Two Docs Talk A-Fib

Narrator: 0:01

Welcome to MedEvidence, where we help you navigate the truth behind medical research with unbiased, evidence-proven facts, powered by ENORE 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 very, very delighted to be talking with my colleague and friend, Dr. Neil Sanghvi, in another episode of Two Docs Talk, which is a series that we're doing for our MedEvidence platform. Neil and I had a fabulous discussion in our first segment, talking about what the heck atrial fibrillation is and ways of diagnosing it, and for this segment, we're going to jump into really how to start treating it. Dr. Neil Sanghvi is the medical director of Rhythm Services at Flagler Hospital here in Northeast Florida. He's the one that's really when it comes to coming up with policies and gearing other people toward the best ways of identifying and treating arrhythmias. Neil's the guy in our town. So thanks for that service, Neil and let's jump into a discussion about the ways that we treat atrial fibrillation.

Dr. Neil Sanghvi: 1:10

Sounds great. Thank you for having me, Mike. I really appreciate it.

Dr. Michael Koren: 1:13

So okay, we make the diagnosis of atrial fibrillation. Tell us what the next steps are and how we think about it as cardiologists. I n terms of what the appropriate level of intervention may be, depending on what we're finding in the clinical scenario.

Dr. Neil Sanghvi: 1:29

Yeah. W hat we try to dive into are potential trigger points or contributors that allowed the patient to develop atrial fibrillation. You know we talked about hypertension, we've talked about electrolyte imbalances, and so we try to tackle these in individual formats. So, first and foremost, basic lab work right, let's make sure that you're not deficient in magnesium or potassium or that your thyroid is overactive or hyperactive because that could potentially lend towards atrial fibrillation and correcting those simple deficiencies or overactivity through diet and or supplements or medical therapy if the thyroid happens to be hyperactive. That'd probably be the first, very first step. Then the more difficult journey begins because most of the time, these patients are suffering from a multitude of problems high blood pressure, obesity, sleep apnea, as we talked about before. And these are lifestyle changes that individually need to be tackled and are not easy to tackle but often yield a lot of reward if we do tackle. And that's involving things like losing weight and aerobic activity. What do we talk about? I think you know, Mike, I think you've told me before, you've told your patients what Thirty minutes a day, five days a week at a minimum, right? That's what we're looking for, and so you know that's what we're pushing. That's right. Yeah, right, we admit, that this is easier said than done, but the rewards probably outweigh any of the medicines that we can provide. And so, weight loss management, sleep apnea, managing and monitoring high blood pressure and trying to treat it. W hether it be through a combination of weight loss, diet alterations, right. And then there's dash diet in the past, right, dietary approach to stopping hypertension, and it's, you know, as crazy as it is. What we put into our bodies impacts us, and so if we could change what we put in, that would help, right?

Dr. Michael Koren: 3:22

So in your scope of clinical experience, is there a big percentage that can come in, get diagnosed with a brief episode of A fibrillation and then just change the lifestyle, be it alcohol reduction or treating their sleep apnea or the things and then be fine.

Dr. Neil Sanghvi: 3:38

You know, amazingly, the ones who are successful? The answer is yes. Yeah, there's a number of trials that have been done, both in the US and Europe, actually looking at this very question and saying if we have a very rigorous approach to diet and exercise, can have a meaningful impact. W hether it's completely getting rid of A-fib rillation altogether or to the point where it's not a bother right. And they've shown clearly that that is a powerful tool. The biggest challenge is us being successful at it. Right, the amount of lifestyle change required is a dedication, but the rewards are tremendous. And so any therapy I offer has to be based on that.

Dr. Michael Koren: 4:19

So and, let's get a little more specific. Let's say somebody comes in, and you find out that they overindulge in alcohol. They're not a complete drunk, but it's not unusual for them to drink two, six packs of beer on the weekends. And they notice they're getting some palpitations and other things the next day or maybe later in the day, and they behave themselves and they stick to a very, very strict regimen of one glass of red wine within or every day and that's it. So rate that person.

Dr. Neil Sanghvi: 4:50

Yeah, again, it's very difficult. Unfortunately, I don't have a test that exists to say that this is your trigger, so I can only advise them to say these are the potential contributors. And if it turns out that in this individual, there's a sensitivity to alcohol, which often there is. I've seen tremendous success in just simply changing alcohol intake. I'll take another example just to piggyback off that. In the Starbucks world that we live in right, we live in these worlds where a coffee serving which used to be this, and I saw you pick up your mug right there- Yeah, it's water.

