Welcome, everyone. We're going to get started in just one minute. Thank you everyone for attending. I'm just going to give everyone a couple of minutes before we start. I'm just going to give one more minute, one or two minutes still. I see people dialing in. Thank you everyone, all of those of you who have dialed already. All right. While we don't get started, people are still dialing in, but we're going to have to do some introductions, so that will take a couple of minutes. First of all, welcome to everyone to this webinar titled, What the 2023 AFib Guidelines Tell Us About Risk Factor Modification and Prevention. We're going to dive in deep into the guideline, risk factor modification and prevention, as well as lifestyle intervention. Please let me introduce myself first. I'm Jose Hoglar. I'm professor of medicine and electrophysiologist at UT Southwestern Medical Center here in Dallas, Texas. These are the disclosure slides. Let me introduce you then to, we have two speakers and two panelists. We're going to start with Dr. Lin Yi Shen. He's a good friend and colleague. He's a professor of medicine, director of the Lillehei Heart Institute at the University of Minnesota. And then we have also Dr. Andrea Russo, director of arrhythmia services, professor of medicine, program director of electrophysiology fellowship at Cooper University in New Jersey. We also have Dr. Prash Sanders. He's professor of medicine, director also of arrhythmia services at Adelaide University in Australia. Very early over there. Thank you so much, Prash, for joining us. And we also have the honor to have here with us, Megan Struer. She's a nurse practitioner in electrophysiology, also participated in the guideline. She's assistant professor of the School of Nursing at the University of Washington in Seattle. So what we're going to do, the format is we want to have a conversation with the audience. We want to, the audience will have an opportunity to send questions to the speakers and the panelists, and we'll be happy to track those questions. We're going to have two lectures first by Dr. Russo and Dr. Sanders. And then after that, we're going to address as many questions as possible among ourselves, try to, like I say, dive in into what the guidelines have to say about these topics, and also try to give an insight of what the writing committee members were thinking when they wrote these recommendations. So let's start with the first speaker, Dr. Russo. Please take it away. Great. Thank you so much. Thank you so much, Jose. And let me just pull up my slides here and share them. So really a pleasure to be here tonight. And I thank the Heart Rhythm Society for allowing us to present this information. So this is the document we'll be referring to. So this was published earlier this year, and our moderator tonight, Dr. Hogler, was our fearless leader on the document and really was thrilled to see the emphasis on a lifestyle and risk factor modification. And this here was certainly an incredibly passionate writing group. We divided up the pillars of AFib management into three separate pillars. One is stroke risk assessment and treatment, thrombobolic risk assessment, symptom management, and that includes evaluation of AFib burden with rhythm control and rate control. And you can see here right in the middle is this modifiable risk factors. So this is what we're going to talk about tonight. And these kind of factors are important in reducing AFib onset progression and adverse outcomes, and really the focus of something different than I think most of us are doing, you know, used to been doing in electrophysiology. So in terms of the disease continuum, these factors are very important throughout the disease continuum. And what we thought about and what I think is also different in this document, previously the classification of atrial fibrillation was based on arrhythmia duration. So things like paroxysmal, persistent, long-standing persistent atrial fibrillation, and it was thought that that might have some implications on treatment, but the new classification really recognizes this disease as a continuum. Those who have these risk factors for atrial fibrillation, things like obesity, sleep apnea, alcohol, diabetes, and then maybe some earlier pre-AFib is what we named it, atrial enlargement or some other high-risk features, things like non-sustained atrial tachycardia, and then the more classic paroxysmal, persistent, long-standing persistent, and ablation, right? We don't always say cure right after ablation, but there's still, these patients are monitored closely. And the important thing to know here is that wherever you are at, that it's really important to treat these modifiable risk factors, whether you're in the early stages or even as things go on. And that's because really atrial fibrillation can continue to have progression and it can continue to have substrate remodeling, and you can, early on, you may just have a few triggers and some non-sustained arrhythmias, but later on, based on your genetic predisposition as we age, more likely to have atrial fibrillation, but having more atrial fibrillation, we always said atrial fibrillation begets atrial fibrillation, you can get these changes, structural changes in the heart. And even in the prevention, I think this was also, you know, something very different, right? This is prevention, people have not even had necessarily AFib yet, a class one recommendation, patients should receive comprehensive guideline-directed risk factor modification targeting those things, obesity, physical inactivity, unhealthy alcohol consumption, smoking, diabetes, and hypertension. And I have to say, give a lot of credit really for Dr. Sanders, who has done a lot of this original research, really focusing on prevention and also modification of these risk factors to decrease some of these things that can really impact on AFib and increasing amount of AFib and increasing inflammation and fibrosis, and really has been at the forefront of this. So let's talk, we're splitting up some of these topics, and I'm going to start out by talking about diabetes, and I don't need to tell anyone who's listening here, but diabetes is really common. Type 2 diabetes affects over 9% of the U.S. population, and it's a major risk factor, right? A major risk factor, and is associated with, is a major risk factor for stroke in the setting of AFib, but it's associated with increased cardiovascular events and mortality. But it also increases the risk of developing atrial fibrillation. And once you have, you know, diabetes, it's also associated with, you know, lower quality of life and increased hospitalization, increased mortality. And this, and as well as some of these other, you know, modifiable risk factors, you know, diabetes can have a lot of different effects, either through inflammation or fluctuations in glucose by impacting on the structure of the heart. Fibrosis, increasing fibrosis, increasing, you know, electrical changes and remodeling of the heart, and also changes in the autonomic nervous system, and all of this can kind of, you know, impact on the amount of atrial fibrillation we have. So what about, does it matter, you know, how well our sugars are controlled or, you know, patient's sugars are controlled? Well, you could see if a hemoglobin A1c level is higher, you can see that that is associated with an increased risk of atrial fibrillation. If diabetes has been present for a longer period of time, that's also associated with an increased risk of atrial fibrillation, and these are the odds ratios. We also know that diabetes increases the risk of stroke in patients with atrial fibrillation and independent, one of the strongest independent risk factors, and we include that in our CHADS-VASc scoring system, and you got a point for diabetes, but if we, you know, treat it with anticoagulants, we can reduce that risk. And there's other, just to mention, because I think this is also something new in the guidelines, you'll see is not just using CHADS-VASc score, you can use other scoring systems, and if you have a risk of 2% or more per year, that is something we would consider, you know, patients should be anticoagulated. And we also have now for diabetes so many different treatments, you know, certainly in some of these treatments may have additional impacts. So, for example, the GLP-1 receptor agonists and also the SGLT2 inhibitors, we see a lot of patients on these who have diabetes, and now we see them being used for things without, even patients who don't have diabetes, right, people are using some of these drugs for weight loss and just have a lot of beneficial effects, heart failure, other things too. And I'm just going to show you this one study, although these are one meta-analysis of large randomized trials of some of these drugs, including the SGLT2 inhibitors and the GLP-1 receptor agonists included here, and these are studies compared with placebo, but just to note that there's no, none of these studies had primary outcome measures of atrial fibrillation there. AFib was considered more of a complication, so looking at adverse events, but you can see overall the SGLT2 inhibitors were associated with a lower risk of atrial fibrillation. Again, that's combining all these different studies, and you can see some of the drugs may have different effects than some of the particular, so it's maybe not the entire class of drugs, as far as we can tell, you know, from these studies that don't have AFib as a primary outcome. And the GLP-1 receptor agonists did not in this meta-analysis show any significant effect in reducing, you know, the chance of having AFib, although if you look closely with the ones with the arrows, these are the two different drugs, semaglutide, suggests maybe, you know, that each drug might be, you know, not the same as the other ones in the class. And so there's really like a lot of controversy right now is what the effect of, you know, of these drugs is on AFib, and is it really a primary effect, or is it just the fact that patients are, you know, doing better, losing weight, controlling their blood pressure, and doing all these other good things, but you could see even some of the other, you know, drugs, you know, might have some beneficial effect on atrial fibrillation. These are just observational studies, though we still have a long way to go to get, you know, better studies looking at AFib as a primary outcome. So I think the point is, is not just, you know, treat your atrial fibrillation with all the things we're treating AFib classically for, but to modify, you know, other diseases and other risk factors and lifestyle modifications, these drugs can help reduce some of these things that can increase atrial fibrillation, electrical and structural remodeling, you know, in addition to, you know, potentially reducing the risk of AFib. So what about hypertension? What's the