Good afternoon. We are going to start this session on ear fibrillation strategies. I think that all the speakers do not deserve a bigger presentation. They are already well known, international leaders of opinion, known by all of us. So, the first presentation will be on the lessons learned in paroxysmal ear fibrillation in the World Trial by Dr. Vidal Ezebak. Hello, thank you very much for the opportunity to be with you in the Congress. I am going to present a study that we did in Canada on patients with paroxysmal ear fibrillation. My conflicts of interest. I am going to present the study, AWARE. It is the study of an increased strategy of ear fibrillation compared to a standard strategy of isolation of the veins that we did in Canada with my colleague from Ottawa, Giri Schneer. We know that in paroxysmal ear fibrillation studies we have success rates of approximately 70-75% depending on the study and the way recurrences are defined, the way patients are monitored to detect recurrences. We are looking at how we can possibly improve these results. Issues to consider are, first, if there is any way that we can improve the success rate of the first procedure. Also, the limitations of the strategies and the elements that we have at that moment. It may be that there is a limit to the effect that we can achieve with a strategy that only focuses on isolation of the pulmonary veins. There are also risks of complications when we do ablation. It may be that the strategy of isolation of the pulmonary veins is not for all patients. And also the question of what is the ideal endpoint for these randomized studies. Intermittent monitoring, continuous use of implantable monitoring and the advantages of each strategy. We know that in patients that do have recurrences, in general, it is because they also have reconnections of the pulmonary veins. And that is why, when we do the first procedure, we have to focus on trying to make lesions that will persist without gaps and without the risk of reconnecting. We know that when ablation is done, there are permanent effects and there are also reversible effects. We can have acute isolation, but due to the effect of local edema, which then recovers the conduction and is related to FA recurrences. We did a systematic meta-analysis to compare studies that used a segmental isolation strategy of the pulmonary veins compared to studies that used a strategy more of the WACA, Wide Anteral Circumferential Ablation, a wider isolation that includes the antero of the veins. And the result is superior when a more central isolation is done. The hypothesis that we had was that perhaps if a WACA is good, perhaps doing a double WACA could be better. It could be perhaps better to access a superior durability with the second WACA. It could have as a secondary effect additional modification of the substrate. It could perhaps modify some extra-pulmonary triggers. The manuscript of the design is below. Here you can see examples of the double WACA. The first WACA is done first and then around the first one a second is done. And we hypothesized that this redundancy could perhaps help the effect. The inclusion criteria were patients with paroxysmal FA, anti-arrhythmic refractories and standard criteria. To have objectivity, the workflow included starting with a simple WACA in the patient. And only after completing that same WACA during the procedure, it is randomized, an envelope is opened that is already pre-randomized to say if the patient is going to enter the double WACA and a second WACA is done. Or if it is in the conventional, an adenosine injection is done to confirm if there is a reconnection with additional ablation if required. The primary endpoint was the recurrence of any arrhythmia detected in holters from 14 days to 3, 6 and 12 months. So a total of 42 days of monitoring, which is higher than most studies that were done without an implantable monitor. We randomized almost 400 patients to the simple WACA with adenosine or the double WACA. We did not see any difference in the primary endpoint between the two groups. The results were quite good in both groups. We did not see any difference in the secondary effects. This is the manuscript that we published in JAMA Cardiology that summarizes the results of the study. And we can see, as I mentioned, that in this population, the two strategies, doing the double WACA without adenosine or a simple WACA with adenosine, had similar results. The conclusion of the study is that the double WACA that was evaluated was not superior to the simple WACA with adenosine, that the success rate of 75% with a 42-day monitoring was comparable or better than some other studies, and the absence of requiring a second ablation of 90% of the patients was quite good. But we return to the idea that perhaps there is a roof of the effect that can be achieved with a strategy of just isolating the veins. And the question of whether there is an additional role in looking for other areas, other targets to do ablation. We present a sub-study of the AWARE first, which is scheduled to be published soon, in which we analyze the patients who had their ablations with a