Abstract
Background
Multiple risk factor interventions using counselling and educational methods assumed to be efficacious and cost‐effective in reducing coronary heart disease (CHD) mortality and morbidity and that they should be expanded. Trials examining risk factor changes have cast doubt on the effectiveness of these interventions.
Objectives
To assess the effects of multiple risk factor interventions for reducing total mortality, fatal and non‐fatal events from CHD and cardiovascular risk factors among adults assumed to be without prior clinical evidence CHD..
Search methods
We updated the original search BY SEARCHING CENTRAL (2006, Issue 2), MEDLINE (2000 to June 2006) and EMBASE (1998 to June 2006), and checking bibliographies.
Selection criteria
Randomised controlled trials of more than six months duration using counselling or education to modify more than one cardiovascular risk factor in adults from general populations, occupational groups or specific risk factors (i.e. diabetes, hypertension, hyperlipidaemia, obesity).
Data collection and analysis
Two authors extracted data independently. We expressed categorical variables as odds ratios (OR) with 95% confidence intervals (CI). Where studies published subsequent follow‐up data on mortality and event rates, we updated these data.
Main results
We found 55 trials (163,471 participants) with a median duration of 12 month follow up. Fourteen trials (139,256 participants) with reported clinical event endpoints, the pooled ORs for total and CHD mortality were 1.00 (95% CI 0.96 to 1.05) and 0.99 (95% CI 0.92 to 1.07), respectively. Total mortality and combined fatal and non‐fatal cardiovascular events showed benefits from intervention when confined to trials involving people with hypertension (16 trials) and diabetes (5 trials): OR 0.78 (95% CI 0.68 to 0.89) and OR 0.71 (95% CI 0.61 to 0.83), respectively. Net changes (weighted mean differences) in systolic and diastolic blood pressure (53 trials) and blood cholesterol (50 trials) were ‐2.71 mmHg (95% CI ‐3.49 to ‐1.93), ‐2.13 mmHg (95% CI ‐2.67 to ‐1.58 ) and ‐0.24 mmol/l (95% CI ‐0.32 to ‐0.16), respectively. The OR for reduction in smoking prevalence (20 trials) was 0.87 (95% CI 0.75 to 1.00). Marked heterogeneity (I2 > 85%) for all risk factor analyses was not explained by co‐morbidities, allocation concealment, use of antihypertensive or cholesterol‐lowering drugs, or by age of trial.
Authors' conclusions
Interventions using counselling and education aimed at behaviour change do not reduce total or CHD mortality or clinical events in general populations but may be effective in reducing mortality in high‐risk hypertensive and diabetic populations. Risk factor declines were modest but owing to marked unexplained heterogeneity between trials, the pooled estimates are of dubious validity. Evidence suggests that health promotion interventions have limited use in general populations.
Keywords: Adult, Humans, Coronary Disease, Coronary Disease/mortality, Coronary Disease/prevention & control, Counseling, Health Promotion, Patient Education as Topic, Primary Prevention, Randomized Controlled Trials as Topic, Risk Factors
Plain language summary
Multiple risk factor interventions for coronary heart disease
In many countries, there is enthusiasm for 'healthy heart programmes' that use counselling and educational methods to encourage people to reduce their risks for developing heart disease. These risk factors include high cholesterol, excessive salt intake, high blood pressure, excess weight, a high‐fat diet, smoking, diabetes and a sedentary lifestyle. This review is an update of all relevant randomised trials that have evaluated an intervention that aimed to reduce more than one risk factor (multiple risk factor intervention) in people without evidence of cardiovascular disease. The findings are from 55 trials of between six months and 12 years duration conducted in several countries over the course of four decades. The median duration of follow up was 12 months (with a range of six months to 12 years). Multiple risk factor intervention does result in small reductions in risk factors including blood pressure, cholesterol and smoking. Contrary to expectations, multiple risk factor interventions had little or no impact on the risk of coronary heart disease mortality or morbidity. This could be because these small risk factor changes were not maintained in the long term. Alternatively, the small reductions in risk factors may be caused by biases in some of the studies. The methods of attempting behaviour change in the general population are limited and do not appear to be effective. Different approaches to behaviour change are needed and should be tested empirically before being widely promoted, particularly in developing countries where cardiovascular disease rates are rising. Further trials may be warranted.
Background
As the incidence of cardiovascular disease is largely explained by modifiable risk factors (serum cholesterol and reduced high‐density lipoprotein (HDL) cholesterol, blood pressure and cigarette smoking), reducing risk factors through health promotion focusing on lifestyles is a logical way of preventing disease. Randomised controlled trials of the effectiveness of multiple risk factor intervention using counselling and education in addition to, or instead of, pharmacological treatments to modify major cardiovascular risk factors have been carried out in primary care and in the workplace. The findings of these trials have been equivocal; effectiveness in reducing cardiovascular disease incidence appears to be associated with the degree of risk factor control achieved (Editorial 1982a; Editorial 1982b; Appel 2004). Taken with evidence from quasi‐experimental studies, such as the North Karelia project (Puska 1976; Puska 1981) and the Stanford Heart Disease Prevention Programme (Farquhar 1977; Farquhar 1990; Fortmann 1993), it is widely believed that multiple risk factor intervention using counselling and educational methods is both effective and cost‐effective and should be expanded. Recently this idea has been extended to people with diabetes (Davey Smith 2005; Sartorelli 2005) and hypertension (Pickering 2003; Little 2004; Svetkey 2005).
In many countries multiple risk factor counselling and health education is embodied in guidelines produced by professional groups (NSF‐CHD 2000; AHA 2002; NSF‐CHD 2006; European Task Force 2007) and government (Kickbush 1988; NSF‐CHD 2000; Muto 2001) recommending use of behavioural counselling for stopping smoking tobacco, making healthy food choices and increasing physical activity.
Alongside the guidelines, health services have acted by developing health promotion as a specialty (Editorial 1984) and in the UK extra payments are now made for the routine collection of data on cardiovascular risk factors in primary care, and issuing of primary prevention policy (NSF‐CHD 2000).
Non‐systematic reviews have promoted the notion that multiple risk factor intervention is effective (McCormick 1988; Schoenberger 1990). However, a systematic review of the randomised trial evidence involving almost a million person‐years of observation, using Cochrane Collaboration methodology, demonstrated no impact of multiple risk factor intervention on coronary heart disease mortality (Ebrahim 1997). Since this systematic review was published in 1997 more randomised trials and community evaluations have been published, predominantly with disappointing findings (Tudor‐Smith 1998; Berglund 2000; Pickering 2004). A recent non‐systematic review has again claimed benefits for multiple risk factor intervention (Daviglus 2006). With the rising burden of cardiovascular diseases in developing countries, there has been a strong view that multiple risk factor intervention should be the cornerstone of primary prevention (Ebrahim 2008; Vartiainen 2009), although it is acknowledged that interpretation of the findings from the randomised trials makes this problematic in poor countries (Ebrahim 2001; Lim 2007). In view of the continued policy importance of multiple risk factor intervention a further update of the review was needed to incorporate several new trials.
Objectives
To assess the effectiveness of multiple risk factor intervention using counselling or educational approaches (or both) aimed at behaviour change, with or without pharmacological interventions, in adults assumed to be without prior clinical evidence of heart attacks, stroke or peripheral vascular disease in reducing:
total (all‐cause), CHD and stroke mortality;
non‐fatal CHD and stroke events;
systolic and diastolic blood pressure;
blood cholesterol levels; and
smoking rates.
Methods
Criteria for considering studies for this review
Types of studies
Randomised controlled trials (RCTs) of at least six months duration of follow up with parallel‐group design. Trials could be randomised by individual or by group (e.g. family, workplace site).
Types of participants
We included trials which recruited an adult population whose mean age was 35 or above.
General populations included workforce populations and high‐risk groups (hypertension, obesity, hyperlipidaemia, type 2 diabetes or a combination of these) as well as subjects that did not have a high risk of developing CHD. We excluded trials where the percentage of participants with evidence of CHD was more than 25%.
Types of interventions
A health promotion activity to achieve behaviour change; more specifically counselling or educational interventions, with or without pharmacological treatments, which aim to alter more than one cardiovascular risk factor (i.e. diet, reduce blood pressure, smoking, total blood cholesterol or increase physical activity).
Types of outcome measures
Primary outcomes
Total (all‐cause) mortality, fatal CHD and fatal stroke events.
Secondary outcomes
Non‐fatal CHD (including myocardial infarction, unstable angina, need for coronary bypass grafting and or percutaneous coronary intervention) and stroke events requiring hospital admission, net change in blood pressure, total blood cholesterol and smoking.
Search methods for identification of studies
For the original review we searched MEDLINE from 1966 to April 1995 using a RCT filter (Dickersin 1994) (see Appendix 3). We checked reference lists of identified papers, sought expert advice and undertook citation searches.
We updated these searches by searching the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (2006, Issue 2), MEDLINE (2000 to June 2006) and EMBASE (1998 to June 2006), using a RCT filter for MEDLINE (Dickersin 1994) and EMBASE (Lefebvre 1996) (see Appendix 1 and Appendix 2). Reports of RCTs from MEDLINE and EMBASE are added to CENTRAL on a regular basis; to avoid duplication of effort we did not search earlier years of these databases.
We checked references of identified studies and made searches for additional follow‐up papers if the studies published up until 2006 did not provide all of the data required for the review. We applied no language restrictions.
Data collection and analysis
For the searches in 1997 and in 2006, two review authors checked all titles and abstracts obtained through the searches independently to eliminate studies that were definitely not relevant to the review. In the 2001 update, one review author checked the results of searches and eliminated all those definitely not relevant to the review. Two review authors checked the remaining papers independently. For all versions, two review authors obtained and read each paper thought to be of possible relevance to determine whether it fitted the specified inclusion criteria. We discussed disagreements and resolved them with a third review author.
Two review authors performed independent data abstraction using a data extraction form and resolved disagreements by discussion or by consultation with a third review author. We contacted chief investigators to provide additional relevant information where necessary.
We attempted to contact study authors. However, when information was not available from trialists, we assumed missing data to occur at random.
The main aspects of quality which were formally assessed included the adequacy of concealment of randomisation, comparability of baseline characteristics, blinding of outcome assessors and completeness of follow up. It was not possible to include blinding of intervention allocation since this is not possible in lifestyle interventions.
For continuous variables (i.e. blood pressure, blood cholesterol) we used mean differences with 95% confidence intervals (CI) to ascertain net changes (i.e. control group minus intervention group differences). We used the longest duration of follow up that was reported in the primary publications. For studies where subsequent follow‐up data were published, we did not update data on continuous variables since it was considered likely that long‐term findings would reflect attrition bias, effects of co‐treatments with drugs and possibly publication bias (publication of positive findings). Similarly, we used smoking levels from the primary publication of the trial and did not use any subsequent published follow‐up data in analyses.
We expressed categorical variables (e.g. mortality, clinical event rates and smoking) as odds ratios (OR) with 95% CI. We used fixed‐effect models except in instances where there was significant heterogeneity of effects, where we applied a random‐effects model. For studies where subsequent follow‐up data on mortality and event rates were published, we updated these data in the review. We applied intention‐to‐treat analysis to these outcomes.
We quantified statistical heterogeneity using the I2statistic which describes the percentage of total variation across studies that is due to heterogeneity rather than sampling error (Higgins 2008). We summarised the findings using a fixed‐effect model unless there was significant heterogeneity (I2 statistic > 75%) in which case we applied a random‐effects model. In case of significant heterogeneity we sought to identify and explain possible causes by exploring the effect of participant, drug treatment, era of study and study design characteristics.
We confined subgroup analysis to co‐morbidity (diabetes, hypertension, hyperlipidaemia and obesity and one other co‐morbidity (e.g. obesity and diabetes), no co‐morbidity), and evidence of prescribed drug treatment (prescribed medication during trial and no prescribed medication or drug treatment not stated).
We used meta‐regression methods to examine the effects of age and blood pressure and cholesterol‐lowering drug treatments on outcomes. We also examined the effect of level of coronary heart disease risk using the control group incidence rates to determine whether trials recruiting higher‐risk participants were more likely to demonstrate beneficial effects.
We confined sensitivity analysis to method of randomisation (cluster, cluster analysed as individual, individual), allocation of concealment (adequate, unclear, inadequate) and age of trial (publication of trial before 2000 and after 2000). We used funnel plots to ascertain publication bias for each outcome.
Results
Description of studies
Results of the search
The updated search (2001 to 2006) resulted in 3926 references, after removal of duplicates. From these we excluded 3844 and obtained 82 full‐text papers for further inspection. Of these we excluded 55 papers reporting on 50 studies. Thus in total, including studies already listed as excluded in previous versions of the review, we excluded 128 references, reporting on 117 studies (see Characteristics of excluded studies). One additional paper was a design paper for an ongoing study (Roderigues 2005)
Citation searching of included studies identified two further papers for these studies (Look AHEAD 2003; Toobert (MLP) 2005) thus we added 29 papers reporting on 16 studies to those studies already included in previous versions. In total we included 55 trials (reported in 91 papers). Details of these studies are shown in the table of Characteristics of included studies.
