So, if you've been with me for the first two videos, you know the drill. I'm going through the dense ACC AHA dislabetime guidelines, so you don't have to. And you've already seen that, we've established a good baseline. If you haven't seen those videos before, I recommend going and watching those, they may be helpful. But if you just want to watch today, that's fine. We're talking all about sections 4. 2. 3 through 4. 2. 10. We're talking about algorithms, risk enhancers, and everything you need to know to start to risk stratify your patients. So let's dive into it. So, first things first, we have to start with an individualized risk-benefit discussion, right? The guidelines make it very clear that we have, before we write any prescription or do anything, we need to have a real conversation with patients, right? We're not just. Giving a carte blanche, here's a medication, and they actually gave a pretty helpful tool to help you do this. They have a checklist, which is table 10 in the document. It kind of walks through how to think about talking with your patient about managing their dyslipidemia. They recommend the first step is a comprehensive ASC VD risk enhancement, which includes using the calculators we talked about and we will talk about more in a second here: the prevent calculators. And then, on top of that, considering: hey, do they have any additional risk-enhancing factors or reproductive age risk markers or more things we'll talk about in the future? And then you explain the risk in absolute and relative items to them. So you say, hey. What's your absolute risk? What's your relative risk? We look at the prevent scores, kind of think of it together. And then I always mention that: hey, we want to emphasize healthy lifestyle as the foundation for everything. So we're viewing their lifestyle habits, including diet. Physical activity, BMI, tobacco use, and point them to resources if need be. Then, and only then do you recommend talking about potentially Pharmacotherapy, right, and considering statins versus non-statin medications and discussing the potential adverse effects. And then, on top of that, they also recommend talking about cost and convenience, right? Meaning, we have to talk about You know, the Pandora's box of hey, what's this going to cost me? Is it going to be covered by insurance? Is it if it's not? And so it has to be a priority, because, right? Because if you say, hey, I have the perfect plan for you, we're going to start on this, this, this, but someone's like, uh. It's not covered, and I can't pay a thousand dollars a month out of pocket, then that's not a good plan. And so, costs and administration have to play a big role. Also, administration, meaning, hey, if someone's like We need to get you an injectable, but they say, I'm never injecting myself with anything. And we've all had patients who do that, and that's okay. Well, then your perfect plan is not great. So, once again, working with the patient to understand what they want to do, ask the patient questions, express their values. Preference them is telling them what you want and then work together and collaborate to come up with a therapy. And this is the ultimate goal of any conversation, right? It's to have a well-balanced conversation with you know the patient being heard, everyone feeling like they're on the same page and going from there. And so, the new standard is the prevent ASCBD equations, right? They're much better calibrated. They integrate kidney function and metabolic health. And table 11 is a great example of the new features. You can see it here in the video version. There's a lot going on, so I will walk through those. So, first, It's very large. There's a lot more representation. It's 3 million adults that are more reflective of the diversity actually here in America. Next, they lower the limits to 30 instead of 40. And it also provides sex-specific equations, but they've also removed race or ethnic variables as well. So they say, hey, they got rid of those. They also provide a base model of risk prediction that includes commonly available risk factor measurements: things like age, sex, blood pressure. Total NHGL cholesterol, diabetes status, tobacco use, kidney function by EGFR, all those things. On top of that, they ask: Are you on a satin, are you on antihypertensive, what their BMI is? And so. This allows you an opportunity to provide additional inputs as well. And on top of that, they also say, Hey, you can put in A1C, you can put in your urinary, you know, albumin to creatinin ratio, and also zip code looking for social determinants of health. And these risk factors are not necessary to generate the risk estimate, but they may enhance the risk prediction. It also gives a hard percentage for each patient looking for their ASCBD, looking at that, heart failure, and total CBD risk. Which, once again, total CBD is the AS CBD plus heart failure. So they give you three different percentages for those specific outcomes. And finally, they say that the new equation is as accurate as the old one. At separating high risk versus not high risk, but it provides a significantly and substantially more accurate risk estimate than the previous equations that we're talking before. In fact, they're about 40 or 50% lower than the 10-year risk estimates from the pool cohort equations for the same risk factors. So they're saying, hey, these are better equations, they're more accurate. And so that's where this whole prevent thing came from, just to give you guidelines there. And so the guideline also gives a Class 1 recommendation for adults aged 30 to 79 with an LDL between 70 and 189. So they're saying this is the target we can get this calculator from. So between 7189 and that age, that's where we can use this. So Once again, this table here that we're looking at is what are the percentages, meaning, hey, what are the risks that we have? And you can look here