Risk assessment and lipid modification for primary and secondary prevention of cardiovascular disease: summary of NICE guidanceBMJ 2008; 336 doi: https://doi.org/10.1136/bmj.39554.624086.AD (Published 29 May 2008) Cite this as: BMJ 2008;336:1246
- Angela Cooper, senior health services research fellow,
- Norma O’Flynn, clinical director
- on behalf of the Guideline Development Group
- 1National Collaborating Centre for Primary Care, Royal College of General Practitioners, London SW7 1PU
- Correspondence to: N O’Flynn
Why read this summary?
Cardiovascular disease remains a leading cause of morbidity and mortality in the United Kingdom. Randomised controlled trials have shown benefit from modifying risk factors in people at risk of developing cardiovascular disease and in those who have evidence of established disease. Currently patients are often assessed opportunistically and treated on the basis of individual clinical or laboratory results rather than on their overall level of risk of developing cardiovascular disease. This article summarises the most recent recommendations from the National Institute for Health and Clinical Excellence (NICE) on the effective identification and assessment of people at risk of cardiovascular disease, and on the modification of lipids in primary and secondary prevention. The detailed consideration of the evidence is available in the full guideline (www.nice.org.uk/ CG67).1
NICE recommendations are based on systematic reviews of best available evidence. When minimal evidence is available, recommendations are based on the guideline development group’s opinion of what constitutes good practice. Evidence levels for the recommendations are given in italic in square brackets.
Identifying those at risk of cardiovascular disease for primary prevention
Use a systematic strategy rather than opportunistic assessment to identify people at high risk of the disease.
Exclude patients known to have established cardiovascular disease or who are already considered at high risk, such as patients with diabetes or lipid disorders.
Estimate risk of cardiovascular disease using risk factors already recorded in primary care records, such as age, sex, and blood pressure.
Use the estimated risk value to prioritise patients, and arrange a full formal risk assessment for patients whose estimated 10 year risk is ≥20%.[These first four recommendations are based on results from health economic modelling]
Assess risk (both estimate and formally) using the 1991 Framingham 10 year risk equations, with the following variables: age (30-74 years), sex, systolic blood pressure (mean of previous two systolic readings), total cholesterol concentration, high density lipoprotein cholesterol concentration, smoking status, and presence of left ventricular hypertrophy.2 [Based on the experience of the Guideline Development Group]
Fasting lipid levels are not needed for risk assessment.
Record factors important for development of cardiovascular disease, such as ethnicity, body mass index (kg/m2), and family history of premature heart disease.
Adjust the risk score for factors important for development of cardiovascular disease but not included in the risk score as follows:
-If there is one first degree relative with premature coronary heart disease, increase the estimate by 1.5; if there is more than one first degree relative with premature coronary heart disease, increase the estimate by up to 2 [Based on good quality evidence from cohort studies and on the experience of the Guideline Development Group]
-Increase the estimated risk for men with a South Asian background by 1.4.
Use clinical judgment to decide on treatment if the risk score is near the threshold for treatment and evidence exists of other factors that may predispose a person to premature cardiovascular disease, such as socioeconomic status, severe obesity (body mass index greater than 40), or the patient is already taking antihypertensive medication or has recently stopped smoking.
Consider further investigations and specialist review in people in whom familial hypercholesterolaemia or other monogenic lipid disorders are suspected because of clinical findings, lipid profiles, and family history of premature coronary heart disease.
When using risk estimation tools for identifying risk of cardiovascular disease, note that these tools:
-Can give only an approximate risk value, and interpretation of risk scores should always reflect informed clinical judgment
-Do not include people aged 75 years or older, but people 75 years and over may benefit from statin treatment, particularly if they smoke or have high blood pressure.
Communicating cardiovascular risk with the patient
Explain the process of risk assessment and the meaning of risk in everyday, jargon-free language.
Provide information on absolute risk rather than relative risk, and use graphical and textual formats to inform patients on risks and benefits of interventions.
Explore prior information given and patients’ personal beliefs on health and their readiness to make lifestyle changes and develop a shared management plan.
All patients at high risk of cardiovascular disease should be advised to:
Eat a diet low in saturated fat and dietary cholesterol and replace saturated fats by monounsaturated and polyunsaturated fats
Eat at least five portions of fruit and vegetables a day and at least two portions of oily fish a week
Take 30 minutes of physical activity a day, of at least moderate intensity, at least five days a week; activities should include those that can be incorporated into everyday life, such as walking, using stairs, and cycling
Limit alcohol consumption (for men to up to 3-4 units a day, for women up to 2-3 units a day).
