Avoiding Afib Strokes: Top 10 Things to Know — Mintu Turakhia, MD, FHRS

September 10, 2015

In his talk about Avoiding Afib Strokes at the 2015 Get in Rhythm. Stay in Rhythm.TM Atrial Fibrillation Patient Conference, Dr. Mintu Turakhia of Stanford University discussed how our thinking about afib and stroke, and when to treat, has changed over the last couple of years.

Dr. Turakhia covered the Top Ten Things to Know about AF and Stroke:

  1. Determining the risk of stroke in AF, including the CHADS2 and CHA2DS2-VASc risk scoring tools
  2. How precise are stroke risk scores for people with AF
  3. Who should get stroke prevention therapy?
  4. What medicines can reduce the risk of stroke in AF?
  5. What about aspirin? Isn’t it safer?
  6. Is stroke risk affected by choosing rate control vs. rhythm control?
  7. Will ablation lower stroke risk?
  8. Ways to reduce risk of stroke without medication, including three options for left atrial appendage (LAA) exclusion
  9. Why do patients with appendage occlusion still have strokes?
  10. What the future holds

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    About Mintu Turakhia, MD, FHRS

    Dr. Turakhia is a cardiac electrophysiologist, outcomes researcher, and Assistant Professor of Medicine and of Health Research and Policy at Stanford University. He is

    Chief of Cardiac Electrophysiology at the Palo Alto VA Health Care System and is an Associate Investigator at the Center for Innovation to Implementation.

    In his clinical role, Dr. Turakhia performs complex catheter ablation (primarily for AF), device implantation, and left atrial appendage occlusion. Dr. Turakhia has an active clinical research program, with funding from AHA, VA, NIH, the medical device industry, and foundations. His research program aims to improve the treatment of heart rhythm disorders, with an emphasis on atrial fibrillation, by evaluating quality and variation of care, comparative and cost-effectiveness of therapies, and predicting outcomes such as stroke.

    Dr. Turakhia has extensive expertise in using large administrative and claims databases for this work. His other research interests include technology assessment of new device based therapies and the impact of changing health policy and reform on the delivery of arrhythmia care. Dr. Turakhia has over 70 publications and is a Fellow of the American Heart Association, American College of Cardiology, and Heart Rhythm Society.

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    Video Transcript:

    Time markings are approximate

    So, again, my goal is to be informational. It’s a lot to cover. It’s too much to cover. This is to give you an overview on how our thinking around afib and stroke, and when to treat, has changed over the last even couple of years. So, here’s what we know, and how we’ve classically thought about things. When you get that electrical chaos in the atrium, as you heard from Dr. Day, you lose coordinated mechanical activity. It doesn’t empty. You get something called stasis, which is when blood doesn’t move. What happens when blood doesn’t move? It clots.

    What happens when it clots? It leaves, and you get a stroke. We know that stroke is a major, major problem. In fact, the thing we worry about most in afib.

    [00:01:00] Because of its burden, 15% of the strokes that occur in the U.S. are AF related. If you don’t treat or don’t prevent stroke, the risk of stroke per year can be as high as 12% or 15%, even.

    It’s expensive to the healthcare system. And AF-related stroke tends to be more disabling and more morbid, and more fatal, as you’ve also heard, than non-AF-related stroke. We do know that we can make a difference by preventing these with drugs, and more recently, devices. So I did this Letterman style, but I won’t be as funny. What are the top ten things I need to know about AF and stroke? One, how do I determine my risk of stroke in afib?

    This has also changed. We used to use a score called the CHADS2 because this is the best thing we have. So the way we think about your risk of stroke in afib is that you take the risk factor shown here.

    [00:02:00] Let’s focus on the top one. Cardiac failure, hypertension, age greater than 65, diabetes, and stroke. Cardiac failure is also congestive heart failure. And you add those points up and you get a score. And what you can see here is that that risk in blue goes up as you accumulate more points.

    There’s a more recent score which has become more commonplace, which is the CHA2DS2-VASc score. It essentially adds to that risk score a couple of things, one is vascular disease, the other is two age categories. And unfortunately – not fortunately – you get one point just based on sex. So, women get one point, as long as that’s not the only risk factor.

