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Coronary heart disease: risk factor management pages 47-54 Multiple choice questions and submission instructions page 55 Practice profile assessment guide page 56

Coronary heart disease: risk factor management

NS271 Foxton J et al (2004) Coronary heart disease: risk factor management. Nursing Standard. 19, 13, 47-54. Date of acceptance: November 9 2004. Aim and intended learning outcomes The aim of this article is to provide an overview of coronary heart disease (CHD) risk factors and their management. After reading this article you should be able to: Explain the rationale behind the treatment targets to reduce the incidence of CHD in the population. Describe the risk factors for CHD. Use the coronary risk calculator to identify people at high risk of developing CHD. Identify those who are at moderate risk of CHD. Discuss the role of lifestyle advice in the management of cholesterol. Describe the drug therapy that may be used to reduce cholesterol. Incidence and prevalence CHD is the leading cause of mortality and morbidity in the UK and the single most common cause of premature death. Despite a fall in CHD mortality in recent years, the UK death rate is among the highest in the world at around 120,000 per year (British Heart Foundation (BHF) 2003). CHD, together with cancer and stroke, accounts for 35 per cent of life years lost before the age of 75 (BHF 2003). In addition, more than 1.5 million people in the UK are living with angina and 500,000 have heart failure (Department of Health (DoH) 2004) frequently, although not exclusively, caused by CHD. This high incidence is not unique to the UK and a similar pattern is being observed worldwide (Yusuf et al 2002). The World Health Organization (WHO) has predicted that by 2020, CHD will be the greatest cause of death and disability throughout the world (Tunstall-Pedoe et al 1999). The increasing number of people living with the disease is of concern to healthcare professionals. Strategies to prevent this are therefore of great importance. The National Service Framework (NSF) for CHD (DoH 2000a) laid the foundations for dramatic improvements in the prevention and treatment of heart disease, and 1.8 million people are now receiving lipid-lowering drugs, with lifestyle advice a key feature of primary and secondary prevention appointments. However, there is room for improvement and the NHS Improvement Plan (DoH 2004) sets an ambitious target to reduce death rates from CHD and stroke in the under-75s by at least 40 per cent by 2010. Pathophysiology CHD can develop at any age. Initially, an area of atheromatous plaque forms in the coronary artery. The mechanism for plaque formation is unclear, although the predominant view is that lipid accumulates under the lining of the coronary artery (Samar 1999). Because the lipid infiltrate is a foreign matter, white blood cells called macrophages engulf it, and create foam cells (Samar 1999). Smooth muscle cells then invade the area, which enlarges. It is not until the plaque obstructs more than 50 per cent of the lumen of the coronary artery that the flow of blood to the heart muscle, the myocardium, is reduced. This usually means that when resting, or undertaking minimal activity, the blood supply to the heart is adequate. However, when the heart requires a greater supply of oxygen, as occurs during exercise or emotional episodes, the blood supply cannot increase sufficiently and the person will experience chest discomfort. This is referred to as angina pectoris. Once plaque has

This article has been supported by an educational grant from:

In brief Author Julie Foxton RGN, RM, is senior nurse adviser, HEART UK, Maidenhead, Berkshire; Michaela Nuttall RN, DipN, MSc, is CHD Co-ordinator, Bromley Primary Care Trust, Kent; and Jillian Riley RGN, RM, BA(Hons), MSc, is head of postgraduate education for nurses and allied health professionals, Royal Brompton Hospital, and honorary lecturer, Imperial College, London. Email: jf@heartuk.org.uk Summary Coronary heart disease is the leading cause of mortality and morbidity in the UK. Nurses have a pivotal role in the management of high-risk patients and the modification of risk factors. Key words Cardiovascular system and disorders Health promotion These key words are based on subject headings from the British Nursing Index. This article has been subject to double-blind review. Online archive For related articles visit our online archive at: www.nursing-standard.co.uk and search using the key words above.

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formed, the wall of the coronary artery is damaged and irregular in shape and platelets cluster around the obstruction. This reduces the size of the lumen still further and consequently the blood supply is also reduced. Sometimes platelet aggregation can be sudden causing an abrupt and total occlusion of the coronary artery. At this time the person will experience a myocardial infarction (MI). level of less than 2.0mmol/l (Williams et al 2004). The risk of developing CHD can be calculated using a risk chart. This forecasts the risk of developing CHD over the next ten years. High risk is identified where the risk is calculated as 30 per cent or higher, whereas moderate risk is calculated as a 10 per cent risk of developing CHD over the next ten years (Wood et al 1998).

