Chapters Transcript Video Cardiovascular Longevity Dr. Luke Gambill discusses the pillars of cardiovascular longevity. I'm excited to be here. This is going to be an ambitious talk for 15 minutes, but we're gonna, we're gonna try to get through it. This is something yeah, near and dear to my heart. Um No pun intended and uh something we should all be striving for. All right. Where is it? What I do in deep Greenland? Cool. All right. So objectives. I want y'all to think about why it's important that we um collectively start thinking about um AC A S CBD um uh on a causal model. We're going to go over some risk factors today. Um I want to um enlighten or give people in the audience an appreciation for two biomarkers, Apo lipo protein B as well as lipo protein A. Um And uh I want um uh to everyone to leave here today realizing that exercise truly is the best medicine and that um sleep is absolutely crucial. So big bad stats for um A S CV D. It's the leading cause of death worldwide. About one person every 33 seconds in the US dies from heart disease. It's responsible for about 20% of deaths costs us a boatload of money, $240 billion annually, about 20 million deaths annually worldwide. Um This is inevitable and ubiquitous if you live long enough, it's not a question. If you're going to die, um, uh, with, uh heart disease or a CV SD, it's gonna be if you die from it. Um And so delaying the onset of this problem should be the goal for everybody who wants to live a long and healthy life. All right. So these are the guidelines that the AC C has put out from 2019 about primary prevention. And uh you know, the class one recommendations here uh for 10 year risk model is kind of what they focus on. They give it their highest level recommendation if you're a younger person though. Um everything else is kind of a A um two B or two A recommendation. And uh right here, this is the um the one recommendation I I wholeheartedly disagree with, this is for adults that are young people, 20 to, you know, basically 60. Um uh they say you can consider doing a 30 year risk model on patients. Um you know, depending on what risk factors they have. And I would argue, you know, these patients benefit the most from early recognition of risk factors and treatment. And um and so this should be mandatory. And so I think this should be right up here with, with this, with this guideline right here. Um We need to be thinking bigger. All right, the 10 year risk model, which is the standard. There's, this is the one on the AC C uh web page, but there's Framingham, there's score. Um It's basically powered for age, which is nonmodifiable as we know. But depending on what your age is that pretty much drives the whole show here. They say low risk, less than 5% borderline 5 to 7.5, intermediate 7.5 to 20 high risk 20. And the guidelines right now basically don't say that you should be taking aspirin or statin therapy as primary prevention until your risk gets greater than 5 to 10%. Um This is a, um we don't do this for smoking, right? So you don't have uh patients you see in your clinic who are smoking and you let them smoke until they're 10 or 20 or 30 year risk for lung cancer goes up. And so, um again, I think this is the wrong idea. I think a, a longer risk model 30 plus years is probably more appropriate for a lot of our, a lot of our patients. So, uh the causal model um of A S CV D takes into account the duration of time, the arterial wall is exposed to risk factors and this is a compounding risk over time. Um The analogy here is, listen, you know, you'd be a fool to not save any money in your bank account. From the time you, you know, twenties, thirties, forties, fifties and expect to retire in your sixties and seventies, um, comfortably financially. Um, we do this all the time with our health though. Um, you know, we take for granted when we're younger. Um, you know, um, we don't exercise maybe. Right. We, you know, we abuse our, you know, we don't take care of our bodies. We don't, you know, treat our risk factors aggressively or even identify them. Um and this compounds over, over time um to the point where it would, you'd be foolish again to, to think that you could drift into your sixties and seventies with um you know, with um good cardiovascular health, if you're not actively um putting the time and the energy um you know, to, to improve of this, it's, you know, it's an investment in your, in your health. And, and so the majority of people who are at short term um uh risk, low risk for the short term are actually probably at high risk over the long term. And this is why I think that, you know, you know, early treatment um uh of risk factors once they're identified is, is actually um you know, is crucial here. So these are the pillars of A S CV D metabolic health, um Apo lipo protein B, hypertension smoking and um sleep, I added, it's not really a conventional one, but I, again, I, I think that um sleep is um is, is, is um probably undervalued for how important it is in affecting all aspects of your health. Um I'm not really gonna go over smoking just because, you know, it should be abundantly clear that um you know, that that's, that's bad and um you know, you're pressing on the accelerator um of death if you, if you, if you smoke um so metabolic health, um it encompasses a lot of things. Um um these are the general things that I like to think about. So, you know, the classic syndrome X, which we'll talk about in a second, uh lipid metabolism, how sensitive to insulin you are, what your exercise capacity is and what's your body composition um out in Suffolk where I practice and we have a lot of um overnourished people. Um as