer's not working. And the, okay, perfect. So no timer and no clicker. So thank you again. I have no disclosures relevant to this talk. So today our goal is to look at the pros and cons of the transvenous versus the subcutaneous ICD. But I don't think we can do that without briefly reviewing the history of the athlete with a defibrillator. And we'll touch again on the emergence of shared decision making in the care of the athlete and go through the role of both types of devices in our athlete patient population as well as consideration about device selection and programming as it pertains to the athlete. And I'm gonna start with a thought provoking question. So if you have an asymptomatic 17 year old basketball player that comes to you with this ECG, are you going to allow them to return to play? And what if he has a defibrillator in place? Does your thought process change at all if your patient has an ICD in place? And if the patient's appropriate for a device, how do you make decisions around what type of device to place? Are you gonna choose a traditional transvenous system for which we have a lot of history? Or are you going to choose a subcutaneous system for example? So a lot of the time that I spend in clinic and I think for many of us, we think about this question, should my patient with a defibrillator even return to sport? And this is a question that we've really only been asking for a little while. So if we look back at 2008, which really wasn't that long ago, I graduated from medical school in 2008 and that feels like yesterday. But that was still the era of if in doubt, kick them out. So universal, unconditional disqualification from competitive sport in athletes who'd had a previous cardiac arrest or who had an ICD in place. But I think even in that short amount of time, we've come a long way. We've seen this data today already, but Rachel Lampert has really helped us understand the athlete patient population with a device and it seems as though things aren't quite as bleak as we'd feared. So in our athlete patient population with an ICD in place, there were no tachyarrhythmic deaths and there were no externally resuscitated tachyarrhythmias during or after sports participation. And while some athletes had shocks, they weren't all during competitive sport. And really this concept of shared decision-making in the care of the athlete with an ICD really has only been around since 2015, which is only 10 years ago. And that's when the door really opened to even have the question, can my patient with an ICD return to sport? So what are the options? Well, these are them. So we have our traditional transvenous ICD system, we have subcutaneous ICDs, and more recently there's the extravascular ICD, but we're not gonna touch on that one now. But the challenge is if you go to PubMed and you try to find data on defibrillator in the athlete or which configuration to choose, you're not gonna find a lot. And just like kids aren't just mini adults when they come to clinic, athletes are a bit of a unique patient population and there's not a lot of data to help make us inform those decisions specific to the athletes. We have to extrapolate. So if we look at something like the ATLAS trial where patients were randomized to receive either a subcutaneous ICD or a transvenous ICD, it wasn't about athletes in particular, but it included the types of patients that we're seeing in our clinics who are having these discussions about return to sport. So it included patients with hypertrophic cardiomyopathy and idiopathic VF and the channelopathies ARVC and CPVT. And what studies like ATLAS helped us understand is that there's certainly a good side and a bad side. So it's obvious and it's funny that we needed a large RCT to tell us this, but there's a significant reduction in lead-related complications with a subcutaneous ICD system and particularly in our younger patients who we hope are gonna have long lives and hopefully many devices over the course of decades, it's nice to avoid tricuspid valve insufficiency. And it was reassuring to find out that there was no increase in failed appropriate shocks. But with good comes bad and there was a trend towards more inappropriate therapy in these patients. They have more surgical site pain. We don't have pacing options. At that time, there was no option for anti-tachycardia pacing. And as much as we may want to put a subcutaneous ICD in a patient, 7.5% of the patients in ATLAS failed their screening and weren't eligible for a subcutaneous ICD. Well, what about leads? Do they fracture more in the athlete-patient population? Well, at least in the transvenous lead, it seems that that's not the case. So again, data from Rachel Lampert and her group show that the five-year survival of ICD leads, so now the transvenous lead, was 95%. And it really wasn't any different than in the non-athlete-patient population. Sports with heavy arm use and contact sports didn't show higher rates of malfunction. And maybe the only exception was in weightlifters. So there was a higher rate of lead failure in people who lifted significant weights, but small numbers. So if we look at patients in general receiving an ICD, are younger athlete patients