Dr. Michael Koren: 5:19

Yeah, it's water. It's turning to this. It's turning to this right. Unlike Johnny Carson, there's nothing alcoholic in there.

Dr. Neil Sanghvi: 5:27

There are no two carbon molecules.

Dr. Michael Koren: 5:29

I swear to it.

Dr. Neil Sanghvi: 5:30

Okay, very good. So you know, oftentimes I'll ask a patient. I was like, how much coffee do you drink? They'll say a cup. I was like, tell me how big that cup is. And it turns out it's this guy (showing large cup). There you go, so and so that's not a single serving of caffeine, right? And so a successive caffeine can be a trigger as well.

Dr. Michael Koren: 5:45

Yeah, yeah, okay, perfect, and we're still engaging in lifestyle there as well. Okay, so run us down the spectrum of different levels of intensity in terms of the treatment of atrial fibrillation.

Dr. Neil Sanghvi: 5:56

Yeah, so we talked of lifestyle. That's foundational, you know it's the hardest goal, but it's the foundation of anything that we build on. So the patients, who are doing a good job, are trying to do their best, but yet we're still having episodes of atrial fibrillation. Then we'll move toward things that are pharmacologic. So there's a classification of medicines known as beta blockers and there's another class called calcium channel blockers. They come under common names metoprolol, an d verapamil, these are meds that are meant to try to have an impact on the electrical properties of the heart in a mild way, and sometimes we'll be successful in suppressing these triggers that are triggering atrial fibrillation. So, to backtrack just for a moment, A-fib has to be triggered in many instances, and that trigger is a series of misfires in the heart that initiate it. So we're trying to suppress the triggers, and it's through lifestyle changes that we just talked about, or some of these meds that try to suppress the triggers. So that would be the next strategy. Now, the success rate in these meds varies from patient to patient. Okay, but they're not the most powerful meds and oftentimes, they may not be successful in suppressing the trigger, but what they can do is help make the symptoms less evident to the patient. So many times, patients here, they feel the irregularity, they feel the racing, and the meds will help calm that. So it's not so debilitating, and so the botoprolos and the dothylatisans can help in that regard.

Dr. Michael Koren: 7:22

Let me explore that with you a little bit more. And I think that this speaks to physicians who may be really focused on underlying triggers, versus physicians that are just kind of checking boxes when they make their decisions about what meds to use. So in my experience and obviously as a general cardiologist, I treat atrial fibrillation. One of the tricky parts is to understand the triggers and then to pick the therapies that are most likely to offset that effect. So, for example, if somebody may be a driving executive and we think that adrenaline surges are causing atrial fibrillation, maybe a beta block is a good choice. If you have perhaps an African-American female that has high blood pressure, maybe a calcium channel block would be better because that will reduce blood pressure to a greater degree in an African-American patient compared to a beta blocker, and that might be a good choice. So targeting your therapy to the specific circumstance of the patient is such an important part of what we do as cardiologists.

Dr. Neil Sanghvi: 8:24

I wholeheartedly agree. I think we are not all built the same and each of us we do require some tailored therapy, and there's definitely tailoring that goes along with ethnic background, personal circumstance, physical circumstance, situational right. So the history becomes such a big part of this. When do you have your AFib episodes? Some will say it occurs while I sleep. Well, those are triggered by a vagal response, a nerve that's in the body, And so you're now trying to treat vagally mediated atrial fibrillation, and there's certain therapies for that. There's the executive, as you described, which are adrenaline or exercise-induced AFib, and so those are adrenaline-induced, and so I agree, there are tailored therapies, for sure, and I try to dissect the patient a little bit to understand which may be a specific trigger to decide which medicine may be effective.

Dr. Michael Koren: 9:18

Okay, so let's jump from that class to the more stronger anteroid mix.

