this webinar that is entitled My Patient Has Atrial Fibrillation, What Now? My name is Thomas Dynnecker and I'm very happy to have you all join this important session on what to do acute management of atrial fibrillation. This webinar is a component of the HRS Compass Early Rhythm Control Project, which is supported by Sanofi and Biosense Webster. Thank you all for registering and attending today. I hope you'll have a good meeting. First of all, I'd like to introduce Dr. Andrea Russo to you. She is the past president of Heart Rhythm Society and currently a professor of medicine at Cooper Medical School of Rowan University. She's the academic chief of the division of cardiology, director of EP and arrhythmia services, and director of the Clinical Cardiac EP Fellowship Program at Cooper University Health System. With no further ado, I'll hand it over to Andrea and have a good meeting. Thank you very much. Great, thank you. Thank you, Thomas. I'm really excited to be here for this webinar. We really have an incredible group of internationally recognized speakers and investigators who study atrial fibrillation throughout the globe. We're going to talk today about the practical aspects of the diagnosis and contemporary management of atrial fibrillation in this webinar that's entitled, My Patient Has Atrial Fibrillation, What Now? I'm going to run through everyone's disclosures here and then tell you specifically about our incredible speakers and panelists. Then we will go to the specific talks and then we'll have plenty of time for a panel discussion and question and answer session. Our first speaker will be Dr. Prash Saunders, who serves as director of the Center for Heart Rhythm Disorders at the University of Adelaide. He's the director of cardiac electrophysiology and pacing at the Royal Adelaide Hospital and the group leader for heart rhythm disorders at the South Australian Health and Medical Research Institute. He has published numerous papers and also been awarded numerous accolades. He currently chairs the digital education committee for the Heart Rhythm Society. Dr. Gerhard Hendricks is professor of cardiology at the University of Leipzig in Leipzig, Germany. He has one of the largest EP departments in Europe, providing services to up to 5,000 patients and performing almost 2,500 interventions for arrhythmias every year. He served the European Heart Rhythm Association in lots of different functions and is currently the editor-in-chief of the EP Europace Journal. Dr. Nasir Marosh is director of the Heart and Vascular Institute at Tulane University School of Medicine and he's also the executive director of the Tulane Research Innovation for Arrhythmia Discoveries. He has led multiple initiatives to improve the integration of digital technology is really at the forefront of this field and has also published his research findings in numerous peer-reviewed articles in medical journals. I'd also like to introduce our esteemed panelists. Dr. Thomas Denecke, who you met briefly, is the director of clinical interventional electrophysiology at the Heart Center of Rhone Clinic Campus in Bad Neustadt, Germany, one of Germany's largest EP centers. He specializes in complex ablation of atrial and ventricular arrhythmias and is the educational director of multiple era educational courses. Dr. Denecke is a board member of the German Cardiology Society, a member of the era National Society Committee and serves on digital scientific committee for the Heart Rhythm Society. Dr. Thomas Deering is the chief of the Arrhythmias Center and chief quality officer at Piedmont Heart Institute in Atlanta, Georgia, where he also serves as chair of the Cardiovascular Governance Center at Piedmont Health. He has served in various roles for the Heart Rhythm Society, including president from 2018 to 2019. He has moderated and spoken throughout the world at several conferences and cardiology meetings and has authored numerous publications addressing cardiac arrhythmia and cardiovascular quality issues. In fact, Dr. Deering is currently the chair of the Quality Improvement Committee of HRS. And finally, Dr. Kathleen Kenney is a primary care physician with a special interest in both women's health and cardiology. She is presently on the teaching faculty and a key member of this group today. She is at Stanford University and is a clinical associate professor of medicine and is the recipient of many teaching awards and other prestigious honors. She is a fellow of the American College of Physicians and co-director of Stanford Primary Care's CME program. So we'll have the three talks in the webinar today, followed by the Q&A and discussion. So you can enter your questions at any time, but we're going to hold the questions to the discussion period. You can use that Q&A function on the screen. And without further ado, I'm going to go ahead and turn this over to Dr. Saunders to give us the first talk on really what we need to know about atrial fibrillation mechanism, risk factors, and screening. Thank you, Andrea. Let's see. Okay. Thank you for the invitation to participate in this session. We've gone through my disclosures. So I want to focus on the mechanisms of atrial fibrillation. And very early on, we've learned that cardiac disease, as shown in the four corners of this figure, have an important role in contributing to the development of atrial fibrillation. These change the atrial structure. They change the electrical properties. They affect the autonomic nerves and iron channels, all of which gives rise to triggers, which initiate atrial fibrillation, but also alter the substrate of the atrial myocardium to give rise to atrial fibrillation. Now, once atrial fibrillation occurs, it can then feed back on itself to self-propagate itself by altering these same mechanisms. Now, we know that this cardiac disease is kind of well established. We know about heart failure. We know about valvular disease and also coronary artery disease that contribute to getting atrial fibrillation. We know there are risk factors that are frequently associated with this. Hypertension, the highest attributable risk for atrial fibrillation in our community, and diabetes. We also recognize that this is a disease that occurs as individuals get older. There's significant data on alcohol excess, particularly in terms of binge drinking. We've got well-established guidelines there, but we're recognizing also that habitual regular levels of alcohol use can lead to the substrate for atrial fibrillation. Probably importantly also, we're recognizing in the current community that we're seeing newer factors, obesity, physical inactivity, sleep apnea, a variety of forms of early hypertension, and also genetic factors that contribute to atrial fibrillation. Some of these factors are becoming more important, and I'm going to show you some of the data related to that. Here's some recent work in relation to alcohol. What we see is that perhaps in terms of incident atrial fibrillation, up to seven drinks a week seems to be favorable, but then you have an exponential increase in your incident atrial fibrillation with greater consumptions of alcohol, and there may be some mild differences between the type of alcohol that's consumed. In terms of physical activity, we see that as someone's cardiorespiratory fitness improves, so does that there's a decrease in the incidence of AF, and so it highlights the importance of avoiding a sedentary lifestyle, and for us as healthcare practitioners to promote increased physical activity. We've got a large amount of data in terms of obesity now, and obesity is important not only because it's associated with a number of conditions that are known to cause atrial fibrillation, but they in itself can cause injury to the heart, mechanical effects, inflammation also due to adipose tissue itself. Importantly, these result in significant