the same as older patients? And of course, the answer is no. They have more problems. They have more device-related complications. They have more inappropriate shocks. They have more lead-related issues. They have more infections. And the numbers are quite significant. And when we think about the rate of complications in young people with defibrillators, and that's generally the athlete-patient population that we're seeing, it's a pretty high rate of complications. So the ICD is not a benign intervention. And particularly when we're thinking about transvenous devices, we can't ignore the fact that some of these patients at some point may need their device extracted, and that's not a benign intervention. So there's procedure-related mortality to consider, and all cause in-hospital mortality between 1.8 and 3.4%. Well, so that all sounds a bit terrible for our young patients. So how do subcutaneous ICD leads perform in the athlete? That's a really excellent question for which we really have no data at this point in time. But we have questions. We have athlete-specific factors that we can consider that are hopefully hypothesis-generating for future research. So you have to question whether the long path of the subcutaneous electrode from beyond the lat dorsi through the subcutaneous tissue is at higher risk of fracture. And what does that look like for a patient who might be a weightlifter? What about for swimmers? What about for golfers? Are golfers gonna be bothered by their swing if there's a huge generator in their axilla? Is there an increased risk for far-field noise during strenuous sport? So is a 19-year-old high-level hockey player different than my 74-year-old sedentary post-MI patient with a device? Probably. Is there an increased risk of lead damage from a collision with a player or a ball? So if the subcutaneous device, for example, is extra thoracic, is it more susceptible to outside forces? And what about inappropriate shock? So particularly for non-beta-blocked athletes, and I'll tell ya, athletes don't like being beta-blocked particularly. Are they at a higher risk of inappropriate shocks? So I'm hopeful that studies like Sports SICD will help us inform some of these questions, but the jury's out and we need more time and more data. And we've talked today that really a one-size-fits-all approach really doesn't work to any part of the care of the athlete with a defibrillator, so we really have to be extra thoughtful when we think about how to program devices with ICDs. And a lot of the original programming trials really weren't thinking about young patients with CPVT who might have a defibrillator. But our young patients can absolutely achieve very rapid heart rates. So 220 minus your age, that's a pretty high heart rate. And we want to make sure that we avoid things like inappropriate shocks, which can have devastating consequences in the CPVT patient, for example, and precipitate a shock storm. And will the EV-ICD be a game-changer for the athlete? It avoids the tricuspid valve, it avoids transvenous leads over time, and again, time will tell, and it's an exciting new technology that has the potential to really change the game, if you will. But I think it's important for us to remember that we all may sleep better at night if our athlete has a defibrillator in place, but ICD monotherapy really shouldn't be a replacement for condition-specific therapy. We would never take a heart failure patient and give them a defibrillator instead of GDMT. So if we have patients with Long QT syndrome, CPVT, for example, we really have to make sure that our patients have the rest of their treatment program tailored specifically to them. And in an athlete, this has already been brought up today, but ICD implantation solely for the purpose for return to play should really never be done. So we're really talking about our athletes who have a standalone indication for ICDs in the first place. So if we go back to transvenous versus sub-Q, I think both have pros, both have cons. For the transvenous ICD, we certainly have a long history of implanting and following patients with transvenous systems. We've got good evidence to support their use, and they have the added benefit of bradycardia support, anti-tachycardia pacing, and even biventricular pacing, for example. And the batteries have excellent longevity. But there is the trade-off that a transvenous system has a higher risk of infection, there's more lead-related complications, and we can't ignore extraction-related risk. For the subcutaneous ICD, it's an attractive option, but particularly my female patients, they don't love them. The generator's big, it's in the way. But there is a lower risk of infection, there's lower lead-related complications. But we have to deal with the short-term issues of post-operative pain and the absence of bradycardia support, for example. So we're certainly in an era of paradigm shift when we're considering athletes with defibrillators. This is a concept that really didn't exist even 20 years ago. And we're no longer in the if-in-doubt, kick-them-out, paternalistic, maternalistic era where we just disqualified everybody from sport. But I think we really need to be extra