Thanks very much. I also have been working in this space for quite some time, but not as long as perhaps Dr. Saxena, and it's an area of interest that I've been working on for over a decade. So when we talk about heart failure and atrial fibrillation, one of the things that sometimes people confuse is the symptoms. So people say, oh, I have a patient, they have heart failure, they have atrial fibrillation, they have no symptoms. Well, the symptom is the heart failure, right? So that's what we need to remember when we treat our patients with this problem, is not necessarily palpitations. What we're trying to modify here is actual LV remodeling and changes that could stem from atrial fibrillation itself. So there's some questions that we do need to answer, and even with the trials that we have so far that I'll be discussing, we may not have completely answered them. Is AF an instigator of heart failure or a mark of disease? Does elimination of AF improve heart failure? How much AF needs to be eliminated to improve heart failure? Should all patients with heart failure and AF undergo an ablation? So I just want to set the stage, and many of you may be heart failure specialists in the audience, but if not, to understand what is the risk reduction we get with guideline-directed medical therapy. So you take a patient with heart failure, you give them their GDMT, what do you get? Well, if you have optimal guideline-directed medical therapy, you have a 23% relative risk reduction in all-cause mortality, and a 21% relative risk reduction in cardiovascular mortality. So just keep those numbers in your mind. That's what we achieve with medication. Now when we think about atrial fibrillation and heart failure, we have to start way back. This was the original study that looked at AF and heart failure and treatment with amiodarone versus medical therapy. The AFCHF trial published by Denis Roy in the New England Journal back in 2008. And no difference in their primary outcome of death from cardiovascular causes compared to a rate-control strategy. But if you look at the amount of atrial fibrillation that they were able to reduce, it really wasn't that great. It was something, but it wasn't great. So now let's move on to the current area. So this is a summary of the trials that have been done, looking at sort of not the heart endpoints, sort of what we would call surrogate endpoints, like ejection fraction, VO2 max, recurrence of atrial fibrillation. And we started with PABA-CHF, a small trial done out of Bordeaux, randomized 81 patients, and the comparator was catheter ablation versus AV node ablation and CRT. And in that trial, the EF went up by 8% in the ablation arm. So a winner there. And that kind of set the stage for all of this. The McDonald study was small, only 41 patients. It was negative, showed no difference in rate control. Then we come a slew of studies, all of which were positive for these surrogate endpoints. And then the AMICA trial, which looked at rate control or amiodarone versus atrial fibrillation, showed no difference. And then we have the larger studies. As you know, Dr. Maroosh has published the CASTLE-AF trial. It was 363 patients, EF less than or equal to 35%. The comparator was rate control or amio, and the outcome was heart failure mortality. And they were able to achieve a relative risk reduction of 38%. I mentioned the CABANA study because they did a post hoc analysis of their heart failure patients. Now, although they didn't have all the ejection fractions, they did find a relative risk reduction of 36% in their primary outcome. And then we did the RAFT-AF study predominantly in Canada. We had 412 patients. The EF was less than 50%. Rate control was the comparator to catheter ablation. We demonstrated a relative risk reduction of 37%, but did not quite reach statistical significance. Although all of our secondary endpoints were in the right direction. And then we have CASTLE-HTX, which is the most recent trial, also showing a significant benefit in patients with advanced heart failure. And so this is what the curves look like. There's just a couple things I want to point out here. One is the time it takes to actually exert an effect. The CASTLE-HTX trial is a little bit unique. The time it took to exert an effect was immediate. But in RAFT-AF and CASTLE-AF, the time it took was approximately 18 months. So you do the ablation, you've got to remodel the LV, and then you might see an effect. And so one of the things in the RAFT-AF studies, it was stopped prematurely because of what was thought to be futility. But when they looked at the study, they only looked at, I don't know if you can see my pointer, no, you can't. But anyway, they stopped it at around 18 months. Unfortunately, they didn't see the separation of the curve, so we were underpowered because of that. But when you look at the reduction in AF burden, it was significant. So when you think about what do we need to do to actually reduce AF in these patients, I'll show you what the number needs to be. It was out of Dr. Maroosh's study and some other data out of in vivo studies. We probably need to get about 50% reduction in atrial fibrillation at least. In the RAFT-AF study, we did a combination of PVI plus something. PVI alone was very rare. In the CASL-AF study, half the people got PVI alone and other lesions. In the RAFT-AF, a third of patients underwent redo and 23% in the CASL-AF study. The mean increase of ejection fraction was 8% in CASL-AF and 10% in RAFT-AF at 24 months, but also a slight increase in the rate control population of 3%. So this is what I was getting at about AF burden. So it's a sharp inflection point of reducing your primary endpoint at a burden of around 50%, and that holds for the primary endpoint in CASL, all-cause mortality, and hospitalization due to heart failure. And this is an in vivo study that exposed cells, pluripotent stem cells, to atrial fibrillation. And again, the burden came around that number. So in terms of reducing calcium current, action potential duration, and sarcomere organization in the LV, or in the cells. Now when you put this all together, this is a meta-analysis