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British Medical Bulletin 59:3-16 (2001)
© 2001 Oxford University Press
Asymptomatic individuals – risk stratification in the prevention of coronary heart disease
Department of Cardiology, Charing Cross Hospital, London, UK
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Abstract |
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Top
Abstract
IntroductionThe report of the World Health Organization Expert Committee on Prevention of Coronary Heart Disease considered that a comprehensive action for coronary heart disease (CHD) prevention has to include three components:
- A population strategy – for altering, in the entire population, those life-style and environmental factors, and their social and economic determinants, that are the underlying causes of the mass occurrence of coronary heart disease
- A high risk strategy – identification of high risk individuals, and action to reduce their risk factor levels
- Prevention of recurrent coronary heart disease events and progression of the disease in patients with clinically established coronary heart disease1
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Prevention targeted at patients with established coronary disease and the high risk strategy targeted at healthy individuals at high risk are an integral part of clinical practice. The clinical approaches and the population approaches for coronary heart disease prevention are complimentary, but the population strategy is fundamental to reducing the burden of cardiovascular disease.
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Introduction |
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While recognising the importance of the public health strategy embodied in the UK Government's Health of the Nation document2
, which outlines a policy seeking to reduce morbidity and mortality from CHD and other atherosclerotic disease in the population, it is essential that specialists and general practitioners also recognise their responsibilities for preventive medicine in routine clinical practice. Clinicians regularly see patients who have either presented with CHD or other atherosclerotic disease, or are found to be at high risk of developing atherosclerotic disease because of hypertension, dyslipidaemia, diabetes or a combination of these risk factors. In defining the objectives for CHD prevention in clinical practice, it is implicit that priority is given to those patients who are at highest risk of developing CHD, rather than attempting to reach every adult in the population. Therefore, risk stratification is required.
In 1998, the Joint British Societies' Recommendations on Prevention of Coronary Heart Disease in Clinical Practice3 set an order of priority for CHD in clinical practice:
- 1(a) Patients with established CHD
- 1(b) Patients with other major atherosclerotic disease
- 2 Individuals with hypertension, dyslipidaemia, diabetes mellitus, family history of premature CHD, or a combination of these risk factors, which puts them at high risk of developing CHD or other atherosclerotic disease. Patients with diabetes mellitus are at particularly high risk of CHD.
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Concept of coronary heart disease risk |
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The biology of atherosclerotic disease, its determinants and complications, is a continuum of risk in the population. At one end of the spectrum are young individuals without atherosclerotic disease who have not yet been sufficiently exposed to the life-style and environmental factors responsible for this disease and its complications. Then there are an increasing number of individuals who develop asymptomatic atherosclerosis as a consequence of their exposure to smoking, an unhealthy diet and sedentary life-style which result in obesity, hypertension, dyslipidaemia, diabetes and other risk factors for atherosclerosis and its complications. Finally, at the other end of the spectrum are patients with symptomatic atherosclerosis – angina, myocardial infarction, stroke and peripheral arterial disease – whose subsequent risk of recurrent disease and death is in part driven by those factors responsible for the diseases initial manifestation. Given this continuum of risk exposure and disease, the traditional division of prevention into tertiary, secondary and primary is artificial. While patients with symptomatic atherosclerotic disease are at high absolute risk of a further event (or a new event in another arterial territory) compared to the healthy population, some individuals without any clinical manifestation of atherosclerosis, such as those with diabetes mellitus, may be at greater risk because of multiple predisposing factors which have not been addressed. For example, a man with an uncomplicated inferior myocardial infarction and well preserved ventricular function may actually be at lower risk of a further coronary event compared to a man of the same age, currently smoking, with an elevated systolic blood pressure of 156 mmHg, a total cholesterol of 6.4 mmol/l, high density lipoprotein (HDL) cholesterol of 0.8 mmol/l and impaired glucose tolerance. Therefore, it is appropriate to address life-style and other risk factors for atherosclerotic disease for patients with symptomatic atherosclerotic disease, and those at high risk of developing symptomatic disease in the same way. This view does not conflict with the clinical priorities for CHD prevention.
