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.
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. Okay I have nothing to disclose. And this is a little bit of a road map of today's presentation on prevention of atherosclerotic cardiovascular disease. My number one focus today is going to be to help 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 personalize their care. I'm going to talk about the role of L. D. L. 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 and 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 after a sclerotic 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 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 our mandalorian randomization studies that are really helpful. The lower your magnitude of exposure. 12 deal which is in the X. Axis. The less proportional the more proportional reduction in L. In coronary heart disease. So these medallion 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 L. D. L. results in a proportional reduction of risk of heart disease. That's that gray line there. And then the last one is randomized controlled trials that are beginning to have more and more data follow up of about five years um 96,000 patients in this um ah meta analysis actually. And we see the reduction of the magnitude of exposure um with risk. So all of these taken together give you a pretty good sense of it's wrong. Um This is a slide to convey wide 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, for example, pack years for tobacco exposure. Or um the cholesterol can be viewed as an exposure as well. So over here, that line, the the horizontal line that I am 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. Okay, 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 in 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 is 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 Disl epidemiology can reduce their cardiovascular risk or can reduce the onset of cardiovascular disease by 50% just by uh having good lifestyles throughout their lives next here. So why assess risk? Here's a rationale for why we do this risk estimation. So here's another composite trial done by the cholesterol treatment. Trialist. They took 27 randomized control 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 graphed up to 2.5 million malls per liter. That's 85 mg per deciliter. So in those very high risk patients who have an estimated five year risk of major cardiovascular events, more than 30% estimated risk. Right? Hi 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 five years. If you lower the SDL slow 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 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 pulled cohort equations where we estimate this 10 year atherosclerotic cardiovascular risk. And you see that people who are low risk uh and high risk have pretty good streamlined 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 step here. Um is the flow chart for primary prevention guidelines. We see that these guidelines that there are, oh, I'm hearing an echo there. Okay, so the guidelines acknowledge that for this intermediate group that is borderline intermediate risk, there is uncertainty on to how to treat these patients what to do. So, the guidelines um offer these risk enhancing 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 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 pre eclampsia and gestational diabetes. Um Other risk factors such as south asian ethnicity uh elevated crp levels greater than two mg per disa. Later they all um identify these high the subset of patients and who 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 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 1 75 mg per deciliter. I'm looking here oops go back oops! All right. Higher than 1 75 mg per deciliter in non fasting lipids. Um Done at least three times. Uh This is a subgroup that is at increased cardiovascular risk. Even if you control their LDL. There is also, let's talk a little bit about these lipid biomarkers. The high sensitivity crp that I met mentioned is a marker of low grade inflammation. It's a downstream protein that liver makes um in response to inflammatory cytokines um that are circulating in 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 L. P. P. L. A. To um it's also called the black 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. It is produced by the macrophages, the lipid laden macrophages when they are stressed and it is a marker of black progression. So when I see elevated cRP levels and it doesn't really make sense. Um I sometimes order this L. P. P. L. A. To just to clarify if it's more of vascular inflammation or a low grade inflammatory marker that might have less. Um wait for risk management. L. P. A. Is a very very important risk factor. It is emerging. It is now become clear that it's independent risk factor for the development and progression of cardiovascular disease. Two main mechanisms one is that it increases um thrombosis um and the second one is that it um induces oxidation of LDL. So it makes um your particles or your lipid profile more pathogenic. And at the same time when there are plaque ruptures the fiber and the license is not as effective and you might have more events uh be at greater risk. Um When the cell P. A. Is extremely elevated um more than um 300 or um 500 animals per leader. Um we typically think that these patients are very very high risk and we put them on aspirins even when they are low risk in any other um conditions. Also LPA. might be a market for preeclampsia in women. So all these things are emerging and they're very interesting. Appleby is a very um uh huh. Nice molecule to know about 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 the more pathogenic lipid profile in general I don't use the NMR. Um to assess risk I use triglyceride levels and non HDL cholesterol non HDL is the poor man's apo B. It is a very good um assessment of risk. In fact the european guidelines use non HDL cholesterol and it makes more sense. Uh For us we kept L. D. L. 