Good morning and welcome, everyone. This is a session on lifestyle and risk-effect modification in atrial fibrillation, and also a joint session with Korean Heart Rhythm Society. I am Seil Oh from Seoul National University, Korea, and president of Korean Heart Rhythm Society, and my co-chair is Professor Boyoung Jung from Yonsei University, Seoul, Korea. He is the vice president of Korean Heart Rhythm Society. We have four distinguished speakers in this field from Australia and Korea, and they will inform you about coffee, alcohol, exercise, obesity, and so on. I think these are very essential for ourselves as well as patient education, because some doctors have bad habits, especially in alcohol drinking, so I frequently recommend to my friends like this, you must do as doctors say. You must not do as doctors do. We will have 12-minute presentation and three-minute Q&A for each topic. I will introduce first two speakers. The first speaker is David Cheng from Alfred Hospital, Melbourne, Australia. He will talk about coffee. Please. Good morning, everyone. I have no relevant disclosure. Thank you to HRS for the opportunity to present this morning, and what a perfect topic to kick off the last day of HRS. I think we all need a bit of coffee to stay awake on Sunday. My task is to talk about the associations between coffee consumption and arrhythmia. Coffee is ubiquitous in most societies, and therefore, unsurprisingly, there's significant public interest in coffee as a modifiable lifestyle risk factor. There's a general perception that arrhythmia risks increase in those who consume coffee. However, if you look at the EAC guidelines from 2021, coffee consumption at three to four cups per day has been suggested as being potentially moderately beneficial. One of the major limitations in current literature is a lack of large-scale population studies or even randomized studies looking at the associations between coffee consumption and arrhythmia outcomes. The first question to answer is, why should coffee have any beneficial effects from a cardiac point of view? Because, after all, the main ingredient, which is caffeine, is a stimulant. It increases the release of adrenaline, noradrenaline. It also inhibits the reuptake of calcium in the cells, both of which are potentially proarrhythmic. However, caffeine can also inhibit adenosine receptors in the heart, which can reduce arrhythmia risk. It also contains antioxidant properties, and also it releases endothelial nitrate oxide as well. And not just that, coffee itself is a very complex beverage. It contains more than 100 biologically active compounds, including polyphenols, such as catechins, and also chlorogenic acid, both of which contains antioxidant and also anti-inflammatory properties as well. This was a paper that we published a few years ago looking at the impact of coffee on cardiovascular disease and arrhythmias, based on data from the UK Biobank. So the UK Biobank is a large-scale population-based cohort, which recruited more than half a million participants from 2006 to 2010, and participants were invited to report their coffee consumption based on a weight-based questionnaire. And for this study, we divided that into six intake categories, which were zero cups per day, less than one, one, two to three, four to five, or more than five cups per day. And outcomes, which were measured for over 10 years, were linked to ICD-10 codes. So for this study, we looked at participants who had an incident diagnosis of any arrhythmia, which includes atopy, atrial fibrillation or atrial flutter, SVT, ventricular tachycardia, or ventricular fibrillation. We also included a cohort which did not have any incident diagnosis of arrhythmia during a 10-year follow-up. We excluded those who did not provide any responses to questions based on their coffee consumption, tea, lifestyle risk factors, and also demographic factors as well. From a statistical point of view, we used Cox proportional hazard modeling, adjusting for confounding covariates, including demographic factors, lifestyle risk factors, as well as comorbidities. So the final cohort consisted of more than half a million participants, with a median age of 58 years, and more than half were females. It's important to point out that the majority of the study population were Caucasian, and just under a quarter were considered obese, with the most common comorbidity being hypertension. This is the finding for the main outcome, which was any arrhythmia. If you look at this graph here, the colored graphs represent the different levels of coffee consumption, with purple being zero cups per day, and yellow being more than five cups per day, and every other color in between representing the other intake levels. If you look at the symbols here, the cross represents a p-value of less than 0.01, and the double cross representing 0.001%. The main finding was that there's a U-shaped relationship between increasing levels of coffee consumption and the risk of developing any incident arrhythmia. Consumption between one to five cups per day was associated with a significant reduction in the risk of developing any arrhythmia, with the lowest risk seen at two to three cups per day, which represents a 9% risk reduction. A similar pattern was also seen for atrial fibrillation and flutter, with a risk reduction seen between intake from one to five cups per day, with the lowest risk at four to five cups per day, which represents a 12% reduction. With regards to SVT, we also saw a significant reduction in the risk of developing SVT in those who consume between four to five cups per day, which represents a 16% reduction. And for VT and VF, again, a similar pattern was seen, with the most significant reductions seen between those who consume four to five cups per day. Also we also look at participants who had an underlying diagnosis of cardiovascular disease at baseline, and what was reassuring was that there was no signal for harm in those who consumed coffee at any level. In fact, between two to three cups per day is associated with a reduction in risk of developing any arrhythmia on long-term follow-up. This was a paper published by the UCSF group a few years ago, looking at coffee consumption incident arrhythmias, again based on the UK Biobank data. In this graph here, the dotted blue line represents zero cups per day, whereas the other colored lines represent different levels of coffee consumption. And the conclusion was that each additional cup of coffee consumption was associated with a 3% lower risk of developing any incident arrhythmia. What