Good morning. My name is Julie Mobate. I'm the product manager for the LIA registry and the moderator for this session. And we're pleased to have Dr. Thomas Dooland. He is a cardiac electrophysiologist and an associate professor of medicine at the University of California, San Francisco. He's a left atrial appendage occlusion device implanter and is a member of the American College of Cardiology LAO Steering Committee. And he is an alumnus of Dartmouth College and Yale University. And we're happy to have him here. Thank you. All right. Good morning. Let me get this pulled up here. All right, great. So good morning. My name is Tommy Dooland. Thank you for having me and thanks for coming. So I want to start off by saying that my sort of involvement with left atrial appendage closure is that of a clinician who implants these devices. But I understand, obviously, our audience is very diverse in terms of what our relationship is to left atrial appendage occlusion. So the majority of this talk will be fairly clinically based, but I hope this will be valuable to you in that this will help sort of put some of these metrics that we or some of the data that we gather in the left atrial appendage occlusion registry into context and understand sort of why this data is so important for advancing care of our patients who undergo this procedure. So my hope is that by the end of this talk, we will understand what left atrial appendage occlusion is and why it is performed to recognize why post-implant medications are important. And finally, I hope that we'll be able to discuss some of the strategies, at least that I believe, can enhance medication adherence post-implantation. All right. So the first topic. Let's just briefly touch on atrial fibrillation. You are all likely aware of this arrhythmia diagnosis. This is the most common arrhythmia that we deal with as cardiac electrophysiologists in cardiology in general. So if you have the distinct privilege of living to be 40 years of age, your lifetime risk of developing atrial fibrillation before you die is roughly one in four. This is data from the Framingham Heart Study. So many of us in this room will unfortunately be diagnosed with atrial fibrillation, and I would argue that everyone in this room will know somebody, whether it's a spouse, a significant other, a parent, a close friend, that has or will have a diagnosis of this arrhythmia. And so atrial fibrillation is worth knowing something about. Now when I talk to my patients, when we talk to our patients about atrial fibrillation, I tell them that there's really three main treatment goals. First, we want to eliminate or reduce symptoms that they're having related to their atrial fibrillation. Number two is we want to prevent arrhythmia-associated cardiomyopathy. And the third atrial fibrillation treatment goal, the one that is relevant to this talk, is stroke prevention. And when I talk about stroke prevention or when I talk about atrial fibrillation-associated stroke with my patients, I explain to them that during atrial fibrillation, the top chambers of the heart, the atria, are beating very, very rapidly. They are electrically depolarizing 300, 600 times per minute, and they are electrically depolarizing so fast that mechanically, the atrium are not contracting in any significant fashion. That leads to stagnant blood flow in the left atrium. Stagnant blood tends to clot, and if a clot forms in the left atrium and embolizes to the brain, that's what causes a stroke. Now the real sort of explanation about what's going on is probably a little bit more convoluted than that. We certainly love to make things more complicated than they perhaps really are in medicine. But I think that's a reasonable conceptualization of what's happening in atrial fibrillation. And I often show patients diagrams like this of the heart, you know, cartoon diagrams showing them the right and the left atrium, explaining that the arrhythmia is arising within these structures. We often use these diagrams to explain, you know, atrial fibrillation catheter ablation, for instance. But many of these figures leave out one very important structure, and that is the left atrial appendage. So we all have a left atrial appendage. It's a pouch that comes off the left atrium. It's shown here sort of in this figure as this sort of nice round structure here. But in reality, the left atrial appendage is usually a very complex structure. Why do we have a left atrial appendage? I don't know. It's kind of like the appendix of the GI system. It certainly has some reservoir function and hemodynamic function, maybe some neuroendocrine function. But bottom line is we all have it. And prior data from echocardiography and then, you know, more recent data from these left atrial appendage closure clinical trials indicates that the vast majority of clots that form in the left atrium and then embolize to the brain to cause stroke come from the left atrial appendage. So in reality, the left atrial appendage is this very complex structure. There is dramatic variation in size and morphology between patients. There has been some attempt in the literature to kind of have a classification scheme, although the nomenclature is still, I think, a little unusual. So there's things like chicken wing, cactus, windsock, cauliflower, all sort of ways in an attempt to classify these different morphologies. But in general, you can see that these appendages become very complex structures, very highly trabeculated as you get more