clinical impacts to our patients. We know there's a greater incidence of atrial fibrillation. We know that there's a greater incidence of post-operative atrial fibrillation, and we also know that it curtails our efforts to try and maintain sinus rhythm, and so it's important for us to focus on these risk factors and whether we can manage these to try and improve things. Now, what do these risk factors actually do, and I want to take you through one of our studies, which is really looking at taking sheep, feeding them, making them overweight, and then obese, and quite dramatically, what we see is an increase in atrial fibrosis. This is picroserous red staining. When you can see in the obese atria, there is significantly greater amount of fibrous tissue that's formed. What's also unique in this model is these fat cells on the outside of the pericardial region invades into the myocardium. Now, these sort of structural changes alters the conduction properties of the atria, and not surprisingly, as the animal becomes overweight, there's more atrial fibrillation that occurs, and so this is sort of what's happening at a cellular level in terms of the atrial structure. Now, the exact mechanisms at a cellular level may be slightly different. In high blood pressure, for example, it may be that we're dealing with greater amount of fibrosis. In obesity, there may be a greater amount of adipose tissue, but what we've seen uniformly in the phenotype getting atrial fibrillation is a loss of muscle, an increase in atrial scar, an increase in atrial size, variable degrees of fat infiltration, and conduction abnormalities that result from this that give rise to atrial fibrillation. Now, so what we have learned is that in atrial fibrillation, you have initial episodes, they get more frequent, they get longer, and then they become persistent in a large number of patients. Now, what we know is there are a number of risk factors that can contribute to this, and in red here, I've shown the gradual increase in the substrate abnormalities that are seen that promote a greater persistence of arrhythmia, and there are a number of pathways that have now been identified. Now, importantly, we've seen treating these risk factors and emerging some upstream therapies for the pathways, which may actually reduce the substrate that's seen, and we've seen an improvement in the burden of arrhythmia with a change in the disease course itself, and this is important in terms of addressing the patients that we have in front of us. Now, here's a nice depiction of this. So on the top, we see paroxysm YF going to persistent and then permanent atrial fibrillation. Early on, we're dealing with the triggers of atrial fibrillation. These frequently burst from the pulmonary veins to maintain atrial fibrillation. As we traverse this time course, we start to see the importance of the substrate and more permanent arrhythmia. Now, the substrate can be divided into those that are non-modifiable, age and genetic related. The modifiable ones that I've been talking about, things that we can do something about. Now, I want to introduce this new thing, which is that AF itself contributes to the substrate, and we're starting to see early evidence that treating atrial fibrillation early may actually alter some of this substrate as well and alter therapies for patients. This is the East AF Net study. They took a large group of patients, randomized them to either rhythm control or to standard of care. And although rhythm control was done with ablation in some people, but antiarrhythmic drugs in others, what they were able to show is a dramatic change in heart endpoints, particularly a reduction in cardiovascular death, stroke, hospitalization for heart failure, and also hospitalization for acute coronary syndromes. This has changed our focus and suggested that we need to focus more on maintaining rhythm in this population also. More recently, Jason Andrade and the early AF investigators have presented data on ablation early compared to antiarrhythmic drugs. And what they were able to show is that when they followed these patients for three years, there was less often that a patient progressed to persistent forms of atrial fibrillation if they were ablated early compared to if they were managed with antiarrhythmic drugs. And so, again, showing us a focus that perhaps that element of the substrate we may be able to eliminate by treating atrial fibrillation early. Now, this is what I've talked about so far is the tip of the iceberg in terms of clinical atrial fibrillation that we're dealing with. As we start to see consumer products that monitor rhythm, whether that be armbands, watches, we're starting to see an earlier phase of the disease where we're getting information from patients directly. We're also using more in our clinics, whether it's patch technology, whether it's implantable loop recorders, whether it's handheld devices. We're using more of these in terms of recognizing and monitoring our patients. And while this has been a useful tool in extending our clinics, it also comes with an increased workload and some new definitions of what we need to be dealing with in terms of continuous monitoring. Thankfully, there have been some randomized studies that have come out more recently. I want to highlight just two of them. This is the loop study, which looked at implanting loop recorders in individuals who are high risk of thromboembolic events. It was an uneven split, more patients were in the control group than in the loop recorder group. They detected three times as much atrial fibrillation as a result of having a loop recorder. And they defined atrial fibrillation as more than six minutes. And therefore, they anticoagulated much, much more patients. But surprisingly, they did not find a difference in stroke or systemic embolization. And it tells us that we don't fully understand what we need to do when we're screening patients in this format of what to do. And there's much more to learn. Similarly, the stroke stop study really looked at really high risk patients. This was in Sweden. They used a handheld device and used 30 seconds of atrial fibrillation. You can see the very large numbers of patients that were recruited in this study. And again, in terms of the primary endpoints shown in the first graph, which is a composite, there was no difference. And in terms of the endpoint of ischemic stroke, shown in the second graph, there was no difference. And so here, using 30 seconds of AF as the guide. We have much to learn in this area. There are a number of unanswered questions. Who should be screened? And perhaps we think it should be a person at risk of thromboembolic event. But what's the optimal method of screening? And how much AF is important before we start to anticoagulate? There is a move in our field, at least, to look at AF burden and to start to evolve some strategies on how much AF is needed before symptoms occur, stroke occurs, whether there's future AF and also for heart failure. But one of the things we can do is to manage the upstream factors if we identify atrial fibrillation early. And I want to leave you with this last slide, which is a schema that we've introduced into the literature this year, which is to say, look at the patient from their head to their toe, identifying the reversible factors. This is heart failure, exercise, arterial hypertension, diabetes, tobacco smoking, obesity, ethanol, and also sleep apnea. And I put here what would help in terms of incident atrial fibrillation and also the guides for what we do in a person who already has atrial fibrillation. With that, I'd like to close. Thank you for your attention. That was terrific. Thank you so much, Dr. Sanders. And I'm going to turn this over now to our second speaker, Dr. Hendricks, who will talk about what to do with a patient with atrial fibrillation, but