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National Collaborating Centre for Primary Care (UK). Lipid Modification: Cardiovascular Risk Assessment and the Modification of Blood Lipids for the Primary and Secondary Prevention of Cardiovascular Disease [Internet]. London: Royal College of General Practitioners (UK); 2008 May. (NICE Clinical Guidelines, No. 67.)

  • This publication is provided for historical reference only and the information may be out of date.

This publication is provided for historical reference only and the information may be out of date.

5Lifestyle modifications for the primary and secondary prevention of CVD

[Hyperlink to Introduction]

5.1. Recommendations for lifestyle

Cardioprotective diet

[Hyperlink to Evidence Statements & Narratives]

5.1.1.

People at high risk of or with CVD should be advised to eat a diet in which total fat intake is 30% or less of total energy intake, saturated fats are 10% or less of total energy intake, intake of dietary cholesterol is less than 300 mg/day and where possible saturated fats are replaced by monounsaturated and polyunsaturated fats. It may be helpful to suggest they look at http://www​.nhs.uk/Livewell​/healthy-eating​/Pages/Healthyeating.aspx for further practical advice.

5.1.2.

People at high risk of or with CVD should be advised to eat at least five portions of fruit and vegetables per day, in line with national guidance for the general population. Examples of what constitutes a portion can be found at http://www​.nhs.uk/Livewell​/healthy-eating​/Pages/Healthyeating.aspx and www​.5aday.nhs.uk

5.1.3.

People at high risk of or with CVD should be advised to consume at least two portions of fish per week, including a portion of oily fish. Further information and advice on healthy cooking methods can be found at http://www​.nhs.uk/Livewell​/healthy-eating​/Pages/Healthyeating.aspx

5.1.4.

Pregnant women should be advised to limit their oily fish to no more than two portions per week. Further information and advice on oily fish consumption can be found at http://www​.nhs.uk/Livewell​/healthy-eating​/Pages/Healthyeating.aspx

5.1.5.

People should not routinely be recommended to take omega-3 fatty acid supplements for the primary prevention of CVD.

Plant stanols and sterols recommendations

[Hyperlink to Evidence Statements & Narratives]

5.1.6.

People should not routinely be recommended to take plant sterols and stanols for the primary prevention of CVD.

Physical activity

[Hyperlink to Evidence Statements & Narratives]

5.1.7.

People at high risk of or with CVD should be advised to take 30 minutes of physical activity a day, of at least moderate intensity, at least 5 days a week, in line with national guidance for the general population10.

5.1.8.

People who are unable to perform moderate-intensity physical activity at least 5 days a week because of comorbidity, medical conditions or personal circumstances should be encouraged to exercise at their maximum safe capacity.

5.1.9.

Recommended types of physical activity include those that can be incorporated into everyday life, such as brisk walking, using stairs and cycling (see ‘At least five a week’)16.

5.1.10.

People should be advised that bouts of physical activity of 10 minutes or more accumulated throughout the day are as effective as longer sessions (see ‘At least five a week’)16.

5.1.11.

Advice about physical activity should take into account the person’s needs, preferences and circumstances. Goals should be agreed and the person should be provided with written information about the benefits of activity and local opportunities to be active, in line with ‘Physical activity’ (NICE public health intervention guidance 2).

Combined interventions (diet and physical activity)

[Hyperlink to Evidence Statements & Narratives]

5.1.12.

Advice on diet11 and physical activity12 should be given in line with national recommendations.

Weight management

[Hyperlink to Evidence Statements & Narratives]

5.1.13.

People at high risk of or with CVD who are overweight or obese should be offered appropriate advice and support to work towards achieving and maintaining a healthy weight in line with ‘Obesity’ (NICE clinical guideline 43).

Alcohol consumption

[Hyperlink to Evidence Statements & Narratives]

5.1.14.

Alcohol consumption for men should be limited to up to 3–4 units a day. For women, alcohol consumption should be limited to up to 2–3 units a day. People should avoid binge drinking. Further information can be found at http://www​.nhs.uk/Livewell​/healthy-eating​/Pages/Healthyeating.aspx.

Smoking cessation

[Hyperlink to Evidence Statements & Narratives]

5.1.15.

All people who smoke should be advised to stop, in line with ‘Smoking cessation services’ (NICE public health guidance 10).

5.1.16.

People who want to stop smoking should be offered support and advice, and referral to an intensive support service (for example, the NHS Stop Smoking Services).

5.1.17.

If a person is unable or unwilling to accept a referral to an intensive support service they should be offered pharmacotherapy in line with ‘ Smoking cessation services’ (NICE public health guidance 10) and ‘Varenicline for smoking cessation’ (NICE technology appraisal guidance 123).

5.2. Introduction – lifestyle modification for the primary and secondary prevention of CVD

There is a substantive and consistent body of epidemiological, physiological and observational evidence demonstrating that changes in diet modify blood lipids and other risk factors and that these changes are associated with reductions in morbidity and mortality from CVD. Similarly epidemiological, physiological and observational evidence supports the association between cardiovascular health and levels of moderate or greater physical activity and associates a sedentary lifestyle with increased cardiovascular risk.

It is difficult to design, fund or organise randomised trials sufficiently large and rigorous that can yield evidence for the effect of diet, physical activity, smoking cessation or multifactorial lifestyle interventions on cardiovascular events. The observational literature on diet, dietary modification and physical activity provides a large body of evidence that has been periodically reviewed for major national initiatives. It is beyond the resources of this guideline to attempt such a review and we have referenced national reports and systematic reviews and cross referred to appropriate national advice.

To maintain consistency of reporting across both pharmacological and lifestyle interventions, we have limited formal searches for evidence to randomised trials with outcomes that include cardiovascular events. Such studies are few and we are acutely aware that this limited trial evidence does not adequately reflect either the strength or breadth of evidence that can be derived from epidemiology and other observational work.