into the distal appendage. And this has some implication for left atrial appendage closure. This is a 3D reconstruction of a CT scan performed on a patient prior to atrial fibrillation catheter ablation. You can see, again, the appendage sticking off the left atrium. And you can appreciate how this particular appendage has a quite narrow neck. And while it's not, you know, multilobular, it's relatively straightforward from that standpoint, there's still a lot of sort of craters and lobules to it. So clinically, we use CT scans to look at left atrial appendages. We also use a technique called transesophageal echocardiography. So luckily for the cardiac imagers, although this is really bad for us in cardiac electrophysiology when we like to burn on the back of the heart, but luckily for the imagers, the left atrium sits directly adjacent to the esophagus. There's no bone or air or other structures that impair echo images in between. So our echo colleagues are able to get these beautiful images of the left atrium and the left atrial appendage. And you can see the left atrial appendage here is sort of this triangle-shaped structure. And this is a relatively simple morphology, especially in this echo view. But that's what we're looking at when we do these TEs for Watchman candidacy. And this is what a thrombus looks like. So you see this sort of serpiginous structure here in the left atrial appendage. These little tick marks on the side are one-centimeter markings. So this clot is maybe three centimeters by one centimeter. And you can imagine if this leaves the heart and goes to the brain, this can do some real damage in the form of a stroke. And even if it doesn't go to the brain, but it could go to a limb and cause limb ischemia, it could go to the gut and cause gut ischemia, it could infarct the kidney. So when these thrombi leave the heart, they cause a lot of problems. Now, the good news is, is that anticoagulation works, and anticoagulation works really well. There are few pharmacologic treatments in medicine that have as profound a treatment effect as anticoagulation does for atrial fibrillation stroke prevention. So this was a clinical trial done, or published now, over a decade ago. But in this trial, they took patients who the providers thought were poor candidates for long-term anticoagulation, and they randomized them to either aspirin or apixaban. And they felt that there was sort of clinical equipoise to do this, because it was felt that these patients maybe couldn't take anticoagulation. And interestingly, they had to stop the study at one year. They had to stop the study at one year because they felt it was unethical to continue to randomize patients to aspirin, because the stroke prevention effects of apixaban were so profound. So we prescribed a variety of anticoagulation medications to our patients in 2022. Some of them are listed on the right, warfarin being the sort of tried-and-true drug that's been around for many, many decades, with the newer medications, although, honestly, they're certainly not so new anymore, listed below that. But it's important to remember that anticoagulation only works if it is prescribed, and anticoagulation only works if it is taken by the patient. So this is interesting data. This is NCDR pinnacle data from my colleague John Suh, who works at the University of California, San Diego. They looked at a variety of cardiology practices that enrolled patients in the pinnacle registry, and they quantified the proportion of patients within each cardiology practice that were prescribed an oral anticoagulant. And interestingly, the median practice treatment prevalence was only about 50%. So only about 50% of patients in these practices are receiving this very potent, very effective anticoagulation therapy for atrial fibrillation stroke prevention. And why is that? Well, the maybe obvious answer would be these cardiologists don't know what they're doing, and they need to be educated that these patients need to be on anticoagulation. But I don't think that's really the case. I think, you know, clinically caring for these patients, I can tell you that many patients, most patients, don't want to be on an anticoagulant medication because they're worried about the risk of bleeding. And then there are many patients that can't be on an anticoagulant medication because they've had a prior bleed. And so we see these patients very frequently in clinical practice. Maybe an elderly patient who's a fall risk in their family, and maybe their primary care provider are very worried about putting them on anticoagulation. Heaven forbid they fall and hit their head. We see many patients who have already had prior head bleeds prior to their atrial fibrillation diagnosis. People are very appropriately so, very reluctant to put them on an anticoagulant medication, which may worsen the likelihood or increase the likelihood that this could recur. Patients with prior GI bleeds, patients who engage in hobbies or have a profession that puts them at high risk for traumatic injury. These are all examples of individuals for whom anticoagulation and atrial fibrillation may be problematic. So who do we consider for left atrial appendage occlusion? Well, patients have to have atrial fibrillation to start off with. They have to be at elevated risk of stroke. As you're probably aware, the risk of stroke is not shared equally among all individuals with atrial fibrillation. And we use this CHADS-VASc scoring system to assign a point score to an individual