data like there? Well, we have also a class one recommendation for patients with AFib and hypertension, optimal blood pressure control is recommended to reduce AFib recurrence and AFib-related cardiovascular events. And, you know, what data is out there, not necessarily data for hypertension alone. Now, this is one of the studies, and you'll see others that Dr. Saunders will show us, but this study looked at a lot of different risk factors, right, and looked at risk factor reduction is resulted in modifying these risk factors resulted in greater reduction in blood pressure. So you could see this group here and less, you know, and also the arrhythmia-free survival was better with risk factor modification compared to the control subjects, pretty dramatic. And you could say, well, does blood pressure mean anything? Well, if you look here, again, it doesn't say it's not causing an effect per se, but you can see here in the control group, not as much, there's a significant drop in blood pressure. We're doing all these healthy things and weight loss we know can help with blood pressure control, but you can see here a much more dramatic effect here when, you know, in blood pressure reduction with the risk factor modification group. So it's not just, you know, so there's more to it here. So controlling blood pressure suggests controlling blood pressure is beneficial. And then renal denervation. So this is one study looking at catheter ablation alone versus catheter ablation with renal denervation. So, and the impact on AFib recurrence. So you could see here, these are atrial arrhythmias of all sorts of recurrence, and this was randomized PBI alone to PBI plus renal denervation. And you could see here that there was a longer time to recurrence of atrial fibrillation in those who also had renal denervation, which we would assume would reduce blood pressure. And you could see here that it did in this study at 12 months, you look at the PBI only group, not much change in blood pressure, but in the renal denervation group, it was 150 down to 135 millimeters of mercury. So again, then that was a significant difference, but, you know, between the groups. Another study looking at, you know, blood pressure intervention, and this is looking at in SPRINT, it was looking at intensive blood pressure lowering to less than 120 millimeters of mercury systolic compared to just standard lowering, and looked at the risk of AFib in this study also. They were originally a randomized study, but this was, you know, a subgroup analysis, and you can see intensive blood pressure lowering was associated with a 26% lower risk of developing nuance at AFib, again, suggesting that this is important in reducing AFib blood pressure control. And aldosterone pathway blockade, and this is using either spironolactone or a plurinone, and this is randomized in observational studies, but, you know, a large number of patients overall, and then you can see a significant overall reduction in AFib risk in patients who received these drugs versus those who did not. You know, so blood pressure seems to be important. And then alcohol, what about alcohol? Well, we know that in the guidelines, we gave it a class one recommendation with some randomized data here, too, with those seeking AFib rhythm control should minimize or eliminate alcohol consumption to reduce AFib recurrence and AFib burden. So what data do we have? So this was actually an interesting study looking at acute alcohol consumption with discrete AFib events, Dr. Marcus did this, and 100 participants, and they wore this continuous ECG monitor as well as this ankle transdermal ethanol sensor for four weeks. And they also documented the alcoholic drinks that they were consuming and self-reported that, too, and there was also some blood tests looking at this, you know, ethanol component here to corroborate their assessments of what they were drinking. Anyway, overall, an AFib episode was associated with a twofold higher odds of one alcoholic drink and actually over threefold odds of at least two drinks in the preceding four hours. And individual AFib episodes were associated with a higher odds of recent alcohol consumption, suggesting the role of alcohol here in causation of AFib. So here's a meta-analysis. These were seven prospective studies, over 12,000 AFib cases, and looking at alcohol consumption. And alcohol consumption, at least even at moderate intakes, is a risk factor for AFib as shown here. So if you look at compared to non-drinkers, these relative risks were higher. So one drink was higher than compared to non-drinkers. And then you can see if you get up to four or five drinks, that the relative risk was even higher. And then abstinence. So if, you know, alcohol causes it, what does abstinence do? So this was a multicenter prospective randomized study performed in Australia. Australia is certainly, our investigators there have certainly been ahead of the times here in looking at these kind of things. But these are adults who consumed at least 10 standard drinks per week, and they had either paroxysmal or persistent AFib, but were in sinus rhythm at baseline. And they were randomized to alcohol abstention versus just doing what they're continuing to do. And you can see here, the abstinence group had a longer period of time before recurrence of AFib compared to the control group. And you could also see this is AFib burden over 5%. Abstinence group is here. AFib burden over the six-month follow-up was significantly lower in the abstinence group. This was no AFib. So they're more likely to have no AFib. Caffeine. Now, this is one that I'm very happy to say that the guidelines give it a class three, no benefit. So for patients with AFib, recommending caffeine abstention to prevent AFib episodes is of no benefit based on the data we have. Now, if someone tells you they're having, you know, they drink a lot of caffeine and they're feeling palpitations, you know, in that case, you'd probably still tell them because even if they're feeling APDs and not feeling well, but the data does not suggest that caffeine causes AFib per se. So these are observational studies. And this is a meta-analysis, seven observational studies over 115,000 individuals, cohort studies and case control studies. You could see overall that caffeine exposure was not associated with the increased risk of AFib. And so I was happy to see that. And, but it's actually interesting too, if you look at these studies and they divided it up into low caffeine intake, moderate or high caffeine intake, and actually those who had lower caffeine intake, the caffeine exposure may even potentially decrease the risk in these, again, it's observational studies, but it doesn't seem to make it worse. So thank you. I want to actually turn this over to my colleague, Dr. Sanders to continue from here. Thank you, Andrea. And again, we're going to do the questions at the end. So Dr. Sanders, take it away. Can you mute it? You can see the slides okay? Yes. Thank you. So thanks, Jose and Andrea. And what I'm going to do is to kind of follow on some of the risk factors that we've talked about to kind of bring out the remaining risk factors that we thought should be mentioned as modifiable factors. And one of the most important ones that we're faced with is that of obesity. And this is important because it's almost at a point where this is gonna take over from hypertension as the highest attributable cause for atrial fibrillation. And so it becomes really important in the kind of community context. The picture on the right shows the various ways in which obesity can lead to changes in the myocardium to give rise to the preference to be in atrial fibrillation. But the bit that I wanna highlight with this is actually the fact that it is often associated with other conditions that cause atrial fibrillation on their own. And so it's very rare in the AF patient to have an isolated risk factor that causes AF. And most often we're dealing with a scenario of multiple factors that need to be attended to. And so I think that highlights it in the obesity population. From a clinical perspective, there are big issues here. It causes more incident atrial fibrillation. There is more post-operative atrial fibrillation. And from our ablation strategy perspective, there's a greater incidence of recurrent AF after AF ablation. So this is important from the perspective of our patients. Now, the approach we've taken is really to treat each of these risk factors, recognizing early that isolating at one risk factor had limited benefit. And so we try to treat each risk factor that's important for that given individual. And shown on this slide are some of the factors that we think are reversible, but together with the targets that we have been using in our studies. So weight is critical. We try to lose at least 10% of weight. Exercise is important. We're trying to increase the amount of exercise one does. The blood pressure, as mentioned, crucial. Diabetes, crucial. We also target sleep apnea in those who we're trying to maintain sinus rhythm in. Lipid lowering to guideline levels. We aim to stop smoking and we try to reduce alcohol consumption. And we've talked about this, ideally like to eliminate it, but in our studies, we've targeted less than three standard drinks for a week. And so this is the schema that we've used in terms of our risk factor management group. And as highlighted, our studies have all been about managing all risk factors. It's not just isolated obesity, but this is a randomized study in an obese population where we got them to lose weight over a 15 month period. And what we see is a significant reduction in the intervention group where we have a reduction in the symptoms of atrial fibrillation. And then when we undertake continuous monitoring, there are fewer episodes of atrial fibrillation and these last for a shorter duration of time. So we can really see that there is a benefit at least in that short to medium term in terms of managing weight and risk factors. Now in legacy, we continue this, but in a larger cohort of patients in an observational series. And again, I'll highlight that the weight here is used as a measure of the overall risk factor management. And we were able to show two important things here. The first is that there's a graded response. The better you manage your risk factors, the more likely you're going to remain in sinus rhythm. So that I think gives us a guide as to what we can achieve. But one of the other things this study showed was we should try to avoid fluctuations in weight as we try and lose weight. And so that becomes important in terms of strategies and counseling that we need to be providing to our patients in order to achieve the benefits of weight reduction. And this I think is probably the most important one in our series, which is looking at how AF disease can be changed altogether by managing risk