This data-driven presentation from cardiologist Eveline Stock, MD, will give you a better grasp on how to identify at-risk patients; how to assess cholesterol types and numbers; and how to take advantage of the multiple benefits of plaque imaging via CT coronary calcium scans, including applying the scores to decisions such as initiating statins or other preventive therapies. Bonus: a look at new guidelines on hypertension.
Uh, my topic today is going to focus on cardiovascular prevention, on lipids for risk assessment and use of coronary calcium. Um, Let me see if I can advance my slide. It seems to be stuck here. OK. I have nothing to disclose, and this is a little bit of a roadmap um of today's presentation of prevention of atherosclerotic cardiovascular disease. My number one, focus today is going to be to help, um, clarify how to identify those at risk. I see that that is the first step and the most important so that we can get adequate treatment to the adequate populations and the adequate patient and personalized their care. I'm going to talk about the role of LDL and non-HDL cholesterol. As a causal risk factor for developing and progression of atherosclerotic cardiovascular disease, going to talk a bit about the guidelines and evaluation of risk, considering the risk enhancing factors that are now part of the guidelines and that have been very helpful. Um, the use of CT coronary calcium score. To aid in preventive strategies to reduce cardiovascular risk, going to talk about imaging of subclinical atherosclerosis, which is central to preventing cardiovascular disease. And uh emerging indications for coronary calcium scoring such as people on statin, young patients, and repeat testing. So, let's dive in. And this first slide, I put in so that you have some real evidence and real strong that you feel that there is overwhelming evidence that low density lipoproteins actually cause atherosclerotic cardiovascular disease. I can't tell you how many times patients and clinicians have confusion about this, but there's ample evidence, not only from, um, you know, the, um, Trials and Framingham data, but large genetic, epidemiologic, and clinical studies. So here, um, This graph is a little bit um to show you the proportional reduction in risk of coronary heart disease. So, in the Y axis, you see proportion of reduction with lowering exposure. So the blue line are Mendelian randomization studies that are really helpful to lower your magnitude of exposure to LDL, which is in the X axis, the less proportional, the, the more proportional reduction in in coronary heart disease. So these Mendelian randomization studies allow us to follow patients for about 52 years, putting all the studies together. Um, so that's very strong data. Then there's prospective cohort studies that have a medium follow-up of about 12 years. They give us a perspective on how um the reducing the exposure to LDL results in proportional reduction of risk of heart disease. That's that um gray line there. And then the last one is randomized control trials that are beginning to have more and more data follow up of about 5 years, um, 96,000 patients in this, um. Uh, A meta-analysis actually, and we see the reduction of the magnitude of exposure um with risk. So all of these taken together give you pretty good uh sense of Its role. Um, This is a slide to convey why lowering the LDL cholesterol is important. Not only is there data from all these trials, but we're starting to think of cholesterol exposure, um, not only thinking about the duration, not only about the magnitude, but the amount of duration of the exposure. So we're thinking of cholesterol. As an exposure, as much as we think about, uh, for example, pack years for tobacco exposure or, um, The cholesterol can be uh viewed as an exposure as well. So, Over here, that line, the, the horizontal line that I um highlighted in red is uh the clinical threshold for onset of cardiovascular disease. And at the bottom, you see age. So advancing age in the X axis, exposure to um different magnitudes of cholesterol years. OK? So, The patients, for example, who have severe hypercholesterolemia from birth, the FH patients, you see that this curve is very sharp and steep. They reach this threshold very early in life, on average, 30 years earlier than their counterparts who don't have this. Then we see that people that have moderate hypercholesterolemia, if this extends long enough in somebody's life, you will reach this threshold where you will see clinical cardiovascular disease. It it's estimated that this exposure is about 5000 mg per deciliter years, um. Um, with modest exposures, you're going to be delaying the onset of clinical cardiovascular disease. And then people who have lifelong low LDL cholesterol either from genetics or from really good lifestyles, um, from an early age, they may never reach it. Um, Uh, it's important to realize that people who have genetic dyslipidemia can reduce their cardiovascular