patient to estimate their yearly risk of stroke off anticoagulation. The higher the CHADS-VASc score, the greater the risk of atrial fibrillation-related stroke. So when these devices were approved by CMS, it was deemed that patients should have a CHADS-VASc score of three or greater. In addition, they must have a suitability for short-term anticoagulation, but they have to be deemed unable to take long-term oral anticoagulation. So these are the devices that we are currently implanting. There are other devices, but these are the two FDA-approved devices for percutaneous left atrial appendage closure. Shown on the left is the Boston Scientific Watchman Flex. And on the right is the Abbott Amplacer Amulet, which is a newer addition to the armamentarium. These devices are put in typically under general anesthesia. We go through the femoral vein, usually the right femoral vein. That brings us to the right atrium of the heart, where we perform a transeptal puncture to gain access to the left atrium. And that's, of course, where the left atrial appendage is. These devices are placed via a catheter and sheath, and we position them in the left atrial appendage. We make a lot of measurements to make sure that the appendage is adequately sealed, that there's no leaks, that the device is well compressed. We tug on the device to make sure it doesn't come out when we apply some, hopefully, gentle counter traction to the device. And as long as everything looks good, we then loosen the screw, and the device is on its own. As the device is coming out, the device stays in place, and hopefully the patient remains free from stroke. So this is what a Watchman device in the left atrial appendage looks like. This is on a transesophageal echocardiogram. You can see the Watchman device sort of sitting down here, and it's flexing with the heart. And this is sort of where the appendage would have been if there was no closure device. And I'm not going to go through much of the data supporting the efficacy of Watchman, but this is pooled data from the two randomized clinical trials that got the Watchman device approved, Prevail and Protect. And you can see when you combine all the data and follow these patients out for five years, that at five years, all strokes or systemic embolisms was about the same between the two groups. However, Watchman randomization was associated with a reduced risk of hemorrhagic stroke because these patients are able to come off long-term anticoagulation, presumably. But maybe there's a little bit of a price to pay. Maybe there's a little bit of a price to pay in terms of increased risk of ischemic stroke or systemic embolism. But nonetheless, when you look at all-cause mortality, and this is as randomized at five years, there was a reduction in all-cause mortality with randomization to Watchman versus Warfarin. One of the main things I want to emphasize, what I spend a lot of time talking to patients about, and frankly what I spend a lot of time talking to referees about, is that percutaneous left atrial appendage occlusion is a treatment strategy. We do not put these devices in and patients get off the table and we say, have a nice life, see us back in clinic if you have any problems. It is a treatment strategy. This is the initial post-implant medication regimen that was assigned to the original Watchman device, and we'll talk a little bit more about this later. But you see that these patients are pretty heavily anticoagulated or treated with antiplatelet agents out through at least six months. The second goal of this talk is to recognize why post-implant medications are important. Why do we prescribe anticoagulant and antiplatelet therapy after percutaneous left atrial appendage occlusion? We do so because we are concerned about device-related thrombus. So we took a look at these devices a few minutes ago, but these devices are basically a metal scaffold, and in the case of the Watchman, it's a nitinol scaffold, so it's a nickel titanium alloy over which there's a fabric cap. And this fabric cap is what faces the left atrium. And it turns out that our blood, when it encounters any foreign material, loves to clot on that foreign material. And we've learned this lesson with cardiac stents, right? That's why after putting in a cardiac stent, patients need to be on antiplatelet therapy to prevent their platelets from forming clots on this stent scaffold that's in their coronary artery. So two, do we have to protect our patients from clot formation or device-related thrombus on the face of these devices as they are healing into place? So this is what device-related thrombus looks like. These are four, on the left, are four transesophageal echocardiogram pictures of device-related thrombus, and on the right are four CT scan pictures. So if you look down here in panel F, you see this Watchman device with this big, fat thrombus right here on the face of the device, shown by the star. Maybe down here in panel G, you see an amulet device with this dark structure right here. That's a clot on the face of the amulet device. This is really bad. This is really bad because these clots can embolize, they can break off the device, travel to the brain, and cause a stroke. If that sounds familiar, that's the exact reason why we're putting in these devices, to prevent that process. Now, in these patients, we have, unfortunately, given them the disease or the problem that we're trying to prevent or protect them from. Now, the good news is that our bodies heal