was different from our study was that there doesn't seem to be a sling effect. Based on this graph, it seems like the more coffee you drink, the lower your risk of getting any arrhythmias. In terms of the specific arrhythmias, very similar to our study, they showed that the risk of developing atrial fibrillation, atrial flutter, and also SVT is reduced with coffee consumption. This is another study from the Physicians' Health Study. This is looking at just under 20,000 participants, which are all males, with the average age of 66 years and a mean follow-up of nine years. And it showed that consumption between one to three cups per day was associated with a significant reduction in the risk of developing atrial fibrillation. Similar to our study, they showed that there was a U-shaped relationship between increasing levels of coffee consumption and the risk of developing atrial fibrillation. The lowest risk seems to be at those who consume one cup per day. The CRAVE trial, which was published by the UCSF group a few years ago, is the only randomized study to date that I'm aware of, which is to look at the association between coffee consumption and arrhythmia. So this was a prospective randomized case crossover trial involving 100 participants, and they all wore this ZioPatch continuous ECG monitoring device, which measured the ECGs continuously for two weeks. And for this study, participants received text messages on a daily basis over a two-week period, and they were randomly instructed to either consume coffee or to not consume coffee. And for this study, no participant was allowed to have two consecutive days of coffee consumption. And what was reassuring was that there was no evidence of a higher incidence of atrial or ventricular atrophy with coffee consumption. This was a study from the Multi-Enix Study on Atrial Sclerosis, or MISA study. This study involved a much smaller cohort involving just over 6,000 patients with a mean age of 62 years, with just under half consisting of males, and a mean follow-up of 8.5 years. What it showed in this graph here, so the black line represents those who do not consume any coffee, whereas they look at those who consume between one to three cups per month, and more than one cup per week. And what it showed was that those who drank between one and three cups per month did not have an increased risk of developing atrial fibrillation. However, any consumption above one cup per week was actually associated with a significantly higher risk of developing atrial fibrillation. When they deep dive into the data, this graph here just shows all the different levels of coffee consumption. And what it showed here was that the highest risk of developing atrial fibrillation was seen in those who consumed six or more cups per day, at a risk of 9.8%, with a p-value of 0.02. But when it adjusted for core variants, including age, gender, smoking, hypertension, and diabetes, only those that consumed between two to four cups per week, two to three cups per day, and more than six cups per day, was associated with a significantly higher risk of developing atrial fibrillation. However, for the other levels of consumption, there was no significant association with the risk of developing AF, which I think is a bit unexplained here. Now in terms of the different types of coffee and how it affects your risk of developing arrhythmia, this was, again, a finding from our study. Based on the UK Biobank, we have information in those who consume decaffeinated, those who consume ground coffee, and those who consume instant coffee. So if you look at the graphs here, the purple line represents those who consume instant coffee, the green represents ground coffee, and decaf is represented by the orange line. And what we see here is that there's a significant reduction in the risk of developing any arrhythmia or atrial fibrillation in those who consume ground or instant coffee between one to five cups per day, as shown by this cross and double cross signals, which represents significant P values. However, decaffeinated coffee was not associated with any reduction in arrhythmia or atrial fibrillation incidence. So I'll conclude by saying that based on current population-based studies, regular coffee consumption is associated with a reduction in incident arrhythmia or atrial fibrillation, and I think the most consistent benefit is seen in those who consume multi-moderate levels per day, around two to three cups. And we've also shown that in those with prevalent cardiovascular conditions, coffee consumption remains safe. Ground or instant coffee is associated with reduced risk of developing arrhythmia, but we don't see a signal for benefit in those who consume decaf coffee. And based on this, I think we can say that daily coffee consumption should not be discouraged, but rather considered part of a healthy diet. So thank you for your time today. We are now open for questions. Any questions? Okay. Thank you for wonderful presentation. I have a question about the analysis of UK Biobank, like the code, maybe we have to think about the healthy user bias in the copy kind of thing, because someone who have the symptom maybe they avoid the copy, so what do you think about that? Yes, I think the advice that we will provide in our clinical practice is in those patients who have symptomatic palpitations with any coffee consumption, that first I think it's important to try ascertain whether they truly have arrhythmias at the time of the palpitation symptoms. But if they do feel that coffee consumption reliably triggers palpitations, then perhaps in this patient, they should be the ones to try and reduce or perhaps avoid coffee consumption. But we can also reassure them and say that based on the evidence that we have so far, that regular coffee consumption is not really associated with a significant risk of developing arrhythmias or atrial fibrillation, and perhaps there's a signal to benefit based on studies so far that it can be beneficial for them. So I think it's very important to try and obtain symptom-rhythm correlation just to show them that there is a relationship between their symptoms and also documented arrhythmias with coffee intake. Thank you, Dr. Chen. Let's move on to the next speaker. Next speaker is Dr. Jongil Choi from Korea University. He will talk about alcohol. Please. Thank you, Professor Oh. Professor Jeong, it's a great honor to be here. Yes, my topic is alcohol consumption and atrial fibrillation. I would like to review and introduce the main Korean data. This is OECD data recorded in the alcohol