Thank you all for attending. The QR code was up, but hopefully most of you have already gotten the app by this point for any questions, audience response, as well as submitting questions to us for the end of the talk. And so we're very pleased to present the Challenging Arrhythmia Cases for the Allied Professional Session. And we will go ahead and start with Megan Labreck, a PharmD from OhioHealth. Good morning. Thank you guys for coming, and happy day three of HRS. All right, so today I'm going to briefly review some adverse effects related to anti-arrhythmic drugs, present a patient case, and then evaluate some of the risks and benefits of the anti-arrhythmic drugs. So, as you all know, all of the anti-arrhythmic drugs that are on the market are high-risk medications. They all have black box warnings, multiple drug interactions, narrow therapeutic index. So it's really difficult to ascertain what the percentages of patients that come in to the hospital or the ER with pro-arrhythmia. Unlike patients, for example, we have numbers that are reported annually for patients that have adverse events related to, for example, anticoagulants, the number of patients that come in with bleeds, the number of patients that come in with strokes. Those things are reported. However, it's difficult to analyze the patients that come in with adverse events related to anti-arrhythmic drugs because what does that look like? Is it recurrent VT? Is it atrial flutter? Why complex tachycardia? Is that arrhythmia progression? Is that new disease? Is that worsening heart failure? Is that sudden cardiac arrest related to anti-arrhythmic drugs? So it's really hard to determine some of those things and differentiate between disease state progression, new cardiac disease versus medication effects. We do know, however, that AFib burden on health care, and particularly AFib, is significantly higher than patients that are non-AFib patients. $16,000 higher annually in patients that have AFib without some other cost data here. So average total health care costs for patients with AFib, $27,000 more per patient per year than a non-AFib cohort. So despite increases in diagnosis, earlier detections, improved technology for screening, we have improved ablation technologies that you've all sat in on these sessions over the past several days. We haven't had many improvements in drug therapy. So the last drug that was approved was dronetarone in 2009. Previous to that was ticasin in 1999. We still use drugs, however. Every day we are prescribing patients anti-arrhythmic drugs. So if we look at the compound annual growth rate of anti-arrhythmic drugs, all of them on the market, we're seeing about a 6.4% growth in the U.S. So you can see here our expected growth. But what does that really mean? So this is kind of just to pull out some information. So if we're looking at about $1 billion in drug therapy of last year, compare this to PFA. So PFA took over the market last year and is exponentially rising. Their compound annual growth rate is about 32%. And so this is initiating last year. So they're going to be expected to hit the $4 billion by 2030. So PFA is exponentially taking over our ablation market. So comparing that to our anti-arrhythmic drug usage, again, we're still using these medications. So we still have to keep in mind the importance of monitoring adverse effects and prescribing patterns. So a patient that was referred for me for SOTA law is a patient who is a 78-year-old gentleman who has a significant history for HFREF, coronary disease with 3-vessel CABG. He had VT with a secondary prevention ICD that was placed in two previous VT ablations. And he has other significant history that's listed in this slide as well. He is a 90-kilo, 70-inch male. He has had several medications in his history as well. He had an allergic reaction to imiodurone. And then he had reinitiated SOTA law after an ablation at our standard starting dose that we practice at my institution. It's 120 milligrams twice a day. So this patient, unfortunately, had recurrent monomorphic VT in May, and ATP failed on his device. So he was delivered a shock. So when he had follow-up with his primary electrophysiologist, the discussion for what to do next was dose increase. So as you all know, SOTA law is a reverse-use-dependent potassium channel blocker. So it increases their action potential and prolongs repolarization. So it has dose-dependent QT prolongation. And our guidelines recommend that SOTA law has this loading dose recommendation here and a maintenance dose recommendation at anywhere between 80 and 160 twice a day for patients with normal renal function. So we have two options. Generally speaking, we can put our patient inpatient to initiate this dose increase to 160 with monitoring and electrolyte optimization. Or do we do this as an outpatient? Other questions to consider in this situation, this patient was already stable on 120, regardless of renal function previously. So if we looked at this patient's labs, his estimated cranium clearance was about 48, using Krokroft's natural body weight. So electrolytes were already optimized in this situation. So something that I think is a little bit in a controversial state at this point is, do we care about renal function when we're dose increasing, if they're already stable? And when do we deem patients drug refractory? So I think that there might be a time when some patients would have been deemed drug refractory to SOTA law, and we would have discontinued it. So practice patterns are different at every institution, but do we optimize dosing higher if patients have recurrent arrhythmia on a dose that they were already stable on? So when the patient came to me for his up titration of the medication, his ECG showed stable, normal, rhythm-based sensory pace. His hand-measured QT, QTC was 424, using the Bizette's formula. And most recently, ESC and ERA put out a