Narrator:
0:01
Welcome to MedEvidence, where we help you navigate the truth behind medical research with unbiased, evidence-proven facts, powered by ENOCORE Research Group and hosted by cardiologist and top medical researcher, Dr. Michael Koren.
Dr. Michael Koren:
0:16
Hello, my name is Dr. Michael Koren and I'm delighted to be part of this wonderful series with my dear friend and colleague, Dr. Neil Sanghvi, who is an electrophysiologist who is talking with me about A-fibrillation.
Dr. Michael Koren:
0:30
This is a series called Two Docs Talk AFib, part of our MedEvidence platform. We've been having just a fabulous and fun and educational discussion about managing A-fibrillation. In the last segment, we talked a lot about a hypothetical soccer player who was diagnosed with A-fibrillation that had a lot of issues with regard to anticoagulation and managing the arrhythmia and ultimately making sure that this person did not miss penalty kicks on the field because of A-fibrillation, which was the proximal cause of his referral. So Neil is a national expert. He's been on a lot of different panels from different venues around the country talking about rhythm issues and he's the medical director of the heart rhythm section at Flagler Hospital here in northeast Florida, so very, very well-versed in this and just a wonderful speaker and somebody that can help us really understand these issues. With that, Neil, we were talking in the last segment about the decision between anticoagulation and using a left atrial closure device, and this is an area where there's a lot of current research going on and maybe you can help us start to explore that?
Dr. Neil Sanghvi:
1:40
Oh, absolutely. So give us your perspective. Yeah, you know, I think the arena of stroke prevention in AFib is a tremendously large area because of the issues obviously the morbidity for the patient and the suffering that they suffer and the cost to the health system in managing these patients, and so we are trying to do the best we can to help protect these patients. And so, right now, there are two strategies on managing AFib patients. T here is a patient who needs to be on some form of anticoagulation. We talked about these NOACs that are currently existing warfarin back in the day, which tended to be the only agent that's out there. And, you know, clinical trials. I think, Mike, you're involved with some of these, right?
Dr. Michael Koren:
2:22
I've done a few in my day.
Dr. Neil Sanghvi:
2:24
Just a little bit right, involving alternative ways of looking at the delivery of anticoagulation for these patients. And so, you know, I think the area of research is ripe in this arena. There's some monoclonal antibodies that I believe that are being explored right now in this arena to see if there are easier ways of delivering anticoagulation. So right now we're required to dose patients on a daily or twice daily basis with a regimen to try to help get them the anticoagulation that they need. And that comes with its own right? You've, got to remember, I've got to take my pill. Did I take it today? Did I take it yesterday? And so some ease of therapy might be an issue. And so there's research going on in that arena. You know, I'm going to dive in a little bit on the other side of it right now, which is that left appendage closure which we were talking about, that pouch closure.
Dr. Neil Sanghvi:
3:18
As of today, its indication is mainly for patients who are considered to be not candidates for long-term anticoagulation because of risk profiles. Right, that patient that falls, that patient was active, right. But what we're learning is that its effectiveness is quite powerful. And that perhaps it really ought to be not simply meant for the patient who's excluded from anticoagulation, but rather a choice for the patient who doesn't want anticoagulation, right? So the patient who says, yeah, I understand, I have a risk of stroke and I need something to treat that risk. Perhaps I could be considered for this in implantation of a device versus being on a day-to-day anticoagulate.
Dr. Neil Sanghvi:
3:58
So the Watchman device, which is a Boston scientific device. They have a trial called the Champion trial right now which is enrolling patients, looking at effectively patients who are considered for anticoagulation and then randomizing to say, okay, you stay on a de-coagulation, you get the Watchman and we're gonna see what happens. And the goal is to show that the rate of stroke is no different whether you are on a blood thinner every day. Or if you got the device put in. So that's going on, you know as a therapy.
Dr. Michael Koren:
4:25
I'm gonna break that down a little bit more with you, because you brought up a lot of really really good things and research questions and I have to prevent myself from getting too nerdy here, but a little bit of background will probably be helpful for people who are listening in on us. So Just remind everybody in the medical field and people in the non-medical field is that we develop clots through this coagulation cascade and there are a number of different factors and we use these numbers to describe all the different factors. And Warfarin, or cumin, in which we mentioned, which was originally developed as rat poison in Wisconsin, based on cattle that were eating certain types of grass and having bleeding problems, which is, you know, really interesting trivia and interesting ways of looking how drugs are developed. But nonetheless, that particular drug hits a lot of these clotting factors non specifically, and the newer drugs are now looking at factors very, very specifically, and the Noax, or the novel anticoagulation Agents that we were just talking about, often hit factor 10. But there's also other factors that lead to the development of something called thrombus, which is required for a blood clot. That may be better targets for Anticoagulation than what we have currently on the market. So one of the clinical trials that we're doing now is looking at something called factor 11 that we hope is more specific for preventing thrombus but less likely to cause bleeding that may come from your glass, your glass cutter person or other people that are involved in day-to-day activities, including soccer, that may put people at risk for Bleeding, complications or very bad bruising.