consumption. As you can see, there is a huge variability across the whole country. And interestingly, in Korea and the U.S. and Australia and New Zealand, the similar alcohol consumption annually, 8 to 10 liters annually. What is the standard alcohol drink? WHO defined 10 grams per pure alcohol. This is the United States definition, and 14 grams of pure alcohol. The average, you know, one drink, one can of beer and one glass of wine is the standard dose of daily alcohol drink. This is the Korean style of heavy drinking. Interestingly, heavy drinkers are defined as men and women consuming more than 40, 20 grams of pure alcohol per day. Interestingly, in Korea and the U.S. and Canada, the similar number, 33 to 35% of heavy drinkers. I'm so surprised that this number is very high in our society. I would like to talk about alcohol consumption and atrial fibrillation. As you know, traditionally, text-wise, we know holiday alcohol syndrome is alcohol consumption that may cause atrial fibrillation. This is a potential mechanism for acute alcohol consumption as trigger, the cellular effect, and the autonomic effect. The cellular effect is damage to gap junction, intercellular channel, and direct myocyte injury and inflammation and acute oxidative stress. Autonomic effect is sympathetic activation and vagal inhibition, and reduced heart rate variability. And then, the electrophysiology effects occur, and the shortening of atrial and pulmonary vein action potential and atrial effective refractive period, and enhanced AV nodal conduction, leading to the reentry mechanism. This is a habitual alcohol consumption and atrial fibrillation pathophysiology. Alcohol-induced atrial inflammation and oxidative stress may cause hypertension, sleep apnea, and LV remodeling. And then, atrial substrate remodeling, and AA dilation, and fibrosis. And also, triggered by acute binge. Binge drinking is defined as more than five standard drinking on a single occasion. And the cellular effect, as I mentioned, and the cellular effect and the sympathetic activation, electrolyte imbalance, and leading to, finally, atrial fibrillation. Let's talk about alcohol and risk of atrial fibrillation. So far, there are many major studies examining the effect of alcohol consumption and atrial fibrillation. Based on this data, we conclude that alcohol is an important risk factor for atrial fibrillation through direct effect, and by contributing hypertension, obesity, and habitual drinking at moderate level, as well as binge drinking, predispose atrial fibrillation with an increase in atrial fibrillation recurrence. And as you can see, atrial fibrillation is linearly increased, but other heart failure, cardiovascular mortality is a U-shape. Although a small amount of alcohol is cardioprotective, these benefits do not extend to atrial fibrillation. This is Korean data, and as you can see, the sudden cardiac arrest, the alcohol consumption is significantly associated with reduced incidence of sudden cardiac arrest. However, atrial fibrillation, as a heavy drinker, showed a significant higher incidence of new onset atrial fibrillation like this. Interestingly, the p-interaction, this analysis showed that p-interaction is less than 0.05 in smoking, hypertension, diabetes, and dyslipidemia. This comorbidity is important in atrial fibrillation in addition to alcohol consumption. This data is done in the Scandinavian countries, in Finland, Germany, and Sweden, in a community-based pooled quota. As you can see, the one number of drinks per day, alcohol is 20 grams, 12 grams, and the hazard ratio is 1.16. In addition, associations were similar across types of alcohol, and in contrast, alcohol consumption at lower doses was associated with a reduced risk of incidence of heart failure. This association between the alcohol consumption and incidence of AF was neither fully explained by cardiac biomarker, BMP, and concentration, nor by the occurrence of heart failure. This subgroup analysis showed that very interesting, and the amount of alcohol is the incremental effect, and the higher alcohol amount showed a higher incidence of atrial fibrillation. However, the frequency is not clearly demonstrated in this study. This is Korean data. We analyzed about 1 million patients who participated in the national health check-up. As you can see, the amount of alcohol per week significantly increased in new onset atrial fibrillation. Interestingly, the number of drinking sessions per week is more important. So dividing alcohol consumption to avoid binge drinking may not be an appropriate strategy for preventing new onset atrial fibrillation, and preventative effects of mild drinking observed in this study require further validation. This is very interesting data in Korea, and they analyzed a large-scale UK biobanker. As you can see, the heavy drinker showed a higher incidence of new onset atrial fibrillation, and in addition, combining the polygenic risk score, this means that with genetic predisposition to alcohol metabolism, they concluded that individuals with genetic predisposition to low alcohol metabolism were more susceptible to atrial fibrillation. So far, as you know, the alcohol consumption is significantly associated with the risk of new onset atrial fibrillation. However, we wonder whether alcohol abstinence can reduce the risk of atrial fibrillation and the subsequent stroke. This is beautiful data done by an Australian group in a multicenter prospective randomized trial. They compare the recurrence of atrial fibrillation between abstinence group, two drinks per week, versus control group, 17 drinks per week. Baseline alcohol intake is 16.8 versus 16.4, the same. And they conclude that after a two-week blank period, atrial fibrillation recurred 15.3% in the abstinence group versus 17.3% in control group. Kaplan-Meier curve showed that abstinence group showed significantly lower incidence of recurrence of atrial fibrillation. And also, abstinence group had a longer period before recurrence of atrial fibrillation, and atrial fibrillation burden over six months followed was significantly lower in abstinence group. This is very interesting data done in Korean group. And they analyzed the cardiovascular outcome related to the atrial fibrillation. And the primary outcome was defined as a composite of a thromboembolic event and atrial fibrillation-related hospitalization to the progress on the progress of atrial fibrillation. Interestingly, they showed that J-shaped association between alcohol intake and adverse event in atrial fibrillation. And this is published in the European Heart