compendium of antiarrhythmic drugs. If you haven't had a chance to view that, it's a very comprehensive review of antiarrhythmic drug therapy. And there's recommendation of up titration to twice a day may be performed based on recurrent arrhythmia or AFib burden as noted by a patient's device. So I have here a patient's initial SOTA law dosing, or not patients, I'm sorry, the package labeling for initial dosing. And as you see, it's varied based on arrhythmia, whether it's AFib or ventricular arrhythmias. And the dosing recommendation is based on creatinine clearance. And I find it very interesting that daily dosing, we decrease frequency when patients have declining renal function. So with the package labeling, it indicates starting at a low dose and up titrating after the patient is stable for at least three days. I'm not sure that that's now in practice at that model, because we would have patients in the hospital for probably weeks if we wanted to get them on a up titrated stable dose. Package labeling also recommends decreasing frequency with renal adjustments, which in practice, we see less effective dosing, breakthrough arrhythmias, and treatment failure earlier. So again, with this compendium that was released, the monitoring longitudinally recommends keeping the QTEC less than 500. So no mention necessarily of renal function in up titration of doses after maintenance therapy. So despite lack of current literature, SOTA law is probably underdosed in a lot of situations in many scenarios. IV SOTA law is available, and it provides an increased time to steady state. The QT QTC is directly proportional to the serum drug concentration during the time of the load. It is costly, however, and so it may not be available at every institution, and there needs to be a dedicated provider to review those every 15-minute ECGs during the infusion. So what is this 21st century dosing? So this is sort of the dosing that our institution follows in regards to renal function. And again, this is something that is anecdotal, I would say. This is kind of how we follow in practice and how we start patients. We don't really decrease to daily dosing, and we follow QT QTC longitudinally and make sure that patients, of course, are not having breakthrough, and we make sure that patients are not having QT prolongation. But we generally start patients always at a standard dose of 120 unless they have bradyarrhythmias without a device. Of course, that would be a whole other conversation. But if they have declining renal function in that 30 to 40, 50 range, we would maybe start at 80. But above 50, we really start at 120 twice a day. So a little bit varied from what the package insert says, but we always consider the indication for the medication, whether it's ventricular or atrial arrhythmias. We always look at baseline heart rates and if they need to be on a concomitant beta blocker for, like, GDMT. And those conversations are had then with the provider of that medication. So overall, I think that some things like the anirhythmic drugs, with the lack of available or limited options and available high-quality data, refractory ventricular arrhythmias may be an area that we can get a little bit creative with or we have to think about when do we deem a patient refractory. It's important to, you know, document or even publish your reports of combination medications as there's not a lot of information on that either. So we all know that maxilatine is a great adjuvant drug for ventricular arrhythmias. So there are case reports out there of other medication combinations, but documenting and allowing our colleagues to learn from one another about medication successes is going to just further improve our learning and our practice for our patients. Thank you. APPLAUSE Thank you. That was a great discussion. We'll take some of the questions at the end, but I'm happy to introduce Ms. Tiffany Andrade-Hermann, I believe physician's associate at Brigham and Women's Hospital. Thank you. Good morning, everyone. Thank you for choosing to spend your morning with us bright and early. Again, I'd like to echo Megan to welcome you to day three of HRS. Thank you to the co-chairs for inviting me to speak today, and thank you to my co-panelists. Today, I will be presenting a case called what is a slam dunk for ablation, a case that's demonstrating the basic principles of ablation and optimal patient selection. Here are the learning objectives. So I would like to review the current guidelines for AFib ablation, review a patient case, and describe the basic principles of catheter ablation. Just to see what everyone's experience is with treating folks with atrial fibrillation, I'm curious to see what patient profile or characteristics do you consider when recommending a patient for AFib catheter ablation. So there should be a QR code that should populate. It is a short answer question, so I am looking for a response. Do you all see the QR code? Did it populate? No. It's all right. I'll give you some answers anyway. So some things to consider would be failed rate control strategy, failed or folks being intolerant to anti-arrhythmic regimens, athletes, history of heart failure, longer durations of AFib episodes, or anyone who's really interested in ablation as a therapy for AFib treatment. So we'll come back to this. So as of 2023, the ACC, AHA, ACCP, HRS, I love saying all that, guidelines for AFib management have recommended for AFib rhythm control that ablation be served as first-line therapy, making it a class one indication for patients who have symptomatic AFib despite prior anti-arrhythmic use. So we'll start off with the case. This is a 55-year-old gentleman with no significant past medical history who presents to his primary care wellness visit, reporting palpitations and elevated heart rates up to 150 beats per minute that he captured on his wearable device. Labs are ordered and he is ordered. This