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I don't got it. How, how will be everybody? Is everybody? OK. Today I see MS Patel Assad. I see Irene Lola is a new person called Mr Ridge Winder. We've got Shereen Tabo. Okay. All right. So, you know, we talked about hypertension and this is a continuation of our discussion on um disorders of lipid metabolism and the principles by which we uh do screening and risk reduction of uh patient's that we detect uh to be at risk of developing um cardiovascular disease. So putting it very simplistically, I thought we do a brief talk on disorders, a lipid metabolism because this would build up from our token hypertension. Um because you don't alter anybody's cardiovascular risk by just controlling the BP. You have to control all the risk factors. The very big principle is um ensuring that you're managing the patient holistically. Uh We haven't had a lecture and I think you haven't had any lectures on screening. So I'll take up a lecture on screening whenever I can squeeze um a lecture through maybe at the end of cardiology. Um So let's look at the physiology of um lipid metabolism in the body. So there are mainly two sources of um lipid production in the body. One of it is from dietary fat. Um and it's not illustrated here, but there is another cycle that runs in the body and from carbohydrates and the Krebs cycle and acetyl coa a you can convert those also into lipids. And because lipids are not water soluble, you can't just absorb them. So what happens in the body as the uh dietary fat is absorbed, um they get packaged into what are known as Kylo microns. And uh Kyle comes from the gut and Mike run means they're small microscopic particles. So what really happens is that the triglycerides get hidden inside and this is covered by a forceful lipid um coat and because it's forceful lipid and the molecules are small, they can get absorbed and they go directly from the lymph into the bloodstream and straight from the bloodstream, they go into the liver and then they get broken up into various components, whether it's triglyceride, LDL, VLDL, intermediate Density ideals and the hdl's. Um so that's just a very basic um basic schematic of what's happening with the lipids. So you can then therefore understand that a proportion of the, the facts that are appearing in any patient's bloodstream must be coming from the diet. Okay. And then there is an independent pathway inside the liver of the manufacturer of lipids that is coming from the Krebs cycle, which is the carbohydrates. So, if you're somebody who's eating a lot of carbohydrates, then that will also the excess of that will also be converted into lipids. And the rest of it is, of course, coming from the diet. Now, the way somebody handles these and the levels of lipids that are circulating in the gut, circulating in the bloodstream will determine um the available um lipids that are there for the cells. And we all know, I mean, all the studies have shown that an excess of um lipids um are associated with a higher risk of atherosclerosis and cardiovascular disease. Uh That evidence is absolutely certain it's there. So if we look at the next slide, um we can see that lipid metabolism in the liver is regulated by an enzyme called H MG co A reductive. Okay. So in the liver here, this is where HMG coa a reduct eases operative. And if we were very clever people imagine if we wanted to reduce somebody's cholesterol, where do you think that we could manufacturer or engineer a drug that would affect the lipid metabolism or the amount of lipid that is available to um uh to us in the body? Any ideas you can um mute yourself because this is interactive. Anyway, uh the liver itself for a chylomicron. Yeah, that, that, that is quite, quite, quite right. You are. So you can manipulate that, but also you can do a bit of dietary manipulation. So this is where we use cholestyramine and what cholestyramine does is it increases the bile acid re absorption. Sorry, the bile acid excretion causes a diarrhea. And then what the body does is it takes the endogenous cholesterol to manufacture more bile acids. So, um those are the two main sites where we can manipulate the lipid levels. So we did this before when we were talking about the hypertension. So let's look at the drugs again. So we've got um statins and what statins do is to basically blocks this enzyme. And this is a rate limiting enzyme. It's one of the last steps in uh lipid synthesis in the body. So if you block this, you automatically just reduce the available cholesterol that is um available to uh to the body. And the plasma lipid is going to be a combination of both nutrition and genetic factors. So you might have to people that are having the same type of diet, but some people are genetically programmed to make more cholesterol and the more cholesterol that's available, the total amount of cholesterol than that would increase your risk of um uh atherosclerotic heart disease. And um Kylo Macron's as I explained there, manufactured in the small intestine and they are a molecule that enabled uh transport uh within the splanchnic circulation to deliver. Um And you've got three or four types of sub components that will make up your