talking more about acute management. Yeah, thank you so much, Andrea. Atrial fibrillation is everywhere and is increasing. So wherever you work in the healthcare sector, you will see more patients approaching you with atrial fibrillation. And acute treatment of the arrhythmia is an issue that you will meet and see everywhere in healthcare. That's why I would like to share with you some perspectives on the approach to the patient with atrial fibrillation, some questions that you should address in finding the right way for acute treatment of atrial fibrillation. Okay, this is now better to see. I have nothing to disclose related to this talk. I think some of the general rules in approaching atrial fibrillation have been nicely outlined in the 2020 ESC guidelines. And one of the main messages from these guidelines is to systematically approach atrial fibrillation in the acute setting as well as in the chronic setting. And the ABC pathway that was introduced makes it really easy. ABC is so intuitive, is so easy to remember, and it gives you so good guidance to treat atrial fibrillation. A stands for anticoagulation and avoid stroke, which is important in the acute treatment. And also, and the third speaker in this webinar will refer to that, Nasir Maroosh, when it comes to chronic treatment as stroke is one of the most devastating complications of atrial fibrillation with hundreds of thousands of patients affected every year around the globe. The B stands for better symptom control. And as we have learned from Parash Sanders, it may also be turned to better outcome in patients with atrial fibrillation in the lights of the East AF data. But for the moment, I think the orientation on symptoms still is leading in guiding therapy. However, as pressure has indicated, that may change in the future. And there is increasing evidence that rhythm control may affect endpoints in patients with atrial fibrillation. So if you see a patient with atrial fibrillation, the first and most important key element is to ensure the diagnosis. And for the moment, it's still the ECG recording of atrial fibrillation that gives you a solid basis to have a diagnosis and to go into treatment of atrial fibrillation. There are a couple of questions that I consider particularly important when it comes to the acute treatment. And in general, as in many, many situations in medicine, it's easier if you know the patient who approaches you with atrial fibrillation as compared to an emergency setting where you see a patient with acute atrial fibrillation where you do not have any information about the patient history and the comorbidities which are important and comortalities of these patients. So some of the key questions that are really important to me in order to get quickly oriented and find the right path for the patients are listed on the left side. Is the first episode of atrial fibrillation or is it something that the patient has developed recurrently? So the second, third, fifth episode of atrial fibrillation, is the patient hemodynamically stable or is the patient hemodynamically unstable? That is one of the key elements that guides the acute treatment of atrial fibrillation. When it comes to the therapeutic options, and we will go through the medical and non-medical options that you have for the acute treatment of atrial fibrillation, it's important to get quickly oriented as good as one can in an acute situation whether or not there is known structural heart disease in the patient or heart failure known in the patient, whether there are signs and symptoms of acute heart failure when you see the patient with atrial fibrillation. I've already mentioned the key element of stroke prevention in patients with atrial fibrillation and it's important to assess the risk factors for stroke and also take a quick look on the risk factors for bleeding. So we will go through a case with the first episode of atrial fibrillation who is hemodynamically stable but symptomatic. The patient is a male patient, he's not known for having structural heart disease but he knows that he has hypertension and then the risk factors for stroke can be nicely assessed using the CHA2DS2-VASc score. The CHA2DS2-VASc score is not optimal for stroke risk prediction but for the time being it's the best that we currently have in the same accounts for for the HES blood. If you prioritize the two elements, the stroke risk and the bleeding risk, it's good to have the key focus on the stroke risks first and not over emphasize on bleeding risks. One of the innovations that we introduced with the 2020 guidelines is the atrial fibrillation characterization to get a quick, better picture on where the patient stands with atrial fibrillation and the 4S characterization sums up on four different dimensions of atrial fibrillation. It includes the stroke risk, which can be measured by the CHAT score, the symptom severity, the ERAS symptom score can be used. The burden of atrial fibrillation perspective-wise plays a key role, not so much in the accurate situation, but for finding the best chronic path of the patient with atrial fibrillation. It's an important element and last not least for the chronic management of patients with atrial fibrillation, the substrate severity. Press Sanders has nicely outlawed the role of the substrate for patients with atrial fibrillation and the importance of the substrate and the modulating factors for the substrate. Nassir will give you the details on stroke prevention, but it's also important in the acute phase of treatment of atrial fibrillation and it is really not so complex to get access to the good therapeutic paths for the patient with respect to anticoagulation and stroke prevention. The CHAT score gives us a clear guidance there and for most of the patients with factors that do not have a very, very high bleeding risk, introduction of oral anticoagulation, preferably with NOACs, may be considered or should be considered also in the acute treatment of patients with with atrial fibrillation. How to introduce the right treatment opportunity in patients in the light of the symptoms of the patients, the structural heart disease, the hemodynamic situation of the patient. The first element in the acute treatment of patients with atrial fibrillation has been mentioned already, stroke prevention, when atrial fibrillation occurs in the patient is not protected by an established oral anticoagulation and then the key is symptom control, improvement of symptoms and then attach that to the right path of introducing chronic and long-term treatment of this patient. So in the acute setting of atrial fibrillation, the decision on rhythm or rate control as the initial path is important and I've already addressed the question of hemodynamic stability or instability in hemodynamic, instable patients. Cardioversion, to me, is the key option to bring the patient out of a potentially dangerous situation. If the patient is stable, then there is a question whether or not additional rate control to pre-existing drug therapy may be necessary. In most patients or many patients, this is not the case. However, if the atrial fibrillation is conducted with high rates to the ventricles, additional rate control may be necessary to be introduced. I always consider pretty early in the decision-making process of the patient whether or not the patient fulfills these criteria. To find the direction for the patient, is that a patient that may preferably profit from a rhythm control strategy and I introduce and include that into my initial decision-making of the acute treatment of the patient. Then, of course, it's the question of patient desires and patient preferences for acute and chronic management. In many, many patients, there is no really emergency situation with the patient and you have the freedom to consult with the patient and to include that into the