factors. So the figure here in the left shows what we expect that AF goes from paroxysmal to persistent to permanent AF. And in green, 48% of people progress over a five-year period if they don't manage their risk factors, but only 3% who lost more than 10% of weight progressed over that time. But the important one is on the right-hand side of this screen, where if you manage your risk factors well with 10% of weight loss, 88% went from persistent to either paroxysmal or to no atrial fibrillation. That is, we can actually change the disease course in these patients. And I think this is giving us insights into where the risk factor management could take us in our patients with atrial fibrillation. These are not isolated. And one of the things that we're concerned about is that morbidly obese patient, are they going to have the same sort of results in terms of weight loss? And this is a neat series of studies that came out of the Cleveland Clinic, which looked at post-AF fibrillation, those who'd undergone bariatric surgery compared to those who did not. And what they found was if you lost weight and the greater number of risk factors you managed as part of that bariatric surgery experience, the time to recurrence of atrial fibrillation was significantly delayed. And the need for repeat ablation was also significantly lower. So it suggests that this population may also benefit. And I guess we're waiting for studies on some of the weight loss medications as to whether we can expect similar sort of results. We did not have any of that at the time of the guideline writing. The Cleveland group also extended this in a very similar study to what we saw in reversing the type of atrial fibrillation, where they looked at the type of gastric surgery that was undertaken in terms of what happened to atrial fibrillation. And you can see the best benefits were seen with true gastric bypass down on the bottom row in orange, 43% had no atrial fibrillation, 27% had a change from persistent to paroxysmal atrial fibrillation, and only 2% shown in the green had progression. So there is some difference based on the degree of weight loss and the type of surgery that was undertaken. And so this provides some insight into the management of the morbidly obese patient. We were very prescriptive in the guidelines, really trying to provide some useful things for the clinician to be able to use. And really, we've said in overweight and obese individuals with a BMI greater than 27, we recommend weight loss, and we actually put an ideal target of at least 10% of weight loss and to reach some hard endpoints. And this was a class one recommendation with some randomized data as I've demonstrated here. And so this is an important risk factor for us to manage. I wanna change our attention now to physical inactivity, because again, this is something that's becoming much more common in our community, and we're starting to face this more and more with our patients. Our lifestyles are forcing us to be less active. I wanna highlight a couple of things from this UK Biobank study, is that this is looking at incident atrial fibrillation. Exercise reduces the risk of atrial fibrillation, but here's the kind of conundrum in men especially, is as you keep exercising and you reach the kind of more athletic side of things, your risk does go up, and that's also been well described. And so this is one of the issues we face with exercise. Most of our patients, however, as you would expect are on the lower end of this scale. And so for most of them, we're gonna be recommending increasing exercise. Now, women, completely different story. All exercise is good exercise here. And so there is no increase in actually none of those endurance athlete studies demonstrated that women had a greater risk. And so again, we might be seeing differences in the two sexes in terms of how much and the targets that we have as we move into the future. And I'll show you a little bit of the data related to that. Now, most of the data we have is actually on self-reported physical activity. And we have very few that have evaluated this in terms of formal cardiorespiratory fitness, but the story is pretty similar. This is a review article, and the size of the circles really show the size of the populations that have been studied in this. And there are only really three major studies. As you go to lower cardiorespiratory fitness, your AF incidence increases, and that's a consistent story. And it is consistent with what we've seen with the reported physical activity. Now, thankfully, we have got data in terms of what happens if we try to improve people's physical activity level. On the left-hand side is a cardio fit study, which, and on the right-hand side is the morbidly obese patients who lost weight and the physical activity levels that were assessed on there. And what we see in both these studies is a consistent story. The better your cardiorespiratory fitness, the more chance that you have of maintaining sinus rhythm, and there is a graded response. And in cardio fit, what we were able to show was that this was additive to what we saw with weight loss. And so this brings another realm of something that the patient can do themselves in terms of improving their health in terms of atrial fibrillation. Now, the guidelines was affected by this study, which was the randomized study in this field. And we've had very little directly randomized studies in this field. And so this was active AF, and it randomized patients with symptomatic atrial fibrillation to either standard of care, which is what are 150 minutes of exercise on education. And the patient was allowed to do what they could. And the exercise group who had an intensive, moderate to significant endurance type of exercise of vigorous aerobic activity in a bid to try and improve outcomes. We increased the amount of exercise duration to 210 minutes per week. And there was a six month training period after which the patient dealt these habits to be able to continue this. And this really did show a significant improvement in the time to recurrence of atrial fibrillation in this population. And it also significantly improved the symptom score from atrial fibrillation. And so this did inform in terms of randomized evidence to our guideline recommendations. I wanna just put this out there as a teaser because I think this is an area that we're going to see the difference. And so if we look at the difference between the two sexes, men and women both have a benefit in terms of exercise. But if you look at the symptoms, men have less of a benefit than women in from exercise. And so there may be specific tools that we need to start addressing. And I think we will see a lot of data coming out in the next few years relating to this. So what did we say in the guidelines with regard to this? Again, we tried hard to be prescriptive. We did suggest that people needed to do moderate to vigorous exercise training. And we gave a target of 210 minutes per week. And again, with hard end points in terms of what we might expect from this. This is a class one level of evidence, with randomized data for this recommendation. Now I wanna turn our attention to sleep apnea because this did create a lot of discussion in the guidelines. And I'm gonna show you why it created discussion and why we came up with our recommendations as we did. The data has been around for quite some time now. AF patients have a greater risk, sleep apnea patients have a greater risk of atrial fibrillation. And if we look at our patients with AF, they have a high incidence of sleep apnea, but it does depend on where you measure this. So with an AHI or apnea hypopnea index of five per hour, almost eight out of 10 of our patients have sleep apnea. If we use what's now being used in terms of the standardized classification, four out of 10 have a significant sleep apnea, but this data is quite variable. They're based on questionnaires in some, they're based on home testing in some, and then there are sleep studies, which has become what's called the gold standard. Now I'm gonna show you why this may change in the next few years, and again, why it informed guidelines. And there are various levels of this polysomnography that can be done in order to assess sleep apnea, and it's quite variable in the literature. Our enthusiasm for this come from consistent observational studies that have evaluated a role in patients with atrial fibrillation. And there are numerous of these, and there are meta-analyses to go along as well. I've taken this out of the Heart Rhythm Journal. It's from a Japanese group. They looked at patients undergoing AF ablation. One week after the ablation procedure, they did a formal sleep study, and then they allowed patients to choose whether they went on to CPAP or no CPAP. So it becomes an observational design. Now, if the Kaplan-Meier curves, in terms of recurrence after AF ablation, you can see if you have sleep apnea and you don't have CPAP therapy, this is the green line, you have the worst outcome. If you treated the sleep apnea patient with CPAP, you push this curve up towards the same as the patients who have no sleep apnea. And this is really very encouraging and why our field continues to look at this as whether we can manage this in terms of our patients with atrial fibrillation. Now, I'm gonna give you some of the downsides now, because I think it needs to be put into perspective. And one of the things that our sleep services need to do is they need to show symptoms associated with sleep apnea. And all of our polysomnography is guided by whether they have symptoms. This is a series of patients from our own laboratory, consecutive patients who had the Epworth sleepiness scale and the blue line shows where that becomes significant. And the sleep study formally assessed down the bottom. And one of the things to point out here is 88% of those people with sleep apnea would not have been picked up with just the questionnaire. So this is one of the issues that is facing the controversial data that's coming out in this field that we need to be keeping in mind. I also wanna show you this because we're starting to understand more as we have methods to continuously monitor day-to-day sleep apnea. This is from Dominic Lins. He's used a pacemaker that has a validated algorithm for look for sleep apnea. And actually patient A here is gonna have sleep apnea whenever you test them. This is a great scenario. Patient B is never gonna have sleep apnea when you test them with a single sleep study. Actually, most of our patients that patients see where depending on how much sleep they've had, how much alcohol they've had, how much meals they've had, how much exercise they've done, they may have sleep apnea on different nights. And if we look through this pacemaker, what we see in a given individual, red shows where they have severe sleep apnea. And so really suddenly