Included studies
We found a total of 55 trials of multiple risk factor intervention, comprising 61 distinct study groups; a dramatic increase on the 14 trials identified for the original review. The total number of patients recruited amounted to 163,471 with data on clinical endpoint for 139,256 participants. The trials with clinical endpoints comprised approximately 909,500 patient‐years of observation and those with risk factor endpoints 321,000 patient‐years of observation. The duration of follow up ranged from six months to 12 years; the median follow‐up time was one year. Sixteen studies (with 17 arms) recruited patients with hypertension and five trials were of patients with diabetes.
Fourteen trials reported total or coronary heart disease mortality as outcomes and two trials from the original review (the Swedish RIS 1994 study and the WHLP 1998) reported extended mortality follow up. Only four trials were sufficiently large to have adequate power to show meaningful changes in total or coronary heart disease mortality (HDFP trial 1970; MRFIT Study 1982; Gothenberg Study 1986; WHO Factories 1986). In the Rachmani 2005 trial the number of fatal and non‐fatal clinical events outnumbered the number of participants recruited to the study. For the purpose of this review, we used the number of participants who experienced one or more events in this analysis. However, most recent trials did not include clinical event endpoints but focused on the following outcomes: blood pressure, serum cholesterol, physical activity, diet, control of diabetes and weight loss.
In general, the trials compared an intervention comprising some form of counselling and education with control groups, which either received usual care or nothing was described. The type and intensity of behavioural intervention used was seldom reported in the older trials. Very few studies reported the theoretical approach used to underpin the intervention. When stated, the Stages of Change model (Prochaska 1983; DiClemente 1991) was the most common approach used. A person‐centred and self‐directed psychological approach was used by one study (Meichenbaum 1993) and another one relied on a combination of social cognitive theory, goal systems theory and social ecological theory (Toobert (MLP) 2005). Most education and counselling intervention strategies targeted a combination of risk factors including diet, exercise, weight loss, salt intake, alcohol use, stress management, smoking cessation, adherence to medication or specific clinical regimens, particularly in patients with hypertension or diabetes.
Interventions included workshops, lectures, individual sessions, personal counselling, provision of written material, assignments, shopping tours and cooking sessions. Some studies required family members, partners or both to participate in the intervention. The intervention strategies were commonly provided by a variety of health professionals including physicians, nurses, nutritionists, dieticians, nurses, exercise trainers, cooks, psychotherapists and physiotherapists. The intensity varied and ranged from four to 54 sessions over periods of time ranging from two weeks to three years.
With the exception of two studies recruiting men and women over the age of 60 years (Applegate 1992; Garcia‐Pena 2001), the oldest subjects included in the trials were 75 years of age. The majority of trials randomised only middle‐aged adults, although younger adults were recruited by some studies. The mean age in all the trials was 50 years.
Few studies looked at quality of life (Oslo Diet Exercise; Toobert (MLP) 2005) and only one examined cost‐effectiveness of the intervention; in this case a nurse‐led intervention for elderly hypertensive patients (Garcia‐Pena 2001).
Excluded studies
We excluded 116 trials identified as involving multiple risk factor interventions from consideration for the following reasons: no relevant risk factor changes measured and/or reported (n = 159), non‐random allocation to intervention and control groups (n = 315), no specific multiple risk factor intervention (n = 6), control group received substantial intervention (n = 210), follow up to at least six months was not reported (n = 12), the mean age of participants was less than 35 (n = 88), over 25% of participants had CHD (n = 110), numbers in groups were not reported (n = 1), baseline or follow‐up data were not provided (n = 6), or no comparable control group was identified (n = 6). A large number of older studies were set up in what was then the Soviet Union but it appeared that allocation to intervention and control groups was not random. Attempts to trace the investigators were unsuccessful. Three studies appeared suitable in the latest update but missing data precluded them from inclusion in the review update, as attempts to request data from the original authors were unsuccessful (Boylan 2003; Kisioglu 2004; Elliot 2007).
Risk of bias in included studies
The quality of the trials examined deserves comment. Very few of the older published trials provided sufficient detail to replicate the intervention used, and in several trials the intervention varied between sites and over time. It is likely that the quality of the intervention, in terms of intensity and frequency, person carrying out activities, and the theoretical framework of behavioural change used, will determine the impact of the intervention. One third of studies (n = 18) used an intention‐to‐treat analysis on both categorical and continuous variables. Some explained that the last available reported measurement was used for the final endpoint measurement. Of these 18 studies, the loss to follow up ranged from 1% to 42% (median 13%). As such, losses to follow up were a particular problem as changes in risk factors cannot be reliably assessed in an intention‐to‐treat analysis.
Random allocation methods were not usually reported. In only 13 out of 55 trials we considered the methods used as adequate and in nine they were inadequate. We made specific enquiries of investigators for the original review predominantly to obtain event data but did not make these in this update as most of the new trials had measured clinical events. In the large trials it is unlikely that the allocation method was suspect but was simply inadequately reported.
Blinding of intervention allocation for the participants is not possible in lifestyle interventions and this inevitably raises the possibility of bias. Only 12 out of 55 trials blinded the assessors to treatment allocation. As such outcomes were usually assessed with knowledge of treatment allocation and this too makes biased assessment of some outcomes possible. It seems unlikely that lack of blinding may have had any effect on clinical event outcomes, but it is possible that participants randomised to a control or usual care group might have been more likely to take health preventive activity as they may have felt they were missing potential benefits. Lack of blinding in assessment and or relying on self‐reported smoking histories may have resulted in a reporting bias with those allocated to interventions more likely to say they had stopped smoking, as seen in previous studies (West 2007). Validation of self‐reported smoking outcomes using biochemical assay of serum thiocyanate was reported in only three of the older trials and none of the new trials.
Effects of interventions
Total (all‐cause), coronary heart disease (CHD) and stroke mortality
Total (all‐cause) mortality
From the 14 studies that reported total mortality, there was no strong evidence of any reduction in the pooled analysis (RR 1.00; 95% CI 0.96 to 1.05) using a fixed‐effect model (Analysis 1.1). Follow up of mortality ranged from six months to 12 years.
1.1. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 1 Total mortality.
A significant reduction in all‐cause mortality was seen in trials where patients were recruited with either hypertension or diabetes (RR 0.78; 95% 0.68 to 0.89) (Analysis 1.4) and in those trials where patients were being prescribed either antihypertensive or lipid‐lowering drugs during the trial period (RR 0.86; 95% CI 0.78 to 0.96) (Analysis 1.5) using a fixed‐effect model.
1.4. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 4 Total mortality (by co‐morbidity).
1.5. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 5 Total mortality (by drug treatment).
Coronary heart disease mortality
Eleven trials reported on coronary heart disease mortality; the pooled OR was 0.99 (95% CI 0.92 to 1.07) using a fixed‐effect model (Analysis 1.8).
1.8. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 8 Coronary heart disease mortality.
Stroke mortality
Six trials reported on stroke mortality (HDFP trial 1970; Finnish men 1985; Gothenberg Study 1986; Oslo Diet Antismoking; Swedish RIS 1994; Rachmani 2005). Only one of these trials reported a significant reduction in stroke mortality but the pooled relative risk favoured intervention (RR 0.75; 95% CI 0.60 to 0.95) (Analysis 1.15) using a fixed‐effect model. This may be explained by better monitoring and adherence of drug treatment as five of the six trials were given drug treatment during the study.
1.15. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 15 Stroke mortality.
For total and coronary heart disease mortality, funnel plots suggested no evidence of small study bias in trials (Figure 1; Figure 2). Evidence of significant statistical heterogeneity was not apparent in the pooled RR for total mortality, coronary heart disease mortality or stroke mortality.
1.
2.
Modelling the effects of age using the mean age of study participants and proportion of patients on antihypertensive treatment and cholesterol‐lowering drug treatment did not reveal any significant interactions between age, drug treatments and outcome. There was a significant interaction between intervention and level of coronary heart disease risk estimated from control group incidence, indicating that trials recruiting higher‐risk participants were more likely to demonstrate beneficial effects. This effect was explained by the inclusion of the two trials which studied hypertensive patients rather than general population or workforce subjects. It is impossible to separate this effect of baseline coronary heart disease risk from the benefits of pharmacological treatment of hypertension.
Allocation concealment had little effect on total mortality although the trials with inadequate allocation concealment reported stronger evidence of an effect on total mortality, however this was driven by the HDFP trial of hypertensives (Analysis 1.3).
1.3. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 3 Total mortality (by allocation concealment).
Fatal and non‐fatal clinical events
Nine trials reported on fatal and non‐fatal clinical events which required hospital admission (HDFP trial 1970; MRFIT Study 1982; Oslo Diet Antismoking; Finnish men 1985; Gothenberg Study 1986; WHO Factories 1986; Swedish RIS 1994; Garcia‐Pena 2001; Rachmani 2005) and four trials reported on stroke events (Oslo Diet Antismoking; Gothenberg Study 1986; Swedish RIS 1994; Rachmani 2005). The follow‐up period ranged from six months to 11.8 years.
All analyses showed considerable heterogeneity of effect (I2 above 75%) so findings must be viewed with caution. Overall, a reduction in events was observed (RR 0.84; 95% CI 0.73 to 0.98) (Analysis 1.21) using a random‐effects model. This effect was explained by inclusion of patients with either hypertension or diabetes in whom the combined event relative risk was 0.71 (95% CI 0.61 to 0.83) (Analysis 1.24). No effect was seen in participants without a co‐morbidity.
1.21. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 21 Fatal and non‐fatal clinical events.
1.24. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 24 Fatal and non‐fatal clinical events (by co‐morbidity).
Changes in risk factors
For all analyses of risk factor changes very high levels of heterogeneity of effect were found (I2 between 85% and 97%). Although we applied random‐effects, we cannot draw conclusions regarding the consistency of effects on risk factors. We explored this heterogeneity and it could not be attributed fully to the effects of pharmacological treatment or study design effects. There was some evidence of possible regression to the mean effects as risk factor net changes were strongly correlated with the initial level of blood pressure, smoking and blood cholesterol. The sample size weighted correlation coefficients between initial level and magnitude of risk factor reduction for diastolic blood pressure, smoking and blood cholesterol were 0.73 (P = 0.006), 0.63 (P = 0.01) and 0.74 (P = 0.004), respectively. In other words, those studies with the highest baseline diastolic blood pressure, smoking prevalence and blood cholesterol levels demonstrated larger falls in these risk factors at follow up.
Systolic and diastolic blood pressure
For both systolic and diastolic blood pressure, 48 trials (53 arms) indicated a significant reduction favouring intervention. The weighted mean difference between intervention and control was ‐2.71 mm Hg (95% CI ‐3.49 to ‐1.93) for systolic blood pressure and ‐2.13 mm Hg (95% CI ‐2.67 to ‐1.58) for diastolic blood pressure using random‐effects models (Analysis 1.36; Analysis 1.42). In total, 24 trials reported that patients were on medication for high blood pressure. When analysis of outcomes was confined to these trials, strong evidence of reductions in both systolic and diastolic remained. This was also seen when the analysis was confined to trials where no medication was prescribed (Analysis 1.39; Analysis 1.46).
1.36. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 36 Systolic blood pressure (individual analysis or cluster).
1.42. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 42 Diastolic blood pressure.
1.39. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 39 Systolic blood pressure (by drug treatment).
1.46. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 46 Diastolic blood pressure (by drug treatment).
Not all trials reported, or were able to provide data on, blood pressure at follow up. Investigators from the Oslo study stated that there were no changes observed (Hjermann I, personal communication, 1996). Overall, changes in blood pressure were small. For both outcomes there was no evidence of small study bias in the trials as shown by the funnel plots (Figure 3; Figure 4).
3.
4.
Both subgroup and sensitivity analysis had no effect in reducing heterogeneity or on the overall but inconsistent findings of a reduction in blood pressure.
Blood cholesterol
Forty‐four trials (50 arms) reported blood cholesterol as an outcome. Blood cholesterol levels showed a small but highly significant fall (weighted mean net difference ‐0.07 mmol/L; 95% CI ‐0.08 to ‐0.06) (Analysis 1.49) using a random‐effects model. This is a bigger effect on cholesterol‐lowering than previously seen in the 2001 update of this review. Nineteen trials reported that patients were on cholesterol‐lowering medication and when analysis was confined to this group the reduction in cholesterol was almost identical to the pooled result and was similar to that seen in those trials in which no cholesterol‐lowering drugs were used (Analysis 1.53). Cholesterol levels were lower in the trials in which both antihypertensive and cholesterol‐lowering drugs were used (‐0.18 mmol/L; 95% CI ‐0.22 to ‐0.14 mmol/L).
1.49. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 49 Blood cholesterol.
1.53. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 53 Blood cholesterol (by drug treatment).
Trials with inadequate concealment showed a non‐significant reduction compared with those with adequate or unclear concealment (Analysis 1.51). Figure 5 shows no evidence of small study bias.
1.51. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 51 Blood cholesterol (by allocation concealment).
5.