Journal, Dr. Seil Oh and the Wigan Chair Group. And they are based on the nationwide court data. And as you can see, this Kaplan-Meier curve will show that abstinence group and non-drinker, the lower incidence of stroke compared to the current drinker. And they conclude that ischemic stroke risk reduction is 14%. So they suggest that lifestyle intervention, including attention to alcohol consumption, should be encouraged as part of a comprehensive approach in the management of a patient with new diagnosis of atrial fibrillation to improve clinical outcome. This is the ESG guideline. As you know, alcohol consumption is a cause of atrial fibrillation and stroke and also the significant risk for bleeding on anticoagulation patients. So alcohol is a very hazardous lifestyle. And so ESG recommends that they finally reduce alcohol consumption to less than three standard drugs. I think it's based on the Australian IHT data, less than 30 grams of alcohol per week is recommended as a part of comprehensive risk factor management to reduce atrial fibrillation recurrence. And the class of recommendation one, level of evidence B. And finally, alcohol consumption has a high burden of disease. And alcohol is an important risk factor for atrial fibrillation through direct effect on the atrial substrate. Although a small amount of alcohol is cardioprotective, these benefits do not extend to atrial fibrillation. The frequency of drinking is also a significant risk factor for new onset atrial fibrillation. Individuals with genetic predisposition, polygenic risk score to low alcohol metabolism were more susceptible to atrial fibrillation. And regular alcohol consumption is a potentially modifiable risk factor for atrial fibrillation. And abstinence group showed a reduction in both burden and risk of recurrence of atrial fibrillation compared to control group. And abstinence after diagnosis of atrial fibrillation could also reduce the risk of ischemic stroke and other cardiovascular outcome. Thank you for your attention. APPLAUSE OK, this topic is open for questions. By the way... Thanks for a lovely review on the role of alcohol. In Australia, it's quite easy for us to do that study because it is such a big issue. Is it a common risk factor in Korea? People drinking too much alcohol and having atrial fibrillation? Oh, you mean the Korean? Korean population. Yeah, and the alcohol drinking is very popularly... ..the lifestyle in Korea, as you can see the picture in the heavy drinker. However, it's the data... We see data and the level of data is similar. I think Western countries enjoy more the toxic and the spirit and more the strong alcohol, and the Korean is a little bit weaker. And so, yeah. So I suppose one of the challenges we have in Australia is we have this data, and around the world, and I think that's why a lot of doctors don't talk to patients about alcohol, don't know how to bring it up. A lot of people find it really important as a social tool. Do you have any insights in terms of how you get people to stop drinking? Yes, and stop drinking is more important, but in terms of only the atrial fibrillation, as you can see the U-shaped curve, this is other cardiovascular mortality, including heart failure, and possible mechanism is improve the lipid profile and reduce the platelet aggregation and inflammation. And so still I think we have the controversy in terms of alcohol consumption and all kinds of cardiovascular outcome. However, in terms of atrial fibrillation, alcohol is toxic and modifiable risk factor in our data. I'll just make one last comment about the less than three standard drinks as a recommendation. It's a relatively arbitrary number. That number was taken from the sort of lifestyle risk factor management program. When we did that study, the randomized study, we found that those that completely abstained had a better outcome and freedom from AF than those that continued to drink small amounts. So I think just to take note, that's kind of a bit of a pragmatic approach because people find complete abstinence very difficult. Please visit in the Korea in the next year that we communicated alcohol small amount. Thank you, Dr. Chen and Dr. Kiston. Thank you. So speaker is Dr. Sigan Ruiz from Alfred Health Hospital and she is really excellent. This HRSB team, she has five presentation and this is her last presentation. I'll celebrate the last of the presentations with a big strong coffee. So I'd just like to thank Heart Rhythm Society and also the Korean Heart Rhythm Society for the kind invitation to present today. I have no disclosures. I'll be tackling two challenging modifiable risk factors which are obesity and sleep apnea in the AF population. And when I saw this talk, I thought, I'm not sure how I'm gonna talk about these two things for 12 minutes. And then I found in fact that my talk was way too long. So I am gonna try and condense the data as much as I can and hopefully leave you with the important message that no one risk factor in isolation is the only important thing to be thinking about with the patients, but I'm gonna take you through that shortly. We have this QR code, but we've got a question coming up which hopefully will invigorate some audience participation. My slides seem to be out of order. Okay, I'll do my best with this, but anyway, ablation remains the cornerstone of AF management. And despite advances in catheter ablation technologies and increased durability, we have seen a relative plateau in the success of ablation alone. But in saying that, obviously we've had a lot of discussion in this meeting about how we define success, but it really requires us to think a little bit more about how we tackle AF beyond just treating rhythm on its own. And that takes us back to the origins of the disease process. So much so that the most contemporary American guidelines has really looked at AF more as a disease continuum. And with that comes an opportunity to see how we can possibly target important milestones in this AF trajectory to reduce the risk of AF developing and the disease progressing over time. And we know this is of critical importance. AF is associated with significant morbidity to our patients, costs to the healthcare system, and it's a global public health crisis. So it really requires significant attention. And the focusing is increasingly coming towards shifting our focus towards earlier intervention. And the challenge for us as electrophysiologists is we often see patients once they have AF, but really probably the best time to intervene is when people don't have AF, but are at risk