decision-making process what to do acutely and chronically in these patients with atrial fibrillation. What are the options for acute rate control? There are two types of drugs that sets the screen as a first-line treatment. That's IV beta-blockers and that's calcium antagonists. Depending on the situation where the patient is in, IV treatment may be preferable as long as the patient is hemodynamically stable. Whether you prefer beta-blockers or calcium antagonists, the non-dehydropuridine class of calcium antagonists depends on the comorbidities of the patient and we'll take a look to the guidelines in a minute from now to get some guidance in the decision-making process. Second-line drugs are digitalis and amiodarone in rare instances for rate control, not for rhythm control, for rate control in these patients. If a single drug is not effective, combinations of drugs may become rate control. This has been taken from the guidelines and that summarizes the settings in the upper part of the slide for acute treatment. Consider the comorbidities of the patient. If patients have non or hypertension or half-path, beta-blockers and calcium antagonists can be chosen. In HFRAF, there is a preference for beta-blockers. Also, in the acute treatment, as long as the patient is not severely decompensated. If there's pulmonary disease, the calcium antagonists should be preferred. And as I've outlined before, if you are not successful with a single type of drug application, combinations of drugs are recommended in order to achieve a good rate control. What are the options for acute rhythm control? I already shared with you that in hemodynamically instable situations, my preference clearly is cardioversion, as long as a patient is in a setting where cardioversion can be performed. So, if you have the patient outside a medical environment, bring the patient into the medical environment and treat the patient with electrical cardioversion. I personally prefer electrical cardioversion in any emergency setting over any type of pharmacological cardioversions, because it's fast and it's always, almost always, effective. Pharmacological cardioversion can be approached when the patient is relatively stable, preferably with class one enterythmic drugs, as long as there are no anticoagulations for the use of these drugs. When it comes to cardioversion, a quick look to the guidelines and the flowchart, it gives good orientation how the cardioversion in patients with acute onset of atrial fibrillation can be performed. And we have good data, again, from the people of the race clinical trials that have investigated whether an early or delayed cardioversion in stable patients with acute onset of atrial fibrillation can be applied. And we will take a look to the results that guide this setting in a minute. One thing is important when atrial fibrillation, the onset of atrial fibrillation, has a duration of more than 48 hours, then the considerably elevated stroke risk in patients, according to the Charles Vass score, must be taken into consideration. And the rhythm control and cardioversion may be delayed until TEE has been performed in order to exclude left atrial thrombi, not to put the patient on an unacceptable risk for thromboembolic complications. I think that is particularly important that the race trial shared with us the outcome of the two cardioversion strategies, early versus delayed cardioversion in patients with recent onset of atrial fibrillation. And these are the key data from that trial. The primary endpoint of the trial was sinus rhythm at four weeks in patients with acute and recent onset of atrial fibrillation. And they compared an immediate cardioversion strategy within hours to a cardioversion strategy, which was delayed for one or two days after the onset of atrial fibrillation, again, as long as the patient is hemodynamically stable and the stroke risk has been appropriately addressed. And it's interesting to see, and please focus on the lower right or the B panel of this slide, that the spontaneous cardioversion rate in the patients that were in the delayed cardioversion group was significantly higher as compared to the early cardioversion group and approaches almost 70%. So it gives benefit to the patient, it benefits to the physicians, it reduces the utilization of infrastructure for cardioversion, and the outcome sinus rhythm at six weeks is comparable in both groups. So my preference in stable patients really is the path of delayed cardioversion. Clarify the issue of stroke prevention, apply a beta blocker if necessary to reduce ventricular rate, and then wait and see until the patient may spontaneously convert into sinus rhythm once rhythm control is the goal of treatment in this acute phase. So these are some of the bullet points that I would like to summarize. Follow the ABC pathway. ABC has proven beneficial effects on main outcome. It's easy to follow and it can be applied in acute as well as in chronic settings. Stroke risk is substantial in many patients with atrial fibrillation. This has to be considered before we go into acute and chronic treatment. Also take a look to bleeding risks to have checked that you don't run in a situation where a patient with substantial bleeding risks may have contraindications to oral anticoagulation. For acute rate control, beta blockers and calcium antagonists from the non-deuteropyridine group should be taken. My preference, and almost my personal preference, as long as there are no contraindications, is a beta blocker of the calcium antagonists. But I have to confess that the clinical data given preference to either drugs are not so strong for beta blockers or for calcium antagonists. Electrical cardioversion for acute rhythm control is my preference for over medical anterithmic drug cardioversion as it is highly effective and it is faster than the application of anterithmic drugs and for me in my personal perspective also the safer way to proceed and to go. Consider early or delayed cardioversion. I have a preference to delayed cardioversion as long as the patient is stable because it may be more comfortable for the patient and also for the environment. And then last but not least, share the options for rhythm control or rate control with the patient in order to put the patient from the acute treatment to the chronic path that serves the desires and the expectations of the patients best. Thank you very much for your attention. Well, thank you. Thank you so much, Dr. Hendricks. That was fabulous and I'd like to move on to our last speaker is Dr. Maroche, who will talk about more of the diagnostics and stroke prevention in patients with atrial fibrillation. And then we'll have the panel discussion. Feel free to put in some questions in the Q&A part of this. Hi, everybody. My great honor to be here with you today. And after you heard the two top five masters in afib in the world, Hendricks and Sanders, it's very hard to add anything to the two great lectures from diagnostics to prevention and guidelines. But I want to actually, while they were talking, I started because we have a great panel here together. I cut my slides a little bit so we can allow some time. So I'm going to be just summarizing in terms of diagnostic, you know, Andrea and Thomas asked me to briefly talk about diagnostic and stroke prevention. This is a slide I brought with me today. This is a recent guidelines ESC where 30 seconds is only needed to diagnose atrial fibrillation. And I keep this in mind today with the new tools we have. I think if you see any irregularity, afib should be considered and it should be alarmed with the tools available. But that's a guidelines-based diagnostics, at least 30 seconds in a 12-lead. Now, asymptomatic afib, and that's important. This slide is very important. It's mentioned in the guidelines that Gerd put together. We detect this a lot. With the