Smoking
Twenty studies reported on smoking prevalence. Pooled analysis indicated a non‐significant reduction in smoking prevalence (RR 0.87; 95% CI 0.75 to 1.00) (Analysis 1.28). Most of the studies relied on self‐reported smoking status at end of follow up. In the Hypertension Detection & Follow up Program quantitative data were not available but no changes in smoking rates were found (HDFP trial 1970). Smoking rates fell particularly sharply in the Multiple Risk Factor Intervention Trial and in the Change of Heart 1999 study. The former used individual smoking advice given by a physician (MRFIT Study 1982) and in the latter large baseline differences between groups were noted and losses to follow up were high (Change of Heart 1999). Validation of self‐reported smoking rate reductions in the Multiple Risk Factor Intervention Trial (MRFIT Study 1982) by comparison with serum thiocyanate levels suggested that the improvement might be overestimated. None of the more recent trials indicated a significant reduction in smoking status.
1.28. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 28 Smoking prevalence.
Subgroup analysis indicated no change in the results in the other studies which had recruited a low number of participants with cardiovascular disease (CVD), where the risk reduction was 15% (RR 0.85; 95% CI 0.79 to 0.92) (Analysis 1.33) using a random‐effects model.
1.33. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 33 Smoking prevalence (by era).
Allocation concealment had no effect on the results. Figure 6 shows no evidence of small study bias.
6.
Sensitivity analysis
Age of trial
Age of trial did not have a significant effect on trial outcome other than fatal and non‐fatal clinical events. Studies published before 2000 reported similar effect sizes compared with those published after 2000. Net differences were small: ‐0.45 mm Hg in systolic blood pressure, ‐0.49 mm Hg for diastolic blood pressure, 0.04 mmol/L in blood cholesterol (RR difference of ‐0.26 for total clinical events).
Cluster‐randomisation
In meta‐analysis the weighting given to trials with a cluster design may be over‐estimated. Only one trial used a cluster design where analysis was confined to the clusters (Change of Heart 1999) and no benefits were demonstrated other than a 57% risk reduction in smoking prevalence (RR 0.43; 95% CI 0.28 to 0.64) (Analysis 1.29) using a random‐effects model. In trials with a cluster design which provided analysis by individual significant benefits were observed in reductions of systolic and diastolic blood pressure and cholesterol (Analysis 1.36; Analysis 1.43; Analysis 1.50), all using a random‐effects model. Overall benefits tended to be in trials with randomisation by individual.
1.29. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 29 Smoking prevalence (individual analysis or cluster).
1.43. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 43 Diastolic blood pressure (individual analysis or cluster).
1.50. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 50 Blood cholesterol (individual analysis or cluster).
Quality of life and economic costs
Oslo Diet Exercise used the General Health Questionnaire and found that exercise had a significant effect on enhancing self‐esteem, competence and coping for the intervention group but that other quality of life dimensions remained unchanged. Toobert (MLP) 2005 used the Medical Outcomes, Short Form General Health questionnaires together with the Problem Areas in Diabetes scale. When the results were combined, quality of life did improve for the intervention group particularly in enhancing competence in self‐care. Garcia‐Pena 2001 evaluated a programme whereby a nurse made weekly or fortnightly home visits to elderly patients with hypertension. In applying a cost‐effectiveness analysis, the authors concluded that the reduction in blood pressure obtained may justify the small incremental cost of the intervention.
Discussion
As reported in the earlier review, multiple risk factor interventions comprising counselling, education aimed at behaviour change and drug therapies for the primary prevention of coronary heart disease were ineffective in achieving reductions in total or cardiovascular disease mortality when used in general or workforce populations of middle‐aged adults. The pooled effects of intervention were statistically insignificant but a potentially useful benefit of treatment (about a 8% reduction in coronary heart disease mortality) may have been missed despite the very large sample sizes in several of the trials. It is surprising that despite the continued popularity of these interventions no further large‐scale randomised studies, powered to detect clinical event endpoints, have been carried out. Any coronary heart disease (CHD) mortality benefits of these multiple risk factor interventions was confined to those trials recruiting people with hypertension and diabetes. Similarly, benefits in stroke mortality were confined to those trials recruiting patients with hypertension and taking drug treatments. Such participants may well be more highly motivated to act on counselling and education interventions and may also benefit because they were more likely to adhere to their drug medications.
Our rationale for focusing on mortality outcomes rather than non‐fatal event outcomes is that counting deaths and comparing them by random allocation group is unlikely to be biased, but once attribution of causes of death is involved there is some potential for bias to occur as events were not necessarily assigned causes blind to random allocation group, particularly in the older, large trials. Similar potential biases arise in counting and assigning causes to non‐fatal events.
The risk factor changes associated with interventions were modest but are probably optimistic estimates as changes could only be measured in those remaining in the trials. All risk factor change analyses were heterogeneous, making pooled estimates of effect questionable. Habituation to blood pressure measurement and self‐reports of smoking will also tend to exaggerate the changes observed. It is, however, not possible to separate participants' level of risk from the use of antihypertensives in the present set of trials, as studies with high‐risk participants tended to be the ones which included participants with high levels of antihypertensive drug use. Furthermore, there are many problems in relating trial outcome to a risk measure which is itself dependent on the outcome in meta‐analysis (Egger 1995). We are cautious in our interpretations of these risk factor changes because, if these effects were real, they would have been reflected in reductions in CHD mortality given the size of some of the trials. Furthermore, as the average duration of follow up was 12 months, the risk factor changes that were observed are unlikely to be mirrors of the broad secular trends occurring over much longer time periods. Our conclusions are that observed risk factor changes are likely to be over‐estimates and are probably, in the main, due to bias in design and effects of pharmacological treatments.
Although we did observe weak evidence of benefits on combined fatal and non‐fatal cardiovascular disease (CVD) events, this was explained by trials which included hypertensives and diabetics, supporting the conclusions based on the mortality findings. Heterogeneity of intervention effects on non‐fatal clinical endpoints is probably caused by two factors: the participants included in the trials and the use of pharmacological treatments. Hypertensives, at highest risk, were more likely to benefit from counselling and education, and effective drugs. We stand by our interpretation that these interventions are not beneficial in general populations. These findings suggest that targeting of current health promotion activities to high‐risk individuals might be of more value than more general health promotion for everyone.
Our findings are relevant to middle‐aged adults who are seen in general practice or occupational health practices. Although our inclusion criteria were focused on trials of primary prevention we found that some studies had recruited participants with some evidence of prior heart attack, stroke or peripheral vascular disease. These trials contribute important data to our analyses so we did not wish to exclude them but decided to reject trials that comprised more than 25% of participants with prior CVD events. These trials did not report findings by prior CVD and even if they had the comparisons would not be by randomisation as none of the trials deliberately set out to randomise patients with prior diseases. However, their inclusion in this review would tend to bias our findings towards finding positive effects of intervention given that these health promotion interventions appear to be more effective in people with established cardiovascular disease (Oldridge 1988; O'Connor 1989; Mullen 1992).
Although missing data could affect the conclusions of this review, we consider that the proportion of loss at follow up was not that substantial, and its impact on fatal events (primary outcomes) is perhaps lower than that observed for non‐fatal events.
The interventions used
The benefits of drug treatments for lowering blood pressure and cholesterol are clear (Davey Smith 1993; Collins 1994; CTT 2005). However, those people at highest risk of disease in both hypertension control (Mulrow 1995) and cholesterol‐lowering (Davey Smith 1993) benefit most. Treatment of low‐risk populations may result in small treatment benefits being outweighed by small treatment risks (Davey Smith 1994), which may have occurred in both the Multiple Risk Factor Intervention Trial and the Finnish businessmen's trial (MRFIT Study 1982; Finnish men 1985). There were strong associations between baseline levels of risk factors and net falls experienced, suggesting that intervention may be more effective in populations with particularly adverse risk‐factor profiles.
More intensive interventions might be expected to produce better effects although those used in many of the trials would far exceed what is feasible in routine practice. A meta‐analysis of dietary modifications found that increasing intensity of dietary intervention was associated with greater falls in blood cholesterol levels in high‐risk participants (Brunner 1997). In the Minnesota Heart Health Programme, a non‐randomised community trial of intensive health promotion, both risk‐factor and mortality changes showed virtually no difference between intervention and control communities (Luepker 1996). The continued enthusiasm for health promotion practices given the failure of these community intervention trials is curious, especially given the huge resources which have been put into them.
Latency of effects
It is possible that benefits cannot be detected in the early stages but emerge over time. Longer‐term follow up of the Multiple Risk Factor Intervention Trial participants has demonstrated increased divergence between control and intervention group mortality rates (MRFITRG 1990) which has also been found in the Tromso Family Trial (Professor S. Knutson, personal communication). However, evidence from pharmacological trials suggests benefits from reduction of blood pressure and blood cholesterol are observed within two to four years (Collins 1994; Scandinavian 1994). The effects of giving up smoking vary depending on the clinical outcome considered: stroke risk falls rapidly after stopping (Wannamethee 1995), but coronary heart disease risk may be less reversible (Cook 1986; Ben‐Shlomo 1994).
Evidence of benefit
The quasi‐experimental North Karelia study has been very influential in supporting multiple risk factor intervention. Examination of the trends in both risk factors (Puska 1985; Vartiainen 1994) and coronary heart disease mortality (Valkonen 1992) observed in North Karelia and comparison regions shows similar patterns occurring at the same time, suggesting that the interventions in North Karelia were not instrumental in causing the improvements observed (Ebrahim 2001). Indeed, the North Karelia and similar projects may be viewed as effects, or epiphenomena, of the very high coronary heart disease mortality rates experienced in many countries in the 1960s.
In secondary prevention following myocardial infarction and angina, trials of multiple and single risk factor interventions have suggested substantial benefits (Oldridge 1988; O'Connor 1989; Mullen 1992). It is probable that intervention aimed at lifestyle modification following myocardial infarction is effective because participants are much more likely to change their behaviours.
Limitations of randomised controlled trials
The interventions reviewed were essentially individual (49 trials), family (three trials) or work site (three trials) approaches. Randomised controlled trials impose limitations on the nature of interventions that may be tested and are of more value in examining high‐risk rather than population and social approaches to prevention (Rose 1992).
Context
The majority of included trials (47%) were undertaken in Europe and in the USA (29%) whilst the remaining were undertaken in other countries including Australia, Japan, Brazil, Mexico, Israel and Taiwan. Over the past decades, whilst there has been a decline in deaths from heart disease and stroke in developed countries, especially in Europe and the US, increasing trends are being experienced in developing countries, particularly in India and China (Callow 2006). The US alone has experienced a decline in deaths from CHD by as much as 60% to 63% during 1965 to 1998 and a decline in cerebrovascular death by 59% to 63% during the same time period. In Europe similar trends have been observed: a decline in deaths from CHD of 30% to 32% and a decline in cerebrovascular death by 55% to 57% between 1965 and 1998 (Levi 2002). These declines have been attributed to lowering of risk factor distributions and better treatment (Bejot 2007; Ellekjaer 2007; Fang 2007). Our results must be viewed within the context of the falling trends seen in CHD and stroke deaths. Replication of these multiple risk factor intervention studies in countries where the cardiovascular disease is increasing should be a high research priority.
Authors' conclusions
Implications for practice.
The use of 'health promotion' techniques for one‐to‐one, work site or family‐orientated information and advice on a range of lifestyles (exercise, smoking cessation, diet) given to people at relatively low risk of cardiovascular disease is not particularly effective in terms of reducing the risk of clinical events. The costs of such interventions are high and it seems likely that these resources and techniques may be better used in people at high risk of cardiovascular disease and those with established cardiovascular disease, where evidence of effectiveness is much stronger.
Policy implications
Health protection through national fiscal and legislative changes that aim to reduce smoking, dietary consumption of fats, 'hidden' salt and calories, and increase facilities and opportunities for exercise, should have a higher priority than health promotion interventions applied to general and workforce populations. It is essential that the current concepts and practices of multiple risk factor intervention, primarily through individual risk factor counselling, are not exported to poorer countries as the best policy option for dealing with existing and projected burdens of cardiovascular disease (Pearson 1993). Health protection should be promoted as the mainstay of chronic disease prevention in poorer countries (Ebrahim 2001; Asaria 2007).
Implications for research.
It is unlikely that any further large‐scale multiple risk factor intervention trials will be mounted in high‐income countries in the future. It is also unlikely that uncontrolled or quasi‐experimental study designs will produce more robust answers to questions about the effectiveness of multiple risk factor intervention by means of individual or family health information and advice.
Research on the effects and costs of health protection (i.e. fiscal and legislative approaches) and primary prevention would be of direct policy relevance, particularly in low and middle‐income countries.
Qualitative studies examining how participants perceived and responded to the advice and treatment given in these randomised controlled trials could be very helpful in shaping future interventions. For example, the availability of foods and better access to recreational and sporting facilities may have a greater impact on dietary and exercise patterns respectively, than health professional advice. The effects of new approaches need to be examined in a wide range of people and in different contexts as it seems likely that the poor, socially excluded, specific ethnic groups and older people may all react in different ways and that interventions offered in developing countries where cardiovascular disease rates are increasing dramatically may be accepted more readily.