Patients with symptomatic atherosclerosis are the top priority for CHD prevention in clinical practice for pragmatic reasons3. Such patients present themselves to medical services because of symptoms and are at high risk of recurrent coronary disease or death. Risk stratification of these patients is unnecessary in relation to life-style and risk factor intervention. They all require professional intervention on smoking, diet and physical activity and appropriate management of weight, blood pressure, lipids and glycaemia. In addition, there are cardioprotective drugs – aspirin or other platelet modifying agents, ß-blockers, ACE inhibitors, lipid modification therapies and anticoagulants – which reduce the risk of recurrent disease and improve survival. However, in contrast to symptomatic patients, high risk asymptomatic individuals have to be sought through population screening, whether systematic or opportunistic. Attendance in general practice or hospital is an opportunity to risk-stratify a healthy individual by assessing absolute risk of developing CHD – that is, the probability of developing non-fatal myocardial infarction or fatal CHD over a defined time period given a particular combination of risk factors – and then, depending on the degree of risk, to intervene appropriately. Taking account of all major cardiovascular risk factors avoids undue emphasis being placed on an individual risk factor at the expense of overall or absolute risk. Risk factors exert an accumulative effect on absolute CHD risk. Therefore, an individual with a number of mildly abnormal risk factors may be at a level of absolute CHD risk greater than that of someone with just one high risk factor.
For example, using the Framingham risk equation, a man of 50 years, who is a non-smoker, with a systolic blood pressure of 125 mmHg, a serum cholesterol of 8.2 mmol/l, and an HDL cholesterol of 1.0 mmol/l, has an absolute risk of developing CHD of about 15% over the next 10 years. A man of the same age who smokes cigarettes, with a systolic blood pressure of 140 mmHg, cholesterol of 6.2 mmol/l, and an HDL cholesterol of 0.8 mmol/l and is diabetic has an absolute CHD risk of about 30% over the same period. In other words, his risk of developing a CHD event compared with the first man (relative risk) is increased 2-fold, despite the fact that none of his risk factors considered individually (apart from smoking) would be thought sufficiently high to merit action. In contrast, by taking a unifactorial approach, the first man's cholesterol level may be considered sufficiently high to require treatment by diet, and possibly even drug therapy, despite his absolute CHD risk being low.
Therefore, in assessing healthy individuals' risk stratification by estimating absolute risk of developing CHD, or other atherosclerotic disease, is necessary to identify those highest risk individuals requiring the most intensive life-style intervention and, where appropriate, drug treatment. Specifically, prescribing antihypertensive and/or lipid lowering medication should reflect both absolute CHD risk as well as individual risk factor levels, and not just individual risk factor levels alone. The man of 50 years already described with an absolute CHD risk of less than 15%, and a cholesterol level of 8.2 mmol/l. would not be a candidate for lipid lowering therapy in the absence of familial dyslipidaemia. In contrast, the man with an absolute CHD risk of greater than 30%, and a cholesterol level of 6.2 mmol/l, would be given lipid lowering therapy if there was no response to diet despite his cholesterol level being lower than that of the first man. This absolute multifactorial risk approach fundamentally challenges the traditional medical model focused on single risk factors, as evidenced by hypertension4 and dyslipidaemia5. Undue emphasis in the past has been placed on elevations of single risk factors rather than on overall multifactorial coronary or cardiovascular risk. In practice, physicians deal with the whole patient rather than one aspect of his or her risk. Clusters of risk factors have a multiplicative effect and thus an individual with a number of modest risk factors can be at considerably greater risk than a person with one very high risk factor (Table 1).