Dr. Neil Sanghvi: 9:22

Yeah. So the anteroid mix is a second tier of therapy that I will turn to when our basic therapies are ineffective. Now, these are drugs that are designed to specifically manipulate the electrical properties of the heart. Okay, the channels that actually help the heart beat are what they're manipulating, and they come into a different set of categories. W e choose agents based on specific patient criteria. So, for example, certain anteroid drugs can be used safely in all patients, some patients who have severe coronary disease, blockages in their heart arteries, weakness in the heart muscle. We can't turn to certain meds because they've been shown to be more harmful than good. But their effectiveness as a whole, in aggregate, tends to be about 50%. Okay, so 50% of patients that get put on these meds will see medical benefit right and have suppression of their atrial fibrillation because the direct therapy is now suppressing the misfires that are allowing this A-50 trigger. That's not 50% lifelong, it's 50% for, you know, certain durations. Unfortunately, there are patients who've been put on these meds works for a while and then the body adapts. And so all of a sudden they're breaking through the medication. There's others where we use a certain med but because this time goes on, the patient may develop another ailment, which then makes that med prohibitive. So we have to come off and go to something else. Unfortunately, the best odds are 50-50, you know, and those aren't great, right? I mean those aren't great, but that's the best that we have in medical therapy. I'll turn to an agent, droneterone, also known as Motak. It's the last agent that came onto the market for atrial fibrillation. There was hope in the medical community that it was going to be this panacea. It was going to be this powerful medicine that was going to help us manage atrial fibrillation, be very effective, without any toxicities, and unfortunately it ended up becoming one of the weakest ones that's out there on the market. It's power, it works for patients in the right patient, but it doesn't work for everybody, and so we just haven't made headway in this anti-arhythmic drug therapy. But drugs do make effect in patients. We try them in certain patients, but they do come with some side effects, like any medicine would, and so we balance them.

Dr. Michael Koren: 11:34

Yeah, motak's an interesting product. A s you bring up Droneterone, we did a lot of research. I personally did a lot of research with that over the years and the thought process it was a safer anti-arhythmic because it really worked just in the atria rather than the ventricle. But, as you point out, we get the data, it turns out maybe not to be the best anti-arhythmic agent and probably something that we don't use nearly as much as we thought we might use. So, moving from drugs to devices, I know you do a lot of that work, so it sounds like that's become more a common approach for a lot of patients with AFibylation.

Dr. Neil Sanghvi: 12:03

Yeah, so anybody who looks up A Fib, they're going to see the term Obylation come across, and so it's a minimally invasive technique where we take catheters through veins in the legs to attempt to eliminate misfire and tissue. So conceptually, anatomically, you and I have talked about this atrial fibrillation comes from the upper chamber, the atrium of the heart, and what we've learned through years of research is that the source of the misfire, the trigger, oftentimes comes from structures known as pulmonary veins. And these are vessels that drain blood from the lungs. As they empty the oxidated blood from the lungs back into the heart ambriologically, these vessels actually form for the heart itself. As they stretch out from the heart, they pull along some conducting tissue. But the problem is that the cuff of conducting tissue ends up being not as well regulated as the rest of the heart is, and as a result, misfires will trigger. So what catheter ablation is is a technique, and we can do it with either heating the tissue or supercooling the tissue, but effectively we're destroying that cuff of tissue, and by doing that we're not impacting the overall function of the heart in any way. So patients really worry am I kind of hurting regular heart muscle? The answer is no. All we're doing is taking away that cuff and by doing so we suppress in many patients the misfire. The success rate 70 to 75% in patients who otherwise have a healthy heart in preventing atrial fibrillation. So much more powerful than the medications that exist out there, but not 100%. I wish it was, but it's not there.

Dr. Michael Koren: 13:38

So interesting and so impressive, and the technology just gets better and better. As I understand the data, the success rates have improved dramatically over the last decade or two.

Dr. Neil Sanghvi: 13:48

Absolutely, the key here was the heart, as the rest of the body wants to heal itself, and I just mentioned that I'm trying to actually cause a scar. I'm trying to destroy tissue, and so the tools we had weren't as effective. So we would get some inflammation and what we thought was destruction, but over time it would re-heal, and then the problem comes back again. The way I like to explain it to patients is I'm trying to build a wall, and if a door develops in the wall because something heals, it's very difficult for misfires to come through. The tools we have now are much more powerful than before. The success rates are going up, I said 70, 75%. And in the right patient it could be even upwards of 85%. And the procedure is not very taxing, so that's why it's become much more favorable for patients to turn to inablation versus other therapies that exist that we talked about. So let's go from very high tech, which is really, really cool, to low tech.