What's new
| Date | Event | Description |
|---|---|---|
| 23 January 2013 | Review declared as stable | This review will not be updated. The last two updates showed no substantive trials and few clinical events were found. It is highly unlikely that any further large scale, adequately powered trials will be conducted in the future. Small trials using only risk factor changes continue to be published but these do not contribute robust evidence to guide policy and practice due to inherent biases in their design. Owing to the development of very strong evidence to support pharmacological prevention of CVDs though use antihypertensives and statins there is much more emphasis on this approach used in conjunction with life‐style modification, making the findings from this review of much less relevance to contemporary public health practice. It is possible that new trials of multiple risk factor interventions will be mounted in low and middle income countries in the future and a separate review of their effects would be useful should this occur. |
History
Review first published: Issue 2, 1999
| Date | Event | Description |
|---|---|---|
| 11 November 2010 | New search has been performed | The search has been re‐run to June 2006. We identified and included 16 trials from the updated search. |
| 11 November 2010 | New citation required and conclusions have changed | A total of 55 trials are included in this update. We applied the new criteria of including studies with at least six months follow up. New authors are introduced to this update. |
| 1 October 2008 | Amended | Converted to new review format. |
| 16 February 2007 | New search has been performed | Revised plain language summary. |
| 18 August 2006 | New citation required but conclusions have not changed | Substantive amendment: updated with a new search from 1995 to September 2001. An additional 21 trials were found and were incorporated into the earlier version of the review. The findings and conclusions are essentially unaltered from the previous review. |
Notes
This review will not be updated. The last two updates showed no substantive trials and few clinical events were found. It is highly unlikely that any further large scale, adequately powered trials will be conducted in the future. Small trials using only risk factor changes continue to be published but these do not contribute robust evidence to guide policy and practice due to inherent biases in their design. Owing to the development of very strong evidence to support pharmacological prevention of CVDs though use antihypertensives and statins there is much more emphasis on this approach used in conjunction with life‐style modification, making the findings from this review of much less relevance to contemporary public health practice. It is possible that new trials of multiple risk factor interventions will be mounted in low and middle income countries in the future and a separate review of their effects would be useful should this occur.
Acknowledgements
We are extremely grateful to the following investigators who provided us with data: M. Shipley (WHO Factories 1986), L. Wilhelmsen (Gothenberg Study 1986), I. Hjermann (Oslo Diet Antismoking), J. Shaten (MRFIT Study 1982), T. Miettinen (Finnish men 1985), J. Muir and T. Lancaster (OXCHECK 1994), J. Baron (Abingdon 1990), S. Pyke (Family Heart 1994 M), S. Boles (Take Heart 1995), T. Ekbom (CELL Study 1995), A. Goble and M. Worcester (FARIS). The following investigators replied to our request but were unable to provide us with further data for various reasons: G. Payne (HDFP trial 1970), D. Morisky (Johns Hopkins), R. Stamler (Stamler 1989), S. Knutson (Tromso 1991 M), C. Connell (Connell 1995), P. Whelton and M. Espelund (TONE 1998), A. Steptoe (Change of Heart 1999), G. Berglund (Persson 1996) and K. Emmons (WHP 1999). We would also like to thank M. Napoli (Center for Medical Consumers) for her help with the plain language summary.
We would also like to thank the following people for their help with the translation of papers so that we could complete the data extraction from non‐English papers: M. Podinovskaia (Immunology Unit at the London School of Hygiene and Tropical Medicine) ‐ Russian translation, C. To (CRASH Trials Co‐ordinating Centre at the London School of Hygiene and Tropical Medicine) ‐ Chinese Translation, E. Gohil (Global Change and Health at the London School of Hygiene and Tropical Medicine) ‐ Polish Translation, C. Pizzi (Medical Statistics Unit at the London School of Hygiene and Tropical Medicine) ‐ Italian Translation and R. Houben (Infectious Disease Epidemiology Unit at the London School of Hygiene and Tropical Medicine) ‐ Dutch Translation.
Appendices
Appendix 1. Search strategies 2006
CENTRAL
#1 MeSH descriptor CARDIOVASCULAR DISEASES this term only #2 MeSH descriptor CORONARY DISEASE explode all trees #3 cardiovascular in All Text #4 (coronary in All Text near/3 disease* in All Text) #5 (heart in All Text near/3 disease* in All Text) #6 MeSH descriptor HYPERTENSION this term only #7 hypertension in All Text #8 (atherosclerosis in All Text or arteriosclerosis in All Text) #9 (hyperlipidaemia in All Text or hyperlipidemia in All Text) #10 MeSH descriptor ARTERIOSCLEROSIS explode all trees #11 MeSH descriptor CHOLESTEROL explode trees all trees #12 MeSH descriptor HYPERLIPIDEMIA explode all trees #13 cholesterol in All Text #14 multiple next risk next factor* in All Text #15 coronary next risk next factor* in All Text #16 (#1 or #2 or #3 or #4 or #5 or #6 or #7 or #8 or #9 or #10) #17 (#11 or #12 or #13 or #14 or #15) #18 (#16 or #17) #19 MeSH descriptor HEALTH EDUCATION explode all trees #20 MeSH descriptor HEALTH PROMOTION explode all trees #21 MeSH descriptor HEALTH BEHAVIOR explode all trees #22 MeSH descriptor PRIMARY PREVENTION this term only #23 MeSH descriptor COUNSELING this term only #24 counsel* in All Text #25 (health in All Text near/3 educat* in All Text) #26 (patient in All Text near/3 educat* in All Text) #27 (education* in All Text near/3 program* in All Text) #28 (health in All Text near/3 promotion* in All Text) #29 (health in All Text near/3 behaviour* in All Text) #30 (health in All Text near/3 behavior* in All Text) #31 primary next prevention in All Text #32 (multiple next risk in All Text near/3 intervention* in All Text) #33 (multifactor* in All Text near/3 intervention* in All Text) #34 (multifactor* in All Text near/3 prevention in All Text) #35 (risk next factor* in All Text near/3 reduc* in All Text) #36 (risk next factor* in All Text near/3 manag* in All Text) #37 (risk next factor* in All Text near/3 intervent* in All Text) #38 (lifestyle in All Text near/3 intervention* in All Text) #39 (lifestyle in All Text near/3 advice in All Text) #40 (life‐style in All Text near/3 intervention* in All Text) #41 (life‐style in All Text near/3 advice in All Text) #42 (life‐style in All Text near/3 alter* in All Text) #43 (lifestyle in All Text near/3 alter* in All Text) #44 (lifestyle in All Text near/3 educat* in All Text) #45 (life‐style in All Text near/3 educat* in All Text) #46 (life‐style in All Text near/3 chang* in All Text) #47 (lifestyle in All Text near/3 chang* in All Text) #48 (behavior* in All Text near/3 chang* in All Text) #49 (behaviour* in All Text near/3 chang* in All Text) #50 (health next care in All Text near/3 advice in All Text) #51 (healthcare in All Text near/3 advice in All Text) #52 nonpharmacologic* in All Text #53 non‐pharmacologic* in All Text #54 (#19 or #20 or #21 or #22 or #23 or #24 or #25 or #26 or #27 or #28 or #29) #55 (#30 or #31 or #32 or #33 or #34 or #35 or #36 or #37 or #38 or #39) #56 (#40 or #41 or #42 or #43 or #44 or #45 or #46 or #47 or #48 or #49 or #50 or #51 or #52 or #53) #57 (#54 or #55 or #56) #58 (#18 and #57)
MEDLINE on Ovid
1 cardiovascular diseases/ 2 exp coronary disease/ 3 hypertension/ 4 exp Arteriosclerosis/ 5 exp Hyperlipidemia/ 6 (cardiovascular adj3 disease$).tw. 7 (cardiovascular adj3 (fit or fitness)).tw. 8 (Coronary adj3 disease$).tw. 9 heart disease$.tw. 10 hypertension.tw. 11 hyperlipid?emia.tw 12 cholesterol.tw. 13 atherosclerosis.tw. 14 arteriosclerosis.tw. 15 coronary risk factor$.tw. 16 multiple risk factor$.tw. 17 cardiovascular risk factor$.tw. 18 or/1‐17 19 health promotion/ 20 exp health education/ 21 exp health behavior/ 22 exp counseling/ 23 primary prevention/ 24 (multifactor$ adj5 (intervent$ or prevent$)).tw. 25 ((lifestyle or life‐style) adj3 (intervention$ or educat$ or advice$ or alter$ or change$)).tw. 26 ((lifestyle or life‐style or behavio?r$) adj3 (intervention$ or educat$ or advice$ or alter$ or change$)).tw. 27 ((healthcare or health care) adj3 advice).tw. 28 primary prevention.tw. 29 (risk factor$ adj3 (reduc$ or manage$ or managing or intervent$ or program$)).tw. 30 (educat$ adj3 (program$ or patient$)).tw. 31 ((health or healthcare or health care) adj3 (educat$ or advice or promot$)).tw. 32 (nonpharmacologic$ or non‐pharmacologic$).tw. 33 ((lifestyle or life style or life‐style or behavio?r$ or risk factor$) adj3 modif$).tw. 34 or/19‐33 35 18 and 34 36 randomized controlled trial.pt. 37 controlled clinical trial.pt. 38 Randomized controlled trials/ 39 random allocation.sh. 40 double blind method.sh. 41 single‐blind method.sh. 42 or/36‐41 43 clinical trial.pt. 44 exp Clinical trials/ 45 (clin$ adj25 trial$).ti,ab. 46 ((singl$ or doubl$ or trebl$ or tripl$) adj (blind$ or mask$)).ti,ab. 47 placebos.sh. 48 placebo$.ti,ab. 49 random$.ti,ab. 50 research design.sh. 51 or/43‐50 52 exp animal/ not humans/ 53 42 or 51 54 53 not 52 55 54 and 35
EMBASE on Ovid
1 cardiovascular disease/ 2 exp ischemic heart disease/ 3 (coronary adj3 disease$).tw. 4 heart disease$.tw. 5 Hypertension/ 6 hypertension.tw. 7 (cardiovascular adj3 (disease$ or fit of fitness)).tw. 8 exp arteriosclerosis/ 9 exp hyperlipidemia/ 10 hyperlipid?emia.tw. 11 cholesterol.tw. 12 arteriosclero$.tw. 13 atherosclero$.tw. 14 coronary risk factor$.tw. 15 multiple risk factor$.tw. 16 cardiovascular risk factor$.tw. 17 or/1‐16 18 exp health education/ 19 exp health behavior/ 20 primary prevention/ 21 exp counseling/ 22 (multifactor$ adj5 (intervent$ or prevent$)).tw. 23 ((life‐style or life style or lifestyle or healthcare or health care) adj3 (intervention$ or educat$ or advice or alter$ or change$)).tw. 24 primary prevention.tw. 25 (risk factor$ adj3 (reduc$ or manage$ or managing or intervent$ or program$)).tw. 26 (educat$ adj3 (program$ or patient$)).tw. 27 (non pharmacologic$ or nonpharmacologic$).tw. 28 (risk factor$ adj3 modif$).tw. 29 ((lifestyle or life‐style or life style) adj3 modif$).tw. 30 exp behavior therapy/ 31 (behavi?r$ adj3 (intervention$ or program$ or modif$ or change$ or alter$)).tw. 32 (promot$ adj3 (health or healthcare or health care)).tw. 33 or/18‐32 34 17 and 33 35 random$.ti,ab. 36 factorial$.ti,ab. 37 (crossover$ or cross over$ or cross‐over$).ti,ab. 38 placebo$.ti,ab. 39 (double$ adj blind$).ti,ab. 40 (singl$ adj blind$).ti,ab. 41 assign$.ti,ab. 42 allocat$.ti,ab. 43 volunteer$.ti,ab. 44 Crossover Procedure/ 45 Double Blind Procedure/ 46 Randomized Controlled Trial/ 47 Single Blind Procedure/ 48 or/35‐47 49 exp animal/ 50 nonhuman/ 51 exp animal experiment/ 52 or/49‐51 53 exp human/ 54 52 not 53 55 48 not 54 56 55 and 34
Appendix 2. Search strategies 2001
MEDLINE on Ovid
<Mid 1998 to August Week 2 2001>