total cholesterol. So you've got VLDL, very low density lipoprotein, intermediate density lipoprotein, low density lipoprotein and high density lipoprotein. Okay. Now, these lipoproteins that is VLDL and I L D L, they are um they are regulated by apple proteins. So apple proteins are small signature proteins. Um they are present on, you know, can you see these little blebs that are on top of the kylo microns. The apple proteins are actually regulators that sit on top of this um Chylomicron protein. And these pro apple proteins then regulate the metabolism of the L deal. And I I L D L okay. Low density lipoprotein is the main carrier of cholesterol and it delivers it both to the liver and the peripheral cells. And HDL is produced in the liver and the intestines through a transporter mechanism. So when we look at cardiovascular disease, there's a strong association of cardiovascular risk with the total amount of cholesterol. Now, the non HDL cholesterol is the total cholesterol minus the HDL and that is most of the LDL and the LDL is really intimately linked to the cardiovascular disease. So, if the total cholesterol rises, the cardiovascular risk rises, it's very, very simple. And the lab will report your total cholesterol HDL ratio. There's a weaker association between triglycerides, VLDL or intermediate density lipoproteins and cardiovascular risk. But we know now that high density lipoproteins are protective against cardiovascular disease, there is a rarer condition of hypertriglyceridemia, which is an inherited uh metabolic disorder. And in these patient's, if the triglycerides are over 10 millimoles um and that is because they are not processing the kylo microns, this increases the risk of pancreatitis. So, these are the rarer inherited metabolic conditions and they have quite rare and, and really speaking, they present as acute emergencies. That's something that we need to take up if we're doing an acute medicine module. So you've got primary and you've got secondary hyper lipidemia. So, imagine that somebody has um hypothyroidism, then hypothyroidism or diabetes itself, obesity, all of these contribute to secondary hyper uh dyslipidemia and hyper lipidemia because the the uh blue coast metabolism's especially in diabetes um is not um uh not well um uh the sorry, the total amount of sugar that's available in the body in patient's were diabetic activates the acetylcholine way pathway. And that's a parallel pathway for the manufacturer of lipids. So that gets activated in people that are poorly controlled. But we also see secondary hipaa lipidemia in all of these conditions, alcohol, anorexia, nervosa, um and certain drugs and these are all sort of MCQ topics, right? Combined contraceptive pill retinoids, thiazide diuretics, corticosteroids, beta blockers, Demox and anti retroviral drugs. So this, this is a, this is an MCQ uh sort of hot topic. Now, primary hipaa lipidemia xaz are genetic. Um and they are mainly disorders, like I said of hypertriglyceridemia, their disorders of VLDL and Chylomicron packaging. And then you've got the hypercholesterolemia says, which are disorders of LDL and there are two types, there's homos I kiss and there's heterosis and that just tells you how they are inherited disorders of HDL are very, very rare. And then you have combined hyperlipidemia is, which have a bit of everything. So when you look at, uh, the, when you look at the risk of cardiovascular disease, and this was, um, I think the seven countries trials very old trial. But basically what it showed is that as your cholesterol level rises and you're following up a cohort of patient's that are um showing a high cholesterol, their cardiovascular mortality rises in this particular talk. I've not looked or rather, I've not done a talk on the, um, I've not done a talk on the pathology of atherosclerosis. Um, and that would need an extra five or six slides. This is a very, very busy talk. I think it has exceeded my time limit of one are in this one particular lecture. And if it does happen that we need to carry on, because I, I do want to get across to you the principles by which we can manipulate people's cardiovascular risk and it's important in primary care. So when, when you see the, the, the, the cardiovascular risk and that it's rising with the amount of cholesterol and this is a lifetime study. So they have looked at people over a long period of time and they've shown that the cardiovascular risk is rising. So even before we start, um, uh using drugs, um, there is a component in patient's who don't have a genetic risk factor. To say, for example, if you take, if I, if I make myself a patient, um, and I say to you, I have a family history that my father and my mother both had ischemic are disease and both had high cholesterol's. Then it's more likely that the kind of hyper lipidemia that I'm having is, is, uh, it's either heterosis, I guess, or it's a homozygous hyper dyslipidemia because I must have inherited the gene. But suppose you've got somebody that doesn't have a family history of high cholesterol, but they have any of these risk factors, which we talked about here. So we're talking about people who are diabetic. They have obesity nephrotic syndrome that