is his baseline EKG. So we see that they're in sinus rhythm, narrow QRS complex, no pre-excitation, and no evidence of intraventricular conduction delay. So we undergo some diagnostic studies including lab work, which were all normal, a two-week patch monitor, which identified a 23% atrial fibrillation burden. He did have periods of RBR up to 125 beats per minute. Subsequently, underwent an echocardiogram to identify any structural heart disease. He had a normal LV size with normal wall thickness, had severely reduced left ventricular ejection fraction of 20 to 25%, and a severely dilated LA with a LAVI of 49. He did have some moderate mitral regurgitation, but no other valvular disease. So this is his EKG in AFib. And as you can see, he's in AFib with RBR. Ventricular rate is about 124 beats per minute. So he meets with cardiology, who then refers him to EP. We have an initial conversation about lifestyle modification. He had been on a couple benders, and so we had to counsel him on alcohol reduction. And we discussed rate control versus rhythm control. The patient ultimately elected to pursue rhythm control with dofetilide. And he was on aspirin at the time, given his low travasc, and then that was discontinued. We had initiated therapeutic eloquence dosing for him. So he was loaded on dofetilide. I just want to take a moment to discuss the guidelines with regards to AFib management in patients with heart failure. And so in the most recent guidelines, catheter ablation was considered to be a class one indication, was upgraded as a class one indication for patients with heart failure with reduced ejection fraction. And this was due to some recent randomized control trials that demonstrate the superiority of catheter ablation over drug therapy for rhythm control in patients with HFREF. And so we'll review this in the next slide. Kind of the landmark trial, those small case series, a small patient population, about 200 patients in CasLAF demonstrating, or patients with end-stage heart failure and AFib. And these patients were randomized to either ablation or goal-directed medical therapy alone. And the primary outcome was assessing for composite death, implantation of an ALVAD, or urgent heart transplant. Here we see some Kaplan-Meier curves with regards to the outcome here. So on the left, we can see that patients in the ablation group, which is this red line here in both, did have a lower incidence, a lower incidence of the primary endpoint. And so the incidence of death from all-cause mortality was significantly lower in the ablation group versus the goal-directed medical therapy group, with a hazard ratio of 0.29. And this went on to be used for subgroup analysis, particularly in the Cabana trial that did confirm the beneficial effect of catheter ablation regarding morbidity and mortality for patients with reduced EF. And so this allowed for the upgrade from the 2019-2020 consensus statement of a class 2B indication for ablation to now be upgraded to a class of 1 indication for AFib ablation in these patients. So his treatment strategy is revised. He progresses, unfortunately, from paroxysmal to persistent AFib, despite T-casinoidophetalide. He started on metoprolol, of which we uptitrated, and then digoxin was added for further rate control as a bridge to ablation. And he subsequently underwent an AFib ablation via PFA. I don't know how many of you guys scrub cases or see, or are part of the workup in terms of preparing patients for ablation, so I figured I wanted to go into this just a little bit. But generally speaking, from a pre-procedure planning standpoint, we do assess lab work similar to our patients, where we're looking at biomarkers, their coags, type and screen. We do get an EKG, with hopefully being able to capture the AFib episode, the patch monitor, or some sort of device interrogation if they have an implanted device, so that we can assess for the total burden, and also assess for whether or not there's more instances of regular tachycardia versus irregular tachycardias, and also being able to correlate them with the patient's symptoms. Getting a structural assessment with an echocardiogram to assess the RV, LV size and function, as well as the biatrial size, and any evidence of any valvular disease, especially mitral valve disease, as it can have outcomes in terms of recurrence and approach. And so, also excluding the left atrial appendage, making sure there isn't a thrombus, can be done with either TEE or CT scan. At our institution, we're more favorable of doing CT scans, just because we can also get the cardiac anatomy for the pulmonary veins, and being able to assess for some suboptimal epicardial coronary disease. In terms of what to consider when having a conversation with the patient about ablation, certainly discussing a catheter select, or maybe not with them, a catheter selection, that's something that the operator's thinking about, whether that be an irrigated catheter with saline, a non-irrigated catheter, or contact force catheters, where you're getting feedback from the catheter in terms of how much force you're putting on the tissue. Energy source would be, it could be cryogenic, or what we call cryo-balloon, so here on the top right, there's a cryo-balloon catheter that essentially expands at the antrum of the pulmonary vein, and provides an arctic front that then allows for fibrosis to take place. The radiofrequency ablation was, you know, the standard for quite some time, until PFA came along, and so that's what's displayed here, where we're delivering heat energy, or cautery to the tissue, to ultimately form those scar lesions. Pulse field electroporation, a lot of the talk around this conference about PFA, so delivering these high vibration sequences to be able to form pores in the cells that maintain structure, but obviously destroy the cell, allowing the scar to form without collateral damage to neighboring