that we did. We do get favorable effects on heart failure events, very significant relative risk reduction of 34%, and then a significant reduction in cardiovascular mortality. So when we put all these trials together, everything is favoring ablation. But what are the sort of downsides? We need to think about the consequences of an ablation in these patients. There are ablation-related events. In the RAFT-AF study, it was 10.8%, pretty minor, but there was a death due to an atrial esophageal fistula. Contemporary data using pulse field ablation has been looked at in the heart failure population. This is a study done by Turgam et al that looked at the outcomes with respect to atrial fibrillation, as well as the acute adverse events, and they were pretty favorable. So PFA may be a very promising modality in this sicker, albeit sicker, populations. Long term, though, these patients can develop atrial flutter. And atrial flutter in a heart failure patient can be devastating. You can get one-to-one conduction if you're not enough for rate control. You can have even two-to-one conduction can aggravate their cardiomyopathy. And the presence of atrial fibrosis actually increases the risk of atypical atrial flutter post-ablation. So we need to think about these types of things down the road when we ablate these patients. It's not that common, but it's certainly more common in the heart failure population than it is in the non-heart failure population. So as we improve our ablation techniques, perhaps this can be mitigated. When you look at long term outcomes overall in patients with atrial fibrillation that undergo ablation, they generally do better. This is very good data to suggest that we're not harming our patients by ablating them, and I think that's important. A couple of final points, one is time to ablation. I think this is emerging as a very important topic. This is a study done using retrospective data where they looked at the time from diagnosis of atrial fibrillation and performing catheter ablation and found that an increasing diagnosis to ablation time was associated with procedural success. And so all of this idea that we have with respect to progression of atrial fibrillation that Jason Andrade has taught us from his study called Early AF, this is real. And I think we need to really get at it with our heart failure colleagues to say that atrial fibrillation needs to be targeted early. And then, of course, the East Age AF study did a heart failure sub-study. They were targeting early ablation, or early rhythm control, I should say. It was not everybody had an ablation. But over a very long follow-up, they had a significant reduction in their primary outcome in their heart failure population, a composite of cardiovascular death, ischemic hemorrhagic stroke, hospital admission with worsening heart failure, acute coronary syndrome. But only 18% of patients got ablation, with 7% in the usual care receiving ablation. So still some work to tease out there, but I think the message is fairly clear that early intervention is important. Last point, are there any particular subgroups that may be a benefit? And again, in the RAF AF study, albeit it was a negative study, but we did have a signal that patients who were paroxysmal or type 1 persistent, meaning persistent due to a cardioversion, did better. And so again, early intervention, that's the message there. So this is a summary of atrial fibrillation and heart failure, kind of where we stand with respect to ablation. And the data that we have for us, we have small numbers of patients that have been studied, we need to do more to ensure. Although I think that the HEF-REF population probably benefits, although the data are from a highly selected population. When it comes to preserved EF, I'm gonna leave that for Dr. Pacini to address. And then finally, this is a summary of what I've just said. Likely improvement in heart failure outcomes, especially in HEF-REF. Possible improvement in stroke, highly select population in the studies that we've done so far. And we need to do this earlier. Not just about tachymedia and cardiomyopathy. There is an actual effect on the LV itself in restoring sinus rhythm. So even if people are rate controlled in atrial fibrillation, restoring sinus rhythm has a benefit. Thank you very much. Maybe walking will cure everybody. Thank you. that's this stuff, that's right. Great. Thank you very much, appreciate the invitation. My disclosures, I think, are two major ones. One is I am not an electrophysiologist. I like to think I know a little bit about HCM and AFib. And two, in comparison to a lot of other fields, there's really a paucity of randomized clinical trials as it relates to AFib management in this disease. And so all the data I'm going to be showing is really retrospective, observational. That said, AFib is the most common and a very important clinical pathway in HCM. About 20% of HCM patients develop atrial fibrillation that is clinically identified, making it the most common sustained arrhythmia in this disease. And when you compare it to age-matched populations, AFib occurs four to six times higher. That being said, when you look at subclinical AFib episodes seen on implanted devices, an additional 20 to 25% of HCM patients have these episodes, meaning that up to 40 to 45% of HCM patients may develop atrial fibrillation. That said, the management implications and impact of asymptomatic AFib only on implanted devices remains unknown. So the focus of my talk here is going to be on clinical AFib. Why does AFib develop in HCM? And I think there's a complex mechanism in this disease, and this is my hypothesis. One is you have outflow obstruction and dynamic mitral regurgitation from that, as well as diastolic dysfunction, all of which increase left atrial pressures. In addition, we know that some genes, MYH7, have higher rates of AFib, and thought is that there might be a primary atrial myopathy. In addition, atrial fibrosis in HCM is more extensive than in other forms of heart failure. And all of this combined with comorbidities, most prevalent in HCM in terms of a driver for AFib is obesity and obstructive sleep