Dr. Michael Koren: 14:38

How about supplements? A lot of people think that there are different types of supplements. A lot of people think that there are different supplements that can work for A fibrillation.

Dr. Neil Sanghvi: 14:48

That's much more challenging, right? I think the electrolyte supplements magnesium, potassium there's been some role in helping A fibrillation. In that regard, there aren't any other major supplements that I've come across. I mean, Fischwell has been mentioned as a possible tool, you know, variable success. To me where the supplements come into play is that there isn't much harm in going on them, you know, assuming you don't have any major kidney issues or liver issues, and so it's a compliment to that lifestyle change that we were earlier addressing. The challenge with AFib, as you and I know it's not one thing often that's the trigger. It's a multitude of things that come in constellation.

Dr. Michael Koren: 15:32

So maybe for a limited population there can be some role, but maybe not something you should put too much hope in. Alright, so let's get to a clinical case. This is a hypothetical. It's a completely hypothetical, but I played soccer for a number of years and periodically people would come up to me knowing that I was a cardiologist and a soccer player, mostly a defenseman. But we had this one occasion where somebody missed a PK, a penalty kick. And they were, I think, coming up with an excuse that they were having some palpitations that seemed to have distracted them from their goal of scoring a goal and winning the game for our team. But nonetheless, I took the person at their word and noticed that he did have an irregular heartbeat that led to my evaluation that showed that this person in fact had paroxysmal A Fibrillation. So, with this person in mind, who, let's say, he's in his fifties, hypothetically. I'm very curious in our next segment to see how you would manage that person. And hopefully get that person back to the soccer field and actually scoring goals when they were asked to take a PK. Sounds like a good plan.

Narrator: 16:44

Thanks for joining the MedEvidence podcast. To learn more, head over to MedEvidence. com or subscribe to our podcast on your favorite podcast platform.

Narrator: 0:01

Welcome to MedEvidence, where we help you navigate the truth behind medical research with unbiased, evidence-proven facts, powered by ENORE Research Group and hosted by cardiologist and top medical researcher, Dr. Michael Koren.

Dr. Michael Koren: 0:17

Hello, I'm Dr. Michael Koren here with another episode of Two Docs Talk A-Fibrillation on our MedEvidence platform. I'm delighted to be speaking with my friend and colleague, Dr. Neil Sanghvi, who is the medical director of heart rhythm services at Flagler Hospital here in Northeast Florida. W e're excited to have this conversation. We've been having a really informative and fun conversation. So thanks, Neil, for this. And we end our last section by talking about a hypothetical person who we both know, by the way, a guy in his 50s who was discovered to have atrial fibrillation during a soccer match when he missed a penalty kick, at great consternation amongst all of his teammates. But in fact, he had a good excuse. He had an irregular heart rhythm on the soccer field and fortunately it settled down there for a little bit, but then ultimately, I evaluated him and sent him over to you. So tell me what your analysis of this type of person might look like in general, and then we'll sort of dig into some specifics about the care of people like him.

Dr. Neil Sanghvi: 1:22

Sure, Yeah, absolutely. You know, it's unfortunate, it happened on the soccer field and it cost the team a game. So I'm sorry about that.

Dr. Michael Koren: 1:30

I'm still a little upset, I must admit he was too.

Dr. Neil Sanghvi: 1:35

Yeah, no. So this is the patient, right, he's noticing, he's in physical high stress level and he says my heart's beating wrong, right? And then, it's not constant. So you know, the first question is, what situations causes this to happen? So we kind of try to get to that underlying understanding of triggers. And then the most important thing for me is I have to see it. I have to see it to know what's going on. And so typically what we'll use is some form of a wearable monitor which records the rhythm of the heart, so that way I can actually see what the heart is doing when the patient is having the symptom that they're having. And the type of monitor will vary based on the frequency of the symptom. And so patients may have heard of things called Holtres, which are somewhat shorter term monitors, anywhere from 24 hours to like a week. And then they have other long term monitors, which are called event monitors, which you can wear upwards up to a month. And what's nice about these monitors these days is that historically these monitors had a lot of wires and it would be fairly burdensome to wear, But nowadays we have these little patches or stickers that come on board. They just stick it on themselves. They can wear it all the time. Many of them are actually even water resistant, so you can shower with it, and it has the ability for the patient to push a button or somehow indicate to us that, hey, i'm in the middle of a symptom, and I can pay special attention to that period of time to see what is the heart doing when the patient is having their symptom. The other benefit is that the monitors also have the capability of recording arrhythmias or irregular heartbeats that are of significance even when the patient's not pushing the button. Say you're asleep, and so that will be a tool I would use to try to determine what is going on when the patient is feeling what they're feeling.

