UPMC Physician Resources
Watchman™ Device for Stroke Prevention in Select Patients with Atrial Fibrillation: New Devices for Rhythm Management
Dr. Sandeep Jain discusses stroke prevention in patients with atrial fibrillation.
Upon completion of this activity, participants should be able to:
- Improve management of anticoagulation in patients with atrial fibrillation based on current guidelines.
- Improve recognition of non-pharmacologic options for atrial fibrillation management.
- Risk of Stroke and Death in Atrial Fibrillation by Type of Anticoagulation: A Propensity-Matched Analysis. Pacing Clin Electrophysiol. 2015 Nov;38(11):1310-6. doi: 10.1111/pace.12695. Epub 2015 Aug 7.
- Patient outcomes according to adherence to treatment guidelines for rhythm control of atrial fibrillation.J Am Heart Assoc. 2015 Apr 6;4(4). pii: e001793. doi: 10.1161/JAHA.115.001793.
- Comparative effectiveness of antiarrhythmic drugs for rhythm control of atrial fibrillation.J Cardiol. 2016 May;67(5):471-6. doi: 10.1016/j.jjcc.2015.07.001. Epub 2015 Jul 29.
Dr. Jain has financial interests with the following proprietary entity or entities producing health care goods or services as indicated below:
- Grant/Research Report: Medtronic
- Clinical Research Trial PI: Medtronic, Boston Scientific, St. Jude
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Release Date: 11/1/2016 | Last Modified On: 11/1/2016 | Expires: 11/1/2017
Like most talks I think I committed to being onboard several months ago and this was the title that Dr. Fallert gave but like most manipulative people I'm going to kind of talk about whatever I want to, so you'll bear with me. But atrial fibrillation and watchman will be mentioned somewhere in there. And so these are my disclosures for research support.
I think many of you may have seen me give this slide and maybe all of the others too at some point, but what kind of physicians go into electrophysiology? If you remember the concerned mother bringing her infant toddler in to the doc, can he lead a normal life? And the doc says I'm afraid not, he'll be an engineer. And the mother begins to cry. And that's really not too different than the path most electrophysiologists have gone through in their social lives. And so forgive me for that.
So what is atrial fibrillation? I think most of you know when you think about atrial fibrillation it's this chaotic mess in the top chambers of the heart that then leads to irregular and rapid ventricular response rates. And you see that on a rhythm strip with a normal regular P wave followed by Q, R, S and T versus no real defined P wave or atrial activity. It's the supraventricular arrhythmia with no effective atrial contraction, with irregular and often rapid ventricular response rates and the stasis that happens in the atria predisposes to thrombus. Most of the thrombus that occurs, the most likely place in the heart is in the left atrial appendage and we'll talk more and more about that and how the strategies have evolved over the years to try and deal with that.
This is a disorder of aging, the prevalence increases with age and it's the most common sustained arrhythmia with 1% of those over the age of 60, 5% of those over the age of 69 with about a 3 million American prevalence in the U.S., with about 1 to 1/2% of the population having atrial fibrillation with a 25% lifetime risk. So you don't have to look far or wide amongst your friends and family circles probably to know somebody with atrial fibrillation.
So why does it matter? The quality of life is lower in patients with atrial fibrillation with lower total functional capacity, lower global life satisfaction and really on the order of those that undergo an angioplasty or post-MI but we think of these I think a lot differently and sometimes think of you know MI, often people can tell you the day it happened, they view it as an acute event. Once they are "fixed" they may view this as a low risk thing going down the road whereas with atrial fibrillation many patients are reminded of this from the symptoms every day or very commonly in their life, it's unpredictable and they are often waiting in anticipation of the next event to happen.