    It’s been shown that women can have a higher risk of stroke in afib, but even that data is mired in some controversy. Nonetheless, the risk goes up gradually as those points accumulate.

    [00:03:00] Number two: How precise are these stroke risk scores for people with AF? Are they as good as we think, or are they as good as they sound? The answer is no, they are not. But unfortunately, they are the best we have.

    So this complicated graph on the left is intended to show you how well this classifies things. So this is a form of discrimination. When we think of screening tests or risk scores, we look to see how well they often can discriminate those who have stroke and those who don’t have stroke.

    The graph isn’t important. The area under the curve of those graphs is the measure of discrimination, and they are shown there. Now, if you were to just flip a coin, you automatically get 0.5, because lower than 0.5 means you’re incorrectly predicting. You’re actually doing worse.

    So flipping a coin is a 50% agreement score, and these do barely better than flipping a coin.

    [00:04:00] The way to think about this is that if you were to use very primitive risk tools, there are some patients who remain untreated because they’re thought to be “low risk” and they may actually get a stroke. There are some patients who are considered high risk, who may get a major bleeding event before they experience that stroke, or in place of stroke. So the scores, as stated, are not very good.

    One thing to just note is that even the decision around anticoagulation really has to be individualized, particularly in lower risk patients, because the data are so poor. So, whenever there’s a score we think, “Oh, this must be very precise and very scientific,” but in fact, the CHADS2 score came from the 1990s from 1,700 patients, age 65 to 95, who were sick enough to be admitted to a hospital with afib and were discharged.

    These were from seven hospitals in the south. The data was from billing sources, not from real record review.

    [00:05:00] And it was limited in followup. So, here we are taking this old score of CHADS2 and applying it to people who have 15 minutes of afib, who are otherwise healthy, who are age 40. You can’t do that. They’re apples and oranges.

    So the data was poor, and until recently, it was the best we had. The reason we were so prescriptive, perhaps to a fault, with this score, was that it was specific. It missed a lot of people who could have strokes. It wasn’t sensitive. These are terms that we use in screening tests.

    But specific means that it really could identify…so it really was able to find the patients who were definitely at high risk, and at least treat them. You missed patients who didn’t fall on the radar screen who were at risk for a stroke, but it did get the high risk patients.

    [00:06:00] A decade ago, two decades ago, warfarin, or Coumadin, was only reserved for high risk patients. We were not very good at managing it. INR lab tests were not well controlled; it’s still a problem. And on top of that, we were very bad at controlling blood pressure, and the two together would increase the risk of intracranial hemorrhage.

    So, as we got better with warfarin, and as new drugs came along, which I’ll talk about, the goal was to find something that was more sensitive, to actually find anyone who would likely get a stroke and treat them, because the benefits now started outweighing the risks. The upside of being on therapy was far better than the downside because we’ve done such a great job at getting the bleeding risk as low as we have. And I’ll talk about that.

    So the problem with the CHA2DS2-VASc score is that even so – I’m sorry this is not showing – the numbers of events in this group were really low.

    [00:07:00] So we’re basing some of our information on what to do in low risk patients based on having counted one stroke, four strokes maybe, in 600 patients. And again, it’s just hard to know what to do when the numbers are that small. So, this is the best we have, but you have to realize that even these scores have limitations. Sometimes we as physicians, our colleagues, often don’t see this.

    This, again, has to be a personalized decision. Where there’s less controversy, is when you start accumulating those points. So when your score is two, three four and up, that’s when it becomes very clear that there is benefit, and that’s what the clinical trials have shown. In this score, which is sort of our version 2.0 score, is better. It’s more sensitive. It tends not to miss people with strokes. But we have to be reserved with our enthusiasm, because this was also derived in a highly-selected population.

    [00:08:00] The reason this gets important from a public health standpoint is when you look at apples, and then you apply the rules you derived in apples to oranges, you can get different results. So, as Dr. Day showed you, if rates of afib vary across the world, they vary across populations, we’re the highest in the U.S. and we’re using data from other countries, is that really going to be on target? So, of course, a lot has been done. There’s a lot of followup studies to show that we are on target, but they’re not perfect. That’s the only point.