TIME OUT 1
Write down, in no more than one paragraph, your own definition of CHD. Risk factors A number of factors are thought to increase the likelihood of developing CHD. The three major risk factors are smoking, hypertension and abnormal cholesterol levels. However, additional risk factors include a family history of CHD, diabetes, abdominal obesity, lack of fruit and vegetables in the diet and lack of exercise (Yusuf et al 2004). These risk factors are common, regardless of sex, ethnic group or age and are frequently not found in isolation, thereby increasing the risk (Yusuf et al 2004). Some risk factors are modifiable, for example, cholesterol, diabetes, hypertension, obesity, physical inactivity and smoking, and efforts should be made to increase awareness of how to reduce the likelihood of developing CHD both in the person who has identified risk factors and in the population as a whole (Yusuf et al 2004).

TIME OUT 3
Look at the risk calculator on the following websites: www.hyp.ac.uk/bhs/Cardiovascular _Risk_Charts_and_Calculators.htm Consider a patient you have cared for over the past week, who does not already have a diagnosis of CHD, and use the calculator to assess his or her risk of developing CHD over the next ten years. You may need to read the patients notes to find some of the details. The nurses role The role of the nurse has extended to meet the changes in health care where increasingly the emphasis is on health promotion and disease prevention. This is outlined in the documents Making a Difference (DoH 1999a), the NHS Plan (DoH 2000b), and Shifting the Balance of Power in the NHS: Securing Delivery (DoH 2001). Government policies to improve the health of the individual and the population have emphasised that nurses have a significant contribution to make. The nursing profession can assist the shift in responsibility for health to patients by empowering people to improve their health outcomes. Diabetes and obesity are also increasing in the UK (BHF 2003). The nurses role is pivotal in helping to address this increase. Nurses can proactively implement preventive strategies and advise on many aspects of health promotion. They are increasingly using clinical guidelines to ensure a higher quality of care (Puffer and Rashidian 2004). This means that while nurses are ideally placed to provide information, the advice given can be more consistent and evidence-based through the application of local and national guidelines. This also helps to improve equity of care. In CHD the proactive role of the nurse has been further reinforced by the publication of the NSF for CHD (DoH 2000a), which suggests that the ideal way to implement secondary prevention is through nurse-led clinics. While nurses in almost all areas of care have the opportunity to assess and advise on CHD risk factors, it is particularly pertinent for nurses working in primary care and the community. This is because many people who have CHD or who are at a high or moderate risk of developing the disease are cared for in primary care settings. For those people with CHD, there is now

TIME OUT 2
Using a separate piece of paper for each risk factor identified above, write down what you are currently doing to reduce that risk factor either in your own life or in a patients life. Once you have done this, compare your answers with the suggestions below. Modification of risk factors There are a number of ways in which the risk of developing CHD can be modified. They include lifestyle advice as well as the prescription of advice regarding medication. Abnormal cholesterol levels are a major risk factor for CHD and are responsible for at least 46 per cent of all new cases of CHD (BHF 2004). Consequently, efforts are being made to lower cholesterol levels in the population to a target level of 5.0 mmol/l or less for total cholesterol. This may seem hard to achieve certainly among some sections of the patient population and in some areas of the country, for example, where patient concordance with therapy is poor, there is an inability to tolerate therapy or where sections of the community are unable or unwilling to access medical services but the most recent British Hypertension Society guidelines go further and suggest a total cholesterol of less than 4.0mmol/l and low-density lipoprotein (LDL)