risk or can, uh, reduce the onset of cardiovascular disease by 50% just by, uh, having good lifestyles throughout their lives. The next here. So, why assess risk? Here's a rationale for why we do this risk estimation. So, here's another composite trial uh done by the cholesterol treatment trial list. They took 27 randomized controlled trials and put together these um this graph. So here we see that people um And the, there are major cardiovascular events avoided per 100 per 1000 people in the Y axis. So the higher the bar, the better off you are. So you avoid. The most risk by lowering. LDL cholesterol with statins. Um, at the X axis, you see graft up to 2.5 millimoles per liter. That's 85 mg per deciliter. So in those very high risk patients who have an estimated 5 year risk of major cardiovascular events, more than 30% estimated risk, right? High. High-risk patients. The major cardiovascular events avoided are the highest. But not only the high risk patients benefit. You see here those uh light blue um. Um, The bars. Even in those people who have less than 5% risk estimated at 5 years, if you lower their LDLs low enough, they are going to be showing you in a stepwise manner, decreased cardiovascular event. So, how do we think about this, when to start, and how do we do this? So, the 2019 guidelines for a primary prevention give us, I would say, a pretty good idea of how to do this. First, I'm sure you're all familiar with the um pooled cohort equations where we estimate this 10-year atherosclerotic cardiovascular risk and you see that people um who are low risk. Uh, and high risk have pretty good streamlined, uh, approaches. You go for lifestyle or lifestyle and drug therapy. That was the prior, um, risk estimation, um, major cardiovascular events avoided with successive reductions in LDL cholesterol with statin. Here, um, is the flow chart for primary prevention guidelines. We see. That these guidelines acknowledge that there are um Oh, I'm hearing an echo. There. OK. So the guidelines acknowledge that for this intermediate group that is borderline intermediate risk, there is uncertainty on how to treat these patients, what to do. So the guidelines um offer these risk enhancing uh factors that can give us ideas about the net net benefit of our therapies. And these are things that you will normally have from the clinical history or laboratory tests. So here's a list of the um risk enhancing factors. And as a physician who's interested in women's health, I was very pleased to see that these guidelines include conditions that are specific to women, such as history of premature menopause before age 40 and history of pregnancy associated conditions. that down the road will increase your cardiovascular risk such as preeclampsia and gestational diabetes. Um, other, um, risk factors such as South Asian ethnicity, uh, elevated CRP levels greater than 2 mg per deciliter, they all, um, Uh, identify these, the subset of patients in whom you want to pay more attention because they are at increased risk. The other ones are, for example, chronic inflammatory conditions that we see more frequently as well as women, um, in women, such as rheumatoid arthritis or lupus. Um, The Um, elevated triglycerides and metabolic syndrome are also kind of novel. Um, you, when you have triglycerides higher than 175 mg per deciliter, I'm looking here. Oops, go back. Oops. All right. Higher than 175 mg per deciliter in non-fasting lipids um done at least 3 times. Uh, this is a subgroup that is at increased cardiovascular risk even if you control their LDLs. There is also, let's talk a little bit about these lipid biomarkers, the high sensitivity CRP that I mentioned. is a marker of a low grade inflammation. It's a downstream uh protein that the liver makes um in response to inflammatory cytokines um that are circulating. And these inflammatory cytokines can come from the blood vessels or can be um non-specific. There is another marker that is not mentioned in the guidelines that is the LPPLA2. Um, it's also called the plaque marker. Some of you might have seen me order this test when you refer patients to me. It is what I like to call the angry macrophage test. Uh, it is produced by the macrophages, the lipid-laden microphages when they are stressed, and it is a marker of plaque progression. So when I see elevated CRP levels and it doesn't really make sense, um, I sometimes, um, order this uh LPPLA2 just to clarify if it's more of vascular inflammation. Or a low-grade um inflammatory marker that might have less um weight for risk management. LPA is a very, very important, uh, risk factor. It is emerging. It has now become clear that it's an independent risk factor for the development and progression of cardiovascular disease. Two main mechanisms, one, is that it increases thrombosis. Um and the second one is that it um Induces oxidation of LDL, so it makes um Your, uh, particles or your lipid profile more atherogenic and at the same time when there are