    The most important thing about the way we think about stroke and afib, as your providers, has to do with treatment. So, prior to the NOACs, the new oral anticoagulants, everything was hinged upon warfarin. And warfarin, as I mentioned, was not the greatest. The bleeding rates were very high. The rates of brain hemorrhage from bleeding were really, really a problem with warfarin.

    [00:09:00] And a lot of times, we just were more afraid to treat because of the risks than we are now. So now we’ve moved towards high sensitivity, low risk, high upside with these drugs. And we know that you don’t need to have a ton of risk factors to get that stroke over time, so we have lowered our treatment thresholds.

    That goes to number three: Who should get stroke prevention therapy? This is a complicated question, and there’s a tug of war that you need to be aware of between the European Society of Cardiology and the three cardiovascular societies in the U.S. – the AHA, the ACC, the HRS. So even all of us can’t get along in the way we think about this. And the controversy about who should get treated is not in patients at high risk. We all believe that they should be treated. It has to do with when you start getting into lower risk patients.

    [00:10:00] So in 2011, the European Society of Cardiology proposed that we use treatment thresholds based on the CHA2DS2-VASc score and OACs, oral anticoagulation, and you would give it if the score was two or more for sure, and you probably should give it if the score was one. But you don’t need to give anticoagulation if the score is zero, and not even aspirin. And we’ll talk about aspirin. In 2014, the three U.S. societies got together and agreed with ESC that if the score is two or more, you should get anticoagulated. We all agree. That risk is substantial.

    But if the score is zero, you still should not get anything. But the controversy was around this low risk, a risk score of one, one single risk factor. That could be age, that could be hypertension, that could be diabetes. What if you just have one risk factor?

    [00:11:00] That’s where there’s a little more discussion you have to have about what is best for you. The other thing that I want to say is, we don’t really know how much afib should qualify to pull the trigger. All these scores were based on people who came with a clinical diagnosis.

    So the anticoagulation scores were defined by the treatment, not the disease. They came in, either in the hospital or in these surveys, to be seen for afib. It wasn’t that they were wearing some monitor and somebody found four minutes of afib one day and never again. Those are incredibly difficult and incredibly challenging situations where the decisions have to be well thought out, but also highly personalized.

    What medicines can reduce my risk of stroke in AF? Well, again, I’ve told you there’s been a shift. This is the emphasis I want to make. That’s why I keep saying it.

    [00:12:00] The new agents and better warfarin control have tilted in favor of us being more willing to treat, because we see a lot less bleeding, a lot less fatal bleeding, a lot less serious bleeding, and much better outcomes with preventing stroke.

    The numbers on this slide are not important. I put them here so that they’re in your handout and you can take them home: dabigatran is Pradaxa; rivaroxaban is Xarelto; apixaban is Eliquis; and edoxaban is a new drug that’s just come on the market, as well, by Daiichi Sankyo, and it’s been released now for about two months. Very few people are…are any of you on edoxaban? Yeah. It’s very, very new.

    The important thing here is that the major bleeding rates, not including brain hemorrhage, were lower in two of the trials, and at least as low as warfarin in all four. So these are low.

    [00:13:00] The most important thing, though, is brain hemorrhage. Intracranial hemorrhage, when you bleed in your brain and you get a stroke because you bled in the brain, and the tragedy and the irony of getting this because this is the one thing you were trying to prevent, they’re even lower than with warfarin.

    So, number one, appreciate that the risk of warfarin is 0.74, 0.74, 0.47, 0.85. It’s lower than 1% per year. That’s low. A decade ago it was even as high as 3%, 4% in some patients, so we’ve done a really good job there. Intracranial hemorrhage with the new agents is below a half percent. So there is a small risk, and this is a risk that’s important, because it’s not zero. And you have to think about this if you’re extremely low risk of having stroke and AF.

    [00:14:00] But in general, we’ve done a really good job, and these drugs have done much better in this case. And at some point, we’ve been able to prove that all these drugs are at least as good as warfarin, and in some cases maybe better. The other thing to note, and the most important part about warfarin, is to have a periodic assessment of how well you or your family member is doing on warfarin.

    It turns out that the patients who are at highest risk of stroke, as seen by the CHADS2 score table up here, and at highest risk of bleeding based on a bleeding risk score that we tend not to use, have progressively lower time in INR range. So if you’re on warfarin, you know that you generally need to keep your INR between two and three. And these numbers here, these percentages, are the percentages of time that these patients were on these drugs and had an INR in that range.