The focus of today is the stroke risk ranging 3 to 5 times that of the general population. If you have atrial fibrillation 15% of strokes that occur occur in patient with AF with a signal of increased risk mortality in patients with AF from primarily old retrospective data. And the hard thing to sort out with this is AF goes along with a lot of other disorders, and is it really a cause of mortality is always hard to say and really actually we go around telling patients that it's not going to kill you but we really don’t' know that. It's hard to separate out the hypertension, the diabetes and everything else that comes with AF of how much additional risk there is for mortality.
These are the risk factors that we think about for causing AF and what I tell my patients is it's a difficult thing to treat or diagnose even because it's rare that we can point to one cause as to why somebody might have AF. Other risk factors that I view as more like triggers usually don't cause AF unless there is an underlying substrate there, hypothyroidism, alcohol abuse, severe infections and pulmonary disease and even anger and hostility. And I tell Dr. Buffer this every time he answers the phone from that 2 a.m. page to be a little more calm when he does it. But he's learning.
So the lifestyle cascade I think is what we are realizing more and more. We kind of at least as electrophysiologists always view this as there is some electrical problem in the heart, we should be able to fix that electrical problem like we do with WPW or AV node reentry or even ventricular tachycardias where we can define a focal source and treat it with a catheter or a medicine. The difference here is that it's taken us a long time to really come to the realization that this is a conglomeration of different disorders, the biggest being aging that we can't reverse, hypertension, sleep apnea, stress, alcohol that all leads to this common end point of fibrosis in the atria and then you get secondary electrical disorder from this. And you know some of the efforts that are made on that end from pulmonary vein isolation and catheter ablation to try and treat it but I think it's important to note that that is a treatment not reversing the underlying cause and not uncommonly we see patients who will undergo a "successful catheter ablation" that several years down the road that underlying process advances and we see more and more of AF. So this is something that you know goes along with this whole idea of stroke risk as well that we'll touch on.
So three different types of AF that we talk about, paroxysmal, persistent and permanent and it's really as simple as what they sound like. Paroxysmal is AF that patients go in and out on their own without us doing anything about it. Persistent is one that's stays in for you know longer than 7 days or doesn't convert and it requires us to do something whether it's an electrical cardioversion or an antiarrhythmic drug. And permanent AF is really the same thing is persistent where patients stay in it without us doing anything but we've given up, we've decided there is no point in trying to maintain sinus rhythm or there is no longer the ability for us to even try because we can't do it. So again the three main concerns with AF you all know, thromboembolism, the symptoms that patients have and the possibility of a tachycardia induced cardiomyopathy which is luckily relatively rare and important to diagnose early on because usually reversible.
So anticoagulation how do we treat this? Anticoagulation to prevent thromboembolism, medications to control the heart rate and in some patients that are highly symptomatic respiration of normal rhythm. So I'm going to kind of shift focus on stroke which is really the biggest morbidity and potential mortality of this rhythm that again another feature that I think in the EP world we have been very late to come to the game to really focus on what needs to be done for this rhythm as far as stroke prevention and stroke treatment as opposed to just what the P wave is or isn't on the EKG. There is a 5-fold risk of increase in stroke in patients with AF, it's the most common and devastating complication of atrial fibrillation. The all cause stroke incidence is about 5% and atrial fibrillation is a clear important risk factor for stroke like we mentioned. This risk goes up with age. Ischemic stroke is associated with atrial fibrillation and often more severe than strokes from small vessel disease or even carotid disease. And this stroke rate is - it persists even when you are not in atrial fibrillation or symptomatic from it. So this is a big important take home point that I try to stress every time is that the reason to anticoagulate when we use these scores is a history of atrial fibrillation with the risk factors, not necessarily the rhythm that you are seeing the patient in today or in the office that day, so that it's not that which we fall into the trap of all the time of feeling comforted by seeing somebody in sinus rhythm that day and thinking that their stroke risk is low. It really comes back to the history of having that AF with these risk factors.