conscious and mindful about the type of device that we select and the potential short-term advantages and long-term consequences of our decisions. And our device programming has to be specifically tailored to these patients. And we always have to be mindful of the fact that the defibrillator should never be viewed as an alternative to medical therapy and as a vehicle to return to play. So thank you so much. Thank you. That was another really great talk. We already have somebody ready to go. This will be my last question, I promise. Ziggy from Temple. One of the things that occurs to me for the use of a transvenous device is putting the device in the submuscular space. Because in my brain, for the active athlete, there may be less movement of the device in the lead there. So you still don't eliminate the extraction-related risks of a device. But maybe some of the lead-related complications would be reduced with submuscular implant. I recognize that in a young population, the generator chains in the submuscular space that are inevitable over time are gonna be, at best, a nuisance and, at worst, more than that. But I wonder what your experience is with the submuscular implant in these patients. I'd be curious what everybody has experienced, but I really haven't found an appreciable difference in the submuscular implant versus a traditional subcutaneous implant for the transvenous system. And I think we know, in general, that our patients, particularly who are younger, more active with normal ejection fractions, in general, have a higher rate of fracture and lead-related issues over time. And it's a real challenge. If you put a device in a 15-year-old and they have something like CPVT and they should have a good life expectancy, that's many, many, many decades of wear and tear and many, many gen changes and many, many opportunities for pocket infections, bacteremia. So it's a real challenge. So I think before we even consider the defibrillator in the athlete, the first question should always be, does my patient have a reasonable indication for an ICD in the first place? Because what we're setting them up for is really a lifetime of device-related. We give them a new condition, right? They have CPVT, but they also have the disease of defibrillator. And that's not nothing. And that can become a bigger problem than their first substrate. Yeah, I think that that's such an important point, to make sure that the indication is really solid and, of course, the shared decision-making. But regarding the submuscular space, my experience is that it's great for people who don't have a lot of subcutaneous tissues, so you're worried about threatened erosion. Some people want it for cosmetics, but it is still in a space that can be a problem for people who exercise. It's usually secured to the underside of the pectoralis muscle rather than the top side. And it also can interfere with the neurovascular bundle. In my long life of putting these things in, I certainly had one patient that had really severe problems related to that as an outcome. So there's always issues with every single type of defibrillator. And certainly, the transvenous devices for older people still are a reasonable option for lots of reasons. If they need CRT or they need antibradycardic pacing, because neither the EICD nor the subcutaneous ICD currently have antibradycardic pacing, that will be overcome soon enough in the Boston Device Hover with their leadless device. I also have a nose to difference or benefit from the submuscular. Frankly, I usually try to steer the patient away from doing the submuscular, because it sounds great at that moment, especially at the initial implant. But 10 years later, it's not so great usually. I will say in the pediatric world, I probably put the majority of submuscular in adolescent girls. I think that is a big question that they have. They don't want this thing sticking out when they're wearing tank tops. And it's just a reality of it. I do think there's a lower infection risk in the submuscular. We certainly see that in our Down's patients, because they tend not to pick at the pocket as much. So I do think there still is some role for it. Go ahead. Wouldn't you say in the era of the EVICD that the sub-QICD is obsolete with the antitachy pacing, the half size? Or is there, or do you still implant those in some patients? I think it's too soon to say that the sub-QICD is obsolete. And I think there's certainly gonna be patients in whom we just can't get into that space. So I think we need a longer history with the EVICD. I think like any technology, it sounds amazing. But even if we think about PFA today versus PFA two years ago, like eventually we regress towards the mean. So I hope it's wonderful. And I hope we can eventually have smaller generators, particularly for female patients who are really honestly bothered by the size of the sub-QICD. But I imagine there will be room for both technologies. I mean, the subcutaneous ICD is a great device. I just wanna sort of put that out there. And it does have its issues, of course, that have been discussed. But it's been FDA approved since 2012, a lot of the over-sensing issues have been overcome, the noise issues still are