    [00:15:00] It’s the number of days while on warfarin that the INR was in two to three.

    Again, this is ironic, because the higher your stroke risk and the higher your bleeding risk, the less likely that you may be able to achieve that because of all the other factors that go into play. It turns out that, even in the trials, where you were having your warfarin managed made a difference. So now this is on a global scale, and this is just the warfarin users in the RE-LY trial, which looked at warfarin against dabigatran, which is Pradaxa. And in fact, the U.S. was not on top. Sweden had the best INR control in their group: 77%. That’s extremely high.

    Sweden has a national healthcare system that effectively has one anticoagulation clinic for the entire country, and everyone gets it the same way.

    [00:16:00] The U.S. was in the lower part of the top third, or in the top part of the middle third, I don’t know, but it was at 66% in the average. And in the real world, it’s even less than this. And other countries, like India, that I put because I’m originally from India, is even lower.

    So if you’re not going to get good INR control, you’re not going to get the benefit. Where is that line in the sand? What does the TTR [time in therapeutic range] need to be? If the TTR is below about 58% or 60%, the warfarin may actually not be doing anything. It may not be any better than aspirin or placebo, and may be increasing your risk for stroke. If you look at real world data in the world, in the U.S. we’re not good at this. We’re probably hovering around 55% to 58%. We’re just barely there. So, for you as a patient, you have to look, “What is my TTR?” You talk to your anticoag clinic and you try to improve that. And if you can’t, you think about other strategies.

    What about aspirin? Isn’t it safer?

    [00:17:00] This is a question we get all the time. Can’t I just take aspirin? It’s easy. It’s safe. The answer has changed. The answer is no. It is not as good, and it’s not any safer. So, we have to remember that aspirin causes bleeding. It’s not low. Eric Topol did this ten years ago now. He looked at 192,000 patients in 31 trials of all types, and he found that even at low doses, baby aspirin doses, there’s an appreciable bleeding rate that exceeds that if you’re not on anything.

    This is not trivial. There is bleeding with aspirin. You might think, “Okay, well, maybe there is bleeding, but I’m sure it’s less than anticoagulation,” right? We’ll talk about that in a sec. But what we do know is that aspirin, when compared to warfarin, it’s clear.

    [00:18:00] If you now do a study of studies, as Dr. Day showed you from another meta-analysis, that when you take all the aspirin and warfarin combination trials together, you get at least to 45% reduction over aspirin.

    So warfarin is clearly better than aspirin at preventing stroke. We also know that warfarin is better than the combination of aspirin and Plavix for the purposes of treating afib. These are often drugs that are prescribed for other conditions of the heart, but if afib is the only problem, anticoagulation is better.

    Now, here’s the other thing. Well, what about the new oral anticoagulants? Well, this study, Averroes, looked at aspirin versus apixaban, or Eliquis, and found that when you compared aspirin to apixaban, the apixaban did much, much better at preventing stroke. You can see the cumulative risk here over time was much lower with this.

    [00:19:00] And this difference started to emerge within the first month of followup. This doesn’t take that long to see that benefit. And then here’s the other hook. Look at major bleeding. Aspirin was no different than apixaban for major bleeding. So you got no benefit from aspirin, and you incurred the same risk.

    So our way of thinking about aspirin in intermediate to low risk population has really changed. We’ve really moved away from prescribing aspirin. And in fact, in all of cardiology, we’re trying to de-implement aspirin, even in non-afib patients who have no heart disease. There’s no clear benefit, and there’s bleeding risk.

    So if you’re on the fence between aspirin and anticoagulation, aspirin may be very, very tempting to think about, and it still may be right for the truly low, low risk patients. But even in those situations, we have no data to suggest that aspirin is often better. So, this is a tough area.

    [00:20:00] The treatment has to be highly individualized. But the point here is to dispel the notion that aspirin is giving you benefit without risk; it’s not the case.

    Number six: Is stroke risk affected by whether I choose rate control or rhythm control? If I have an ablation, if I’m on antiarrhythmic drug therapy, is my stroke risk going to be lower? Another common question.