of developing AF. Why is this a problem? Well, we know AF is only on the rise and it's a global problem affecting all countries and all ages. And in part, we thought this was due to our aging population but increasingly we're seeing it's also due to increased accumulation of lifestyle risk factors. And I've included here a slide from our colleagues from Adelaide who have done a huge contribution to this work and also added in sleep apnea. And we see that all of these factors are increasing in concert with the rising AF prevalence. The recognition of risk factor modification has become so highly prioritised in the guidelines that in fact, only a few years ago, it was elevated to the first pillar of AF management. And more recently, it's been centralised as the central pillar of AF management. So it's corded on the two sides by rhythm control and anticoagulation, but really at the core, the importance is tackling modifiable risk factors. So now I have a question to open up the sort of, us delving into the literature. We have a 67-year-old gentleman with paroxysmal AF but increasing severity and frequency of episodes, BMI of 40, severe sleep apnea confirmed on a sleep study, hypertension, alcohol. As you can see, there's a lot of things that we could tackle here. He's been referred to you specifically to be considered for AF ablation. So what should be the priority in this patient's management? We'll just give you a minute to give your responses. I'm not quite sure how long, how this works, but let's see. So you have four more seconds. All right. Okay, well, this is nice to see. So we'll talk about this more later in the presentation. So we know that each individual risk factor is independently associated with AF risk. But we know that these risk factors rarely occur in isolation. And moreover, those risk factors don't just contribute directly to AF pathogenesis, but they can have indirect effects. So for example, someone who is obese may be more likely to be sedentary and they may be more likely to develop diabetes or heart failure. And all of these factors contribute to the accumulation of processes that can promote AF development. This is a very nice review article, again, from our Adelaide colleagues, really highlighting how these risk factors share common pathways. And importantly, I wanted to highlight that patients with sleep apnea also commonly are overweight, but not always, often have hypertension and may become sedentary. And importantly, as was highlighted by our earlier speaker, alcohol consumption is commonly linked to sleep apnea. So you can see this really close relationship. And that's why it's important when we're thinking about identifying risk factors and then treating those. We don't just treat one thing in isolation. Our group has contributed some work to this field. What we really wanted to do is harness the power of clinical risk tools, which we could utilize at the bedside for motivational counseling and individualized decision-making with our patients and say to them, if you have these risk factors, this is the risk of AF developing or progressing over time. And so we developed from the UK Biobank and externally validated this clinical risk tool, the Framingham Heart State, the HARMS-II AF Risk Score. And you can see it's a little bit small, but you can see that this risk model performed well, both internally and externally with regard to AF risk prediction in a population who had not had AF before. And we compared this risk model to other existing risk tools, which importantly do not comprise modifiable risk factors. Therefore, there's no tangible targets to intervene. And it outperformed two historical risk models and performed comparably to the well-recognized CHARGE-AF Risk Score. So now let's look at sleep apnea. We know that sleep apnea has acute and chronic effects and can affect AF pathogenesis through various pathways, including hemodynamic effects, affecting left atrial hemodynamics, causing left atrial fibrosis and scarring, electrical remodeling, structural remodeling that can promote AF development. And this is really nicely illustrated in work from our colleagues at the Royal Melbourne Hospital, where they nicely performed a mapping study in patients with sleep apnea, at least moderate severity. And they showed patients with more severe sleep apnea had also more advanced left atrial electrical remodeling. And it was interesting to see that there was this inverse association between sleep apnea severity and tissue voltage in patients with paroxysmal but not persistent AF. And they followed up this with a small randomized study published a few years ago now, looking at patients with AF and at least moderate sleep apnea. And they looked at treatment versus no treatment. And you can see to the right that treatment of sleep apnea with CPAP resulted in significant improvements in these electric anatomical characteristics, increase in tissue voltage in the left atrium, increase in conduction velocity and reduction in fractionation. So it really showed us some promise that perhaps treating sleep apnea even in isolation may have favorable outcomes in our AF patients. Now, this is a small observational study published now a few years ago, but in circulation. And they looked at patients who underwent cardioversion, had AF and sleep apnea. And they looked at comparing patients with AF with no sleep apnea, patients with AF with sleep apnea, untreated patients with AF and sleep apnea that was treated. They wanted to see the relative risk of AF recurrence over 12 months. And you can see that in patients with sleep apnea treated with CPAP, they had no significant change in terms of that 12 month arrhythmia recurrence risk compared to controls. However, those with untreated sleep apnea had a doubling of their risk. And it'd be really nice to see this reproduced in some more recent and larger data. A recent meta-analysis of seven prospective studies, again, these were not randomized, looked at patients with AF and sleep apnea and looked at what happened if you treat their sleep apnea and they may have an ablation or they may not need an ablation. And what is the outcome in these patients showed whether or not these patients had an AF ablation, the outcomes were favoring those who had CPAP treatment for sleep apnea. And in fact, there was a 42% relative reduction in AF risk across all groups. Again, it's important to note these are relatively small and non-randomized data. And then came a larger randomized study. And I think we were all hoping that this would be the study to change practice. Now, this