and see the new risk thresholds because the math has shifted, right? So low risk is now less than 3%. Borderline is three to five, intermediate is five to less than ten, and high risk is anything 10 or greater. And so, because prevent estimates are, once again, about 40 to 50% lower than the old pool cohort equations. These new lower thresholds actually capture a very similar group of patients that were treated on the old guidelines. So, it's also important to understand that we will be treating about the same amount of people. I've explained more about that in previous podcasts, but we'll talk about it. But they're looking at that. And on top of that, it's also vital to look at the 30-year risk for younger adults, right? It helps us explain to a 40-year-old why we care today, even if their 10-year risk looks totally fine on paper. And so now that you say, you know, we can consider starting a medication at that borderline, which is between 3% and 5%, which is lower than previous guidelines. Previous guidelines were 5%. Now we're saying, hey, 3% to 5%, you can consider it. And once again, it's because the lower The lower percentage is from the new equations, but they wanted to have the same amount of people have access to these medications if possible, and that's why they kept it there. When you first read the new guidelines and see that we are now considering lipid-lowering therapy at 3% for a 10-year risk, your initial thought might be: are we just trying to put sentins in the water? Like, is that what we're doing? It sounds so low, but We're going to talk about why they made this decision. So, first, the old PCEs were notoriously bad at overestimating risk, right? The old calculators overestimate it, and these prevent ones are better. And the risk estimates, like I mentioned before, generally 40 to 50% lower than the old calculator would have given us. So mathematically, a 3% on the prevent calculator captures roughly the same population of U. S. adults. That the old 5% of the pooled cohort equations would do, right? So that's all they're saying. They're saying, hey, the same threshold we had before, we actually have the same threshold that's just a little lower because our calculator is better. That's what we're saying. We're not just blindly treating more people. We have a more accurate ruler. And second, and this is the crux of how to evaluate interventions. It comes down to a risk versus reward and cost matrix, right? So in this case, they had a really good table in there that I'm going to show here, a chart. In this case, though, specifically for statins, the cost we worry about is private prevention, right? That's what we're hoping for, versus diabetes. Creating diabetes. So, if you look at the randomized controlled trials, the math is pretty clear. Right at that 3% 10-year risk mark, the curve starts to cross over. So, the number needed to treat To prevent one ASC V D event with a moderate intensity statin becomes lower than the number needed to harm, meaning the risk of triggering a new diabetes. So, what they're saying is that, hey, at that 3%, It's kind of our washout. We're like, hey, we're going to have one case of diabetes, but we're going to prevent one ASCBD event. That's like why their whole math works out. And that's the whole, all these things you can see on the charts. And so. Why does it matter? Well, it's important because it proves that there is a definitive strategy behind this. It wasn't just made up saying, we'll do it. It gives us, you know, the understanding that. For younger patients, we're trying to explain their true risk, and we're also trying to understand what the other side effects could be. And so, we're kind of working together to get this. So, and It didn't make a lot of sense to me until I looked at the graph. So, the graph I think is really helpful. We'll look at it together. And I know this is not trying to be a dense statistics lesson, but this is, you know, why we Do this and why the recommendations are for this. So we'll start with it. So if you look at the axes, the bottom x-axis are the patient's 10-year cardiovascular event rate, and the vertical y-axis is the number needed to treat. There's a red swooping line you see on both panels. This is our number needed to treat to prevent one ASCBD risk, so, or ASCBD event. And as a patient's baseline risk goes up, the number of people we have to treat to prevent a heart attack goes down, right? So if your risk is high, we feel much better that, hey, Treating you will help prevent something, right? But we have to be academically honest: statins definitely carry a risk of bumping blood sugars up and causing incident diabetes. And that is our harm, right? That flat Horizontal black line represents the number needed to diagnose, or essentially the number needed to diagnose diabetes, one new case of diabetes over 10 years. And so if you look at panel A, panel A represents moderate intensity satins. So the black line is sitting at 100. That means if we treat 100 people for a decade, we might cause one case of diabetes. Now, follow the red curve down until it intersects with that black line. And where does it cross? Right at the 3% risk mark. So that blue circle is the tipping point. If we treat patients below a 3% risk, we're mathematically causing more diabetes than we're preventing heart attacks. But the second they cross over that 3% line, the net clinical benefit flips. And we're preventing more disease than we're causing. And then if you move over to panel B, this is for high intensity statins. And because higher doses carry a slightly higher risk. For causing diabetes, the flat back black line drops down to 33. So because the harm threshold is lower, the red curve doesn't cross until about 7% 10-year risk mark. So it tells us exactly why we don't use high-intensity statins. For a patient at 4% risk, the math simply doesn't protect them. So, we're saying when we