plaque ruptures, the fibroanalysis is not as effective and you might have more events, uh, and be at greater risk. Um, when this LPA is extremely elevated, um, More than um 300 or um 500 nanomoles per liter. Um, we typically think that these patients are very, very high risk and we put them on aspirins even when, um, they are low risk in any other um conditions. Also, LPA might be a marker for preeclampsia in women. So all these things are emerging and they're very interesting. Apple Bee is a very um Uh, Nice molecule to know about. Um, when you have elevated triglycerides and metabolic syndrome, your particles are going to become smaller because the triglycerides displace the cholesterol in them. And so, you are going to have for the same levels of cholesterol, more particles and a more atherogenic lipid profile. In general, I don't use the NMR um to assess risk. I use uh triglyceride levels and non-HDL cholesterol. Non-HDL is the poor man's apple bee. It is a very good um. Uh, assessment of risk, uh, in fact, the European guidelines use non-HDL cholesterol, and it makes more sense, uh, for us, uh, we kept LDL because our clinical trials are done with LDL goals, and it seemed. You know, difficult to change, but if I had my pick, I would use non-HDL cholesterol as a marker of effectiveness of my treatment of risk. Um, acid is more accurate because LDL might miss those, uh, lipoproteins that transport triglycerides such as VLDL and remnant lipoproteins that are very etherogenic and you might think that you're at goal with your LDL, but you're missing that residual risk because you're not considering the um The non-HDL cholesterol or um measuring apple B. Apple B is like a bean counter. There's one apple B in each molecule that is bringing cholesterol into the body, so apple B containing lipoproteins, um. Are your atherogenic particles. So, if your apple B is below 90, uh, in general, it's lower risk. And if your non-HDL cholesterol is less than 100, you are very well controlled. In general, it's 30 mg per deciliter higher than LDL targets, 30. Um, OK. So, having said that, when you have risk enhancing, uh, factors, you might, uh, want to, uh, start these patients on lipid lowering treatments, have these conversations with your patients. And so when that is not enough, when, let's say you have this borderline risk, you did your patient clinician um discussion, and you're still on the fence, so your patient is not convinced. Um, And then you, the guidelines endorse the use of coronary calcium score to help refine the risk. So, I want to make clear that this is not a screening test, it's a risk, um. It's for risk evaluation. Uh, coronary calcium has not demonstrated that when you do coronary calcium and base your treatment therapies, Um, in prospective studies, um, that you assign to people who have high calcium versus, um, using coronary calcium to guide therapy and trials, um, Those um trials have not been done in the US because um. They're very costly. They're being done in Europe, so we will have that data. But for now, it is for risk assessment and it's very useful. So it's a class 2A indication to help you refine your risk. So how do we do this CT coronary artery calcium scores? So, they're done in Your general CT um suite, uh, the more modern, uh, scanners all have the capability of doing heart gating. Gating is done by pla placing your electrodes on the patient's chest and detecting the cardiac cycle and the chest CT. Um, images in diastole. So it's a very um fast test. It only takes about 10 minutes in the room and very low radiation, about 1 millisievert, which is about a half of the um background exposure over a year. So imagine just living on this planet gives you radiation exposure. Half of that over a year is about that. Number. Uh, it might be a little bit, uh, higher in people who are very big and you need more penetrance to see the heart. So, but it's equivalent to a mammogram, to a bilateral mammogram, if you can, um, discuss that with your patients. Uh, the beauty of this test is also that it's highly reproducible. It has an, um, it's not um operator dependent like an echocardiogram or an angiogram. Um, these are done with um softwares that know exactly what to do. You get your number and you're good. And anywhere you do it, those numbers are gonna be comparable. Um, the estimated variability is about 12% between tests done at different times and I mean, at the same time, but in different machines or um. And that's about the variability of LDL cholesterol. So overall, a very good. Tests very accurate and fast. Um, so, how does coronary calcium help us? So here you see a um picture of a coronary calcium score of 0. As you can see, you see the spine in the back of this uh square and then everything else is not lighting up. On the next panel where it says CAC score of 1200, you do see the coronary artery light up and that is what you will be, what will be uh scored and Um Reported in your study. The nice thing