introduces an independent risk. Now, if we look to altering this component, which is the dietary fat, and then we come back to this, then we know that there is a proportion of the cholesterol that we can knock off by changing their diet. Does anybody know what kind of proportion we might be thinking of? Does anybody know what kind of proportion? So, if I were to give you a figure, say, ranging from 5% to 20% let's say 5% to 30%. How much do you think that we can knock off from somebody's diet? We just diet alone. So, and then this happens a lot in patient's that have, um, intolerance to statins or any of the other drugs. Any idea? It's about 15 to 20%. You're absolutely right. Thank you. That was that Mr Azad? Yes, ma'am. Yes. Well done then. Thank you, Mr Azad. Yes. It's about 15 to 20%. Um, so you can look at lipid lowering and you can counsel your patient's. Um, and obviously that should be culturally sensitive. Um You have to take a dietary history and you need to be able to explain to them that what might be contributing to this problem and then they can go on, you know, a fat free diet. But what is the problem if we were to rely on diets alone in people? And, and I, I would point you to this, um, this sort of um, graph, any idea what would be the problem if we were to rely just on somebody's diet. So if a patient of mine says to me, yep, I'm going to be really good. I'm going to reduce my diet, I'm going to work really hard on my diet. And that's just what I'm going to do. Do you think that that's a good idea to rely just on diet? I think physical use of the fact as well as also contributory. So just removing the diet is not enough, whatever the fastest stored we have to remove by physical activity. Yeah. So, yeah. So you can do that by asking them to lose weight, reducing the total amount of calories, smaller portions lower glycemic index foods because the lower glycemic index foods will turn off the acetylcholine a pathway that's coming through the Krebs cycle. And of course less red meat, let's process needs less refined sugars because refined sugars get absorbed really um quickly, you can replace the saturated fats with more unsaturated fats and reduce the amount of trans fats. But no, I think the point I was trying to drive home here is that cardiovascular disease does not happen within a day or two if you're looking at 15, 20 years. So this is a slow burn. This is um uh something that you're not going to change in a day. It's a bit like buying a life insurance policy if you um advise the patient on that and then the patient comes back after three months and then the cholesterol has come down. That's, that's very pleasing with the difficulty here with patient's. And this is how I explain to my patient's is that you're going to have to sustain this now lifelong, meaning you're going to have to sustain this change in your diet for the next 20 years. Uh because we don't know when the cardiovascular disease might happen, but we know that it is that time is a factor. And what most people find really hard. And I've seen this in real life is that they will be really good for the first six months. And then after that, when I test them again in the year the cholesterol has gone out the window because unfortunately, food is so readily available and it's so tempting that they can do this for a day or two, maybe three weeks, 10 months. But then after that, once they're off the GPS radar, if they start eating again, uh, we don't have the consistency of reduction that we would find with medication. It's a terrible thing to say because, um, really speaking, we should be relying on overall um, weight loss and reduction of um the glycemic load that we're giving the body because then there are other dangers like developing diabetes, etcetera, but human nature is very hard to control. So we can't really rely on that. So you have to see the patient who's sitting in front of you. Now, if we look at the medication, then, um, we've got statins and as I said, they're working on the liver and so does Ben Pedrick Acid. These are working on Heggie and Co A BMP do like acid is a newer drug and it decreases the total cholesterol synthesis. Uh Is it in B is um reducing the intestine absorption? So it gives you a kind of a diarrhea, coolest tyramine is sorry, doctor quick questions. Sorry to interrupt. Yes, of course. Please interrupt. Just wondering. And you know, you said that patient's may actually, um, look after the diet for like, say up to up to 10 months, 12 months or so ever. So would you start with me, would you counsel them to keep up with that or would do you actually also introduce medications to them just in case they fall back into their old habits? Yeah. But here is the, here, here's the deal. You see, you've got to talk to them and we're going to come to when we go to the law, when we go to the, the latter slides. Uh, this is the problem because the science is not precise and you're absolutely right. Um, there are tools and I'm going to show them to you the, in the European uh countries, they use the score tool and then we use the to risk and it's how you talk to your patient. And it's about you doing that cardiovascular risk assessment when you're talking to