give a higher dose of statins, we're more likely to cause diabetes. And so, when patients worry that we're just putting medications, we want everyone to take it. You can say, Hey, this is why they did it. You can have a discussion with them, right? You can show them this graph and say, Hey, this is why we think we want to do this. It's just there. But moving on from that, let's talk about risk enhancers now. This is the personalized step, right? So, CPR, right? Calculate, personalize, reclassify. We all know that calculators are imperfect and they're just looking at a 20,000-foot lead, right? The pre-vent equations are great, but they don't capture everything. And so, we need to. Dive deeper. So, when you have a patient sitting in that borderline 3% to 5% risk category, you have to look for risk enhancers, right? We're seeing a lot of Patients coming in worried about inflammation because you know what they see on social media, but we can actually use that to our advantage. The goal is to identify high-risk individuals not captured by the calculator. And the guidelines state that if you measure high intensity CRP and it is two or higher on two successive occasions without an underlying cause, that is a Class IIA recommendation to utilize a high intensity satin to reduce ASC B D events. The presence of these enhancers tells us Other, you know, their individual risk is much higher than the algorithms might suggest, right? So that's the thing. The algorithms are great, but they don't capture every human being. Talk to the person in front of you, figure out the risk. Other risk enhancing factors include a history of premature ASCBD in a parent or sibling, meaning an onset before the age of 55 for men or 65 for women, high-risk ancestry, for example, South Asian or Filipino. High polygenic risk, if ever measured, chronic inflammatory diseases like lupus, rheumatoid arthritis, or advanced psoriasis or inflammatory arthritis. You know, if you also have LP little A with a greater than 125 nanomoles per liter or 50 milligrams per deciliter. Triglycerides persistently greater than 175 milligrams per deciliter if non-fasting, and if greater than 150 fasting, if you have a CKM syndrome or LDL persistently greater than You know, 160 to 189, and 9 HCl greater than 190 to 219, or APOB greater than 120 milligrams per deciliter. That's a lot. I just went through the table. Table 13 has this all laid out. In case you're listening, I wanted to at least mention those, but there are quite a few risk-enhancing factors that we have, and this is what we're going to talk about. And the final risk-enhancing factor that I do want to talk about are reproductive age risk markers, which we'll talk a little bit more in depth here. So Guidelines also give a class to a recommendation to consider these markers when assessing ASCBD risk and considering lipid-lowering therapy. Reproductive risk markers associated with ASCBD include hypertensive disorders of pregnancy, so that could be a bunch of different things. It could be preeclampsia or gestational hypertension. Also, gestational diabetes, small for gestational age, meaning birth weight below 10%. Preterm deliveries before 37 weeks, recurrent spontaneous pregnancy loss, and also other reproductive risk markers, including early menarchy, less than 10 years old, early menopause, which is less than 45. And especially premature menopause, which is less than 40, and also things like PCOS or irregular menses. So, once again, this is very different in these guidelines compared to previous guidelines, but talking about hey, If you had pre-clempy in a previous pregnancy, that is actually a potential risk-enhancing factor. You can have that discussion. And once again, it's just a discussion of: hey, you've had this, you may be at high risk, let's talk about it. Next, let's move on to section 4. 2. 3. 5, polygenic risk scores. So this is definitely newer here. We haven't seen a lot of this yet. We're starting to see these scores and assess these patients for Genetic risk for CAD. And this, once again, this is not standard yet. We're not going to see a whole lot of it, but I don't want you to get overwhelmed or need to order these risk scores on every patient. We reserve this mostly for people who've already gotten this done with a strong family history, right? So the data shows that a high polygenic risk score is most impactful at predicting risk in adults younger than 55, right? So if you're younger, That may tell something if you're older, not as much. And having a high CAD polygen risk score is basically a risk equivalent to other Major risk enhancing factors, right? So doubling the potential risk of ASCBD events. And so if a patient brings you a high score, it's a great opportunity to get buy in for optimizing everything else in their lifestyle because they have a higher risk and the clinical benefit may be better. Then moving on here, let's talk about selective imaging. So, specifically, are we talking about coriary artery calcium or CT? And let's talk more about that. If you have someone who has an intermediate or borderline risk and neither of you are sure about starting a statin as a CAC scan, it may be helpful in this situation. It's a Class 1 recommendation. And if that score comes back zero, we essentially say, hey, the power of zero, as long as they don't have diabetes, aren't a smoker, and don't have a severe family history, a score of zero essentially gives a warranty period saying, hey, like, We can defer treatment for about three to seven years and focus on lifestyle. But I do have to, I feel like I have to mention that, once again, CAC is not perfect. A CAC of zero does not necessarily mean you don't have atherosclerosis, right? We can't detect soft plaque, which is actually the more dangerous and unstable plaque, from a CAC scan. But it does have decent data supporting short-term deferral of lipid-lowering therapy and