it brings into question the value of doing a single sleep study as our means to assess sleep apnea. And so this is one of the conundrums that we're dealing with in this field of sleep apnea and atrial fibrillation. Now, things that influenced our decisions and how we geared our recommendations in the guidelines. And there's two important studies, both from the same group in Norway. This is a three study. It was phase one and phase two. And I'm gonna show you this. I'm also gonna show you the limitations of this study, but nevertheless, these were randomized designs. Paroxysmal AF, AHI of greater than 15, so significant sleep apnea. They went to the effort of looking at AF burden by loop recorders. This is preablation. Their patient characteristics show an AHI of 21, so it's significant here. But here's the downside of this, is that the assumption here was there was a 34% mean burden. Now, if you look at our AF ablation population and circadosis, probably a really good example of that, it was 1.5 to 3.7%. So they were expecting a huge incidence of atrial fibrillation in the group and a 25% reduction with CPAP therapy. And so it's perhaps not surprising then that they found no difference in this group, particularly when the mean burden in their population was nowhere near the 34%. It was more like the 5%. So this is one of the things that in a randomized design has been presented and so really does require further studies to evaluate. The second phase of this study was published in Heart Rhythm and it looked at patients who were still symptomatic from phase one and randomized them for what happens with ablation itself. Now, there's a couple of things here. And again, the sample calculation shows that in paroxysm AF, they're expecting a recurrence rate of 70%. That seems a little bit excessive for what we're used to and that's what based this study on. And they also included patients who had prior ablation. So it's unfortunately not as clean as what we would like. They had 55 patients with CPAP, 54 without CPAP and followed through to a 12 month outcome. And I think not surprisingly, again, there's no difference but it does provide us that limitation of the data that we have. And again, you see here the differences between the group in terms of the burden that they have. It's very low in this population of patients. So in terms of our guidelines, we had to now take into account the fact that we have two randomized studies that have informed us. Although we have all of these studies that are observational understanding that there were limitations in this study. And so we've given this a 2B and a non-randomized kind of level of evidence to suggest that number one is the prevalence of AF is high, sleep apnea is high in the AF population and maybe worth screening that, but the role is still unknown in terms of what our therapy is. And I think this is one of the areas where things will change as we get more data in this field. Now, I wanna bring out a couple of other factors that we brought out in the guidelines. And I wanna do this in the context of showing you a case from our laboratory. This is a gentleman who had a businessman, 48, so young, 10-year history of atrial fibrillation. It's paroxysmal, increasing in frequency. And at this stage, the episodes were less than 24 hours in duration. He was pre-sinkable, particularly after exercise. And you can see his baseline ECG already has some evidence of some conduction disease there. It's not completely normal, but as a very typical of the patients that we see. You can see this is a picture of him on the right-hand side. It's very typical of the patients that we have for atrial fibrillation. He did not know of any of the risk factors that he had at the time he presented with atrial fibrillation. He was hypertensive. He had an element of glucose intolerance. His cholesterol was elevated and he also was drinking alcohol excessively, 25 standard drinks for a day. You can see his weight is up with a BMI of 29.3. And in terms of his echocardiogram, we can see that there are some early signs of remodeling. AEF is 53. There's a little bit of left ventricular septal dimension increase, and the left atrial volume is slightly increased. So this is not uncommon in the population that we see. So he is placed on a Pixivan, Fleconide, and a Torvastatin prior to, by the general cardiologist when he's referred in. And I wanna just take you through one approach, which is what we use in Adelaide. And we've recently put this in Europace so that it can be seen as what we do. And one of the key features that we do is we divide these clinics up into two. The arrhythmia clinic and the risk factor management clinic. And the main reason for that is to not give information overload for the patient who's having to take in a lot of information at this point. I wanna focus now on the risk factor management clinic, because that can be run really by anyone, but it needs to be run in a systematic way. And it's that one-on-one relationship, and it really requires a bit of time. And the first appointment you can see here is 60 minutes. And we put four steps in terms of how we achieve this. And the first step, I think, is probably the most important. It's relationship building. It's understanding the educational level, the way information needs to be communicated, the priorities for the person and their family. We also introduce various diaries that the patient keeps in order they become aware of their weight, their blood pressure, what they're eating, their exercise levels. And then we can use that to make adjustments. It's crucial to identify risk factors. I'm gonna show you this again, the head-to-toe concept towards the end of this talk, of an acronym to use at the bedside in order to identify reversible risk factors. And then each of these needs to be provided achievable targets that can be reviewed by you as a trainer in order to come up with new targets at each visit. And then we have the end final targets. And this is how we kind of achieve the habitual change. So I think this is kind of important in terms of understanding one way that has worked. There may certainly be multiple ways that this can be done. So this person's given some rate control medication and we start referring him to the risk factor management. And we're always thinking when should we be ablating this person? And certainly with the data coming out about early rhythm control, that's something that we should continuously evaluate at each of these visits. And as mentioned, we start them off on a variety of diaries so that they become aware of their treatment. Now, over a six month period, this gentleman reduced significantly his risk factors. And I think the biggest risk factor for this man was his alcohol consumption. By cutting it down to three standard drinks for a week, you reduce the amount of calories that go in, your weight comes down. He's clearly exercising already and his symptoms improved dramatically. And so we held off that ablation strategy and we reviewed them every three months. Now, then he presents with now increasing amount of atrial fibrillation and episodes that have gone on for more than 24 hours and he's become symptomatic again. And so at this point, we do undertake AF ablation for this man. It is something that should be done concurrently with the risk factor management. And this is now 14 years after AF ablation. This is what we started with. And he's a completely different person in terms of his lifestyle that he's managed to achieve. He's had no AF, his weight's normal. He's now abstaining from alcohol and we continue to manage his hypertension. And I think an important thing to be able to follow is their atrial size. Atrial size has come down to 60 mils from 80 mils and that's a good indication of the benefits that we're seeing. And we've only got him on a couple of medications. He's no longer on any anticoagulants or antiarrhythmic drugs. So I wanna show this really because we did introduce two other things into the guidelines, which I think is crucial. A 1A recommendation is that patients should receive comprehensive care addressing guided directed lifestyle and risk factor management. This is concurrently with each of the other pillars that we've mentioned. And the second one is that there needs to be clinical care pathways. I think that's probably the goal here because I think anyone can do this. We have really good data now that nurse-led clinics actually achieve this pretty well because actually our nursing colleagues are very good at following these pathways, perhaps more so than some of us do. And it has been shown to not only improve guideline adherence, but also improve hospitalization and mortality. And so I wanna show that there's a partnership here that needs to evolve. And we're starting to recognize this in many of our services. So let me bring this to a close here. We did, as Andrea pointed out at the start, we put lifestyle and risk factors as a central pillar to our management here. And in the base of this house, we did introduce the head-to-toe concept as risk factors that each clinician at the bedside should look for and consider treating. And I think that that's important in terms of having a tool that you're able to use when you see each patient. So thank you for having me and we look forward to the discussion time. Thank you. All right. Thank you so much, Brush. All right. Let's open the floor to discussion. Please, to our audience, send your questions via the question Q&A format in the Zoom application. And otherwise, we're gonna start with our panels. I just wanna throw an idea here to you all. Perhaps Lingyi and Megan can comment since they're our guests, but I tell you one thing that you probably do not know is that the joint committee or clinical practice guidelines were coming at me to cut this guideline shorter. And the first thing they told me is, why do you have to have a recommendation for exercise training since exercise should be applied to anyone? It's a general cardiovascular health. And the answer that I had is because we have specific data or specific exercise efforts that is specifically beneficial for a population with a specific disease process. And you see these in other conditions, for example, in hypertension, if you do HIIT training, the blood pressure lowers to a higher degree. We know that for effects of longevity walking, 8,000 steps, we saw that paper in the New England is beneficial increase of longevity. So what do you think of having a specific prescriptive approach to training when we have strong data suggesting that with a specific exercise effort, you have a specific benefit? Lingyi and then Megan. And then I'm gonna open like that, the conversation about that. Okay, great. First of all, congratulations to Andrea and Prash for two excellent presentations. And Jose, thank you so much for that question. On one hand, I can see