I'm sure you can all attest to um so metabolic syndrome as it's classically defined and listen, I'm not also a huge fan of, of this, but um I think it, you know, it, it, it frames things uh reasonably well. Um So weight circumference in men, greater than 40 inches in females, greater than 35 triglycerides, greater than 1 50 or on medications to treat HDLC. Less than 40 mg per deciliter in men or 50 mg per deciliter in women, blood pressure greater than um 1 30/85 or medications to treat fasting glucose, greater than 100 mg per deciliter or medications to treat uh fasting glucose is, um, I don't think the best marker for this. Um, you know, only because a lot of people will have um mildly elevated fasting glucose from having a cortisol surge in the morning. Um, but when you go on, you further check under the hood and A one C and fasting insulin levels, they're actually, um, they're actually um, quite insulin sensitive um in this country, uh over about the last decade or so, the prevalence for uh metabolic syndrome increased from 36 to 47%. So that's about half the people uh in the country. This was a meta analysis and Jack from 2010, it looked at 87 studies and had roughly 950,000 people. And the big takeaway from this is if you have metabolic, oh, the other thing to point out metabolic syndrome, you only need three of those things. By the way, you don't need all five, you need three. And so that's important to keep in mind too. Um But if you have metabolic syndrome, your risk of A S CV D increases by about 135% your mortality increases by about the same, your all cause mortality increases almost to 60%. Your risk of having a heart attack increases almost to 100%. Your risk of stroke by 100 and 27%. If that's not bad enough. These are all the malign that you're more likely to get if you have metabolic syndrome. All right. Well, in this country, we, as I mentioned, we have a bunch of overnourished people. Um, uh, almost 70% of the population in this country now is either overweight or obese. Um, not everybody who is obese has metabolic syndrome, but it, um, a large majority of them are, um, overweight people again, 22%. Um, I would, um, I would argue that if you have a patient in your office who is overweight, or most certainly, if they're obese, the burden of proof is on the provider to prove that they're metabolically healthy. All right. Um cholesterol, um something we're probably all familiar with. So, um A S CV D is, is, is essentially driven by the deposition of APO lipo protein B containing um um um particles that get trapped in the arterial wall. Over time, we've traditionally assessed this by measuring LDLC concentrations and non HDLC concentrations. And uh it's probably worth noting that um when you're born, your LDLC level is in the 20 to 40 mg per deciliter range. Um If you keep it at that for the course of your life, um the likelihood that you're going to have a, a cardiac event or have any problems with A S CV D is incredibly, incredibly low. Um This slide here, this just kind of outlines like over time here on the Y axis. Um you get progressive more inflammation and Othella dysfunction and that's a signal for batty streaks to form which, you know, over time can progress into a more aggressive aroma and then eventually can rupture and that's where your mis typically occur. All right. So this was um, uh, a big study that was put out um by the European um uh society of Cardiology. It was a meta analysis, meta analysis that looked at over 200 studies, roughly 2 million people and 20 million people years. Um And what they did was they looked at um um all the um trials looking at lipids and mortality and whatnot and it included uh randomized cohort trials, um randomized trials, cohort studies as well as Mendelian randomization. And the big takeaway here is um um the longer you're exposed to lower levels of LDLC, um typically the, the less likely you are to die of any cardiovascular events. And this is, you know, almost a log linear relationship. When you look at the Mendelian randomization, these are people who have genetic predispositions to having low cholesterol. Um They did, they did great out here. Um And these are the cohorts and the randomization trial. So I, I don't think it's controversial at this point to, to, to say that um that um LDL and A OB containing pro um particles are what drives AC A CV D over time. Um APO lipo protein B and so all the sinister aro cholesterol in your body is carried around by this by this lipo protein. It's um and so, uh you can see out here um these a OB 100 particles, this includes the VLDL, um remnants of VLDL which are quite AIC um kind of the ID LS, the intermediate lipo protein ones and LDL and then LP little lay out here. And what I want you to notice is generally the, the degree of agen of these particles is, is driven by how concentrated their cells are with cholesterol. All right. All right. LP. Little A, this is the most dangerous particle in the world that no one's ever heard of. All right. I, um, this is, um, something that brings close to home with me. I have one of the highest LP Little A levels of anybody. I've, I've ever checked this on. Um, and this is not something that, um, is, is, is routinely checked by people. I, I might be one of the only cardiologists routinely doing it. Um, at least that I can see it is an independent risk factor for A S CV D and aortic stenosis. It is genetic predetermined, right? And so, um, um, once your levels are determined by birth or whatever, they rarely change up the course of, of your life, it's got about a 10 to 15% prevalence worldwide. So you can look around, there's a fair amount of people in here