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- [00:00]
A
If you've got an ldl, where, where are you in the high risk?
- [00:04]
B
Yeah. And that's been, you know, this controversial topic that has spanned the last few decades because before people used to think that having a cholesterol level of 130 or so is normal, but now we know the lower your cholesterol, the lower your LDL cholesterol again, that bad cholesterol, the better it is for you. So the initial studies looked at this 130 cutoff, but now we know that for people like you and I, your LDL cholesterol should really be a hundred milligrams per deciliter or less.
- [00:36]
A
Yeah.
- [00:37]
B
If you're higher than that, you have a substantially higher risk of developing heart disease.
- [00:43]
A
This episode is brought to you by Element. You guys know how much I love electrolytes because we need them for our brain and body to work. Well, that's why I'm so excited that I've partnered with Element LMNT Electrolyte drink, which gives you everything you need and nothing that you don't. It actually contains a science backed approach to the electrolyte ratio. You've got a thousand milligrams of sodium, 200 milligrams of potassium and 60 milligrams of magnesium. So none of the junk. So I've started taking a little bit more than usual. I now take two to three sachets a day of Element and that's purely because I live in New York City. Right now it's very hot. I'm going to the gym and I'm also sweating a lot. If you haven't done so yet and you really want to try this out, go through to element lmnt.com neuro because right now they're offering a free sample pack with any purchase that's each single serving pack with an Element order. So I'm obviously obsessed with the Kiwi one. I have it during the day. So if you guys want to try this, just head on over to element.com neuro it's completely risk free. PK, welcome to welcome to New York and welcome to the Neuro Experience podcast.
- [02:08]
B
Thank you so much, Louisa. So good to be here.
- [02:12]
A
I'm fascinated by your world, but I know about you. Why don't you tell everybody else about you?
- [02:17]
B
Yeah, sure. So I'm PK or Prakrithy. I'm a cardiology fellow at the Brigham and Women's Hospital and Harvard Medical School in Boston. And you know, I want to be an interventional cardiologist. So focusing on heart Disease and sort of the highest risk patients that do come in with things like heart attacks. And then from a research perspective, I do want to stay an academic, so I want to be a researcher and specifically a clinical trialist, where we're at the forefront of solving unanswered questions in cardiology, such as. So some things. I think, you know, there's several areas to explore, but I think the lipid space is one particularly interesting space. And then also for the highest risk patients, patients that are still having heart attacks, I want to understand, you know, what we can do to decrease their risk before they come in with. With those types of extreme problems. And then in patients that do have those problems, you know, what can we do from, you know, a device perspective or procedural standpoint to make their overall health better?
- [03:20]
A
Okay, well, this is exciting. Okay. And the reason being is that cardiology has been somewhat of a mystery to me.
- [03:30]
B
Yeah.
- [03:31]
A
Okay. The brain, not a mystery to me. Cardiology. And this entire world of cardiovascular disease, disease has been something that this year of trying to understand more about. And that's because, you know, I'm. I'm on social media a lot, and I follow a lot of physicians and scientists, and I just see so many things relating to diet. There's like, diet wars that happen. And these diet wars are really aimed at, are you a. A carnivore person? Are you a vegan person? This is all in the name of preventing cardiovascular disease. So I think there's so much, much information out there that for me, even I'm like, okay, if it's about cardiovascular disease and we're trying to prevent that, and how do we do that? So why don't we talk about what cardiovascular disease is to start with?
- [04:24]
B
Yeah, I mean, I think, you know, you've covered some of the hot topics in the field already, but cardiovascular disease is sort of this big bucket term for problems that can happen in the blood vessels of the heart and the vasculature of the body and then create bad things. For example, if you have disease that builds up in the arteries of the heart, you can have a heart attack. Heart attacks can sometimes just be heart attacks in themselves, or they can cause death in the most severe cases. Then you can also have patients who build up disease in the vasculature of the brain or the arteries of the brain, and they can develop strokes. So that still fits in this term of cardiovascular disease. And then patients can develop, you know, blockages and other parts of their bodies to their kidneys, the blood vessels of their kidneys. And other important organs. So it's really a big umbrella term for disease and different vascular and arterial beds of the body.
- [05:22]
A
Okay, so vascular disease.
- [05:24]
B
Yeah.
- [05:24]
A
You know what I think would be really interesting? I just taught a two day course on the weekend and we went into the vasculature of the brain and I saw myself describing the difference between capillaries, blood vessels, veins. So why don't we take that path? Because I'm actually interested to know if these blockages or diseases occur in. In just arteries or are they in veins as well? Yeah, so let's separate them and talk about them.
- [05:54]
B
Yeah, for sure. So I think they can happen in both the blockages can happen in arteries, and that's sort of the peripheral or even sort of central arterial disease. That's arterial disease because the blockages is. The blockage is happening within the blood vessel. And you also have venous disease where you can develop clots in the veins. Now, the highest risk diseases are usually found in the arteries. When the veins are blocked, you can develop some problems.
- [06:21]
A
Is that deep vein thrombosis.
- [06:23]
B
Yeah. So one example of it is deep vein thrombosis. So the classic example is somebody takes a long flight for, you know, 14 hours to India or Dubai or something like that, and then they have sort of swelling in one leg, and so they present with pain or swelling in one leg. And then you get an ultrasound and you find that they have developed a clot in the vein of their legs. Now, that clot in itself is not so problematic if it's handled and addressed quickly with a blood thinner. But if that clot is not handled appropriately and that patient is at higher risk for developing more clots because of their genetics or some of their hormone levels, things like that, then that clot can go to the lungs and cause what's called a pulmonary embolism. And that can be fatal. So people can die from it, which is really bad. So that would be sort of the extreme of venous disease. But arterial disease is sort of what we were talking about earlier, which is when you have disease that progresses over time. So, you know, if people have risk factors of heart disease, like high cholesterol or diabetes, high sugar levels, or a family history of disease, meaning that their genetics just predispose them to this kind of disease, then what can happen is plaque can build up in the vessels of those arteries. They can build up in the distal arteries, meaning the small arteries that lead into the capillaries or in sort of the more proximal arteries, which are sort of the larger arteries and cause catastrophic events if those are blocked significantly. So what happens is over time you have some of the blockages, but then eventually, if that entire artery is blocked and it's supplying your heart or your brain, then those areas can be significantly damaged or even cause death or extreme disability.
- [08:21]
A
Yeah. So the. Obviously we'll take a really low level understanding. We know that blood is, you know, getting profused through these arteries like a. Like a pipe, if you will. And evidently we need blood flow 24 7. And then over time, we get narrowing. So, you know, closing up of those arteries and it makes it harder and harder. And then eventually what. Maybe that. That plaque just kind of builds up and it occludes.