The use of plant sterols and stanols is not to be routinely recommended for patients at high risk. [No evidence found of benefit to patients at high risk of cardiovascular disease]
Drug treatment for lipid modification in primary and secondary prevention
Measure fasting total, low density lipoprotein and high density lipoprotein cholesterol concentrations, and triglyceride concentrations once before starting drug treatment (if fasting concentrations are not already available) except in patients with acute coronary syndrome, where fasting concentrations should not be measured until three months after acute coronary syndrome.
When the decision has been made to start statin treatment, prescribe a drug shown to be of clinical benefit and with a low acquisition cost (taking into account the required daily dose and the product price per dose).3
When starting or increasing statin treatment, discuss with the patient the risks and benefits of treatment and take into account comorbidities, multiple medications, life expectancy, and the patient’s own preferences.
Statins for primary prevention
Consider all other modifiable risk factors for cardiovascular disease, comorbidities, and secondary causes of dyslipidaemia, and optimise their management if possible. Consider therefore smoking status, alcohol consumption, blood pressure,4 body mass index or other measure of obesity,5 fasting blood glucose concentrations, renal function, liver function (transaminases), and thyroid stimulating hormone concentrations (if dyslipidaemia is present).
Offer statin treatment as part of primary prevention for adults with a 10 year risk of ≥20%.3 [Based on good quality evidence from a meta-analysis]
Treat with simvastatin 40 mg. If this is contraindicated or drug interactions are possible, choose a lower dose or an alternative such as pravastatin.
Do not routinely offer higher intensity statins—that is, statins used in doses producing greater cholesterol lowering than simvastatin 40 mg (for example, simvastatin 80 mg). [No randomised controlled trials have compared high and low intensity statins in relation to cardiovascular outcomes in people without cardiovascular disease]
Do not set a target concentration for total or low density lipoprotein cholesterol in primary prevention. [No randomised controlled trials have compared high and low intensity statins in relation to cardiovascular outcomes in people without cardiovascular disease]
Once a patient has started taking a statin, repeat lipid measurement is unnecessary. Clinical judgment and the patient’s preference should guide the review of drug treatment and whether to review the lipid profile. [Based on the professional opinion of the Guideline Development Group]
Statins for secondary prevention
Consider all modifiable risk factors, comorbidities, and secondary causes of hyperlipidaemia, and optimise their management. Do not delay treatment until optimisation of risk factors has been achieved.
Offer statin treatment to adults with clinical evidence of cardiovascular disease.3 Start treatment with simvastatin 40 mg. If there are potential drug interactions, or simvastatin 40 mg is contraindicated, choose a lower dose or an alternative preparation such as pravastatin. [Based on good quality evidence from a meta-analysis of 14 trials]
Offer people with acute coronary syndrome a higher intensity statin. [Based on results of health economic modelling of cost effectiveness]
Consider increasing the dose to simvastatin 80 mg or a drug of similar efficacy and acquisition cost if a total cholesterol concentration of <4 mmol/l or a low density lipoprotein cholesterol concentration of <2 mmol/l is not attained [Based on results of health economic modelling of cost effectiveness]
Use an “audit” concentration of total cholesterol of 5 mmol/l to assess progress in populations being treated for secondary prevention, as more than half will not achieve a total cholesterol concentration of <4 mmol/l or a low density lipoprotein cholesterol concentration of <2 mmol/l. [Based on results of health economic modelling and on the professional opinion of the Guideline Development Group]
Monitoring statin treatment
If a person taking a statin starts taking additional drugs or needs treatment for a concomitant illness that interferes with metabolic pathways or increases the propensity for drug and food interactions, consider reducing the statin dose or temporarily or permanently stopping it.
Advise people taking statins to seek medical advice if they develop muscle symptoms (pain, tenderness, or weakness); if this occurs, measure creatine kinase concentrations.
Do not routinely monitor creatine kinase in those who are asymptomatic.
Measure baseline liver enzyme (transaminases) levels before statins are started, within three months of treatment starting, and at 12 months, but not again unless clinically indicated. People whose levels are raised but are less than three times the upper limit of normal should not be routinely excluded from statin treatment.