who have this that probably don't even know it. Um, there are some ethnic considerations this appears to be uh uh higher concentrations of LP Little A in um Southeast Asians as well as African American population or uh um, and so, uh how this plays out for, for some populations is unclear but certainly for um, most Caucasians and, and um most other people that um if you have an elevated level, it, it is a harbinger of badness. Um The current ac cah A guidelines um only recommend checking this if individuals have a family history of a premature ischemic heart disease or a personal history of this. Um You know, when you take a good history on patients, you can almost know whether LP Little A was going to be elevated or not based on, based on their family history alone. LP Little A is, does a bunch of bad things. So it's pro agentic, it's pro inflammatory, it's prothrombotic again, it's an LDL molecule, it's attached to this Apo A Tao here, which has got all these little pringle domains on it and it's a scavenging molecule that basically clears out oxidized phosphor lipids. But in doing so, it can get embedded in the heart walls a little bit more easily. And we also think that's the same mechanism for why it affects the aortic valve as well and leads to premature aortic stenosis. If you have someone who's got aortic stenosis and they're in their fifties, young sixties and they have coronary disease check an LP little A level, it's going to be elevated, almost certainly. That's not it. We, oh, ok. Here we go. All right. So, the Europeans, they're, they're, they're a bit more, um, forward thinking about this. Um, I like their, um, uh, I like their, uh, consensus about this so they think it should be checked in every adult at least once. Um, and you interpret the LP little, a concentration in the context of kind of their other, um, uh cardiovascular risks and then you can intensify treatment based on that. Um And uh this is uh shows that basically the higher your little A concentrations go. Um uh the likelier hazard hazard ratio has increased for your likelihood of having um A S CV D. This is a busy slide, but again, this is part of that same study. And so here's patients who have baseline risk of A as CVD events and the actual risks here. So no matter what your baseline risk are, if you have elevated LP little A levels, it's just, it's a force multiplier for your risk. And even if you have levels out here that are elevated and you basically have no other risks. You know, you should still act accordingly and, and, and be as aggressive as you can with management of all your other risk factors. There are treatments for this. Um I'm not really diving into a lot of the treatments or therapies for this stuff today. Um But um NIACIN does it most people would recommend you probably don't need to take niacin, it's hard to take. Um And there's been a couple of older studies um that, you know that debunk the, that nisin is beneficial PC KS nine inhibitor. So this is repatha and will actually reduce this anywhere from 15 to 40% in some people. And then there's a bunch of phase two and phase three trials that are coming out looking at these little oligonucleotides. So that's coming. So we will have more targeted therapies um down the road here, hopefully sooner rather than later. All right, this is the only um slot, I'm gonna talk about insulin resistance. Um but it is the root cause for a lot of A S CV D and chronic disease that includes PC os hyperlipidemia, gout, et cetera, et cetera. When you have excess insulin, uh floating around, it decreases the bio bio bioavailability of nitric oxide and impacts the expression of A OC three which decreases the expression of lipo protein lipa, which um basically leads to accumulation of triglycerides. As I showed you earlier, having a lot of triglycerides circulating in your bloodstream and stuff in your cholesterol is a bad thing, ultimately leads to endothelial dysfunction. About 50 to 75% of all deaths seen in patients with diabetes or complications of cardiovascular disease. Um I think we are late to the party identifying people with insulin resistance. And um and um the reason it is, is because if you're using the standard marker of an A one C, um, you're, you're, you're, you're missing out. All right. And so we don't really do the, the OGT test anymore. I think pregnant women will still get it, but we don't routinely do it in the clinic because it's time intensive and you don't need to keep someone around for two hours and, uh, and measuring their insulin levels and, and, and glucose. So we mainly now rely on fasting glucose and a one C. Um I've been checking fast and fasting insulin levels in my patients for years now. Um because that's gonna be the canary in the coal mine when your fasting insulin level is increased. Um uh that is the first sign that you're becoming insulin resistant and I would argue that we shouldn't wait, you know, for someone's a one C to get 5.65 0.7 you know, 5.8 by the time that's happened again, the, the train left the station uh years ago. Um I see a lot of um prediabetics also that um that are just are not being treated with any pharmacotherapy, which to me, um, you know, I I'm always on the other side of the coin here as you know, we should be, again, treating these risk factors aggressively and early. Um because again, I, I think that the earlier we can identify insulin resistance and, and get to them and get it better than the better likelihood of patients going to do over the long term. Published October 17, 2023 Created by Related Presenters Michael (Lucas) Gambill, D.O. Sentara Cardiology Specialists View full profile
BROADCASTMED