- [08:47]
B
Yeah. So there's actually several theories out there, so I'll just refer to the heart because I know that the best. But there you can have what's called plaque rupture. So, you know, somebody has all those risk factors, their arteries narrowing and narrowing, as you're saying, but then there's some stressful event that happens or some stressful trigger in the body. Like, you know, for example, someone could have an infection or they could, you know, be exercising and have sort of stress to their. To their body. And what can happen is that plaque, if it has a lot of cholesterol in it or lipids in it, it can rupture because high cholesterol content and plaques make them unstable. And so if they rupture, that elicits this whole cascade or series of events in the blood vessels that cause your platelets to sort of come and aggregate there. And so what will happen is that small area through which blood was able to pass through then gets. And so you have no blood supply going to whatever part of the heart that blood vessel supplied. And that causes a big heart attack or death if you know, it's supplying a big area of the heart.
- [09:53]
A
And then what's the difference then between having a minor heart attack and having a really big one?
- [10:00]
B
Yeah, no, that's an excellent question. And I think it's something that we don't always think about. We just think about heart attack being sort of this bucket term. But a minor heart attack would be one where the blockage is perhaps more distal. So meaning it's lower down in the blood vessel. And the blood vessel that it's sort of impacting is one that supplies less of the heart muscle, or the myocardium, as we call it. Now, if you have a larger heart attack, then usually we're thinking of more proximal blood vessels, so blood vessels sort of that supply a greater territory of the heart muscle or myocardium. And so if you have, for example, I'll just use some of the terminologies. There's three big blood vessels in the heart that we care about. There's the right coronary artery, then there's the left anterior descending artery and the left circumflex artery. The left anterior descending and the left^. The two left sided arteries come from an artery called the left main artery. And so that supplies more than 2/3 of the myocardium of the heart. So you can imagine if you have a narrowing in that left main and then you have some stressful trigger, some event that causes that plaque to rupture, then you're essentially blocking more than 2/3 of blood going to the heart. And the heart needs blood to pump just like any other part of the body needs blood to function. And so that is sort of the most severe type of heart attack one can have. And it usually leads to death.
- [11:34]
A
That is scary. I'm going to ask a. Probably sounds like a dumb question.
- [11:38]
B
No, no.
- [11:38]
A
But if in this event does it end up, up unblocking somehow or does it just stay there, blocked?
- [11:45]
B
Yeah, that's actually a great question because in some cases that clot is able to resolve a little bit because there's sort of so many different cells at play. You'll have your platelets that, that will come to the area and cause the clot. But then you'll also have sort of muscular cells and fibroblasts. So all these different types of different components coming together. And so there can be sort of some of that clot there. Usually it doesn't work so quickly unless the patient's given medication. So if anyone has come into, has sort of dealt with the situation, you'll know that the first thing that happens when someone comes to the hospital is they're given aspirin and a high dose aspirin. And it's basically to prevent this clot from like progressing or potentially even cause it to resolve a little bit. But when you have such a big clot, it's, it's unlikely that it'll resolve on its own.
- [12:42]
A
How many STEMI's do you see?
- [12:44]
B
We see quite a lot. Especially being at like a large academic center in a city, you tend to see quite a few. Now in Boston there are several hospitals, just like in New York. So I think the STEMI volume is distributed between them. But it's still a real problem that we're seeing day to day.
- [13:02]
A
Well, that brings us to the main topic. I'm really happy that you, you spoke about cardiovascular disease and for, you know, the reason why we want to know more about it. I always believe education is probably at the first point of prevention. Yeah, that's in my, in my humble opinion. So now that we understand that, hey, cardiovascular disease, it exists as a vascular disorder of some kind, we need to prevent it because we are. We don't want it. So let's talk about the world of lipoproteins and cholesterol, because I'm guessing that this is at the forefront of cardiovascular disease, right?
- [13:43]
B
Yeah, I think that's absolutely correct. Sort of managing cholesterol is one of the best things we can do to help our cardiovascular health.
- [13:51]
A
Okay, what is cholesterol? Let's talk about it.
- [13:55]
B
Yeah, that's a great question. So cholesterol, I mean, you know, when you think of it, you've probably heard of it in multiple contexts and sort of a negative context. Everyone thinks of sort of cholesterol in two different ways. There's good cholesterol and bad cholesterol. But I'll first distill it down a little bit more. So cholesterol, it's just this sort of waxy, like, substance, and it's produced in the liver, and it makes up several parts of the body essentially to allow your body to conduct important functions. So it helps build the cell walls of our cells. It helps generate some hormones in the body. It helps, yeah, vitamin D. And also is important in sort of the generation of bile acids, in the way we process certain foods. So it's an important component that we do need some of in the body. But I think the problem arises when you have too much of it. And so that's probably what we're going to focus on.
- [14:53]
A
Too much of the bad one or too much of the good one?
- [14:56]
B
Yeah, too much of the bad one. So then when we think about sort of what we refer to or what we measure in cardiology as cholesterol, we actually measure a few different parameters. So there's something called a lipid panel, which is what a lot of us will get when we go to the doctor just to see what our cholesterol is. And that has a few key components. You have your total cholesterol, which is sort of this umbrella term for all of the different cholesterol components that we're measuring. And then that lipid panel will break it down into other components. You'll have your bad cholesterol, your Good cholesterol and triglycerides to keep it sort of simple.
- [15:37]
A
Okay, so what's. But, okay, so we've got the good cholesterol, bad cholesterol, which we'll get into. But what's triglycerides?
- [15:42]
B
Yeah, so triglycerides are sort of a different component of not necessarily cholesterol. They're made up of sort of these fatty chains, and they also can lead to higher cardiovascular risk, but they're independent from your cholesterol.
- [16:00]
A
So it's not under the cholesterol umbrella.
- [16:03]
B
It's not under the cholesterol umbrella. But then when you look at the good and bad cholesterol, what are they? So bad cholesterol is ldl, or low density lipoprotein cholesterol. And low density lipoprotein cholesterol is actually made up of a significant portion of cholesterol, but also a little bit of triglycerides okay, so triglycerides in themselves can be a risk factor, but then they also make up lipoproteins and lipo. The bad lipoprotein, the low density one, has some level of triglycerides in it. And this can get kind of complicated, but essentially, lipoproteins just help transport cholesterol and triglycerides and other proteins that are within these molecules across the body because cholesterol can't travel sort of on its own as well. Then there is good cholesterol, and that's hdl, or high density lipoprotein cholesterol. And that is actually beneficial in some cases, although some people can have too much of it. But we don't care about that as much in cardiology in terms of having medications that target it. At one point, people believed it was important. But a lot of the drugs that have targeted HDL or high density lipoprotein in particular, have not been shown to improve those areas of cardiovascular disease we just talked about. So things like heart attacks, strokes, or even death.
- [17:34]
A
Okay, so the. So let's go back to ldl. Is this the. Is. Does this result in the plaque that builds up in the arteries?
- [17:41]
B
Yes. Okay, so LDL cholesterol is one of the main components that makes up that plaque that we don't like in the arteries. And it is specifically the part of the plaque that I was talking about, that lipid core that tends to be unstable and can rupture in people that have high levels of cholesterol that isn't controlled.