that critique, right? That in a sense, what we are recommending here is a preventive cardiology clinic, right? This is almost like the seven healthy lifestyle factors or now the eight healthy lifestyle factors, including sleep. And by the way, if we optimize all those risk factors, we will probably reduce the risk of every single adverse health outcome in the world, right? Because all of these risk factors are also risk factors for cancer, arthritis, frailty, et cetera. So why is it so unique that it needs to be put in a special position in the AFib guidelines? I think the response to that, in addition to what you just said, Jose, that there are specific data in the field of atrial fibrillation is that we need to highlight and underscore that in the management of AFib, in addition to all the different pharmacological therapeutics we have, as well as catheter ablation, first and foremost, we need to think about atrial fibrillation as being a systemic disease. That it is not just purely an electrical phenotype, but one might say that it is a vascular phenotype. So that really changes mindset, changes the paradigm, and maybe changes management in the future, right? So not only in Adelaide, but hopefully across the broad continents of Asia, Africa, North America, we will all start to shift towards trying to prevent it, trying to reduce the progression in addition to treating it electrically by catheter ablation. So I think it is entirely apt in the 2023 guidelines for lifestyle and risk factor modification to take such a prominent position. And also, Jose, in the next iteration, perhaps it will even take a more prominent position with more data. I will pause here. Thank you. Because when you started having the conversation, I'm going to let Megan comment. She's a nurse practitioner. I'm sure she manages these patients. Then you start having conversations. Now you start having research. GLP agonies, you know, for example, for AFib patients, you start, you open the door to more, how do we make patients exercise and things like that? And so, like you said, we wanted to change the paradigm. We were not naive enough to believe that everybody was going to start exercising from reading the guideline. We were not that naive, you know, I've been a cardiovascular specialist for many years and I exercise and I believe in that, in the benefit. So, but we wanted to change the conversation. Exactly right. Megan, do you want to say anything about exercise? What do you see? Yeah, well, I work in electrophysiology. So, and, you know, I think a lot of times I'm seeing people post-ablation. I might see them pre-ablation, but sometimes only, you know, after they've already decided to have ablation, they come back for maybe a pre-op discussion of some sort. So, a lot of the care that I'm doing is post-ablation, but it's, I think, a really good time to talk about or follow up on the conversations that patients have had with their electrophysiologist and hopefully general cardiologist at that point, because if they're free from AFib, they're feeling really good. And that tends to make people feel motivated to continue feeling good. So, it's a great time to talk about how do we continue to keep you in and maintain sinus rhythm and continue the kind of reversal of the progression and, or the pausing, at least, of the progression of your atrial fibrillation. So, I really just focus on, like, what are people motivated to do? And now that they're feeling good, what are they capable to do? And so, I take a, you know, starting slow or starting low and going slow. So, for a lot of folks, especially if they have comorbid conditions like heart failure, I know there's some question about lifestyle changes for heart failure in the Q&A. You know, if someone has heart failure and AFib, and now they're finally free of AFib, it might be a time that they can actually start making some changes. So, sometimes I say, start with a five-minute walk, you know, five minutes. And then if you get to where you can do five minutes a few days a week, then go up, you know, make it seven minutes. So, I try not to start with 150 or 200 or 300 a week goal, but it is a good time where people are motivated. And I think before people get to me, you know, or us in electrophysiology, I think it's really important to start the conversations earlier in general cardiology about the importance of lifestyle change so that before they get to us, they're already maybe starting to at least think about it, hopefully do it, and to improve their chance of success with their rhythm control medication or their ablation. So, that's- I like to say, oh, we're starting slowly for sure. And that's in the text, we talk about gradual effort and Dr. Sanders' studies also, the methodology is gradual effort. So, but, you know, of course, you know, why don't I expect anybody to start running 200 minutes a week for sure, especially many of our patients don't even own a pair of shoes. But let me, we're starting to have questions in the audience and I want to get to those. And I just- Can I just add one quick comment also on that? I want to say is that the answer is, it's because this isn't really, why do we put it in the guidelines? It's not really widely known, even, you know, for general cardiac, that this prevention of AFib, that there is something that you can help to prevent. So it's, that's not really, you know, apparent. And then I was, you know, interested even with rehab, right? With cardiac rehab, you know, in fact, I had a patient, there was an advertisement from a rehab center saying AFib, and I'm thinking, oh, someone's covering it for AFib, but no, you have to pay out of pocket. So I think raising awareness of the importance to the general medical community is so important. I think we wanted to change the paradigm. What we wanted to say is AFib is not a rhythm disorder, but a metabolic disease. It's a comprehensive illness, a cardiometabolic, an expression of cardiometabolic illness. So I think that's kind of what we have in this conversation, but of course, we're not naive enough to believe, because, you know, exercise has been part of hypertension management for years and things like that. Let's go to this question, Andrea, for you. Any particular antihypertensive agent associated with AFib burden reduction beside MRA, or we just go to management of hypertension as per hypertensive guidelines? Go ahead, Andrea. That's a great question. I don't, I'm not aware of any, you know, there's, those kinds of studies aren't there. It's really just getting the blood pressure down, controlling the blood pressure. And that was just one example of a study. There's not a lot of studies, really. Again, as Prashanth alluded to, it's a comprehensive risk factor modification, and you're doing a lot of things at the same time. So I'm not aware of any particular benefit of one drug over the other, although maybe in the future, we'll find out more about that. What the guidelines say, manage the hypertension per goal as per hypertension guidelines. We really didn't go into the specific of, like you said, there was no specific therapy. That, you know, that's never been shown. I agree with you, Andrea. Prash, lifestyle changes for heart failure patients. Yeah, I think this is an important one. So we have on the head-to-toe schema, heart failure is an important one, mainly because it's a modifiable disease that we can treat and we can see significant benefit in our patients. But from a lifestyle perspective, I'm gonna say this is gonna become a bigger issue because as we recognize HEF-PEF in most of our patients coming with AF, okay? So, and it turns out the exercise is one of the biggest determinants of how stiff your left atrium is and your risk of delving HEF-PEF. So that's going to be your modifiable that means of risk factor change to modify a heart failure. And so, although when we wrote this, it was more about HEF-REF, I think we're gonna be focusing much more in our population in HEF-PEF where lifestyle is gonna play a crucial role for this. Thank you so much. HEF-PEF, here I see a comment, shouldn't there be more of an effort for patient-clinical engagement overall? And shouldn't that be part of the plan to focus on more shared decision-making to affect the relationship? Go ahead, Raj. So, look, I'm happy to tell you the patient-clinician relationship is the essential component here of how lifestyle is done. If you don't have that relationship, it's just not gonna work. It's one of the crucial things of the arrhythmia clinic which the patient considers when they come as the most important clinic because that's what they're symptomatic from, arming the patient to want to undertake lifestyle changes. And then, then it's the relationship building and that first column in our four column strategy that I put, I'd highlight that is the crucial thing. And it's why one trainer with the patient and that relationship is and it's shared decision making through the whole thing. One of the things that we addressed just before was how much of a target we should give. And I can tell you, patients set harder targets on themselves than we would. And actually in part of the role, when you say, look, how much exercise we think this is where we need to get to, how much would you like to have achieved by next time, they always said something that they're going to fail on. And so it's really important from our perspective to give them a target they can achieve, because that's when they're more motivated to keep going. And each time you can extend that, but that's part of the role. And so that relationship is crucial. So I completely agree with you. It's focused on that relationship and what you can build in terms of therapy out of that. Let me mention that the guideline acknowledges that it might not sound obvious based on the questions I see from the audience. For example, if you push too hard, the patient you're going to lose, they're going to find somebody else. Okay, we know that we don't want that. And that's why we use language in the guideline that we use targets. And for example, in alcohol, we talk about alcohol cessation or moderation. So we don't use a specific target, say you cut it to zero in the guideline, because we acknowledge that for some people, they still want to drink because they find pleasure and joy. And we don't want to be judgmental either, because we don't want to lose our patients. So the guidelines does offer that kind of language that understands that we need to get there slowly, be kind to your patients. And like Dr. Sanders said, set realistic targets, realistic parameters. We're just putting, like I said, the conversation out there, but we get that we have to be kind and non-judgmental. I see Lingyi nodding here. Do you agree, Lingyi? Yes, completely. I don't think more needs to be said than what Prashanth has already mentioned, that in the end, especially when it comes