strategy of high power short duration against a strategy of normal power. And we saw that in the patients treated with high power short duration, the procedures were significantly more efficient, and with less use of fluoroscopy. Now, moving on to the role of extra-pulmonary triggers, we know that there can be triggers of the right side, fibrosis, and in this slide you can see the rates of different types of triggers that can be seen, extra-systoles, nodal reentrances, atrioventricular reentrances, flutters, and the fibrosis scar on the posterior wall. We know that when there are triggers at the beginning of the disease, with time, it becomes more of a problem of the substrate, and depending on where the patient is in this evolution of the disease, it may be that with time, attacking or treating the substrate is important. Both with speech treatments or pharmacological treatments, or modifying the patient's substrate, which has hypertension, diabetes, sleep apnea, overweight, etc. All of this is important. We already have funding to do an AWARE 2, whenever there is a study, we like to do another one to evaluate other points, and in this study, we want to see if there is value in doing something more than pulmonary veins in patients with paroxysmal FA. So, the strategy is PBI versus PBI+. The idea is, in patients with an additional strategy, to see the effect of doing an electrophysiological study, looking for dents, nodules, accessory veins, flutters that can be flattened, areas of fibrosis, either in the posterior wall or elsewhere, that can be considered for speech or triggers. So, to sum up, there is potential to improve the results of speech in patients with paroxysmal FA in the first procedure. There are current and future studies that have to evaluate if there is a ceiling effect, a maximum effect that can be achieved by isolating the veins, and maybe if we have to look for additional strategies or not, that has to be checked. In patients with paroxysmal FA, the most important point that we think explains the recurrences are the reconnections of the pulmonary veins, so we have to use strategies in the first procedure to obtain a persistent isolation rate without long-term reconnections. The role of the extra-pulmonary triggers is something that has to be evaluated in these patients. To increase the success rate, we also have to be careful not to increase the risks and, on the contrary, improve the safety of these procedures. Maybe new types of energy, such as pulmonary field, can improve the safety part, although it may not have an efficiency effect. If it can be safer, it is already a step forward. And strategies, point by point, or more broadly speaking, these are also things that we are evaluating. With that, my time is up. Thank you very much for your attention. Thank you very much, Vidal. We will leave it for the end, if there are any questions, if we have time. We are going to give way to the second speaker. Is Dr. Mon connected? Yes, here I am, can you hear me? Luis, good afternoon. It is a pleasure to have you with us. Likewise. Likewise, how is everything? Very well, Luis. Dr. Luis Mon, from Hospital Clínico de Barcelona, as he said, also known by everyone. So we are going to give him the floor for his presentation. Luis, we are going to hear you talk about sports and auricular fibrillation. Well, thank you very much for the invitation. I am very sad not to have been able to be here for personal reasons in this Congress, but I hope to be able to be in the next one. And it is really a pleasure to share with all of you these topics on sports and auricular fibrillation. I am going to go over the history of this a little bit. And the fact is that, although this topic, we already started working with it in 2002, that is, 20 years ago, I still think there is little knowledge. Probably because we all have a certain bias towards the promotion of sport and everything that is a negative effect, we try to undervalue it. In this initial observation, what we did was, in our clinic of outpatient patients, to see that most of the patients we looked for, consecutive patients, had auricular fibrillation without any other cardiopathy, totally idiopathic, even without hypertension. And we saw that almost 50% of them, who had no risk factor for auricular fibrillation, none at all, practiced sports of resistance regularly. And we thought, this is a lot for a population of between 25 and 65 years. And we went to look for, in a population, using the Regicor study, which is an epidemiological study, in Catalonia, and we saw that, at this age, more or less, the proportion of males, because these patients were all males, who practiced sports of resistance, was 15%. And in this first observation, we said, well, this cannot be casual. There has to be an association here that has to do with auricular fibrillation and sports of resistance. From these initial publications, came many others. I put here some examples. This is a study we did in patients who had run the marathon, who were studied, and, at 10 years old, this population already existed, we analyzed what had happened with it, and we saw that, in