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 As it is more accurate because L. D. L. Might miss those uh lipoproteins that transport triglycerides such as V. L. D. L. And remnant lipoproteins that are very uh thorough genic. And you might think that you're a goal with your L. D. L. But you're missing that residual risk because you're not considering the um the non HDL cholesterol or measuring Appleby Appleby is like a bean counter there's one Appleby in each molecule that is bringing cholesterol into the body. So Appleby containing lipoproteins um are your pathogenic 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 Okay so having said that when you have risk enhancing uh factors you might want to uh start these patients on lipid lowering treatments. Have these conversations with your patients. And so when that is not enough for it let's say you have this borderline risk. You did your patient clinician 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. 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 U. S. 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 two way 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 C. T um sweet. The more modern scanners all have the capability of doing hard gating gating is done by placing your electrodes on the patient's chest and detecting the cardiac cycle and the chest ct um images in DS. Tole. So it's a very um fast test. It only takes about 10 minutes in the room and very low radiation about one millisecond vert. Which is about a half of the background exposure over a year. So imagine just living on this planet gives your radiation exposure half of that over a year is about that number. Uh It might be a little bit higher in people who are very big and you need more penetrates to see the heart. So but it's equivalent to a mammogram to a bilateral mammogram if you can 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 Softwares that know exactly what to do. You get your number in your good and anywhere you do with 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 test. 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 zero 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 scored. And um reported in your study, the nice thing about coronary artery calcium is that it's integrating a lifetime of exposure of your traditional and non traditional risk factors for A. S. C. D. D. 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. Okay 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 nineties. The first studies by dr Ramberg um We're done in 19 9 were published in 1995. He did autopsies where he looked at calcium that is plotted in the X. Axis. So he took these coronaries measure calcium and then he did the plaque um correlated this with how extensive the plaque was these in these autopsy. Um People who came for, they didn't come for autopsy but they were 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 and population. So not you can have very high calcium scores in young people. Um In both women and men you see green as present in men even in the first uh 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 um older age is above 75. You still have a group of the population that has a calcium score of zero. So just basing your risk assessment and age which is a very strong predictor in the A. S. C. V. D. Pulled equations. Doesn't give you the full picture when you want to go and personalized for your patient that risk assessment and give him the best advice onto if to need treatment or not. Um This slide. Um As I was saying that 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 page person years for each coronary artery calcium category with each age group. So age is plotted in the X access, the coronary calcium score is in the Z axis. So calcium of zero. 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 calcium scores the higher you go, the the higher your mortality at different ages. So, um elderly people who have zero calcium have very low mortality rates. And this 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 cardiovascular diseases. Right? So this is data from messa the the multi ethnic study in populations where we see that the calcium score above 400 at each strata. So even a calcium scores from 1 to 400 greater than 400. We see increases in cancer and chronic kidney disease and 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 graphs 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 zero they may not never reach this 7.5%. 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 follow them from the baseline exam at time zero for 10 years or 12 years. If your calcium score was between one 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 you're a guest since course or above 100. Um we consider that to be the threshold to start treatment. So the cholesterol guidelines from 2018 also show us um these concepts. So for people ages 40-75 and LDL cholesterols between 70 and 190. Um we uh ended our at borderline risk. You use your risk enhancers like we talked about. And if the decision is uncertain, you consider measuring coronary calcium and selected adults. Now for calcium scores of zero, The Calcium score of zero doesn't mean zero risk. But um in low risk populations you're pretty comfortable, you know, withholding treatment or waiting right in people whom you might, who you need to be careful. Are people with calcium score of zeros with diabetes with who are active smokers or who have a family history of coronary disease. These are the people that um despite a calcium score of zero, you have a patient discussion and you probably would recommend statin treatment regardless of the calcium score because you know that in these patients is 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 two, a 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 we use these calcium scores to predict risk. Right? So this is a cumulative major cardiovascular events in the upper panels, we see people with calcium scores of zero. You see that as time goes by these lines do not diverge 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 endorsed the selective use of coronary artery testing 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, deceased 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 A. S. C. B. D. 