to an intervention that's going to require effort from the patient, you need the patient by it, right? So I think at the very start, you need to win that trust and that the patient actually sees you as a partner, rather than somebody who is just going to be completely prescriptive. So even, and I think on the point about targets, yes, yeah, it is good to have the targets in the guidelines, what we want to work towards, right? Those are the aspirational goals. But whatever the patient can do, we take, right? If the patient is able to lose 5%, we take it, right? Although we say, hey, and then when they lose 5%, they come back, we congratulate them, we motivate them, hey, how about just another bit more, right? So I think that's the way to, in incremental ways, that would be the most effective way. Thank you. Let me, thank you, Lingyi. Let me throw another question here from the audience. Any indication that anti-inflammatory diet modify AFib evolution? Okay. Thank, thank you for that question, Jose. So observational studies have shown certain anti-inflammatory, such as polyunsaturated fatty acids, omega-3, may be beneficial in reducing atrial fibrillation, but randomized controlled trials have not shown that to pan out. I agree with that. Yeah. And then I think there are other isolated studies on vitamin C or ascorbic acid, where these studies have been, the results have been conflicting. So as the guidelines state, you know, there are no specific recommendations in terms of dietary supplements or nutritional supplements in order to modify the risk of atrial fibrillation. But that, with that being said, I think our recommendation as physicians, and we get asked that all the time, right? Then our standard response would be a healthy diet, right? Where it emphasizes more plant-based diet, less red meat, et cetera, et cetera. Right. To me, that would be the basic, right? If you have a basic diet, low calorie, Mediterranean style, that has a lot of protein, exactly. That has shown to keep your weight down, things like that. Yeah. Okay. I'm seeing other questions here. Some of them Prash has already answered online. Let's go to another topic. I want to hear the controversy of sleep apnea. We had that controversy. I want to see what Prash says. The problem with sleep apnea is also the company that it keeps, you know, everybody with sleep apnea usually has four additional risk factors. And also sleep apnea patients are very motivated. The ones who get into the treatment are really very motivated. And those observational studies on sleep apnea tend to be very biased for that reason. Patients who actually do have access in the first thing, in the United States, you have to wait like a year for a good sleep study, for example. So the patients who actually get access to the sleep study and get on treatment, I'm very motivated. And that's always been a criticism. Like you say, Prash, when you do randomized study, then there's divergence of results compared to observational studies. We saw that a little bit in heart failure too, that everybody was hopeful of sleep apnea heart failure. And when you did a randomized study, it didn't turn out to change heart outcomes. So go ahead, Prash. And then I'll let the panel comment on that. Look, I think this is an area that could potentially make a big difference, but we need to pick our patients better. We've certainly had patients with severe sleep apnea whose AF have gone away when you treat with CPAP, but they're far and few between. Okay. And so the bigger question is, do all people with AF need treatment of sleep apnea? Major issues, you know, have we got the way we diagnose this correct? You know, is apnea hypopnea index, the best indicator, a one day indicator, is that useful? How do we monitor this? You know, how much treatment of sleep apnea is adequate? You know, so, you know, many of the trials, for example, the big randomized trial SAVE was criticized because they only achieved two to three hours of CPAP therapy. And maybe that's not adequate to prevent enough episodes. So any randomized study here is going to be set to fail more than it's going to set to succeed, which is one of the problems that we're going to be faced with in terms of moving the field forward. The biological feasibility is huge. We have preclinical studies that show fibrosis occurring, we saw autonomic changes occurring, and we can show that it all reverses by treatment, treating sleep apnea. So we'd like to try and work out which patient now is going to benefit the most from this in order to be able to treat it. So, and that's going to be patient factors as well. And hopefully we're going to have more treatments available. I think we're getting more data now in terms of mandibular splints, which people are much more tolerant to use. There are certainly patient forums that are talking about how to tolerate CPAP therapy. And there's even a really interesting thing coming out of China, really fascinating, because in China, there's a, just the jaw structure makes people more prone to sleep apnea. So the incidence is higher and you don't have all of these other risk factors that go with it. And they're using a sclerosing agent at the back of the tongue to, as a one-off treatment to reduce the risk of the tongue falling back. And as that gets evaluated more, there may be some interventional treatment that can be offered for this as well. So, and obviously device therapies are being evaluated, medical therapies are being evaluated. And I think this field is just going to change, but we need the studies to change the recommendations. Thank you so much. All right. Let's see, what do we have here in the question and answer? Let's see. I'm going to throw one at you, Andrea, and then Megan too, to comment. What happened, one problem with the CHAS-DAS score too, is it doesn't take into account, like I said, the guideline is a little bit, you know, ambitious in trying to hope that the conversation changes and patient's lifestyle interventions work and those are adopted widely. What happens if they are adopted widely and the patient blood pressure normalizes and they lose weight and the diabetes goes away, then what happened to your CHAS-DAS score? What is the effect of those interventions? And the patient will tell you, you asked me to lose weight, you asked me to exercise, I did. Can I come up with a PIXIVAN, for example? That's a tough one. And that's, so, so go ahead, Andrea, another debate for our panelists. Yeah, no, that's a really good question. I have a little better feeling, you know, that we're, might, you know, have, if it's heart failure and the cardiomyopathy goes away and the heart failure goes away, but if you have a history of hypertension, diabetes, I think we do have some, at least some impact of, we know that treating it will reduce the risk of, you know, obviously, AFib and we're treating hypertension well, but I kind of separate the whole thromboembolic, you know, preventive part of it from the rhythm control part of it. And I guess part of that is because I think some of the damage is done, I guess, from AFib and causing some atrial changes and causing some other, you know, structural autonomic changes on the atria. And I don't know that we completely reverse all those things. You know, so, yeah, maybe you're at reduced risk when you get rid of, you know, you treat the hypertension, but did you have some structural changes? Did you have some other changes from, you know, epicardial fat, things like that from diabetes and other things? So I don't have a good answer for that. We certainly don't have a randomized trial or anything like that to say, now you're safe to stop, you know, your anticoagulant. And I actually don't clinically, if they have a history of hypertension and diabetes, you know, even if it's controlled, I still count that as diabetes. Do I think they're worse off if the hypertension is poorly controlled? Yes. If the diabetes is poorly controlled, yes. But I just don't know that it's safe to stop, you know, the anticoagulation. Yeah, I'm the same. If it's treated and controlled, I'm not stopping anticoagulation. Now, if there was a scenario where they have such great lifestyle, yeah, change, but it disappears without treatment, I, you know, in that situation, I would consider it and have a, you know, a shared decision-making discussion with the patient. I think obviously it would depend on their other risk factors. But I actually have this conversation more about age. So folks who maybe had an ablation, this is going to circle back to your case study, Prash, but, you know, they have a successful ablation, maybe they're five years out in your case, you know, this was 14, they're under 65, their only risk factor is hypertension. So technically based on their CHADS-VASc, they could come off, you know, their anticoagulation for their, you know, less than 2% risk per year, but then they turn 65, and they still have hypertension, and they still have a history of AFib, even though it's been gone for 14 years. So, you know, and maybe they're having a lot of PACs, or something like that. So I come across that question more related to age than I do lifestyle, which is not really the question you asked. But I'm curious if anyone else has had this kind of, you know, people age into now qualifying for anticoagulation, even though they have been free of AFib for many years, but they have enough. The guideline, the guideline, we don't have all the answers for sure, Megan, and I agree with Andrea, but the guideline did move away from the rigidity of the CHADS-VASc again, to open the conversation, to open the future research, because you were so rigid about CHADS, we cannot have an opportunity for research to come up, that people come out with a more personal approach to risk management based on degree, for example, use AFib burden, for example, as one of the variables. We know there have been some observational studies that say if you have isolated AFib, like meaning AFib that happened once three years ago, the risk of stroke is much less than the risk of AFib that is paroxysmal, but ongoing or permanent or persistent for sure. So, so that kind of, we don't have all the answers, but again, the guidelines serve two purposes. One is to provide recommendations, what to do today, but also open the door for future research and discussions. And you point out, I think, you know, in addition to the AFib burden, and you know, you point out also in our, in the guideline discussions, we pointed out other, other risk factors, right, that aren't included in any, you know, it might not be in other scoring systems either, but you might have, age is a really important one, right? Age is, that's a continuous risk. It's not like on your 65th birthday or your, you know, it's a continuous risk. It continues to go up. So that's an important one, but other things like left atrial enlargement, renal