repeating it three to seven years. That's what it is. But the other type of imaging is coronary CT. So that's what we're looking for. We just talked about the power of the standard CAC score, and while it is Helpful. It only tells us a little bit, right? About the hardened calcified plaque, where it doesn't show the whole picture. I always explain to patients like this: the standard CAC only lights up when we see old, stable calcified plaque, but the Coronary CT lets us look at the active formation of the soft non-calcified plaque, as well as the high-risk features like positive remodeling, which are actually most volatile, right? So the guidelines specifically call this out. As a class IIB recommendation for adults who don't have pirate AS C V D, but are likely to be hiding a large burden of soft black, specifically patients with diabetes, HIV, or chronic inflammatory disorders, right? We might not see that, they may have more aggressive disease. Earlier in life, in these cases, where the standard tools leave us with more uncertainty, it may be helpful to do coronary CT. This one is kind of like ah, they shrug their shoulders, but it's worth looking at. To me, this is going to be much more expensive. It has a little radiation. So that's why they recommend CAC. But ultimately, CAC is an interesting one because let's say you're young and you have a positive CAC. Well, that's florally, that's good to know. But let's say you're kind of middle-aged and the CAC is negative. Are you super confident? Like, once again, not really, maybe for those three to seven years. And so they're all about the CAC, but that's what we're looking at. But I do want to highlight a big update here as well in terms of incidental plaque. If you get a lung cancer screening or non-cardiac CT scan, And the radiologists noticed: hey, there's a coronary plaque here. That's a class one trigger to consider starting or intensifying lipid-lowering therapy. The plaque is disease. We don't have to wait for other symptoms. We say, Hey, yeah, you got it. Let's go treat it. And that's been something that I've done for a while in my practice. I go through scans with residents and say, Hey, what do we see here? And they say, Oh, you know, it's Even like you can knee x-rays, you can see like calcium everywhere. You say, oh, this person has like significant peripheral vascular disease. What is it? What are we worried about risk factor-wise? And so, yeah, we see it all the time. And so. Kind of seems weird we didn't include that before, but now it is something we can do and can consider them as having atherosclerosis just based on incidental findings. Next, let's talk about our algorithms right here. So, Section 4. 2. 3. 7 is the bread and butter for this. Everything's primary prevention for adults 30 to 79. With an LDL between 70 and 189. And it's an algorithm kind of going through what we're looking at in terms of low risk versus high risk. Can look a little intimidating, but we'll break it down section by section here. Let's dig in first. This is the core algorithm for our primary prevention. Once again, age 30 to 79, who have LDL between 70 and 189. If it's not between there, We don't have the good data, so we kind of have to use our brains and figure it out. But before we look at the specific risk buckets, notice what's happening at the very top of the algorithm, right? So that I took a picture here, took it off top of the algorithm. Every single pathway starts with a health behavior counseling and individualized risk-benefit discussion. That's super important. That's our foundation. We can't out-prescribe a poor lifestyle. And so we do have to do with the heavy lifting of asking and talking about diet and exercise and all those things, right? Now, let's look at the left side of the tree, the low 10-year risk group, which is less than 3%. Historically, we might have just high-fived these patients and sent them home, but this can be deceptive, especially for someone who's younger. So, guidelines give us recommendations to look deeper. If their 10-year risk is low, but their 30-year risk hits 10% or higher, or their LDL is hanging out between 160 or 189, it is reasonable to potentially talk about lipid lowering therapy. So We do this to hopefully blunt their cumulative lifetime exposure, you know, because we're hoping that, hey, we can prevent them before it gets there. That's kind of a new thing. Before we say, hey, low, no problem, let's go. Here we say, well, like your 10 year is low, but your third year might be actually high, so we can consider for that. Next, we move to the middle of the algorithm. This is the messy middle, right? This is where we live in primary care. Nobody's ever low risk, or you know, these are the ones you see all the time, right? For the borderline group, 3% to 5%. This is entirely dependent on clinical judgment and the patient's preference. So if you and the patient decide to treat based on those numbers and risk-enhancing factors, that's reasonable. And they say, hey, a moderate intensity statin. Is something you can consider. For the intermediate group, however, the 5% to 10%, the evidence is a little bit stronger, and there's a class one recommendation to initiate at least a moderate intensity statin. Pushing to high intensity satins for folks in the upper end of that range. The goals here are pretty concrete. We want at least a 30% reduction, driving LDL under 100%. But what if you're stuck, right? What if your patient is hesitant? You're not sure if lifelong pharmacotherapy is the right call today. Well, once again, that's where we can utilize the CAC if you want to. If the CAC is zero, you can say, Hey, we'll see you in a couple of years. If it's greater than zero, then you have your answer and you can initiate a medication or talk about being very aggressive. So, we can use these tools to bridge the gap a little bit, although, once again, not perfect. Next, let's