them and it's how you as a doctor because of course, you're supposed to give the information to the patient and if the cholesterol is very high, if there's a family history, if the diet and the lifestyle can't be modified, um, then definitely I offer both. Um, I tend to offer both because there is a, um, almost as much as there's a commercial reality. There is a practicality that people, um, and certainly GPS. Um, unless you, you have a very small private practice and you're monitoring your patient every three months or so, the truth and the reality is that people go off of the radar, we don't get to see them, the government, um uh you know, cannot reach out to so many people. What is really important is to empower your patient. And that is where lifestyle medicine comes in. We'll talk about that briefly when we get to the latter stages. But diet as well as the medicines are, I think they are important. Um um, and, and, and, and, and not just because of the 15% but because you have to sustain that lifestyle change for the next 20 years. And there are patient's who will completely change their lifestyle and I've seen it, they will lose weight, um that lipid profile dramatically changes. Um And then it's also what everybody's eating in the whole household, you know, they change, they change and there are people who are motivated and you're really lucky if you have patient's like that. Now, remember what we're talking about here, applies both to primary and secondary prevention. So secondary prevention and tertiary prevention is where somebody has already developed ischemic heart disease. And then all of these targets, they go out the window because in those patients', we would use drugs, medication as well as diet and all the good stuff around exercise, etcetera for overall cardiovascular risk reduction. But that the primary prevention is very, very different from secondary prevention. And hopefully, if we have a little time, what I'm I'm thinking of doing is that if we overrun this, uh um what we might do is we'll go into the next lecture and we'll pick this up and then we'll pick up the next lecture maybe on a subsequent occasion. But there are some key things in here that are really important to understand. So, thank you for asking that question. Yes, you would use lipids as well as diet. You would use the two together because at the end of the day, as a doctor, what you are looking at is you're looking at overall, um, lipid improvement and you have to employ whatever means that you have available to you. Um, you have to give patients the choice. It's their choice. And some people, unfortunately, they develop side effects. So the best will in the world, the, I think the most soul destroying consultation is you have a patient, you put them on the medication and then the next thing you know, they bring you back after two weeks and they've had side effects and then what you do is you try a different one and you try a different one. So we do have patients that are intolerant to a whole range of lipid lowering therapies and then your hands are really tied and then they can only rely on, uh, weight loss and all the other, all the other stuff that is given over here. So if we look at the medication, you've got, uh, police tyramine, this is actually quite effective, but these are quite, um, okay. So before I, um, go for the, what do you think in this, if we go back to here, where do you think your lipid lowering therapy will be most effective? Do you think it'll be effective if we were to work hard on here or would it be most effective here? Any idea by medication on the liver? Yes. By diet on the dietary fact. Yeah. But this, this results in a much lower lowering of the total cholesterol compared to blocking stuff in the liver. So when and, and, and this is the sort of principle that you will employ even when you're treating somebody with diabetes. Because when we do the endocrinology lectures, we're looking at diabetic control and diabetes drugs, not all the drugs are equally effective. So in some patient's, you would use a combination of medication. You see, but the most powerful are these two that are working at the level of the liver. The statins and rented a weak acid Lampwick acid is is the new kid on the block. Very expensive given only in secondary care, not initiated in primary care. But I think once it comes off of patent, it has a unique um metabolism and it works in a unique pathway and it doesn't have the side effects that we have with statins. So if you look at this drug as it can be, it takes a very small proportion of it gives you gi side effects, but it will also give you muscle cramps and aches and pains. Cholestyramine is effective. Um And basically what it does is it depletes the body of um bile acids. So, what the liver does is it draws down the endogenous cholesterol to manufacture more bile acids and it depletes the endogenous cholesterol pool fibrillates. They are useful in hyper dyslipidemia, hypertriglyceridemia. But they're actually also, they've got loads of side effects and they're not always very effective. Nicotinic acid causes a lot of flushing. I've used this in patient's and really speaking it, it's not, it's not our mainstream