about coronary artery calcium is that it, it's integrating a lifetime of exposure of your traditional and non-traditional risk factors for ASCBD. So it will funnel genetics risk factors into this integrated risk. And Just the presence of calcium tells you a lot about the biology and the interaction of these factors. Um, you know, having cardiovascular, um, risk factors is almost like living in a bad neighborhood. You know, that something could happen, you're not sure, you take precautions, but when the coronary calcium is present, you know there's been a break-in. Your risk immediately is highlighted, and you know that you must act. OK. So, what is the relationship of coronary calcium to coronary atherosclerosis? How do we know that these two are related? So, we know this since the mid 90s. The first studies by Doctor Rumberg. Um, were done in 1990 were published in 1995. He did autopsies where he looked at calcium, uh, that is plotted in the X axis, so he took these coronaries, measured calcium, and then he did the plaque, um, correlated this with how extensive the plaque was these in these autopsy, um. Uh, people who, who came for, they didn't come for autopsy, but they were met, um, studied in the autopsy. So that's when the relationship between the coronary calcium and extension of coronary plaque was established. And then, um, we know, um, from The experience we have with coronary calcium is that the distribution of coronary calcium is very heterogeneous in population, so not, you can have um very high calcium scores in young people, um, in both women and men, you see green is present in men, even in the first uh Um, bars from 45 to 54. And in women as well. And as we advance in age, you see that the amount of people who have a coronary calcium score greater than 100 increase in both men and women. But even at um Older ages above 75, you still have a group of the population that has a calcium score of 0. So just basing your risk assessment in age, which is a very strong predictor in the ASCVD pulled equations, doesn't give you the full picture when you want to go and personalize for your patient that risk assessment and Um, given the best, uh, advice. Onto if to need treatment or not. Um, this slide, um, As I was saying, the coronary calcium number can be used for predicting mortality, and it can extend to both elderly patients and those less than 45 year olds. So it's not only a test for old people, it has been proven to be useful in young patients. And I will show you more about this, uh, using a clinical case a little bit later. So here we see all-cause mortality per 1000 person years for each coronary artery calcium category with each age group. So age is plotted in the X axis. The coronary calcium score is in the Z axis, so calcium of 0. You see that the all-cause mortality is low. Not only does it predict coronary heart disease and atherosclerotic deaths, but it also predicts all-cause mortality. And so, in people with high uh calcium scores, the higher you go, the um The higher your mortality at. Different ages, so, um. Elderly people who have zero calcium have very low mortality rates. And this um brings us to that um thought that you are really as old as your arteries and we have a chronological age and we also have a biological age, right, that we can estimate. So, um, as I mentioned briefly, the, there, the coronary calcium can also be used. Um, Or can translate. Into non-carddiiovascular diseases, right? So this is data from MSA, the, the multi-ethnic study in um populations where we see that the calcium score. Above 400, and at each strata, so even a calcium scores from 1 to 400 and greater than 400, we see increases in cancer, in chronic kidney disease, in COPD, mortality from pneumonia, from DVT, dementia, and even hip fractures. So, it seems to be a Marker for biological age and for susceptibility of your tissues to injury. Um, here's um, A um Graph showing in females and males, how the coronary calcium can be used to predict the cardiovascular risk. So the green line that I highlighted at the bottom of both of these graphs shows you that If a person has a coronary calcium score of 0, they may not never reach this 7.5% ASCVD risk that we know is cost effective for statin treatment or for lipid lowering. And so Um, The and as the calcium score starts to increase, you see how useful it becomes. Um, In people as you, as you um follow them from the baseline exam at time zero for 10 years or 12 years, if your calcium score was between 1 and 100, by the end of 10 years, you're already reaching this threshold. So, this tells you that um you can start treatment in these patients and you will be cost-effective. Especially in people with higher than 300, right? So the threshold to consider treatment based on a calcium score is 100. So if your Gatson scores are above 100. Um, we consider that, um, to be the threshold to start, um, treatment. So, the cholesterol guidelines from 2018 also show us um these concepts. So, for