- [18:06]
A
So I am also, you know, when I, when I research this and what we've found, I think, 20 years ago, right. You'd go and do a standard measurement from the doctor and you'd get back your LDL hdl. Now we know about something else, which is a lipoprotein B. Yeah. And there's also a lipoprotein A. Yeah. And I'd love to understand what they are also referred to as APO A and APO B. Yeah. Because I think that they fall under this LDL pathway. Do they?
- [18:37]
B
Yes. So that's a great question, because I think now that we know some of the basics of cholesterol and people have explored this for decades, not even longer than that, we're able to measure these different particles very well now. And so let's just start with apob. So APOB is a protein that can be found on LDL cholesterol. So as I was talking about before, LDL cholesterol has the cholesterol component, it has the triglycerides, but it also has some proteins, some phospholipids and other things. One of the proteins is apob. And in a recent study that was performed in the UK Biobank, which is sort of this big biobank of, you know, hundreds of thousands of patient data from the United Kingdom, what investigators found was that the APOB particle, if you actually measure that directly, which you can do, is associated with those bad things like mi. So, like heart attacks, death, strokes, even more so than, you know, triglycerides or the LDL itself. So measuring APOB is now something that some argue should be prioritized in addition to sort of, sort of some of the more traditional things we look at, just because of that association with these high risk issues that we want to.
- [20:02]
A
Solve, why are we not. Why are we not just getting those in a standard measurement?
- [20:08]
B
That's a great question. Yeah. I think that hadn't been the tradition, but I think now we have more data that suggests it's important. So, you know, in our hospital, we are measuring it for a lot of our patients.
- [20:19]
A
Standardized.
- [20:20]
B
It's not standardized across the board, but I think for patients where, you know, you think that their LDL cholesterol is high or they have higher risk, you just go ahead and measure that as well. The apob.
- [20:31]
A
Okay, so if apo. So it's not enough to just get back your lab results and it says you've got a high ldl, you want to know if it's, you know, if I've got a high APOB as well.
- [20:42]
B
Yeah, I think because a lot of the guidelines and the Traditional teaching had been LDL cholesterol. A lot of, you know, what treatments you use and what you do is centered around ldl. So that's still the mainstay of measurement. But in terms of assessing someone's risk in more detail, the APOB can give you that additional information. So I'd measure both if I was particularly concerned about a patient. You can start with your lipid profile in general, and then you can add on apob.
- [21:12]
A
And what about apoa?
- [21:14]
B
Yeah, so APOA is a very interesting area. And so there's this molecule called lipoprotein. And lipoprotein is another risk factor for heart disease. So we talked about LDL cholesterol and HDL cholesterol and triglycerides a little bit. But lipoprotein A is sort of its own entity. Lipoprotein A is a molecule that, that consists of a LDL or a low density lipoprotein like particle that is bonded to apoa. And so the combination of those two together forms lipoprotein little A.
- [21:56]
A
Okay.
- [21:56]
B
And this molecule has been studied for quite a while, but there's no therapy until recently that has been shown to target lipoprotein directly and reduce its levels. And so, you know, people used to measure it, but there wasn't anything you could do in terms of acting on it and decreasing one's risk. So what the prior studies had done was essentially understanding what does lipoprotein A do to sort of those bad things we were talking about earlier, like heart attacks, strokes, cardiovascular death. And a lot of genetic studies have shown that high levels of lipoprotein A are actually associated with higher levels of cardiovascular death, higher levels of stroke.
- [22:44]
A
Is that through plaque buildup? Is that because of plaque buildup?
- [22:48]
B
So the way that lipoprotein A actually works is still being fully elucidated. It's not fully known.
- [22:55]
A
So we can go to Mars.
- [22:56]
B
Okay.
- [22:57]
A
Or wherever Elon's taking the world, but we can't understand LP exactly.
- [23:02]
B
We don't know all the details of that yet. We don't know what's going on inside our bodies. And what's especially scary about this is that this lipoprotein little A is primarily genetically mediated. And so while for LDL cholesterol, the sort of isolated LDL cholesterol, you can do certain things and we'll get into that. Lipoprotein little A, until now, there hasn't been too much you could do because diet and exercise tend to not affect its levels substantially.
- [23:36]
A
So is this the reason why? You know why? We used to hear that maybe a 35 year old triathlete who's at the peak of his sport or Tour de France. I do remember the Tour de France guy, maybe 42 years old, high VO2 max, thinks absolutely healthy, just dies suddenly of a heart attack. But having a completely clear lipid panel.
- [23:58]
B
Yeah, I think that is exactly right. I won't say it's the only reason because there are several things that can, you know, lead to that unfortunate consequence. But lipoprotein A is one particular risk factor that has been implicated in sort of these unpredictable deaths. Because you can have a relatively normal LDL cholesterol level, but a high lipoprotein A level, and that high lipoprotein A level will still put you at a higher risk for heart attacks, death, stroke and even this other area of heart disease called valvular disease. So like aortic stenosis, we can get into that later. But yeah, it has a lot of implications and is something that we need a therapy for because when, when bad things happen with it, it's, it's quite drastic.
- [24:50]
A
But would it make sense, regardless of pharmacological interventions right now, would it make sense then if you have a, if you're in a, the moderate risk for lp, let's just say, or even high risk lp, you get back a reading and you have a high lp, would it make sense then to do everything you can to lower APOB and ldl?
- [25:14]
B
Yeah, that's also an excellent point. You know, I think right now the guidelines, and especially the European Society of Cardiology guidelines, they just came out last year with this type of recommendation. What they said was if you do have elevated lipoprotein, first of all, they said that everybody should get lipoprotein A levels measured once in their lifetime because it doesn't change. Right.
- [25:39]
A
Because I did mine, we were talking offline and.
- [25:41]
B
Exactly.
- [25:42]
A
I don't have. And I was, I was low. I don't have to go back and do it next year.
- [25:46]
B
Yeah, the, the general learning, the traditional learning has been that lipoprotein A levels don't change drastically over your lifetime. That 70 to 90% of them is just, it's all genetically mediated because you have this LPA gene and it just determines what your LP levels will be. Now, there are some studies that show that lipoprotein A can be an acute ph reactant, meaning in instances of stress or inflammation in the body can go up. But again, for the most part it remains the same over the course of your Lifetime. So sort of measuring it that one time is very helpful. And then understanding whether you are, you know, in the majority and just have low lipoprotein A levels and don't need to worry about it is important. And then also understanding if you're very high risk and have high levels of lips, lipoprotein A is very important.
- [26:39]
A
I want to just go back to arteries for a moment.
- [26:43]
B
Yeah.
- [26:43]
A
Okay. Because you just said the word inflammation.
- [26:46]
B
Yeah.
- [26:46]
A
And this is a question I have now. The walls of these artists. Would you say that they have muscles along them?
- [26:52]
B
Yeah, they're made up of smooth muscle cells.