1 cardiovascular diseases/ 2 exp coronary disease/ 3 hypertension/ 4 exp Arteriosclerosis/ 5 exp Hyperlipidemia/ 6 (cardiovascular adj3 disease$).tw. 7 (cardiovascular adj3 (fit or fitness)).tw. 8 (Coronary adj3 disease$).tw. 9 heart disease$.tw. 10 hypertension.tw. 11 hyperlipid?emia.tw. 12 cholesterol.tw. 13 atherosclerosis.tw. 14 arteriosclerosis.tw. 15 coronary risk factor$.tw. 16 multiple risk factor$.tw. 17 cardiovascular risk factor$.tw. 18 or/1‐17 19 health promotion/ 20 exp health education/ 21 exp health behavior/ 22 exp counseling/ 23 primary prevention/ 24 (multifactor$ adj5 (intervent$ or prevent$)).tw. 25 ((lifestyle or life‐style) adj3 (intervention$ or educat$ or advice$ or alter$ or change$)).tw. 26 ((lifestyle or life‐style or behavio?r$) adj3 (intervention$ or educat$ or advice$ or alter$ or change$)).tw. 27 ((healthcare or health care) adj3 advice).tw. 28 primary prevention.tw. 29 (risk factor$ adj3 (reduc$ or manage$ or managing or intervent$ or program$)).tw. 30 (educat$ adj3 (program$ or patient$)).tw. 31 ((health or healthcare or health care) adj3 (educat$ or advice or promot$)).tw. 32 (nonpharmacologic$ or non‐pharmacologic$).tw. 33 ((lifestyle or life style or life‐style or behavio?r$ or risk factor$) adj3 modif$).tw. 34 or/19‐33 35 18 and 34 36 randomized controlled trial.pt. 37 controlled clinical trial.pt. 38 Randomized controlled trials/ 39 random allocation.sh. 40 double blind method.sh. 41 single‐blind method.sh. 42 or/36‐41 43 (animal not human).sh. 44 42 not 43 45 clinical trial.pt. 46 exp Clinical trials/ 47 (clin$ adj25 trial$).ti,ab. 48 ((singl$ or doubl$ or trebl$ or tripl$) adj (blind$ or mask$)).ti,ab. 49 placebos.sh. 50 placebo$.ti,ab. 51 random$.ti,ab. 52 research design.sh. 53 or/45‐52 54 53 not 43 55 54 not 44 56 44 or 54 57 35 and 56 58 limit 57 to yr=2000‐2001
EMBASE on Ovid
<1996 to August Week 2 2001>
1 cardiovascular diseases/ 2 exp coronary disease/ 3 hypertension/ 4 exp Arteriosclerosis/ 5 exp Hyperlipidemia/ 6 (cardiovascular adj3 disease$).tw. 7 (cardiovascular adj3 (fit or fitness)).tw. 8 (Coronary adj3 disease$).tw. 9 heart disease$.tw. 10 hypertension.tw. 11 hyperlipid?emia.tw. 12 cholesterol.tw. 13 atherosclerosis.tw. 14 arteriosclerosis.tw. 15 coronary risk factor$.tw. 16 multiple risk factor$.tw. 17 cardovascular risk factor$.tw. 18 or/1‐17 19 health promotion/ 20 exp health education/ 21 exp health behavior/ 22 exp counseling/ 23 primary prevention/ 24 (multifactor$ adj5 (intervent$ or prevent$)).tw. 25 ((lifestyle or life‐style) adj3 (intervention$ or educat$ or advice$ or alter$ or change$)).tw. 26 ((lifestyle or life‐style or behavio?r$) adj3 (intervention$ or educat$ or advice$ or alter$ or change$)).tw. 27 ((healthcare or health care) adj3 advice).tw. 28 primary prevention.tw. 29 (risk factor$ adj3 (reduc$ or manage$ or managing or intervent$ or program$)).tw. 30 (educat$ adj3 (program$ or patient$)).tw. 31 ((health or healthcare or health care) adj3 (educat$ or advice or promot$)).tw. 32 (nonpharmacologic$ or non‐pharmacologic$).tw. 33 ((lifestyle or life style or life‐style or behavio?r$ or risk factor$) adj3 modif$).tw. 34 or/19‐33 35 18 and 34 36 cardiovascular disease/ 37 exp ischemic heart disease/ 38 (coronary adj3 disease$).tw. 39 heart disease$.tw. 40 Hypertension/ 41 hypertension.tw. 42 (cardiovascular adj3 (disease$ or fit of fitness)).tw. 43 exp arteriosclerosis/ 44 exp hyperlipidemia/ 45 hyperlipid?emia.tw. 46 cholesterol.tw. 47 arteriosclero$.tw. 48 atherosclero$.tw. 49 coronary risk factor$.tw. 50 multiple risk factor$.tw. 51 cardiovascular risk factor$.tw. 52 or/36‐51 53 exp health education/ 54 exp health behavior/ 55 primary prevention/ 56 exp counseling/ 57 (multifactor$ adj5 (intervent$ or prevent$)).tw. 58 ((life‐style or life style or lifestyle or healthcare or health care) adj3 (intervention$ or educat$ or advice or alter$ or change$)).tw. 59 primary prevention.tw. 60 (risk factor$ adj3 (reduc$ or manage$ or managing or intervent$ or program$)).tw. 61 (educat$ adj3 (program$ or patient$)).tw. 62 (non pharmacologic$ or nonpharmacologic$).tw. 63 (risk factor$ adj3 modif$).tw. 64 ((lifestyle or life‐style or life style) adj3 modif$).tw. 65 exp behavior therapy/ 66 (behavi?r$ adj3 (intervention$ or program$ or modif$ or change$ or alter$)).tw. 67 (promot$ adj3 (health or healthcare or health care)).tw. 68 or/53‐67 69 52 and 68 70 random$.tw. 71 randomized controlled trial/ 72 trial$.tw. 73 compar$.tw. 74 follow‐up.tw. 75 blind$.tw. 76 double blind procedure/ 77 placebo$.tw. 78 placebo/ 79 doubl$.tw. 80 nonhuman/ not human/ 81 exp child/ not exp adult/ 82 or/70‐79 83 82 and 69 84 83 not (80 or 81)
Appendix 3. Search strategy 1995
MEDLINE
randomized controlled trial.pt. randomized controlled trials/ random‐allocation.sh. double‐blind‐method.sh. single‐blind‐method.sh. 1 or 2 or 3 or 4 or 5 clinical trials.pt. clinical trials.sh. clin$ near trial$.ti. clin$ near trial$.ab. placebo.sh. placebo.tw. random.tw. 7 or 8 or 9 or 10 or 11 or 12 or 13 limit 14 to human coronary disease.sh. cerebrovascular disorders.sh.
Data and analyses
Comparison 1. Multiple risk factor intervention versus control.
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
|---|---|---|---|---|
| 1 Total mortality | 14 | 139232 | Peto Odds Ratio (Peto, Fixed, 95% CI) | 1.00 [0.96, 1.05] |
| 2 Total mortality (individual analysis or cluster) | 14 | 139232 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.96, 1.05] |
| 2.1 Individual | 12 | 70355 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.89, 1.00] |
| 2.2 Cluster randomisation ‐ analysis by individual | 2 | 68877 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.12 [1.04, 1.22] |
| 3 Total mortality (by allocation concealment) | 14 | 139232 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.96, 1.05] |
| 3.1 Adequate allocation concealment | 3 | 18729 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.86, 1.21] |
| 3.2 Inadequate allocation concealment | 4 | 13388 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.71, 0.94] |
| 3.3 Unclear allocation concealment | 7 | 107115 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.03 [0.98, 1.09] |
| 4 Total mortality (by co‐morbidity) | 13 | 138010 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.96, 1.05] |
| 4.1 No co‐morbidity | 7 | 120158 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.04 [0.99, 1.09] |
| 4.2 Co‐morbidity (hypertension and diabetes) | 6 | 17852 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.78 [0.68, 0.89] |
| 5 Total mortality (by drug treatment) | 13 | 139091 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.01 [0.96, 1.05] |
| 5.1 No drug treatment | 4 | 76589 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.12 [1.04, 1.21] |
| 5.2 Antihypertensives OR lipid‐lowering drugs | 6 | 26113 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.78, 0.96] |
| 5.3 Antihypertensives AND lipid‐lowering drugs | 3 | 36389 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.92, 1.06] |
| 6 Total mortality (by era) | 14 | 139232 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.96, 1.05] |
| 6.1 Low rate of CVD | 7 | 18818 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.73, 1.18] |
| 6.2 High Rate of CVD | 7 | 120414 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.01 [0.96, 1.06] |
| 7 Total mortality (by age of study) | 14 | 139232 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.96, 1.05] |
| 7.1 Before 2000 | 11 | 133228 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.01 [0.96, 1.05] |
| 7.2 After 2000 | 3 | 6004 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.90 [0.51, 1.60] |
| 8 Coronary heart disease mortality | 11 | 132564 | Peto Odds Ratio (Peto, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 9 Coronary heart disease mortality (individual analysis or cluster) | 11 | 132834 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 9.1 Individual | 10 | 69102 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.96 [0.87, 1.05] |
| 9.2 Cluster randomisation ‐ analysis by individual | 1 | 63732 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.08 [0.94, 1.23] |
| 10 Coronary heart disease mortality (by allocation concealment) | 11 | 132834 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 10.1 Adequate | 1 | 12866 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.72, 1.20] |
| 10.2 Inadequate | 3 | 12853 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.85 [0.67, 1.07] |
| 10.3 Unclear | 7 | 107115 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.94, 1.11] |
| 11 Coronary heart disease mortality (by co‐morbidity) | 11 | 132834 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 11.1 No co‐morbidity | 7 | 120845 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.94, 1.11] |
| 11.2 Co‐morbidity (hypertension or diabetes) | 4 | 11989 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.66, 1.01] |
| 12 Coronary heart disease (by drug treatment) | 11 | 132834 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 12.1 No drug treatment | 1 | 1232 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.44 [0.17, 1.15] |
| 12.2 Antihypertensives OR lipid‐lowering drugs | 5 | 88079 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.89, 1.10] |
| 12.3 Antihypertensives AND lipid‐lowering drugs | 5 | 43523 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.01 [0.90, 1.13] |
| 13 Coronary heart disease (by era) | 11 | 132834 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 13.1 Low rate of CVD | 4 | 12420 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.66, 1.49] |
| 13.2 High rate of CVD | 7 | 120414 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 14 Coronary heart disease mortality (by study age) | 11 | 132834 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 14.1 Before 2000 | 10 | 132693 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.92, 1.07] |
| 14.2 After 2000 | 1 | 141 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.57 [0.13, 2.50] |
| 15 Stroke mortality | 7 | 56931 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.75 [0.60, 0.95] |
| 16 Stroke mortality (by allocation concealment) | 7 | 56931 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.75 [0.60, 0.95] |
| 16.1 Adequate | 1 | 12866 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.18 [0.53, 2.64] |
| 16.2 Inadequate | 2 | 12172 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.58 [0.37, 0.91] |
| 16.3 Unclear | 4 | 31893 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.60, 1.05] |
| 17 Stroke mortality (by co‐morbidity) | 7 | 56931 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.75 [0.60, 0.95] |
| 17.1 No co‐morbidity | 4 | 45342 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.87 [0.66, 1.14] |
| 17.2 Co‐morbidity (hypertension or diabetes) | 3 | 11589 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.54 [0.36, 0.83] |
| 18 Stroke mortality (by drug treatment) | 7 | 56931 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.75 [0.60, 0.95] |
| 18.1 No drug treatment | 1 | 1232 | Odds Ratio (M‐H, Fixed, 95% CI) | 2.08 [0.19, 23.03] |
| 18.2 Antihypertensives OR lipid‐lowering drugs | 3 | 23947 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.66 [0.45, 0.97] |
| 18.3 Antihypertensives AND lipid‐lowering drugs | 3 | 31752 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.80 [0.60, 1.06] |
| 19 Stroke mortality (by era) | 7 | 56931 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.75 [0.60, 0.95] |
| 19.1 Low rate of CVD | 2 | 649 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.49 [0.17, 1.46] |
| 19.2 High rate of CVD | 5 | 56282 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.77 [0.61, 0.97] |
| 20 Stroke mortality (by study age) | 7 | 56931 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.75 [0.60, 0.95] |
| 20.1 Before 2000 | 6 | 56790 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.76 [0.60, 0.95] |
| 20.2 After 2000 | 1 | 141 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.65 [0.10, 4.00] |
| 21 Fatal and non‐fatal clinical events | 9 | 121381 | Odds Ratio (M‐H, Random, 95% CI) | 0.84 [0.73, 0.98] |
| 22 Fatal and non‐fatal clinical events (individual analysis or cluster) | 9 | 121381 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.88, 0.96] |
| 22.1 Individual | 8 | 57649 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.89 [0.84, 0.93] |
| 22.2 Cluster randomisation ‐ analysis by individual | 1 | 63732 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.06 [0.97, 1.17] |
| 23 Fatal and non‐fatal clinical events (by allocation concealment) | 9 | 121381 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.88, 0.96] |