So the risk factors that we all know of, the CHADS score is the original score that was used, congestive heart failure, hypertension, age over 75, diabetes and prior stroke or TIA. You add up the score that a patient has and the more the risk factors the greater the risk ranging from 2 to 18%. And the guidelines are 0 risk factors, aspirin or really nothing; 1 risk factor is dealer's choice, aspirin, Warfarin or nothing; and 2 or more risk factors Warfarin. And again Warfarin or a NOAC wherever you see Warfarin.
And that has changed now with the CHADS2 VASc score which it really came about because it was realized that CHADS2 score of 0 and 1 were often underestimating risk so that the CHADS2VASc is really the same thing as the CHADS2 except now age over 75 gets you 2 points, 65 to 74 is a risk factor, vascular disease as well as female gender. So you can imagine it doesn’t take long to add up to a score of 2 in a female who is 65 or a female that has hypertension that then would be indicated for anticoagulation. And the guidelines have kind of moved to reflect this as far as a CHADS2VASc again of 0, no antithrombotic; 1 is really any of the above and 2 or greater oral anticoagulation. And it's important that all of these scores are thought of in nonvalvular atrial fibrillation, in valvular atrial fibrillation you don't do a score, they by themselves an anticoagulant. And how you define valvular is a mechanical mitral valve or mitral stenosis, not 2 plus MR or 1 plus aortic insufficiency. It's really the mitral valve pathology that's been shown to cause these kind of - to have a much higher risk because of stasis in the left atrium.
We all that the difficulty with Coumadin is what we are struggling with and really to find that sweet spot of 2.0. If you go down to 1.9 the ischemic stroke rate significantly goes up, and you start going over 2 and the atrial cranial hemorrhage rate goes up. And this is the whole reason we have novel anticoagulants and we have a lot of options for blood thinners that I've listed here and we'll talk a little bit more about them. But my overall take on this and I'll be interested in hearing the panels as we talk about cases is you know the advantages of these new medications are their disadvantages. So fixed dose, no monitoring sounds like a great thing but fixed dose, no monitoring may not be a great thing when you are trying to bring somebody in for a cardioversion or you are trying to assess compliance and figure out have them been taking this; whereas with Coumadin you can see what their INRs were doing.
Short half life is a good thing in the sense of if somebody bleeds you just stop the medication. It may not be a great thing if one or two doses missed could be a significant issue whereas a dose of Coumadin missed usually won't affect your INR, and what little it does affect it would be 2 days down the road. There is really no dire drug interactions which is I think the biggest convenience factor of a NOAC over Warfarin in addition to the lack of needing monitoring.
The antidote story is no longer true, there is a clear antidote at least for Pradaxa and others coming, so that I think that that is going to really alleviate a lot of the concerns of bleeds and I think most patients though even now that have bleeds on a NOAC if they had the same type of bleed on Coumadin their management wouldn't be all that different as far as blood products or basically transfusion and waiting for the anticoagulant effect to be - to wear off.
So with that I want an introduction, I want to move on to a case which I'll open up to the panel for discussion. So given the following patient characteristics in which setting would switching from Warfarin to say Dabigatran be appropriate and supported by clinical data? So A, ejection fraction of 30% with class II heart failure; B, a normally functioning mechanical mitral valve replacement or C, LVH with an ejection fraction of 55%; chronic renal insufficiency with a creatinine clearance of 10? So maybe I'll ask Dr. Davis to start with this. Okay, great. I realize I didn't ask a show of hands but maybe we can ask it now. Anybody want to disagree with Dr. Davis? I think in general that's a wise choice not to disagree with her; but you know I think Lydia brings out all the important points of how these medications are approved. How are they approved? They are approved form the trials that were done to gain FDA approval and if we look back at a lot of these "exclusions" I think it's important to remember it's usually just because those patients weren't included in the trial, not necessarily because we have negative data on it. Although the mechanical mitral valve story at least with mechanical aortic valves we do have data that's negative, so any mechanical valve would definitely be taken out. Anybody I switch or even start now on a NOAC I kind of forewarn them that they'll figure out what your co-pay is going to be in a year because that problem comes up a lot, and it's almost you know everything that's been seen about the increased stroke risk for example with Xarelto after the study was closed was in the switching period where that monitoring isn't as intense people were stopped on the Xarelto, started on the Coumadin there was a week there where they were not anticoagulated. On a high CHADS patient you do enough patients you'll see that. So I think it's an important point, I think there is definitely a little less push to switch upfront. I'll show you one reason why you might think that it's still an open question and maybe there is a signal there or a reason to switch.