control cases, the marathon gave 8 or almost 9 times more risk of auricular fibrillation in a 10-year follow-up. But other groups also saw similar things. For example, this is a little earlier, in 1998, in Finland, the field runners, again, had a 5.5 more risk of auricular fibrillation. The risk is very high, for example, in the background skiing, in this series, in this cohort, 13% of auricular fibrillation, 10% in veteran cyclists. This led us to publish a review in the Nature Reviews of 2016, which we published with Eduard Wasch, who worked hard on this review, it is very good, if you want to look for it, it is really very complete. Here we mark in green the positive studies of association and the negative studies, starting with small cohorts of less than 1,000 individuals, in which almost all are positive and establish this association, in large studies of more than 2,000 individuals, there is still a large majority that find this association, some do not find it, because they are studies that have been done in patients who enter the study at a very old age, when they have already selected those who do not do ear funding. For various reasons there are studies that have not been so conclusive, and some meta-analyses that also go in this direction. But I also want to bring you a very recent study, a meta-analysis, which includes 13 studies that met the criteria, among them three of ours, made in Barcelona, in our center, and with a very different number of patients. Some are cohorts, others are control cases. For example, the study of Acer was the American Physician Study, which looked at American doctors who did sports, what was their rate compared to those who did not, and they also saw an increase in this rate. Later we will see the results. There were even studies with 50,000 patients who practiced Nordic skiing. The network does not let me see. Hello? Yes. So, really, in this meta-analysis they saw that all of them, and we are talking about men, because this phenomenon, at least until now, has been seen little in women, almost all of them had a clearly positive association between resistance exercise and risk of auricular fibrillation, which on average was 2.5 times compared to the controls. So, how is it explained that the exercise has so many positive effects and, on the other hand, the case of auricular fibrillation, the auricular fibrillation is promoted? So, here there are several explanations. One of them is, for example, the U-shape. That is, if here we consider sedentary individuals as a reference, we see that this is the accumulated hours of high-intensity sport. This is a study that we did in 115 patients seen in emergency. And you see that, from a certain level of exercise, this protective effect of exercise disappears. It even tends to increase the risk of fibrillation. In this case, in addition to sport, other independent factors were associated with height. That is, the taller an individual is, the higher the probability of having auricular fibrillation, and then the amnesia in this study. In any case, you see that this could be an explanation of the difference between men and women. Height really also plays a role, curiously. This wave, or this form of association in U, has been seen in other studies, much larger, with more patients, like the ones we mentioned here. And we see that it is reproduced, both if we call it exercise MEDS, as well as the level of activity, etc. This beneficial effect is reproduced when the exercise is moderate, and negative when the exercise is very high. There are several studies here that show that this type of pathology is much more prevalent in men. That is, the auricular fibrillation generated by exercise in women is much more infrequent. And it is still not clear what the difference is. It could also be that the degree of exercise that women did at this time was lower. We are now seeing patients in their 40s or 50s. Now young people do much more exercise, as do women. The result of this is to be seen. In any case, for example, in this study that was done in England, with the famous UK Biobank, which has impressive cohorts, there were 400,000 individuals between the ages of 40 and 70. They concluded that the risk of auricular fibrillation is lower among physically active patients, who exercise. Therefore, this would really favor exercise. But then, when you look at the paper in detail, you see that when they talk about vigorous physical activity, if one is that there is no increase, it increases proportionally when you increase the meds per week, for example. Something that is not seen in women. Women do have a beneficial effect, which is not observed in vigorous exercise or in normal exercise. That is, we cannot draw general conclusions because it is a complex relationship. To study this, we saw some animal models, and I'm not going to go too far, and we saw that rats that exercised very intensely had more fibrosis in the auricle, had a higher parasympathetic index, and had a higher inducibility of auricular fibrillation. And this was not entirely reversible, but it could reduce the inducibility when a detraining was done. In principle, this