| 23.1 Adequate | 2 | 13584 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.76, 0.88] |
| 23.2 Inadequate | 2 | 12172 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.73 [0.62, 0.86] |
| 23.3 Unclear | 5 | 95625 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.96, 1.08] |
| 24 Fatal and non‐fatal clinical events (by co‐morbidity) | 9 | 121381 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.88, 0.96] |
| 24.1 No co‐morbidity | 5 | 109074 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.90, 0.99] |
| 24.2 Co‐morbidity (hypertension or diabetes) | 4 | 12307 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.71 [0.61, 0.83] |
| 25 Fatal and non‐fatal clinical events (by drug treatment) | 9 | 121381 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.88, 0.96] |
| 25.1 No drug treatment | 1 | 1232 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.57 [0.33, 0.97] |
| 25.2 Antihypertensives OR lipid‐lowering drugs | 5 | 88397 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.88 [0.84, 0.93] |
| 25.3 Antihypertensives AND lipid‐lowering drugs | 3 | 31752 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.93, 1.08] |
| 26 Fatal and non‐fatal clinical events (by era) | 9 | 121381 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.88, 0.96] |
| 26.1 Low rate of CVD | 3 | 1367 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.60 [0.44, 0.84] |
| 26.2 High Rate of CVD | 6 | 120014 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.89, 0.97] |
| 27 Fatal and non‐fatal clinical events (by age of study) | 9 | 120011 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.89, 0.97] |
| 27.1 Before 2000 | 7 | 119152 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.90, 0.98] |
| 27.2 After 2000 | 2 | 859 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.46 [0.25, 0.85] |
| 28 Smoking prevalence | 20 | 51586 | Odds Ratio (M‐H, Random, 95% CI) | 0.87 [0.75, 1.00] |
| 29 Smoking prevalence (individual analysis or cluster) | 20 | 51586 | Odds Ratio (M‐H, Random, 95% CI) | 0.87 [0.75, 1.00] |
| 29.1 Cluster randomisation ‐ analysis by cluster | 1 | 520 | Odds Ratio (M‐H, Random, 95% CI) | 0.43 [0.28, 0.64] |
| 29.2 Individual randomisation | 16 | 31506 | Odds Ratio (M‐H, Random, 95% CI) | 0.89 [0.76, 1.04] |
| 29.3 Cluster randomisation ‐ analysis by individual | 3 | 19560 | Odds Ratio (M‐H, Random, 95% CI) | 0.98 [0.89, 1.07] |
| 30 Smoking prevalence (by allocation concealment) | 20 | 51586 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.76, 0.82] |
| 30.1 Adequate allocation concealment | 4 | 12136 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.58 [0.54, 0.63] |
| 30.2 Inadequate allocation concealment | 5 | 4365 | Odds Ratio (M‐H, Fixed, 95% CI) | 1.03 [0.91, 1.17] |
| 30.3 Unclear allocation concealment | 11 | 35085 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.89 [0.84, 0.94] |
| 31 Smoking prevalence (by co‐morbidity) | 15 | 49681 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.75, 0.82] |
| 31.1 No co‐morbidity | 15 | 49681 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.75, 0.82] |
| 32 Smoking prevalence (by drug treatment) | 20 | 53491 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.76, 0.83] |
| 32.1 No drug treatment | 9 | 10724 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.78, 0.93] |
| 32.2 Antihypertensives OR lipid‐lowering drugs | 6 | 31599 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.72 [0.68, 0.76] |
| 32.3 Antihypertensives AND lipid‐lowering drugs | 5 | 9263 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.91 [0.83, 1.00] |
| 32.4 Co‐morbidity (hypertension or diabetes) | 5 | 1905 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.89 [0.70, 1.12] |
| 33 Smoking prevalence (by era) | 20 | 51586 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.76, 0.82] |
| 33.1 Low rate of CVD | 15 | 16120 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.85 [0.79, 0.92] |
| 33.2 High rate of CVD | 5 | 35466 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.76 [0.72, 0.80] |
| 34 Smoking prevalence (by age of study) | 20 | 51586 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.76, 0.82] |
| 34.1 Study before 2000 | 15 | 50166 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.79 [0.75, 0.82] |
| 34.2 Study after 2000 | 5 | 1420 | Odds Ratio (M‐H, Fixed, 95% CI) | 0.89 [0.68, 1.18] |
| 35 Systolic blood pressure | 53 | 64809 | Mean Difference (IV, Fixed, 95% CI) | ‐3.38 [‐3.63, ‐3.13] |
| 36 Systolic blood pressure (individual analysis or cluster) | 53 | 64809 | Mean Difference (IV, Random, 95% CI) | ‐2.71 [‐3.49, ‐1.93] |
| 36.1 Cluster randomisation ‐ analysis by cluster | 1 | 504 | Mean Difference (IV, Random, 95% CI) | 2.5 [‐0.79, 5.79] |
| 36.2 Individual randomisation | 45 | 38261 | Mean Difference (IV, Random, 95% CI) | ‐2.99 [‐3.87, ‐2.11] |
| 36.3 Cluster randomisation ‐ analysis by individual | 7 | 26044 | Mean Difference (IV, Random, 95% CI) | ‐1.79 [‐3.54, ‐0.04] |
| 37 Systolic blood pressure (by allocation concealment) | 53 | 64809 | Mean Difference (IV, Fixed, 95% CI) | ‐3.38 [‐3.63, ‐3.13] |
| 37.1 Adequate allocation concealment | 14 | 18950 | Mean Difference (IV, Fixed, 95% CI) | ‐4.32 [‐4.69, ‐3.96] |
| 37.2 Inadequate allocation concealment | 9 | 4669 | Mean Difference (IV, Fixed, 95% CI) | ‐2.03 [‐2.84, ‐1.23] |
| 37.3 Unclear allocation concealment | 30 | 41190 | Mean Difference (IV, Fixed, 95% CI) | ‐2.65 [‐3.03, ‐2.26] |
| 38 Systolic blood pressure (by co‐morbidity) | 53 | 64809 | Mean Difference (IV, Fixed, 95% CI) | ‐3.38 [‐3.63, ‐3.13] |
| 38.1 No co‐morbidity | 29 | 52275 | Mean Difference (IV, Fixed, 95% CI) | ‐3.70 [‐4.01, ‐3.38] |
| 38.2 Co‐morbidity (hypertension or diabetes) | 24 | 12534 | Mean Difference (IV, Fixed, 95% CI) | ‐2.81 [‐3.23, ‐2.38] |
| 39 Systolic blood pressure (by drug treatment) | 53 | 64809 | Mean Difference (IV, Fixed, 95% CI) | ‐3.38 [‐3.63, ‐3.13] |
| 39.1 No drug treatment | 29 | 15846 | Mean Difference (IV, Fixed, 95% CI) | ‐2.74 [‐3.19, ‐2.29] |
| 39.2 Antihypertensives OR lipid‐lowering drugs | 17 | 34517 | Mean Difference (IV, Fixed, 95% CI) | ‐3.89 [‐4.28, ‐3.51] |
| 39.3 Antihypertensives AND lipid‐lowering drugs | 7 | 14446 | Mean Difference (IV, Fixed, 95% CI) | ‐3.31 [‐3.81, ‐2.80] |
| 40 Systolic blood pressure (by era) | 53 | 64809 | Mean Difference (IV, Fixed, 95% CI) | ‐3.38 [‐3.63, ‐3.13] |
| 40.1 Low rate of CVD | 49 | 30562 | Mean Difference (IV, Fixed, 95% CI) | ‐3.07 [‐3.38, ‐2.75] |
| 40.2 High rate of CVD | 4 | 34247 | Mean Difference (IV, Fixed, 95% CI) | ‐3.92 [‐4.34, ‐3.51] |
| 41 Systolic blood pressure (by age of study) | 53 | 64809 | Mean Difference (IV, Fixed, 95% CI) | ‐3.38 [‐3.63, ‐3.13] |
| 41.1 Study before 2000 | 36 | 53606 | Mean Difference (IV, Fixed, 95% CI) | ‐3.59 [‐3.90, ‐3.28] |
| 41.2 Study after 2000 | 17 | 11203 | Mean Difference (IV, Fixed, 95% CI) | ‐2.97 [‐3.41, ‐2.54] |
| 42 Diastolic blood pressure | 53 | 75400 | Mean Difference (IV, Fixed, 95% CI) | ‐2.41 [‐2.55, ‐2.26] |
| 43 Diastolic blood pressure (individual analysis or cluster) | 53 | 75400 | Mean Difference (IV, Random, 95% CI) | ‐2.13 [‐2.67, ‐1.58] |
| 43.1 Cluster randomisation ‐ analysis by cluster | 1 | 503 | Mean Difference (IV, Random, 95% CI) | ‐0.30 [‐2.86, 2.26] |
| 43.2 Individual randomisation | 46 | 49255 | Mean Difference (IV, Random, 95% CI) | ‐2.36 [‐2.94, ‐1.77] |
| 43.3 Cluster randomisation ‐ analysis by individual | 6 | 25642 | Mean Difference (IV, Random, 95% CI) | ‐0.79 [‐1.42, ‐0.16] |
| 44 Diastolic blood pressure (by allocation concealment) | 53 | 75400 | Mean Difference (IV, Fixed, 95% CI) | ‐2.41 [‐2.55, ‐2.26] |
| 44.1 Adequate concealment | 14 | 18969 | Mean Difference (IV, Fixed, 95% CI) | ‐2.38 [‐2.60, ‐2.16] |
| 44.2 Inadequate allocation concealment | 10 | 15644 | Mean Difference (IV, Fixed, 95% CI) | ‐3.70 [‐4.01, ‐3.40] |
| 44.3 Unclear allocation concealment | 29 | 40787 | Mean Difference (IV, Fixed, 95% CI) | ‐1.60 [‐1.85, ‐1.35] |
| 45 Diastolic blood pressure (by co‐morbidity) | 53 | 75400 | Mean Difference (IV, Fixed, 95% CI) | ‐2.41 [‐2.55, ‐2.26] |
| 45.1 No co‐morbidity | 28 | 51891 | Mean Difference (IV, Fixed, 95% CI) | ‐2.33 [‐2.52, ‐2.13] |
| 45.2 Co‐morbidity (hypertension or diabetes) | 25 | 23509 | Mean Difference (IV, Fixed, 95% CI) | ‐2.51 [‐2.73, ‐2.29] |
| 46 Diastolic blood pressure (by drug treatment) | 53 | 75400 | Mean Difference (IV, Fixed, 95% CI) | ‐2.41 [‐2.55, ‐2.26] |
| 46.1 No drug treatment | 28 | 15449 | Mean Difference (IV, Fixed, 95% CI) | ‐2.09 [‐2.40, ‐1.79] |
| 46.2 Antihypertensives OR lipid‐lowering drugs | 18 | 45505 | Mean Difference (IV, Fixed, 95% CI) | ‐3.05 [‐3.25, ‐2.85] |
| 46.3 Antihypertensives AND lipid‐lowering drugs | 7 | 14446 | Mean Difference (IV, Fixed, 95% CI) | ‐1.41 [‐1.70, ‐1.13] |
| 47 Diastolic blood pressure (by era) | 53 | 75400 | Mean Difference (IV, Fixed, 95% CI) | ‐2.41 [‐2.55, ‐2.26] |
| 47.1 Low rate of CVD | 48 | 30200 | Mean Difference (IV, Fixed, 95% CI) | ‐1.70 [‐1.90, ‐1.49] |
| 47.2 High Rate of CVD | 5 | 45200 | Mean Difference (IV, Fixed, 95% CI) | ‐3.15 [‐3.36, ‐2.94] |
| 48 Diastolic blood pressure (by age of study) | 53 | 75400 | Mean Difference (IV, Fixed, 95% CI) | ‐2.41 [‐2.55, ‐2.26] |
| 48.1 Study before 2000 | 36 | 64197 | Mean Difference (IV, Fixed, 95% CI) | ‐2.76 [‐2.93, ‐2.59] |
| 48.2 Study after 2000 | 17 | 11203 | Mean Difference (IV, Fixed, 95% CI) | ‐1.38 [‐1.67, ‐1.10] |
| 49 Blood cholesterol | 50 | 71776 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 50 Blood cholesterol (individual analysis or cluster) | 50 | 71776 | Mean Difference (IV, Random, 95% CI) | ‐0.24 [‐0.32, ‐0.16] |
| 50.1 Cluster randomisation ‐ analysis by cluster | 2 | 2475 | Mean Difference (IV, Random, 95% CI) | 0.01 [‐0.01, 0.03] |
| 50.2 Individual randomisation | 43 | 49428 | Mean Difference (IV, Random, 95% CI) | ‐0.28 [‐0.39, ‐0.17] |
| 50.3 Cluster randomisation (analysis by individual) | 5 | 19873 | Mean Difference (IV, Random, 95% CI) | 0.01 [‐0.03, 0.04] |
| 51 Blood cholesterol (by allocation concealment) | 50 | 71776 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 51.1 Adequate allocation concealment | 12 | 13108 | Mean Difference (IV, Fixed, 95% CI) | ‐0.16 [‐0.19, ‐0.13] |
| 51.2 Inadequate allocation concealment | 11 | 16876 | Mean Difference (IV, Fixed, 95% CI) | ‐0.13 [‐0.16, ‐0.10] |
| 51.3 Unclear allocation concealment | 27 | 41792 | Mean Difference (IV, Fixed, 95% CI) | ‐0.04 [‐0.06, ‐0.03] |
| 52 Blood cholesterol (by co‐morbidity) | 50 | 71776 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 52.1 No co‐morbidity | 34 | 55462 | Mean Difference (IV, Fixed, 95% CI) | ‐0.08 [‐0.09, ‐0.06] |
| 52.2 Co‐morbidity (hypertension and/or diabetes) | 16 | 16314 | Mean Difference (IV, Fixed, 95% CI) | ‐0.06 [‐0.08, ‐0.03] |
| 53 Blood cholesterol (by drug treatment) | 50 | 71776 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 53.1 No drug treatment | 31 | 19210 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.05] |
| 53.2 Antihypertensives OR lipid‐lowering drugs | 13 | 43070 | Mean Difference (IV, Fixed, 95% CI) | ‐0.06 [‐0.08, ‐0.04] |
| 53.3 Antihypertensives AND lipid‐lowering drug | 6 | 9496 | Mean Difference (IV, Fixed, 95% CI) | ‐0.18 [‐0.22, ‐0.14] |
| 54 Blood cholesterol (by era) | 50 | 71776 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 54.1 Low rate of CVD | 44 | 25887 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.05] |
| 54.2 High rate of CVD | 6 | 45889 | Mean Difference (IV, Fixed, 95% CI) | ‐0.09 [‐0.11, ‐0.07] |
| 55 Blood cholesterol (by age of study) | 50 | 71776 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 55.1 Study before 2000 | 33 | 66040 | Mean Difference (IV, Fixed, 95% CI) | ‐0.07 [‐0.08, ‐0.06] |
| 55.2 Study after 2000 | 17 | 5736 | Mean Difference (IV, Fixed, 95% CI) | ‐0.14 [‐0.18, ‐0.10] |
1.2. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 2 Total mortality (individual analysis or cluster).