So RE-LY, as Vickie mentioned you know the INR in therapeutic range in the Warfarin group, 18,000 patients, was 64% which is really - it seems low but it's actually one of the best. 55 to 65 is thought of as a great time in therapeutic range with Warfarin. So it just highlights how poorly we do even in a well run trial where people are watching things closely. And what was seen, I'll just kind of skip through this, but they had to have one of these higher risk factors, a prior stroke, lower EF, class 1 or greater heart failure, age over 75 and if they were younger one of the high risk factors. Exclusion was severe valve disease, recent stroke, increased bleed risk which is obviously a little difficult to objectively assess, active liver disease and a low creatinine clearance in addition to pregnancy. But anyway the combined end point, stroke, systemic embolism was equal to Warfarin in the lower dose Pradaxa group and in the higher dose Dabigatran group an improvement over Warfarin. And this led in 2011 to updating the guidelines for atrial fibrillation to offer as a class 1 indication Dabigatran and subsequently the other NOACs.
So just going back to the question Lydia was absolutely right that A would be the right answer. Low EF patients with heart failure were studied in RE-LY but none with a mechanical valve and none with a creatinine clearance that was that low.
So I'm going to skip over this to ROCKET-AF just to get moving with a couple of the other cases. The bottom line was it's a similarly designed study, the main difference between this and RE-LY was the CAHDS-VASc score and the baseline characteristics was higher, the CHAD score actually was mid-3s, I think 3.5 where it was 2.5 to 2.7 in RE-LY, so arguably a little sicker population group and the Rivaroxaban group had you know on par improvement in overall composite end point if not better especially in stroke and systemic embolism. There was a signal of increased non-life threatening bleeds but overall life threatening bleeds were less or equal, mostly driven by intracranial hemorrhage and that has kind of come through in most of the studies as well. In post-op analysis I think the GI bleed risk, which we'll talk about some more, is really where some of this separates out.
So I'll touch quickly on ARISTOTLE, which looked at Apixaban, again similar study, 18,000 patients randomized to Apixaban or Warfarin with the primary end point of stroke or systemic embolism. And this is a study where there was clear superiority of Apixaban over Warfarin to this end point, and a decrease in major bleeding as well as a mortality improvement signal. So I guess I would re-ask that question of if stable on Warfarin with this type of data do we have some push to think about switching based on improved outcomes at least by this one trial? This is definitely something food for thought. The only piece that at least I don't understand from this is we have no clear answer why there was a mortality benefit. It wasn't all driven by those intracranial hemorrhages or you know severe bleed risk. And I think that's still a little bit of an open question of what is the mechanism by which patients may be - you know if we knew 100% that this is a mortality benefit then I think the discussion is a lot different of well why are you keeping them on Coumadin you know? And I think we just don't necessarily have that answer.
So I think that's a segue to another case. A 73 year old male with a history of hypertension and COPD who first presented with recurrent symptomatic atrial flutter. He underwent a successful catheter ablation of atrial flutter and follow-up event monitoring showed no recurrence of atrial arrhythmia three months post-ablation. He was maintained on anticoagulation with Xarelto through this and now you are seeing this patient in follow-up in the office in sinus rhythm and what do you decide to do with their anticoagulation? A, continue Xarelto; B, stop the Xarelto and start the aspirin; C, stop the Xarelto and no aspirin, D, stop the Xarelto and start Plavix? So I'm going to take a show of hands before we ask our panel to answer. So how many of you would say you need to take Xarelto? Raise your hands. Okay. Remember the number has to add up to more than 10 by the time I'm done with this, so otherwise you are all going to pick D, and I'm going to tell you right now that's the wrong answer. B, stop Xarelto, start aspirin? Okay. All right. C, stop Xarelto and no aspirin? Okay. And D, stop Xarelto, start Plavix? Okay. All right, so I think most people said B, stop Xarelto, start aspirin. So I think those are all good points. We'll come back to the question, I mean I think the highlighting no evidence to suggest that as I said before that what the rhythm is at the time mitigates stroke risk. Now we like to think so, but we just don't have that data yet that at least by ablation we can do that.