apnea combined to this high AFib rate. Can we identify patients, though, with HCM at increased risk for AFib? And with the help of Rick Carrick, we created the HCMAF score, which is the first externally validated risk-predicted tool for AFib specific to this disease, imputes four easy-to-identify clinical features, left atrial size, age you're seeing the patient, age when HCM was diagnosed, and whether or not they have heart failure symptoms. And with that, computes risk for AFib at two and five years. And this was recently incorporated into the 2020 4HA guidelines for HCM, and they created a nice online tool where you can put in those features, and then, again, it tells you risk for your individual patient for AFib development. And for those individuals who have a high-risk score, they recommend extended ambulatory monitors, which is what we do in clinical practice as well, but also counsel those patients on AFib symptoms with the hopes that they would come to clinical attention earlier. Why does AFib matter in this disease? And this is data now going back 25 years, looking at outcomes in about 100 patients with AFib, and showed that they were really abysmal. Almost 60% of patients developed chronic or permanent AFib over about a six-year follow-up period. At the end of that follow-up period, 50% had class III or IV heart failure symptoms. Embolic event rates were particularly high, almost 20% of the cohort, and particularly high HCM mortality. And that really raises the question as to whether or not prognosis of AFib and HCM with contemporary treatment is the same. You're going back from that study in 2001, where treatment was really warfarin for anticoagulation and amiodarone for rhythm control, which was often avoided for both of those given those challenges of management. And to this purpose, this is what we saw when we went back and looked at our cohort of HCM patients with AFib followed for about six years. And in our patients, we found AFib was not always progressive, often highly symptomatic, though. Sorry, I have five minutes left, right? Okay, okay. We found that AFib was not always progressive, but it's often very highly symptomatic in HCM, and therefore, for our patients, very aggressive rhythm control. And in this era, which was now also eight years ago, it was predominantly antiarrhythmetic drugs. Also, though, in patients with symptomatic obstruction with AFib, myectomy, which relieves left atrial pressures with MACE procedure, and then also AFib ablation. And in those patients, AFib was not progressive with only 25% of patients over follow-up with aggressive rhythm control, ultimately developing permanent AFib. Which antiarrhythmetic drugs can you use in HCM? And to that purpose, this is the most recent guidelines for that. In my clinical practice, I most frequently use Sotalol for rhythm control, also use disoperamide in those obstructive patients with paroxysmal AFib as disoperamide also decreases outflow gradients. We use dofetilide less, but other centers use that more frequently in their HCM cohorts, obviously needs a lot of QT monitoring. And then last line for us is really amiodarone, because it's a young patient population and obviously concerned about the long-term toxicity profile. That being said, it's probably the most efficacious of the antiarrhythmetic drugs in HCM. How about catheter ablation in HCM? And that's gotten a really poor name in HCM, and that is in part because of the very high risk of AFib recurrence after ablation in this disease. 50% in one year in this multi-center cohort for patients with paroxysmal AFib, and almost 100% in two years in patients with persistent AFib in HCM patients after ablation. This nice meta-analysis from Mayo looks at risk in HCM after AFib ablation, outcomes in HCM after ablation versus non-HCM patients, and shows that recurrent AFib occurs at 1 1⁄2 times higher rates in HCM, almost threefold more use of antiarrhythmetic drugs after ablation to control AFib, and a 1 1⁄2 times need of repeat ablation in HCM patients versus the general population. That being said, I think it's fair to ask, is AFib recurrence really the correct measurement of treatment success, particularly in a complex disease like HCM? And this nice multi-center cohort from Italy looked at longer-term outcomes after ablation, but not just looking at AFib recurrence, but also what the long-term treatment was. And they started with a third of patients with proxismal AFib, two-thirds with persistent AFib. Again, high rates of AFib recurrence, almost 50% in one year. That being said, they then underwent a repeat ablation or added antiarrhythmetic drugs, and you can see over a long-term follow-up, two-thirds of those patients maintained sinus rhythm, and just 20% ended up going on to develop permanent AFib. I think there's a lot of interest to say the least in pulse field ablation and how that translates into HCM. And this nice study out of France and Switzerland, three centers comparing patients who underwent pulse field ablation retrospectively versus thermal catheter ablation, showing lower rates of AFib recurrence at one year, only 70% recurrence rate after PFA versus, again, about 50% after thermal ablation. But again, that is probably in part because of a much more extensive ablation procedure being done with 60% of those patients having extra pulmonary vein ablation with pulse field. And our EP group, LAE, has really moved to using pulse field as their first line for our HCM patients, and almost always going extra pulmonary vein ablation as well. Stroke risk in HCM, I think it's important to note. The prediction models don't work. Still high rates of embolic events in HCM patients with Lochette's VASc score, and therefore the guidelines really recommend anticoagulation, typically DOACs after all, after the first episode for all HCM patients with symptomatic AFib. And with anticoagulation, stroke risk can really be minimal in our cohort retrospectively. That's 0.3% per year, dramatically lower than prior errors. And I like to think that this is in part because of our modern treatment with being very aggressive. If you compare our outcomes in this study