over these devices and sort of seal them off over time. So this is data from a canine model. You see that even at three days, the body starts to form granulation tissue over the face of the Watchman device. And at 45 days, the device is largely endothelialized. So the body has formed a layer of cells over the face of this device and is really going to prevent blood from directly interacting with the fabric mesh and preventing the risk of device-related traumas. These are two examples from human autopsy, one at 200 days, one at close to 900 days. I don't believe these patients died of complications related to their Watchman or stroke. You see there is nice endothelialization of the device at 200 days, although for some individuals, the device does not completely endothelialize or does not endothelialize as fast as in other individuals. We don't have a perfect understanding of who that is, why that is, what factors affect how quickly these devices sort of seal off. And there's sort of this arbitrary six months of protection that we prescribe for these patients. But the truth of the matter is we don't know the right duration of therapy. No one studied four months versus eight months, six months versus 18 months, et cetera. So how common is device-related traumas? Well, it depends, frankly, on how you're treating patients after Watchman implant and how often you look, not surprisingly, right? So in the Protect and Prevail clinical trials, when there were transesophageal echocardiograms done at 45 days and at one year, the risk of device-related traumas was about 3.5%. I think it was 3.7% in these patients. But in other clinical settings, when people are looking more frequently or perhaps anticoagulating or prescribing antiplatelets with less frequency or at lower doses or less dual antiplatelet therapy, the risk of device-related traumas is higher. So in this setting, it was 7.2% per year. And higher rates are seen among those who were discharged either on no therapy or single antiplatelet therapy. So device-related thrombus, as we mentioned, as you may expect, is bad. It's bad because it causes stroke or systemic embolism. So patients with device-related thrombus are at much lower likelihood of remaining free of ischemic stroke or systemic embolism. And that's been shown in this study. It's been shown in other studies such as this one as well. If you form a clot on the face of your device, you are at really high risk of having an ischemic stroke or TIA. And at the risk of stating the obvious, device-related thrombus is very difficult to treat. It's difficult to treat because the reason we are putting these devices in patients is that they are poor candidates for anticoagulation, poor long-term candidates. So now you take a patient who's had a prior brain bleed and doesn't want to be on anticoagulation, you don't want to prescribe anticoagulation, and you get this TE and you find, oh man, now they have a clot sitting right on their device. And presumably, the treatment is going to be escalation of anticoagulation or antiplatelet therapy. But that patient may not be able to tolerate it. Or you may be trading the benefit of getting rid of this thrombus with an increased risk of intracranial bleeding. So we don't like to treat device-related thrombus. We like to prevent device-related thrombus. So what are the recommended post-implant medications? And this is very relevant to the NCDR, left atrial appendage occlusion registry. So if you go to the FDA website and look up these devices, you can find their directions for use, the pamphlets. And this is for the amulet device. So for the amulet device, it's recommended that patients receive aspirin and clopidogrel, so two antiplatelet agents, for six months after implant. Again, that is to prevent device-related thrombus while the endothelial layer is forming over the face of the device. Why six months? Why not four months? Why not eight months? Because that's how they did it in the clinical trials that got this device approved. So there was someone, obviously, with understanding of how this endothelial process works, with a lot of thought going into this. But six months was picked somewhat arbitrarily. And we don't know, again, the exact time course that patients need to be treated for to maximize results, to minimize bleeding, and to minimize device-related thrombus. So when the Watchman device first came out, this was the regimen. I call this the old school Watchman regimen. So the Watchman clinical trials, Prevail and Protect, used warfarin and aspirin for the first 45 days. At 45 days, the patients got a transesophageal echocardiogram to look for appendage closure, or continued appendage closure, to make sure there's no clot on the device, to make sure the device has sealed off the appendage. And if that is the case, warfarin was dropped and clopidogrel was started. And that was continued out through six months. Now, after a year or two on the market, I would say most of us were implanting these devices not with warfarin, but with direct oral anticoagulants, like apixaban, rivaroxaban, dabigatran. They're just much easier to take than warfarin. They don't require the monitoring. There's not all the drug-drug and drug-food interactions. So this is what we had been doing up until 10 days ago. All of our patients were being treated with, or most of our patients were being treated with this regimen. 