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evidence of benefits from four randomised controlled trials of nurse-led secondary prevention (Allen et al 2002, Cupples and McKnight 1999, Moher et al 2001, Murchie et al 2003). Three of the trials were in primary care in the UK and one in secondary care in the United States (US). These show that nurseled secondary prevention clinics can improve secondary prevention of CHD risk factors. Wright et al (2001) also found that nurse-led risk factor management is acceptable to patients. There is less evidence that nurse intervention is effective for those people who are at high or moderate risk of developing CHD but have not been diagnosed with CHD. The Cochrane Library reviewed multiple risk-factor interventions for primary prevention of CHD and concluded that effective interventions on a general population basis would be mostly ineffective and costly (Ebrahim and Davey Smith 1999). Therefore, targeting health promotion activities at high-risk individuals should be considered the first step. Targeted CHD prevention is also advocated by the joint British recommendations on CHD prevention (Wood et al 1998). Lifestyle and pharmacological interventions and goals for those people at high risk of CHD are similar to those for people with CHD. with improvements in cardiovascular risk (Han et al 1997). Unlike BMI, which does not take into account body fat distribution, waist measurement can give a better indication of android obesity (central distribution of excess adipose tissue) (Donahue et al 1987). It is recommended that weight reduction is required when waist circumference is more than 102cm in men and more than 88cm in women (Lean et al 1995). Dietary advice Nurses can also advise on a healthy diet (Figure 1) which may include the following: Calorie intake 1,200-1,600kcal per day, moderate fat intake by eating less fatty meat, fatty cheese, full-cream milk, fried food and lard (Tang et al 1998). Consider eating more vegetables, fruit, cereals, wholegrain bread, poultry, fish, rice, skimmed or semi-skimmed milk, grilled food, lean meat or pasta. Fried food should be discouraged, but steam frying or using a vegetable oil high in polyunsaturates, such as sunflower or rapeseed oil or one containing plant sterols or stanols could be considered (see below). Use low-fat spreads suggest considering a low-fat spread that contains plant stanol/sterol esters. These and other plant stanol/sterolcontaining foods may be useful adjuncts in lowering cholesterol levels. Plant sterols and stanols are sourced from either wood pulp products or soya bean distillates, rapeseed and sunflower oils. They inhibit the absorption of cholesterol in the intestines and may achieve total cholesterol reductions of up to 14 per cent (Miettinen et al 1995). They are safe and tolerable and are contained in a variety of ready-to-buy products ranging from milk and milk drinks, yoghurts and spreads. However, these products should be used as described as a constant circulating level of stanols or sterols is required to achieve maximum efficiency and effectiveness. Box 1. Benefits of 5-10kg weight loss Mortality 20-25 per cent fall in overall mortality 30-40 per cent fall in diabetes-related deaths 40-50 per cent fall in obesity-related cancer deaths Blood pressure 10mmHg fall in diastolic and systolic pressures Diabetes Up to a 50 per cent fall in fasting blood glucose Reduces risk of developing diabetes by more than 50 per cent Lipids Fall of 10 per cent total cholesterol, 15 per cent low-density lipoprotein and 30 per cent triglycerides Increase of 8 per cent high-density lipoprotein
(Blenkinsopp 2004)

TIME OUT 4
In Time Out 3 you calculated a patients risk of developing CHD over the next ten years. List this patients risk factors for CHD. Under each risk factor, identify some of the ways in which you might help him or her to reduce this risk. Lifestyle management Weight loss There is a twofold increase in the risk of developing CHD in people who are obese or overweight. For those who are obese, CHD is the main cause of excess mortality (British Nutrition Foundation (BNF) 1999). This is in part because obese or overweight individuals are more likely to have hypertension, diabetes and high triglyceride and cholesterol levels, and other abnormalities of clotting that increase the risk of thrombus formation or MI (Meade et al 1993). Weight control is important and can be achieved in a variety of ways. Eating less fat, sugar and alcohol is helpful but, to achieve a healthy body weight, it is also important to incorporate regular, moderate exercise into a daily routine. Various benefits are associated with weight loss (Box 1). In people with a body mass index (BMI) greater than 25kg/m2 (calculated by dividing weight in kilos by height in metres squared), referral to a dietician or nutritionist should be considered. Strategies should be considered that gradually reduce weight by about 0.5kg per week through a combination of diet, exercise and behavioural changes. Reduction of waist circumference is associated

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Figure 1. The HEART UK diet sheet