tools we have, patients come to us without any symptoms. I put the screen box up there, what symptoms means. Probably if you dig deeper, talking to your patient, you find most really some symptoms associated with afib. But nevertheless, today's and now, we have a patient of an ICD, pacemaker, implantable loop, a wristband, or a Fitbit, or Apple Watch, or Samsung, and so on. And you diagnose any kind of atrial fibrillation without the symptoms associated with that. We consider this as asymptomatic afib. And obviously, there were the box of Pandora of diagnostic. I'm looking at the reasons, and monitoring goes on, but that's the definition of asymptomatic atrial fibrillation. That's why I call it wearable afib. I think what everybody listening to me, especially in primary care today, will see two or three patients a week in their clinics who show up with alarm from their devices, either they have afib. Now we have this in Apple Watch, for example, FDA-approved detection, a LifeCore, a Samsung, Fitbit, on and on, using PPG, simple PPG waveforms to detect atrial fibrillation. So that's something we need to deal with as physicians in the community. And then we had two days ago a big convention in Park City just talking about that. I think a couple of people in the panel here discussed three hours trying to figure out what to do with these patients. But that's something we cannot neglect, you and me. We need to take this seriously, not only what to do with these patients, but also what they mean in terms of outcome, in terms of patient outcome, long term and short. Is this the early detection? Is this a sign of something else going on? We're learning as we go, but that's something you're going to see in your clinics day on and day out, and take them seriously. So when we see a patient with atrial fibrillation without diagnostics, you heard a beautiful review, beautiful review from Gerd, who, by the way, wrote the guidelines that you heard. It's not like he's showing people's data, but he saw this as the 4A concept and so on. Symptoms, quality of life, comorbidities, Prash talked in details about the comorbidities, and by the way, he is the guy who opened our eyes in this whole lifestyle, comorbidities as part of our treatment options and guideline changing concept that he put together. That's something we need to assess, you know, work on those, and you heard a lot about this, and from Gerd as well. The AFib burden is, for me, as a new kid on the block, and we agree, all of us, we've seen this recently in the last couple of years, that's what we're looking for, because of the tools we have today to assess the AFib burden. We didn't have them before. We had the 12-week ECG, and that's it. You go to the clinic, they have your ECG written. Now my daughter, 10 years old, have an Apple watch, shows it to me once a week. They're, Daddy, I don't have AFib. That's what we're dealing with, and that's, she's recording all the time. So we have a burden data, and we can assess them. We have information on this, and last but not least, substrate. Now we have imaging tools. We have a way to assess this. So when we diagnose atrial fibrillation, these three boxes have to be fulfilled. You heard a lot about this, you know, the symptom score, and how level of symptoms. I'm going to spend time on this. You heard the whole lecture about this from Prash, lifestyle modification, and we can't finish repeating this. Again, lifestyle modification, sleep apnea, losing weight. It's, I'll leave it up to you, especially me living here in New Orleans, what the alcohol consumption means, but he showed you some data on this. AFib burden, that's a summary slide, very important slide. I'd like to show this. We know that AFib burden, the more AFib we have, the higher the risk for mortality and outcomes and strokes, and adjusted, unadjusted. Child vascular, no child vascular. This is done, this is known. Your patient comes with more AFib. We showed this the first time with association mortality and hospitalization in CALSAL-AF. They tried to look at heart failure population with defibrillators. So we showed that if you lower the burden, the less than 50% in the patient population with an ablation procedure in this case, the people will live longer and have less chance going to the hospital. So burden is becoming, has been, but now in prospective fashion, we're showing this, it's important. And now we have something called the SMIR that we talked about this recently. This is a data from the D-CAF2 trial, where we took 800,000 sets of ECGs. And daily ECG means a lot. If you put them in this equation of your patient time in AFib in a 32nd day over a month, and what does it mean? And why this is important, we showed that this correlates very well with long-term outcomes. And that's something on your wrist. Every one of your patients who come to see you in your primary care clinic, your EP clinic, cardiology clinic, can apply the SMIR, the rule, which is some semi, or I call it burden light assessment, because it's not continuous, obviously, but the daily recording means a lot. The patient has this on their wrist. Substrate, you heard this from Gerd, and he was, I think, instrumental in bringing this through his guidelines to talk about substrate. All of us, we deal with the atria to deal with atrial fibrillation. Until now, we look at the 12-lead ECG or STRIP to deal with this disease or maybe patient symptoms. But that imaging tools that see here in the middle, all of those can assess the structure, function, shape of the atrium where AFib is harbored. And we're treating that disease, we have to consider what's the home of atrial fibrillation to make it simpler. And we've been talking a lot of work on MRI scan. And why this is important, when we predict stroke today, we're using CHAD-VASc stroke, and everybody on this call and you listening, you know that this AOC is very, very primitive, very low, 0.68, the best one we use, 0.68, 0.67. So you can tell from this here, even patients with CHAD-VASc 1 and 2, we still have significant risk of stroke per year. So we're using a score, which is mediocre in my opinion, that's why we need more. The burden is a way to look at the patient with AFib. But also, we know a lot now, not only from our group and others around the world, that this atrial imaging using looking at myopathy, by the way, this is a historic picture looking at the myopathy in the atrium, the blue is a lot of fibrosis and collagen in the atrium, red is very healthy tissue, but which is the more fibrosis you have, the higher risk of stroke, we've shown this. The same thing applies with the function and the shape. Strain, you have a strain, you have an echocardiogram, all these major companies today, GE, Philips, and Siemens, they offer the strain imaging software. Within a simple echocardiogram, you can click, ask your technician to add it. And this tells you a lot about the atrial function, and the shape of your appendage, which all of those has been shown to predict strokes, more so than simple stroke ACG. And that's what the guidelines show us, we need to look at that. This myopathy has been shown, for example, in Denimite, from Dr. Betts and his group, that if you look at your atrial myopathy, and put links in your patient, you will see more AFib, the higher the myopathy burden, the higher the fibrosis burden in MR, that's important. So when you see this in your patient as a screening test, as an imaging screening tool, we need to be alarmed for the incidence of AFib, that's an important study published in JAG in 2020, I'm not sure it doesn't take a lot of press. We also showed, this is Dr. King's work, that the higher the amount of myopathy, the higher the incidence of stroke in your patients with atrial fibrillation. Not only the CHAD-VASc, which in this case was corrected for, rather the amount of myopathy. If you