versus the past, much lower rates of adverse events. Five-fold decrease of advanced heart failure at last follow-up, only 10% of our cohort. Three-fold decreased risk in embolic stroke. And HCM mortality in our cohorts with aggressive AFib treatment is low. So in conclusion, AFib and HCM, often highly symptomatic, impacts quality of life. Contemporary therapy, though, allows AFib to be treatable for most of our HCM patients, low threshold for anticoagulation, and obviously strive for better outcomes. Thank you. So thank you very much, Lassire. So these are my disclosures, but I have nothing to disclose regarding this talk. So let's first start with some epidemiological data. And in patients with cardiac amyloidosis, the prevalence of AFib has been reported to range from 40% to 88%, depending on the studies, which is much, much higher. That's what we see in the community, as well as in major heart failure trials. Now, the prevalence of AFib is also higher in those patients with a poor heart failure functional class and cardiac amyloidosis. And this also holds true when we look at the different stages of the disease, with the prevalence of AFib being more important in terms of prevalence in those patients with a more advanced stage of the disease. Now, we know also that the overall mortality is higher in patients with cardiac amyloidosis in those with more advanced disease, which means a greater columnar class or heart failure functional status, which is in this right part of the panel here. You don't see my arrow here. Now, since we saw the relationship between AFib and staging categories as well as heart failure functional status, we may wonder what is the prognostic implication of AFib in patients with cardiac amyloidosis. And here you have two studies in which you see that there is no impact of AFib on all-cause mortality. So this may seem weird, and you may wonder whether this really reflects the reality, but we have an old bench of studies which are in the same direction, and you see the list of these different studies here. And in those studies, the presence of AFib has not been associated with differences in overall survival in cardiac amyloidosis. And this could possibly be explained by the poor overall prognosis and limited life expectancy of the disease itself. If you see the graph on this slide and the two graphs on the previous slides, you notice that nearly 50% of the patients died after a mean follow-up of two to four years. But, however, we have some interesting data and such in this publication, and you see that the maintenance of sinus rhythm in patients with persistent AFib, who underwent a DC shock, and all those patients at cardiac amyloidosis, you see that the maintenance of sinus rhythm was associated with a better life expectancy. But the other side of the coin is that the maintenance of sinus rhythm was only achieved in 13% of the patients, which is pretty low. And when we look at this likelihood of maintenance of sinus rhythm, you see an inverse relationship with the stage of the disease, and so the most benefit was seen in terms of maintenance of sinus rhythm in patients at the early phase of the disease. Now, importantly, the management of AFib in patients with CA is very challenging. If we just look at the rate control in those patients, as you know, cardiac amyloidosis is a restrictive disease in terms of profile, and this results in a low, virtually fixed shock volume. And the consequence is the cardiac output depends mainly on the acceleration of heart rate in those patients. As a result, rate control strategy is very challenging because the different medications that you may use to control heart rates, in the great majority of the cases, they have to be stopped after a while just because of patients' poor tolerability. Now, if we move to rhythm control, many antiarrhythmic agents are contraindicated in patients with cardiac amyloidosis, and this means that the choice is very limited to amiodarone. Now, as you know, of course, ablation is the alternative to rhythm control as compared to antiarrhythmic drugs, so we have to have a look at the arrhythmogenic substrates of the arrhythmias in patients with CA. And due to the infiltrative process in these patients, it has been shown that these patients on the left panel have a mean endocardial voltage which is lower in each atrial segment as compared to a group, a matched control group of patients with persistent AF undergoing a catheter ablation. And in addition, they also have a significantly higher proportion of low-voltage area in each segment. So this means that they have a diffused substrate in terms of arrhythmogenic... of arrhythmogenicity, and this results also in a greater number of inducible atrial tachycardias as compared to the other group. Now, the likelihood that you have a non-PV trigger at the first time of AFib ablation is also increased in those patients with cardiac amyloidosis and in the multivariate analysis, it is absolutely clear here. And this leads to the Lassa risk score, which was introduced by the UPenn group. And when you have amyloidosis, you get four points, which means in terms of risk fortification for non-PV triggers that you have one-third of risk to have non-PV triggers. So the arrhythmogenic substrate both in the left atrial and in the PVs is completely different as compared to what you observe in patients who have no CA. In addition to that, AFib ablation is associated with a higher in-hospital all-cause mortality and adverse events, both at index admission and up to 30 days of follow-up in those patients with cardiac amyloidosis. So the procedure is more risky in those patients. Now, in terms of results of catheter ablation in those patients, we have a meta-analysis, which is to be published very near future in the Heart Rhythm Journal. And they summarize here eight studies, all observational studies with 168 patients. The great majority of those patients had AFib, but in addition to that, you have 50% of the patients with atrial tachycardia. And when you look at the results, you see that after a mean follow-up of three years, the recurrence rate of AFib in those patients who