structures. Laser and stereotactic ablation, which is probably more common for VT as opposed to, or factory VT as opposed to AFib. There are some ways to map the heart with electro-anatomical 3D images, and there are some systems for PFA specifically that allow for integration of mapping and ablation. Image guidance, certainly you're using intracardiac echocardiograms, or ultrasounds, that allows us to see the images real time, or fluoroscopy if you're a fluoro center, which I feel like the field of EP is moving towards an ultrasound-guided ablation process. And then newly, AI integration with an assistance that allows us to assess for any non-pulmonary vein triggers, or any re-entrant tachycardias. This is a photo of what you see at the beginning, at the end of the case, generally speaking on the left, so we're looking at the heart from the back. And the purple, this is all activation timing, and so the purple is normal tissue, red is scar, and the left veins are on the left, and the right veins are on the right. And so we can see that this patient had some degree of scar along the antrum, and then some degree of scar along the back wall, but given his persistence, we figured that he would benefit from a pulmonary vein isolation and a posterior wall isolation. The image on the right just demonstrates all red, meaning that we've actively isolated the back wall, as well as the pulmonary veins. So again, as I mentioned, he undergoes an ablation. He's continued on metoprolol and digoxin. He has an implantable loop recorder implanted to allow us to trend his AFib burden post-procedure. He did not have any recurrence within his blanking period. He continued to be monitored monthly, and at eight months post-ablation, he did have a 10-hour episode of AFib without recurrence. We got a repeat echocardiogram to assess whether there was any improvement in his ejection fraction, and there was, from the 20 and 25 percent to 48 percent, and there was reverse remodeling of his left atrium that went from severely dilated to normal. So overall, a positive, you know, patient response. It certainly still has some degree of a mild cardiomyopathy, and unfortunately, as of late, he's been having more symptomatic episodes of AFib, and so we're going to pursue a repeat ablation. So overall, the take-home messages are that patient selection does involve a comprehensive assessment of AFib class, so whether someone's paroxysmal, persistent, or long-persistent. Any additional comorbidities that perhaps would be worth optimizing is beneficial. Their left atrium, you know, for folks who have a left atrial index greater than 50, sometimes it can be more challenging and offer opportunities for more ablation or have some impacts in terms of the long-term success. The individual patient factors, so their motivation to have an ablation and hopefully get their AFib under control certainly is part of the conversation, and then how they've responded to previous therapies, such as antiarrhythmics or weight control or cardioversion. The bottom line is the sooner you have an ablation, generally speaking, the better the success rate, and so if you're paroxysmal, you have better outcomes than someone who's long-standing persistent, and I can't stress this enough, but lifestyle modification conversations pre- and post-ablation are really important because certainly it can reduce the burden beforehand in terms of how many episodes of RVR they're having, but also how symptomatic they are, and then enhances the chances that they remain rhythm-free or AFib-free post-ablation, and the routine assessment of arrhythmias that is now happening with a combination of technology, whether that be wearables, patch monitors, device interrogations, can be helpful in deciding what's the appropriate next step for the patient. Thank you for your time. Here's my contact information, and thank you to my group. I appreciate it. Thank you, and our final speaker is Javed Legacy from Boston Scientific. He'll be talking about what's new in the EP Lab. Hi. Thank you for attending the talk. I look forward to sharing this talk with you. So today's talk is what's new in the EP Lab, a case that highlights novel ablation techniques. My name is Javed Legacy. I currently work for Boston Scientific as an EP Clinical Specialist. I graduated from the HRS LEAP program in 2024, and I'm still currently involved with HRS 3-LEAP. So the burning question is what's new in the lab. It's pulse-field ablations, and I found this profound quote out of Nature Review's cardiology that stated, the advent of pulse-field ablation is revolutionizing the field of AFib ablations. I thought this was so important, and I wanted to understand why. So I looked at what happened before PFA, and we had one modality. We had a thermal mechanism, and thermal had two techniques. It had a heat technique and a cold technique. So heat would be RF, cryo would be cold. In the advent of pulse-field ablation, the new modality is electroporation. Electroporation is now used with the pulse-field ablation technique. So just come back to this real quick. So if you look at this, we mentioned earlier that there was a redo AFib case. So now a physician can look at a complex AFib patient, and they can say, well, they had a thermal, they had an RF procedure, they reoccurred. So now they have a choice with a different modality. They can choose pulse-field ablation to help that This is a very novel idea, and this is why I think that there's a revolution of pulse-field ablation occurring with our ablations. So today's objectives are to look at what is pulse-field ablation, the mechanisms for PFA, the improved PFA safety factors, and the overview of PFA techniques. So what is pulse-field ablation? Pulse-field ablation is a non-thermal ablation modality. It uses a high-voltage therapy delivery system, and you can think of it like creating a cloud around the catheter, kind