have more than 25% of your atrium scarred or diseased, then your chance of stroke is way high. Dr. Akuma, University of Washington in Seattle, corrected even patients having strokes with myopathy, in patients with AFib and non-AFib, and showed that this is a very powerful predictor. These patients, independent of their arrhythmia, they have a higher risk of stroke. You put patients who have embolic strokes and look at their atrium. So that's a source of stroke, a substrate that got presented in the guidelines, that we should start taking it more seriously, especially with us getting in the atrium and doing more and more ablation, extensive ablation, don't forget that. How to manage this? Simply, you heard from Greg, extensive lecture on this. NOACs took over from Warfarin, based on these multiple trials, the Aristotle, the Rocket, and the Engage. All of them shows either non-inferiority or superiority as Apexaban, for example. And now the guidelines are straightforward, 1A, 1A, NOAC versus Warfarin. And I'll spend time on this, but this is a recent paper, and it's under debate, but showed striking data that we can neglect. Around 20,000 patients presented by Dr. Khatib and her team, multiple investigators looked at the Medicare database and associated the use of left atrial occlusion devices for the appendage for mortality benefit in our patient population. This is a lot of trials going on today to compare this to blood thinners, but something to keep in mind as we go, we have tools now to really be superior, to elevate the breathing risk, not only stroke risk, our patient, and using a tool like this. I wanted to bring this with me before I give it up to the panel to discuss practically my simple take home message here, 30 seconds rule, maybe diagnostic, define AFib, or maybe less than that, but go deeper, look at the burden when you treat your patient, AFib alone, yes or no is not enough. AFib, not only the arrhythmia itself, there's more to this, look on the atrium, image it, not only in a patient AFib, but without atrial fibrillation and high risk for arrhythmia or stroke, you should look at the atria and hopefully try to treat them or monitor them. Thank you, guys. That was great. Thank you. Thank you so much, Nasir. That was terrific. I want to start the discussion with the group, and I want to actually, as questions are coming in, I want to start out with Dr. Kenny, because I think going more up to where we're not as cardiologists or EP docs, we're certainly not seeing people primarily. You're seeing probably the vast majority coming into the office and maybe with, as Dr. Mosh described, as they're coming in with their watch and they're coming in with a rhythm strip and it says AFib, kind of curious, what should we be doing with those patients? What do you do with those patients? I suspect you're not sending every one of them to an EP doc. How do you manage? What does the patient ask? What do you talk to them about? Yeah. So, great. Thank you for all the talks. These have been really educational and interesting for me. I do get a lot of patients that come in with Apple Watch readings. I wouldn't say three times a week, which was purported, but I probably get at least one every week or two. So I think when you look at the Apple Watch trial, I think when they found AFib in about half a percent in the study group, it was like a three to six-month monitoring period, but I think only one-third ended up having AFib on the subsequent Zyopatch equivalent monitoring. So maybe it's because it's sporadic, but maybe also there's some false reading on the Apple Watch. And I'm not just singling out that one device, but that's what I'm most familiar with in my panel of patients. So I think what I do when I see these kinds of patients is I order a Zyopatch, which is again, the maker that we use for a 14-day monitor to see if we can then capture the AFib. Again, we know that AFib can be quite sporadic, so it may be that some of these folks have legitimate AFib on their Apple Watch and we're not capturing it in 14 days. And so I think that that's always an interesting question is, are we missing it and is it clinically significant? I think that the old teaching was that you needed to be in AFib for 48 hours before you would have a stroke. I don't know if that's sort of changing over time. Now we've got this interesting new data that the atrial fibrosis itself may be a big factor, and then also the burden. So I think what I'm doing is the Zyopatch. I don't know if that's sufficient based on what I've heard today. Yeah. Yeah. Dr. Danicki, please. Yeah. No, I think this is a very, very important thing that we're discussing. So what I do if I see a patient with AF on a wearable, of course, I first of all look at the rhythm strip itself. So if you have an EKG, that is very, very important to look at it. Like in the Apple watch where you have a single lead EKG and this can be diagnostic for atrial fibrillation. The next thing I would do is actually, I would use this as an alert sign to look for any cardiac abnormalities. So just do an echo, do blood pressure measurements, just to make sure that we're not dealing with a secondary phenomenon and actually we're having some thought of cardiac abnormalities that would warrant further diagnostic. And I think that's, when you look at the data that is out there, we don't have a good indication for using these wearable detected AF episodes as an indication to start any sufficient treatment for AF. But I think it is a starting point to look deeply into these patients and see if there is any structural abnormalities. I'm not sure how the rest does it. I can weigh in there a little bit, and Drea too. You know, Thomas, I do something very, very similar to that. I first of all want to make sure I've got the diagnosis correct. I mean, these devices are very good, but they're not perfectly accurate, nor are we. And I've seen many times how people have gotten a diagnosis of atrial fibrillation that is not correct. So I think my first thing is to make sure the diagnosis is correct. I, like you, Thomas, then look for substrate abnormalities because it's usually either congenital with risk factors that develop as one ages, or there's an intrinsic underlying substrate that leads to the atrial fibrillation. So I try to do that first. The third, secondly, the third thing that I do is I also use this as a wake-up call. Most of the time when subclinical AF is detected, it's short in duration, and the symptoms are relatively minimal. But if they are asymptomatic and it's short in duration, I look for modifying risk factors. I engage my primary care physician. Is their hypertension controlled? Their diabetes controlled? Have they been worked up for sleep apnea? And if those things are operative, then I usually, as part of a team, like to engage them to make sure that those components are addressed effectively. So those are the three things that I do up front. The fourth thing that I really do is, although it's usually asymptomatic, sometimes that's not always the case. I mean, the patient might have the classic racing of my heartbeat, but sometimes if they have a fair amount of AFib and they have exercise intolerance that parallels that, that could be symptomatic. So I try to have them record when they're having symptoms. So those are kind of the four things that I do, but I still think we don't know what to do in terms of when to anticoagulate and when to get more aggressive. We need more studies. Yeah, I think these are all great points. So look further, first of all, confirm the diagnosis, look further, try to find out, you know, make sure it really is AFib and to see how much it is, and then look for modifying the risk factors that, you know, it really, Australia and Dr. Saunders, you've done such an incredible job, better than we've done in, certainly better than the U.S. and