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Because CHD risk rises with increasing age, older individuals are more likely than younger ones to qualify for intervention based on an absolute CHD risk approach. Given a proportionate reduction in risk for an intervention, the benefit will inevitably be greatest in those at highest multifactorial risk – namely the older and elderly patients. Yet, life expectancy in these older, high risk patients is shorter than younger patients and the benefits of intervention need to be considered in the context of a life-course approach. Although younger individuals are at lower absolute CHD risk, they will certainly accumulate more benefit from effective life-style and therapeutic interventions over a life-time. To take account of life-time exposure to risk factors, the European recommendations on coronary prevention6
,7 advocate estimating absolute CHD risk today and projecting that risk to say age 60 years, assuming no change in risk factor levels. In this way, accumulative exposure to risk over a life-time can be estimated and individuals tracking towards a high risk category in later life can be identified earlier and appropriately managed.
The risk stratification of asymptomatic individuals in the population identifies those at highest risk who should be targeted first. As a minimum, the Joint British Societies3 recommend that healthy individuals with a 30% or higher CHD risk over 10 years should all be identified and treated appropriately and effectively now. As the scientific evidence clearly justifies risk factor intervention in healthy individuals with a CHD risk lower than 30%, it is entirely appropriate, as the next step, for physicians to expand progressively opportunistic screening and risk factor intervention down to individuals with a 15% CHD risk over 10 years, as long as those at higher levels of risk have received effective preventive care. Taking a progressive, staged approach to coronary prevention ensures those at highest risk are targeted first, and delivery of care is commensurate with medical services being able to identify, investigate and manage patients properly over the long-term. As there is evidence from randomised control trials that, for some risk factor interventions, drugs significantly reduce the risk of CHD events, and all cause mortality, in individuals with a risk as low as 6% over the next 10 years, it would be appropriate to extend risk factor intervention to individuals with a CHD risk lower than 15% as long as there are resources to do so.
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Calculation of coronary heart disease risk |
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The concept of calculating absolute CHD risk as the clinical context in which decisions about the management of individual risk factors are made was first proposed for the management of hypertension in New Zealand in 19938
. The Joint European Societies – European Society of Cardiology, European Society of Hypertension and European Atherosclerosis Society – then proposed, in 1994, that absolute risk should be the basis for prevention of coronary heart disease in the healthy population embracing blood pressure, lipids and diabetes6. The Joint European Societies produced a coronary risk chart based on age, smoking, systolic blood pressure and total cholesterol. A separate coronary risk chart was produced for patients with diabetes mellitus. This was followed by the New Zealand cardiovascular risk chart which employed a combination of systolic and diastolic blood pressure values, the ratio of total cholesterol to HDL cholesterol and a 5-year rather than 10-year risk model8. The Sheffield Risk and Treatment Table differed from these initial risk assessment charts in that its first use was to determine whether total cholesterol and HDL cholesterol need be measured and, if so, whether the lipid ratio confers an absolute 10-year CHD risk of 30% or more in the context of other risk factors. Subsequently, a Sheffield Table was published to identify individuals at 
15% CHD risk9. The Joint British Societies produced a coronary risk prediction chart (see 
http://www.hyp.ac.uk/bhs/riskpv.htm
) and an associated computer programme Cardiac Risk Assessor, the latter calculating both 10-year CHD risk and cardiovascular risk (including stroke) over the same period3. The Joint British Societies chart is based on age, smoking, systolic blood pressure and the ratio of total cholesterol to HDL cholesterol and diabetes. The chart risk stratifies healthy individuals into three categories: those individuals at highest CHD risk (30% or higher, red band); those at the next level of CHD risk (15% or higher, orange band); and finally those whose CHD risk is less than 15% (green band). When a physician sees a patient, an intuitive assessment of cardiovascular risk will take place based on their age, exposure to tobacco, visible obesity including central obesity, blood pressure, a measurement of lipids (cholesterol, HDL cholesterol and triglycerides) and glycaemic response to a glucose load (impaired glucose tolerance and frank diabetes), family history of CHD, especially premature CHD, and clinical evidence of end organ damage such as retinopathy, renal impairment, micro-albuminuria, left ventricular hypertrophy on ECG or echocardiography, and so on. This intuitive risk assessment is formalised by using coronary risk charts or computer programmes and, because clinical judgement can be imprecise, it is important to estimate risk as objectively as possible. However, this does not exclude the need for clinical judgement as the risk charts do not incorporate all of the risk factors for atherosclerotic disease and it is necessary to adjust the risk obtained to take account of these other factors. For example, clinical evidence of end organ damage will increase the risk, as will a family history of premature CHD. Therefore, in making a decision about whether to introduce antihypertensive or lipid lowering medication, the absolute risk assessment from the chart or computer programme has to be interpreted in the context of other information and ultimately clinical judgement about an individual's management is required.