of what you see here between these two things, this blue haze. Think of it like an electrical cloud. And when you bring that electric cloud in proximity to the myocardium, it electroporates the myocardium cells, it subselects it, and it forms, the key here is non-thermal nanopores in the myocardial cell memory. When you form these non-thermal nanopores in the cell memory, you electrically isolate the cell. So really, what are the benefits here? So if I told you that you could have an ablation, and you could subselect just the myocardium and avoid collateral damage to adjacent structures, like the esophagus or the phrenic nerve, this would be a novel idea. This is what pulse-field ablation offers. So the safety factors with thermal modality included pulmonary vein stenosis, phrenic nerve palsy, and atrial esophageal fistulas. So here you can see that we're isolating the pulmonary vein. And whenever we were in contact with the esophagus or adjacent to the phrenic nerve, we were concerned about damage to these structures. Because thermal mechanisms spread like a free spirit, we can't tell it to subselect the myocardium, it just spreads and it affects anything that it touches. With pulse-field ablation, you also have pulmonary vein isolation with an electric field. And whether you're in contact with the esophagus or the phrenic nerve, it does not affect the phrenic nerve, no damage, it just subselects the myocardium. So let's look at this. Let's take a metaphor. Let's assume the house is a myocardial cell, and the tree represents the esophagus, and the fence represents the phrenic nerve. Let's assume that we ablate the house with RF. So the house burns. The house spreads like fire to the trees, to the fence, and it damages the phrenic nerve and the, apologies, the esophagus and the phrenic nerve. When it's over, you're left with a pile of ashes. If you looked at the cell after you ablated it, you have no clue what, there was a cell there. There's just a lesion. Now take the same mechanism and use PFA, and let's ablate the house with pulse-field ablation. So this is the electric field that surrounds it. When it's over, what you see, you still see a house. The structure of the cell still exists. You've blown out the doors, you've blown out the windows, you've blown out the roof, and you still have a house that's no longer functional. This is what pulse-field ablation offers. It offers the ability to maintain the structure of the cell, but the lesion electrically isolates it and leaves that structure there. And if you notice, we haven't affected the trees or the fence, so the esophagus and the phrenic nerve have been spared without having to titrate, so titrate power. So why is this? So the myocardium has a really special property of the electric field. And if you look at the electric field. And if you look at the electric field properties of other structures in the heart, the myocardium is very special. It has a very low electric field property. The myocardium electric field properties are four times weaker than smooth vascular tissue, nine times weaker than a nerve cell. So if we tune the electric field so that it's strong enough to affect the myocardium, weak enough to not affect the adjacent structures, we can effectively tissue sub-select the myocardial tissue for the ablation. So now let's review the current catheters that are on the market for pulse field ablation. There's actually a wide range. When you look at pulse field ablation, the systems are categorized in the same way as RF. There's one-shot techniques which ablate the vein all at once. There's point-by-point techniques that ablate the vein point-by-point as you go. So I've broken this down as the overview, the workflow, the company, and the PFA system. In the one-shot category, you have Boston Scientific with a ferripulse system, you have Medtronic with a pulse-select system, you have Biosense Webster with a varipulse system, and in the one-shot category, you have Medtronic with a SPIR9. So let's first look at the one-shot technologies for pulse field ablation. Biosense Webster has the varipulse PFA system. In the United States, the trial was called ADMIR. It was indicated for paraxysmal AFib. The adverse event rate was 2.9%, and if you notice, there were zero pulmonary vein stenosis, zero atrial esophageal fistulas, and zero furnic nerve paralysis. The overall primary effectiveness for this clinical trial was 74.6%. Next we have Medtronic with the pulse-select PFA system. The clinical trial was called PULSE-AF. It's indicated for paraxysmal and persistent AFib. The event rate, safety event rate, was 0.7, and they also documented zero esophageal offense, zero pulmonary vein stenosis, and zero furnic nerve injuries. Then you have Boston Scientific with the varipulse PFA system. The clinical trial was ADVENT. It was indicated for paraxysmal AFib. The primary safety endpoint was 2.1%. There were zero documented atrial esophageal fistulas, zero persistent furnic nerve palsies, and zero pulmonary vein stenosis. Overall effectiveness, primary effectiveness of this trial was 73.3. So in the point-by-point category, we have Medtronic with the SPHERE-9. The trial was called SPHERE-PER-AF. The indication was for persistent AFib. The primary safety event rate was 1.4, and they also documented zero pulmonary vein stenosis, zero furnic nerve palsy, and zero atrial esophageal fistulas. So we are in a new era where we now, physicians have the choice between different modalities to help treat patients with complex AFib, either in a de novo setting or a redo setting. And it's very exciting, and it's a unique time to be a part of this history for pulse field ablation. Thank you for your time. Thank you. Thank you to our panel. Do we have any questions? Do we have any questions that have come through on that? Yes, we do. Okay. So I'll start with, and I think this is for our last two speakers. How do patient