move over to the far right side of the algorithm, right? So the high-risk group of the prevent. This is above 10%. So the nuance essentially disappears here. It's not like, hey, let's figure it out. It's like, well, there's their class one recommendation to start AI. Medications, right? So we're treating these primary prevention patients with very similar intensity to our secondary prevention folks. So the goal here is aggressive. We want to cut their LDL by 50% or more with an absolute target of under 70. And this is where we have to be completely honest with ourselves and patients, right? For a lot of these high-risk individuals, one medication is probably not going to do it, right? So a statin may only get them halfway there. If you max it out and they're still not hitting that sub 70 goal, the algorithm instructs for us to escalate. So, first, add a zetamide. That's usually recommended first line. If there's still not a goal, then you can add on PCSK9 inhibitor like or bempitoic acid. We don't just shrug and say, hey, you're close, your LDL is 95. Here they say, yep, definitively, let's try to get it to the goals and use the tools available to get them all the way there. Next, we're going to mention section 4. 2. 4, which is looking at severe hypercholusteralemia, or like the 190 plus club, right? So it's not like bowling where a higher score is better. But if a patient walks in with LDL above 190, this is what we're talking about, right? So the prevent should not be used here. It's actually a classy recommendation saying, hey, That's not what the that's not made for that. The lifetime risk is already assumed, and the calculator is not set for that number. But before we jump to writing prescriptions, we have to look at foundations, right? So we have to be careful and take a careful dietary history and rule out secondary causes. Specifically, If a patient is on a high saturated fat, ketogenic, or carnivore diet, some of these patients will manifest with a severe hypocholesterolemia purely from their diet, right? That's a whole other thing. I have a lot of content on that whole discussion, but that's one thing that we can see. And if we rule that out, then the guidelines recommend we lean into panel testing for genetics, right? Looking at familial hypercholiolemia. And identifying, do they have that? So that's kind of the general rule. From here, once we've diagnosed, you know, it is actually, you know, pretty severe, greater than 190, primary hypercholesterolemia. The first step is: you know, they recommend maxually tolerated statin. But Here's the reality. Once again, statin probably not going to cut it for people over 190 in terms of getting two goals. And this is where, once again, we split our primary prevention targets. If the patient is simple, meaning they don't have ASCBD, they don't have. You know, familiar hypercholesterolemia that we know of, and they don't have subclinical plaque, we're recommending to add therapies like azetamide, PCSK9, bempidoic acid to get lower than 100. However, if they're complex, meaning confirmed familial hypocholmia, like maybe a heterozygous, or they have other ASCB risk factors or a positive MCAC score, their risk is significantly higher. And for this group, we must escalate our combination therapy with a goal of less than 70. And finally, we have to talk about the risk tiers of this 190 club, right? If the patient has severe hypercholesterolemia and they already had a clinical event. They're at a big risk for recurrent events, right? So for these patients who are throwing the kitchen sink at them and using maximally tolerated premiums, everything to get LDL less than 55. And that can happen. But then there is the rarest and most dangerous phenotype, homozygous feminine hypocholmia. And these patients often develop coronary obstruction early in their life, really early, meaning like teenage years and as extreme lifetime risk. The absolute best thing you can do for these patients in primary care is to bridge them to a clinical lipid specialist. This is not necessarily something we have to handle. You know, we can start the foundation, get them on medications, but they'll probably need advanced therapies like lipoprotein apheresis potentially. And so. Identify that and ship them out. But we can start the therapy because that's what we do. We know how to do that. Next, let's talk about our diabetic patients who haven't had cardiovascular events yet. So Our core adult demographic, age 40 to 75, the guidelines do a lot of the heavy lifting for us, right? The rule is pretty simple. If you have diabetes, you get a statin. It's a class one recommendation, and we want to drive that LDL under 100 because we know that diabetes is such a risk factor for it. But we have to also look at the individual in front of us. If they have multiple ASCBD risk factors alongside diabetes, they're standing much closer to having an event, right? And so that scenario, maybe we step it up and try to have the goals of LDL under 70. And if they experience statin-associated side effects, we don't just throw our hands, we add and pivot. We do, you know, azetamide, bamido acid, PCSK9, whatever we need to do. I sound like a broken record, but the goal is we have lots of tools, get them to their goal. And on the edges of the bell curves though for age-wise, let's talk about it. For younger adults ages 20 to 39, their 10-year risk might look deceptively low. But if they've had type 2 diabetes for 10 years or type 1 for 20 years or showing signs of microvascular damage like albinuria or neuropathy, their lifetime risk is much higher, right? So we need to consider. Potential earlier intervention to protect the vascular foundation earlier on. On the flip side, for our patients over the age of 75, if we look at frailty and life expectancy, if they have a life expectancy of at least two and a half years. Modern intensity statins is reasonable