only had AFib initially is 35%, which is a pretty good result. And when you look at the whole population, the recurrence rate is at the same follow-up period is 43%, which means that the percentage is higher in those patients who had atrial tachycardia initially. And it has been reported that atrial tachycardia ablation in patients with CA is sometimes very, very difficult. Interestingly, one study reported, because it's the only one who evaluated that, they reported a higher success rate in those with the earlier stage of the disease. Now, the authors of this meta-analysis also evaluated in only two studies, which reported mortality outcomes comparing ablation and non-ablation among CA patients. That's atrial arrhythmia ablation was associated with a 64% reduction in all-cause mortality. Well, these are observational studies, so we cannot draw any conclusions from this slide and from this data, but I wanted to share these results with you. Now, as a conclusion, ladies and gentlemen, I would say that the prevalence of AFib is high in patients with cardiac amyloidosis and even higher in those with more advanced disease or poorer heart failure functional class. Both rate control and rhythm control are challenging in those patients. For rate control, this is related to the portability of drugs due to restrictive cardiomyopathy, and for rhythm control, the choice of antiarrhythmic drugs is limited to amiodarone, low maintenance of sinus rhythm, and DC shock in advanced disease, and ablation is limited in terms of success when case of atrial tachycardia in presence of a diffused substrate. But many experts suggest that rhythm control should be preferred over rate control, and you have some data showing that the success rate is high in those with an earlier stage of the disease. I thank you for your attention. We go on to our next talk, which is on catheter relation of AF in persons with FPEP. Can we all breathe easier now? And will you give it back? Thank you, guys. Professors, ladies, gentlemen, it's my pleasure and honor to give this talk, and I apologize for being late. I did not realize 29 was all the way at the other end of the convention center. I'm going to talk about catheter relation of atrial fibrillation in patients with heart failure and a preserved ejection fraction. These are my disclosures. So we're facing an avalanche of atrial fibrillation, but we're also facing an avalanche of heart failure with preserved ejection fraction. And so the topic of managing atrial fibrillation in persons with FPEP is going to become increasingly important moving forward. And this is one of my main messages today. FPEP in our AFib clinics is often hiding in plain sight. And these are data from an aggregate of studies compiled by our chief fellow in a recent review that she submitted. And what you can see is the prevalence of atrial fibrillation in persons with FPEP is very, very high. And it's something we – sorry. The prevalence of FPEP in persons who come to our clinics for evaluation for atrial fibrillation is very, very high, and it's something we need to consider. And there's a bunch of ways you can approach this. We know that people who have dyspnea have a much higher likelihood of having FPEP, and so you can send a natriuretic peptide level in these patients. There are also several artificial intelligence add-ons for your echo lab that can give out pretest probability and posttest probability for the presence of FPEP and guide future testing. We know that patients do better in sinus rhythm across a large variety of illnesses. That includes FPEP, and these are data showing that patients maintaining sinus rhythm have better neurohormonal levels and improve myocardial performance. These are data from Get With The Guidelines Heart Failure and Nationwide United States Quality Improvement Registry that doesn't necessarily look at catheter ablation but looks at rhythm control versus rate control in persons with FPEP. And in this analysis was able to account for a very large number of comorbidities and patient characteristics in over 15,000 patients with heart failure and ejection fracturing greater than or equal to 50%. You can see that there was an association with improved mortality. In our center, very early on, quite some time ago now, we compared how patients with HFREF did after ablation. We compared patients with FPEP to those with HFREF after ablation, and as you can see, maintenance of sinus rhythm is fairly similar, perhaps a difference as the cohort dwindled. But more importantly, you can see that symptomatic resolution in persons with FPEP treated with catheter ablation is very equivalent to those with HFREF. And I think this is important because, as has been previously shown in this session, we have a very good evidence base for catheter ablation in persons with heart failure and reduced ejection fraction. Similarly, we saw very significant improvements in functional capacity in persons with heart failure with preserved ejection fraction. Other centers have also reported their data. This is a very nice study that showed the adjusted risk of hospitalization was significantly reduced in persons managed with a catheter ablation approach relative to medical therapy only. And in the CABANA primary trial, in the sub-analysis of individuals with heart failure, essentially 80% of four out of every five persons with heart failure in CABANA had HFPEF among those who had ejection fraction data. And as you can see here, the primary endpoint, which was neutral in attention to treat in the overall CABANA population, was significantly positive in those persons with heart failure, again, with a very sizable minority of patients with HFPEF, or majority with HFPEF. So the question is, for the baseball fans in the audience, can we reverse the curse? And I truly believe in that because I'm a Chicago Cubs fan, so if we can win the World Series in contemporary times, anything can happen. So what's the evidence for that? Actually, there's quite a bit of evidence from small studies. This is one of my favorite studies that's been performed in the past decade by Dr. Sugamar and colleagues, where they asked a