I suspect better than many other countries. I want to address, actually, there's two questions that kind of in the Q and A section there that are kind of overlapping and people talked about symptoms. People talked about, you know, maybe what we might talk about subclinical AFib and the million dollar question is, we talked about AFib burden. A couple of the speakers did, you know, what is that amount of AFib that we have to worry about? We're talking about anticoagulation. How much do we need to worry about to anticoagulate chronically? And then I think, you know, at least one of the questions I'm getting from, you know, the ER docs a lot too is, do I believe that they had symptoms for just 24 hours? Am I okay to cardiovert without looking further? So maybe different people could address different parts of that question. Yeah. Please. Let me, let me, let me take this, this question, Andrea. So if we have today with the, with the, with the initiation of NOAC into our clinics and our life a couple of years ago, I think it's the, the, the, the road for the patient to see us in the EP clinics rather than be admitted in ICUs and TEs changed a lot. Does the patient, they call me from the ER, patients have AFib. Is he hypotensive? No. Give him NOAC, see him in a clinic tomorrow, unless he's symptomatic, highly symptomatic. Rate control of 24 hours. I think that changed a lot. And I hope in the past you used to cover him with the, you know, low microweight heparin and give him subcutaneous care two days until he comes in or admit him to a floor, do TE and cardiovert him. I'm, I'm the fan of seeing them in the clinic, especially now with the early intervention becoming a very hot topic for us, all of us here realizing early intervention. So we have to see them in the clinic and prepare them for either ablation or the group of people doesn't apply a major myopathy, another reason for, for, for exclude them out. But I'm realizing I'm, I'm real, I'm using the NOACs through the ER a lot, sending patient home same day, I feel they're protected and then bring him back the same day for further management and take it step by step in terms of under the ER setting. And the reason I'm mentioning this because our system in the US, maybe the others watching us from outside, that's a big deal. The time in the ER is a big challenge for us in America. And then we need to take this as seriously. And that's why I mentioned the use of NOACs to save the system hassle and keep patients safe first of all, send them home, see him next day in the clinic. I really would like to hear Tom Dearing input on this, how he applied this patient who comes to not hypertensive need to be cardioverted. If he will admit him or just give him a NOACs team in the clinic next day for further diagnostics and testing and processing. No heart failure is stable otherwise, Tom. When a patient comes to the ER, my general perspective is that we should try to expedite excellently using that term. So basically I feel that if they can be cardioverted because I'm confident that their atrial fibrillation has been short in duration, and I'm usually not, then we will do that and we will expedite their discharge. Conversely, if we cannot ensure that, we can either get aggressive with the imaging CT or TEE to find that out and then aggressively cardiovert them and discharge them. Or we put them on a drug that will lower their rates sufficiently and have them seen in our APP, AFib clinic the very next day. So we try to get them out of the ER, ERs right now are overwhelmed, overworked, the hospitals are as well. So we try to keep the patients out of the hospital, leaving that only for those who are profoundly symptomatic and need to be there. Now, having said that, like you said earlier on in your presentation, Gerd, if I'm not sure about the duration of atrial fibrillation, and even for the patients who's profoundly symptomatic, I went into it on 2.37 a.m., you know, on a Saturday night, I'm not confident. I figure if we cardiovert without knowing how long, without imaging to determine what it is or an appropriate period of anticoagulation, we're potentially doing them a disservice. So if I can control rate and I can discharge them, I will send them home unless I'm absolutely sure because they're monitoring themselves every day or they have an implantable device or a wearable that they check every hour. I don't know, do you do it similarly or differently, Gerd? You wrote the guidelines on all this. I do it absolutely in the same way. I fully agree with everything that has been said. We have to make sure that the emergency units are not flooded with atrial fibrillation patients because it's not a good place for them, usually, outside an emergency situation. So the strategy, take a look to the patient, consider stroke risk, give a beta blocker, either acutely IV or calcium antagonist, give it as an oral drug, and send the patient home for 24, 48 hours and then see what you can do in the atrial fibrillation treatment unit outside the emergency settlement. I think that the evidence is there that this is good quality for the patient and it's a safe mode of treatment. When the patient then comes back, I am, based on the data that Prash and Asir have shared with us, I'm moving more and more to a consideration of rhythm control strategy. And my preference in that field is ablation based on the data, the early AF, stop AF trial and everything we've seen. I'm still hesitating with the question whether we need an east AF ablation trial in order to see whether or not there may be more, maybe even less benefit as compared to anthrax drugs. I think it would be reasonable to do that. We cannot just transfer the east data with 80%, 90% drug treatment to the ablation field. And I'm glad you brought that up. Actually, we're going to have a whole webinar talking about the early treatment and benefits and preventing this reverse remodeling. And I appreciate that comment. I have two questions. One is, well, actually it could either be, so Dr. Hendricks kind of knows all this because he wrote the guidelines and led the guidelines. Or Dr. Danicki, maybe you could start with the one question related to subclinical AFib and burden. Do we have an answer? Like how much do we need? Does it matter if there's symptoms? What do we need in terms of anticoagulation to kind of institute that in the chronic situation, not just in the ER? Either, yeah, either Dr. Danicki. I think that the relation of stroke risk and atrial fibrillation burden is one of the most complex questions that we need to address in the years to come. This is very complex to understand as well as the other complex thing is sudden cardiac death. But we are talking about burden of atrial fibrillation and stroke risk. I believe that the importance of burden should be different for patients with different comorbidities. I believe that we will not be able to define a generally applicable time window for patients that are good for patients if we grade them with CHATS-WASC-2 and CHATS-WASC-5 or 6. I believe that the duration of atrial fibrillation in higher CHATS-WASC, higher substrate patients as Nassir shared with us, must be handled different as compared to patients with a low substrate intensity and with low comorbidities. Thomas? Yeah, I get it. I completely agree. I think it's a mixture of AF burden, CHATS-WASC score, other risk factors, and all of this needs to put into an equation. So that's really a major task. And we're now just getting ready to measure AF burden adequately. So we're still on the verge of learning, I think, and I think we need to wait a couple of years until we have the answers for that. But very good question. Yeah, totally agree. We are still learning. I think that's a great thing about our field is that we're just, you know, have so much to learn. And as we learn more, we realize how much