is a fact that is accepted. However, there is still little knowledge. When people do a patient survey, they ask, well, is this hypertensive? As we see this patient at 50 years old, when perhaps he no longer does as much exercise as when he was 20, maybe he does only three hours a week, three days a week, four hours. This is much more than the general population. There are other aspects that we will talk about tomorrow, about exercise and coronary disease, which are relatively new. But in the end, to summarize, I would say that high-intensity exercise is a clear risk factor for auricular fibrillation, and that this type of association has not been seen in women. And I think I would leave it here to give a little time to discussion and not cover up with too much data. Thank you very much. Thank you very much, Luis. I would ask you to stay connected for the final session of questions. Now I turn to the third speaker, Dr. José Luis Merino, who will try to answer this question, because all patients need rhythm control. All patients with auricular fibrillation. Thank you, José. Thank you very much for the opportunity to speak here today. These are my conflicts of interest. And to frame the subject, when one sees a geography of the left auricle in auricular fibrillation, I think we all know that this cannot be good. So, if one asks the question if all patients should be subjected to a rhythm control strategy, the simple answer is yes. And we know that it should be yes, because we know that auricular fibrillation is associated with some bad consequences. The contribution of the auricle to ventricular filling is lost, the heart rate is increased, the adaptation of the heart rate to exercise is lost, and very important, which is often not taken into account, is irregularity. Irregularity in itself is associated with deleterious effects. This is a classic article, where, after a nodal ablation, a step marker was implanted on the patients and at the same frequency the regular and irregular step marker was programmed. So, as you can see, irregularly, the heart rate drops and the pulmonary capillary pressure increases. It is not the same simply because of the irregularity. We also know that heart failure and auricular fibrillation are two entities that are imbricated with each other. There is the classic aphorism of atal fibrillation begets atal fibrillation, the classic aphorism begets heart failure and heart failure begets atal fibrillation. We also know that patients can start with parasitic auricular fibrillation and, if nothing else is done, they end up with persistent auricular fibrillation. We also know, from recent studies, that if we make a precode rhythm control strategy, this is better than frequency control. So, well, I think it is clear that all patients should receive a rhythm strategy. The next question is, ok, but how? That is the next question. And we know that drugs have not been a good choice. This is the study of AFIM 20 years ago and drugs were not superior to frequency control. They could even be a little worse, almost touching the meaning. On the other hand, studies with ablation, as I bring you just two, the study of AFIM, ablation was clearly superior to conventional treatment. In the combined endpoint in this study of patients with heart failure, ablation was better. This has just come out of the oven. The worst patient we can imagine. This randomized study had to be interrupted because patients with ablation were clearly better. Perfect. But these results are extrapolable to other populations with auricular fibrillation because maybe patients with heart failure are doing very well, but maybe others are not. And, well, this question of whether they are extrapolable, we have Dr. Packer here, maybe he can answer it. The study of CAVANA, another population, there were no differences in the frequency control strategy with ablation compared to drugs. So, here we have our doubts. Other populations, persistent auricular fibrillation, this is the STARA-F and there is not much difference, depending on what we do. Or the study of CAV, again, persistent auricular fibrillation, they see that the efficacy is really low in the follow-up. We also know that there are patients who respond very well, like this patient with an auricular fibrillation that came from a single vein and this is not the same, a young patient, 25 years old, pulmonary micro-veins, no, pulmonary micro-veins, no, macro-auricular fibrillation, and the pulmonary veins become... Of course, here the ablation is not the same as in the previous patient. We also know that ablation is not free. This is from the CAVANA study, 9% complications, clinical complications, but we also have subclinical complications. Patients who have a subclinical embolism and this is a recent study of ours that with new ablation techniques can reach 60%. Therefore, it is clear that we need, before recommending the generalized ablation of all patients, we need to improve the efficacy and we need to improve the safety, especially in patients in which the symptoms are less clear. But the last question that I would like to ask you is phenomenal. Ablation to