an issue, but definitely overcome. The majority of people, even adult females, in my experience, do actually really well with it, and it will be great if we have an option for a smaller generator for that device, of course. The EVICD, it has also a lot of potential, but I agree, we just need more data and more time with practical use of it. I would say for our congenital heart patients, they've all had sternotomies, so we still need it. The EVICD is not really an option yet for our TETs and our Fontans that have VT, so we still need it. Okay, we're going to have to move along in the interest of time. I encourage you to submit your questions, we'll try to get to it, but the final presentation is on pharmacotherapy for athletes with ICDs by Dr. Darden from the Kansas City Heart Rhythm Institute. Okay, well thanks for the introduction. I'll be able to breeze through a couple of these slides to avoid repetition. But this talk focuses really on a group that sits at the intersection of high performance and high risk athletes with ICDs. ICD may protect you from sudden cardiac death, but pharmacotherapy is really what stops the arrhythmia from happening. So I'll walk us through how we tailor medications specific to the condition, reduce shocks, and touch briefly a little bit on return to play too. So I have no disclosures. We talked about this. I'll briefly go through this. So it's kind of, you know, this whole field of sports cardiology is really, really cool in a way because we've gone through, we've gone from complete blanket restrictions to now return to play guided by shared decision making and risk stratification. I was fortunate enough to be part of the expert consensus statement from Heart Rhythm Society led by Dr. Chung and Dr. Wampert. But we really focus on a few things. We of course focus on shared decision making, but also a few important things in order to allow patients to return to play. The arrhythmic genic substrate needs to be treated. They should be free from recent arrhythmia and they should be stable on medical therapy. So that's where this talk comes into play. And we talk a lot about, we talk quite a bit about athletes, right? Pediatric athletes. A lot of times when people think of sports cardiology, you think of a professional athlete or division one college athlete, but really it's anybody who puts a high premium on exercise. So somebody like me as an adult EP, we see a lot of masters athletes, weekend warriors and whatnot. They all kind of have the same goals and can fall under this category. Athletes with ICDs fall under kind of two broad categories, primary prevention and secondary prevention. Primary prevention, of course, you never want the ICD to fire. So these may be patients with CPFD, with syncope, hypertrophic cardiomyopathy with a massive septum. Usually beta blockers are the cornerstone of therapy for these patients. Secondary prevention, of course, you already know that there's a malignant substrate there. So the ICD alone is not enough. You want to combine anti-rhythmic drugs on top of beta blockers, for example. You want to reduce another ICD shock, but you also want to help restore the athlete's confidence to exercise again, perhaps at some level. So as we go through condition specific strategies, I'll start off with Long QT syndrome. So beta blockers are the foundation of therapy for Long QT syndrome. It's not just any beta blocker, we're talking non-selective beta blockers, specifically Natalol, sometimes Propanolol. And dosing and compliance, as we talked about in previous talks, is critical with this. Got to make sure patients are compliant with this. So the once daily dosing of Natalol can definitely help with compliance. And also the timing of the dose may play a role too. So if you're competing or exercising in the afternoon, it's probably best to take it in the morning compared to the afternoon. And some athletes don't tolerate beta blockers, they notice a blunted heart rate response, but that can be a sign that the dose is actually effective. That may be more effective than actually evaluating the QT interval. If you do have Long QT type 3, that's where myxilatine can come into play, that can shorten the QTC. So if you do notice ectopy, ventricular ectopy on your device, myxilatine should be added. We talked briefly about cardiac sympathetic denervation. And that can be particularly helpful if you continue having breakthrough despite medical therapy or if you cannot tolerate medical therapy too. Now most patients with Long QT syndrome will have an ICD for secondary prevention. Of course, some select patients with Long QT may have it for primary prevention. But there's good news. Appropriate shocks with Long QT is actually quite uncommon. You're probably just as likely to have an inappropriate shock from T-wave oversensing, sinus tachycardia. So that's where the smart programming comes into play, higher thresholds, higher detection rates and whatnot. And to touch briefly on this, there's a lot of data when we think about the observational data with regard to return to play. There's quite a bit of data for Long QT syndrome. Most recently, the LIV Long QT syndrome, which was mentioned previously by