BEST CHOICE
Cereals and starchy foods

IN MODERATION

BEST AVOIDED

Potatoes

Vegetables and fruit

Fish

Meat

Vegetarian choice

Eggs and dairy

Oils

Spreads

Meals

Cakes and biscuits

Puddings

Flavourings, sauces, jams and sweets

Reproduced with the kind permission of HEART UK

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Physical activity Thirty seven per cent of CHD deaths in people under the age of 75 are attributable to physical inactivity (BHF 2003). The cardiovascular benefits of regular physical activity include reduced blood pressure and less likelihood of obesity, both of which help to reduce the risk of developing CHD. However, the Health Survey for England 1998 (DoH 1999b) identified that approximately 70 per cent of people were not taking regular physical activity. Recommended levels to gain cardiovascular protection, if you are physically able, are at least 30 minutes of steady activity on five or more days a week (American College of Sports Medicine (ACSM) 2000). This can take the form of walking, jogging, swimming, cycling and dancing, which can easily be fitted into a regular day. Smoking Smoking is the single biggest cause of preventable death in the UK. Each year, tobacco smoking accounts for more than 30,000 deaths from cardiovascular disease (Callum 1998). It is essential that nurses take a proactive role in helping people to stop smoking and provide advice on smoking cessation. Key features of individual smoking cessation are: Ask about smoking at every opportunity. Advise all smokers to stop. Assist smokers to stop. Arrange follow-up. Stopping smoking will reduce CHD risk even if a person has smoked for many years. There are short and long-term benefits. Within eight hours nicotine levels will be reduced by half and within 24-48 hours carbon monoxide levels will be comparable to those of a non-smoker. The long-term benefits are considerable; excess cardiovascular risk from smoking reduces by half within one year and after five years reverts to about the same level as someone who has never smoked (Critchley and Capewell 2003). Alcohol In moderation (one to two units daily for women, two to three units for men), alcohol may reduce the risk of CHD by potentially increasing high-density lipoprotein (HDL) cholesterol slightly and reducing thrombotic tendencies (Mukamal et al 2001). A unit is defined as a half pint of beer, lager or cider, or a pub measure of wine, sherry or spirits. However, consuming too much alcohol places health at risk in a number of ways. When taken in excess, alcohol can damage the cardiac muscle, cause arrhythmias, stroke and coagulopathies (Lindsay and Gaw 2004). Additionally it may contribute to obesity, high triglycerides and hypertension, risk factors for the development of CHD (Lindsay and Gaw 2004). Men should drink no more than three to four units of alcohol and women no more than two to three units a day. Stress A certain amount of stress may be desirable as it keeps people alert and motivated. However, as stress levels increase and especially if prolonged, they can be counter-productive. Stress can exacerbate symptoms in people with pre-existing heart disease, and can contribute to hypertension (Blenkinsopp 2004). Additionally, it may lead to the adoption of poor eating habits, smoking and increased alcohol consumption and non-concordance with prescribed medication. The nurse can help people to find time for relaxation or teach them simple breathing exercises to help reduce the risk of developing CHD (Blenkinsopp 2004). Drug therapy This section examines methods used to control and correct the lipid profile (Box 2), other than diet and lifestyle. Statins These are the most common form of drug therapy for reducing raised cholesterol levels. The first statins were produced more than 20 years ago from fungi, but newer versions are man-made. Statins include atorvastatin, cerivastatin (now withdrawn), fluvastatin, lovastatin (not available in the UK), pravastatin, rosuvastatin and simvastatin, and others are undergoing clinical and scientific study. Statins work by inhibiting the action of 3-hydroxy3-methylglutaryl-coenzyme A (HMGCoA) reductase, an enzyme which is involved in cholesterol synthesis in the liver (BNF 2004). Statin therapy can reduce low-density lipoprotein (LDL) cholesterol by up to 60 per cent (McTaggart 2003). Additionally, statins lower triglycerides (fatty acids attached to glycerol) in proportion to their LDLlowering effect. Different statins vary in their effect on HDL cholesterol but they generally cause a small rise and because HDL is cardioprotective this is a beneficial action (Assman et al 1995). Statins have been proven to be effective at lowering mortality and morbidity for cardiovascular disease (DoH 2000a, Gordon 2000, Hebert et al 1997, Minhas 2003, Shepherd et al 2002, Wood et al 1998). The Simvastatin Survival Study (also know as the 4S study) in the late 1980s was the first trial to provide this information (Shepherd et al 1995). Trials such as this have continued over subsequent years and prove the safety and efficacy of statins and a reduction in cardiovascular events following statin therapy (Athyros et al 2002, Downs et al 1998, Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group 1998, Sacks et al 1996). A more recent study examined people with type 2 diabetes who were therefore at high risk of developing CHD. It demonstrated Box 2. The lipid profile Total cholesterol Low-density lipoprotein cholesterol High-density lipoprotein cholesterol Triglycerides december 8/vol19/no13/2004 nursing standard 51