characteristics impact transeptal crossing complexity and choice of crossing device? Great question. So I think that if someone has a huge left atrial appendage or a mobile intraatrial septum, that can often make the transeptal puncture very challenging. Ideally, it's a structure that is amenable to being bent, and so we see tenting when we're going across with the needle or going across with any transeptal sheath. But if there is already some fluidity to that structure or a lipominous intraatrial septum where there's some pouching, oftentimes that can pose a challenge. It's hard to appreciate that, I think, on any pre-procedure imaging, in particular echocardiogram or CT scan, so it's something you encounter when you are in the case. But having the imaging modality certainly is beneficial because you can kind of project what would be your best place to go across. That gives you the most beneficial reach to get to the pulmonary veins or the posterior wall. Great, thank you. The next question is how do we approach ablation in patients with severe obesity and the accumulation of epicardial fat? Yeah, that's the never-ending issue, right? I think that actually brings importance to doing the lifestyle modification. Certainly not everyone is a candidate for GLP-1s or SGLT-2 inhibitors, but that's something to consider pre-ablation. We generally tell our patients that they have to lose at least 10% of their weight prior to being an ideal candidate for ablation because they have to understand that there can still be significant recurrence after the ablation, even if it's acutely successful, just because of their weight alone. And generally speaking, obesity does enhance the fibrosis and the degree of scar that can take place afterward as well. So I do think it's something that you should counsel your patients on or refer them to a weight loss clinic beforehand to make them optimized, however we categorize that, prior to ablation. But I do think that it poses a risk to general anesthesia. And from a procedural standpoint, sometimes there can be more venous access issues. We don't really do epicardial access for AFib ablations, but for VT ablations, certainly that can pose a challenge where you might need to prepare to have cardiac surgery on standby just in case. So that's something to consider. If you're a center that has our resource, great. But I think that's operator-specific as well in terms of their comfort in getting into that space when someone has more epicardial fat. Just a follow-up question to that. From a practicality standpoint, you mentioned referring to a weight loss clinic. Not every center has that availability. And our primary care colleagues are completely overwhelmed. The cost inhibition of the GLPs. What are your suggestions for how to manage that? It's not ideal to be managed in an EP clinic, obviously, but if it is a requirement to get the procedure, what onus does that put on us as EP professionals? Yeah, it's a great question. I think building a partnership with, and I totally understand it's not a resource available at every institution, but I think education becomes a big part of it, too. If we're able to collaborate with our primary care colleagues or able to collaborate with our cardiologists who have a little bit more comfort, perhaps, with folks on GLP-1s, it is important for us to start to establish those relationships because that does improve outcomes for our patients. So if that doesn't exist already in your center, that's a project idea. And then the other piece is sometimes external referrals is helpful, just because I do think, as an overall risk factor, it certainly poses cardiac risk regardless, but if folks are pretty motivated to get their AFib burden under control, it's going to be a huge factor that should be considered preablation or for antiarrhythmic therapy or anything, really, because if our end goal is to get an AFib-free person, I think it makes it challenging if the underlying risk is still there. Indeed, yeah. This next question is for Dr. Lebrecq. Can you please comment on best practices for initiating flecainide in the outpatient setting as well as Sotilol in a patient with an ICD? So for flecainide in outpatient setting, if it is daily dose scheduled flecainide, I think it's really important just to make sure that your patient is thoroughly evaluated in regards to having an updated recent echo to ensure that their heart function is normal, and then having a recent stress test, whether that's treadmill or nuclear, whatever the patient can handle, to make sure that they don't have any coronary disease. I think that, of course, there's controversy there that could take a whole nother talk, which we won't go into, but I think that in the outpatient setting, starting at a relatively, starting a scheduled low dose is, not necessarily a low dose, but what would be appropriate for the patient, with, of course, the AV nodal on board with that mechanism of use dependence is important. If you're doing pill-in-the-pocket, however, and it's the first time the patient has taken that dose, I think it's important to make sure that patient is monitored in some fashion, whether that's bringing them into the ER, bringing them into a pre-procedure area, like your PCU, as if they were going to be cardioverted so that they're under some sort of monitoring so that they don't have any sort of adverse effect to that one time, or first dose of their pill-in-pocket, either flecainide or propafenone, just because of that risk of the atrial flutter with rapid ventricular response, and then potentially wide complex tachycardia. I think if the patient tolerates that after their first dose, then they are free to then do subsequent doses at home. So we know that the patient is safe, and avoid those adverse events. In regards to SOTA law and ICDs, if you have a busy throughput center like we do, if there wasn't a dedicated provider