    It’s really challenging to know. At this point, we’re erring on the side of probably not. It may be the case that there’s some benefit. The reason I say probably not is we just don’t have great data. There have really been no trials where people on antiarrhythmic drugs have been discontinued from their anticoagulation to see if they accumulate events. So there’s been no randomized trials. And the toxicities of the antiarrhythmic drug therapies are a problem here, that they’ve not shown benefit, because there is a risk of those.

    [00:21:00] When you look at just real world patients, there is an excess stroke risk seen in patients who stop anticoagulation, who are still on rhythm control. And although one trial of dronedarone demonstrated a decreased stroke risk on those who were treated with dronedarone as a rhythm control, another trial showed that there was an increased risk of stroke, but that was in permanent afib.

    So we have really no data around here, but we’re very, very cautious and reluctant to strip away the anticoagulation in cases where you’re on rhythm control and you’re having less afib. If you’re having no afib at all, it’s an even more challenging issue because there is a temptation to stop it. And again, that could be the right answer, but we don’t have a ton of data there.

    What about ablation, though? That’s a better treatment, as you’re going to hear about in the afternoon, than antiarrhythmic drug therapy, in the right patients. Won’t that lower my stroke risk?

    [00:22:00] The answer is, we don’t know. But right now it’s very difficult to count on that. Again, there have been no randomized trials on stopping anticoagulation after an ablation. Unless you have a randomized trial, you can’t prove that it was causal.

    There have been a lot of great small studies that have shown that in truly low risk patients who have no afib in follow-up…so they have their ablation and they get very good monitoring. They have shown that they don’t have strokes. And I believe the data. I’m sure they really didn’t have strokes. But what does that really mean?

    Maybe it means that the people who responded to pulmonary vein isolation had a lower burden of stroke factors. Are there ways to reduce risk of stroke without medication? So this I’m going to talk about briefly. This has been in the news very recently because of FDA approval. We do know that LA(left atrial) appendage is a source of clot in 90% of patients.

    [00:23:00] And we know that if you take it out, you’re going to prevent a blood clot from forming.

    There’s really three ways you can do this. You can surgically ligate it. This is often reserved for adjunctive therapy with CABG valve and even surgical Maze procedure. Or you can go into the heart and occlude it, or you can go around the heart and tie it off without opening the chest. This is something that has been around a very, very long time, and many technologies in parallel have emerged and are in place. And now with FDA approval of at least one nonsurgical option, there is a choice.

    This is the Watchman device that was FDA approved. It’s delivered through the left atrium by means of an expanding plug that covers the appendage. This is now in the right atrium looking at the inside of the heart, and it goes into the left atrium in the exact same way that you would do an afib ablation.

    [00:24:00] But then what you do is you find the left atrial appendage – that is the left upper pulmonary vein – and just below that, this highly trabeculated structure, all these little formations, is the left atrial appendage, and that’s where blood clots form.

    And eventually, you make your way down there by several tools that allow you to get down, find that left atrial appendage, and then deliver the Watchman device to occlude it.

    There’s some things here that are shown on how you do this more technically, but what you’ll see – this is contrast being injected so you can see it on X-Ray – is that the sheath will come back and it will deploy this device.

    What that does is it occludes the appendage. So you withdraw, and this device expands.

    [00:25:00] Over a couple of months, weeks to months, would lead into complete occlusion of that as a source of blood clot in the left atrium in afib.

    There have been several trials that have been done. The first was the PROTECT-AF Trial. And this compared warfarin, which is the control, to this. And there were very, very few patients. And what we learned from the first trial was that it was at least as good as warfarin, statistically.

    But there was an increased risk of complications here, looking at the primary safety endpoint. So you were sort of taking an upfront risk. I view this as buying a house versus renting a house. There’s an upfront risk when you buy a house. There’s an upfront risk when you get a procedure. There’s a chronic risk of paying rent. So you’re paying rent every day, you’re doing that.

    And that is really how you think of a drug; there tends not to be an upfront risk. Over time, we’ve learned that these are viable options.

    [00:26:00] And over time, it seems that the device may do even better than warfarin in select patients as well. There’s some followup data, as well, that shows that the device is at least as good.

    So, another device on the market is a Lariat device, which is not FDA approved to prevent stroke; it has an approval to close soft tissue. So this is a gray area where some people are doing this, but it doesn’t have the approval, the endorsement, by the FDA that it reduces stroke, because there hasn’t been a study.