study was, again, a modest sample size. All patients had pulmonary vein isolation. They were all paroxysmal AF. And in fact, originally they'd planned to include 130 patients randomized to, patients with AF and sleep apnea randomized to standard care versus CPAP. And they also had a control group who had AF without sleep apnea. And importantly, about a third of the patients with sleep apnea who were allocated to CPAP treatment were actually excluded from the final analysis because they did not require an AF ablation. Now, the authors didn't explain why this is the case, but you can possibly infer maybe their symptom profile improved to an extent that it was felt it wasn't needed. And I think that's really important limitation here when we're interpreting this data. But you can see to the left, there was no significant difference in arrhythmia recurrence. In the middle, you can see all groups experienced a significant reduction in AF burden. And to the right, all groups experienced a significant improvement in AF symptom severity. So this conclusion of this randomized studies, there was no difference between these groups. But I think there are these key limitations. If you have a third of patients who are in the active arm that are excluded in an already small population, I do think that is a problem. Also important to note that adherence with CPAP in the active arm was only at best four hours. So I'm not sure how many of you can survive on four hours sleep, but I think that is something we need to look at. And so if we think about the guidelines and how that's changed or rather not changed, you can see that there's a class 2B level of evidence in terms of treating sleep apnea. So there's this recognition that we should be looking for it but the question is, is treating it with CPAP going to translate to meaningful outcomes in terms of improvements in AF outcomes? And I think there's more work to be done in this area. So now let's pivot over to obesity. Obesity we know is independently associated with AF risk and it's also common coexistence with hypertension, metabolic syndrome and alcohol as well as other factors. Each one standard deviation increase in BMI is associated with a heightened and incremental risk of AF development and disease progression. And this has been shown in multiple population-based studies and again, there's indirect and direct effects. And we know that people who gain weight can have coinciding other lifestyle behaviors that may not be ideal for AF and other cardiovascular disease conditions. And these all culminate in structural and electrical changes in the heart that can promote AF development and disease progression. Our colleagues in Adelaide have done a lot of work in this field, particularly with regard to weight reduction. So the legacy trial, this was a non-randomized study but looking at patients with AF and raised BMI and offered them weight loss intervention. And this is not with surgery. And they showed that patients who underwent weight loss and achieved weight loss of 10% or more had the most favorable outcomes. And this is both single and multi-procedure success meaning they subsequently underwent AF ablation. And you can see in the box to the right that it's not just important to lose weight but it's important to maintain that weight loss. So patients who did the worst were those who gained weight subsequently and the second worst were those who had fluctuations in their weight. And in fact, the greatest fluctuation seemed to have this dose dependent response where greater fluctuations in weight up and down resulted in the worst outcomes. Not only did they show that but they also showed there is this interesting relationship with the AF disease trajectory. So in patients with paroxysmal AF who achieved 10% weight loss or more they were far less likely to progress from paroxysmal to persistent AF, only 3%. And then the reverse was also true. So those with persistent AF who achieved 10% or more weight loss were far more likely to exhibit reversal to a paroxysmal AF phenotype. So really promising in terms of protective benefits with the AF trajectory, potential reversibility of the AF phenotype. And now we'll look at the other ways of weight loss other than lifestyle measures. So a group looked at bariatric surgery pre-AF ablation and they found that patients underwent bariatric surgery had greater arrhythmia-free survival both with single and multiple procedures. And there was this relationship between the, again, the degree of weight loss. Thank you. The degree of weight loss and arrhythmia outcomes. And importantly, there was also an association between weight loss and the amount of weight that you had and epicardial fat, which we know can be proarrhythmic. I'll try and skip to the last few slides in the interest of time. I know GLP-1s are very topical at the moment. Thankfully, GLP-1s don't seem to be associated with increased AF risk. This has been shown in a couple of meta-analyses. The question really is, is there a protective benefit? We know that patients with AF and obesity probably would benefit, but what about the broader AF population? We really don't have any randomized data thus far, but it's probably coming. And recent meta-analysis show, suggested, these are small studies published last year, that there was potentially a protective benefit after catheter ablation in terms of AF recurrence risk. However, in that same year, a large non-randomized study, this is a propensity match study of more than 1,000 patients showed no difference in patients on GLP-1s versus those not on GLP-1s. So I think with that said, we need to study GLP-1s more in this space. So you can see the guidelines have really shifted over the last five years, really prioritizing risk factor management more. And some of these risk factors have now been elevated to class one in terms of optimizing these parameters. You might say, if a patient's gonna have an ablation anyway, do I really need to address these risk factors? Well, the answer is yes. Our Adelaide colleagues have shown that when you undergo ablation, if risk factors are optimized, these patients do far better than if we just treat the AF in isolation. So these are the recommended targets. And of course, it's really important these are individualized to the patient. And as was discussed earlier, we take a pragmatic approach. So if you have a patient in front of you and they are very unlikely to abstain from alcohol, we look at what is a tangible target that they can get to that is gonna alter or mitigate their risk. So going back