everyone, even if we manage to have 100% efficacy. We increase the efficacy to 100%, the risk to 0%, can we offer it to everyone? Is it realistic? Well, we know that pulmonary fibrillation is increasing. This is already a first problem. This is a more rational analysis. I thought about it years ago and I analyzed 2000 data from 2016-2017. At that time in Spain there were about 46 million people living. Assuming a prevalence of pulmonary fibrillation of 2%, that represented that we had approximately 1 million patients with pulmonary fibrillation. How many of these were treated with ablation? It was less than 0.3% of patients. That is to say, even if we duplicated, triplicated, multiplied by 10 our laboratories, it is totally realistic. It is true that not all patients will need ablation with the current technology, but even if we said no to everyone, it is impossible. At that time, I calculated that the number of ablations in general in Spain would reach 18,000 in 2025. The proportion of patients treated with FA would also be 40%. That would give us that by 2025 18,000 patients with pulmonary fibrillation would be treated in Spain. That is to say, more or less the trend is there, but even exceeding my predictions. This implies that in 2025, assuming an increase of 5% would be 12,000 patients and we would not reach 1.4%. It is totally realistic that we will be able to treat all patients. In my opinion, all patients with pulmonary fibrillation should be treated with ablation of pulmonary fibrillation and rhythm control, but with ablation. In an ideal world, the prognostic data of some studies cannot be exported to others. The efficacy needs to be improved, as well as the safety, particularly in patients with FA and if they have few symptoms. And, above all, the epidemiological data strongly advocates the hypothesis or the desire to be able to ablation all patients. However, we have to be a little selective, but I want my message to be positive. I am an optimistic person and 25 years ago, remember how we were. Who would have told us that we would be here today talking about ablation of pulmonary fibrillation, talking about some FA patients that would be unthinkable years ago? So, perhaps, forget everything I have told you in 25 years. We are talking about all of them. Thank you very much for your attention. Thank you very much, José Luis. We are going to move to the last presentation. Dr. Packer is from Mayo Clinic. It is a real pleasure for us. Dr. Packer is being here. We really appreciate the effort to be with us today. The title of the presentation is Effective Ablation vs. Drug Therapy on Quality of Life Results from the CABANA Trial. It's an honor to be here. I appreciate very much the invitation. I appreciate being on a program with the previous two or three talks that you heard. There's a little bit of overlap, but I think that that'll be okay. You know, when we talk about quality of life, there was a lot that we said about it in CABANA. But there's a lot we didn't say about it in CABANA, and so I'm going to go through and see if I can give you an update on the information that we have about quality of life, and that it's not just adding up some score. Typically with quality of life, you add up some score, and when you're through adding up the score, it gives you some means of knowing just exactly how well the patient did. Now this is not quality of life. This is my disclosures, but I'm not going to say anything about them because I don't think it makes any difference with what's going on with this presentation. So quality of life in atrial fibrillation, we talk about it in the way that we feel with palpitations. We talk about physical, and we talk about mental, and we look at those, and we score those, and it makes us think that that's all there is to it. Well, there's a lot more that's not just beyond those numbers. There's a lot more that's causing the atrial fibrillation. So the first thing is, we've known for some time that obesity creates a big problem. So how much of the quality of life problem in atrial fibrillation is quality of life, and how much of it is really obesity? And you can see from 1990 to 2000 to 2010, at least in the United States, the obesity problem just kept getting bigger. And just so that nobody feels bad, it's kind of the rest of the world too. And so it's an issue that's, yes, it's quality of life, but it's not just counting up numbers to see how somebody feels, because there's so much that contributes to the quality of life above and beyond simply you feel palpitations, or you feel short of breath, or something like that. So let's look at contributing factors. Now, if you look above, it talks about aggressive risk factor management. And it could be that we would do nothing whatsoever with atrial fibrillation, and patients could still feel pretty good, and their quality of life would be better, if they would manage their risk factors. If they worked on weight management, that's the next one there, and the one after that is hyperlipidemia, and it looks like this is not good. It could be obstructive sleep apnea, it could be hypertension, it could be diabetes. Each