simple question. People who came in to EP clinic referred for catheter ablation with atrial fibrillation. What percentage among patients who had dyspnea had HFPEF? And guess what? It was about 65%. They underwent ablation, and as you can see on the right panel in green, they experienced a wide variety of improvements, including decrease in cardiopulmonary congestion, improved hormonal profile, and a decrease in arrhythmia recurrence. This is not the only study. We can't present 10 studies in a short talk, but here's another one. Here's a very nice analysis using propensity matching, looking at patients with medical therapy versus ablation therapy, and two big things to point out. The first is that progression of atrial fibrillation was dramatically lower in those persons treated with catheter ablation. And the second important point is that there were, remember, everyone in this cohort met diagnostic criteria for HFPEF at baseline, so the number of persons that fulfilled criteria after therapy was much lower in the catheter ablation arm. So I'm not suggesting that catheter ablation cures every shred of evidence of HFPEF, but clearly in a very significant group of patients it dramatically improves symptoms, and in some cases patients won't even meet diagnostic criteria. It's important to remember that there are heart failure guidelines. For those of us who have our nose buried deep, deep, deep in the AFib guidelines and may not peruse the other guidelines as much, and there are several medical therapies we should keep in mind for the treatment of HFPEF. This is from the guidelines, and the summary is provided by Dr. Sanjeev Shah at Northwestern, suggests that afterload reduction, decongestion with SGLT2 inhibitors, MRA, ARNI therapy in persons with EF less than 55% to 60% are very important, and PD inhibitors and nitrates do not appear to have as much benefit. If we look specifically at the SGLT2 inhibitors, these are data from the China AF registry that show among patients undergoing catheter ablation, outcomes are improved in those treated with these medications. So a really important part of your protocol for catheter ablation and HFPEF patients should be making sure they're on guideline-directed medical therapy. You certainly don't want to send them out to the door and say, well, address your guideline-directed medical therapy with your general cardiologist. This is something you want to address right away. And I know as electrophysiologists we're very confident, but these patients really need every single therapy that can be brought to their attention to improve outcomes. What are the pitfalls? Well, we just heard a really nice talk about how difficult managing atrial fibrillation is in persons with cardiac amyloid. One way to make that even more difficult is if it's not diagnosed or you bring someone to the lab who has amyloid and you don't know that. Rhythm control can be very appropriate in these patients, but certainly they need to be staged. They need to be seen in an amyloidosis clinic and get on any disease-modifying therapy as part of their overall care. And a pre-procedural MRI for both patients with cardiac amyloidosis and hypertrophic cardiomyopathy can be very, very helpful to give you an idea of the scar burden. Inadequate afterload reduction and persistent hypertension is another pitfall in the management of these patients, and you need to be meticulous and make sure their I's and O's when they're discharged, either same day or next day, that they don't have any fluid accumulation from their ablation procedure. There are scores that can help you risk stratify what the likelihood of adverse cardiovascular outcomes are after ablation and can help you risk stratify what the individual's likelihood of recurring atrial fibrillation. Although I think we need to be a little bit careful with risk scores that are based on recurrent atrial fibrillation because, as we know from CasLHF for HF-REF, sometimes reduction in atrial fibrillation can result in a significant improvement in outcomes even if the patient's still having recurrent arrhythmia. There are some unanswered questions. What's the best energy modality? What's the optimal lesion set? Is adjunctive renal sympathetic denervation very helpful in hypertensive HF-PEF? What's the optimal paraprocedural management? The wonderful thing about heart rhythm medicine is we all work really hard as a community to answer unresolved questions. And as you can see here, there is a plethora of planned or ongoing clinical trials, including the Cabana HF-PEF trial that's just been submitted to the NIH under the leadership of Dr. Packer. So in conclusion, HF-PEF is underdiagnosed in patients with atrial fibrillation. Freedom from AF decreased symptoms. Improvement of functional class are similar in persons with HF-PEF compared to HF-REF. Observational data and post-hoc analyses suggest the benefit might even be greater in HF-PEF. And fortunately, we have lots of large multi-center trials going on to help answer these final questions. So thank you for your time and attention. Thank you. Our next speaker is Dr. Chris Bain, all the way here from Australia, to talk to us about paraprocedural management of AFib ablation heart failure patient. And please scan the QR code that Sanjeev has made me work on. So without everybody, I'm going to check that. Thank you, everybody. It's a great pleasure to be here, and I'd like to thank faculty for inviting me to present on this increasingly important topic. I have no conflicts of interest that are clear related to the specialties of cardiology or cardiac electrophysiology. Apart from that, I'm an anesthetist, not an electrophysiologist or an anesthesiologist. I must acknowledge the organizations that have provided me with support for my own research. My current practice is based at the Alfred Hospital in Melbourne, Australia, and that is a major quaternary institution that specializes in the management of heart failure and a leading center for ventricular assistance and heart transplantation. The electrophysiology service is integral, completing more than 500 AFiblations annually, of which 30% are for HEF, for heart failure with reduced ejection fraction. The service offers a mixed approach of RF and pulse field ablation that is tailored to care for the patients with complex cardiovascular issues and multiple comorbidities. 