To identify individuals at high multifactorial risk requires screening which for the most part is undertaken in general practice, either as new patient checks or opportunistically at other consultations. Other contacts with medical services through occupational health screening or specialised hospital clinics can afford the same opportunity. Risk estimation is based on an interview and some physical measurements including blood tests.
To estimate CHD or cardiovascular risk as accurately as possible, the statistical models should be derived from prospective epidemiological data from the population to which the model is to be applied. The model should include all the important risk factors which are easily and routinely measured in clinical practice. The following variables are considered important: smoking, blood pressure, total cholesterol, HDL cholesterol, diabetes, family history of premature CHD and ECG evidence of left ventricular hypertrophy. The Framingham Study from the US is the epidemiological model used in the European, New Zealand, Sheffield and Joint British Societies charts and related computer programmes10.
With this information, it is possible to calculate an individual's absolute risk of developing CHD – that is, the risk of a non-fatal myocardial infarction (MI) or coronary death over 10 years. As risk increases exponentially with age, the risk will be closer to the lower decennium for the first 6 years of each decade – for example, at age 45 years, the risk will be closer to that at age 40 years but at age 47 years it will be closer to that at age 50 years. Family history of premature CHD (for example, in men under 55 years or women under 65 years) increases risk by a factor of approximately 1.5-fold and should also be taken into account in assessing an individual's risk.
The Framingham risk equation is based on measurements made at baseline on a single occasion and, therefore, it is appropriate to estimate risk in clinical practice in the same way. However, the slope of the relation between the true mean risk factor level and risk of developing disease is steeper than that of a single measurement and risk because of regression dilution bias. The slope of the regression line relating CHD risk to risk factor measurements based on a series of recordings is steeper because the effects of biological variation are largely abolished. Therefore, CHD risk will be somewhat higher than the estimate based on the first blood pressure or cholesterol measurement made at an initial screening visit. Absolute risk will also be underestimated by using values of blood pressure on treatment, or cholesterol recorded after dietary intervention, because the true risk is likely to be closer to the life-long habitual levels of these risk factors. By the same token, it would be inappropriate to classify a cigarette smoker, who has recently stopped, as a non-smoker because risk will reflect life-time exposure to tobacco. Whilst it is appropriate to estimate absolute CHD risk on the basis of single risk factor measurements, a decision to treat requires a series of recordings of say blood pressure or cholesterol over a period of time. So it is important to distinguish risk assessment from the final decision to introduce antihypertensive or lipid lowering therapy. The latter is dependent on both the context provided by absolute CHD risk and the long-term levels of individual risk factors observed over time. Life-style intervention will also impact on these levels.
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Healthy individuals and management of risk |
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For individuals without clinical atherosclerotic disease, the absolute risk of developing CHD (non-fatal MI or coronary death), or other atherosclerotic disease, during the next 10 years should strongly influence the intensity of life-style and therapeutic intervention. As the absolute CHD risk increases, so should the intensity of intervention, thus maximising the potential benefit from risk factor reduction. In addition, as the absolute risk increases, so the threshold for drug treatment of blood pressure and dyslipidaemia should be lowered. With advancing age, the absolute risk associated with any one risk factor, or combination of risk factors, may over time become sufficiently great to justify intervention.