more we have to learn there. I love this other question. And I have to ask, you know, Prash, this is in your realm. And I think you've been one of the few people I know who've really done this very successfully in putting these collaborative processes together. We're working on this in the U.S. in a very formal manner. Compass, this whole program that we're doing here today, you know, how far away are we or how did you do it? I should say you're not so far away because you've been doing it between, you know, this integrated care approach to treatment of atrial fibrillation, plus the things you talked about. I mean, some of the hardest things, you know, to do is some of these risk factor modifications, you know, how did you do it basically? Yeah, I mean, I think this is a important question that's been raised because we're busy and we need kind of nurse practitioners to be working with us to be able to deliver a large component of this. And that's where we've kind of introduced this whole integrated care, because I think similar to many health sides of things, we don't get adequate funding to be able to achieve these targets. And so by combining this where we have a nurse running parallel with our clinics and then we pop in for the last part of that consultation. So they might have spent an hour with the allied health person going through each risk factor. And then we really take care of the AF component for about the 15 minute consultation. And we kind of absorb the cost of doing that. So we've kind of found a way to work around the system in getting that. But this is clearly something that healthcare systems have to evolve because there's no way we're able to achieve all that. And I think even as a primary care physician, it'll be almost impossible to go through all of these factors within the time frames that have been allocated in primary care. And so that's why we've taken it on in a nursing clinic to be able to do that. And it works very, very well. And initially, I had reservations as to whether it would have the same results. It has absolutely the same results as us having a physician undertaking those clinics. So I think it's where we need to move. And hopefully, programs like this will kind of push the needle a little bit further to enable funding for this kind of clinics. Great. I know we need our primary care doctors involved in these things, too, because it's really a team approach. This is really a systemic disease, really, when you think about it. I love this other question here, too. And I think Dr. Maroche, although everyone's introduction in this group was pretty modest compared to what everyone's done. But Dr. Maroche has been involved. He was the initial chair of the Digital Health Committee when it wasn't even a committee yet. But talking about the diagnosis of AFib using patches and algorithms and devices, and so how is that whole process going? And do we need to confirm things? I mean, just if you can comment a little bit about that. First of all, before I comment, I mean, Tom and you, by the way, this whole digital health concept at HRS, it's not us. You started this. And thank you. We have to say that. Tom Deering came in and you executed. You started this for us. And now here we are some eight years later. Thank you, guys. It's a wild west, Andrea. It's a wild west, all I can say. Since Tom looked at me and said, can you do this and help us with these tools and get it together and start the first white paper, the white paper became a group of people. What's a group of people? And it became a committee. And then we tried to understand what's going on, to be honest. Since then, we're still trying to define the subclinical AFib. I put the site called Wearable AFib to guide our colleagues at primary care who calls us every day. What should I do with this 30-second strip? And I probably have three sessions this week. I'm talking just about that. And to be honest, we have to wait for the trials. We have to wait for the trials to finish and give us some more solid data. All we know now, when you see an AFib on one of your devices, and that's a question. People ask me which device I should use. People come to me. We did the survey last week. I think everybody on this call have this data, probably similar to ours. 68% of our patients in my clinic today, they come to me prepared with a digital device to measure the atrial fibrillation or the rhythm. That's unheard of. I mean, today, if you asked me this question five years ago, six years ago, it was like, what? We encourage people to buy devices. Now they have the devices. They have the rhythm with them when they come to the clinic. So what to do with this? We're trying to use platforms, softwares, all of us. Now there's tools to manage this data with the patient, communicate with them. That's a new platform of information we never had before, which is great for the patient's sake, because I really believe and feel we're preventing a lot of issues with heart failure and strokes. We're going to see this in 5, 10 years from now, when we start utilizing early detection of AFib, for example, which we never knew about before. I think there's a lot of advantage. But the question we're dealing with now as a society, as a community, working with our colleagues in primary care, is how to streamline this information? Where should they go? What to do with the next? Now we're finishing guidelines from us as a society and in Europe as well, is what to do with the wearable AFib first detection? What to do with it? And thus, we're waiting for some data. There's some primary data and some later data. For now and yet, at this moment, if I see an AFib, I have to take it seriously and to prove it otherwise. If I see 30 seconds of AFib on a strip or 10 seconds of AFib, I have to take it seriously and to prove it otherwise. I'm not sure anybody on this call would agree with, disagree with me, but if somebody come to me today and said, this is an Apple watch or Samsung watch told me 8 minutes of AFib or 10, 15 seconds, 20 seconds of AFib, I have to do a monitor. I have to put a patch, like Kathleen would do, and maybe an echo, and maybe look at the history, if I have any comorbidities, go further. If there are no comorbidities and no issues, just a finding, do a simple monitor and do an echo. If they have a diabetes, hypertension, I go deeper and stress test and all this stuff. That 10, 15 seconds on their wearable, it's triggering a positive Pandora. And I have no choices because I have no data yet. Until the data generated, that's the only option I have in my clinic today. That's great. Thank you. Thank you so much. So we are winding down and I want to just give anyone the opportunity to make any last comments, in particular, Dr. Denecke, because he really put these speakers, this wonderful group here together today. If you have some other last comments or pearls to give the audience. Well, I think my last pearl that I want to give out is thank you everyone for helping me out with this. This was a great session. And Prash said it best that seven standard drinks per week are okay. So a standard drink is one liter of beer. So cheers to everyone. Thanks a lot. Remember to claim credit for this presentation. 1.25 ACE credit is available for today's presentation. To claim your credit, please complete the session evaluation, which will be available after you've viewed the content of today's presentation. Upon completion of the evaluation, you will be able to view and download your certificate for your records. This will also appear in your transcript, which can be accessed at any time by selecting transcript from the left-hand navigation menu within HRS 365. Thank you.

acute management

diagnosis

stroke prevention

atrial fibrillation

AFib

risk factors

screening methods

early diagnosis

management

acute treatment options

patient history