people ages 40 to 75 and LDL cholesterols between 70 and 190. Um, we, uh, and that are at borderline risk. You use your risk enhancers like we talked about, and if the decision is uncertain, you consider measuring coronary calcium in selected adults. Now, for calcium scores of 0, The calcium score of 0 doesn't mean 0. Risk, but um in low-risk populations, you're pretty comfortable, you know, withholding treatment or waiting, right? And people who you might, who you need to be careful are people with calcium score of zeros with diabetes, with uh who are active smokers, or who have a family history of coronary disease. These are the people that Um, despite a calcium score of 0, you have a patient discussion, and you probably would recommend statin treatment regardless of the calcium score because you know that in these patients, it's more likely than not that they're going to advance in their calcium scores. When you repeat the test, if you repeat it. So for um It is a class 2A recommendation that an intermediate risk or selected borderline risk adults, if the decision about statin use remains unclear, it is reasonable to use the calcium score in the decision to withhold, postpone, or initiate statin therapy. So this is um A graph showing us how um we use these calcium scores to predict risk, right? So this is a cumulative major cardiovascular events. In the upper um panels, we see people with calcium scores of 0. You see that as time goes by, these lines do not diverge. Uh, significantly, however, in people with these higher coronary calcium scores, we see diversion quite early, showing you that it is, um, A marker of severity and a marker of major cardiovascular events, um, that would warrant treatment. The 2019 primary prevention um guidelines endorse the selective use of coronary artery testing. Uh, for shared decision making, and it's ready for prime time. Um, it's been ready for prime time for a number of years, but, you know, our payers are not catching up with this yet. And there are a lot of people who would benefit from a calcium score but don't, um, have one because it needs to be paid out of pocket. In explaining the rationale for the inclusion of calcium scores, the authors of the guidelines stated that the identification of subclinical atherosclerosis rather than the use of serum biomarkers is preferred. Because of the extensive body of evidence demonstrating the superior utility of atherosclerosis disease assessment, particularly with coronary calcium measurements over any serum biomarker. Isn't that interesting? Um, it is better than lifestyle, it is better than genetics, it is better than any single biomarker. So for the prediction of future ASCVD events, including both coronary heart disease and stroke. And as you saw, it has utility for non um coronary diseases as well. So, I'm going to um talk a little bit about what's new um for calcium scores for guiding other preventive therapies. So, um, The idea that a calcium score can identify a group of patients who you thought were at moderate or borderline risk, and with your calcium score, you actually see that they have advanced subclinical atherosclerosis, right? You Measure your calcium score, it's above 100 or even worse, above 300, and you know that that patient is really um somebody who has advanced their coronary calcium uh subclinical atherosclerosis. And I'm gonna show you how the risk is comparable to doing secondary prevention. So, um, like I said, coronary calcium shows you a group of people in where the break-in has already occurred, right? So they're higher risk patients. So there's a continuum of atherosclerotic cardiovascular disease from um Uh, subclinical atherosclerotic disease, uh, turns into clinical disease when somebody has an MI, a cardiovascular event, peripheral arterial disease, heart failure, or sudden death. And definitely, we don't need to wait for the patient to have an event to know that we need to be aggressive. So that is one of the values that's identifying the subclinical atherosclerosis. In the US we use mostly coronary calcium scores. The European guidelines have incorporated the carotid ultrasounds as well. And I sometimes use it in my practice when, you know, the patient um um would like to have a better risk assessment, uh, better know the risk and the calcium score is 0, sometimes the, the plaque is already forming in the carotid arteries, and, and we have another indication that this patient has a clinical disease. They're not always concordant. Um, one of the things that coronary artery calcium is being used for is for not only statin and lipid lowering, uh, therapies, it's being used for decision making, um, on aspirin treatment, so. Now that we know that the therapeutic window for aspirin is much narrower than we thought, right? We have these recent clinical trials, at least 3 of them showing that there's high risk of bleeding when you look at ASCVD risk course and try to decide using that um um that measurement