to look at those interrogations in real time, or any sort of dynamic QT, then I think it's difficult to do that. If you have somebody in the time to look at transmissions, then I think it would be reasonable to do that in patients with an ICD and check them after several, three days. I think this is commonly done in the outpatient setting without necessarily being reported. So I think that being judicious about appropriateness in dosing makes you sure electrolytes are optimized before doing so, and renal function is relatively normal and hasn't been labile. I'm gonna field this question to Javed. Is the percentage of secondary ablation or reoccurrence, I guess the question is, is there a comparison to reoccurrence after cryo versus RFA? Is that something that's been studied? It's a good question. There are studies out there. I would probably refer you to your local teams to find out specifically about those studies and those techniques. Each study is unique to that catheter and that technology. And the therapy for either de novo or redo rates are specific to that clinical study, so I'd recommend you to that local team. Okay, great. I do have a follow-up question because I always think if I lived in a perfect world and I had the access to any tool in my EP lab, to you when you're selecting that modality, what is, I guess I wanna know, how do you pick the perfect tool? Point, PFA, RFA, cryo? Are there certain, if you could give me a five-second rundown of how you pick the right tool for your patients? So I don't get to pick the tool. No, in a hypothetical world, if you would. Yeah, I mean, if you're looking at safety factors and the concern for the age group or the disease state or how long the AFib has been there, these may play factors in which technique you decide to use. There's real concerns with safety when you're ablating the left atrium, the pulmonary veins. The esophagus can be displaced in different parts. It could be on the right side of the left atrium. It could be on the left. And having to monitor either the temperature of the heat or putting cooling balloons in there for RF. And these are factors that you have to, real concerns. And in the older age groups, you don't want them to come back. And you try and want them to have the best procedure as possible. And I think really what physicians are doing is they're just looking at the case of the patient and they're deciding that, you know, I really want this patient to have pulse field ablation because they're coming back after a convergent procedure and they really need help with that. Other physicians prefer their point-by-point technique and like to use RF. So it's a really good question. And I think safety drives a lot of those decisions. It kind of points to now we have more tools, right? We can do better at patient selection, different tools for different patients. So thank you. Different tools and in different ways to affect the cell. Right, and this last question, oh, go ahead. This gentleman's been standing here. I want to make sure that we get that. Thanks, I just had a quick question on repeat. So it seems like a lot of times, quite a few times, the pulmonary veins are isolated and then those patients end up going back for redo, touch up. When is it too much? I mean, when do we quit bringing these patients back? Because in my mind, you can only ablate so much tissue, correct? I mean, eventually you're going to have, I mean, theoretically stunned atria or dead atria and then what have you accomplished? So is there a line in the sand where it's kind of gone in practice where maybe twice, maybe three times and then that's it? I can comment, but feel free to take it. Yeah, I would say that at our center, we probably max out around like five ablations, generally speaking. But you're right that, going back to your question about modality choice and what influences your option, I think being mindful that, generally speaking, you're right that the pulmonary veins are isolated by the time you get in there. You confirm bidirectional block, but then you may have posterior wall triggers. You may have to do a mitral isthmus line or a lateral anterior line. So I think you don't really know until you get in there. It's hard to interpret that from an EKG or from a device interrogation. And so just being, you're almost approaching it like a new procedure every time in order for you to find the circuit that perhaps is contributing to the clinical arrhythmia. But after a while, especially if the patient hasn't been on any antiarrhythmics or any rate control, I think that introductions, that conversation starts to be had in terms of utility because we still want that atrium to contract, right? And we run the risk of standstill, which is not helpful for anyone. It increases their thrombotic risk. They have to be on lifelong anticoagulation where there may be a possibility of them coming off of anticoagulation if they maintain rhythm. But I do think that if we identify that on their EKG, perhaps they're in an atypical flutter or they're in atrial tachycardia, I think our operators at least go in with an approach that we're probably gonna do more of an RF situation there. We're hardly using cryo anymore. We don't use them for redos. But we have been seeing an advent of using the PFA catheter to do these reentrant circuits, which I know there were a couple talks today about that. So I think it's promising and it seems safe so far. I would just say, I don't know that there's a number for how many ablations a patient can have. What we see is a lot of times, especially with pulse field techniques, is that patients have had reoccurring AFib and physicians would like to treat them with PFA to see if that improves their outcomes. And I think a lot of those decisions for repeat ablations is largely driven by the patient's symptoms and quality of life and an attempt for that physician to give them better