medication, Omega three, they do reduce the hepatic VL deal. But all of these actually, all of these are very weak, including that one, the strongest uh potent drugs that you have are these. Um and then in somebody with secondary um uh cause is then you're going to want to throw everything in. Um Let's look at the score ing tools. Now, does anybody and some of my students who might be on this lecture already know this uh that uh what, what is the difference between primary secondary prevention? What's the difference between primary secondary tertiary prevention, do we know? So, primary prevention is where you've detected somebody, whether it's opportunistically or whether it is through a screening program and you have found somebody that has already got a high cholesterol but has not developed any clinical evidence of cardiovascular disease. So you're looking at somebody who's 40 who might have a total cholesterol or say seven and a family history of strong family history of ischemic heart disease. Now, these this is the score tool um and they use this in Europe and all of these are based on studies that were conducted in people. So that then what they did is they took the data and retrospectively, they tried to develop a kind of a score ing tool that would be used in conjunction in a consultation to give uh patient's a kind of figure as to their risk. So overall, you can see that men at all ages have a higher risk than women. Okay. Men at all ages have a higher risk than women. Women after the menopause have the same risk as men. And if you're a nonsmoker, then your risk is much lower than you are a smoker. Okay. So when we come down to the latest slides and I'll show you the slides on um the q risk tool, you will understand that the the score ing tools are only a means of giving a kind of quantitation to the patient. And a kind of discussion that allows you to um explain to the patient where they might be sitting on risk. So if I say to somebody, they have a greater than 10% risk, what does that mean to the patient if I said to you that somebody has a 10% risk? So and and this is another nice way to illustrate risk to people that if you are a smoker and you're a man of 40. Your risk at the age of 40 is the same as somebody who's a nonsmoker at the age of 65. You see. So these are visual tools that we use to counsel people when we are talking to them about cardiovascular risk and the risk of a difference. Yeah, 20 years difference. So what that means is that if you're smoking, you're increasing your risk, fast forward, top gear, you're going to get there 20 years faster because we know that cardiovascular disease develops slowly insidiously untreated people over 15, 20 years. So it's very unusual unless you have got a lipid metabolic disorder or what we call an eye MD inherited metabolic disorder to get cardiovascular disease before the age of 40. And that's one of the questions that we've got in our curious scoring tool. So when we look at the classes of evidence, so we, um, so the European Society of Cardiology, um these are slides by the way that I've taken off of the European Society of Cardiology. If you go onto the website, you can download them, they're, they're, they're there for the public. So they're different um classes of um uh evidence. And when we, hopefully, if I get time and I do a lecture on evidence based medicine and screening and classes of evidence and how we develop guidelines, we will see that if the evidence is very, very strong, then it's you know, the the treatment is recommended. So the classes, so we're going from uh the lowest class to the highest class that it could be considered should be considered and is recommended to indicated. So you can see that the the language is changing from maybe should be two is recommended and this is based on the levels of evidence. So if we look at the the next slide, there are grades of evidence. So the lowest grade of evidence is small case studies and consensus consensus of opinion. So if a whole load of experts think that yeah, that's the right thing to do a smaller studies, retrospective studies, uh disease registries, cohort studies and then uh stronger grades of evidence are single randomized clinical trials or very large non randomized clinical trials. With the larger the number of the patient's on the study, the less you're the less is the possibility that that result has arrived by chance. And then the highest level of evidence are the randomized control trials or the data that is uh gathered by meta analysis. Okay. So this is what all the guidelines are based on. So the E S C recommends that um and and for us, these are people who have already got cardiovascular disease, but this is what was useful for our lecture that at least once in somebody's lifetime, you should be doing a lifetime risk of atherosclerotic coronary vascular disease. Okay, by doing a blood test. So within the UK. Over the age of 40 we have something called the NHS Health checks and the NHS health checks are offered to people to uh bring them in measure their BP, talk to them about their family history, their smoking, um their obesity, their diet, their weight and offer them uh fasting lipid testing. And um what the