- [26:54]
A
Yeah. Not the same as capillaries, by the way, which are just like a hairline by one cell thick, like a hairline in diameter. Would you then say that another cause of a heart attack or this vascular disease would be if the cell. If the. The lining, the smooth muscle cells were attacked by inflammation, for example? Does that. Like, is there something to be said of the. The walls of the arteries as well?
- [27:24]
B
Yeah, I think that's an excellent point. You know, the two main theories for why not theories, I guess this has been explored. People develop heart disease, and art, specifically arterial heart disease, is high levels of cholesterol and also inflammation. And those are sort of the two major hypotheses that we talk about a lot in cardiovascular conferences. And what we've learned is we've gotten pretty good with some of the medications that we have now and the lifestyle modifications that have been sort of really emphasized in the cardiovascular community at lowering that LDL cholesterol risk. So the decreasing the cholesterol levels and sort of reducing that as a primary issue that causes heart disease. But inflammation is something we're still not great at addressing. And in part, I think the mechanism is not fully understood. And there are several different ways in which you can have inflammation arise in the body. And we're not routinely measuring markers of inflammation. Inflammation in all our patients, but we should be. We should really be measuring things like CRP levels in our patients just to understand if they do have that residual risk that we're not addressing, and that puts them at high risk for heart disease.
- [28:48]
A
But also TNF alpha.
- [28:50]
B
Exactly.
- [28:51]
A
Measuring this inflammation is this. I actually want to talk about what type of, you know, inflammation or cytokines are going in and.
- [29:00]
B
And.
- [29:01]
A
And really attacking the vessels. Are they. What type. Like what. What are we talking about? Is it, like, because we're getting inflammation low levels when we run. When. You know, I live in New York City. Yeah, it's. I'm Con, you know, it's a stressful. It should be the state of an inflammation because you're just, everyone's like stressed here. Are we talking about that type of inflammation?
- [29:22]
B
Yeah, cortisol. Yeah, I think, I think it's probably a mixture of several kinds of inflammation. There are a few specific targets that are being explored in detail and the one that comes to mind, apart from CRP, which has been explored in the past is IL6. So IL6 is getting me started on Aisle 6. Yeah, well, so you're familiar with it, but it's a important molecule, acute phase reactant that has been implicated in inflammation in several different areas of the body but is now being specifically targeted also for heart disease. So there are new drugs on the market that are sort of being studied now as potential additional targets for reducing or mitigating adverse cardiovascular disease.
- [30:16]
A
I literally drink AG1 every single day. I was super tired of taking so many supplements and wanted a single solution that supports my entire body and brain and covers my basic nutritional needs. I also wanted better gut health, a boost in energy and I wanted to support my immune system. And to be honest, I have the tin of AG1 right next to my kettle every single morning. So I see it right there, I have one scoop, I mix it up with ice cold water and I'm ready to go. I now also chuck in an afternoon boost at around 2pm when I'm feeling that afternoon slump. If you are time poor like me and you want to take ownership of your health health, it starts with AG1 and you can try AG1 and get a free one year supply of vitamin D and also get five free AG1 travel packs with your purchase. Just go to drinkag1.com neuro that is drinkag1.com neuro I don't know if you know this. You probably do because you're a very smart cookie. Did you know that it can actually, it's. I call it the bipolar molecule because it's, it can be pro inflammatory. Inflammatory just like you said but it can also be anti inflammatory dependent on where it's released from and we now know that it can actually also be released as a myokine, like a muscle based protein.
- [31:44]
B
I've actually heard of the myokines which is a very fascinating topic.
- [31:48]
A
Yeah, that's what I'm currently researching and just the, the whole outlook of IL6 being secreted from the skeletal muscle and acting as a say anti inflammatory makes it so bipolar. Right?
- [32:02]
B
Yeah, yeah.
- [32:03]
A
In my opinion.
- [32:04]
B
No, I agree and I think you know that's such an interesting space, and I'm not an expert in all aspects of IL6 by any means, but I think that it's something that we need to understand and we need to know how to harness. And I think, you know, now we're living in this exciting space where you have AI and these, like, targeted. I went to this conference recently, and they were talking about, you know, using, like, nanoparticles to specifically target, get, you know, areas of the body with certain medications. If you could do that for something like IL6 or for, you know, a host of other things, we could change a lot of sort of the disease in our body and also improve other things that. That could benefit from these risk factors that we traditionally consider bad.
- [32:51]
A
Yeah, the operative word being could.
- [32:53]
B
Yeah.
- [32:53]
A
I don't know where the idea is going.
- [32:55]
B
We'll see. We'll see.
- [32:57]
A
Okay, so we've. Okay, so what. What I want to now understand. I'm really happy that we cleared up the inflammation. I want to understand diet because, oh, my God, you know, it's like, if I eat a stick of butter, am I increasing my cholesterol? I'm hearing on social media that dietary cholesterol doesn't affect serum cholesterol. So I'd love to understand if what we eat is actually affecting our LDL and apob.
- [33:29]
B
Yeah, that's an excellent question. And I think, you know, 100% what you eat will affect your cholesterol levels. And so one of the. So the American Heart association, which is this sort of overarching body that gives individuals in cardiology and lots of cardiologists the guidelines, the basis on which to advise our patients on what to do to decrease their heart risk. That organization, that body suggests as like their top pillar, that mitigating your cardiovascular disease risk starts with diet. And so I think, you know, a lot of people have sort of tried to look at this in different ways, but eating foods that are high in cholesterol will increase your overall body cholesterol.
- [34:16]
A
What is this? Okay, this is now. We're now talking about saturated fat as well.
- [34:21]
B
Well, yeah. Saturated fats in particular will lead to increases in your bad cholesterol, that LDL.
- [34:30]
A
Cholesterol, but something like an avocado.
- [34:34]
B
Yeah, right.
- [34:35]
A
Yeah. Because we hear about avocados being good fats. Isn't this the same thing?
- [34:39]
B
So avocados have some fats, but they have good fats, and they also have other components in them that can be sort of. Of beneficial to the body in different ways. So sort of target going along with this anti inflammatory pathway. Now the exact mechanism, I don't know all the details of that, but. But I think that there are some anti inflammatory effects there as well. And then there's this whole other category of like eating fish and you know, other types of nuts that have, that are high in omega 3 fatty acids and those have a completely different mechanism of action in, of how they influence your cardiovascular risk. And again, they target your inflammation as opposed to the reducing the LDL cholesterol level in itself.
- [35:32]
A
Okay, so more cholesterol in diet equals higher risk of raising APOB and ldl.
- [35:41]
B
Yep. The bad cholesterol. The bad cholesterol.
- [35:43]
A
So we know that. So evidently we need to be looking at lifestyle interventions. Yeah. My question now is can exercise just so you got a high ldl.
- [35:54]
B
Yeah.
- [35:54]
A
And you're doing. We're not even talking about statins right now. We've gotten back the reading. We're at high risk. High ldl, high apob.
- [36:02]
B
Yeah.
- [36:02]
A
Let's just say we start to exercise. When we exercise, we pump more blood through the body. Therefore we've got more profusion of blood through these vessels. Does this clear plaque?