one of those has to add to the quality of life. I'm going to get to the numbers. So if you're all here because you want to hear the numbers, then I can show you how Cabana demonstrated that atrial fibrillation ablation really is a big deal for quality of life. Some of its ablation approaches, if you look on the left-hand side, ablation is just about dealing with anatomy. So it's a matter of ablating around pulmonary veins, say around the posterior wall. It's also about physiology. It's about everything from triggers and drivers to perpetuators and rotors and complex fractionated electrograms and fibrillatory conduction. And so when we go in and we ablate, then it's important that we take care of those. But if you didn't have the problem with the fibrosis and the obesity and other issues in the first place, maybe it wouldn't have been as big of a problem. One of the things that we're working on is what happens when you take care of fibrosis. Now, you can see fibrosis in this slide from Pierre Halifa and Hezegar. It's actually Pierre Zeiss and Halifa. And you can see the white areas that are strictly the areas of scarring. And you can see where the atrial fibrillation occurs, where it's yellow and it's orange. So now what here is contributing to the problem with quality of life? Well, we're going to check on some numbers again in just a second. The problem is it may just be as similar or as important as fibrosis. So what we're doing is we're looking at fibrosomes. Fibrosomes go through a receptor, and then what they do is they look at cyclotrons. They're not cyclotrons, but cytokines. And then they look at what happens with interleukins and what happens with different forms of triggers that create fibrosis. So if we could do something about that, then that maybe would have a very, very big deal about quality of life because people don't feel good because they can't breathe. And if they can't breathe, part of it's because of fibrosis. And it's probably a lot more due to that than it is to recurrent atrial fibrillation. Well, let's keep going. Well, you just heard about the CASTLE trial. The CASTLE trial showed that if you ablated, that those patients did substantially better than did those that didn't get ablated or who were treated with conventional therapy. In this case, patients who were treated with mostly amiodarone. And the difference in terms of overall morbidity and mortality were significant. So let's talk about cabana, and we'll get to the fibrosis, and we'll get to the fibrosomes, and we'll get to the quality of life. In the upper left-hand corner, you see the composite endpoint of intention to treat. And if you look at the intention to treat endpoint, it didn't look like there was a lot of difference between the two, whether you were treated with drugs or whether you were treated with ablation. That's not completely true, but the problem was with the crossovers. In the upper right-hand corner, the thing that you see is that if you look at the composite endpoint or protocol or how patients were treated, there was a large difference. And there's a difference in mortality and a difference in stroke and a difference in the variable components that create problems with quality of life. In the lower left-hand corner, if you look at the endpoints of all-cause mortality and cardiovascular hospitalization, ablation patients still did better. There was a significant difference in the hazard ratios. On the right-hand side, you see propensity scoring, and Peter Noseworthy did that study, and he did look at propensity matching, and he looked at a whole bunch of different components of propensity matching. And they looked at about 180,000 patients, and they looked at the composite of mortality, stroke, major bleeding, and cardiac arrest, just like we did with cabana. And the thing that they found out is about 12,000 were ablated, 170,000 weren't ablated. And if you get down to the bottom of it, the cabana outcomes demonstrated that there was a significant improvement in quality of life, yes, but a more important improvement in total mortality. So let's look at a little bit more here. You see composite outcomes in cabana, upper left-hand corner. Patients who are under the age of 65 had lower event rates, and when they had lower event rates, then they did better from the standpoint of whether they died or not, whether they felt better or not, whether they had cardiac arrest or not, whether they had strokes. Another one is in the upper right-hand corner, and that's heart failure. So you see blue, what's blue? Blue is patients treated with drug therapy. What's red? Red's treated with ablation. So in patients that had heart failure, the thing that happened that's quite important is the patients who had cabana-type ablation lived substantially longer. They had fewer strokes. They had fewer event rates. This is what you just heard a few seconds ago about AF begets heart failure and heart failure begets AF. It's not just anymore AF gives you problems with sinus rhythm. If you get sinus rhythm back, then AF goes away. It's not just that. It's this whole heart failure business. That's why we're doing cabana-HF. If