E S C and these are the 2019 guidelines. Obviously, they are saying that high risk patient with hypertriglyceridemia with levels between 1.5 to 5.6, they should be considered for combination therapy with statins. People who have heterocyclic this familial hypercholesterolemia because remember the familial variety can be homozygous as well as heterozygous. Um They, they should also be considered for primary prevention. So there's a difference between primary prevention. Primary prevention is somebody who has never had an atherosclerotic cardiovascular event. So, if I am somebody who has a cholesterol of six or seven, and I, I have no family history of cardiovascular disease, then um I would still be considered a high risk patient because we haven't done my genetics and we've not done my typing. So if I've never had a cardiovascular occurrence, you'd be looking at primary prevention, secondary prevention over somebody who's already had a heart attack or they've had a mini stroke, they've had a T I or they've had a stroke or they've already got some other uh cardiovascular pathology like chronic kidney disease may have already developed and treatment of. Um, now when we get to the older patient's, um the evidence is actually uh in some of the studies, it's a bit, it's a bit harder to get now. Okay. And, and here it is, it is recommended for primary prevention in people who are older but below the age of 75. And the reason for that is we never ran trials and people who are older because people who are older and this is where the evidence gathering, the evidence becomes difficult because people who are older have a much higher prevalence of cardiovascular disease. So how are you going to gather the evidence for primary prevention? Because really speaking, what you'd have to do is you'd have to take people over the age of 75 who are, who don't have any cardiovascular disease. Give them all statins, make sure they live for 25 or 30 years and then draw the inference of whether you were able to reduce the cardiovascular outcome or not. But, but you really can't do that because they already have disease unless you go and Doppler everybody or you do calcium score ing or you do some invasive angiography, you're not going to find evidence in people of that age who don't have cardiovascular disease. I'm sorry if this is complicated. Just stop me and ask me if what I'm saying is complicated. Does that make any sense? What I'm saying? What you're trying to say? Is how we can identify, someone needs a primary care about how to prevent the primary reasons. Yeah, you can't do it in the elderly. What I'm saying is it's very hard to run a trial in the elderly people because really primary prevention, but truly speaking, it's not primary prevention because it would have already developed a level of cardiovascular disease. Anyway. So you're not going to get somebody who has virgin i arteries with no atherosclerotic disease at the age of 75 or 80 that you're going to be able to put them on statins. So common sense tells us that if the cholesterol is high, you can offer it to them and that's where the discussion will come in. So if there's somebody of high risk to say, for example, they've got chronic kidney disease that diabetic, the hypothyroid, they've got loads of other risk factors. Then yes, it should be considered because green is uh straightforward recommendation and the orange is uh it's a recommendation. Um It should be considered um two doctors in inevitable that we're all going to get high cholesterol. Is that what you're saying? I think it's not inevitable that we'll all get high cholesterol, but the Fatty street can even be found in the post mortem of babies. So the fatty street pathology is already there in Children from the time that they're born. What is inevitable is, yes, we will all get a tear, a sclerotic um narrowing of our arteries, whether it's of our kidneys or of our cardiovascular system. Our brain, the atherosclerosis is a slow insidious process because going back millions of years, we didn't have so much processed food. We just didn't have the currency. So the, the diet has considerably changed. Uh, and we are less mobile. We don't get up, we don't walk around. Um, because what exercise does is it opens up the blood vessels of the heart and it Marshall's in all the, um, all the, how do I put it? All the um, so coronary arteries are terminal end arteries and it brings in all the collateral circulation. So it marshall's in all the collateral circulation. So, um, I, I suppose atherosclerosis, as I mentioned is inevitable unless you take somebody and I think the signs is now and the guidelines are now moving into lower and lower risk. So, years ago, about 10 years ago, we used to offer statins to people with a Q risk of 20%. Now it's 10%. And the government is now saying you can give it at a Q risk of even much lower because we recognize that this is a slow insidious process and no doubt, arthrosclerotic cardiovascular disease is preventable, isn't it? So, it doesn't make sense not to offer it. Yeah. And certainly in patient's with type two diabetes, my own clinical practice is that I will uptitrate the statins too, quite, quite a high tolerable does because