The 1976 Doll and Peto study based on 20 years observation of smoking among British doctors (Doll, R. and Peto, R., 1976) remains a seminal descriptor of a clearly defined and modifiable risk factor. The 50 year prospective follow up study (1951 to 2001) showed that men born between 1900 and 1930 who continued to smoke cigarettes died on average about 10 years younger than those who were lifelong non smokers, while those who stopped at around 60, 50, 40 or 30 gained, respectively, on average 3, 6, 9, or 10 years of life expectancy compared with those who continued (Doll, R. and Peto, R., 1976). For men born between 1900 and 1930, the absolute difference between cigarette smokers and non smokers in the probability of death in middle age increased from 18% (42% versus 24%, a twofold death rate ratio) for those born in the first decade of the century, and for those born in the second decade the probability of death increased to 28% (43% versus 15%, a threefold death rate ratio) (Doll, R. and Peto, R., 1976). The authors concluded that among men born around 1920 prolonged cigarette smoking from an early adult age tripled age specific mortality rates, but at age 50 halved the hazard and at age 30 avoided almost all of it (Doll, R. and Peto, R., 1976).

There is extensive and robust trial evidence that smoking cessation programmes are effective in reducing smoking (Wu, P., Wilson, K., Dimoulas, P. et al, 2006). However, no randomised controlled trials with cardiovascular outcomes resulting from smoking cessation have ever been conducted, though there is clear evidence from observational studies that smoking cessation is associated with 40% lower morbidity and mortality (Aberg, A., Bergstrand, R., Johansson, S. et al, 1983). Differences in the prevalence of smoking between the higher and lower social classes has been estimated to account for over half the difference in the risk of premature death faced by these groups (Jha, P., Peto, R., Zatonski, W. et al, 2006). Consumption of tobacco in forms other than smoking should also be noted. High consumption of alcohol is also associated with substantially increased rates of coronary heart disease and all cause mortality (Emberson, J. R., Shaper, A. G., Wannamethee, S. G. et al, 2005).

For secondary prevention most trial evidence relates to patients following myocardial infarction and that evidence is covered in the NICE guideline: ‘Myocardial infarction: Secondary prevention in primary and secondary care for patients following a myocardial infarction’, CG48 (2007) http://guidance.nice.org.uk/CG48. Trial literature is almost completely absent for lifestyle interventions in secondary prevention of stroke and peripheral arterial disease.

5.3. Cardioprotective dietary advice

[Return to Recommendations]

5.3.1. Evidence statements for cardioprotective dietary advice

Low fat diet

5.3.1.1.

No randomised controlled trials were identified in people at high risk of CVD that compared low fat diet with usual diet for the outcomes mortality or morbidity.

5.3.1.2.

One small randomised controlled trial in people at high risk of CVD with elevated cholesterol and triglycerides found that advice to reduce consumption of fat, sugar and alcohol was associated with reduction in total cholesterol and fasting triglycerides compared with control.

5.3.1.3.

In patients with suspected CHD, one small randomised controlled trial found that adopting a lipid–lowering diet reduced total cardiac events compared to usual care but did not confer any benefit for the outcomes of cardiovascular mortality, MI, stroke, coronary surgery or angioplasty. Lipid–lowering diet was associated with decreased total and LDL cholesterol compared to baseline levels.

5.3.1.4.

No randomised controlled trials were identified that compared low fat diet with usual diet in patients with peripheral arterial disease or following stroke.

Increased fruit and vegetable diet

5.3.1.5.

No randomised controlled trials were identified that compared increased fruit and vegetables diet with usual diet in people at high risk of CVD.

5.3.1.6.

One randomised controlled trial in patients with angina found that advice to increase consumption of fruit and vegetables was not associated with a reduction in all cause mortality, cardiac death or sudden death compared with advice to eat sensibly.

5.3.1.7.

No randomised controlled trials were identified that compared increased fruit and vegetables diet with usual diet in patients with peripheral arterial disease or following stroke.

5.3.1.8.

One randomised controlled trial in patients with angina found that advice to eat oily fish or take omega 3 fatty acid supplements was not associated with a reduction all cause mortality or cardiac death.

5.3.1.9.

One randomised controlled trial in hypercholesterolemic people without and with coronary artery disease found that omega 3 fatty acid supplements was associated with a reduction in the primary outcome of any major cardiovascular event, and the secondary outcomes of unstable angina and non fatal coronary events (HR 0.81, 95%CI 0.68 to 0.96)

5.3.2. Clinical effectiveness of low fat diets for the primary prevention of CVD

No randomised controlled trials were identified in people at high risk of CVD that examined the effectiveness of low fat diet versus no change in diet for the outcomes of all cause mortality, cardiovascular mortality or cardiovascular morbidity.

One small randomised controlled trial was identified on the effectiveness of low fat diet versus no change in diet to modify lipid profiles in people at high risk of CVD (Hjerkinn, E. M., Sandvik, L., Hjermann, I. et al, 2004).

The participants in this trial were a sub-sample from a population of 1232 men aged 40–49 years selected for a previous study (Hjermann, I., Velve, Byre K., Holme, I. et al, 1981) according to the following criteria: mean serum cholesterol = 7.5 to 9.8 mmol/l, coronary risk scores (based on cholesterol, smoking and BP) in the upper quartile of the distribution and systolic BP < 150 mmHg. The sub-sample of 104 men were further selected for this trial (Hjerkinn, E. M., Sandvik, L., Hjermann, I. et al, 2004) if fasting triglycerides > 2.5 mmol/l.

A total of 104 men were randomised to either the intervention group which received dietary advice over a five year period or to the control who received no advice.

Participants in the dietary intervention group were given advice to reduce total energy intake (mainly by reducing sugar, alcohol and fat), reduce saturated fat consumption and slightly increase polyunsaturated fat consumption. Participants in the intervention group also received anti-smoking advice.