- [36:14]
B
Yeah, that's an excellent question. And people have actually looked into this exact question. So what exercise can do, is it can. You know, we've been talking about inflammation a lot exercise in the period that you're doing it. Sure, there's more stress in the body, but overall it decreases that inflammation, that stress in the body. And so in that sense, what it can do is decrease some of that residual risk we have and it can actually stabilize some of those plaques. So we know that people that exercise tend to have more stable plaques than those vulnerable or unstable plaques with the, those high, highly sort of cholesterol, those high cholesterol content, sort of less fibroblast composition. And so, so the, the, the stability of the plaque is really important in terms of whether or not it goes on to cause cardiovascular disease. And so exercise is one of those things that leads to increased stability of the plaque and can be very helpful.
- [37:20]
A
Interesting. Okay. Because I was, I, I always think about that. I'm like, should you just be exercising? But it doesn't have the same effect as, you know, completely eliminating bad cholesterol and saturated fats. Diet would have a greater intervention. Right.
- [37:35]
B
I think both are helpful because one is preventing the cholesterol from actually circulating in the blood and getting to those arteries. And that's really the diet or the medications. And then the second is, is stabilizing what's already There. So a lot of times when we see people or we see patients, you know, they're coming in their 50s, 60s, sometimes younger, in their 40s, but they already have some level of plaque. And so you really want to stabilize that plaque and also prevent more plaque from coming in. So I think targeting this sort of the reduction of plaque from both angles is important. Now, if you're talking to someone that's, you know, in their 20s.
- [38:15]
A
Yeah.
- [38:16]
B
Then I think the conversation really is important about sort of ensuring the diet is really good, measuring their risk and understanding how high risk they are. And if they are high risk, potentially intervening earlier.
- [38:31]
A
Okay, so then would it make. Okay, that's. There's so much going through my head and I wanted to understand and more. So in terms of diet, how does fiber play a role in this? Because we. There is a wonderful study that was done that I can't think about now, but it showed that high fiber intake can help reduce A, or cause mortality, and B, it can reduce cardiovascular disease risk.
- [39:01]
B
Yeah. I mean, I think, sort of just thinking about it mechanistically, fiber. If you're having foods that are high in fiber, they're going to satiate you for longer. You're going to eat less of those highly saturated foods. Highly. Foods that are high in saturated fats, foods that are high in carbs or sort of those unprocessed sugary items that we try to avoid. And so if you're decreasing your overall sort of intake of those bad fats of those processed sugars, then you're decreasing your risk of developing heart disease because you're reducing the amount of cholesterol that's circulating in your body and you're decreasing the amount of sugar in the body. And we know that high sugar consumption is associated with pre diabetes and diabetes, and both of those are associated with heart disease. So I think in that sense, having diets that are high in fiber can be beneficial for heart disease.
- [40:00]
A
Oh, that's upset me now. I thought there was a more like radical thinking behind this, like pathophysiologically thinking that fiber actually goes in and clears the blood vessels. Okay, so that doesn't help.
- [40:12]
B
Pills of fiber.
- [40:13]
A
Yeah, I'm like, that doesn't help.
- [40:15]
B
Not as much. Not. Not that we're using right now in our practice. But if it's something that you know will come around the corner, be interesting to see.
- [40:25]
A
Okay, let's talk about preventing and treating cardiovascular disease. We've already obviously spoken about top two, which is obviously lifestyle. So diet, exercise. Can you. Is There a way to actually build stronger arteries, like the walls of the arteries?
- [40:43]
B
That's a good question. Actually, I've. I've never been asked that question. And I'm thinking about it from a.
- [40:50]
A
Look from I'm talking. We've spoken about muscles. I'm like, yeah, there is muscles on the. Can we build stronger arteries?
- [40:56]
B
Stronger arteries, Yeah. I mean, theoretically, you think that there may be a way to sort of target those muscles, but as of now, I don't think that's a target that we look at in heart disease or in mitigating heart disease, but perhaps something to consider for the future.
- [41:11]
A
Well, maybe we'll elaborate on a research project. Okay, let's talk about testing somebody gets their. What would be a high reading. Let's talk about if you've got an ldl, where are you in the high risk?
- [41:26]
B
Yeah. And that's been, you know, this controversial topic that has spanned the last few decades because before, people used to think that having a cholesterol level of 100 or so was normal, but now we know the lower your cholesterol, the lower your LDL cholesterol. Again, that bad cholesterol, the better it is for you. So the initial studies looked at this 130 cutoff, but now we know that for people like you and I, your LDL cholesterol should really be 100 milligrams per deciliter or less.
- [42:00]
A
Yeah.
- [42:01]
B
If you're higher than that, you have a substantially higher risk of developing heart disease.
- [42:07]
A
At neuro athletics, we say below 90.
- [42:11]
B
Yeah, that's out. I like that.
- [42:12]
A
That's out. But that's LDL.
- [42:14]
B
Okay, LDL.
- [42:15]
A
Yes, we do LDL cutoffs at below 90. What about APOB?
- [42:21]
B
APOB? So that's a good question. There is. Because it's not routinely measured, people don't go by specific cutouts offs on APOB in terms of, you know, whether or not to start medications or to intensify your exercise. But, but if you think of it as, you know, APOB makes up LDL cholesterol, you would have essentially the same types of target. So if you're looking at a target of 100mg per deciliter in terms of being reasonable LDL, then your APOB should also be less than. Than that. So less than 100 milligrams per deciliter.
- [43:00]
A
I mean, what's it. Doesn't it, you know, this. The. It's like, you know, if you had to model someone, you'd model a kid, right? Yeah. What's their like what is like a 10 year old, an average 10 year old? Has they got an APOB reading of what?
- [43:12]
B
That's it. I actually don't know. It should be low.
- [43:16]
A
Yeah.
- [43:16]
B
But then we're also learning that now people that are 10 years, 12 years old are starting to develop metabolic syndrome and are, are having these high LDL cholesterol levels and require earlier treatment because otherwise you can imagine if they're already having these high levels of cholesterol roaming around in their body at 10 years of age, then if they, once they get to their 30s, they're already, you know, having this plaque progress and are high risk for developing heart disease early on. So it's not something that only happens to adults. And I think this also goes along with what we were saying earlier. There's genetics at play, there's D at play, there's inflammation at play. So if you have these factors at play at an earlier age, then you're still going to potentially have high LDL and APOB levels when you're younger.
- [44:09]
A
So is there a genetic component to ldl?
- [44:13]
B
Yeah, there is a genetic component to LDL cholesterol and there is a dietary component to ldl.
- [44:20]
A
What's the, what's the, what's. Okay, okay. What's the genetic component of ldl?
- [44:26]
B
So there's a few different enzymes that are at play. So, you know, one of the enzymes that's been looked at is HMG, CoA reductase. And that is an enzyme.
- [44:38]
A
I'm Ronnie.
- [44:39]
B
HMG, CoA reductrase. And that is the enzyme, or actually its receptor is the enzyme that's the target of statin medications.