dysfunction, some of those are included in some other scores. You may not be easily able to calculate it, but you can consider those things also. Yeah, it's just hard because I've been seeing this, you know, more and more as people are coming back and they're having maybe a lot of palpitations and we do a monitor and there's maybe a lot of ectopy, but maybe not straightforward AFib. They're 68, 70, whatever, you know, it's just, it's something that I'm coming across often more than I'm coming across actually seeing their risk factors so much that they, you know, that I would take them off. So Jose, you wanted to say something, go ahead, Lingyi. Yeah, I'd like to chime in here and back to your question and also Andrea's response, right? So the reason why the CHAT-VS variables are in the CHAT-VS score is because not only do they relate to atrial fibrillation, right? Hypertension, diabetes, et cetera, but they all are risk factors for atrial remodeling. And in the guidelines, it's mentioned atrial enlargement, but I really want to call out increasingly in the last few years, we now know that left atrial dysfunction or impairment of LA function as actually an even more robust and sensitive marker of atrial myopathy. And it's been shown that left atrial dysfunction is independently associated with stroke, dementia, name all the outcomes of AFib independent of atrial fibrillation. We did cover that. We had that conversation, Lingyi, in the guideline, but unfortunately we didn't have any good way to present that concept with a recommendation because the data is early, but we at least opened the door for that concept to be studied further and to be presented because like you say, maybe, you know, that person with atrial dysfunction is a higher risk, all risk factors being equal, you know, with the evidence of atrial myopathy by other, for example, biomarkers, antiprobium, for example, left atrial dilatation. Those are very, you know, but how do we personalize that? We don't know yet, but maybe in the future we will. Right. And also maybe in the future, we won't be asking the question, oh, you know, if the blood pressure is well treated now or the diabetes is well treated, do we stop anticoagulation because a more proximate marker might be measuring the atrial function, but how is the atrial function doing? Because it summates the effects of all the other risk factors. Yeah. Let me, let me, let me, go ahead, Prash. Go ahead. It's super interesting because we use the left atrial size as a, as a really good guide as to how well their risk factor management and the AF burden is going. So if you're seeing it coming down, we haven't used function, which is actually a little bit more variable in terms of its analysis. And you need kind of specialized lab. I want to kind of highlight something Megan said, which is, you know, we've focused on age as an important factor to kind of reevaluate, but someone who gets hypertension, who gets diabetes with weight is at risk of getting that in the future. And so, although we may see all of this going away, it's really important to continually reevaluate that person in terms of their risk of, of stroke, of AF coming back at least on a yearly basis, because they're getting older because they're getting these risk factors. So I think that's important. And we did have that discussion in the guidelines. So it's probably important for people to recognize that also. Let me, let me take a question real quick here. It says from, from one of the audience members in the audience, be sure to make a routine recommendation to stop for AFib. Yes, absolutely. Right. You agree for AFib at least there's no evidence that's beneficial. Do we agree with that? Finalist? Yeah. So that's, that's, that's easy to me. Of course, the patient might have other indications related to cholesterol or other indication. I'm talking about purely for AFib. You agree? Prash? Totally agree. I mean, we do have so many observational studies again, but the big RCT really shows a negative impact. I think one of the difficulties with diet that we faced in terms of giving a hard recommendation in the, in the guidelines is there are so many variables that are affected when, in all of the studies that evaluate dietary changes. And so that's why we, we put it in the text. We didn't actually make a formal recommendation on any of the, of the dietary measures because of that fact. The only dietary thing that is clear to me, and I'm just going to throw it out here to the panel is caffeine. Caffeine gets blamed for everything but the bad weather, my God. Every patient comes to me, dog, my heart is racing, I already stopped caffeine. I say, why do you do that, my God? Go ahead, Andrea. Right, agree. I think that was, yeah, that would be a terrible thing to have to stop. We have evidence that actually does not cause fatigue. Patients with AFib, it does not seem to, you know, worsen their symptoms. And I personally believe caffeine is a superfood. I don't know, what do you think? Rush? I think there's a lot of information online and patients are getting it for themselves. So I think it's, and I think it's not getting refuted by healthcare providers. So I think that it's something that we can give back to patients and try to help them refocus on the more important issues, most of which we've talked about here today in these presentations. And that can maybe help in those shared decision-making discussions. Like, you know, that can be really hard to give up but feel free to have your coffee or your tea and let's talk about what may actually really help you prevent, you know, recurrence. I totally agree, Megan. You were there in the deliberations and I think every writing committee member felt the same way. Everybody said, listen, we have to give this back to our patients, please. You know, you cannot get rid of every single pleasure in life. My God, absolutely not. We're here to help you as healthcare providers. And that's why it was so important to put it as a class re-indicate. You know, it was so important because healthcare providers are not, you know, aren't aware of that, right? So it was important to put it in there. Yeah. I see here something about cannabis discussion. I don't, we didn't touch that in the guidelines. Anybody knows any data on that? Maybe we need to look at my study. I don't know. There's a lot of people there. The only data that has come out of kind of Greg Marcus and the kind of Californian hospitalization data and showing a slight increase in incidence of atrial fibrillation, both with stimulant drugs and also cannabis use. And I think that's been published. But in terms of how that changes in kind of withdrawal, no one knows really. So we didn't make any recommendations on it and it wasn't actually what factor that was discussed. Right. Let me take another audience questions here. Anything on the device monitoring in front for, device monitoring in front for earlier diagnosis and evidence of a fit before becoming symptomatic. Anybody wants to tackle that? I mean, I could just start, but again, I'm sorry. No, no, please, Andrea. I think that is a really, that's a, that's a big, a really important question. And, you know, so monitoring, so we know that a lot of AFib is asymptomatic. We know that a lot of wearables, you know, obviously can pick up AFib that's asymptomatic and sometimes, you know, may not be always so accurate being able to document it and kind of looking at, you know, all the other risks and the things like, you know, other risk factors for stroke and if they're not symptomatic, but how much AFib you're having and to really, you know, to document that. So I think it's an important thing. I think we're seeing this more and more in the office. I think our primary care physicians see this in the office too. It's not just, you know, every EP patient I think has some kind of wearable or if not just another kind of consumer device they hook themselves up to. But we're going to see more and more of this and to know what to do with that data and when to act on it. Is two minutes of AFib enough to cause a problem? Well, probably not, but what else is behind that? But a really important topic. I think it was one of those things that we discussed at length in the guideline committee and we actually, that beautiful figure that Andrea put up of the continuum of AF really brings that in that we're starting to recognize this preclinical AF almost that in populations. We also had a lot of chat about, you know should it be ECG monitored? Should it be, can we use PPG as a means? And really, again, we kind of stayed silent on it because we just don't have enough data other than saying we need an ECG to diagnose AF which is what we put in there. So I think this is one of those areas that may change over the next few years as our understanding and accuracy of these devices get better. But at the moment, I don't think we can kind of advocate for anything other than ECG monitoring. And then the importance based on that figure is really I think where our knowledge base is at the moment. But just to remind everyone that we did have that debate in the guideline by writing committee members and there are two elements here, right? One is the screening for AFib in high-risk populations like the elderly and the data is not robust enough. There's a lot of discordant results. And the idea is also that we're not sure that we have even, we can detect AFib but with the data is soft in changing heart outcomes, right? Yeah, I think there's only one study that modestly decreased stroke from Sweden but other studies have been negative. So we're not ready to make a strong recommendation on screening for AFib. There's some isolated populations that have been like hypertrophic cardiomyopathy especially high-risk populations for AFib where scores exist for screening. And then, the problem with the devices, the wearables if you have those devices in people who have low pre-test probability of AFib then you're gonna have a lot of false positives not just the way Bayesian works. So that's my comments. I see Lin Yi itching to, Lin Yi you wanna say something about that? Actually, nothing more. I think we have discussed this quite well. I think suffice it to say that there will be more that we will learn, right? In terms of what to do with subclinical atrial fibrillation detected from devices. But I agree with Preston that right now we will have to take the ECG confirmation as the diagnosis of AFib for all the management that goes around it. Yeah, so people bring them to your office now. Say my Apple watch told me I have AFib. So sort of that we can now make across the board population-based recommendations. Yeah, all right. Let me see what else I see here. I see you answer some fresh online. We answer a lot of questions. Any, our panelists, any issues that you wanna, we have a few minutes that we should deep dive deeper. We