Dr. Michael Koren: 3:14

Yeah, and that's really, really important is making the diagnosis, and especially in these cases where it happens, it stops happening and people are having a hard time to describe exactly what it is they're experiencing. Sometimes the symptoms are vague. And also, you know, I'm a little bit of a historian and one of the trivial facts is that most people don't know where the term halter comes from. It's actually the name of the doctor who first prescribed this kind of concept Dr. Halter.

Dr. Neil Sanghvi: 3:44

You know, you've just taught me something today, thank you.

Dr. Michael Koren: 3:48

You ever think about that? No.

Dr. Neil Sanghvi: 3:50

I did not. I actually thought of it like almost like a harness halter and walked away with that.

Dr. Michael Koren: 3:56

But I just learned something new. We'll do fact check on that, but I'm pretty sure that's correct. So that's a little trivia question, Trivia answer, I should say. Okay, so let's get back to the guy who I played soccer with, so you do this analysis. Lo and behold, you find out that he is having some episodes of atrial fibrillation in different circumstances. What are the next steps? All right.

Dr. Neil Sanghvi: 4:22

Well, you know, we've diagnosed him with AFib. We figured out a trigger, which tends to be exercise in this individual, And so the next conversation is all right, how do we deal with this? Well, I'm not taking him away from exercise and I'm not taking him off the soccer field because you'd kill me and he would be upset. So we need to figure out ways to manage this and suppress the arrhythmia. And so, you know, assuming he doesn't have anything reversible, so we go back to that earlier conversation of electrolytes, thyroid, all that kind of stuff, to make sure all of that's in balance. We've taken away anything that could be addressed simply, and now it's activity and adrenaline that's triggering it. So then we have the discussion. You know, how do you want to manage this? There are obviously chronic medicines that he could take that could try to suppress the trigger and prevent the episodes from happening. The downside, though he's a young guy, otherwise healthy, and, you know, would be committed to lifelong medications. Or we talk about that ablation that he and I talked about before, to try to deal with the symptoms. But the other side of this, Mike, is stroke. Right? I mean, you and I kind of haven't really touched on that. So besides symptoms? AFib is the number one cause of strokes due to clots in patients over the age of 65 and a common culprit of strokes in patients who come in with unidentified reasons for stroke when they show up to the hospital.

Narrator: 5:41

Dr. Michael Koren: So I've got to manage that.

Dr. Neil Sanghvi: 5:43

Huge point right, and so this patient who now has atrial fibrillation. We have the symptom side that we can address, but I got to manage the stroke side. And that management will vary based on the patient. And really it's based on risk factors and there's several things that we look at. We look at the patient's age. Whether they have high blood pressure or not, irrespective of whether it's well controlled or not, just the mere fact that they've developed high blood pressure, whether they're diabetic, what's the heart function is right? Is it weak? Not weak that kind of thing? Have they ever had a stroke or stroke-like event before? Do they have other vascular disease? Do they have a diagnosis of coronary disease or some sort of blockages in their legs or something like that? These risk factors culminate into something called a CHADS Vascular that we use to stratify patients to determine who are the patients at the highest risk for stroke from AFib versus those who are low risk. Low risk we don't necessarily need to worry about things like blood thinners. H igh risk that's when we're talking about those things that patients have read about in the past or seen commercials about Warfarin or Coomidin that we've all heard about Alakuis, zirelto, cvesa there's a number of them out there that we have to talk about.

Dr. Michael Koren: 6:49

Yeah, and we use the term NOACS for that as novel anti-coagulants. Yeah, so that's a really important point. So when I was serving as Chief Resident at New York Hospital in internal medicine, i used to quote data at that time this is a little while ago, of course that stated that if you had atrial fibrillation versus not having atrial fibrillation, your risk of a stroke went up six-fold. And if you had atrial fibrillation with valvular heart disease compared to somebody without atrial fibrillation and valvular heart disease, your stroke risk goes up 20-fold. Are those still pretty accurate numbers?