- [44:51]
A
Okay.
- [44:51]
B
And we know that people who have a low levels of this enzyme based on their genetics, because they have a knockout of something, etcetera, they tend to have lower LDL cholesterol levels. And they were some of the first people who were studied to understand whether statin use in the long term led to adverse events or had side effects that were sort of prohibitory. And people saw that those people did well and they did well over a long period of time and, you know, tended not to develop heart attacks or strokes or, or die from heart disease. And so that was sort of the premise for why these statin medications, the idea for why the mechanism of statin medications was so good. There's also PCSK9.
- [45:40]
A
Well, that's the inhibitors that.
- [45:41]
B
Yeah, exactly.
- [45:42]
A
That's it. Yeah.
- [45:43]
B
And just like the statins, you know, these are of course totally different mechanism of action, but people that have a loss of function in their PCSK9 gene, they tend to have. Have less risk of heart disease in the long term. And so based on those genetic. The genetics of those individuals, people thought, okay, let's target this particular sort of molecule in the body, and let's see what we can do in terms of reducing people's overall risk. And now we have PCSK9 inhibitors that are able to do just that.
- [46:18]
A
It down regulates the. Does it.
- [46:21]
B
So essentially, PCSK9 is involved in a very complex pathway, but ultimately leads to lower levels, levels of LDL cholesterol when it's inhibited. Oh, wow.
- [46:32]
A
Okay. So would you say then doing something like a 23andMe genetic test or any other genetic test is. Should be standardized as well?
- [46:43]
B
I think that that's the way that we're moving. I don't know if 23andMe measures all these specific targets, and I think there are a lot of other targets that are being explored right now. But once we're at that point where we sort of understand all of the different genetic components that can cause higher cardiovascular risk, no doubt people should have this sort of looked at earlier and then addressed earlier. So if you have sort of, you know, lower levels of PC or if your PCSK9 is already inhibited, then obviously you wouldn't benefit from that kind of a medication. But your lipoprotein A is high. Maybe you need medication to sort of reduce that risk. Right. So I think that'll help us really target what types of therapies people need and also make medicine and cardiovascular medicine much more precise. So this idea of precision medicine and ensuring that we're doing what's best for each individual patient as opposed to sort of everyone on a population level.
- [47:46]
A
Okay, so we've discussed the PCSK9 inhibitor. What about what's a statin? Because this is the standard, like, okay, your LDLs there you can put you on a statin and. Controversial topic.
- [47:56]
B
Exactly.
- [47:57]
A
And there's risk factors as well. Yeah, but they're not all bad. So let's talk about what it is.
- [48:03]
B
Yeah, so this is one of my favorite topics to talk about because statins are such an important medication and they've been around for a while, but there is, as you say, this hesitation by some to take the medication. So what are statins? They are medications that sort of inhibit that HMG CoA reductase and so prevent that enzyme from binding to its receptor factor and therefore decrease the amounts of circulating bad cholesterol or LDL cholesterol you have in your blood. And so by doing that, by Reducing the amounts of bad cholesterol in the blood, they're able to prevent more plaque buildup in the arteries of the heart and the arteries of the brain, and then sort of prevent things like strokes and heart attacks down the road.
- [48:50]
A
So sorry to cut you off. So that doesn't mean that. So the mechanism of action of a statin doesn't go in and ameliorate these plaques? No, it just prevents other ones from building up.
- [49:03]
B
Well, the, the mainstay, I guess, of, of its action is in preventing the plaque progression, so preventing the plaques from getting bigger. Okay, but if the plaques aren't sort of having more and more cholesterol building up within them over time, then they'll be stable. And there's this other sort of theory out there that statins also have an anti inflammatory component to their treatment. So in that sense, they're also, in some studies have been shown to regress plaque so cause that plaque to get better over time and sort of resolve itself because there's decreased inflammation.
- [49:48]
A
Okay.
- [49:49]
B
So it really does, it really does target it from two different sides. I think the primary mechanism of action is prevention of plaque progression because you're having sort of less deposition of cholesterol within the plaques. But over time, once you have sort of that lipid core sort of stabilizing and sort of resolving itself, and you have a lot of those, you know, different, you have a lot of different molecules within the cell wall, the, the arterial wall itself that can sort of help resolve some of the plaque. They, the, the plaque will essentially start to regress over time. And then the statins also have this anti inflammatory capability, so that'll help stabilize the plaque and regress it even more.
- [50:34]
A
So, you know, I, is it true that once you've built up the plaque in these pipes, we'll call them, is there a way to just like, can we ever get just a clean pipe again?
- [50:47]
B
Yeah, that's what everybody hopes for. Yeah. I think right now what we aim to do is we aim to stabilize the plaque and make it, instead of totally clean, as hard or as stable as possible. And so what that means is instead of having the plaques that are high in lipids and very unstable, we want plaques that are fibrotic, calcified, that will never rupture no matter what stress comes around in the body. So right now you aren't getting clean pipes, you're getting more calcified pipes. But those calcified pipes aren't going to rupture and cause problems. And that's the way in which we mitigate heart disease.
- [51:32]
A
Well, that's scary. That's basically saying you're just, you've. You've clogged the pipes and that's. Yeah, we can maybe stabilize it. We can make them smoother. Yeah, because I keep thinking about a water pipe now.
- [51:44]
B
Yeah, I think that's a great analogy.
- [51:45]
A
Yeah, the water pipe. And it's like, it's muddy, but if we make it like more cement, like, then the water that goes through it can just flow through. Through.
- [51:53]
B
Yep.
- [51:54]
A
But that's, that's, that's crazy.
- [51:56]
B
It's not ideal.
- [51:57]
A
It's not. So you just want to just stop. Yeah, just stop with the bad eating. And you know what? I think we, we haven't even. We've still got to stick to the, you know, we've got to stick to the statins right now. I understand that, but I, we've. We've got to talk about how things such as smoking and smoking can affect cardiovascular disease and alcohol too. But, but we'll stay on that. Let's just stay on topic right now because I've got so much going through my head. Okay, statins. Now, with a statin, is it true that you may get things like muscle weakness if you take it?
- [52:32]
B
Yeah. So that's been one concern with statins, which is what we call myopathy, or inflammation of the muscles of, you know, different parts of your. Of your body. And in particular, people will get. Some people may get myopathies in their lower extremities to their thighs or their legs. Now, that is a side effect that a lot of people are concerned about, but the actual incidence is very, very low. So less than 10% or even less than 5% of patients actually develop a real myopathy. And so the tolerability of these stands is very high. And the benefit fits really outweigh the risks for statin medication. So the overall benefit in terms of reducing heart attacks, strokes, death is so much higher than any of these types of side effects that people often are worried about when a doctor talks to them about taking a statin.
- [53:33]
A
So there's different types of statins.