don't have a lot of questions here anymore. Go ahead Lin Yi. Yeah, one quick one. Yeah, so we spent some time talking about sleep apnea, right? But I think it's also important to pay attention to the fact that it's not only sleep apnea but there are many other sleep disturbances, you know, like sleep characteristics that are linked to AFib. Just not having enough sleep, right? Or having too much sleep. Those are linked to higher risk of atrial fibrillation and also sleep fragmentation has also been shown to be associated with AFib. So I think on the topic of sleep, that this is not just with atrial fibrillation but really just with health in general, right? Or with cardiovascular disease. It is more than just sleep apnea. I'll pause here. Thank you so much. Any other topics our panelists wanna dive in? We talk about caffeine, alcohol. Just a reminder. I have a question for Prash, actually. You know, in all the research that you and your team have done in terms of weight loss and physical activity, I know that kind of 10% weight loss is what ended up in the guidelines and also to avoid fluctuations. But how are you defining fluctuations? Like if we're gonna teach a patient about, you know, let's aim for 10% and not have a fluctuation. Yeah, so that's actually in the legacy. So we defined as three, five, 10% fluctuation just the same way as we define the weight loss. And so we went from time point to time point looking at over the year, what sort of changes they had. So, and maximum versus minimum kind of thing to try and determine that. The 10% wasn't anything new. That actually comes out of the AHA guidelines. Okay, so AHA recommends that we use that. And realistically, 10% was the aim, but we actually keep going. We wanna get their BMI less than 27. So I think that's going to be important. One of the other things that is going to come out is the target BMI is gonna be different depending on which population. Okay, we're starting to see data that talks about BMI being linked to metabolic syndromes at a much lower BMI in different populations, such as the Asian population, for example. So I don't think the whole story is known from just BMI. It's very applicable to the white population at the moment, but there may be more nuances that need to come and we will need to include some of these things in the guidelines as we get more information. Let me mention, Megan, also that some of that 10% came also from studies that they use bariatric surgery. Some of the data came from bariatric surgery as well. So, and then branch studies too. There have been some studies also that if you lose less than that, if the weight loss was less robust, also the benefit was not there. Go ahead, Andrea. No, I have one other question for Prash too, is, you know, and so, or for anyone, or for even, you know, as a moderator, one of the things that you've just done amazing things, you know, for the research that you've done, you know, at your group in Australia, and you even said a lot of these clinics can be nurse run and physicians, you know, are part of it, but is our healthcare system in the United States is, you know, I see is something that could be a bit of an obstacle to some of this in terms of we pay for diseases and treatment of diseases. And I guess I'm just trying to, maybe you could share is there, to have someone spend time about prevention. That's what we wanna do. That's what we need to do. That's what we're gonna, and overall the costs are gonna go down, right? You're gonna prevent all these complications of obesity and diabetes and all these other things. So we'll save money in the long run, but is there, do you find any of those obstacles or do you, you know, hiring people to, you know, do education and spending an hour with patients, you know, or is it just, is it a difference? And I'll, or even Jose, or what could we do in the United States to try to promote that kind of focus? Rush. Well, one of the things I would say, I mean, we've made it happen because it's part of an academic program. We've had undergraduates do it. We've had PhD students do it. We've had EP fellows do it. Nurses, pharmacists, exercise physiologists, they're all able to do it. So this is something that's easily translatable with a little bit of education between people. So there's no rocket science in terms of what needs to be done. It's just a methodology to do it. I think the incentives probably need to change. And I think if we go to kind of value-based healthcare, which may be coming like based on outcomes of procedures, you're going to find a lot of people pick this up because this is one way that your procedures success is going to improve dramatically. So it may not be a question of taking away procedures, but rather how do we make it better in terms of the outcomes? And that's actually great advertising for health centers if their outcomes are better. So I think the other one is each geography is probably going to need a different incentive depending on how that structures of payments and things occur. And we actually have the opposite where you're almost incentivized to not do a procedure, which is a negative thing, but just because the hospital gets paid as a bulk amount to look after a population as opposed to per procedure. So it's a slightly different way of looking at healthcare. So every geography will be slightly different. You know, I came from, I gave a talk last year in Costa Rica, Central America, and they pay for cardiac rehab, people with metabolic syndrome. They don't wait for the person to have a heart attack. And I believe cardiac rehab, the purpose when you have metabolic syndrome is like we talk about, it's hard to exercise because people don't even know where to start. I agree with Megan. One thing is you have to start slow. You have to have a process. You have to have also a little bit of confidence. And I think that's the value in a small country like Costa Rica that provides that. But I think Andrea, without getting into politics or anything like that, at some point, if the one problem in the United States, the healthcare is paid by the employer, right? At some point, if the individual has a stake, like when you buy car insurance, right? If you're a good driver, you save a bunch of money, you know, that kind of stuff. I think at some point when the individual has a stake, I think that that will change. That's my opinion without getting into the weeds. I let others comment, yeah. All right. Any final thoughts for each panelist? We have, I don't know, I want to finish at 7.40, seven, eight minutes. Let's start with Andrea. No, I just think that, you know, raising awareness and I think it's just fabulous. We're having this webinar that the, you know, Heart Rhythm Society elected to do something on prevention, right? You know, this is, you know, trying to reduce, you know, risk factors, modify risk factors is just, you know, leaps forward into where we need to be. So hopefully we can continue to disseminate, you know, this information to not just us, you know, speaking to the choir and electrophysiologists but all healthcare providers, including internists and general cardiologists because we have a lot more to learn, but this has been such a great start. Rush. Look, I think that there's been a huge step forward to put this front and center in the guidelines and actually that figure, placing this in the middle of our management strategy is so important. I want to encourage all clinicians to work through the head-to-toy schema because that actually is something that you can do at the bedside that's going to make a difference to your patient. Have a method that you can go through rather than taking potluck on terms of which risk factors you're screening for and which ones you're treating. Be systematic in your approach because it will make a difference to the patient. So I'm glad we put this into the guidelines. Megan? Thank you, Rush. Yeah, I just, I think it's, I agree with all the other speakers and panelists. That's so wonderful to see this, you know, a focus of the care that we provide now and that it's in the guidelines. And I think sometimes it can be hard to broach some of the subjects with patients, especially in a rushed, you know, clinical visit, but patients will appreciate it if they can tell it's coming from a place of concern and care. And so, you know, if it can be hard to bring up weight, it can be hard for patients to talk about it. But ultimately, when they see that we care enough to bring it up, they're generally very appreciative. Thank you, Megan. Lingyi? Yeah, so even though there may be some geographical risk factors that make prevention challenging and, you know, prioritize treatment over prevention, I think these guidelines has taken one important step forward, right? By having a new AFib classification system and lifestyle being relevant across the entire spectrum from stage one to stage four, I think this is a first step in trying to, hopefully, that we can really implement prevention in the spread of work and then implement. Yeah, so I think this has been wonderful. Thank you so much. And for my panelists and the audience, I wanna say a couple of things. Number one is please know that the hope of the Joint Committee of Clinical Practice Guidelines is that in the future, the guidelines become a living document, and we hope that we're gonna start editing these documents on a more frequent basis. And a lot of these comments I hear, a lot of this feedback is taken seriously. I write notes on that stuff, okay? We know that our goal was aspirational when we wrote these recommendations, but like you heard here today, we start with little steps and we continue to have the conversation and move, you know, the conversation forward into understanding the complexity of atrial fibrillation as a metabolic disease and keep getting better and learning. And then as new data and new science comes along, added on recommendations and things like that, but I hope that at least by changing the conversation, the new guideline also not only write recommendations, but also moves the needle forward, promotes research into new arenas, and then ultimately the goal is to make our patients better. So with that final note, I wanna thank all the panelists for being here today and the audience. Please a reminder to the audience that you can claim credit for today's presentation. Here is 1.5 AC credits. How do you get it? And I think Sarah, we're gonna have a recording of this webinar also in high rhythm 365 as well. So you can, guys that kind of, whoever missed it or had to leave early will have access to it later today. So thank you so much and look forward to the next one. Good night. Thank you.

AFib

guidelines

risk factor modification

prevention

lifestyle intervention

hypertension

obesity

diabetes

sleep apnea

exercise

dietary components

patient-clinician relationships

shared decision-making