The concept of intervention based on absolute CHD risk is justified by evidence that a given reduction in blood pressure or serum cholesterol produces a constant proportional reduction in risk, independent of absolute risk. For example, the relative risk reduction with statin treatment is constant at 33%. Therefore, the absolute benefit is determined by an individual's absolute risk. Consider two men aged 45 years with a serum cholesterol of 6.0 mmol/l; one has no other risk factors while the other smokes cigarettes, has diabetes mellitus and hypertension complicated by left ventricular hypertrophy. Absolute risk of CHD in the next 10 years are <10% and > 30%, respectively; both would gain the same relative risk reduction from treatment with a statin, but absolute benefit is more than 3 times greater in the latter individual (>10% versus < 3%).
The threshold for drug treatment of blood pressure and blood lipids in terms of absolute CHD risk is a matter of judgement, and for blood pressure it is necessary to consider cardiovascular risk because of the additional benefits seen for stroke. Considerations include the following: (i) absolute CHD (or cardiovascular) risk of patients in the trials that demonstrated benefit; (ii) the number of at-risk patients at these levels of risk who must be treated for a defined period of time for one individual to benefit; and (iii) the cost of preventing a CHD event at these different levels of absolute CHD or cardiovascular risk.
When considering cost, the cost of drug therapy is only one part as there are resource implications for screening, investigation and follow-up of individuals at different levels of CHD risk, principally in general practice but also in specialised hospital clinics.
The evidence from clinical trials has unequivocally shown that individuals with an absolute CHD risk as low as 15% (equivalent to a cardiovascular risk of 20%) over 10 years do benefit from blood pressure and lipid lowering therapies that reduce coronary and cardiovascular morbidity and mortality. So the scientific evidence justifies life-style and therapeutic interventions in the population, at least down to a 15% absolute CHD risk, but the magnitude of this task and its cost for the medical services would be considerable. The costs would include those of opportunistic screening, follow-up, laboratory and other investigations, referral of some patients for a specialist opinion, etc, as well as the cost of drugs. In advocating an order of priorities for coronary prevention, and having started with patients with established atherosclerotic disease, it is appropriate to stage risk factor intervention in the general population, and audit the results achieved at each stage. As a minimum, all individuals with an absolute CHD risk of 30% or more over 10 years should be targeted now for comprehensive risk factor management, which will include, as appropriate, blood pressure and lipid lowering therapy. When it has been shown that those at highest risk have been effectively targeted, the scientific evidence justifies a progressive expansion of coronary prevention from 30% down to 15% absolute CHD risk, linked to NHS resources needed to deliver effective preventive care. For individuals with an absolute CHD risk less than 15% over the next 10 years, drug therapy is not normally recommended.
The exceptions to treatment in the context of absolute CHD risk are severe hypertension (systolic >160 mmHg and/or diastolic >100 mmHg), familial hypercholesterolaemia or other inherited dyslipidaemia, or patients with diabetes mellitus with associated target organ damage.
The proportions of men and women (excluding patients with reported CHD or other atherosclerotic disease) who are potentially eligible for treatment at different levels of absolute CHD risk in England and Scotland, has been estimated by applying the Framingham Risk Function to the Health Survey for England (1994) and the Scottish Health Survey (Table 2). The Health Survey for England did not measure HDL cholesterol and this has been estimated from the Scottish data. The Scottish Survey is based on people aged 30–64 years whereas in England the population 30–75 years were surveyed. For the age group 64–75 years in England, the average HDL cholesterol at age 64 years in Scotland was used: 28% of men and 9% of women in England have an absolute CHD risk of 15% over 10 years. The corresponding proportions in Scotland are 21% and 6% but for a younger age range which stops at 64 years.