Dr. Lampert, published last year, showed that there's no excess event rates in those who participate in vigorous versus moderate activity. So we move forward, CPVT. This is a high-risk, exercise-triggered ventricular arrhythmia syndrome. So again, NADLOL, non-selective beta blocker, is first-line therapy for this. And flecainide, very low threshold to add that. So if there's still sustained ventricular ectopy on a treadmill when they exercise, low threshold for adding flecainide. So a lot of these patients are on dual therapy. Sympathetic denervation plays a role, too, in CPVT. ICD choice can be tricky in these patients because once they get shocked, that can provoke this adrenergic storm and lead to more shocks. So really, really have to emphasize that they are on maximum optimal medical therapy before putting an ICD in these patients. In return to play, we talked about this, too, but this should be really taken into consideration where an exercise treadmill test should be done. There should be no ventricular ectopy. That should be somewhat of a non-negotiable-type situation. ARVC. ARVC is a unique challenge because it's one of the few cardiopathies where exercise can directly accelerate disease progression. So exercise limitation, not so much restriction, can be quite therapeutic in this situation, too. Beta-blocker is often used, but there is modest benefit with this. And the North American ARVC registry essentially showed that with beta-blockade, there is no difference in the risk of ventricular arrhythmias. So when you go through, other antiarrhythmic drug therapy for ARVC is all guided by observational data. We don't have any clinical trials with guidance. Sotolol is often preferred. There was a study in the early 90s showing that it could be about 70, 80% effective, but there's been conflicting data since then. Flecainide, we can use, too. The Hopkins Group has published their series with flecainide, and you often think, well, you don't wanna use flecainide if you have structural heart disease, but it can be effective from observational studies. Patients can tolerate it quite well. But you're often left with amiodarone. And of course, if you have a young person with amiodarone, you have to evaluate the toxicities and inform the patient of the toxicities, but often combination therapy is what's needed with these people. The UCSF group actually published a small series where they combined antirhythmic drug therapy, flecainide, and sotolol, and achieved better suppression with that. But you're also thinking about adjunctive therapy, right? Ablation, epicardial ablation for ARVC. If there's depressed EF, gotta get them on guideline-directed medical therapy. Return to play is a unique challenge. A unique challenge varies from patient to patient, but when you're thinking more advanced ARVC, elite activity, elite competition is likely not gonna be happening. Hypertrophic cardiomyopathy. Now, unlike channelopathies, we don't have a drug that directly reduces sudden cardiac death risk. Instead, we're focused more on symptom relief and relieving the obstruction if they do have it. So beta blockers, again, first line, but again for symptom relief and preventing or reducing exertional gradients. If they cannot tolerate that, then calcium channel blockers. And can't forget about disopiramide with obstructive cardiomyopathy, too. QT monitoring is needed with this. It can prolong it somewhat, but this can be somewhat well-tolerated in an athlete. It won't have so much of that beta blockade effect, obviously. Arrhythmias and HCM, challenging. Again, not really guided by strong clinical data, just similar to ARVC, but amiodarone and sotolol may be used for VT. AFib is also a challenge with hypertrophic cardiomyopathy. These patients may not tolerate it, so rate control, rhythm control with antiarrhythmic drug therapy, low threshold for ablation with athletes in general, as Dr. Chung mentioned in his talk. We have Mavacampton, which is emerging. It improves gradient. Whether or not that may indirectly reduce the arrhythmic risk is still not completely clear. And return to play with an ICD can be possible, but that can be an entire talk in itself, so I'll move on. Brugada syndrome. This is not so much of an exercise-induced arrhythmia. VF is gonna typically occur at rest, when you're sleeping or in recovery from exercise. Quinidine is the cornerstone of therapy if you do have VF related to Brugada syndrome. And then there is quite a bit of data, emerging data showing that epicardial ablation can be an alternative method for controlling ventricular arrhythmias. But really the key is avoidance, right? You want to avoid fever. You want to avoid sodium channel blockers. That's how we really, ideally, can prevent ventricular arrhythmias in these patient populations with Brugada. And then most of the time, as I mentioned, this isn't really so much of an exercise-induced arrhythmia, so exercise is quite safe in patients with Brugada. Ischemic VT. Ischemic VT is one of the few conditions I'm presenting here that actually has randomized control data behind it. So beta blockers, foundation of therapy, not just for symptom and ventricular arrhythmia reduction, but for mortality