1.6. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 6 Total mortality (by era).
1.7. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 7 Total mortality (by age of study).
1.9. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 9 Coronary heart disease mortality (individual analysis or cluster).
1.10. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 10 Coronary heart disease mortality (by allocation concealment).
1.11. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 11 Coronary heart disease mortality (by co‐morbidity).
1.12. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 12 Coronary heart disease (by drug treatment).
1.13. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 13 Coronary heart disease (by era).
1.14. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 14 Coronary heart disease mortality (by study age).
1.16. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 16 Stroke mortality (by allocation concealment).
1.17. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 17 Stroke mortality (by co‐morbidity).
1.18. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 18 Stroke mortality (by drug treatment).
1.19. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 19 Stroke mortality (by era).
1.20. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 20 Stroke mortality (by study age).
1.22. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 22 Fatal and non‐fatal clinical events (individual analysis or cluster).
1.23. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 23 Fatal and non‐fatal clinical events (by allocation concealment).
1.25. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 25 Fatal and non‐fatal clinical events (by drug treatment).
1.26. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 26 Fatal and non‐fatal clinical events (by era).
1.27. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 27 Fatal and non‐fatal clinical events (by age of study).
1.30. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 30 Smoking prevalence (by allocation concealment).
1.31. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 31 Smoking prevalence (by co‐morbidity).
1.32. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 32 Smoking prevalence (by drug treatment).
1.34. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 34 Smoking prevalence (by age of study).
1.35. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 35 Systolic blood pressure.
1.37. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 37 Systolic blood pressure (by allocation concealment).
1.38. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 38 Systolic blood pressure (by co‐morbidity).
1.40. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 40 Systolic blood pressure (by era).
1.41. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 41 Systolic blood pressure (by age of study).
1.44. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 44 Diastolic blood pressure (by allocation concealment).
1.45. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 45 Diastolic blood pressure (by co‐morbidity).
1.47. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 47 Diastolic blood pressure (by era).
1.48. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 48 Diastolic blood pressure (by age of study).
1.52. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 52 Blood cholesterol (by co‐morbidity).
1.54. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 54 Blood cholesterol (by era).
1.55. Analysis.
Comparison 1 Multiple risk factor intervention versus control, Outcome 55 Blood cholesterol (by age of study).
Characteristics of studies
Characteristics of included studies [ordered by study ID]
Aberg 1989 F.
| Methods | Primary care Random allocation by health centre (centres paired according to size, number of doctors and personnel) Unit of analysis was individual | |
| Participants | Men and women on antihypertensive drugs aged 30 to 69 years Mean age 55 N = 129 | |
| Interventions | Group‐based video‐taped lifestyle counselling: dietary change, stress management, increased physical activity, home blood pressure monitoring Up to 8 group sessions | |
| Outcomes | No clinical event outcomes Change in antihypertensive treatment, weight, hypertension, cholesterol, triglycerides, fasting glucose, life quality | |
| Notes | All patients followed the same schedule for reduction and withdrawal of antihypertensive drugs Concluded that intervention was effective in reducing hypertensive medication ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | Unclear |
Aberg 1989 M.
| Methods | Primary care Random allocation by health centre (centres paired according to size, number of doctors and personnel) Unit of analysis was individual | |
| Participants | Men and women on antihypertensive drugs aged 30 to 69 years Mean age 55 N = 159 | |
| Interventions | Group‐based video‐taped lifestyle counselling: dietary change, stress management, increased physical activity, home blood pressure monitoring Up to 8 group sessions | |
| Outcomes | No clinical event outcomes Change in antihypertensive treatment, weight, hypertension, cholesterol, triglycerides, fasting glucose, life quality | |
| Notes | All patients followed the same schedule for reduction and withdrawal of antihypertensive drugs Concluded that intervention was effective in reducing hypertensive medication | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Abingdon 1990.
| Methods | Primary care Random allocation by individual | |
| Participants | Men and women, mean age 42 years (range 25 to 60) N = 368 | |
| Interventions | Diet, weight control, smoking advice, exercise, alcohol advice carried out by nurse Duration 1 year | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | Main focus was on dietary change, but despite self‐reported behaviour change, no changes in blood cholesterol found | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
ADAPT 2005.
| Methods | Screened volunteers on hypertensive drugs Individual randomisation | |
| Participants | Men and women on hypertensive medication for at least 3 months with mean age 55 to 57 N = 241 | |
| Interventions | Facilitator provided individual counselling, interactive group workshops and handouts on lifestyle modification over 4 months | |
| Outcomes | No clinical event outcomes Systolic and diastolic changes, total cholesterol at 3‐year follow up | |
| Notes | 42% loss to follow up ITT used No significant changes other than an increase in total cholesterol in usual care group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Aldana (CHIP) 2005.
| Methods | Work site volunteers Random allocation by individual | |
| Participants | Male and female employees mean age 46 N = 145 | |
| Interventions | Lectures on diet and exercise delivered by dieticians and medical staff | |
| Outcomes | No clinical event outcomes Systolic and diastolic BP and total cholesterol at 6‐month follow up | |
| Notes | Unclear if ITT used Study focused on increasing health knowledge | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Applegate 1992.
| Methods | Community screening and volunteers Randomisation by individual | |
| Participants | Men and women aged 60 to 85 (mean age 64 to 65) with mild diastolic hypertension and modestly overweight N = 56 | |
| Interventions | Nutritionist supervised Individual weight loss goals, exercise and diet self‐monitoring with behavioural feedback Duration 6 months | |
| Outcomes | No clinical event outcomes Weight, urinary sodium, systolic and diastolic blood pressure, waist‐hip ratio, exercise | |
| Notes | Reduction in weight and systolic blood pressure in those followed up Authors report good compliance with intervention Authors conclusions: results indicate intervention will lower borderline or mild diastolic hypertension | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | D ‐ Not used |
Blumenthal 2000.
| Methods | Volunteers screened Randomisation by individual | |
| Participants | Men and women aged 29+ (mean age 48) with un‐medicated high‐normal blood pressure Overweight and not performing regular aerobic exercise N = 79 | |
| Interventions | Exercise physiologist supervised exercise and behavioural intervention including diet Duration 6 months | |
| Outcomes | No clinical event outcomes Systolic and diastolic blood pressure, glucose tolerance, weight, exercise test | |
| Notes | Another intervention group received only exercise intervention Authors conclusions: exercise alone reduced BP and the addition of behavioural weight loss programme enhanced this ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Brekke 2005a.
| Methods | Screened volunteers of relatives of patients with type 2 diabetes individually randomised | |
| Participants | Men and women mean age 42 with no diabetes N = 77 | |
| Interventions | Dietician delivered educational sessions on diet and exercise followed by group counselling for 4 months | |
| Outcomes | No clinical event outcomes Dietary changes, smoking and total cholesterol at 1‐year follow up | |
| Notes | ITT not used Another intervention group received exercise only | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Cakir 2006.
| Methods | Individual randomisation in outpatient hypertension clinic | |
| Participants | Men and women with hypertension mean age 55 to 57 N = 70 | |
| Interventions | Nurse delivered lifestyle modification programme on diet, exercise, smoking and stress management over a 3‐month period | |
| Outcomes | No clinical event outcomes Systolic and diastolic BP, smoking and total cholesterol at 6‐month follow up | |
| Notes | ITT not used Statistically significant results were obtained in lifestyle modification | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
CELL Study 1995.
| Methods | Primary care screening Randomisation of individuals in 2 x 3 factorial design | |
| Participants | People with at least 2 risk factors in addition to moderately raised blood cholesterol Men and women, mean age 49 years (30 to 59) N = 681 | |
| Interventions | Factor 1: counselling on health problems and risk factor management, food purchasing, exercise versus usual care Factor 2: pravastatin versus placebo versus control without drug Duration 1 year | |
| Outcomes | Total mortality and CHD mortality Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence, exercise score | |
| Notes | At 1 year counselling intervention main effects showed lower blood cholesterol and lower Framingham risk factor scores compared with groups not receiving counselling intervention No significant differences in blood pressures, smoking prevalence or exercise score | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Change of Heart 1999.
| Methods | General practice, cluster allocation by minimisation to balance for social deprivation, practice nurse hours and fund‐holding status 20 practices Unit of analysis was general practice | |
| Participants | Men and women mean age 47 years with 1 or more cardiovascular risk factors No treatment N = 883 | |
| Interventions | Nurse‐led stages of change behavioural counselling on smoking, diet, physical activity. 2 or 3 20‐minute counselling sessions + telephone contact | |
| Outcomes | No clinical event outcomes Diet, exercise, smoking habits, blood pressure, cholesterol, weight, BMI Follow up 4 and 12 months | |
| Notes | Based on stages of change model Fewer smokers at baseline in intervention group (39%) than control (49%) Problems with recruitment and drop‐out ‐ more recruited to intervention than control group ‐ 59% of patients followed up at 12 months Those at higher risk received more intensive treatment | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | D ‐ Not used |
Connell 1995.
| Methods | Work site volunteers Randomisation by work site Unit of analysis was individual | |
| Participants | Men and women age 19 to 67; mean age 39 N = 1432 | |
| Interventions | Health risk assessment and individual health counselling Educational classes and self‐help material Duration 1 year | |
| Outcomes | Total cholesterol, systolic and diastolic blood pressure, BMI, exercise frequency 1‐year follow up | |
| Notes | 47% loss to follow up and no ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Esposito 2004.
| Methods | Obesity outpatient clinic individual randomisation | |
| Participants | Obese men with erectile dysfunction and mean age of 43 N = 110 | |
| Interventions | Small group sessions on diet and physical exercise with individual counselling delivered by nutritionist and exercise trainer over a 2‐year period | |
| Outcomes | BMI, erectile dysfunction, total cholesterol, systolic and diastolic blood pressure at 2‐year follow up | |
| Notes | ITT used Emphasis on erectile dysfunction Significant changes observed in intervention group in BP and total cholesterol | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Family Heart 1994 M.
| Methods | Primary care Random allocation of households to intervention and control groups | |
| Participants | Primary care screening, mean age 50 (40 to 59) N = 3941 | |
| Interventions | Intensity of intervention depended on individual's level of risk Nurse counselling on diet, weight, smoking, exercise, alcohol Duration 1 year | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | 2 control groups used: internal to study used for comparisons in this review Drop‐outs were more likely to have high CVD risk factor levels Overall predicted risk reduction of 12% achieved but thought to be too costly in practice ‐ no cost‐effectiveness analysis conducted, however | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Family Heart 1994 F.
| Methods | Primary care Random allocation of households to intervention and control groups | |
| Participants | Primary care: women age 50 (40 to 59) N = 2619 | |
| Interventions | Intensity of intervention depended on level of individual's risk Nurse counselling on diet, weight control, smoking advice, exercise, alcohol Duration 1 year | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | 2 control groups used but internal control used in this review | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
FARIS 1997 F.
| Methods | First degree relatives of AMI, CABG and PTCA patients Randomised by family | |
| Participants | Families of people with CHD event, age 18 to 69; mean age 61 N = 658 | |
| Interventions | Individualised risk factor advice 3 months dietary advice and lipid‐lowering medication if required | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, cholesterol, smoking, BMI and CVD risk | |
| Notes | Results are for people without cardiovascular disease attending combined primary and secondary prevention clinic Information on baseline and follow‐up smoking prevalence not available No significant effect of intervention on smoking quit rate ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
FARIS 1997 M.
| Methods | First degree relatives of AMI, CABG and PTCA patients Randomised by family | |
| Participants | Families of people with CHD event, age 18 to 69, mean age 57 N = 442 | |
| Interventions | Individualised risk factor advice 3 months dietary advice and lipid‐lowering medication if required | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, cholesterol, smoking, BMI and CVD risk | |
| Notes | Results are for people without cardiovascular disease attending combined primary and secondary prevention clinic Information on baseline and follow‐up smoking prevalence not available No significant effect of intervention on smoking quit rate ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Finnish DPS 2001.
| Methods | High‐risk groups identified from epidemiological surveys, opportunistic screening, volunteers Randomisation by individual, stratified by sex, centre and OGTT result | |
| Participants | Overweight or with family history of type 2 diabetes men and women aged 40 to 64 years (mean age 52 to 53) with impaired glucose tolerance N = 523 | |
| Interventions | Nutritionist‐delivered individual and group dietary advice Weight goal established with physician and nutritionist and regular assessment Supervised exercise Each person had 7 sessions in the first year and 1 session every 3 months subsequently | |
| Outcomes | No clinical event outcomes Development of diabetes, weight, diet, exercise, waist circumference, glucose, insulin, cholesterol, HDL, triglycerides, systolic and diastolic blood pressure Follow up reported end of year 1 | |
| Notes | Study planned for 6 years, recruited 1993 to 1998 In March 2000 study stopped on basis of results regarding reduction in incidence in diabetes in treatment group Significant reduction seen in total cholesterol and BMI in intervention group at 1 year and maintained at 3‐year follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Finnish men 1985.