you're over the age of 75, then red is event rates, and it's a lot higher. So if you're over the age of 75, then the risk factors are higher, and if you're under the age of 75, the risk factors are much lower. And if you look at minorities, minorities did much, much better in terms of risk factors and outcomes in events and strokes and atrial fibrillation. Those that were non-minorities had much, much higher risk rates. So why am I talking about this when we're talking about quality of life? The reason is that it's not how you do isn't just a matter of whether we get rid of atrial fibrillation or not. Quality of life may have to do a lot with if you weigh too much, if you have obstructive sleep apnea or hypertension or diabetes or depending on the minority. So I need to make the point again about cabana and cabana heart failure. That's why we're doing this next trial is because we think that those patients are going to feel a lot better and that their quality of life is going to be even better than that if we can get rid of the heart failure. Heart failure will get rid of atrial fibrillation. Atrial fibrillation, if we obliterate it, will get rid of heart failure. That's what we have to find out. That's what we have to prove. We have to try to find out what the issues are. And I always make the point of everyone knows NEMO. And NEMO was lost for a long, long time. And they finally found NEMO, but NEMO didn't look very good. And so the whole issue is quality of life, you have to find it. But you're not going to find it unless you've done something to deserve it, and that is coming up. Well, other considerations. The burden. You see on the left-hand side of that top slide paroxysm, or paroxysmal atrial fibrillation, then persistent, then long-standing persistent. And we're looking at the months since the end of blanking. And the patients who had been ablated were much more likely to be free from a recurrence. About 65% of them did very, very well. 35% did have recurrence. And if you go all the way over to long-standing persistent, those patients didn't do well. And whether you're ablated or whether you're treated with drug therapy, the quality of life didn't turn out very well, vis-a-vis the burden didn't turn out very well. How about the impact of gender on ablation outcomes? Well, on the left-hand side you see women, on the right-hand side you see men, and the bottom line is there's not really a whole lot of difference there. And more important is that the women had a much, much higher improvement in quality of life than did men. So here's some place where you count the numbers up, and if you count the numbers up, then you find that the quality of life really is substantially better in women than it was in men. So what are their benefits? Well, in the upper left-hand corner, it's the same thing I showed you before, and that is that if you were ablated, then you did better than if you were treated with drug therapy. If you look at the one down below, that's a piece of this from Dan Mark, and you can see over time on the left-hand column is looking at months. On the right-hand is the adjusted mean of the quality of life scores. And in the middle, you basically see that for maybe baseline, there wasn't a lot of difference, but if you look at the patients who were ablated, they're all over there on the right-hand side. So being ablated, the right-hand side, the quality of life was substantially better in every way. Is it the burdens better? Is it there's less atrial fibrillation? Is it less weight? Is it less hypertension? It's a lot of less of a lot of things. But the bottom line is the thing we found in Cabana is that the patients who had AF eliminated did best, and there was a parallel between that and their weight and their hypertension. Now, you look up in the upper right-hand corner, we look at the freedom from atrial fibrillation and quality of life and cost of AF on QALYs. QALYs, I think, is something from Australia or something, I don't know, but it's quality of life years spent. And the bottom line is if you read through all of the numbers there, then the cost of doing an ablation over time was about $57,000, and that's in patients that didn't have recurrence of atrial fibrillation at all. And so the bottom line there is that it's not just quality of life on a score, it's quality of life on how things turn out money-wise. Okay, I'm going to show you just a couple more slides. Here is looking at a study that Anita Waplu did, and here you see the actual numbers of quality of life on the left-hand side. On the right-hand side, you see the physical score. On the right-hand side, you see the mental score. And you see that the patients who had AF control, meaning AF was gone, and they were off antiarrhythmic drugs, did very, very well. They were 17. If they were controlled but they were still on antiarrhythmic drugs, they didn't do as well. They were 13s. And recurrent atrial fibrillation, they did even less well. If you look at mental effect, then it's 13, 13, and 9.7, so maybe not as much of a difference as what you might have expected. Even more important than that is what Anita found