as your indication to start statins, I mean to start aspirin. See, when this graph shows very nicely, um, that the ASCVD risk um in the first group is less than 5, in the middle group is between 5 and 20, and in the uh group most more to the right is greater than 20. And see how in the higher risk groups, um. Or um the coronary um. The threshold for bleeding, so the number needed to treat. For, to prevent cardiovascular, um, to reduce risk is, um, depicted in these bars. So, um, the number needed to harm is that red line, OK? So, number needed to treat versus in the, in the bars versus number needed to harm in that red line. So for the People who have low cardiovascular risk. You can identify a subgroup of people who would benefit from from aspirin, right? So the Green The green bar, so coronary calcium above 100, and especially if above 400, that's dark um. The dark green, um, the dark green um bar show you that that has benefit. The interesting thing is that as you advance your your coronary, your ASCVD risk pool, that number needed to harm becomes smaller, and that's why those trials had such a hard time. Um, and demonstrated, you know, that if you base your aspirin and, uh, prescription on ASCVD score, you're gonna be wrong and you're gonna cause harm. So if you use coronary calcium to find those people with subclinical disease. You are in the, you know, um, in the good zone where you know that your therapy is gonna be safe and effective. OK? So calcium greater than 100. The aspirin use is recommended and it's included in the primary prevention guidelines from the National Lipid Association. Um, what about blood pressure? Can we use coronary calcium scores to help us, you know, determine how aggressive we need to be with our, uh, blood pressure management? We want to personalize risk, uh, based on this approach to initiate anti-hypertensive therapy. Um, the new, um, blood pressure guidelines, um, consider blood pressures between 130 and 139 as stage one hypertension. And if your patient is high risk, you should start pharmacotherapy to reduce the risk. And if your patient is low risk, you can, you know, take your time and do lifestyle and make sure that you control hypertension that way. Um, we have evidence, uh, from the Mesa, um. Uh, cohorts that coronary artery calcium can guide personalized risk-based approach to initiation of this, um. Uh, blood pressure treatment. So, um, Here we see a coronary calcium scores, uh, plotted, um. To show you that the coronary calcium score in people that you're using it for primary prevention. Are, uh, at some point equivalent in the risk to people who are enrolled in the sprint trial. So the sprint trial is a trial in high-risk patients with hypertension where um the intervention arm showed. That if you treat hypertension aggressively, you reduce the risk of future cardiovascular events. Mind you that these are people that are very high risk for cardiovascular disease. Um, when you take, um, General patients and you do a calcium score. The intersection. So as you increase your calcium score, see how this line is very steep at the beginning. So with little increases in calcium score, the risk increases exponentially. When you reach a calcium score of around 270, this is a risk equivalent to those high-risk patients who were enrolled in the sprint trial. And so that is sort of your Uh, threshold to know that you're, um, Uh, facing a high-risk patient and that can help you identify those who may benefit from the most intensive blood pressure therapy reductions. Those patients have advanced subclinical disease and they're at high risk. So then you aim for blood pressure systolics less than 120 if the patient tolerates it. Um, how about intensity of lipid lowering treatment? Can you use the calcium scores to better, uh, assess how low you need to go? Um, this is a study also done by the MSA investigators, um, where You are looking at the analysis of secondary prevention equivalents, right? We're trying to see if the CAC score select a group of patients who are equivalent in risk to secondary prevention. So they're comparing here to Fourier population. Fourier where the trials done with PCSK9 inhibitors. These were high risk patients, um. That had had events already, so. Over here you see that line, um, the red arrow, so showing total Fourier population. Um, these are very high risk people, and the calcium score that corresponds to that is around 700. In a population that is less risk from these trials, um, that have Um, Then intervene and don't have residual obstructive or multi-vessel coronary disease, so this is a single event, one vessel they had their MI, um, that corresponds to around a coronary calcium score of about 500. Single prior MI around 300. And no high-risk features, but uh these are secondary prevention patients are around 270. So, just to give you an idea that a coronary calcium score above 300 is similar in risk to having a patient on secondary prevention and thus