10 days ago, roughly, the FDA granted approval for the WatchmanFlex for patients who get this device to be treated with dual antiplatelet therapy. So now the same regimen as the amulet device. And so patients can, instead of getting the oral anticoagulant plus aspirin for the first six weeks, and then dual antiplatelet out through six months, now they can just go straight to dual antiplatelet therapy. And this is actually, this data directly comes from the NCDR, left atrial appendage registry. This was presented at TCT this year. And so this is the registry in action. So while there are these recommended regimens by the FDA, there are many different off-label anticoagulant and antiplatelet regimens that are being used. And the data supporting one regimen over the other are from observational studies. And in an observational study, you have a health care team that's looking at an individual patient, and they are trying to gauge what is the risk of clot formation, what is the risk of bleeding complication. And there are biases that come in in terms of how you prescribe anticoagulant or what you prescribe for that patient. And so these observational studies, while a lot of statistical wrangling is done to try to minimize the risk of this bias, they all are subject to bias. We do not have large, robust, randomized trials comparing different anticoagulation or antiplatelet regimens to each other within the same device after implant. And so we frankly do not know the best way to treat patients after appendage closure. And I will even go as far as saying that there probably is no one best way to treat patients. Certain patients may have higher risk. Certain patients are definitely at lower risk. And you can imagine a scenario in the future where we have some scoring system or some other clinical metric that dictates how we treat individual patients. To add more complexity to it, there are genetic mutations that change how individual patients break down some of these medications, clopidogrel in particular. So roughly 25% of the population harbors a mutation that renders clopidogrel less than ideally effective. So there's an entity known as clopidogrel resistance. And for those patients, aspirin and clopidogrel may not be the best regimen. So there's a lot more to be learned in this area. The other thing I'll say is that I believe there is an unjustified enthusiasm for dual antiplatelet therapy. People seem to think that dual antiplatelet therapy is better because it protects patients, but it doesn't expose them to the same risk of anticoagulation. But I would argue that there's probably no data to support that. In atrial fibrillation stroke prevention, dual antiplatelet therapy has been compared to warfarin. Dual antiplatelet therapy resulted in an increased risk of bleeding, not a decreased risk of bleeding, an increased risk of bleeding compared to warfarin. And we don't need to look even farther than the left atrial appendage closure literature. So this is the amulet IDE trial. This is what got the amulet device FDA approved. It randomized patients to the amulet device and the Watchman device. Amulet device patients received dual antiplatelet therapy for six months. Watchman patients got the warfarin plus aspirin for six weeks, and then dual antiplatelet therapy through six months. Now, if you look at non-procedure related bleeding, there is absolutely zero difference between these two groups. You would not expect the device sitting in their left atrial appendage to change their risk of cerebral hemorrhage, GI bleed, et cetera. And these patients were randomized. There was no selection. They were randomized. And so the fact that there's no difference in bleeding, in my mind, suggests that there's no real difference in bleeding between dual antiplatelet therapy and this warfarin plus aspirin, followed by dual antiplatelet therapy regimen. So I just bring that up in that anticoagulation gets a bad rap, possibly justifiably so, but I'm not certain that dual antiplatelet therapy is a much less risky intervention. And I'll say that this is very provocative data that's come out of a group in Texas and hints that maybe anticoagulation therapy is something we should be doing more of. So they looked at patients that got a Watchman and they got the standard regimen, which included, I think, mostly apixaban and aspirin through, again, 45 days, and dual antiplatelet therapy through six months. And then they treated another group of patients differently. So they treated them with half dose apixaban and aspirin through 45 days. And then instead of doing antiplatelet therapy, they just continued the half dose apixaban. So they did not receive any antiplatelets after 45 days. And the results are almost too good to be true. And there have been calls for a randomized trial to look into this. I look forward to that data. There was no device-related thrombus in the half dose DOAC group, whereas the dual antiplatelet group had a reasonable amount of device-related thrombus. There was way less bleeding in the half dose DOAC group compared to the aspirin and clopidogrel group. And there was less of the composite endpoint, which is stroke and systemic embolism. Now, again, this is not randomized data. This is observational data. It is prone to certain biases. But there is certainly a suggestion here that anticoagulation, and maybe anticoagulation at a half dose, may be really important. There might be something really important about inhibiting the coagulation cascade and not the platelets that protects patients from device-related thrombus and maybe minimizes their risk of bleeding. So