outcomes and a better quality of life. And that's what's so interesting about why PFA is novel. It's because of how it affects the cell. It's different than heat or cryo. It's not a thermal modality. It's an electroporation technique. It preserves the quality of the cell structure. And there's still a lot of learning that we have, but in terms of redos, I think a lot of physicians like the ability to choose between modalities to help support their patients. Are there any patients for whom PFA is not the best choice for ablation, for AFib specifically? That's a good question. I'm not sure I have the answer. I think physicians would probably, sometimes we kind of stay on standby and the physician will decide after they map the heart, what's the best approach for that patient? Yeah, I would say that if the left atrium is pretty small, generally speaking, getting that ablation catheter across is not that favorable. And then the other piece is if they have mechanical valves, sometimes that's not, I don't know if that's a contraindication per se, but it's definitely a consideration. And then going back to our favorite issue of obesity, do your providers have a BMI cutoff for ablation? I think it's circa 50. Our institution, our providers generally try to cut it but they have hard conversations or crucial conversations with patients at 40. Yeah, I would say that at my practice, it's around 40. You know, it's hard to get a group of VPs to agree to any consensus. If you find that somewhere, that would be an interesting talk for HRS. But I think 40 is our magic number, so. Any other questions? Did everybody hear the question? Yeah, so I think that the general summary is, how do you handle AFib recurrence during the blanking period, in terms of anti-arrhythmic drug cardioversion, all those types of things. I can comment as well. So in our institution, depending on the modality, of course, too, so I try to, I hate using the word fail. Again, because we, did they fail the drug? Especially after an ablation, like, okay, so they had recurrence, but now they have, you know, now we took away some of those triggers. So we can use it for suppression again. So I ask that docs all the time. I'm like, how did they fail it? So, yes. So oftentimes, recently, I had a patient that had recurrence in the blanking period, and so we initiated Sotalol in the outpatient setting with a plan for about three to six months, and he'll be re-evaluated. We also often do cardioversions in the blanking period, but then taking them back to the lab is something that our docs consider it like a, they'll have that discussion at like six months, generally with plans to take them back after a year. But now with PFA, those re-dos are being considered sooner, but oftentimes, short-term antiarrhythmic drug therapy is considered, but often cardioversion, and then, if necessary, drug therapy. Yeah, I'd agree. I think it's variable from provider to provider, given this wonderful world of EP. So I would, generally speaking, I think we would try and attempt at a cardioversion first. We have found that most of our providers are still maintaining them. If they were on an antiarrhythmic prior to the procedure, we're keeping them on for a month, and then discontinuing, just because it sounds like, I've heard this, I'm not sure how true it is, but from a blanking period per with PFA, it may be shorter than our three months. And so I think that's favorable for patients, too, when it comes to catheter selection, that some folks are stopping anticoagulation even sooner than that. So I think that'll be an interesting discussion as we learn more about PFA, but it's definitely patient-dependent in terms of their motivation to come off the antiarrhythmic at the time of ablation. But we certainly try cardioversion first, and then increasing or titrating their outpatient regimen, if possible, to see if they convert medically. If that fails, then I, we rarely, I would say we rarely bring in people in for new-onset initiation of Sotolol or dofetilide, but it happens in less than 5% of patients, if any. So I think it was a little hard to hear, but after PFA, how many lesions do you think about CKD, and how often do you bring them back? I can answer the question about the PFA ablations. Really the technique to ablate, it's different than RF or cryo. You have a certain workflow that enables the therapy, and it's unique to that catheter. Yeah, I would say that we in our center, we've seen a couple of patients who have had hemolysis and acute renal failure, and that's typically, our cutoff is probably above like 60 applications in which we're starting to become concerned, especially if they have some underlying renal disease to begin with. A lot of our patients are coming in dry, they're obviously fasting, so that's obviously playing a role. If we anticipate after delivering 60 lesions, we usually give them a full liter of normal saline afterward to just continue to allow for adequate perfusion to the kidney, and hopefully flush it out. But we have seen instances that upon post-procedure discussion with the patient, they have that tea-colored urine, and then we evaluate, they lab work the day of the procedure. Sometimes we keep them overnight to see what happens the following day. Generally speaking, it starts to trend in the right direction. Very rarely, and some of my colleagues here too, I think we haven't had patients who have actually had to be dialyzed, which fortunately, that's been the case. But I don't know if there are other centers that perhaps have appreciated that sooner. No one's volunteering. All right, are there any other questions for our panel of speakers? Well, thank you all so much for this great discussion and great presentation.

Arrhythmia

Anti-arrhythmic drugs

Catheter ablation

Atrial fibrillation

Pulsed field ablation

Patient selection

Non-thermal mechanism

Clinical trials

Healthcare costs