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that, regardless of cholesterol level, lowering cholesterol even further provides additional cardiovascular benefit to the patient (Colhoun et al 2004). A recent initiative, approved by the Medicines and Healthcare products Regulatory Agency (MHRA), has been launched to target people at moderate risk of CHD in the UK. This initiative aims to reduce their risk factors, including lowering blood cholesterol levels. Approval has been given for simvastatin 10mg (one of the statin drugs) to be dispensed by a pharmacist, following a pharmacy screening protocol, to all men and women where the risk of developing heart disease over the next ten years has been estimated as 10 per cent (moderate risk) (MHRA 2004a). Screening is offered to all men over 55 years of age, with no other risk factors for heart disease, to men 45-54 years of age and women over 55 years with one or more risk factors. These risk factors are determined as smoking, obesity, family history of premature death of CHD (before the age of 65 in female relatives and age 55 in male relatives) and people of South Asian origin (MHRA 2004a). Those who fit the criteria are offered lifestyle advice and a statin may be dispensed. If people do not fulfil the pharmacy screening protocol and are not offered the drug, they should still be offered appropriate lifestyle advice. If on screening, someone is identified as high risk he or she should be given lifestyle advice and encouraged to consult the GP for advice and management, as further investigation and treatment may be required. When using the pharmacy protocol, it is not essential to obtain the results of a cholesterol test before commencing the statin. However, to track how cholesterol levels are responding to the drug, which may be important to ensure continuation of the therapy, as well as to monitor its effectiveness, it may be useful to recommend that a cholesterol test is performed when therapy is started and possibly on a yearly basis afterwards. Statins do differ from each other in molecular structure and each has a slightly different mode of action. They may also have different side effects and cerivastatin was withdrawn, due to excess cases of rhabdomyolysis (muscle breakdown) caused by a previously unknown metabolic pathway. The pathway through which the drugs are metabolised is shown in Table 1, which also outlines variations in the reduction of total cholesterol and LDL cholesterol. It is thought prudent to use the appropriate statin for the patients risk profile and in these days of trying to achieve NHS targets (NHS 2004) some statin drugs are viewed as more able to achieve those targets than others. However, some patients cannot tolerate large doses of statins and this may influence the choice of drug prescribed. Recently, the manufacturers of rosuvastatin advised all prescribers to commence rosuvastatin at the starting dose of 10mg and titrate carefully, while patients requiring doses of 40mg and above should be supervised in specialist centres (MHRA 2004b). This advice was given as a result of several cases of rhabdomyolysis that had occurred at the higher dosage. Statins are safe and generally well tolerated (DoH 2000a, Minhas 2003, Sacks et al 1996, Shepherd et al 2002). The most common side effects are usually transient gastrointestinal disturbance, liver function test disturbance of unknown long-term significance (rare) and a spectrum of muscle-related side effects ranging from myalgia (common), muscle inflammation (myositis) to rhabdomyolysis, a potentially life-threatening event (BNF 2004). A number of risk factors for rhabdomyolysis have been identified: older age; lower body weight; hypothyroidism; concomitant therapy and other drugs, and it is therefore wise

Table 1. Profile of statins Drug Dose range Maximum change (%) LDL HDL TG 50 24 34 34 57 41 6 8 9 12 10 12 29 10 16 24 28 18 Lipophilic Metabolic pathway P450 Metabolism 3A4 2C9 3A4 unknown 2C9/2C19 3A4

Atorvastatin Fluvastatin Lovastatin* Pravastatin Rosuvastatin Simvastatin * Not available in the UK

10-80mg 20-80mg 20-80mg 10-40mg 10-40mg 10-80mg

Yes Yes Yes No No Yes

LDL = Low-density lipoprotein cholesterol; HDL = High-density lipoprotein cholesterol; TG = Triglycerides