If a person develops an unexplained peripheral neuropathy, discontinue statins and seek specialist advice.
[The above five recommendations are based on moderate quality evidence from randomised controlled trials, on reports of adverse effects, and on the professional opinion of the Guideline Development Group]
Other lipid lowering agents
Do not routinely offer fibrates or anion exchange resins for primary or secondary prevention, but consider either of these options if statins are not tolerated. [Insufficient evidence on cardiovascular outcomes to recommend routinely in primary or secondary prevention]
Do not offer nicotinic acid for primary prevention, but consider it for secondary prevention in people who cannot tolerate statins. [No evidence for use of nicotinic acid in primary prevention and limited evidence for benefit only in patients who have had a myocardial infarction]
Do not offer an anion exchange resin, fibrate, or nicotinic acid combined with a statin for primary prevention. [No evidence for beneficial effect of drugs used in combination]
Consider people with primary hypercholesterolaemia for ezetimibe treatment (see the NICE technology appraisal on ezetimibe6).
Effectively implementing the recommendations for primary prevention depends on a structured, systematic approach to identifying people at high risk of cardiovascular disease. Formal risk assessment will require good communication with patients and education on the meaning of the risk and the benefits and risks of treatment. Standard models of care should include advice and support in lifestyle changes for both primary and secondary prevention. The costing tool being developed by NICE can be used to estimate additional costs (www.nice.org.uk/CG67).
Further information on the guidance
The way primary and secondary prevention of cardiovascular disease is managed varies among healthcare practitioners. Practitioners report uncertainty in how to manage blood lipids in patients both with and without pre-existing cardiovascular disease, and the prescribing of lipid regulating drugs in primary care shows wide variation.
The Guideline Development Group followed standard NICE methodology for the development of this guidance (www.nice.org.uk/page.aspx?o=114219). The guideline group comprised patient representatives and experts in treatment of lipid disorders and cardiovascular disease in primary care and secondary care, public health, risk score assessment, health services research, health economics, systematic reviews, nursing, and information science.
Future research has been recommended in the following areas:
The identification of the most appropriate risk assessment tool for use in England and Wales both in terms of validation of the tool and in practical use
How risk should be communicated to patients
The use of decision aids in making decisions about treatment in primary prevention
The clinical and cost effectiveness of using target concentrations of total and low density lipoprotein cholesterol in treatment in primary and secondary prevention
The benefits and risks of use of stanols and sterols; these are widely advertised to patients, but little evidence exists on their benefit for patients at high risk.
This is one of a series of BMJ summaries of new guidelines, which are based on the best available evidence; they will highlight important recommendations for clinical practice, especially where uncertainty or controversy exists.
The members of the Guideline Development Group are John Robson (chair and clinical adviser), senior clinical lecturer in general practice, Institute of Community Health Sciences, Queen Mary University London; Peter Brindle, general practitioner principal, Corbett House Surgery, Bristol; Paramjit Gill, general practitioner and reader in primary care research, Department of Primary Care and General Practice, University of Birmingham; Renu Gujral, patient representative; Maureen Hogg, coronary heart disease lead nurse, Cleland Hospital, North Lanarkshire; Tom Marshall, senior lecturer in public health, University of Birmingham; Rubin Minhas, general practitioner, primary care coronary heart disease lead, Medway Primary Care Trust, Gillingham; Lesley Pavitt, patient representative; John Reckless, consultant physician and endocrinologist, Royal United Hospital, Bath; Alaster Rutherford (until June 2007), head of medicines management, Bristol Primary Care Trust; Margaret Thorogood, professor of epidemiology, University of Warwick; and David Wood, Garfield Weston chair of cardiovascular medicine, Imperial College London. Phillip Bath, Stroke Association professor of stroke medicine, University of Nottingham, was co-opted to the group for secondary prevention. The technical team at the National Collaborating Centre for Primary Care were Norma O’ Flynn, Angela Cooper, Neill Calvert, Leo Nherera, Tim Stokes, Nancy Turnbull, Chris Rule, Rifna Mannan, and Nicola Browne.
Contributors: Both authors contributed equally to drafting and revising the summary. NO’F is the guarantor.
Funding: The National Collaborating Centre for Primary Care was commissioned and funded by the National Institute for Health and Clinical Excellence to write this summary.
Competing interests: None declared.
Provenance and peer review: Commissioned; not externally peer reviewed.