considering having a shared benefit discussion. And finally, let's talk about our residual risk for some patients who are in unique situations. So let's say you have People who have their LDL is at goal, but their triglycerides are hovering above 150. Well, here they recommend adding on omega-3s, specifically icosopent ethyl, so IPE. To further bridge the gap and lower their residual ASCBD risk. Once again, don't just say, hey, take fish oil. This is a prescription grade omega-3 that we're looking at. All right, now we're going to talk about secondary prevention. This is for the patients who've already had their cardiovascular event. So, if they have clinical ASCVD, but aren't considered, quote, very high risk, the goal is 50% reduction in LDL under 70. But if they're very high risk, meaning they've had a recent ACS, multiple major events, or one major event plus multiple high-risk conditions, the rules change. The absolute target drops to an LD of less than 55. And this is a hard target to hit. Monotherapy will pretty much never do it. And as I mentioned before, the guidelines give recommendations to add on whatever you need to do to get them below 55. Our job here is to use every tool we have to stop a future event. That's the main goal, right? So it seems that after Year after year, the targets get lower. And why is that? Well, this is actually here's the method to the madness, or is why they say that. You might be like, Jordan, this seems like another scam by Big Pharma to get people low. Like, well, I don't want to tell you, this is what we see. So, what they found in various studies is that when you get LDL around lower than 60, 60 milligrams per deciliter in patients with known plaque buildup. That level of LDL seems to be the level where we can see no further plaque progression, and sometimes we can even see regression of that plaque. But basically, we believe that if the LDL level can get super low, get below that. It won't make anything worse. And that's the whole goal, right? To prevent where we're at. So it's just, you know, it's not just a random number. It's based on what they have seen in terms of Regards of risk, minimization, and plaque progression. So, if we get LDL low enough, we think it won't progress to the plaque. That's the whole understanding behind this. All right, first, let's talk about incidental plaque. If you get that Chest ET and you see some coronary calcifications by the radiologist read, you say, Yep, that's it. And we actually recommend you have disease, don't ignore it. This is it. So, patients, if you do get a cactus specifically and it's between 1 and 99 or less than 75th percentile for your age, it's reasonable to start a moderate intensity statin with a goal of less than 100. Now, what happens when that calcium score comes back even higher? Well, as the plaque burden scales up, our aggression has to as well. If a patient comes back with a moderate CAC score between 100 and 299, they are in the organizing 75th percentile for their age and demographic. then the recommendations are LDL less than seventy. But when they hit severe, meaning greater than three hundred or between nine to ninety nine, well, we want to get that goal under seventy specifically. You know, getting anywhere up to 999, goal under 70, pretty reasonable. But you can also say, hey, at this point, we're starting to consider: do we even go higher? Because when we talk about the CAC over a thousand, well, the paradigm shifts entirely. We essentially treat it as. Secondary prevention. So we're going to try to get the goals of less than 55. I don't think if you're in the 990s and say, oh, like only seven you can't do 55 You could definitely go to 55 if you want to optimize and do things. But overall, if you have a CAC over a thousand, that's pretty much saying, hey, that's a lot going on. And I do want to mention. Coronair CT as well. And the standard, if the standard calcium score shows us hardened calcide plaque, as I mentioned, the coronair CT shows that soft plaque. And the guidelines give it a recommendation to use it selectively, as I mentioned before, patients with diabetes, HIV, chronic inflammatory diseases like lupus, rheumatoid arthritis. And yeah. That's just going to be, once again, a risk enhancer. There's no like numbers or units that they give there. But once again, if you see subclinical atherosclerosis, you'll treat it as such and you can treat them to 70 or 55 depending on other risk factors. All right, now moving on to section 4. 2. 8. This covers special populations, and this is really where we have to lean into the nuance and understand we'll probably have to be a little bit flexible here as there's not nearly as much data. So, first, let's start off. We're going to talk about our children and young adults in primary care, at least in female medicine. This is right in our wheelhouse, right? So, internal medicine, maybe not so much. But very important to know, regardless. So, for kids and young adults, the absolute foundation is always lifestyle, right? We have to establish those habits early. But if you have a child who's eight years old, And they have a presentation consistent with familial hypercholesterolemia, and their LDL is huge, like up there above 160 or whatever, despite muscle months, three to six months of lifestyle effort. At that time, they do recommend it is time to act in terms of starting a potential medication on them. So, statins are allowed in young children. And specifically, there they say, Hey, if you're above 160, try a lifestyle for three to six months. it's appropriate to start a statin. For our young adults aged 18 to 39, we focus heavily on counseling to once again reduce their cumulative lifelong exposure. As we discussed earlier, we might look at their 30-year risk trajectory here. We aren't jumping to medications right away, unless the lipid burden is severe, but we are aggressively planting the