After five years, the dietary intervention was found to be associated with a reduction in total cholesterol (−10.5%, 95% CI −1.5% to −11.7%) and fasting triglycerides (− 27.2, 95% CI −0.1% to −27.4%) compared with control (Hjerkinn, E. M., Sandvik, L., Hjermann, I. et al, 2004).

5.3.3. Evidence into recommendations

Due to the lack of clinical outcome data in this trial, its small size and problems with generalisibility, it was decided by the GDG that it should be excluded and that recommendations made in the Joint British Societies’ guidelines on prevention of CVD in clinical practice (Wood, D., Wray, R., Poulter, N. et al, 2005) would be adopted (total fat intake should be ≤ 30% of total energy intake and saturated fats should comprise ≤ 10% of total energy intake). These targets are slightly lower for total fat than those set by the Department of Heath for the general population (total fat ≤ 35% of total energy intake and saturated fats ≤ 10% of total energy intake) (Department of Health, 2005).

5.3.4. Clinical effectiveness of low fat diets for the secondary prevention of CVD

One randomised controlled trial was identified in patients with a history of CVD that compared advice to adopt a low fat diet with no dietary advice (Watts, G. F., Lewis, B., Brunt, J. N. et al, 1992). This trial recruited men referred for coronary angioplasty to investigate angina pectoris, or other findings suggestive of coronary heart disease (CHD) (70% with angina, 45% with a history of MI). A total of 90 participants were randomised to one of three groups; usual care, lipid-lowering diet, or lipid-lowering diet plus cholestyramine therapy. Patients in the lipid–lowering diet and lipid–lowering diet plus cholestyramine therapy groups were given the following advice by a dietician: to reduce total fat intake to 27% of dietary energy, to reduce saturated fat intake to 8–10% of dietary energy, to reduce dietary cholesterol to 100 mg/1000 kcal, to increase omega 3 and 6 fatty acid intake to 8% of dietary energy, and to increase fibre intake. Participants were followed up for a mean duration of 39 months.

Lipid–lowering diet did not confer any benefit over usual care for the outcomes of cardiovascular death, MI, coronary surgery, angioplasty or stroke. Lipid–lowering diet did, however, reduce total cardiac events compared with usual care 10/28 (36%) lipid-lowering diet versus 3/27 (11%) usual care) (P < 0.05)) and improve the severity of angina symptoms (P < 0.01 lipid-lowering diet versus usual care). Participants in the lipid-lowering diet group had lower total and LDL cholesterol levels at the end of the trial (39 months) compared with their baseline levels (P < 0.01), while there was no change in HDL cholesterol (Watts, G. F., Lewis, B., Brunt, J. N. et al, 1992).

5.3.5. Evidence into recommendations

This randomised controlled trial recruited small numbers and was the only trial identified in patients with angina, stroke or peripheral arterial disease. The GDG decided to adopt recommendations made in the Joint British Societies’ guidelines on prevention of CVD in clinical practice (Wood, D., Wray, R., Poulter, N. et al, 2005) which recommends that total fat intake should be 30% or less of total energy intake and saturated fats should comprise 10% or less of total energy intake. These targets are slightly lower for total fat than those set by the Department of Heath for the general population (total fat ≤ 35% of total energy intake and saturated fats ≤ 10% of total energy intake) (Department of Health, 2005)

5.3.6. Clinical effectiveness of increased fruit and vegetables diet for the primary prevention of CVD

No randomised controlled trials were identified that compared increased fruit and vegetables diet with usual diet in people at high risk of CVD.

5.3.7. Evidence into recommendations

The GDG decided to recommend five portions of fruit and vegetables per day in line with advice given to the general population. For further information, please refer to the Department of Health’s website: 5aday.nhs.uk, and the Food Standards Agency website: http://www.nhs.uk/Livewell/healthy-eating/Pages/Healthyeating.aspx.

5.3.8. Clinical effectiveness of increased fruit and vegetables diet for the secondary prevention of CVD

One randomised controlled trial was identified in patients with a history of CVD that compared advice to increase fruit and vegetables versus non specific dietary advice (Burr, M. L., shfield-Watt, P. A., Dunstan, F. D. et al, 2003). This trial recruited men under the age of 70 who were being treated for angina (50% also had a prior MI). Recruitment occurred in two phases: Phase I was between 1990 and 1992 and phase II between 1993 and 1996, follow up was in 1999. A total of 3114 participants were randomised to one of four groups:

  1. Advice to eat at least 2 portions of oily fish per week or take up to 3 ‘MaxEPA’ fish oil capsules daily (each capsule contains 170 mg EPA and 115 mg DHA) as a partial or total substitute. In the first phase of the study, participants chose diet or capsules or a mixture, in the second phase, participants were sub randomised to receive dietary advice or fish oil capsules.
  2. Advice to eat 4–5 portions of fruit and vegetables, to drink one glass of orange juice daily and to increase intake of soluble fibre in the form of oats.
  3. A combination of 1. and 2.
  4. ‘Sensible eating’ – non-specific advice that did not include either of the above interventions.

Advice to increase consumption of fruit and vegetables was found to be poorly complied with and the advice did not confer any benefit on mortality (all deaths, cardiac deaths and sudden deaths) compared with ‘sensible eating’.

5.3.9. Evidence into recommendations

Only one randomised controlled trial found on the effectiveness of an increased fruit and vegetables diet in patients with angina (Burr, M. L., shfield-Watt, P. A., Dunstan, F. D. et al, 2003) and no randomised controlled trials were identified in patients with peripheral arterial disease or following stroke. The GDG decided to recommend five portions of fruit and vegetables per day in line with advice given to the general population. For further information, please refer to the Department of Health paper ‘Choosing a Better Diet: a food and health action plan’ (Department of Health, 2005), the Department of Health’s website: 5aday.nhs.uk, the COMA report ‘Nutritional Aspects of Cardiovascular Disease’ (de la Hunty, A., 1995) and the Food Standards Agency website (http://www.nhs.uk/Livewell/healthy-eating/Pages/Healthyeating.aspx) (Food Standards Agency, 2007).