    But the way this is done, just so you can see it – you guys can go ahead and start this – is that you’re in the left atrium and you’re outside in the pericardium, the sack around the heart, and you’re delivering a suture, first by having these two magnets connect.

    One is on the inside of the heart; one is on the outside. What’s in between the magnets is atrial appendage tissue. You essentially pull a loop over and you suture this down, and eventually this is finished.

    [00:27:00] Now, it looks easy here. It’s not. It’s very challenging. It’s not been studied in randomized clinical trials. It is available, but these are some of the discussions, if you’re thinking about this, you have to ask, as well.

    So Watchman is now approved and is available. Lariat, again, is not. It has this intended use on closing soft tissue. We’ve not proven in a randomized way that it reduces strokes.

    However, number 9: Why did patients with appendage occlusions still have strokes? It wasn’t zero. And this is where things are changing. It really gets to what the mechanism of stroke is. We used to think of these first two. The LA doesn’t move well. That may cause afib. You get a stroke. Or the afib comes first. It doesn’t make the left atrium move well. When blood sits around, it forms a clot and you get a stroke.

    [00:28:00] But there’s an emerging view that both of these may be independent of each other. And the most recent view that we’re starting to see in our world as we’re beginning to understand the disease, is that you can still have stroke from other reasons, even if you have afib. Those vascular risk factors, as I’ve shown here, may be the things in the risk score.

    Hypertension, diabetes, all increase your risk of stroke, even if you don’t have afib. So that can also occur in patients with afib. What we know if you close the left atrial appendage is if you isolated the source in afib. What we don’t yet know is if the drugs, the anticoagulants, might be preventing stroke in other ways. What does the future hold? I’m going to get through this really quickly.

    We’re inside of a new era here, and it’s digital medicine. I’m in Silicon Valley at Stanford. We get this all the time. We had a digital medical conference dedicated to afib yesterday.

    [00:29:00] There are so many things we’re going to see, so much to see. We’re never going to be offline. And this is empowering because it’s going to introduce new ways of monitoring and tracking your disease. But it’s also going to be difficult with us as physicians because we’re not going to know what to do with the information. We haven’t figured that out.

    I’m going to skip all this because it’s not as important. But I wanted to close with this slide, which is this era of big data in medicine. This is a cartoon of a doctor talking to a patient, saying, “Our statistician will drop in and explain why you have nothing to worry about.” We’re here. We have more data than we know what to do with. And afib is a prime target for this. So we’re going to learn as much as you are on how we figure out how to manage AF, adherence to drugs, monitoring in the outpatient setting, and what to do with all this information. Thank you.

    [00:30:00]
    Man: Thank you. You didn’t bring into the topic anything on the statin use concomitantly. I’m a neurologist, so we like it from a stroke standpoint. But how does that interplay with AF medication?

    Dr. Turakhia: Yeah. So that’s a really important and interesting question. The question is, what about using statins, and how does statin use tie into afib? Statins are not recommended as a principal treatment for afib currently. Statins are used to treat high cholesterol, principally. And in that role, by preventing heart disease that you see over time…if you were perhaps untreated and had high cholesterol, you may prevent afib indirectly because those things predispose. But we are not in a position where statin use is being used.

    Now, there have been trials and studies on several things — one is statin use, one is fish oil — on whether these can prevent afib or prevent outcomes of stroke in afib.

    [00:31:00] And there have been randomized trials with statins. They have been small. With fish oil, they have been larger. And they have not shown clear benefits.

    So right now we don’t have any strong evidence to indicate that either of those would cause substantial benefit in afib. They probably don’t cause harm, but again, you have to think about a statin and its role in cholesterol and cholesterol transport as a prime motivation to be on it.

    Mellanie: Would you be willing to come to the microphone, please? Thank you. We want to make sure that we get your question on video and through the audio system. Thank you.

    Chris: I’ve done some extensive reading. I’m a practitioner in nutrition. I’ve read a lot about serrapeptase. They use it in Europe sometimes, instead of aspirin. What are your thoughts on serrapeptase?

    Dr. Turakhia: Not been studied. There are a lot of aspirin analogues. Serrapeptase is one. There’s a few herbal supplements.