seeds of lifelong health to protect their vascular foundation before it damages their arteries. That's really what they're going for. Now, let's jump on to the other end of the spectrum: our older adults. This is a population where, once again, it's going to be a little bit nuanced here. The guidelines emphasize that we shouldn't base our decisions purely on chronological age. We have to look at their frailty, pill burden, and what the patient actually values. If you have a patient whose life expectancy is less than a year, we have a Class IIB recommendation to simply deprescribe the statin. Let's avoid the unnecessary medication and focus on quality of life. On the flip side, if they are over 75 and have a life expectancy of at least two and a half years, initiating a modern tensile statin is a reasonable thing to do. To reduce ASCB risk, provided you've had a shared risk of benefit discussion, right? And if you and the patient are still stuck in the chasm of uncertainty, well, then you can grab a cats or right if it's zero or minimal. It gives you evidence that you're pretty much good, right? Like their lifetime, they've lived their whole lifetime and have a negative hack, you feel pretty good about that, and say, All right, let's go. Next, let's talk about pregnancy and lactation. So, this is critical because maternal age is increasing for a lot of people in society, and we're seeing more cardiovascular risk factors facing these populations. So, the standard rule here is that statins need to be stopped. One to two months before the patient attempts to become pregnant or the second they find out they're pregnant, right? So we know that statins are contraindicated in pregnancy. Babies need cholesterol to develop, and statins inhibit that. So, it's not a good mix. We do not want that. There's risks to the baby. But what do we do when they actually need treatment? Well, if they have Severe fasting, hypertriglyceridemia. We're talking in 500 or higher. We're worried about pancreatitis, right? In those cases, the guidelines recommend to use fibrates, but only after the first trimester or high dose prescription omega-3s as an adjunct to lifestyle management. So if we're dealing with high LDL though, we can safely use bile acid sequestrants during pregnancy. And lactation. So we meet the patient where they're at, right? Keeping both them and the baby safe. So, this is actually something I've run into before. We say, hey, what do we do in this situation? There's not a lot of great options. But they're saying, hey, there are indeed some options. And this is what they talked about. Next, let's talk about some very specific comorbidities, starting with our patients living with HIV. Following the reprieve trial, this is a Class I recommendation that we universally prescribe statins to these patients between the ages of 40 and 75. Their inflammatory state accelerates plaque progression, and statins significantly reduce that. So, that's the whole goal. So, if you have HIV, you're on a statin. It's kind of like diabetes. Just be very mindful of drug-drug interactions though with their antiretrovirotherapies. Should be checking that up on drug dosing calculators and make sure there's no interactions. For our chronic kidney disease patients, if they're stage three or higher, the rule is going to be Putting them on a modern intensity satin for primary prevention. But we only push to get them super aggressive of below 55 if they also have clinical ASCVD. Also, If they're already starting dialysis, we do not initiate a step. So, pretty much we're saying, hey, if you have three or above, should be on a medication. And then the goal will probably be, you know, with pretty high risk there. Sub 70, only sub 55 if they have lots of other risk factors or clinical AS C V D. And finally, for our patients with chronic inflammatory diseases like rheumatoid arthritis or lupus, we have to remember that standard risk calculators pretty much underestimate the risk, right? We need to treat them proactively because that is. Systemic inflammation and it can drive astlosis and you're going to have a risk-benefit discussion. You know, most likely they're going to treat that as a risk-enhancing factor. Consider at least under 100, maybe under 70 for these patients. Next, let's talk about heart failure and cancer for heart failure with reduced ejection fraction, so HeFREF. The guidelines are very clear. We do not initiate statins. Solely for primary prevention, saying, hey, there's no proven benefit for reducing events or mortality in that specific scenario. So, what they're saying is, if a patient has hefref, you don't just start a stat and saying, hey, like, we're going to do that. Doesn't seem to be good data there. For our cancer survivors, as long as their life expectancy is at least two years, we should treat their dyslipidemia exactly like we would anyone else. And if you have a patient who's in active cancer treatment, who's already on a statin, you can keep them on it. The only reasons we'd stop is if their life expectancy drops below a year, or if their oncologist flags a specific drug-drug interaction with their chemo. Obviously, we want to protect their heart so they can survive cancer, but also they have to. Make sure they stop the cancer first. So it's kind of this back and forth, but that's the idea is treating them as normal because we want to protect their heart. For the next section, we're going to talk about hypertriglyceridemia. And really, what we're going to do is stratify this by urgency. And what I mean by that is if you're in the moderate range, meaning 150 to 499 milligrams per deciliter. Our primary concern is a long-term risk, right? So, a long-term atherosclerotic risk. We think that if your trailer's high, that typically means you're not metabolically healthy, and that we're worried about your ASCBD later in life. So, that's what we're looking for. But before