5.3.10. Clinical effectiveness of increased omega 3 fatty acids (dietary or supplementation) for the primary prevention of CVD

One randomised controlled trial was identified that examined the effect of omega 3 fatty acid supplements in Japanese hypercholesterolaemia patients (18 645) without and with coronary artery disease (26% of the total number of recruits in the study, of which 21% had a prior history of MI, 61% had angina and 18% were recruited following revascularisation) (Yokoyama, M., Origasa, H., Matsuzaki, M. et al, 2007). Patients in the intervention group were given omega 3 fatty acid supplements (1800 mg/day) plus a statin, either pravastatin (average dose 10 mg/day) or simvastatin (5.6 mg/day). Patients in the control group received a statin alone, either pravastatin (average dose 10 mg/day) or simvastatin (5.6 mg/day). At a mean follow up of 4.6 years and for patients with and without coronary artery disease, omega 3 fatty acid supplementation was associated with a reduction in the primary outcome of any major coronary event (including sudden death, fatal and non fatal MI, unstable angina, angioplasty, stenting and CABG) (HR 0.81, 95%CI 0.69 to 0.95). Omega 3 fatty acid supplementation was associated with a reduction in the secondary outcomes of unstable angina (HR 0.76, 95%CI 0.62 to 0.95) and non fatal coronary events (HR 0.81, 95%CI 0.68 to 0.96) Omega 3 fatty acid supplementation did not confer any benefit compared with no supplementation for the following secondary outcomes; sudden death, fatal MI, non fatal MI, CABG or PTCA, coronary death or MI, fatal MI or non fatal MI, and coronary death (Yokoyama, M., Origasa, H., Matsuzaki, M. et al, 2007).

Analysis of the results for patients without coronary artery disease found that omega 3 fatty acid supplementation had no effect on the primary outcome, or any of the secondary outcomes compared with no supplementation. Analysis of the results of omega 3 fatty acid supplementation in the patients with coronary artery disease for the primary outcome of any major coronary event gave a hazard ratio of 0.82 (95%CI 0.657 to 0.998) compared with no supplementation. Unstable angina was reduced in the coronary artery disease population allocated to omega 3 supplementation unstable angina (HR 0.72, 95%CI 0.55 to 0.95) (Yokoyama, M., Origasa, H., Matsuzaki, M. et al, 2007).

5.3.11. Evidence into recommendations

The GDG considered that for dietary fish, the recommendations made by the Joint British Societies’ guidelines on prevention of CVD in clinical practice (Wood, D., Wray, R., Poulter, N. et al, 2005) should be adopted, which recommends at least two servings of omega-3 fatty acid containing fish per week. The GDG decided that there was insufficient evidence to recommend omega 3 fatty acid supplementation for people at high risk of CVD.

5.3.12. Clinical effectiveness of increased omega 3 fatty acids (dietary or supplementation) for the secondary prevention of CVD

One randomised controlled trial was identified in patients with a history of CVD which compared increased consumption of oily fish or taking omega 3 fatty acid supplements versus no change in diet (Burr, M. L., shfield-Watt, P. A., Dunstan, F. D. et al, 2003). This trial has previously been described in the section on clinical effectiveness of increased fruit and vegetables diet for the secondary prevention of CVD. Trial participants were men under the age of 70 who were being treated for angina (50% also had a prior MI). A total of 3114 participants were randomised to one of four groups:

  1. Advice to eat at least 2 portions of oily fish per week or take up to 3 ‘MaxEPA’ fish oil capsules daily (each capsule contains 170 mg EPA and 115 mg DHA) as a partial or total substitute. In the first phase of the study, participants chose diet or capsules or a mixture, in the second phase, participants were sub randomised to receive dietary advice or fish oil capsules.
  2. Advice to eat 4–5 portions of fruit and vegetables, to drink one glass of orange juice daily and to increase intake of soluble fibre in the form of oats.
  3. A combination of 1. and 2.
  4. ‘Sensible eating’ – non-specific advice that did not include either of the above interventions.

Four way analysis found that advice to eat oily fish or take supplements was not associated with a significant change in total number of deaths, number of cardiac deaths or number of sudden deaths compared with the control group who were told to ‘eat sensibly’.

Two way analysis comparing ‘all fish advice’ (intervention groups 1 and 3) with ‘no fish advice’ (intervention group 2 and control group 4) found that advice to eat oily fish or take supplements was not associated with a change in the total number of deaths but was associated with an increase in the number of cardiac deaths (11.5% ‘all fish advice’ versus 9.0% ‘no fish advice’, P = 0.02) and number of sudden deaths (4.6% ‘all fish advice’ versus 3% ‘no fish advice’, P = 0.02).

Adjusted hazard ratios were calculated for ‘all fish advice’ (intervention groups 1 and 3) compared to ‘no fish advice’ (intervention group 2 and control group 4). ‘All fish advice’ was found to be associated with an increase in the risk of sudden death (HR 1.54, 95% CI 1.06 to 2.23) compared with ‘no fish advice’ but no change was observed for total or cardiac mortality.