Dr. Neil Sanghvi: 7:24

Yeah, yeah, we haven't changed the risk profile at all in that regard, so you're absolutely right. A five to six-fold increase in risk of stroke just simply taking two patients one with the diagnosis A-fib and one doesn't and then if you put concomitant diseases on top of that valve disease, cardiomyopathy, history of having a prior stroke-like event and those numbers skyrocket. So the concern levels are very high when it comes to this, and so generally, what we say is that when we estimate your risk of stroke, if it's greater than 3% per year, using some of those risk factors that I just described, that's a patient who really should be contemplating anticoagulation, whether it be through one of the novel agents that you just described Warfarin, which is something that we don't often turn to as much these days, but certainly still on the table as a tool or some other alternative thromboembolic or stroke-preventing technology that's out there.

Dr. Michael Koren: 8:24

Yeah, so another little trivia question. Warfarin, as we all know, was originally developed as rat poison, and I don't know if you're familiar with this, but the W-A-R in Warfarin stands for Wisconsin Agricultural Research, because it was originally developed as a product to deal with rat issues on farms. That's a bit of history.

Dr. Neil Sanghvi: 8:46

I do know and I'm just gonna piggyback just to get how it came about. You probably know this as well as a farmer. It was a farmer who was sitting there and his cattle was bleeding out and hemorrhaging because they were feeding right, and so he brings the cattle to the university and they were like, what is going on? Why am I a cattle guy? Amazing story. And yep, rat poison is exactly how it started off and unfortunately, some of my patients are like do not give me the rat poison.

Dr. Michael Koren: 9:14

Yeah, and the other crazy trivia question is that President Eisenhower was treated with Warfarin extensively after his heart attack and that was really the main treatment they had back in the 1950s.

Dr. Neil Sanghvi: 9:27

That's right, that's exactly right, actually in secret. They did not want the public to know. That's right.

Dr. Michael Koren: 9:33

Exactly, yeah. So interesting little tidbits, all right. So getting back to our soccer playing buddy, so you're gonna put them on a blood thinner, you know. Can you mention the CHAD Vaskor? I gave you a bit of a sense. Let's say, his blood pressure jumps up and down a little bit.

Dr. Neil Sanghvi: 9:50

You know we're thinking in somebody like this, fortunately for him, he's still in the low-risk profile because he's young, otherwise healthy, heart, strong, and the blood pressure may be a contributor. But he's on a low-risk profile and so for him the hazards of the blood thinner are going to be far greater than the benefits that is offering. So we're able to safely avoid blood thinning in his specific case, though it's not without accepting a little bit of risk, right, but the numbers are small. We're talking about one and a half, two percent risk, and so that's something that we converse about and saying are you comfortable with that? And he says yes, we're good. If he says no, we need to think of an alternative, because I worry about a soccer player being on a blood thinner, playing in a high-contact sport.

Dr. Michael Koren: 10:37

Understood. Yeah, and that's an interesting part of the management, which we'll get to in a second. But just exploring this anticoagulation issue just a little bit more. One of the controversies is that when you newly diagnose somebody, some people would argue and I have to admit that I fall into this category that I want to anticoagulate while I do the exploration of what one's risk is and how do you manage that practically?

Dr. Neil Sanghvi: 11:02

Yeah, no, i don't think that's unreasonable. I mean, fortunately, most of the time, you know, it's colleagues like you actually that make my job a little bit easier because you've done the first steps for me. You know, you've gone through the discovery phase. But if they're showing up to my door and I don't know what's going on, it depends again on them. If they're exceptionally young, because, as I mentioned I have 30-year-olds that show up right and they're young and they have zero risk factors whatsoever and they're lonely, what we call. They're called loan a Fit. They're considered very low risk. That's a patient. I feel very comfortable being off the blood thinner and saying we're gonna go through this discovery phase but we're low risk. Everybody else, you're absolutely right, we will. We may even use transient blood thinner for a short period of time while we're just stratifying the risk. And then, once we've identified where they fall on the platform, then we'll have a informed conversation to say here are the numbers, what are you comfortable with? And I just describe it as it's a set of scales right? And there's risks and benefits in both. The blood thinner is very powerful and helping prevent strokes, elevate your risk of bleeding, though, right, not being on them elevated risk of stroke, but you're not bleeding as much, and so we're just trying to find which balance that we can strike, and in some patients the blood thinner makes sense, others it doesn't.