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 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 in my 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 U. S. 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. Better know the risk. And the calcium score zero. 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 um one of the things that coronary artery calcium is being used for is for not only statin lipid lowering 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 three of them showing that there's high risk of bleeding when you look at a S. C. V. D. 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 A. S. C. B. Dig risk. Um In the first group is less than five. In the middle group is between five and 20. And in the 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. Okay 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 especially above 400. That's dark um The dark green the dark green bar show you that that has benefited. The interesting thing is that as you advance your your coronation your A. S. C. V. D. Risk 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 prescription on a. S. C. V. D. Score you're going to be wrong and you're going to 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 going to be safe and effective. Okay 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 blood pressure management. We want to personalize risk based on this approach to initiate antihypertensive therapy. Um The new blood pressure guidelines um consider blood pressures between 1 31 39 A stage one hypertension. And if your patient is high risk you should start pharma co therapy to reduce the risk. And if your patient is no risk, you can you know take your time and do lifestyle and make sure that you control hypertension that way. Um We have evidence from the messa 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 uh coronary calcium scores plotted um to show you that the coronary calcium score in people that you're using it for primary prevention are 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 arms 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 2 70. This is a risk equivalent to those high risk patients who were enrolled in the spread trial. And so that is sort of your threshold to know that you're 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 advance of clinical disease and they're at high risk. So then you aim for blood pressure systolic lesson when 20 if the patient tolerates it um How about intensity of lipid lowering treatment? Can you use the calcium scores to better assess how low you need to go? Um This is a study also done by the messa investigators um Where you are looking at the analysis of secondary prevention equivalents right? We're trying to see if the cat score, select a group of patients who are equivalent in risk to secondary prevention. So they're comparing here to for ear population for ear were the trials done with pcs canine inhibitors? These were high risk patients um that had had events already. So over here you see that line 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 um I um that corresponds to around coronary calcium score of about 500 Single prior and my around 300 And no high risk features. But these are secondary prevention patients 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 cut off and a good um. Uh huh. Um um Understanding of who you're facing these are patients with advanced clinical disease. So um what about deployment of cardio metabolic therapies? We're seeing more and more the use of um S. G. L. T. Two inhibitors for control of diabetes and GLP one 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 high A. S. C. V. D. Risk you might prefer to go directly as first line therapy to using these S. G. L. T. Two S. And GLP ones um to control your risk and your patience and if the calcium score is negative you can start metformin monotherapy and go down that path. Um Let's see how about using um So this is um the same concept coronary calcium too personal. I risk assessment and primary prevention therapies and patients with diabetes um we know that even within diabetic patients there's heterogeneity of a S. C. B. D. Risk. Same as with age as um you saw there's people with diabetes who are despite their hemoglobin a one C. Are going to have low event rates. And people with lower A. One C. S. Who are going to have high event rates. So it is a good way to see who's a higher risk and personalize your therapies. Um Individuals that have calcium score of zero have low event rates that are less than 75.5% patients who have high coronary calcium above 100 have an A. S. C. V. D. Risk at more than 20 per 1000 persons per year. So I brought a case here that 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 asymptomatic patient this is a 53 year old woman. Nonsmoker non diabetic with um good diet and exercise, Family history of premature coronary disease. Her father had an M. I. At age 62. And her blood pressure is borderline or stage one at 1 39 85. H. D. L. 60 L. D. L. Of 1 45. And her pull co hurt equation A 6.4 10 year risk of HCV. D. 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 L. D. L. 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 few minutes. So for this patient um this is somebody who had a coronary calcium score and it was elevated at 3:15. This is for her age 95th%ile 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 LP little a 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 okay doing lifestyle only or moderate intensity statin right? You could also do high intensity statin and aspirin per the National lipid Association guidelines. You know that if the calcium score is more than 100 you would be justified to begin aspirin. This patient has advance of clinical 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 10 year risk is based on these calcium scores. Right? You get the number but you don't you don't know the the 10 year risk. So messa 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 did it wrong there. But um I plugged in her cholesterol's, 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 some more than threefold increase in her estimated risk of 10 years from knowing the calcium score