And especially in this patient one of the points I should have highlighted, I was talking about an atrial flutter ablation. So if you look at patients with atrial flutter 50 plus percent of them if you watch long enough will have atrial fibrillation. So it's almost arguable whether to do a fluter ablation these days outside of treating AF as well. So that many of those patients may have asymptomatic atrial arrhythmias that you don't know about. I guess I would highlight that even if you decide that you want to come off anticoagulation you should probably do some pretty intensive monitoring to decide that it's safe to do that. And back to the point of determine the anticoagulation really based on that CHADS2-VASc score. So I think we learned some very important - one post-op episode like Sam mentioned or one situational event of Holiday Heart I would classify as sort of a different category. This is - that's exactly right and you probably would not commit them to long term anticoagulation.
Having said that, we still don't know where this is all going in the sense that now there is data that you can take patients without any history of AF, take the CHADS score that's high and look at their stroke rates. And they are higher than they are without this. So that probably makes sense, hypertension, diabetes, age and you add all of those up and they are higher. Now the field in that sense is going in two ways. So is there a role to just start anticoagulating people on a high CHADS score, if you had a great way to anticoagulate without the bleed risk you might think about it. Or now there is some evidence that suggests well maybe we should be looking for AF in patients with just a high CHADS score and no symptoms, and you'll actually find it. There is a nice Swedish study where they put loop recorders, implantable loop recorders in all patients with a high CHADS score and they found 30% of them had some atrial fibrillation, but really high CHADS scores. So I think we don't know, we don't know.
And just to review the CHADS score in this case, Lydia, how would you go around with that? I'm going to go back, 73, hypertension, so he does well until 3 years later when he develops persistent atrial fibrillation and relatively asymptomatic in that rhythm and rate controlled on AV nodal agents. So now he also develops a GI bleed requiring transfusion secondary to angioectasia and the Xarelto is discontinued. So what do you recommend next? A, switch from Xarelto to Coumadin; B, switch from Xarelto to aspirin; and C, discontinue all anticoagulation? So I'm going to take a show of hands. A, how many of you would switch from Xarelto to Coumadin? Okay, good. B, switch from Xarelto to aspirin? And C, discontinue all anticoagulation? This is a tough question because this is all depends on a specific clinical scenario. I think the issue with aspirin I think we do this a lot where we say aspirin because we view it as a more benign agent. But there is clearly a bleed risk with aspirin and the problem is that the benefit of aspirin in atrial fibrillation I think as we learn more about this is really being called into question.
So the data was from the old SPAF trials that showed an improved stroke rates with aspirin, but every retrospective look of large databases of aspirin and atrial fibrillation have not borne that out kind of in the modern ara of treatment. And that's why the guidelines, I mean the European guidelines for 5 years have said this, that CHADS at 0 for example or 1, nothing is fine, better than aspirin because you are just increasing the bleed risk without necessarily impacting the stroke risk. so in this type of situation I don’t think we necessarily know when you don't have another option. But it may not be wrong to say nothing or aspirin.