Dr. Michael Koren: 12:13

Okay so let's go back to our hypothetical soccer player who ruins our entire season by missing a PK and you're talking about whether or not you would do an actual procedure on him, an ablation procedure, and whether or not you would use a watchman, or what would make you decide to use that, given the fact that in a coagulation, in a contact sport, may not be so compatible.

Dr. Neil Sanghvi: 12:40

Absolutely. So let's talk about the way I like to talk about A- fib is symptoms and stroke risk, and we separate the two. How do I get them asymptomatic, how do I make them feel better so he can perform wherever he's looking to perform? A nd for this patient, right, we had of we would have a very strong conversation about ablation, mainly because it's as I mentioned previously. It's the most effective tool I have in my War chest of treatment options for a fit. It also offers the least complexity on needing to be on meds lifelong for a young guy, and so I would certainly mention all of the options. B ut I think ablation would be something that I would be pushing him towards and saying, hey, this may be the best for you, you know, because in otherwise healthy heart the outcomes are quite high, right, I mean, I mentioned 70, 75%. But these young hearts where patients have what we call paroxysmal, A- fib, that's that coming and going of the symptoms not being stuck in them, they have upwards of 85% success with ablation. So that would be the way I would handle the symptoms, stroke wise for him. If he's low risk, we may not want anything, okay, and just say this is, we're fine, we don't need to do anything at all. We'll deal with the symptoms and we don't need anything else. But let's just say this guy happens to be diabetic as well, a healthy diabetic, but and so now he's at elevated risk of stroke because the diabetes plays a role, the blood pressure, as you mentioned, plays a role, and even though I do an ablation, I can't guarantee cure. So just because you get an ablation doesn't mean your risk of stroke goes away, okay, so I have to still protect him. And now he's a soccer player. Or let's take another patient, just as an example. Let's take the patient who's just not stable, much older patient who falls a lot. Right, these patients, they need protection. And so this watchman that you described, which is a device that was devised by Boston Scientific, or there's others that are on the market, but they fall into a category called left atrial appendage closure devices or LAACs. These are devices or plugs that get placed into the heart And what they're meant to do is there's a pouch called the left atrial appendage, in the left upper chamber of the heart, which tends to be the source of the stroke, the clot that forms when patients are in the A-fib. So when we talked about the heart quivering. Blood doesn't move well. Well, blood has a property of wanting to clot when it's still, and it sits in this pouch more times than not. 90% of clots that develop in A-fib sit in the or found in, this pouch. So if we plug this pouch off, close it off through a very minimally invasive procedure, we're able to seal off the pouch, we can reduce the risk of stroke equivalent to as if you were on a bloodbath, and so that would be an ideal solution for this patient, because that procedure 45 minute procedure, risk of complication 1% or less and success rate greater than 95% And so that would be an ideal procedure for this type of patient or any high-risk patient. And those high-risk patients are your sports athletes or vocations that are high-risk for bleeding. I'll tell you. I just put one in a patient. She's a glass worker, she's an artist who works with glass, cuts herself all the time, and she was on a blood thinner and she would just bleed like there was no tomorrow. That's a patient we would consider the watchman on The fall patient that I talked about, or patients who are prone to hemorrhage because they have ulcers and will have bleeding. So we need to those are those scales. And the scales are such that the bleeding risk on the blood thinner is so high that it makes sense to look for an alternative.

Dr. Michael Koren: 16:01

Sure, so the left atrial appendageal closure devices are a great example of recent technology that's been highly studied in clinical trials, and in our next segment I'm gonna explore more clinical trial information with you and also what the future holds for people diagnosed with A-fibrillation. Perfect.

Narrator: 16:21

Thanks for joining the MedEvidence podcast. To learn more, head over to medevidence. com or subscribe to our podcast on your favorite podcast platform.

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. 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. 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. 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. 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. 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. 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. 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. 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. 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.