- [53:35]
B
There are different types of statins. There are four pretty common ones that are used, but I think the most common are atorvastatin, Lipitor or Rosuvastatin. And so these two medications are commonly used. And the nice thing about both of these medications is that you can up titrate the dose to what's called a high intensity statin. So the statins that can reduce your heart or your LDL cholesterol and your cardiovascular risk the most. Just to sort of backtrack a little bit, your statins will usually start, start off as low intensity. So the dose will be pretty low, like 10 milligrams or so for Torvastatin. Then, then as your doctor monitors your, your LDL cholesterol levels, and if they're still not at target for you, then they can up them to a moderate intensity. And if it's still not at level, then they can up them to a high intensity level. Stat. Yeah, yeah. And one other thing I wanted to mention was that, you know, we talked about for you and I, so pretty healthy people, pretty healthy adults, the LDL cholesterol cutoff is less than 100 milligrams per decimal oscillator. But for people that have a high ASCVD risk, which stands for atherosclerotic cardiovascular disease risk, and it's just a fancy calculator that takes into account some of the comorbidities you have, your age and your LDL cholesterol. In those patients that have higher risk, you really want to target even lower LDL cholesterol levels. So in the United States, States, the guidelines say that you should target 70 milligrams or less. And in Europe, they actually say 55 milligrams or less for people with higher risk.
- [55:21]
A
Wow, that's really interesting. Let's talk. Have you ever heard of berberine?
- [55:28]
B
No, I haven't.
- [55:29]
A
Okay. Of course not. Okay. It's a, it's kind of like, okay, have you heard of rapamycin?
- [55:36]
B
Kind of. Yeah, but I don't know.
- [55:37]
A
We won't even go there because this is a, this is something that is, is now getting. It's a, it's a supplement. Okay. We won't even go into it. But there's a lot of people now, you know, in this scientific social media world that are like, okay, if you don't want to take a statin, go off and take a. Take some berberine. Can help, you know, with type 2 diabetes. And, yeah, it's interesting. You'll have to look at that.
- [55:58]
B
Is that like red rice y sex extract or is that different?
- [56:02]
A
I have no idea.
- [56:03]
B
Because that's another supplement that people take. But there's actually at the American Heart association copy conference in 2022, so last November, they presented this trial.
- [56:14]
A
Yeah.
- [56:14]
B
Where someone. As sort of a joke, but also, you know, for practical reasons, because this is what a lot of people come into cardiovascular clinics for. They compared statin use to I think nine different supplements or eight different supplements. You should look at it. But the. And they found what the LDL reduction was for each of them. And they looked at. Looked at, you know, the incidence of cardiovascular events for each of those different supplements, and they actually found. So definitely the statin reduced your LDL the most and also decreased your risk the most. But some of the supplements actually increased your risk of having the adverse event. So I think. Don't quote me on this, but I think that red rice yeast extract, which a lot of my patients, you know, say that they want to take, instead of the statin, it's. It has some level of that HMG CO reductase enzyme or property to it, but it's not regulated. And it has a lot of other stuff that I don't know what's in there, but interesting. Tended to increase their LDL level and it increased their risk. So it was actually counterproductive on both ends. And then a lot of the other supplements had, like, you know, sort of similar situations where there was either a null effect or it increased your LDL.
- [57:33]
A
Level a little bit. By the way, when I said rapamycin, I didn't mean. I meant metformin.
- [57:38]
B
Oh. Oh, okay. Interesting.
- [57:41]
A
Yeah. You have to look that up. Okay. I'm. I'm cautious of the time, but I did want to touch on smoking.
- [57:51]
B
Yeah.
- [57:52]
A
Okay. And the reason I just got back from Europe.
- [57:54]
B
Yeah.
- [57:55]
A
And I'm. I was just blown away by the amount of people in Rome and Greece that are just everywhere I went, signed cigarettes.
- [58:06]
B
Yeah.
- [58:07]
A
So what's happening there?
- [58:08]
B
Yeah. So smoking, as we know, is bad for several parts of our body, but especially the arteries of the heart. Again, going back to this whole inflammation piece, smoking can increase the level of inflammation in the body. There's more stress put on the body and the arterial walls. So you often hear of, you know, patients that have higher risk who were smoking and then suddenly had a heart attack because their body is sort of undergoing this acute sort of stress phase. And that plaque that's unstable with a lot of the lipids in it and less of those fibroblasts that are stabilizing, it just ruptures, and they have a heart attack right away. So I think in that sense, smoking can really lead to acute sort of stress response in the body and then cause rupture of those plaques and then in it is just bad for other parts of the body, too. And so you can have disease that develops over time in your legs, in the peripheral arteries of your legs. So people will come in with claudication, which is just very painful legs. They'll come in with, you know, some symptoms of stroke because their arteries in their, in their, in their brains are starting to narrow and develop disease. And then of course, in their heart as well.
- [59:29]
A
Yeah, I, I think that, you know, every, you've just, you know, we're now looking at Alzheimer's disease as more of vascular disease, obviously. And everything you've, you know, from that now combined with what you're saying, we really need to be talking more about the vascular system and the vasculature and talking about, well, what they are. And this is starting down to medical school.
- [59:55]
B
Yeah.
- [59:55]
A
Really?
- [59:56]
B
Yeah. Where you think that's so true, which.
- [59:58]
A
Is just pharmacology school.
- [59:59]
B
Yeah.
- [59:59]
A
But we need greater education around that and for the broader public to understand that it is, you know, what I've gotten from this is cardiovascular disease is there is. We've got plaque and then we've got the cholesterol, but we've also got inflammation which is affecting the walls of these arteries. So what's your, over the next year to year years? What's your main areas? Is you just going hard on LP or on statins?
- [60:29]
B
Yeah, so I'm actually in a few different areas. So as I was saying, I'm going to end up in interventional cardiology. And so I am doing some studies where we're analyzing trials of patients that have the highest risk heart disease. So that left main disease I was talking about before, and understanding in those patients, patients, what is the best way of managing their heart disease, their left main disease. So as you probably know, you know, you can manage it with surgery, coronary artery bypass, or you can manage it with stents. And there's still debate as to which is the best and what we should be doing the way forward. So we're looking at specific populations. So patients with diabetes, patients that come in with acute heart attacks, what should we be doing for those, those patients? So that's one area of interest. And then the other area. Yeah. Is exploring some of these more prevention things because I think that it's really a spectrum. You can't just focus on one area. I think now we need to be focusing on prevention as the primary mainstay of our patients, but also using some of the sort of high risk patients, or not using the patients, but using the times in which they come into the hospital, like for example, during a heart attack, to sort of explain to them that, you know, you need to reduce your risk. And now we have so Many therapies to do so. And so sort of looking at those risk factors and understanding, you know, whether they really do decrease the heart attack, strokes, et cetera, in certain populations.
- [62:04]
A
I was actually, I didn't get to this, and I'm sure it'd be a whole other podcast, but I was going to ask you in terms of screening what your, what your thoughts on were with a CAC score, like if you do coronary artery, you know.
- [62:18]
B
Yeah, I think that's, that's actually something I do in my practice now more and more routinely.