you all, many in the audience, I should say, are probably familiar with this. This is the data that's collected in the left atrial appendage occlusion registry. And because of these various regimens that are used, we want to learn how patients do after these when they're on these various treatments. And that's the rationale for collecting all this data. But how about our intrepid canyon jumper here? He or she gets a Watchman device put in, goes home, gets on the internet, says, my doctor sent me home on warfarin and aspirin. I can't remember. Is that what they said I should stay on? They start googling the internet. They say, should I be on aspirin? Should I be on clopidogrel? Should I be on apixaban? Should I be on some combination of these things? It can be very challenging. And so I want to spend the last few minutes just discussing strategies that can enhance medication adherence post-implantation. There are a lot of challenges in communication what I would characterize as a diverse health care team in the patient after left atrial appendage occlusion. Some of those challenges include that there are multiple post-implant regimens used. That's what we've spent the last few minutes talking about. Left atrial appendage occlusion is often performed at specialized centers. So many of the patients that we close are referred to us from outlying hospitals or outlying clinics where they don't perform left atrial appendage occlusion. And if I perform this procedure at UCSF in San Francisco and the patient goes home and has some bleeding problem, there's over a dozen emergency rooms that they can go to just within San Francisco in the East Bay. You add in the North Bay and the peninsula, there's over 30 different emergency rooms. They show up at a hospital where they don't perform this procedure. No one there has a great understanding of the rationale for the post-implant regimen. And maybe the patient comes in, they stub their toe, they're having a little bit of bleeding, and they say, oh, you had this Watchman device. You don't need to be on anticoagulation. And then they stop it. And now you're trading maybe a very minor bleeding problem for a very serious or real risk of device-related thrombus and stroke. Furthermore, these patients are at increased risk of bleeding complication by definition. The whole reason we're putting these devices in is to get them off long-term anticoagulation. So we expect that these patients are going to be having more frequent encounters with the health care system than our ordinary patients with atrial fibrillation that we treat with anticoagulant medication. And finally, many providers are involved in the care of these patients. As you are likely well aware, Watchman requires shared decision-making with a non-implanting physician. So there is someone usually referring this patient to us, whether it's a primary care provider, whether it's their general cardiologist, whether it's a neurologist. There's someone else usually heavily involved in this patient's care. And it's very important that we communicate with that other provider. Because when these patients do have complications, and unfortunately they do, we need to be involved in the discussion about what is the best way to manage them, balancing all the risks and benefits. So whose role is it to help guide this care? I'm very upfront that it is the role of the implanting team to do so. And I think it's very important for us to take on that role. I've been in a lot of discussions and meetings. How do we help streamline the care? How do we effectively communicate to all the patient's providers? I really think that there's a strong emphasis on things. It's frequently brought up that we should be utilizing the electronic health record. Artificial intelligence is often another buzzword that's thrown in here. But in my opinion, at least in the short term, the electronic health record will not save us. In our city, many hospitals are on Epic. And despite it being the same health care, EHR, none of them communicate with each other. In fact, our county hospital, San Francisco General Hospital, is also on Epic. But it doesn't communicate with the Epic that we have at the university, or it doesn't communicate very well. And so I really think that in 2022 and in the foreseeable future, we have to rely on perhaps very primitive techniques, which involves directly speaking, if you can believe it, to our patients, their family, and to the referring physicians. Picking up the phone and calling someone seems so dated these days, but it's really, I think, really important. It seems like every time I can't get in touch with the referring physician, those are the patients that present a week later with a problem. And I'm getting these phone calls. Ms. Johnson's in my office and bleeding out of her ear. I thought you put a watchman in her. I thought she should be off anticoagulation. What's going on? And so apart from trying to be as diligent as I can in terms of communicating with the patient and family, communicating with the referring physician, the other thing that we've started doing is giving the patient a form letter. And I think this has been relatively, it's certainly well-received by patients. And this is an example of the letter that we give. This is one I gave to a patient earlier this month when we closed her appendage. So at the top, it says, you underwent a watchman left atrial appendage occlusion on the date. And then we say, everything went well. These are the medications