we want to cardio diabetes when we study diabetes. It is a cardiovascular disease. So, um, type one diabetes, you have to give it to them. That's, that's green, an intensification. Yeah, I, I will use multiple agents in people who are diabetic because, um, diabetes is super high cardiovascular disease. Um, obviously you're not going to give it in pregnancy. Um, that, that's mad because there's no safety established in, in, in, in young, um, in people contemplating pregnancy. But um I'll have to miss that meeting anyway. Um inequalities leads. So, yeah, sorry. So going on, should there be like an age whereby we should just be like, okay, there's a guideline for this, a certain age where everyone should be given a satin or no. I think we are moving towards that. I think the government is certainly moving towards that because um the guidelines are getting lowered and lowered and lowered. But uh the the difficulty there is and let me explain this to you when we come to the cure, risk scoring to I I think because we will be closing this and we'll get on to the next one. Can you please hold on to that question for the lattice slides? That because I think this is slide 15, I have to get us to slide 28. So we'll hop on to the next link and then we'll probably take this lecture on into the next link is how do you counsel somebody and that, that is a very, um it's very interesting. It's really important to understand when you're looking at guidelines in blanket therapy that you have to be honest with your patient and the science is imperfect. So you can just hold on to that question when we get to the end. And that's very useful to illustrate the point that I'm trying to make here. Um And anybody that has had any atherosclerotic disease, obviously, um there, there's no, there's no, um you know, there's absolute consensus on that is that the kid gloves are off. You just have to uh take the maximal tolerable does. So, secondary prevention is where somebody has already had atherosclerosis, cardiovascular disease. In that the cardiologist will say to you, you got to up titrate them to the maximum tolerable. Does you um um you can use multiple agents and I do that because we're not looking for another event. Uh So the way you deal with people who have diabetes, chronic kidney disease, who had previous atherosclerotic cardiovascular disease, if they are much higher risk patient's than um is um is a patient who has, who in whom you're trying to do primary prevention. And uh and there are some faults in all these um in these, these scoring tools, they are not perfect. They are just a means of it's exactly like selling somebody a life insurance policy and, and, and being able to discuss with them that that's the risk adding this medication to you. But then what we don't have is we don't have the genetic means of knowing which patient will actually develop an event. So, so that, that is the drawback in any of this. Um So the score charts for people with. So the good thing about the, the, the score chart is that although they are based on studies that were done in Europe and European populations, they've also got score charts for people with high cardiovascular disease, what we don't have in the UK and we can use these in patient's that are higher. But I tend not to bother with this because I tend to see people who are at a higher risk. Um almost as somebody that you are doing secondary prevention, except for the fact that they have not presented with that because they uh imagine that in order for somebody to be classified as somebody who needs secondary prevention, you're actually waiting for an event to occur. So it's not just semantics, it's also about assessing the risk of the patient when you're actually seeing them, I would uptitrate them to the maximal tolerable dose. Um So what was that? Um So these are recommendations for cardiovascular risk assessment in using the score tool in a symptomatic adults um without any evidence of. Um uh so, so what they, what they're basically saying in this recommendation is that if somebody has not had any evidence of cardiovascular disease, CKD diabetes, blah blah, blah, you can do a score to, you can use the score tool and then you can check the lipid profile and you can do a risk estimation. So the least you can do is offer them a risk estimation. And that's what we do in the UK, we've got NHS health checks. Um and then um people who are moderate to high risk, then you have to use the higher risk scoring tool, which is this one. Um But for me, um in clinical practice, if they are at a higher risk, I would treat them at the same level as I would with people with secondary prevention. Because if they have got multiple co morbidity, then you know that the the odds are stacked against um you and the patient. So then you cannot use a primary risk reduction scoring tool. You can either use that or you can use common sense. But this is only a means of having that dialogue with the patient. I think this link is going to break. So we're going to hop on to the next link, Hannah. Is that correct? Is that okay to do? Yes, we've come to the end of this lecture. So I will end the recording now if that's okay. Well, hop on to the next link then.