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Download PRIMARY PREVENTION OF HEART DISEASE
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Shelagh Cleary Vascular Programme Manager Dudley Office of Public Health Do we need cholesterol? Where do we get it from? Lipid breakdown Very large and dense lipid molecules are broken down to release energy for the cells of the body to use. As this process continues they get smaller and smaller and eventually leave the final circulating particles in the blood stream These are the particles we look at when we look at lipid results from blood test reports Lipid profile Final particles Total cholesterol is the value given for HDL, LDL and triglycerides combined – the “total” If we just look at the total it does not give us enough information, because…. High Density Lipids or HDL is anti-artherogenic Low Density Lipids or LDL is pro-artherogenic Atheroma build up The purpose of analysing lipids is to determine whether there is likely to be a build up of atheroma in the arteries. Atheroma build up leads to the development of CVD and to conditions such as heart attack and stroke. So optimally, we would need: A high level of the anti-artherogenic particles – HDL and A low level of pro-artherogenic particles - LDL Why? Unused LDL is oxidised and then forms atheromatous plaques on the inside walls of the arteries, causing them to become narrowed or even blocked. HDL absorbs the unused LDL and takes it back to the liver before it can become oxidised. So either a low level of HDL, or a high level of LDL (or both) causes more atheromatous plaques to be formed Mismatch So what should the levels be? Target levels Cholesterol - less than 5.0 in primary prevention, but less than 4.0 in secondary prevention HDL - at least 1.0, but at least 1.2 in females and people with diabetes Ratio - less than 4.0 – 5.0 LDL - less than 3.0 in primary prevention, but less than 2.0 in secondary prevention. Triglycerides - less than 1.7 CVD Risk Assessment Just looking at total cholesterol does not tell us enough We need to understand how much of this total is made up of the good lipids and how much of the bad For primary prevention risk assessment we use the ratio of total cholesterol to HDL: Ratio = Total cholesterol HDL Importance of ratio This gives a better indication than TC alone of the overall impact of the lipids on the development of atherosclerosis. E.g. work out the ratios…. 55 year old male TC 5.6, HDL 0.8 = 7.0 55 year old female TC 5.6, HDL 1.2 = 4.6 55 year old female TC 7.0, HDL 1.5 = 4.6 If the target levels are raised The iCAP software will identify anyone with a total cholesterol or a ratio of 5 or more in the workflow. Then: Explain the results Give advice on reducing cholesterol in the diet A repeat test is indicated in 3 months time If the cholesterol is still raised at 3 months and the CVD risk is 20% or more, then the GP may commence lipid lowering medication. But remember ratio….. Remember the ratio is a better guide to the impact of the lipids and the development of atheroma, so: If the total cholesterol is raised but the ratio is normal, then just give advice on a low cholesterol diet If the cholesterol is normal but the ratio is raised, give advice and follow with a repeat blood test in 3 months to re-check Familial Hyperlipidaemia Hereditary condition - heterozygous (approximately 1 in 500 of the U.K.) High levels of lipids are present from birth. The disease is genetic, autosomal dominant. Children of a person with FH have a 50 per cent risk of having FH. The disease does not skip generations which means that children and grandchildren of family members who do not have a defective gene are therefore not at risk from FH In all the cells of the body there is a receptor that allows LDL to be cleared from the bloodstream. People with FH have a defect in the gene responsible for this LDL receptor. This causes an accumulation of LDL in the blood and ultimately in the arterial vessel walls. Well researched area, more than 300 known gene defects that lead to FH. Diagnosis of FH – Simon Broome Criteria TC >7.5mmol/l LDL>4.9mmol/l, plus Tendon xanthoma in the person or 1st/ 2nd degree relative Other signs Corneal arcus Development of premature CVD History of premature familial CVD Premature CVD: Male developing CVD at or below 55 years, Female developing CVD at or below 65 years. Premature Familial CVD: Father/brother-developing CVD at or below 55 years Mother/sister developing CVD at or below 65 years N.B. CVD risk calculators or tables cannot be used to asses patients with familial hyperlipidaemia. F.H. Xanthalasma Tendon Xanthoma Corneal Arcus F.H. The iCAP software will identify anyone with possible FH. ALL patients with suspected F.H. should be referred to the GP urgently for assessment and possible specialist referral / assessment of family members N.B. The risk calculation software cannot be used to calculate risk scores for people with FH Explain this to the patient – it will be underestimated if they have FH What will lower cholesterol? Low cholesterol diet – remember the liver makes it too! Increasing physical activity and exercise Avoiding stress What about ..? Smoking Alcohol Low cholesterol diet Switch to mono or poly-unsaturated fats (30%) Reduce saturated fat (10%) Butter, cream, full fat milk Meat, burgers, sausages Processed foods, pies, ready meals Cakes, biscuits, chocolate, crisps Use healthier cooking methods Coffee time? Sweet success with checking blood glucose results Type 2 diabetes Type 2 diabetes is not a single disorder but part of a much broader metabolic syndrome: This consists predominantly of insulin resistance. Insulin resistance results from hereditary and lifestyle factors involving over nutrition and under activity. It is associated with obesity, particularly abdominal obesity. Nature versus nurture? Insulin resistance Insulin resistance