to our question, it's, oops, no surprise that everybody was correct in the room. And you might find that treating some of these risk factors may not necessarily require the patient to have an AF ablation. So really highlighting the importance of addressing all of these risk factors in combination, and then seeing whether or not the rhythm itself remains an issue. So take home messages are obesity and sleep apnea, they're very common, and they're not just comorbidities. They really should be seen as tangible targets for intervention, not just for general cardiovascular health, but specifically as part of AF management. One risk factor alone can have a cascade effect and produce other risk factors. Ablation is not a substitute for addressing the core problem. And so we really need to hunker down to the root cause and go to the very beginning and see what are the things that we can do beyond catheter ablation that can improve outcomes for our patients. Thank you. Thank you, Dr. Sigan, a wonderful presentation, because we are a little bit behind the schedule, so we'll move to the last speaker. Thank you. Last speaker is Dr. Eugen Choi from Seoul National University. His topic is the clustering of health behaviors in atrial fibrillation from risk reduction to adverse event prevention. Dr. Choi, please. Yeah, thank you for the introduction. My name is Eugen Choi, and it is my great honor to have a chance to present in this session. So I'm gonna talk about the clustering of healthy behavior in atrial fibrillation and how the modification of this healthy behavior has impact on the risk reduction to adverse event prevention. So this is my disclosure. So I'm gonna talk about the introduction and each lifestyle factor modification and the smoking, alcohol, exercise, and combination of these lifestyle factors, and also combining with these life factors. And recently, we are focusing on the aldehyde control, so how this has an impact on the risk of atrial fibrillation and the outcomes. So as you know that the recent guideline, the both ACC and HRS and ESC-AFib guideline has emphasizing the role of modification of this lifestyle factors. There has some kind of a very big impact on the AFib outcome. So this is what we call the head-to-toe, and ESC-AFib guideline is AFib care. So there's lots of types of researching healthy behaviors, such as from the surveyed questionary and case studies and observance study. So actually, it is really hard to do the randomized clinical trial because there's some kind of ethical issue, like smoking or drinking or some kind of that kind of behavior. So maybe the survey or questionnaire is kind of a common method to do some kind of research in healthy behaviors. And in Korea, we have a very well-established nationwide health insurance database because a Korea patient is a single-payer system, so all the Koreans are covered by national insurance. And also, the subject older than 40 years old are recommended to have a biannual health checkup. So we have a national health screen database, which included the smoking, alcohol, physical activity, health behavior, but also not a single time, but we have consecutive data, biannually, cumulative data. So we can follow those patient who has lifestyle change among the follow-up period. So this is how we can check, we can analyze those patient, how this modification of lifestyle can affect on the ephemeris and also the outcome in those patient with atrial fibrillation. So let me start with the smoking. Smoking cessation is a class 1B recommendation in the guideline. So maybe everyone in this room has to stop smoking even though they do not have AFib. And smoking is a well-known risk factor for AFib even though they are under anti-cholesterol therapy. Even though there is a multivariate analysis, there is a risk of atrial fibrillation, the risk of ischemic stroke is about 2.1. And also, we have analyzed those who do not have any stroke risk factors that smoking has a higher risk to develop the ischemic stroke in this low-risk population. It's about 9.1. So as I mentioned in our national health database, we can follow those patient who has developed the atrial fibrillation and the change of lifestyle before atrial fibrillation and after the atrial fibrillation. So I think the lifestyle modification is one of the challenge for the patient who developed the newly diagnosed atrial fibrillation or newly diagnosed hypotension diabetes. They may have some kind of made their mind that I should change my lifestyle to prevent something. So this is kind of a time that we can analyze this data. So we analyzed the newly diagnosed atrial fibrillation and those patients who quit smoking has some kind of risk. And current smoker, when we compare with the never smoked smoker, those two groups has a higher risk of ischemic stroke and all-cause death. However, when we compare with the current smoker, if they stop smoking after when they diagnosed atrial fibrillation, the risk of ischemic stroke and mortality has been lower compared to those who are current smoker. Not only the ischemic stroke and the mortality, the risk of dementia also has been influenced by the smoking cessation in those patient who are newly diagnosed atrial fibrillation. So before and after they change the smoking habit, the ex-smoker or quick smoker seems to have low risk in the total dementia and the Alzheimer's dementia and vascular dementia. So it's very important to stop smoking in those patient who are newly diagnosed atrial fibrillation and we should focus on those patient who were educated in this population. What about the alcohol? I think the alcohol part is a little overlap with the previous speakers. So reducing alcohol consumption is class 1B recommendation in both guidelines. And maybe this is the answer for Dr. Kistler's question that young adult in Korea, alcohol intakes is a very important issue. So habitual alcohol intake shows a higher risk of atrial fibrillation. So in this study, we enrolled about 1.5 million young adult who are less than 40 years old. We have four consecutive health surveillance data and whether their alcohol burden has been changed during the four consecutive change. So we grade it as alcohol burden zero to alcohol burden four. Alcohol burden four means that every time when we take the survey, they drink moderate to heavy alcohol drink. They don't change their habit. So this alcohol burden has a pretty clear or close relationship with the atrial fibrillation risk and the four year cumulative amount of alcohol consumption also show some kind of some relationship with AFib