we Write a prescription. We want to look at all the foundations, right? Evaluate for secondary causes like uncontrolled diabetes or a high-sugar diet, and then heavily push lifestyle management. If the patient already has, though, clinical ASCBD and their triglycerides are elevated, the guideline explicitly tells us to focus on intensifying their LDL-lowering therapy first to address the primary athergenic driver. So, once again, for your patients who has ASCBD or diabetes and is maxed out on a statin, but still has triglycerides, 150 to 499, then they say, okay, let's bring something else in. Let's talk about that, acostopent ethyl to lower risk. But if triglycerides are over 500, and specifically they're getting close to 1,000, our entire clinical focus pivots, right? We aren't trying to prevent any heart attack in the future. We're trying to prevent acute pancreatitis today because that's no fun. This requires extreme dietary fat restriction down to like 10% of calories. Get a registered dietrician involved. That's really what's going to come down to. But on top of that, you can also add on medications like fibric acids or fibrates or prescription omega-3 fatty acids. Those are things you can add on as well. And finally, if you happen to run across someone who has familial chylomicronemia syndrome, which I've never seen or FCS, standard therapies barely work. This is how you identify it. So essentially, if triglycerides are over a thousand while fasting and other lipid-lowering therapies don't touch it, That's when we think about FCS. That's apparently where they say, hey, that's the key: you're trying to treat it and it doesn't work. We now have recommendations where we can use an injectional medication called olazarsin to drive levels down. They do, you know, it can work pretty well, but in primary care, you're going to do the heavy work of saying, Hey, I'm trying to treat this and it's not working. And then you're going to get them to a lipid specialist and they will. Manage that from there. That's not one we specifically see in primary care. Maybe you are. If you are, let me know. Drop a comment. That'd be wonderful. But really, what they say the recommendations are: hey, try and identify it. If you can't treat it, it's not going down, it might be FCS. And finally, this section, we've talked about before about LP little A, lipoprotein little A. We're going to talk about risk enhancing factors. And as you know, in primary care, it's all the internet and it is now recommended that everyone gets it, right? So that's a big thing. We should be getting it at least once in their life. And the guidelines, as mentioned, get it once in the adult life. It doesn't really change, it's genetically heritage. And because it's an independent, genetically stable marker, it generally does not fluctuate with lifestyle changes. That means one measurement. Gets you a lifetime marker of risk, and we are primarily looking for levels of 125 nanomoles per liter or 50 milligrams per deciliter and above. It's above that, that's a risk factor. But here, this is where we have to step into the go a little deeper, right? So, we have to be academically honest that statins, you know, our reflex here is: hey, you know, all the guidelines say statin, statin, statin. Statins don't really lower LP little A, and you can't meaningfully change it. With a diet or supplement or exercise, which is kind of unfortunate. Instead of letting people panic over a number, though, right? So, this is we've introduced this to people before. We tell them, hey, you write a high risk factor. But we don't really have anything to treat it. We're not trying to do that. We're trying to use LP Little A as a clinical marker to be aggressive with controlling things we can control, right? Hammer home with foundations, blood pressure, glycemic control, and driving their APO B to goal. So, if you have a patient who already has clinical ASCB, though, they had an event and they have an elevated LP little A. And their maximally tolerated medications not getting there. Once again, they say, hey, you can lower that. And actually, PCSK9 inhibitors can be recommended for this because they actually do lower it a little bit. We don't necessarily know if that means. Like significant clinical outcomes, but it does lower them potentially up to 20 percent. And we are waiting for more specific LP delay lowering therapies. They're in clinical trials, we should know, but right now, what we're saying is: hey, if it's elevated, another risk-enhancing factor, we'll go from there. And so, to summarize everything we've covered today, modern lipid management requires us to step out of algorithms and programmatic thinking and step into the messy middle of personalized medicine. That's really what we're going for here: kind of make it personalized. The overview is first use the prevent calculator to get your bearings, right? So that's just kind of a good baseline to say, hey, how bad is someone's risk? But then personalize the risk with multiple risk enhancers and talk to patients and come up with a plan. From there, when you're coming up with this plan, we talk about it, then we talk about treating two targets. So it really boils down to that. We're no longer just guessing. It's not just, hey, reduce something by 50%. We want to get there, and in the next session, we talk about the different medications. I know I've mentioned medications before, I think everyone's probably very familiar with some of them, but we're going to go more in depth into specifically what they are: dosing, side effects, all those things. That's going to be the last one to carry things out here for this long guideline. But if you did find this helpful, that'd mean the world to me if you share this with a friend or colleague. But that's going to be it for today. Now get off your phone and get outside. Have a great rest of your day. We'll see you next time.