A subgroup analysis was performed and adjusted hazard ratios were calculated separately for those given fish advice (intervention groups 1 and 3) who were sub-randomised to receive omega 3 fatty acid supplements (a subset of 462 patients were sub-randomised to this treatment during the second phase of recruitment) and all others given ‘fish advice’ who were not sub randomised (n = 1109) compared with ‘no fish advice’ (intervention group 2 and control group 4). It was found that those sub randomised to receive omega 3 fatty acid supplements during the second phase of the trial had an increased risk of cardiac death (HR 1.45, 95% CI 1.05 to 1.99) and sudden death (HR 1.84, 95% CI 1.11 to 3.05) compared with those randomised to receive ‘no fish advice’ throughout the trial. All other participants who received ‘fish advice’ (intervention groups 1 and 3) but were not sub randomised to receive supplements were not found to have an increased risk of total mortality, cardiac mortality or sudden death compared with ‘no fish advice’. It should be noted that this was a post hoc subgroup analysis, and the results should be interpreted with caution because the patient numbers in the analysis indicate that the analysis is statistically underpowered.

A second randomised controlled trial was identified that examined the effect of omega 3 fatty acid supplements in Japanese hypercholesterolaemia patients (18 645) without and with coronary artery disease. Patients with coronary artery disease accounted for 26% of the total number of participants in the study, and 21% had a prior history of MI, 61% had angina and 18% were recruited following revascularisation) (Yokoyama, M., Origasa, H., Matsuzaki, M. et al, 2007). This study has been described in the section on clinical effectiveness of increased omega 3 fatty acids (dietary or supplementation) for the primary prevention of CVD. Patients in the intervention group were given omega 3 fatty acid supplements (1800 mg/day) plus a statin either pravastatin (average dose 10 mg/day) or simvastatin (5.6 mg/day). Patients in the control group received a statin alone, either pravastatin (average dose 10 mg/day) or simvastatin (5.6 mg/day). Analysis of the results of omega 3 fatty acid supplementation in the patients with coronary artery disease for the primary outcome of any major coronary event gave a hazard ratio of 0.82 (95%CI 0.657 to 0.998) compared with no supplementation. Unstable angina was reduced in the coronary artery disease population allocated to omega 3 supplementation unstable angina (HR 0.72, 95%CI 0.55 to 0.95).

5.3.13. Evidence into recommendations

Due to the conflicting results of the two studies described for oily fish consumption/omega 3 fatty acid supplementation (Burr, M. L., shfield-Watt, P. A., Dunstan, F. D. et al, 2003) (Yokoyama, M., Origasa, H., Matsuzaki, M. et al, 2007), and the lack of evidence for patients with peripheral arterial disease or following stroke, the GDG considered that for dietary fish, the recommendations made by the Joint British Societies’ guidelines on prevention of CVD in clinical practice (2005) (Wood, D., Wray, R., Poulter, N. et al, 2005) should be adopted, which recommends at least two servings of omega-3 fatty acid containing fish per week. The GDG decided that there was insufficient evidence to recommend omega 3 fatty acid supplementation in patients with angina, peripheral arterial disease or stroke.

5.4. Plant stanols and sterols

[Return to Recommendations]

5.4.1. Evidence statements for plants stanols and sterols

5.4.1.1.

No randomised controlled trials were identified in people at high risk of CVD that compared giving plant stanols and sterols with usual diet for the outcomes of mortality or morbidity.

5.4.1.2.

No randomised controlled trials with cardiovascular endpoints were identified that compared giving plant stanols or sterols with usual diet in patients with CVD

5.4.2. Evidence into recommendations

No randomised controlled trials were identified which examined the effectiveness of plant stanols and sterols in primary and secondary prevention with respect to cardiovascular outcomes. The GDG therefore decided that there was insufficient evidence to recommend their use.

5.5. Regular physical activity

[Return to Recommendations]

5.5.1. Evidence Statements for physical activity

5.5.1.1.

No randomised controlled trials were identified in people at high risk of CVD that compared regular physical activity with sedentary lifestyle for the outcomes mortality or morbidity.

5.5.1.2.

Two studies found that programmes to increase physical activities were cost effective compared to no exercise programmes in improving outcomes for people at risk of CVD.

5.5.1.3.

No randomised controlled trials were identified in patients with angina, peripheral arterial disease or following stroke that compared regular physical activity with sedentary lifestyle for the outcomes of mortality or morbidity.

5.5.1.4.

In selected patients after an MI, randomisation to an exercise prescription programme reduced the risk of death from MI after 3 years, but not all cause or cardiovascular mortality.

5.5.1.5.

In selected patients after an MI, exercise performed at a level sufficient to increase physical work reduced all cause mortality and cardiovascular mortality in long term follow up.

5.5.1.6.

One small randomised controlled trial in patients with stable intermittent claudication showed that physical training classes were not associated with a reduction in total cholesterol or triglyceride levels compared with usual care.

5.5.1.7.

Two cost effectiveness studies concluded that exercise programmes are cost effective compared to no exercise programme in patients with CHD.

5.5.2. Clinical effectiveness of regular physical activity for the primary prevention of CVD

No randomised controlled trials were identified in people at high risk of CVD that examined the effectiveness of regular physical activity versus sedentary lifestyle for the outcomes of all cause mortality, cardiovascular mortality or cardiovascular morbidity.

5.5.3. Cost effectiveness of regular physical activity for the primary prevention of CVD

Two studies were found which addressed this question, one Canadian (Lowensteyn, I., Coupal, L., Zowall, H. et al, 2000) and one American (Marshall, T., Bryan, S., Gill, P. et al, 2005). None of the studies were done in the UK.

Study (Marshall, T., Bryan, S., Gill, P. et al, 2005) was a cost utility analysis which used effectiveness data from the Framingham study. It was not clear as to the sources of the utility data they used in their decision model however it did use appropriate methodology. The authors did not provide resource use and quantities separately which makes it difficult to reproduce their work.

The authors reported that exercise resulted in 529.8 discounted QALYs over the 30 year follow up. Cost/QALY gained was $1395/QALY. A range of univariate sensitivity analyses were done, and the model was robust to all changes in assumptions that were tested.