it gives you a good cutoff and a good um Uh, Um, um, understanding of who you're facing. These are patients with advanced uh clinical disease. So, um, what about deployment of cardio metabolic therapies? We're seeing more and more the use of, um, Uh, SGLT2 inhibitors for control of diabetes and GLP-1 agonists for treatment of diabetes, given that they have shown substantial reductions in cardiovascular disease events and hospitalizations and mortality. So, can we use this coronary calcium to select higher risk populations? Um, These are the European guidelines. We don't have this kind of guideline yet, but we see that um in patients who are at higher ASCVD risk, you might prefer to go directly as first line therapy to using these SGLT2s and GLP ones. Um, to control your risk and your, um, patients, uh, and if the calcium score is negative, you can start metformin monotherapy and go down that path. Um, Let's see. How about uh using um So this is um the same um concept, coronary calcium to personalized risk assessment and primary prevention therapies in patients with diabetes. Um, we know that even within diabetic patients, there's heterogeneity of ASCVD risk. Same as with age, as, um, you saw there's people with diabetes who are, despite their hemoglobin A1C are going to have low event rates and people with lower A1Cs who are going to have high event rates. So it is a good way to Uh, see who's at higher risk and personalize your therapies. Um, individuals that have calcium score of zero and have low event rates that are less than 75.5%. Patients who have high coronary calciums above 100 have an ASCVD risk at more than 20 per 1000 persons per year. So I brought a case here that uh might not seem very exciting to you all, but that's sort of the point. Uh, these are people that we are going to see in our practices. These are people who come to us or their family members or their friends, and it's uh asymptomatic patient. This is a 53 year old woman, non-smoker, non-diabetic with Um, good diet and exercise, family history of premature coronary disease. Uh, uh, her father had an MI at age 62. And her blood pressure is, uh, borderline or stage one at 13985, HDL of 60, LDL of 145, and her pool cohort equation. A 6.4 10 year risk of HCVD which places her like smack in the middle of that, you know, moderate risk, um. Patient. So what do we do with her? So, When we think about these patients, you know, she seems pretty good, good LDL, uh, that is not so high, HDL, um, that most people would say that's a good HDL. And, um, you might elect to just treat her with lifestyle, right? Or um Uh, we'll see the therapies in a, in a few minutes. So, for this patient, um, this is somebody who had a coronary calcium score and it was elevated at 315. This is for her age, 95th percentile, right? So if you take 100 people from the community and that are her age and same-sex women, Um, Not only 5% are going to have a calcium score higher than hers. So, um, this high risk is probably given by her family history of premature coronary disease. We don't know her LPLA, but that's something that could be contributing as well. So how do you treat this patient? Like we said, if you didn't know the coronary calcium score, you would probably feel pretty. Comfortable and you would, per the guidelines, be OK doing lifestyle only or moderate intensity statin, right? Uh, you could also do high-intensity statin and aspirin per the National Lipid Association guidelines. You know that if your calcium score is more than 100, you would be justified to begin aspirin. This patient has advanced subclinical disease. We were able to determine that and we can personalize her care and go further and protect her from further cardiovascular events. We will talk to her about intensive lifestyle modifications, um, high-intensity statins to reduce LDL by 50% or to a threshold of less than 70. And non-HDL less than 100. Um, we would also consider antihypertensive treatment because of the, um, discussion we had before. So, how do we communicate these calcium scores to our patients, right? We have the calcium score. How do we tell people what their um 10 year risk is based on these calcium scores, right? You get the number, but you, you don't know the the 10 year risk. So Mesa has this available online, you can plug in. Um, the 10-year estimated risk for your patient using your coronary calcium score. So in our patient, I plugged in female, 53 year old, 315 for the coronary calcium. She's Caucasian, no diabetes, non-smoker, no family history of heart attacks. Oh, I She does have, I, I did it wrong there, but Um, I plugged in her cholesterols, her blood pressure, and she's not on lipid lowering or hypertension medication. So for this patient, you see down here in this banner that her um 10 year event rate is 6.2, and if you didn't have the coronary calcium, it would be only 1.8. So there is a more than 3-fold increase in her estimated risk at 10 years from knowing the calcium score.