(Reproduced with kind permission of Dr Michael Schachter, Department of Clinical Pharmacology, Imperial College, St Marys Hospital, London)

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to monitor patients in these categories more closely (BNF 2004). Historically, it was suggested that statin therapy should be taken at night, when the liver synthesises most of the cholesterol. However, the newer statins (atorvastatin and rosuvastatin) have long half-lives, remain in the bloodstream for longer and can therefore be taken at any time of the day. Statins are often perceived as first-line therapy after diet and other lifestyle changes. However, they are not the only drug available to lower cholesterol. There are several other products that can be used in combination with statins and in some cases alone to reduce cholesterol and the corresponding risk of CHD. A 10 per cent reduction in cholesterol leads to a 30 per cent reduction in risk of CHD (Law et al 1994). Other cholesterol-lowering products include nicotinic acid, fibrates, resins, omega-3 fish oils and ezetimibe. Nicotinic acid The main effect of nicotinic acid is to inhibit fatty acid release from fat cells in the body. This reduces the production and levels of LDL cholesterol to 17 per cent, while increasing levels of HDL cholesterol up to 26 per cent (Chapman et al 2004). Doses of 2mg per day are required. One of the major side effects of nicotinic therapy has been the severe flushing that accompanies the start of treatment. However, this has been addressed and newer formulations of nicotinic therapy have included a dose titration pack to minimise the side effects that may be experienced (Capuzzi et al 1998). Fibrates These drugs increase the number of LDL receptors in the liver and have a small effect on the clearance of LDL through the liver. Their greatest effect, however, is lowering very LDL (VLDL) and triglycerides. Fibrates have been safely used in combination with statin drugs in the past, although this has predominantly been in specialist centres where careful and frequent patient monitoring can take place (Frick et al 1987, Rubins et al 1999). Data are awaited from the FIELD trial (due to report in 2005) for more information about these drugs. Resins When cholesterol has been made it is stored in the bile ducts and mixed with food to aid digestion. Preventing the re-absorption of bile salts will reduce the amount of cholesterol that is mixed with the salts being reabsorbed. Hence the small reduction in cholesterol. However, resins are often unpalatable they are in powder form and are mixed with fruit juices or yoghurt and their unpleasant side effects of flatulence, constipation and diarrhoea often mean that patients are not keen to take them. They are, however, licensed for use in children. Their cholesterollowering ability is about 14 per cent. They should be used with caution in patients with raised triglycerides as they can exacerbate this problem (BNF 2004). Omega-3 fish oils The benefits of oily fish in reducing the risk of coronary heart disease are well documented (Stone 1996). However, two separate preparations of polyunsaturated fatty acids (PUFA fish oil supplements) known as Maxepa and Omacor are available on prescrip-

REFERENCES Allen J et al (2002) Nurse case management of hypercholesterolemia in patients with coronary heart disease: results of a randomized clinical trial. American Heart Journal. 144, 4, 678-686. American College of Sports Medicine (2000) ACSMs Guidelines for Exercise Testing and Prescriptions. Sixth edition. Philadelphia PA, Lippincott Williams and Wilkins. Assman G et al (1995) Epidemiological and clinical relevance of triglycerides and high-density cholesterol. Cardiovascular Risk Factors. 5, 1, 4-11. Athyros V et al (2002) Treatment with atorvastatin to the National Cholesterol Educational Program Goal versus usual care in secondary coronary heart disease prevention. The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. Current Medical Research and Opinion. 18, 4, 220-228. Bays H et al (2001) Effectiveness and tolerability of ezetimibe in patients with primary hypercholesterolemia: pooled analysis of two phase II studies. Clinical Therapeutics. 23, 8, 1209-1230. Blenkinsopp J (2004) Heart health: advising customers about OTC

simvastatin. Pharmacy Magazine. 10, 8, 25-31. British Heart Foundation (2004) BHF Statistics Website. www.heartstats.org (Last accessed: November 2 2004.) British Heart Foundation (2003) Coronary Heart Disease Statistics. London, BHF. British National Formulary (2004) British National Formulary No 48. London, British Medical Association and the Royal Pharmaceutical Society of Great Britain. British Nutrition Foundation (1999) Obesity: Report of the British Nutrition Foundation Task Force. Oxford, Blackwell Science. Callum C (1998) The Smoking Epidemic. London, Health Education Authority. Capuzzi D et al (1998) Efficacy and safety of an extended-release nicotinic acid (Niaspan): A long-term study. American Journal of Cardiology. 82, Suppl 12A, 74U-81U. Chapman M et al (2004) Raising high-density lipoprotein cholesterol with reduction of cardiovascular risk: the role of nicotinic acid. A position paper developed by the European Consensus Panel on HDL-C. Current Medical Research and Opinion. 20, 8, 1253-1268. Colhoun H et al (2004) Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin

Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet. 364, 9435, 685-696. Critchley J, Capewell S (2003) Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. Journal of the American Medical Association. 290, 1, 86-97. Cupples M, McKnight A (1999) Five-year follow up of patients at high cardiovascular risk who took part in randomised controlled trial of health promotion. British Medical Journal. 319, 7211, 687-688. Department of Health (2004) NHS Improvement Plan: Putting People at the Heart of Public Services. London, The Stationery Office. Department of Health (2001) Shifting the Balance of Power in the NHS: Securing Delivery. London, The Stationery Office. Department of Health (2000a) National Service Framework for Coronary Heart Disease. London, The Stationery Office. Department of Health (2000b) The NHS Plan: A Plan for Investment, A Plan for Reform. London, The Stationery Office. Department of Health (1999a) Making a Difference: Strengthening the Nursing, Midwifery and Health Visiting Contribution to Health and Health Care. London, The

Stationery Office. Department of Health (1999b) Health Survey for England 1998. London, The Stationery Office. Donahue R et al (1987) Central obesity and coronary heart disease in men. Lancet. 1, 8537, 821-824. Downs J et al (1998) Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study. Journal of the American Medical Association. 279, 20, 1615-1622. Ebrahim S, Davey Smith G (1999) Multiple risk factor interventions for primary prevention of coronary heart disease (Cochrane Review). The Cochrane Database of Systematic Reviews. Issue 2. Chichester, John Wiley and Sons. Frick M et al (1987) Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, incidence of coronary heart disease. New England Journal of Medicine. 317, 20, 1237-1245. Gordon D (2000) Cholesterol lowering reduces mortality. In Grundy S (Ed) Cholesterol-lowering Therapy: Evaluation of Clinical Trial Evidence. New York NY, Marcel Dekker.

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tion and can further enhance cholesterol lowering. The American Heart Association scientific statement on diet recommends that patients at risk of cardiovascular disease would benefit from 2-4mg of omega-3 fish oils per day (Kris-Etherton et al 2002). Ezetimibe This drug blocks the absorption of dietary and biliary cholesterol in the intestines. It works specifically at the brush border of the intestine. It can reduce cholesterol by up to 18 per cent (Bays et al 2001). There is a current licence application to launch a combination of ezetimibe and simvastatin in the next few months. Conclusion CHD remains a significant cause of death and disability throughout the western world. However, many of the risk factors for the development of the disease are modifiable through attention to lifestyle and diet. Additionally, newer drug therapies and the use of plant stanols and sterols can contribute to reducing blood cholesterol levels and thereby assist in the prevention and management of CHD. While much can be done to reduce risk factors for CHD in the community setting, the nurse has an important role to play in raising awareness of the risks of CHD and also in assisting people to make necessary lifestyle changes to minimise these risks

TIME OUT 5
Return to the start of the article and look at the learning outcomes. Reflect also on your aims at the beginning of this article. Write a short paragraph under each of the learning outcomes to indicate how you have achieved these outcomes.

TIME OUT 6
Now that you have completed the article, you might like to write a practice profile. Guidelines to help you are on page 56.