    [00:32:00] We see a lot more of this on the West Coast because they’re coming from China. They’re relatively cheap to import.

    We have large Asian populations. And if you go to these countries, they’re prescribed. I actually have a med student who’s digging through all the literature currently, to look at the evidence between herbal supplements and either the development or prevention of afib, or strokes.

    There’s really no data out there, so we’re in a difficult position where we can’t endorse them. And they probably aren’t going to have the same benefit that you would with an anticoagulant. So I think, again, you’ve got to think about what the role of an aspirin or aspirin-like drug would be. If you’re getting the bleeding, you’re getting the harm, but you’re not getting the benefit, it’s really not the right choice in afib.

    Shelley: I’m a former elite athlete, and I was wondering if you were doing any studies on distance runners now, any type of athletes with afib, strokes?

    [00:33:00]
    Mintu Turakhia: Yeah. That’s a great question of the natural history of afib and athletes. You heard Dr. Day speak a little bit about the paradox, and that the more you train and the higher endurance, the more afib that can occur. And that can come through many different mechanisms, which we’re just beginning to understand. I think this is going to come up tomorrow, because Dr. Link is actually on a panel specifically speaking on athletes. I’m going to let him talk more about that as well. We have very, very little data on stroke and athletes, just because we don’t follow them for long enough. And even if you did, you really need to know how active they are in that process.

    So there are athletic registries, and Mark will be able to speak about this in more detail, but there’s such few stroke events that you can’t say anything. Probably, if they’re capable of exercising and they have extremely good function, and probably they’re not going to have all the other risk factors for stroke, their risk is going to be really, really low. But we don’t know with certainty.

    [00:34:00]
    Mellanie: So, let me ask you a question, Dr. Turakhia. The whole area of people who are labeled as asymptomatic, meaning that they don’t feel their afib, and that it doesn’t impact their lives, and they tend to be relegated to rate control medications, but if the doctor were probing a little bit more, he might find that it really does have an impact on their lives, and that maybe they are symptomatic. We hear all the time in the patient community, folks who say, “It’s not really impacting me at all.”

    But then they get to the doctor and the doctor asks a question, and the wife is there with him, and the wife says…she’s about to have a seizure over in the corner, saying, “But you can’t do this and you can’t do that. You can’t even walk up stairs anymore.” So, truly, patients are symptomatic.

    [00:35:00] So what are the recommendations that you have for the patient community for communicating with their doctors around this whole issue? Because it can totally change how they’re treated, tend to be more rate control than rhythm control.

    Mintu Turakhia: Yeah. So, Mellanie, as always, brings up a fantastic point. I showed you that fork in the road. And that fork in the road of rate and rhythm is largely guided by whether a patient is symptomatic. But the real decision may be guided – if it’s not a shared decision, and it should be, but if it’s not – by the provider’s assessment of whether you or the patient has symptoms. So, again, I think that the provider, the doctor, has to be in tune with the patient.

    Why are they here? What motivated the visit? How many doctors have they seen before? What’s going on? How does this fit with their life? Did the spouse drag in the patient because the spouse was concerned?

    [00:36:00] Is the patient someone who is minimizing their symptoms because that’s just who they are, they just go with things? Are there other motivations? Then in turn, I think the patient and the family that comes with the patient has to be in tune with the doctor. Do they have a broad understanding of how afib might be impacting the disease? Are they really probing heavily for symptoms? I think that’s important.

    Now, the flip side of that, is that you don’t want to be at a doctor who has a hammer looking for a nail. I mean, if someone is truly, truly asymptomatic, objectively and subjectively, perhaps pulling the trigger on an ablation after the first visit isn’t necessarily the right approach, right? It can cut both ways. I don’t want to sit here and say that the problem is only the former. We really have to be really humble and thoughtful on both sides, over treatment and under treatment.

    [00:37:00] So you’ve got to have that conversation. It’s good to track your symptoms. Sometimes the only way you know if someone is having symptoms is you educate them what the possible symptoms are. And then once you’ve educated them, they might think they’re having them all the time, so then you have to tie that in with correlation.

    So a good way of doing that is to wear a monitor for not just a day, not just two days. Have patients keep a detailed diary of how they feel and see if you can put some correlation together