Dr. Michael Koren:
6:10
So, from the medical standpoint, we're trying to get better and better drugs. To get those coagulation factors that are very specific for thrombus or clot that would form in the heart and less specific for other things, and then that is being weighed against this concept of using devices. So just to make sure that people understand that point of view. So again, take, take that information and give us a little bit more insight clinically. You mentioned this a little bit before in the previous segment. But will there? will there be people you know over the long run that you think ultimately would be better for one approach to the other, also realizing that A-fibrillation is one form of developing clots, but there are certainly other medical diseases out there that are associated with the same risk factors of A-fibrillation That also form clots right, yeah, no, I think.
Dr. Neil Sanghvi:
7:06
I think we need both therapies and we absolutely need both strategies. The AFib patient specifically there are people who just don't like the idea of having something inside their hearts right, and so they want to be protected, but they don't want a device. That's your anti coagulation patient that may benefit from whatever anti coagulant that's of use in the market at that time right, whether it be the current NOACs or there's some of the things that are being researched as we, as we just touched on. And then there are Going to be patients who say I want simplicity and I wish to have as minimal amount of meds that I could possibly be on, but I need to mitigate my risk of stroke, and that is that patient who will go towards a device route. One of the other areas of research that's occurring is as it pertains to the device-related methods of AFib.
Dr. Neil Sanghvi:
7:57
Thrombobolic prophylaxis, or protection against stroke, is as I have spoken about before. We use AFib ablation as a tool to manage symptoms. Well, we're looking now to see well, if, at the time, I'm already in the heart, if I'm already there if I place this device at the same time that I'm in the heart, perhaps I can deal with both aspects of AFib the symptom side and the stroke side. And so perhaps that's an area where patients will benefit with one procedure with two benefits, and so that's an area of research that's also ongoing. But you're absolutely right anticoagulation, or anticoagulants more specifically, are not going away. We have indications for intral fibrillation.
Dr. Neil Sanghvi:
8:39
We have indications for patients, as you have alluded to pulmonary emboli or DVTs clots that happen in other vascular beds, that they need to be on blood thinners and they need something that's not gonna increase their risk of bleeding but also prevents that clot from forming again in the future. So I think these are areas are ripe And I'm gonna shamelessly plug research and your organization specifically. We need patients to participate, because the therapies we have today is because of the generosity and unwillingness of other patients to participate in trials to give us the therapies that we have today, and so we need patients today to help us move that needle and to somewhere better right, and I think it's participation through research that gets us there right, and it's the trials that you're participating in or others that we've done in other arenas.
Dr. Michael Koren:
9:28
Yeah, all I consider that is amen And well stated, and this is certainly my passion, so I appreciate that very, very much. So I'm gonna have just a few quick fired technical questions for you to answer. We just have a few minutes left and hopefully you can share your wisdom and insight. So explain to people what actually happens if you put a device in with the goal of not using anticoagulation. Does that mean that from day one you're off of anticoagulant, or how does that work? Explain that to people, that transition.
Dr. Neil Sanghvi:
10:02
Yep, so great question. So the delivery of the device itself it's performed, as I mentioned, what we call percutaneously is done through a vein and the leg. There's no cutting involved takes about 30 to 40 minutes to do, generally speaking. The moment the device is deployed, its purpose is to act as a scaffold so the inner lining of the heart can overgrow it, and so there's always some inherent risk that a clock could form on the device early on. So we're not completely off anticoagulation, but what we're able to do is quickly downgrade, and so typically patients are on your agent of choice, whether it be Warfarin or one of the No-X. They'll come in, they have the procedure done.
Dr. Neil Sanghvi:
10:39
We're often immediately able to downgrade to an aspirin and something called clopidogrel, which is a mild or formal anticoagulation They'll continue for at the moment, continue for six months, and then they're just on a baby aspirin after that, which has a much lower risk of bleeding than any of the potent agents We spoke of. Clinical research One of the other areas that is being explored right now is can we accelerate the elimination of the blood thinning? So maybe, rather than waiting six months, is it just three months that we need for that compenetration therapy, and there's even another trial going on to decide whether we even need the aspirin long-term. Perhaps we don't need anything at all. So that's the areas of research that are ongoing in that space Interesting.
Dr. Michael Koren:
11:18
So thank you for that answer. The next thing that I get a lot is my A-fibrillation. Patients ask me is this congenital in any way? Is there a genetic predisposition to A-fibrillation? And if there is, what do we need to do for family members?