The only other point about bleed in general, if you look at - this was a metaanalysis of sort of all NOACs versus Coumadin on this slide. And although there is clearly an improvement in major bleeding, the GI bleed rate is increased with pretty much overall all NOACs, at least independently shown for Xarelto and Pradaxa. So that there is some school of thought, or there may be some hint to say that you are less prone to GI bleed on Coumadin, but that's again in the setting of perfectly managed Coumadin, which is always hard to do and often these patients are already on a NOAC for a reason that they had trouble with Coumadin.
So let's say somebody decided based on this because they've not decided to do anything else that they are switched back to Coumadin but difficulty with INRs and then they come in with another GI bleed. So what do you do now? Obviously a leading question and the reason I bring it up is I think this is not an uncommon scenario where somebody has had a bleed and now you are left with we don't know what to do. And one of the pushes from new technology has been to treat the possibility or try and prevent a clot from forming in the left atrial appendage or wall it off if you will. And there are a few devices out there, one that's FDA approved now called the WATCHMAN Device in the U.S. that basically involves plugging the left atrial appendage so it forms this blind alley and then it endothelializes over so that even though clot may be in the left atrial appendage chronically that it can't get out. And this is indicated to reduce the risk of stroke from the left atrial appendage and in patients with non-valvular atrial fibrillation that are deemed at increased risk of stroke with "a high CHADS score" which hasn't been defined at least by the payers. They are deemed by their physicians to be suitable for Warfarin, so we've got to talk a little bit about that, what does that mean, and have an appropriate rationale to seek a non-pharmacologic alternative to Warfarin, taking into account the safety and effectiveness.
So this is what the FDA said when the device was approved, and I'll just mention a couple of things about the device, show you a couple of pictures of it. It's this basket-like device, mesh-like device that then is lodged via transseptal approach like you saw from Dr. Smith's talk except then you know positioned in the left atrial appendage with really walling off this blind alley. It's done usually under general anesthesia, 1 to 2 day hospital stay and a 1 hour procedure.
These are more pictures of it, of what happens and really more importantly with time what you are looking for, and these are from animal studies, over a period of 4 to 6 weeks afterwards there is endothelialization over the device so that it's walled off and then you know really not in contact with the vasculature as far as risk of thrombus, etc. But because of this risk of thrombus I'll ask Amanda maybe to touch base a little bit about what the routine is for these patients. Amanda is our clinical coordinator for the Center for Atrial Fibrillation and is sort of the intake person for all of these patients to be referred for it. So Amanda, when you are called about a patient being evaluated for a WATCHMAN what are the things that you want to know or need to be possible as far as anticoagulation in that patient?
Okay, so that 6 weeks is for the period to allow this endothelialization to occur because there is a risk of clot forming on the device. So some testing clearly ahead of time, really careful INR watching. The reason Coumadin, patients have to be switched to Coumadin is all the trials were studied with Warfarin. It was all the trials were done as comparison of the device to Warfarin, the NOAC comparison trials are coming and there will be options to put patients on NOACs into trials but for now they have to go back onto Coumadin and with a minimum of about 6 weeks afterwards they need to remain on Coumadin.
So if we look at the studies done and just the number of patients followed, about 5 to 6,000 patient years over 4 major studies that looked at this device all head to head, I shouldn't say all head to head, all but one, all but the registry head to head up against Coumadin and the - if you look at which patients were involved the mean CHADS2 score was in the mid 2s, so these are not really high CHADS score, but CHADS-VAScs of 3 to 4 and with all the usual risk factors.
And if you look at well did this thing work, or what kind of results did we show when patients received the device and then later their Coumadin was stopped. The first point is as time went on the success rate of implanting the device was 95%, so pretty high. And what's been shown over time is the complication rate is actually dramatically reduced, there is a pretty steep learning curve earlier on, some iterations of the device. This has been a 10 year process to get this approved with at 12 months in the latest trial, PREVAIL, over 99% were off Coumadin.