100% of the patients have AF ablation under general anesthesia, and of course we provide an anesthesia service for other forms of catheter ablation as well. So today I will address the issues that are increasingly evident to me in my current practice. Firstly, the growing demand for AF ablation generally in the era of pulse field ablation and specifically in patients with heart failure, and planning for AF ablation in patients with heart failure. To me, this is really about addressing the important and changing question of which approach, general anesthesia with muscle relaxation and full control of ventilation or the varying approaches of sedation such as propofol-based deep sedation or conscious sedation with light sedatives and analgesics. And whether these approaches differ depending on the ablation method, especially in the era of PFA. The importance of communicating as a multidisciplinary team to optimize procedural risks. In other words, as an anesthesiologist supporting a program of AF ablation for patients in heart failure, what do I really need to know? And conclude by summarizing with what I see as a patient-centered approach to periprocedural management. I am experiencing firsthand the growing demand for anesthesia care of patients having AF ablation for heart failure. And I believe this is due to two key events. The now established safety and efficacy of pulse field ablation and the determination of the latest guidelines for management of AF that catheter ablation for heart failure with reduced injection fraction is now a class one indication. The impact of this being a shift in the complexity and acuity of patients being considered for ablation. And this is supported by the findings of Castle HDX trial investigating the impact of catheter ablation in patients with symptomatic AF and end-stage heart failure. 97 patients assigned to the ablation group and 97 to the medical therapy group with a medium follow-up of 18 months. The trial was stopped early with the primary endpoint of death from any cause, LVAD implantation or urgent heart transplantation, occurring in six, that's 8% of patients. And in the ablation group, compared to 19 in the medical therapy group, representing a hazard ratio of 0.24. And now, emerging evidence supports ablation during hospitalization of acute heart failure with pulse field ablation. Although this is a report of a single center, the data demonstrated a steady increase in ablation procedures for inpatients with low EF with PFA under general anesthesia. The outcomes were good with both improved LVEF in patients with their first manifestation of heart failure as well as those with decompensated heart failure. The main conclusion being that it was safe and associated with good clinical outcomes. So collectively, the current guidelines and clinical evidence indicate why there's a growing demand for anesthesia for catheter ablation in heart failure. Given the increasing demand, this brings me to the issue of planning. Which approach? General anesthesia, deep sedation, or conscious sedation? In the worldwide survey conducted between 2010 and 19, Garcia and colleagues showed that AF ablation procedures more than doubled and that there was a trend of increasing use of general anesthesia and deep sedation and decreasing reliance on conscious sedation. Of course, this was a period when cryoablation was on the rise and patient comfort reduced movement facilitating improved catheter stability and mapping accuracy facilitated the trend to increasing general anesthesia and propofol-based deep sedation. What about outcomes? The Danish registry of nearly 8,000 patients having their first ablation of both persistent and paroxysmal AF from 2010 to 2018 compared general anesthesia, which was approximately 20% of patients, to conscious sedation, which was 80%. And they demonstrated the risk of AF recurrence at one year and five years was 26% higher with ablation under conscious sedation compared to general anesthesia. Of course, in the PFA era, the manifest surveys provide valuable insight into the direction things are going with respect to general anesthesia and deep sedation. Manifest PF, published in 2022, 1,758 patients, 24 European centers, 90 operators, general anesthesia, 15%, deep sedation, 85%. Of course, no mention of conscious sedation. Manifest 17, published in 2024, over 17,000 patients, 116 centers, and 400 operators, representing a very high percentage of the use of the Farrah Pulse catheter at that time. And so with this, a rise in the use of general anesthesia to 44% compared to a reduction in deep sedation to 56%. That is thought to be due to increased access to anesthesiology services as well as a desire for better control of movement, cough, diaphragmatic stimulation, and so on. So in summary, the guidelines and clinical studies not only show why there is a growing demand for AF ablation in patients with heart failure, but also demonstrate an increasing need to involve anesthesiologists to provide general anesthesia. Optimizing procedural risk is about communicating as a multidisciplinary team. Is the baseline cardiac function stable or progressively worsening? Are the symptoms of heart failure adequately controlled? And if not, what further treatments can be done to improve the symptoms prior to ablation? Is cardioversion prior to ablation an option? Is the plan to continue medical therapy and anticoagulation? And if not, what are the implications of ceasing these medications? Are further tests indicated, such as right heart catheterization? Patients with right heart failure and severe pulmonary hypertension represent a risk group with significantly increased risk and may require more specialized planning and support. Is the likelihood of significant hemodynamic decompensation low? And if not, is it safer to delay? So to me, it's all about remembering that the patients are in the center of this. And it's our role and responsibility