Dr. Neil Sanghvi:
11:33
Yeah, that's a much more difficult question. I think genetics comes into play. In the patient that is very young and that shows up with AFib There is some concern that there's some thought that there is some genetic predisposition. Screening becomes very difficult, quite frankly, because AFib, as I mentioned previously, is very prevalent And in the majority of our patients who are showing up to your clinic or my clinic they're much older and they tend to have other comorbidities high blood pressure, obesity and so forth And it's hard to blame genes when you have other risk factors that are coming in.
Dr. Neil Sanghvi:
12:02
So, generally speaking, from a familial standpoint, there isn't any strong screening that I tend to recommend, except for, you know, if there's concern. There are those wearable devices that we talked about before that patients can utilize to kind of screen themselves, including the watches that exist out there today. There's another and again I receive no reimbursement from these companies but there's a on TV you'll see something called Cardio Mobile, which is another device that one can utilize to kind of pair with their phone and they can screen themselves. But the most important thing is it's identifying the problem in the individual, knowing what risk factors are, so they can help inform their family members to avoid the risk factors and then dealing with the risk factors with patients themselves.
Dr. Michael Koren:
12:45
Yeah, and the issue Identifying age fibrillation is a huge area of research interest right now, particularly using artificial intelligence and whether or not there are certain warning arithmias that predict, even amongst patients with age fibrillation, who's gonna have more serious complications. So Just fascinating stuff, particularly in the AI world, and I actually went to this interesting conference at the American College of Cardiology where they were talking about there are signals on the EKG That we didn't even think much about. Like that, the whole space on the EKG between the T wave and the P wave We thought didn't really give us much information. But maybe that's not true And if you have any thoughts for some of these crazy ideas that are now starting to be explored in clinical trials, no, i think.
Dr. Neil Sanghvi:
13:33
I think the aspect of the EKG which gives us that picture, that electrical picture of the heart and Intervals that we otherwise thought were not non-contributory and determining whether or not they give us more insight into the electrical signals of the heart, is very fascinating to me.
Dr. Neil Sanghvi:
13:50
You know, I don't have direct knowledge of the EKG analysis, but I do have experience in the space of when we do ablation. So, as I mentioned to you before, when we do ablations is anatomic, we're hitting these veins, but we realize that we're not, we're not batting a thousand with that right. And so there's AI applications on signal, inter cardiac signal analysis to determine if there's areas of tissue That may be more susceptible to triggering A fib, and perhaps those are areas that should be targeted. So same concept, different application, but helping us give us insight into arenas that we otherwise weren't paying much attention to. So, yes, i think the application of AI, as it pertains to rhythm management of the heart and Cardiology in general, is going to be explosive and probably one of the new Renaissance is of our time as it pertains to managing patients interesting.
Dr. Michael Koren:
14:40
So the last thing I'm going to leave for discussion, and very quickly, because this point a real good answer for this. But one of the things that fascinated me is Something called the coronary drug project that studied niacin for hyperclestralemia. And niacin is, we know, as a supplement and it's pretty much fallen out of favor for treatment of Clestral issues, with just a few maybe exceptions that I won't get into for now. But one of the very interesting things about the coronary drug project study was that patients than niacin may have had a little bit less atherosclerotic complications But they had a higher risk of A fibrillation Which led to an actual Null effect that they cancelled each other out. So niacin was not felt to have any cardiovascular benefits because of the offset. Any, thoughts about that? It's a kind of crazy thing from clinical trials but it's fun to think about and speculate.
Dr. Neil Sanghvi:
15:32
Yeah, you know Nothing. Mechanistically that would make sense to me because there is this concept of inflammatory contributions to triggering atrial fibrillation. But one would think that if you have a lower atherosclerotic burden you are actually mitigating inflammation as it pertains to the coronary tree, and you would think that that would actually lend towards less effort. So I cannot explain, and nor have I read anything that would explain, why you would see a signal towards higher incidence of atrial fibrillation in that particular population of patients.
Dr. Michael Koren:
16:05
Yeah, just an interesting little, yeah, little trivia. Well, Neil, this was amazing. Yeah, thank you for sharing your insights. Thank you for sharing your wisdom. I enjoyed it. It was a lot of fun. I learned a bunch of stuff, so hopefully our audience will appreciate all this wonderful information. And again, thank you for being part of two docs talk, each for ablation, in our med evidence platform.
Dr. Neil Sanghvi:
16:28
I appreciate the invitation and thank you as well, and I hope your patients enjoyed the segment. Thank you.
Narrator:
16:34
Thanks for joining the Med Evidence podcast. To learn more, head over to mede vidence. com or subscribe to our podcast on your favorite podcast platform.