risk. So we should keep in mind in young adults, even though they are very young, their cumulative alcohol burden could affect the AFib risk in the future. And this is the Code AFib Registry, which was led by the Professor Bo-Young Jung who is the chair of this session. And we enrolled about 9,000 patients and analyzed the ischemic stroke and TIS system embolism and AFib related hospitalization. And heavy drinking, heavy alcohol consumption increase the risk of this adverse event in patient with atrial fibrillation. And this is well study already mentioned in the previous speakers. The alcohol abstinence in drinker with AFib has reduced the risk of AFib burden. So it is very important to reduce AFib burden in this high risk population. So based on this study, we think about how the alcoholic habit change has effect on the risk especially for the newly diagnosed atrial fibrillation. So in patient who are newly diagnosed with diabetes, they might have to make their mind that I should keep my drinking habit, I should change my drinking habit. How this affect their AFib risk? In those patient who are moderate to heavy alcohol drinkers, some patient who are keep constant drinking, drinkers, but some patient who abstinence this alcohol drinker. And when we compare, and also there is some patient who do not drink anything in before and afters. So when we compare to the constant drinker, the abstainers shows a 20% lower risk of AFib risk. And this risk is almost similar as non-drinker. So we have to educate those patient who are newly diagnosed atrial diabetes that you should keep in mind that if you wanted to reduce your AFib risk, then you should have to quit your alcohol drink. And this is also, we have done the ischemic risk in patient newly diagnosed atrial fibrillation. Before and after the AFib diagnosis, some patient change their alcohol habit. So no drinkers, and some patient who quit drinker, and some patient who constant drinker, or some patient new drinkers. So when we group into the three category, the alcohol abstinence shows a 14% is lower risk in the risk ischemic stroke risk. Actually, this is the abstainer shows a 14% lower risk, but still it's a higher than non-drinker. So we have to keep in mind that the alcohol burden has a cumulative effect on the outcome of the AFib risk, but also it has some kind of cumulative effect on the outcome when they've developed atrial fibrillation. So when does it happen the alcohol abstinence has some kind of impact on the clinical outcome. In this cumulative incidence curve, you can find that the two groups diverge from after the one year. So after the ones, you have to keep stop drinking more than one year if you wanted to see find the effect. I think this is the well established study that the alcohol amount has some kind of effect on the LA remodeling. So maybe we can speculate on this data that reverse LA remodeling could have some kind of happen in those who quit alcohol. And also this kind of a reverse remodeling have impact on the AFib risk amount and also the ischemic stroke. So what about the exercise? So exercise is recommended as class 1B and more than a target 210 minutes per week is recommended. So regular exercise, AFib related symptom, quality of life recurrence was well recently published in the active AFib study in the Australia group. And they found it that exercise intervention combining home and supervised aerobic exercise over six months showed greater freedom from AFib recurrence and reduction of reburden and improved quality of life. So we focus on this exercise on the AFib patient outcome. So when they were diagnosed as newly AFib and their exercise habit changed before and after the AFib diagnosis, some patients chill on the sedentary lifestyle. Some patients start to do the exercise after when they diagnosed atrial fibrillation. Some patients stop the exercise and some patients keep doing the maintain the exercise. So this cardiovascular event shows a close relationship with the exercise maintenance, exercise new starter and exercise dose was also very important. And this is the risk of dementia is also related to the exercise maintenance and exercise new starters. So this is a UK biobank. We have accelerated dry physical activity and shows that more than 105 minutes per week for moderate to vigorous physical activity performing showed a lower risk of all cause mortality and heart failure. So I will skip this one. And combination of this unhealthy lifestyle in low risk atrial fibrillation patient like a sedentary lifestyle and drinking and smoking show the cumulative effect on the primary outcome and all cause mortality. And also when we change the healthy lifestyle combination, this non-current smoker and non-drinker and regular exercise seems to have distributed like this. And this healthy lifestyle combination well correlate with the risk of MACE in AFib patient. So what about the combining the lifestyle modification and early reading control? Not only the healthy lifestyle, but also the early reading control combining this showed the 50%, almost 50% lower risk when we compare to those who do not do early reading control and no healthy lifestyle modification. And similar risk in the healthy lifestyle only and early reading control only. This is about the 22% or 27% risk reduction in the stroke in AFib patient. And I will skip this one. And this is also very reproducible in young population who are less than 65 years old and who are older than 75 years old. So we have to keep in mind both doing the early reading control and healthy lifestyle modification is very important in the population with atrial fibrillation. So this is my last slide. So ladies and gentlemen, the lifestyle factor play a significant role in the development of AFib and strongly influence its clinical outcome. And modifying this factor is essential to reducing both the risk of AFib onset and the adverse cardiovascular events in patient with AFib. And combining comprehensive lifestyle modification with early reading control may further enhance clinical outcome for this patient. So thank you for your attention. Thank you. Thank you, Dr. Choi, wonderful presentation. We are a little bit behind the schedule, but if there's a question or comment, we can. Okay, so now we wrap up this session and I especially appreciate the wonderful speakers and the participants. Please enjoy the remainder meeting. Thank you.

atrial fibrillation

lifestyle modification

coffee consumption

alcohol intake

obesity

sleep apnea

smoking cessation

cardiovascular events

stroke risk

risk factors