The second study (Lowensteyn, I., Coupal, L., Zowall, H. et al, 2000) was a cost effectiveness which used effectiveness data from a number of different studies published between 1980 and 1999. The authors were very detailed in their reporting and references were provided. Resource use and quantities were provided separately.

The authors reported results separately for men and women and stratified results into three age groups. The results showed that exercise, especially unsupervised exercise was a cost effective intervention compared to no exercise. The benefits were more for younger men and less in the elderly man and women. The cost per life year gained ranged between $645/LYG for the 35–54year age group in unsupervised men to $30704 in the 65–74 year age group attending supervised sessions. For women the incremental cost effectiveness ratios for women ranged between $4915 to $ 87166 respectively.

In conclusion, a programme to increase physical activity compared to no programme is cost effective in improving outcomes for people at risk of CVD. The results from the two studies showed that younger men benefit more from such programmes than older men and women. Results also showed that unsupervised activity is more cost effective than supervised classes. This however depended on the assumption that there is almost 100% adherence to the exercise programme.

5.5.4. Evidence into recommendations

Due to the lack of clinical outcome data, it was decided by the GDG that recommendations would be made based on those of the following documents:

These guidelines recommend that thirty minutes of at least moderate intensity activity should be taken per day, at least five days a week. The chief medical officer’s report (ref) describes what is meant by moderate intensity activity: A person who is doing moderate intensity activity will usually experience:

  • An increase in breathing rate
  • An increase in heart rate, to the level where the pulse can be felt, and
  • A feeling of increased warmth, possibly accompanied by sweating on hot or humid days.

Also, a bout of moderate intensity activity can be continued for many minutes without a feeling of exhaustion.

The typical activity pattern of a moderately active person would include doing one or more of the following:

  • Regular active commuting on foot or by bicycle
  • Regular work related physical tasks
  • Regular household and garden activities
  • Regular active recreation or social sport at moderate intensity.

Examples of the intensities and energy expenditures for common types of physical activity are given in Table 1.

Table 1. Intensities and energy expenditures for common types of physical activity.

Table 1

Intensities and energy expenditures for common types of physical activity.

The Chief Medical Officer’s report also provides useful information on the potential risks associated with physical activity. It stresses that the risks associated with taking part in physical activity at levels that promote health are low and that the health benefits far outweigh the risks. The report states that the greatest risks in terms of sustaining sports injuries are faced by:

  • People who take part in vigorous sports and exercise
  • People to do ‘excessive’ amounts of exercise, and
  • People with existing musculoskeletal disease or at high risk of disease.

In relation to cardiovascular risk, the report states that ‘extremely rarely, inactive and unfit individuals who start doing vigorous physical activity may face increased cardiovascular risks’. In addition, it states that vigorous levels of activity may increase the risk of heart attack, although this increased risk appears to only apply to men with high blood pressure and is largely limited to people who do not exercise regularly.

5.5.5. Clinical effectiveness of regular physical activity for primary and secondary prevention of CVD

No randomised controlled trials were identified in patients with a history of angina alone, stroke, or peripheral arterial disease that examined the effect of regular physical activity versus a sedentary lifestyle for the outcomes of all cause mortality, cardiovascular mortality or cardiovascular morbidity.

One randomised controlled trial was identified on the effectiveness of regular physical activity versus sedentary lifestyle to modify lipid profiles in patients with a history of stable intermittent claudication for at least six months (Gelin, J., Jivegard, L., Taft, C. et al, 2001). The trial recruited men and women from a regional cohort of 400 to 500 people. A total of 264 participants were randomised to one of three groups:

  1. Usual care
  2. Physical training classes (a program of 3 × 30 minute sessions of specific walking training per week for the first six months, supervised by a physiotherapist. From 6 months to 1 year, 2 sessions per week were offered)
  3. Invasive treatment (endovascular or open surgical procedure).

Participants were then followed up for 1 year. Physical training classes did not confer any benefit over usual care for the primary outcome of maximum exercise power in Watts or for the secondary physiological endpoints. Total cholesterol and triglycerides were measured at randomisation and at 1 year and there were no differences between the physical training class and usual care groups. In addition, no difference in the number of deaths was seen between groups however, this was not a pre-specified outcome measure.

Due to the lack of clinical outcome data in this trial, it was decided by the GDG to consider evidence used in the NICE guidance: ‘Myocardial infarction: Secondary prevention in primary and secondary care for patients following a myocardial infarction’, CG48 (2007)

Two studies were identified which examined the impact of regular physical activity to improve outcome in patients with a prior MI. The first study was a randomised controlled trial in 651 men, aged 35 to 64 years with a documented MI greater than or equal to 8 weeks but less than 3 years before recruitment conducted between 1976 and 1979 (Naughton, J., Dorn, J., and Imamura, D., 2000).

The exercise intervention was an individualised exercise prescription based on the patient’s ECG-monitored treadmill multistage graded test (MSET). An exercise target heart rate guided the prescription and was determined as 85% of the peak rate achieved on the MSET. This group performed brisk physical activity in the laboratory for 8 weeks (1 hour per day, 3 times per week). After 8 weeks, participants exercised in a gymnasium or swimming pool (15 minutes cardiac exercise followed by 25 minutes of recreational games). Participants were encouraged to attend 3 sessions per week. Patients in the control group were told to maintain their normal routine but not to participate in any regular exercise.

At the 3 year follow up, randomisation to the exercise prescription programme was found to be associated with a reduction in death from MI (RR 0.13, 95% CI 0.02 to 0.78) compared with control. The exercise intervention was not associated with a reduction in all cause mortality (RR 0.63, 95% CI 0.32 to 1.15) or cardiovascular mortality (RR 0.71, 95% CI 0.34 to 1.33) compared with control. The authors noted that by the end of the trial 23% of the treatment group had stopped attending exercise sessions, whereas 31% of the control group reported that they were exercising regularly (Naughton, J., Dorn, J., and Imamura, D., 2000). A secondary analysis of this data (Dorn, J., Naughton, J., Imamura, D. et al, 1999) presented age- adjusted risk ratios and it was found that at the 3 year follow up point, the exercise intervention was associated with a reduction in all cause mortality (0.86, 95% CI 0.76 to 0.98) but not CVD mortality (0.87, 95% CI 0.74 to 1.02) compared with control.