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Blood pressure |
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In the management of blood pressure, assessing absolute CHD or cardiovascular risk is logical and the Joint British Societies produced an algorithm based on this principle.(Fig. 1). The exception to the absolute risk approach is individuals with a sustained diastolic blood pressure of 100 mmHg or greater and/or systolic blood pressure over 160 mmHg. Such individuals should always be prescribed antihypertensive drugs because of established benefit in reducing total cardiovascular risk, and stroke in particular. In those with lower levels of sustained diastolic or systolic blood pressure, 10-year cardiovascular (CHD and stroke) risk should be calculated. It is important to calculate cardiovascular and not just CHD risk in the management of hypertension because of the additional benefit of blood pressure lowering in relation to stroke. An absolute cardiovascular risk of 20% over 10 years is equivalent to an absolute CHD risk of 15% over the same time and this is the recommended threshold for antihypertensive drug treatment.
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Diastolic blood pressure measurements of 110 mmHg or greater should be repeated over 1–2 weeks to confirm a sustained increase, despite life-style intervention, after which drug treatment should be started. Individuals with diastolic blood pressure in the range 100–109 mmHg, but with no evidence of target organ damage, should be given life-style advice and observed, initially weekly and thereafter monthly. If there is a downward trend in blood pressure (diastolic <100 mmHg), observation should be continued together with re-inforced life-style advice. If diastolic blood pressure is sustained at or above 100 mmHg during this 3–6 month period drug treatment should be started. The management of individuals in whom diastolic blood pressure remains between 90–99 mmHg and/or systolic blood pressure between 140–159 mmHg on repeated measurements should be considered in the context of their absolute risk of CHD and stroke, not CHD alone.
In patients with target organ damage (left ventricular hypertrophy, retinopathy – haemorrhages or exudates – renal impairment or proteinuria, for example) antihypertensive therapy is indicated.
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Lipids |
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To assess absolute CHD risk, a non-fasting serum cholesterol and non-fasting HDL cholesterol are adequate. A measurement of HDL cholesterol is essential to assess accurately absolute CHD risk. This is particularly true in women who frequently maintain high serum HDL cholesterol concentrations long after their menopause, which means that a raised total cholesterol can be misleading. Also, as low HDL cholesterol tends to cluster with other risk factors such as diabetes and hypertension, reliance on total cholesterol alone in such men and women will often underestimate risk. All patients who have a pronounced hyperlipidaemia, or for whom lipid lowering therapy is being considered, should have a fasting lipoprotein profile to include fasting cholesterol, triglycerides and HDL cholesterol. Figure 2 is an algorithm for cholesterol management based on absolute CHD risk. Fasting serum triglycerides are important to measure before introducing lipid lowering drug therapy because a raised cholesterol may not be caused by increased LDL cholesterol. If severe hypertriglyceridaemia is present, an increase in serum cholesterol may be caused by cholesterol transported in very low density lipoprotein (VLDL) and chylomicrons (type V hyperlipoproteinaemia). Secondary causes of hyperlipidaemia should always be excluded. This includes enquiring about possible excessive alcohol consumption and screening for thyroid disorders, renal disease, liver disease, diabetes mellitus and impaired glucose tolerance.
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Patients with familial hypercholesterolaemia are at especially high risk of premature coronary atherosclerosis and its complications. Typically, the patient has a cholesterol of around 9 mmol/l or greater together with clinical signs such as tendon xanthomata, early corneal arcus and the premature development of CHD. Untreated, the majority of male heterozygotes and half of the female heterozygotes will have a clinical CHD event before the age of 60 years. Once the diagnosis is made, the need to screen the immediate family is implicit in view of its autosomal dominant inheritance. Patients with familial hypercholesterolaemia do not require risk stratification using the coronary risk chart. They all require treatment with a combination of diet and drug therapy. The drug class of first choice for familial hypercholesterolaemia is a statin.