- [62:24]
A
Wow.
- [62:26]
B
So especially in patients who don't have typical angina, so typical symptoms of chest discomfort or shortness of breath, which is the classic teaching that we learn in medical school of, you know, whether someone has heart disease or not, if someone is coming in with, say, a slightly higher risk of heart disease, they either have it in their family, they have genetics that suggest that, and they got it tested for some reason, or they have high cholesterol, diabetes, etc. And, you know, they're like middle aged. What I would want to do is understand what their risk is for heart disease. And so one way is to do a stress test. But in a lot of these patients, unless they're having, having sort of some level of symptomatology, you may not find anything on a stress test. A coronary artery calcium score will let you see in any patient what the amount of calcium is in their body or in their heart or the vessels of the heart. And so what I'm finding is in a lot of these patients who are otherwise, you know, healthy, but maybe slightly higher risk, you can use the calcium, the coronary artery calcium scalp score to understand whether they're on like the higher end spectrum of having adverse events down the road or if they're on the lower end and, you know, their coronary artery score is zero, so they don't have to worry about it. Five years. Yeah, it really should be zero. If it's not zero, they should strongly consider being on a statin if they meet the other criteria. And, you know, technically it's not per guidelines, but what we're also seeing is that patients who do have coronary, the presence of calcium on their coronary artery calcium scores on those scans, they tend to develop progression of coronary disease. So even starting those patients on some of these medications like statins earlier is very, very beneficial for them because then you're reducing their risk down the road.
- [64:34]
A
Would your. I know that increasing your risk, risk of a myocardial infarction can Be increased from afib.
- [64:41]
B
Yeah.
- [64:42]
A
For example, and I know that because my father had AFIB and ended up in a stroke, and this was in 2019, and that's how we were like, okay, we need to intervene hard now. And. And look, we've seen a, you know, a cascade of problems that arise after this, which is really sad. However, that isn't on the same lines of cardiovascular disease.
- [65:06]
B
Yeah.
- [65:07]
A
Is it afib? It's a completely different ballgame.
- [65:10]
B
Well, it is, I guess. It is a form of cardiac disease, and it can become. It can be important in cardiovascular disease, because the real problem with atrial fibrillation is that essentially what's happening in the heart is that instead of having your normal pumping, your. The top chambers of the heart that collect blood, the atria of the heart are now fibrillating. So instead of having their little atrial kick with each pump of the heart, they're just fibrillating. When that happens every now and then.
- [65:44]
A
It'S not all the time.
- [65:44]
B
Yeah, well, some people have it all the time, and that's called permanent atrial fibrillation. And some people have paroxysmal atrial fibrillation, which just kind of comes and goes, and both are considered abnormal, and both should be intervened upon, depending on a certain sort of caveats, which we can talk about briefly. But for atrial fibrillation in particular, when you have that fibrillation for sort of extended periods of time in those top chambers of the heart, what happens is instead of sort of blood moving with each heartbeat, as it should, some of it, especially around the walls of the. The atria of the heart, and especially that left atria, tends to remain stable. It's called stasis. So it doesn't really move much. And so when that blood doesn't move in that left atrium of the heart, then the blood there, when it's stable, can form clots. Those clots can then be pumped into the left ventricle of the heart, which is the main pump of the heart, and then be sent to different parts of the body, such as the brain, and cause stroke. But sometimes they can even be sent into the coronary arteries and cause a heart attack. That's rare, but it has. It can happen, and it can cause, you know, a heart attack that's. That's quite bad.
- [67:08]
A
Why is it so hard to diagnose afib?
- [67:10]
B
Yeah, well, we're actually starting to get a little bit better, but some people don't experience symptoms with atrial fibrillation, while others do. And, you know, the heart is an inner. Innervated. So in some cases, you know, you. You won't necessarily know if you're having atrial fibrillation just because your heart is fibrillating. It's more so what it does to the amount of blood that's being pushed out of the heart. So you can imagine if your heart isn't pumping normally, then you may have a little bit less output, and then you can feel that. So some people develop shortness of breath, some people notice palpitation, some people notice develop slight chest discomfort. But some people don't notice anything at all because even with defibrillating, they're able to have enough output. And so that makes the diagnosis really tough. Now, with the whole wearable technology, we're starting to be able to capture these things much earlier. And there's a lot of research being done into this. And there was this big Apple Heart study that looked at, at this because of the Apple watch, et cetera.
- [68:16]
A
Is that from Sex in the City as well?
- [68:18]
B
Is it? I don't know that. So the Apple heart study is sort of this. It was led by, you know, I think Apple and some collaborators at Stanford. And essentially they looked at a host of participants who had their apple watch and looked at a variety of different arrhythmias, and atrial fibrillation was one of them. And they wanted to see if they could sort of predict it earlier or not predict it earlier, but essentially catch it earlier earlier, because people were able to check on their Apple watch when they weren't feeling well and essentially send the tracing of what the Apple watch said was afib to their doctor, and their doctor was able to confirm or deny it. So I think in that sense we're able to catch it earlier. And then there's other people who are doing research and using artificial intelligence to capture atrial fibrillation on EKGs that are otherwise normal.
- [69:08]
A
Yeah.
- [69:09]
B
And so, you know, you can imagine if you merge the two and you have the apple Watch catching some of these more nuanced findings on EKGs better as detected by an apple watch, then you can maybe predict these types of things earlier and inter intervene earlier. Because before a patient develops atrial fibrillation, there are certain risk factors that just put them at higher risk risk to developing it. And these include some common things. And I'm sure, you know, I know in our family, you know, some people have this, and multiple patients I see have this, but sleep apnea is a major risk factor for atrial fibrillation. Yeah. And so if you're able to control your sleep apnea, you can potentially sort of eliminate the chance that you'll have atrial fibrillation down the road or at least reduce your chances of it being clinically significant. Significant.
- [70:01]
A
God.
- [70:02]
B
And then same thing. As you know, we talked about clots in the veins of the lungs. So with pes, those are also implicated in atrial fibrillation. And then also making sure your heart is healthy from arterial disease is also important in terms of reducing your risk of atrial fibrillation.
- [70:20]
A
Gosh, Dr. Gabba, you have. You are just incredible. I could keep going for longer and longer, but I want to thank you for coming on here and giving us basically a cardiology with 101 lecture and you're, you're quite big and interesting to follow on Twitter. So why don't you tell us all where we can find you?
- [70:39]
B
Oh yeah, so you can all find me on Twitter and my handle is at prakrithygaba. It's hard to spell, but we'll put.
- [70:48]
A
That in the show.
- [70:51]
B
Anywhere else, please follow me. Mostly, mostly there. I'm starting, you know, starting to dabble with Tik tok.
- [70:57]
A
Yeah, I've seen that. Which is great. We're going to get you on there too.
- [71:01]
B
Exactly.
- [71:02]
A
We'll link it below. Than you. So much for being part of the Neuro Experience podcast.
- [71:06]
B
Perfect. Thank you so much for having me.