After 3 years of the trial, the patients were followed up for 5, 10, 15 and 19 years examining all cause mortality and cardiovascular mortality. The results of this follow - up were published in the second study (Dorn, J., Naughton, J., Imamura, D. et al, 1999) which was a secondary analysis of the first study. For long term follow up at 5, 10, 15 and 19 years, the age adjusted relative risk reductions for all cause mortality were 0.91 (95% CI 0.82 to1.00), 0.88 (95% CI 0.83 to 0.95), 0.89 (95% CI 0.84 to 0.95) and 0.92 (95% CI 0.87 to 0.97), respectively for the exercise prescription programme compared with control. For long term follow up at 5, 10, 15 and 19 years, the age adjusted relative risk reductions for CVD mortality were 0.91 (95% CI 0.81 to 1.03), 0.89 (95% CI 0.82 to 0.96), 0.89 (95% CI 0.82 to 0.96) and 0.93 (95% CI 0.87 to 0.99), respectively for the exercise prescription programme compared with control.

Thus, improvement in physical work capacity resulted in consistent survival benefits throughout the full 19 years. The authors concluded that exercise performed at a level sufficient to increase physical work capacity may have long-term survival benefits in MI survivors.

5.5.6. Evidence into recommendations

It was decided by the GDG that recommendations would be made based on those of the Chief Medical Officer’s report ‘At least five a week: Evidence on the impact of physical activity and its relationship to health’ (Department of Health., 2004) and the NICE public health intervention guidance no. 2 ‘Four commonly used methods to increase physical activity: brief interventions in primary care, exercise referral schemes, pedometers and community-based exercise programmes for walking and cycling’ (National Institute for Health and Clinical Excellence, 2006) and the Joint British societies’ guidelines on prevention of CVD in clinical practice (Wood, D., Wray, R., Poulter, N. et al, 2005).

Please refer to chapter 5 (lifestyle for the primary prevention of CVD) for further details of the Chief Medical Officer’s report and see the full report at www.dh.gov.uk.

5.6. Combined cardioprotective dietary advice and regular physical activity (primary prevention of CVD)

[Return to Recommendations]

5.6.1. Evidence statements for combined cardioprotective dietary advice and regular physical activity

5.6.1.1.

No randomised controlled trials were identified in people at high risk of CVD that compared combined cardioprotective dietary advice and regular physical activity with usual lifestyle for the outcomes mortality or morbidity.

5.6.1.2.

One randomised controlled trial in people at high risk of CVD found that a combination of low fat diet and aerobic exercise was associated with a reduction in total cholesterol and triglycerides and an increase in HDL cholesterol levels compared with control.

5.6.1.3.

A second randomised controlled trial found that a combination of low fat diet and aerobic exercise was associated with a reduction in total cholesterol and LDL cholesterol compared with usual diet.

5.6.1.4.

A third randomised controlled trial found that a combination of diet and aerobic exercise was not associated with a change in lipid levels compared with control.

5.6.2. Clinical effectiveness of combined cardioprotective dietary advice and regular physical activity for the primary prevention of CVD

No randomised controlled trials were identified in people at high risk of CVD that examined the effectiveness of dietary advice versus usual diet and/or regular physical activity versus sedentary lifestyle for the outcomes of all cause mortality, cardiovascular mortality or cardiovascular morbidity.

Three randomised controlled trials were identified which examined the effectiveness of diet, regular physical activity and the combination of both interventions to improve serum lipid level profiles in people with elevated CVD risk factors (Anderssen, S. A., Haaland, A., Hjerman, I. et al, 1995; Hellenius ML, de Faire U, Berglund B et al, 1993; Stefanick, M. L., Mackey, S., Sheehan, M. et al, 1998).

The first study was a randomised controlled trial of six months duration in 158 healthy men aged 35 to 60 years with moderately elevated CVD risk factors (Hellenius ML, de Faire U, Berglund B et al, 1993). Participants were randomised to one of three intervention groups or to the control group (usual lifestyle). The first intervention was diet whereby participants were given verbal and written dietary advice that total fat consumption should comprise no more than 30% of energy intake, saturated fat no more than 10% of energy, cholesterol consumption should be less than 300 mg/day, polyunsaturated fat up to 10% of energy, monounsaturated fat 10–15% energy, carbohydrates (mainly complex) 50–60% energy and protein 10–20% energy.

The second intervention was physical activity; participants were given verbal and written advice to take regular physical activity of an aerobic type 2–3 times per week for 30–45 minutes at 60–80% maximum heart rate.

The third intervention was a combination of diet and physical activity. The control group was told to continue with the diet and lifestyle as prior to joining the study.

After six months, lipid levels were measured and no significant differences were found in total cholesterol, LDL cholesterol or HDL cholesterol for any of the intervention groups compared to control.

The second study was a randomised controlled trial (Anderssen, S. A., Haaland, A., Hjerman, I. et al, 1995) of one year duration in 198 men and 21 women aged 41–50. Participants who each had several coronary risk factors were recruited in Oslo and were then randomised to one of three intervention groups or to the control group. The dietary intervention consisted of counseling to reduce intake of saturated fat and cholesterol and to consume more fish. Energy restriction advice was given to those overweight.

For the physical activity intervention, participants attended aerobic exercise sessions 3 times per week for one hour where they exercised at 60–80% of their peak heart rate in supervised classes of 14 to 20 people.