improvement if there is depressed EF. The OPTIC trial from JAMA in 2016 showed that amylorone plus beta blocker outperformed both Sotalol and beta blocker alone. And myxilatine can sometimes be layered in as more of a synergistic approach. And then there's more data from the VANISH-1, VANISH-2 trials showing ablation can be additive, sometimes even as first-line therapy for patients with ischemic VT. And of course, we talked about this a couple times, but optimizing device settings is critical in these patients. So these medications apply not just to athletes, but to any patient we see, but they do have a significant impact on the athlete. As we talked about, beta blockers can reduce heart rate, can have an impact on endurance. Sotalol requires QT monitoring. If a patient is an endurance athlete, for example, you gotta be mindful of the electrolyte shifts that may occur. Amyloderone, obviously not ideal if you have a young athlete. And then, so you really have to inform the athlete about these medications and individualize it quite a bit. Now, the regulatory landscape is always have to take into consideration if a patient is competing competitively. Beta blocker is banned in some sports. Diuretics are often banned as masking agents. Most antiarrhythmic drugs, probably all antiarrhythmic drugs are allowed because they're not really going to impact exercise performance, probably hinder it. But if you do need one of these medications, such as a beta blocker, you can obtain a therapeutic use exemption to allow them to continue taking it. Now, what's next? We talked quite a bit about the EVICD. We have wearables and remote monitoring, AI-driven programming. As more athletes we see are wearing these smartwatches and whatnot, we may be able to get a little bit more data from that beyond just step count, calories, recovery metrics, whether or not that may predict arrhythmias could be quite interesting. There's quite a bit of undiscovered genes, right? I mean, think about how much we've learned just in the past decade. So as we learn more about variants of specific genotypes, we will be able to better tailor medications to that too. So conclusion, you know, ICDs really need medications. As we talked about, ICD alone is not therapy by itself. Beta blockers, often the universal backbone, really have to tailor medication specific to the substrate. You can complement these medications with sympathetic denervation, ablation. Keep in mind smart ICD programming and return to play as possible with the appropriate risk stratification. Thank you all for your attention. Thank you. A couple did come in electronically as, how strenuous is too strenuous for recreational athletes with ARVC? Is there a magic heart rate limit? If you look at the document, it says basically six METs, which is the equivalent of a brisk walk, very light jog, like a 10 or 12 minute mile. Any comments on the thinner 4.7 ICD lead for left bundle pacing in young athletes? This is a Medtronic new lead, late breaking clinical trial. Virtually no data in the pediatric population, and it's FDA approved, but not released. Not for left bundle pacing, only at the RV apex. I urge caution with any new lead until we get clinical experience. And finally, and Eugene, I may ask you to comment on this. In shared decision making, is legal responsibility also shared in case some adverse events happens? Yeah, this is why I gave it to you. Legal responsibility isn't always shared. And so I think you have to do your best to document, document, document, and involve all parties up front. And as I mentioned, often you need repeated conversations. Yeah, when I've been involved with it as well, I make sure that the organization that's participating has a legal agreement in which it's abundantly clear that the patient or the patient's family are accepting the risk. Document that you've guided them, but they've decided. And I'd urge all of you, when you get involved with that, to have a legal document so that, unlike Italy, where the physicians are responsible if there's a bad outcome, we don't put ourself in a very vulnerable position. Go ahead, final question or comment. Yeah, kind of unrelated. And maybe this is settled science, I don't know, but any athlete who has an ICD and you're adding an antiarrhythmic drug, particularly amiodarone, and particularly in hypertrophs, do you do follow-up DFT testing? For secondary prevention, probably kind of re-stratify that. I haven't had that situation, but patients who've been on amiodarone, obviously low threshold for doing DFTs in the lab when you implant the device, obviously, too. But that is, I didn't talk about DFTs and the impact of antiarrhythmic drug therapy, but that is something that should not be neglected, too. Thanks. We have speakers, a survey, and chair survey as well. Please fill them out. I wanna thank the participants, Dr. Poole, my co-chair, and actually all of you for participating in a really superb session. Thank you.

Heart Rhythm 2025

athletes

implantable cardioverter-defibrillators

ICDs

arrhythmias

hypertrophic cardiomyopathy

catecholaminergic polymorphic ventricular tachycardia

subcutaneous ICDs

transvenous ICDs

shared decision-making

pharmacotherapy