So then when you compare this with the longer term results, 5 year results of primary efficacy again of a combined end point of stroke, systemic embolism as well as severe bleed and cardiovascular mortality there was superiority seen at least non-inferiorly depending on whether you look at the 5 year versus 4 year numbers of following these patients, and it was mostly driven by decrease in bleed risk. The stroke risk actually wasn't that much less, all right it was actually a signal of being a little bit more in the WATCHMAN group. And that probably makes sense because you are not dealing with aortic heart disease, you are not dealing with carotid disease, but in patients with severe bleeds, at least I view that as some of the sweet spot, this really showed a benefit.
They would receive aspirin for a while, I mean if you did aspirin, Plavix and then they continued aspirin afterwards. But many patients then aspirin is stopped as well. The one study that tried to look at aspirin/Plavix upfront had a greater thromboembolic phenomenon so that's why aspirin/Plavix is done I mean during the procedure.
Because in some way the whole device is empathetical to the theory that -
It's a systemic problem. Absolutely.
So it makes sense that you have it (inaudible)
The stroke rate, the ischemic stroke rate. Exactly. And I think that's really kind of the takeaway point of all of this, is so all stroke or systemic embolism was kind of a wash. The ischemic stroke rate in this not much different, the hemorrhagic stroke rate definitely less in the device group and you know even the ischemic stroke rate greater than 7 days was a little bit greater with kind of equal all cause mortality.
Let me just in the interests of time show - you know one of the other questions that comes up is while there is a stroke rate of doing the procedure itself and a complication rate, actually in the initial trial it approached 10%, which I think would seem high, down to 3 to 4% on the more recent trials. So like any other new procedure there is a learning curve and that needs to be kept in mind.
So I'm going to kind of go through this portion a little quickly just to summarize the FDA approval. So used in patients with AF, not related to valve disease, increased risk of stroke, recommended for blood thinning medications, are suitable for Warfarin at least for that period of time and have a reason to seek a non-drug alternative to Warfarin. And I think I would argue that the FDA unlike many other circumstances somewhat got this right. They didn't open up the whole flood gates of saying Coumadin alternative as the trials were actually run, it was some reasonable thought of why this should be done in that patient because of this stroke rate issue. If they have a blood clot in the heart you can't do it, if they've had anything done to their atrial septum you can't do it, they have to be able to tolerate some blood thinning medicine and can't have a sensitivity to the alloys in the device.
The FDA approval, as you all know, is not always the same thing as CMS, National Coverage Determination and Payor Approval, and that has come down now more recently just in the last month of a CHADS2 score of greater than or equal to 2, or a CHADS2-VASc greater or equal to 3 with what you would consider similar to TAVR and a heart team approach of an independent person, whether it's their primary care doc or somebody else involved that's not doing the procedure saying yes I think that it's reasonable and I want this to be considered for a left atrial appendage closure procedure, and some reason why you don't think they should be on longer term Coumadin, which is usually a bleed. Any comments from the panel? Maybe I'll go to this case and then we can talk about how you would think of a left atrial appendage device.
So this is a 72 year old with a history of hypertension, diabetes, persistent AF, managed with rate control and anticoagulated with Eliquis. Six months after Eliquis admitted with an intracranial hemorrhage and the Eliquis is stopped. What would you recommend next? A daily aspirin; a 1 mg a day daily aspirin at 325; Warfarin; restart the Eliquis or refer for a WATCHMAN procedure? So any reason you do 81 versus 325, let's start with that, in any patient? Forget about this patient, a coronary patient, etc? And actually even in the coronary population I would say we don't know right, that is 325 doing any better than 81 and there is a big trial that's going to be started to look at just that.
So would you ever think about Warfarin in somebody who has an intracranial hemorrhage on a NOAC? So I think that's really important getting that opinion from neurology and neurosurgery. And you know this concept of ischemic event with hemorrhage conversion, so maybe those patients could - that actually maybe you are doing them a disservice by not anticoagulating them. I always find the trouble is really getting that straight answer, there is always a little bit of waffling that we just don't know.
WATCHMAN, Amanda, can we take this patient for a WATCHMAN procedure?