The third intervention group was a combination of diet and physical activity as already described. The control group was told not to change their lifestyle during the trial but as all the other participants they were advised against smoking.

After one year, no significant differences in total, LDL or HDL cholesterol were observed for the diet only or physical activity only interventions compared to control. For the combined diet and physical activity intervention, a significant decrease in total cholesterol and a significant increase in HDL cholesterol were observed compared to control. In addition, triglycerides were found to be significantly reduced in all three intervention groups compared to control.

The final randomised controlled trial (Stefanick, M. L., Mackey, S., Sheehan, M. et al, 1998) was of one year duration and included 197 men and 180 postmenopausal women. Women were 45 to 64 years of age, had HDL cholesterol levels < 1.55 mmol/l, and LDL cholesterol levels between 3.23 and 5.42 mmol/l. Men were 30 to 64 years of age, had HDL cholesterol levels < 1.14 mmol/l, and LDL cholesterol levels between 3.23 and 4.90 mmol/l.

Participants were randomised to one of three intervention groups or to the control group. The first intervention was diet where participants were advised to follow the National Cholesterol Education Program (NCEP) Step 2 diet: total fat less than 30% of energy intake, saturated fat less than 7% of energy and cholesterol less than 200 mg per day.

The second intervention was aerobic exercise: participants attended 6 weeks of supervised 1 hour sessions, 3 times per week (held separately for groups 2 and 3). For the remaining 7 to 8 months of the trial, they could attend supervised classes and/or undertake home-based activities with the goal of engaging in aerobic activity equivalent to at least 16km of brisk walking or jogging each week.

The control group was asked to maintain their usual diet and exercise habits.

After one year, for both men and postmenopausal women, significant decreases in total and LDL cholesterol levels were observed in the diet plus physical activity intervention group compared to control.

In addition, one systematic review was identified that assessed the effectiveness of multiple risk factor interventions which included smoking cessation, physical activity and dietary advice with or without pharmacological intervention on a number of outcomes including all cause and CHD mortality (Ebrahim, S., Beswick, A., Burke, M. et al, 2006). A total of 39 randomised controlled trials were identified in adults of ≥ 40 years of age from general populations, workforce populations and high risk groups. Ten of these trials reported clinical event data and a meta-analysis of these ten trials found that multiple risk factor interventions were not associated with a reduction in total or coronary heart disease (CHD) mortality.

The conclusion of the review was that ‘The pooled effects suggest multiple risk factor intervention has no effect on mortality. However, a small but potentially important benefit of treatment (about a 10% reduction in CHD mortality) may have been missed. Risk factor changes were relatively modest, were related to the amount of pharmacological treatment used, and in some cases may have been over-estimated because of regression to the mean effects, lack of intention to treat analysis, habituation to blood pressure measurement, and use of self-reports on smoking.’

5.6.3. Evidence into recommendations

Due to the lack of evidence on the effectiveness of combined approaches, it was decided by the GDG that cardioprotective dietary advice and regular physical activity interventions would be considered separately.

5.6.4. Cost effectiveness of combined cardioprotective dietary advice and regular physical activity for the primary prevention of CVD

There were no cost effectiveness studies found surrounding the use of combined dietary advice and regular physical activity in the prevention of CVD.

5.7. Alcohol

[Return to Recommendations]

Alcohol consumption for men should be limited to up 3 to 4 units a day, and for women alcohol should be limited to up to 2 to 3 units of alcohol a day. People should avoid binge drinking. Further information can be found on the Foods Standards Agency website http://www.nhs.uk/Livewell/healthy-eating/Pages/Healthyeating.aspx.

5.8. Weight management

[Return to Recommendations]

For guidance in weight management in people at high risk of CVD refer to the NICE guideline:

  • Obesity: the prevention, identification, assessment and management of overweight and obesity in adults and children CG43 (2006) http://guidance.nice.org.uk/CG43.

5.9. Smoking cessation

[Return to Recommendations]

For guidance on smoking cessation refer to the NICE Technology appraisals and guidance on public health interventions:

  • Smoking cessation - bupropion and nicotine replacement therapy. The clinical effectiveness and cost effectiveness of bupropion (Zyban) and Nicotine Replacement Therapy for smoking cessation TA039 (2002).
  • Brief interventions and referral for smoking cessation in primary care and other settings PHI001, (2006)
  • Varenicline for smoking cessation. NICE technology appraisal guidance 123 (2007).
  • Smoking cessation services in primary care, pharmacies, local authorities and workplaces, particularly for manual working groups, pregnant women and hard to reach communities. NICE public health guidance 10 (2008).

Footnotes

10

Department of Health (2004) At least five a week: evidence on the impact of physical activity and its relationship to health. A report from the Chief Medical Officer. London: Department of Health. Available from www​.dh.gov.uk

16

This recommendation has been taken from ‘Statins for the prevention of cardiovascular events’, NICE technology appraisal 94. See www​.nice.org.uk/TA094

11
12

Department of Health (2004) At least five a week: evidence on the impact of physical activity and its relationship to health. A report from the Chief Medical Officer. London: Department of Health. Available from www​.dh.gov.uk

Copyright © 2008, Royal College of General Practitioners.

All rights reserved. No part of this publication may be reproduced in any form (including photocopying or storing it in any medium by electronic means and whether or not transiently or incidentally to some other use of this publication) without the written permission of the copyright owner. Applications for the copyright owner’s written permission to reproduce anypart of this publication should be addressed to the publisher.

Cover of Lipid Modification
Lipid Modification: Cardiovascular Risk Assessment and the Modification of Blood Lipids for the Primary and Secondary Prevention of Cardiovascular Disease [Internet].
NICE Clinical Guidelines, No. 67.
National Collaborating Centre for Primary Care (UK).

NICE (National Institute for Health and Care Excellence)

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