to seek an approach that addresses the patient's expectations as well as create conditions to maximize comfort, safety, and efficacy of the procedure. And remember that patient satisfaction is not solely dependent on procedural success and outcomes. So in conclusion, anesthesia or sedation is an essential component of patient-centered care for catheter ablation, atrial fibrillation, and heart failure. Increasing evidence supporting the value of AF ablation and heart failure increases the need for multidisciplinary periprocedural planning and optimization. Propofol-based deep sedation is safe and feasible. However, general anesthesia is increasingly preferred to enhance procedural conditions and ensure patient comfort and safety. And close collaboration between electrophysiologists and anesthesiologists is essential to deliver patient-centered care and improve procedural outcomes. Thank you very much. Thank you, Dr. Behan. First of all, let me congratulate the faculty for this very interesting and important set of talks, meticulously researched on very important aspects of this overall AF and heart failure population. We have a number of questions. you are? Anastasia. Anastasia, brilliant. Just a quick answer? I'm short of breath. Yes. That's a question to our chair here, which I want to engage with. It's a very important question. Why are so many patients with FPEF not being seen in our atrial fibrillation? You know, atrial fibrillation is half the consultations done by electrophysiologists in hospitals. So as I mentioned to Nasir, we may have shot ourselves in the foot a long time ago. We said the symptoms of atrial fibrillation are palpitations, chest pain, syncope, and dyspnea. What we never thought about was that maybe during that episode of atrial fibrillation, there was a hemodynamic event that caused dyspnea. And there's more and more evidence, as Jonathan's research presentation showed, that there is occult and probably acute FPEF that takes place in this situation. Now, April Slee is here, and her work showed that in patients with atrial fibrillation in a firm, the most important complication that emerged was heart failure in 20% of patients. We never talk about that. And I think there is nobody who comes, and when you see a patient of atrial fibrillation, whether EP or cardiology, and they say, well, I'm a little more short of breath, we ascribe it to the arrhythmia. So this table actually has all the right people here, that this group of patients require a multidisciplinary approach to management. And my heart failure colleagues, I faulted them for this, that 92% of patients with FPEF in top cat were treated with rate control, and AF was only a marker. I think April and some of the work we presented shows that AF accelerates heart failure, in early heart failure, and causes pump failure death in advanced heart failure. So understand PALACE, Andromeda, and all of these trials done in class three, four heart failure, they're already on their way to pump failure death. And the HTX trial shows that you get that immediate acute stabilization of that road to pump failure death when you restore sinus rhythm. That physiology is important. Now, we do have a number of questions, and we will try and get, I'm going to ask everybody to find people. We've been moving away from anti-arrhythmic drugs as first line and really moving towards ablation. That being said, as you saw, the recurrence rates after a single ablation procedure is quite high, and so you are using anti-arrhythmic drugs, but now we're starting to use them more after recurrent AFib episodes after a first ablation, or to get them to ablation. The answer to that is that there's no role for Mavicamtin just for AFib and obstructive HCM. If anything, the long-term extension data suggests that risk of AFib long-term on these drugs is high, so we don't use it for AFib management, we use it for obstructive symptoms. Just a comment for you to consider, you showed no change in total mortality, but the question is, do we look at heart failure? The amount of burden, Rathika mentioned 50% in Nasir's study, I would say in a firm it was 25%. I really enjoyed the discussion. I was just going to pick up on Nazir's comments about why electrophysiologists don't see more heart failure patients. I think it's really complicated. I think we all have to act as ambassadors for AF ablation. I think sometimes as electrophysiologists we hang out too much together and not at general meetings and get our message across. I think we definitely need to get away from this tacky mediated cardiomyopathy. Terrible term because we know that there's a lot more to the way AF drives HF than just ventricular rate control. I think a lot of our heart failure colleagues are still back in the days of if they're rate controlled and they're not reporting palpitations, then AF isn't relevant to their heart failure. So I think we still have a huge role in educating. I think the burden aspect that you've shown with carcel AF in terms of having an impact on LVEF, I think that message hasn't quite gotten through yet, that we don't need a perfect procedure to have big impacts on outcomes. So I think it's sort of incumbent on all of us to drive our message home about the benefits of AF ablation in that community. Okay, let's take another question from a list here. A rejunction ablation for the ablationists in the room. Roll and have left. At what stage? That's a question on the screen. Never. Would you? Almost never. Christian, you agree? Yes. So I think it is a question, you know, I think it is definitely a last resort right now, but maybe with physiologic pacing that could change. So I think the question's open. If Dr. Boryani was here, he would argue that there is a role for CRT and AV junctional ablation in the right set of patients, and he does have control data to support that. The question is, what are the... I've never had this in my life before, and thank you for being here. Thank you all again. Thank you.

atrial fibrillation

heart failure

ejection fraction

catheter ablation

PABA-CHF

CASTLE-AF

CABANA

antiarrhythmic drugs

rate control

multidisciplinary strategies