Han T et al (1997) Waist circumference reduction and cardiovascular benefits during weight loss in women. International Journal of Obesity and Related Metabolic Disorders. 21, 2, 127-134. Hebert P et al (1997) Cholesterol lowering with statin drugs, risk of stroke, and total mortality. An overview of randomized trials. Journal of the American Medical Association. 278, 4, 313-321. Kris-Etherton P et al (2002) Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 106, 21, 2747-2757. Law M et al (1994) By how much and how quickly does reduction in serum cholesterol concentration lower risk of ischaemic heart disease? British Medical Journal. 308, 6925, 367-372. Lean M et al (1995) Waist circumference as a measure for indicating need for weight management. British Medical Journal. 311, 6998, 158-161. Lindsay G, Gaw A (2004) Coronary Heart Disease Prevention: A Handbook for the Healthcare Team. Second edition. London, Churchill Livingstone. Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group (1998) Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. New England Journal of Medicine. 339, 19, 1349-1357. McTaggart F (2003) Comparative pharmacology of rosuvastatin. Atherosclerosis Supplements. 4, 1, 9-14. Meade T et al (1993) Fibrinolytic activity, clotting factors, and long-term

incidence of ischaemic heart disease in the Northwick Park Heart Study. Lancet. 342, 8879, 1076-1079. Medicines and Healthcare products Regulatory Agency (2004a) The Reclassification of Simvastatin 10mg (Zocor Heart-Pro) Over the Counter (OTC). http://medicines.mhra.gov.uk/ inforesources/publications/arm18 outcomeqa.pdf (Last accessed: November 25 2004.) Medicines and Healthcare products Regulatory Agency (2004b) New Prescribing Advice for the 40mg Dose of Crestor (rosuvastatin). http://medicines.mhra.gov.uk/ ourwork/monitorsafequalmed/ safetymessages/crestor_9604.htm (Last accessed: November 26 2004). Miettinen T et al (1995) Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population. New England Journal of Medicine. 333, 20, 1308-1312. Minhas R (2003) Current progress in lipid therapy. British Journal of Cardiology. 10, 1, 59-68. Moher M et al (2001) Cluster randomised controlled trial to compare three methods of promoting secondary prevention of coronary heart disease in primary care. British Medical Journal. 322, 7298, 1338-1342. Mukamal K et al (2001) Prior alcohol consumption and mortality following acute myocardial infarction. Journal of the American Medical Association. 285, 15, 1965-1970. Murchie P et al (2003) Secondary prevention clinics for coronary heart disease: four-year follow up of a randomised controlled trial in primary care. British Medical Journal. 326, 7380, 84.

National Health Service (2004) General Medical Services Contract Regulations. London, The Stationery Office. Puffer S, Rashidian A (2004) Practice nurses intentions to use clinical guidelines. Journal of Advanced Nursing. 47, 5, 500-509. Rubins H et al (1999) Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs Density Lipoprotein Cholesterol Intervention Trial Study Group. New England Journal of Medicine. 341, 6, 410-418. Sacks F et al (1996) The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. New England Journal of Medicine. 335, 14, 1001-1009. Samar A (1999) The pathogenesis of atherosclerosis. In Jairath N (Ed) Coronary Heart Disease and Risk Factor Management: A Nursing Perspective. Philadelphia PA, WB Saunders. Shepherd J et al (2002) Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet. 360, 9346, 1623-1630. Shepherd J et al (1995) Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. New England Journal of Medicine. 333, 20, 1301-1307. Stone N (1996) Fish consumption, fish oils, lipids and coronary heart disease. Circulation. 94, 9, 2337-2340.

Tang J et al (1998) Systematic review of dietary intervention trials to lower blood total cholesterol in free-living subjects. British Medical Journal. 316, 7139, 1213-1220. Tunstall-Pedoe H et al (1999) Contributions of trends in survival and coronary-event rates to changes in coronary heart disease mortality: 10-year results from 37 WHO MONICA project populations. Monitoring trends and determinants in cardiovascular disease. Lancet. 353, 9164, 1547-1557. Williams B et al (2004) Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004-BHS IV. Journal of Human Hypertension. 18, 3, 139-185. Wood D et al (1998) Joint British recommendations on prevention of coronary heart disease in clinical practice. British Cardiac Society, British Hyperlipidaemia Association, British Hypertension Society, endorsed by the British Diabetic Association. Heart. 80, Suppl 2, S1-S29. Wright F et al (2001) Patients and practice nurses perceptions of secondary preventive care for established ishaemic heart disease: a qualitative study. Journal of Clinical Nursing. 10, 2, 180-188. Yusuf S et al (2004) Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 364, 9438, 937-952. Yusuf S et al (2002) The global epidemic of atherosclerotic cardiovascular disease. Medical Principles and Practice. 11, Suppl 2, 3-8.

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