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Risk calculation |
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It should be emphasised that CHD risk calculation may be less accurate in certain groups of patients. Particular attention is drawn to patients with familial hypercholesterolaemia, patients with diabetes and target organ damage, and patients of Indo-Asian descent. All these groups appear to be at greater risk than that calculated from the Framingham equation and clinicians should make allowance for this.
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Diabetes mellitus |
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For individuals with diabetes mellitus, CHD risk is greatly increased with both type I and type II diabetes. Over 70% of patients with diabetes die from macrovascular disease, mainly coronary heart disease. Thus, implicit in the long-term management of diabetic patients is the requirement for multiple risk factor modification for coronary prevention. Hypertension is very common in type II diabetes, is strongly related to obesity and highly predictive of cardiovascular complications. Antihypertensive treatment is required for all patients with type II diabetes and blood pressure
160 mmHg, aiming for a target blood pressure of <130 mmHg systolic and <80 mmHg diastolic. For patients with type II diabetes and systolic pressure 140–159 mmHg but diastolic pressure of <90 mmHg, treatment is recommended if target organ damage or microvascular or macrovascular complications are present, or if the absolute coronary risk is 15% over 10 years. Many patients with type II diabetes are overweight and have high cardiovascular risk. They need intensive and sustained advice on life-style and appropriate treatment to achieve other risk factor targets as well as glycaemic control. Cholesterol lowering therapy is indicated in patients with diabetes if the absolute CHD risk exceeds 15% over 10 years and the total cholesterol is >5 mmol/l. |
Chronic renal failure |
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Hypertension and hyperlipidaemia are common in chronic renal disease and the co-existence of hypertension and proteinuria is a very powerful marker for CHD. Rigorous control of blood pressure is important; a target blood pressure of <130 mmHg systolic and <80 mmHg diastolic is recommended. Hypercholesterolaemia occurs in association with proteinuria, but the management of hyperlipidaemia is often complicated by the unsuitability of many lipid lowering drugs and by complex dietary and therapeutic regimens.
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Special considerations |
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Gender differences The absolute risk of CHD is lower in women at all ages up to the very elderly when disease rates almost converge. Over the age of 55 years, women have more obesity, higher total cholesterol and more diabetes than men, and over the age of 65 years have more hypertension than men. At younger ages, blood pressure and LDL cholesterol are lower among women than men and throughout life women smoke less and have higher HDL cholesterol levels. One further large difference between men and women is that levels of central obesity, as measured by waist hip ratios, are very much smaller among women. Despite these differences, absolute CHD risk estimation is as appropriate in women as in men and the same threshold of an absolute CHD risk
15% over 10 years defines those women who may be eligible for antihypertensive and/or lipid lowering therapy. The elderly The absolute risk of CHD and other atherosclerotic diseases is higher in the elderly compared with any other age group. The same proportionate risk reduction will, therefore, potentially have a much more beneficial impact in the elderly compared with younger age groups.
Ethnic minorities Coronary mortality is significantly higher among South Asian immigrants in this country. In contrast, CHD death rates are profoundly reduced among the Afro-Caribbean population whereas stroke rates are highest among the Afro-Caribbean community. Europeans have the lowest stroke rates and the South Asians have rates between those of the Europeans and the Afro-Caribbean, which is compatible with the prevalence of hypertension among the three ethnic groups. The coronary risk chart will underestimate the absolute CHD risk in the Asian community and overestimate absolute CHD risk in the Afro-Caribbean population. Therefore, this chart should be used with caution in these ethnic minorities.
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Footnotes |
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Correspondence to: Prof. David Wood, Department of Cardiology, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UK
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References |
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- Department of Health. The Health of the Nation: A Strategy for Health in England. London: HMSO, 1992
- British Cardiac Society, British Hyperlipidaemia Association, British Hypertension Society, British Diabetic Association. Joint British recommendations on prevention of coronary heart disease in clinical practice. Heart 1998; 80 (Suppl 2): S1–26
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