when she looked at the PCS improvement on the left-hand side over here for physical quality of life, and on the other side is the mental quality of life. And you see patients who were ablated successfully, patients who were treated with drugs, and patients who had recurrent atrial fibrillation. And again, all of the numbers look better with those that were ablated. So were we told correctly in the last two talks that you probably should be ablated? And the answer is, yeah, probably. It probably makes a difference. And for mental, maybe there's not quite as much of a difference. And the mental part may have to do more with some of the other comorbidities. So that's something we do need to work about more. This one I think is important because on the left-hand side, on the left-hand side you see the SF-36 score. On the right-hand side you see the MAF-C score. And what we're doing here is we're comparing SF-36 to MAF-C. And in both cases, one's preablation and one's postablation. And the bottom line is they both paralleled pretty well. So either score showed that those patients who were treated and lost their atrial fibrillation did significantly better in terms of quality of life, but it's also in terms of burden. Now, if you look here again, if you look here again, and again you're looking at MAF-C score on the y-axis and the x-axis is SF-36. For the most part, the patients did better going up and to the left. But you'll notice down around the bottom there's a bunch of patients that had different colored dots. And the bottom line with the different colored dots is even if atrial fibrillation was not eliminated and even if atrial fibrillation persisted, many patients were still doing very, very well in terms of their quality of life. We call that placebo effect. And I think that no matter what we do here, there is going to be some placebo effect. So the bottom line here is quality of life is really important, but so are the other comorbidities and finding out about the comorbidities and taking care of the comorbidities. Getting rid of atrial fibrillation is important. Getting rid of strokes is important. But there is some placebo effect that occurs that contributes to quality of life. But I think the bottom line is with everything that we're doing, I think it's important for us to stay abreast of the need to keep the quality of life and AF burden up and to improve that. And so I'm going to stop there and thank you again for the invitation of being here. Thank you very much, Dr. Packer. I'm going to invite my colleagues, Dr. José Llorente and Antonio Gallegos to open the discussion. Well, the idea that we want to evaluate is to compare two strategies. A simple strategy that only goes for a vein isolation without doing much more. And the other strategy based more on an electrophysiological strategy, where we do a study, we get rid of accessories via the anodal entrance, flutter, we use isoproteranol to get rid of triggers, we do a detailed mapping of the substrate to see if there are fibrosis areas, and to compare those two strategies in patients with paroxysmal FA, to see if there is a benefit in doing something a little more detailed. Well, I want to ask a question to Dr. Mon, who talked about sport and FA. What implications would you have in a patient that you are going to do an FA analysis, and what implications would homogenization have in patients that have fibrosis in the auricular cavity in high-performance athletes to reduce the recurrence of auricular fibrillation in their experience? Well, in terms of the denervation, it surely has a role, because it is clear that part of the auricular fibrillation in athletes is not only the structural change, but also the hypervagotony. Another thing is the practical management. These people want to continue doing sport, so I have found people who do the evaluation to be able to continue doing sport, with their 50, 60, 70 years, 200 km of bicycle road. My advice is, that is a risk factor, just like hypertension, just like another risk factor, try to control it. Don't make them sit in a chair, but make a rhythm of exercise, less resistance, more of another type of exercise. However, the first thing is to realize that this is the cause. And many times, our fellows today go to a patient and the question they ask is whether they have to be evaluated or not. And, on the other hand, many times they ask us how we can improve comorbidities. And this is one of them, just like obesity, just like sleep apnea. Therefore, it is one more risk factor to consider, to manage, and we have to manage it as best we can, depending a lot on a dialogue with the patient. There will be patients who say, look, I don't care if I have to do three evaluations, but I want to continue doing the level of exercise that I do. Well, up to you, they say. But this is a risk factor. This would be the message. Well, thank you very much, Luis, and we are going to end the session. Thank you very much, Dr. Packer. Thank you.

atrial fibrillation

quality of life

paroxysmal atrial fibrillation

pulmonary vein isolation

electrophysiological approach

obesity

sleep apnea

hypertension

ablation