that are going to be discharged on. I give them a stop date for the medication so they understand this is how long you're going to be on these medications. And I try to use relatively patient-centric language to describe why I am prescribing these medications. And then I think the most important thing, and again, I emphasize this when I give this to the patient, is if you have a bleeding problem, call our office immediately. If you go to an emergency room with a bleeding problem, have them call our office. Or if you're seen in a medical office, call this phone number. And I ask them to take a picture of this and put this in their phone, again, hopefully to remind them that they need to be on these medications. We're prescribing them, not just because, but there is an important reason to do so. Because if there is an issue, if there is a bleeding problem, and they need to come off these medications, we want to be involved in the conversation to help understand or communicate the potential risks of doing so before the medications are stopped. So my hope is that in the last 30 or so minutes, we've grown in our understanding of what left atrial appendage occlusion is and why it's performed. We can recognize why post-implant medication regimens are important. Although we don't know the best one, we know they need to be on something. And there are a variety of options. And then we briefly discussed some of the strategies that I think can enhance medication adherence post-implantation. Thank you. Thank you. We do have a couple of questions. Sure. So one was, is there discussion about making the LAO procedure a first-line treatment instead of going through the failed anticoagulants? Yeah, so there is a clinical trial. I think it's called CHAMPION that's funded by Boston Scientific looking at upfront Watchmen. So Watchmen versus standard anticoagulation in patients who are, I think, to get into the trial, you have to meet some sort of heightened bleeding risk criteria. But half of the patients or part of the patient population is getting randomized to anticoagulation. And the others are getting randomized to closure. Important that several of the clinical trials that got these devices approved did not specifically enroll patients who are at heightened risk of bleeding. That is a CMS addition to things. And so probably appropriately so, there was some concern that bad actors would run amok and put these devices in everyone. And so there's very stringent criteria right now. But whether this should be only limited to individuals who have had bleeding problems in the past remains to be tested and will be tested. Of course, there's a strong financial incentive for the companies that manufacture these devices to get them in more patients. And so they will definitely be looking to expand treatment indications in the future. And then the next question, how do you document your plan medication strategy? So I'm thinking that you have it for the patient once they're done. But prior to, do you have something documented that this is what happened? Prior to implant? I'm thinking that's a hopless question. Yeah, so we have like a dot. So we use epic for better or for worse. And we have a dot phrase that we use in our clinic encounter, that sort of the clinic encounter most proximal to the left atrial appendage occlusion. And if for whatever reason that's not in there, we put it in our pre-procedure history and physical on the day of the procedure. So we typically line out, this is the anticipated anti-coagulation regimen or anti-platelet regimen that we will be using. And then we certainly document it in the discharge summary. And then I think the last question is, have you seen success with the letter that does that bridge the gap between once they leave and they've had their procedure with the PCPs or cardiologists or once they go back for another procedure? Yeah, I mean, I don't see the letter as substituting for that. It's mostly if they end up somewhere where we haven't been effective in communicating with. But it's hard to, thankfully, it's I don't mean to give the impression that every patient's coming and hemorrhaging after we put in these devices. The vast majority of patients do very well. They complete their six-month course. And we stop following them as closely. But I can't think of a large trend or a large difference that we've seen. But in part, we're not a huge number of patients before coming back after having stopped everything. But I think that one patient who has their medication stopped for not great reasons and has a stroke is obviously one too many. And so we want to try every strategy we can. Giving them a form letter that takes me literally 60 seconds to print out, I think, is a reasonable strategy to help mitigate that risk. I think that's it. That's it. Now, and how much time after the procedure and discharge? I give that to them the day after the procedure when I see them. And I ask them to take a picture and put it in their phone. Unfortunately, most of them have their phone with them in the hospital. But sometimes, their phone is in the closet or in the hospital room. But sometimes, we do it right there while we're talking. But yeah, I try to just give it to them in person. I think that's it. All right, great. Thank you. Thank you so much.

Dr. Thomas Dooland

cardiac electrophysiologist

left atrial appendage occlusion

post-implant medication regimens

atrial fibrillation

stroke prevention

LAA occlusion devices

medication adherence