We are, if we are not going to start them on anticoagulation then no.
Okay. So yet another kind of area where you know these absolute contraindications for even short term anticoagulation is I think what we are really looking for for an option and there are no great options, there is an option which has some promise which is called the Lariat procedure. It's a combined endocardial and epicardial procedure that is basically tying a knot around the left atrial appendage and it atrophies off, similar to what's done in the appendix in the abdomen. And actually the device that's approved to do this, that's what it was approved for. So because of that it's got a special kind of back door approval without really hardly any data by the FDA to be able to use this for surgical excision of appendices, wherever that appendix may be. So you know not to editorialize my feeling about the device, but anyway so having said that I think it's got some role and here is a video of how it's done.
So you get epicardial access with the sheath, there is also a transseptal endocardial access through which a guidewire is placed that has a magnet on the end of it. This is placed in the tip of the left atrial appendage, you shoot some die to define where you are. You blow up a balloon to define the proximal end of that appendage, because the idea is you want to tie it off here. Then you have epicardial access where you deliver basically a stitch, a noose that over this wire. The cool thing about this is these magnetic wires stick through the appendage wall, so you are not puncturing anything but it's used as a guidewire to get you over the area that you need to be here. So then there is this noose, you tie the stitch and you remove everything and over the next few weeks this atrophies off. And now you have a nice clean, safe, smooth barrier - sorry, smooth wall on that appendage but you can imagine that if you went a little shallow you may leave an outpouching, if you went a little deep you may not get a complete closure and it can be fraught with some of that.
Having said that this is what we call a dry tap to the pericardial space which is not easy, a higher risk of perforating a ventricle, etc. You can't do this is somebody who has had a prior thoracotomy and this is kind of where we are with this. But it is an option for those who absolutely have no ability to take anticoagulants and usually have had some problem with recurrent strokes, etc. as opposed to just a high score.
So I mean I think that's a great point. I think my personal belief is we are not quite there yet, I think the procedure is new, we are still learning about it and we may get to that point where it's like an SVT ablation, a drugs versus SVT ablation. But I don't think we halve the data to really support it and you are absolutely right, the challenge is this, can they take Coumadin for this 6 weeks or not? And I think that's what we struggle with as well.
I had the some thoughts that Lydia had as well about in patients who are undergoing open heart surgery should we (inaudible). The surgeons used to do that a while ago quite routinely. I'm not sure if Dr. Cook is here I don't know if there is a specific reason why that practice has changed.
Yeah, you know the only thing I'd say about that is on the one, just like the Lariat, we have very little data. And what data we have is actually negative on that front. There is a SERK paper out there of patients that got their appendage dealt with. Now what you call ligation versus stapling versus oversewing and the stroke then pretty cavalier about stopping anticoagulation, the stroke rate was like 6% in those patients. And is it because they have an incomplete closure? They would rather staple and oversew rather than cut off because of the bleeding risk and the bleeds that they get. So that that trial is ongoing now too of what way should we really address the appendage epicardially because I think that's definitely the easiest access, they are already there, it's got to be doable; but we have to find the right way to do it. It does, it definitely does.
On the left atrial size.
Yeah, so does left atrial size have any predictive value in recurrent atrial fibrillation or persistence or how long? The larger the left atria the higher the chance. So that's one of the things we look at when it comes to atrial fibrillation ablation of after about 5 1/2 cm even really after 5 the success rate of the procedure goes down because the heart is remodeled so much.
So I would view them as two different, you know whether to anticoagulate or rhythm control as two different decision trees. If they are not symptomatic I wouldn't cardiovert them in the first place in an elderly population with that. IF they are symptomatic I would keep trying even the recurrence rate is high then maybe needs an antiarrhythmic or a procedure, and the anticoagulation piece is all based on that CHADS score. There is some data that the higher the size, the larger the size the higher the thromboembolic risk, but that hasn't really made it into our CHADS type scores.
Great, well thank you all very much.