causes high levels of glucose and insulin in the blood High levels of insulin cause problems with the lipid profile, raising triglycerides and LDL and lowering HDL. It therefore helps to make more atheromatous plaques develop Impaired glucose regulation The regulation of glucose can be impaired for several years before diabetes is diagnosed. This period is called impaired glucose regulation or a pre-diabetic state. Diabetes may be prevented by management of people with impaired glucose regulation Pre-diabetic state …. how do we find it? Diagnosing IGR Fasting glucose test If the fasting glucose is 6.0 or below, then this is normal If the fasting glucose is 6.1 – 6.9, then this may be impaired fasting glucose or IFG or impaired glucose tolerance IGT If the fasting glucose is 7.0 or more, then this may be diabetes Non-Fasting glucose Using the point of care finger prick blood test Ask when the patient last ate a meal or snack If this is more than 2 hours before the glucose should be 6.0 or less If it is less than 2 hours the glucose should be no more than 11.0 Less than 2 hours More than 2 hours - 6.0 or less No more than 11.0 What is in iCAP? iCAP will highlight any glucose result over 6.0 and recommend a 2nd test to confirm. Explain to the patient that they should see their GP or practice nurse to arrange a 2nd test if this is required Take into account other risk factors for diabetes Where a diagnosis is to be considered the practice may send them for / carry out an oral glucose tolerance test (OGTT) Oral Glucose Tolerance test An OGTT is requested to confirm either diabetes or impaired glucose tolerance What the test involves: Fasting specimen Glucose load 2 hour post load specimen This shows any problems with the way that glucose is processed in the body which may give the diagnosis of IGT or diabetes Referral So…., Arrange for a second test for anyone with A fasting glucose of 6.1 or more, or A non-fasting glucose which is: More than 6.0 if they have not eaten in the last 2 hours, or More than 11.0 if they have eaten in the last 2 hours Ask them to see the practice nurse or GP with the results Dudley Diabetes Website www.dudleydiabetes.co.uk Any questions….? What’s pee got to do, got to do with it…? Kidney function Kidney impairment is a major cause of heart attack and stroke and is associated strongly with hypertension The process by which we measure kidney function is the rate at which the kidneys are able to filter the arterial blood stream This is called the Glomerular Filtration Rate or GFR. It is calculated from levels of creatinine in the blood and so is called an estimated GFR or eGFR Chronic Kidney Disease A diagnosis of moderate chronic kidney disease is made when the eGFR is less than 60 mls/min An eGFR of 59 or less would possibly indicate a CKD stage of 3, 4 or 5 These stages are moderate to severe kidney disease. At these levels the incidence of cardiovascular disease is 10 fold. CKD and CVD CKD causes blood pressure to rise which causes a heavy workload on the heart CKD causes levels of protein in the urine to become raised leading to oedema, also causing blood pressure to rise and further increasing the workload of the heart. CKD and CVD CKD causes calcium to be taken from the bones and into the blood stream where it is deposited in the arteries and heart valves. This causes stiff and narrowed vessels and problems with the pumping mechanism of the heart CKD causes anaemia, which increases the workload of the heart as it has to pump the blood faster to maintain perfusion. There can also be loss of perfusion to the heart itself. What is on iCAP? The eGFR result will be displayed. If the result is lower than 60 then it will stage the level of possible CKD, i.e. Possible CKD Stage 3, 4 or 5 Any result of less than 60 will be included in the workflow along with the next step of the pathway The next step would be to repeat the eGFR test after a period of 3 months – advise the patient What about dementia? The incidence of dementia rises with age The incidence in the UK is rising rapidly The risk factors for CVD are the same as for dementia – especially vascular dementia If the patient is over 65, then icap will prompt you to advise the patient of this additional risk Give leaflet supplied by DoH Any questions….? So what are the odds…..? CVD Risk Calculation Risk scores are automatically calculated on the iCAP software. The risk is displayed as latest risk, relative risk and target risk. Latest risk is the risk calculated on the entries made. This is also called absolute risk. Relative risk is what level of risk would be expected for an individual Target risk shows what happens to risk when values are changed, i.e. smoker to non-smoker Communication of risk Risk of 1-9% is low risk Risk of 10-19% is moderate risk Risk of 20% or more is high risk Use odds, e.g. 1 in 5, 1 in 4 etc Heart age – probably more meaningful and more powerful to communicate risk to patients Bus queue Comparison of absolute risk to relative risk High risk Those found to be at high risk are added to a high risk register They will be called for review annually using the software. People at this level of risk can be prescribed lipid lowering drugs More intensive targeting of risk factors Referral Give advice to: Anyone who is high risk, especially where this is unexpected, i.e. where the relative risk is low and there are clinical indications to account for this, e.g. raised blood pressure or lipids. Anyone who has a higher absolute risk than expected / relative risk level, even if this is moderate or low Risk factors will have been identified which can account for the increased level of risk These risk factors need to be reduced where possible to reduce the level of risk – use target risk to demonstrate this So, what are the risk factors…? Any questions….? Wish I’d done a risk assessment! Risk assessment can be a good thing…….