| Methods | Volunteers recruited Randomisation by individual | |
| Participants | Men only, mean age 48 years (40 to 58) High‐risk N = 1222 | |
| Interventions | Diet, smoking, exercise, antihypertensive drugs, cholesterol‐lowering drugs Duration 5 years | |
| Outcomes | Total mortality, CHD mortality Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | Large reductions in blood pressure and blood cholesterol achieved largely through drug treatments, reductions in smoking prevalence Control group risk factors increased CHD event rates higher in intervention group but stroke rates significantly lower Concluded that adverse effects of drug treatment may explain lack of benefit. ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Garcia‐Pena 2001.
| Methods | Primary care individual randomisation | |
| Participants | Men and women over the age of 60 with hypertension mean age 70 N = 718 | |
| Interventions | Fortnightly or monthly visits from nurse to advise on healthier lifestyles with individually negotiated targets over a 6‐month period | |
| Outcomes | Deaths, weight, sodium excretion, systolic and diastolic blood pressure at 6‐month follow up | |
| Notes | ITT not used BP was significantly reduced in the intervention group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Given 1984.
| Methods | Primary care Selection of hypertensives by screening Randomisation of individuals | |
| Participants | Men and women with hypertension on a prescribed regimen of diet or medication, mean age 47 years (18 to 65) N = 86 | |
| Interventions | Educational handbook on risk, impact and benefits of controlling hypertension Individual problem‐solving sessions on medication, diet and exercise Duration 6 months | |
| Outcomes | Systolic and diastolic blood pressure, weight, patient beliefs, symptom severity | |
| Notes | Authors note reduction in diastolic blood pressure Intervention affected patient beliefs | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Gothenberg Study 1986.
| Methods | Population‐based Selection of high‐risk people by screening Randomisation of individuals | |
| Participants | Men only, mean age 51 years (47 to 55) N = 30,022 | |
| Interventions | Diet, smoking, antihypertensive drugs, cholesterol‐lowering drugs Duration 11.8 years | |
| Outcomes | Total mortality, coronary heart disease mortality Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | Large falls in risk factors occurred in both intervention and control groups Concluded that other strategies in high‐risk men are required to have a major impact on incidence of disease in the general population | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
HDFP trial 1970.
| Methods | Population screening Randomisation of individuals | |
| Participants | Men and women, all hypertensives, age range 30 to 69 years (mean age 50) N = 10,940 | |
| Interventions | Stepped care: antihypertensive drugs, diet, smoking advice, weight control, exercise versus Referred care: usual primary care Duration 5 years | |
| Outcomes | Total mortality, CHD mortality, stroke mortality Non‐fatal CHD and stroke events Diastolic blood pressure | |
| Notes | No reductions in smoking prevalence or blood cholesterol (data not published) but significant reductions in blood pressure Total mortality, CHD and stroke mortality significantly lower in intervention group Benefits attributed to treatment of high blood pressure and sustained over prolonged follow up ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Hellenius 1993.
| Methods | Randomisation of individuals in a 2 x 2 factorial design | |
| Participants | Men only, mean age 46 years (35 to 60) Moderately raised CVD risk factors ‐ already involved in a primary prevention programme N = 158 | |
| Interventions | Diet and exercise advised Duration 6 months | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, blood cholesterol Data also given on BMI, waist‐hip ratio, HDL/LDL/VLDL cholesterol, triglycerides, dietary intake, physical activity | |
| Notes | Only data from control group (N = 39) and diet and exercise group (N = 39) used in this review | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Iso 1994.
| Methods | Community screening Randomisation by individual using permuted block method, stratified by blood pressure | |
| Participants | Untreated hypertensive men and women age 35 to 69 years (mean age 58 to 59) N = 111 | |
| Interventions | Physician, public health nurse and nutritionist‐led education, counselling and practical sessions Individual goals for sodium intake, weight control, walking and alcohol intake Duration 18 months | |
| Outcomes | No clinical event outcomes Urinary sodium and potassium, sodium reduction behaviours, alcohol intake, calcium intake, BMI, systolic and diastolic blood pressure | |
| Notes | Intervention associated with reduced systolic blood pressure, reduction in sodium excretion, alcohol consumption No change in BMI, diastolic blood pressure Greater use of antihypertensive medication in control group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Iso 2002.
| Methods | Community screening Randomisation by individual | |
| Participants | Hypercholesteraemic men and women men and women age 40 to 69 years (mean age 54 to 55) N = 104 | |
| Interventions | Physician, public health nurse and nutritionist‐led education, counselling and practical sessions Individual goals for sodium intake, weight control, walking and alcohol intake Duration 12 months | |
| Outcomes | No clinical event outcomes 8‐year follow up of BMI and total cholesterol | |
| Notes | 20% loss to follow up ITT not used Significant reduction seen in total cholesterol in the intervention group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Jalkanen 1991.
| Methods | Patients from hypertension clinic Randomisation of individuals | |
| Participants | Men and women, mean age 49 years (range 35 to 59) With hypertension and overweight N = 50 | |
| Interventions | Individually planned diet (1000 to 1500 kcal per day) Advice on exercise and weight reduction, weekly meetings for 6 months then 3‐weekly Duration 12 months | |
| Outcomes | No clinical events outcomes Systolic and diastolic blood pressure, blood cholesterol, weight, food intake, urinary sodium and potassium | |
| Notes | Intervention led to reduction in weight | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | D ‐ Not used |
Johns Hopkins.
| Methods | Clinic attenders Randomisation by individual to a complex factorial design with 8 groups | |
| Participants | Men and women, all hypertensives, mean age 54.1 years N = 400 | |
| Interventions | Antihypertensive drugs, weight control, general health advice versus No extra educational interventions Duration 5 years | |
| Outcomes | Total and CHD mortality | |
| Notes | Better control of blood pressure (but values not reported), weight and better adherence with treatment and appointments in intervention group Concluded that educational programmes for hypertensive patients were beneficial ITT used 28% loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Kastarinen 2002.
| Methods | Primary care Randomisation by individual | |
| Participants | Hypertensive men and women mean age 54.3 N = 715 | |
| Interventions | Trained nurses provided counselling in behaviour modification in diet and exercise with individualised targets over 21 months | |
| Outcomes | No clinical events outcomes. Smoking, systolic and diastolic blood pressure, blood cholesterol, weight, food intake, urinary sodium and potassium at 2 years | |
| Notes | ITT used. Significant reductions in weight loss, alcohol consumption were seen in the intervention group. | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Lin 1996.
| Methods | Primary care screening 4 villages randomly assigned. Unit of analysis was individual | |
| Participants | Men and women aged 40+ (mean 60) N = 1102 | |
| Interventions | Home visits by public health nurse students aimed at weight reduction, physical activity, compliance with medication Trained volunteers and community leaders involved Education classes and speeches Duration 6 months | |
| Outcomes | No clinical events outcomes Blood pressure, behavioural changes | |
| Notes | Hypertensives received more intensive intervention 35% loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Lindahl 1999.
| Methods | Participants in health survey screened for abnormal glucose tolerance | |
| Participants | Men and women with abnormal glucose tolerance and high BMI mean age 55 N = 301 | |
| Interventions | 1‐month stay in full‐board wellness centre Scheduled aerobic physical activity, stress management, diet modification, smoking cessation encouraged | |
| Outcomes | No clinical events outcomes Systolic and diastolic blood pressure, cholesterol, fibrinolysis, BMI, physical fitness Follow up of 12 months | |
| Notes | Not all participants were followed up Intense programme compared with usual care group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Look AHEAD 2003.
| Methods | 16 clinical diabetes centres screened and individually randomised diabetic patients | |
| Participants | Diabetic men and women who were overweight aged 45 to 74 (mean age 59) N = 5145 | |
| Interventions | 1‐year programme of educational sessions on lifestyle modification (diet and exercise) plus support sessions delivered by counsellors, dieticians, behaviourists, exercise physiologists | |
| Outcomes | No clinical events, weight loss, systolic and diastolic blood pressure, triglycerides, HDL cholesterol, urine albumin to creatinine ratio at one 1‐year follow up | |
| Notes | ITT not used 9 deaths (4 in control group) but not explained Significant weight loss and reduction in blood pressure in intervention group was observed | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Mattila 2003.
| Methods | Work site screening (n = 45) Individual randomisation | |
| Participants | Men and women with mean age of 49 and with hypertension N = 731 | |
| Interventions | 1‐year programme of practical training for lifestyle changes aimed at hypertension with group support Delivered by doctor, dietician, physiotherapist, cook and psychologist | |
| Outcomes | No clinical events, smoking, weight loss, systolic and diastolic blood pressure, physical activity, BMI, HDL cholesterol, at 1‐year follow up | |
| Notes | ITT not used Significant reduction observed in BP in intervention group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Meland 1997.
| Methods | Primary care opportunistic screening Randomisation by general practice (N = 22) Unit of analysis was individual | |
| Participants | Men aged 30 to 59 (mean age 43 to 44) at high risk for CVD by infarction score N = 127 | |
| Interventions | Counselling on health promotion and behaviour change Self‐help and self‐monitoring Duration 1 year | |
| Outcomes | No clinical event outcome Systolic and diastolic blood pressure, weight, resting pulse, cholesterol, lipid profile, smoking habit, thiocyanate, C‐peptide | |
| Notes | Kanfer and Gaelick (1986) and Meichenbaum (1986), person‐centred and self‐directed psychological approach Self‐efficacy was related to exercise change | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | D ‐ Not used |
MRFIT Study 1982.
| Methods | Work site, population and volunteer screening Randomisation by individual | |
| Participants | Men only, mean age 46 years (35 to 47) N = 12,866 | |
| Interventions | Diet, smoking, weight, antihypertensive drugs Duration 6 years | |
| Outcomes | Total mortality, coronary heart disease mortality Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | Small reductions in blood cholesterol concentration Large reductions in blood pressure and smoking rates No significant reduction in disease events Concluded that possibly effective in subgroups but no net benefit because of potentially harmful effects of antihypertensive drugs used Small benefits emerging after prolonged follow up ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Muto 2001.
| Methods | Work site screening Individual randomisation | |
| Participants | Men with mean age of 42 and with at least 1 abnormality in BMI, BP, total cholesterol, triglycerides or fasting blood glucose N = 302 | |
| Interventions | 6 health promotion seminars in health promotion and education, lectures in nutrition, exercise, stress Individual counselling offered, group discussion and self‐education tools Programme delivered by dietician, doctors and exercise trainer over 18 months | |
| Outcomes | BMI, BP, total cholesterol, triglycerides or fasting blood glucose at 6 and 18 months | |
| Notes | ITT not used Significant reductions observed in intervention group in BMI, total cholesterol, triglycerides and systolic BP | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Nilsson 1992.
| Methods | Randomisation of hyperinsulinaemics by individual within cross‐sectional study of treated hypertensives and normotensive controls | |
| Participants | Men and women, mean age 56.1 years with hyperinsulinaemia but not diabetic N = 59 | |
| Interventions | Group education and individual counselling on diet and physical activity by nurse, dietician and physiotherapist Duration 1 year | |
| Outcomes | Systolic and diastolic blood pressure, blood cholesterol, LDL/HDL cholesterol ratio, weight, waist‐hip ratio, blood glucose, insulin, c‐peptide, urate, glucose tolerance | |
| Notes | 63 randomised Intervention group had reduced weight, waist‐hip ratio, blood pressure and LDL/HDL ratio, also dietary improvements Controls informed of hyperinsulinaemic status | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Nilsson 2001.
| Methods | Work site screening Randomisation by individual | |
| Participants | Men and women, mean age 50 years (range 28 to 65) N = 89 | |
| Interventions | Multidisciplinary education and counselling Weight reduction in obese, diet, physical activity, stress management, smoking cessation Duration 18 months | |
| Outcomes | Risk scores, BMI, waist‐hip ratio, sick days, sedentary behaviour, heart rate, smoking, CHD risk factors, glucose, insulin, liver function, cortisol, dehydroepiandrosterone (DHEA) | |
| Notes | 128 randomised (intervention group: 5 did not attend baseline, 16 drop‐outs or excluded for medical reasons at 12 months, 1 lost to follow up at 18 months; control group corresponding figures 10, 5, 2 respectively) 30% loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Okayama 2004.
| Methods | Work site screening Individual randomisation | |
| Participants | Men and women with mean age of 44 and 45 (range 30 to 64) with cholesterol levels of < 300 mg/dl N = 191 | |
| Interventions | Health professionals provided sessions on lifestyle behaviour modification and personalised plans were regularly reviewed Intervention lasted 6 months | |
| Outcomes | BMI, cholesterol, triglycerides, apo‐protein A1 and B at 6 months | |
| Notes | ITT not used Significant reduction seen in cholesterol and BMI in both the intervention and control groups | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Oldroyd 2001.
| Methods | People with impaired glucose tolerance identified in research studies, hospital databases and by GPs Randomisation by individual | |
| Participants | Men and women aged 24 to 75 (mean age 58) years with impaired glucose tolerance identified in 2 OGTT N = 78 | |
| Interventions | Dietician and physiotherapist counselling on diet and physical activity Targets set by Stages of Change Duration 6 months | |
| Outcomes | No clinical event outcomes Diet, aerobic physical activity, glucose tolerance, insulin sensitivity, blood pressure, cholesterol, weight, BMI, waist‐hip ratio | |
| Notes | Intervention group showed increased physical activity, decreased fat consumption but no change in glucose tolerance | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Oslo Diet Antismoking.
| Methods | Population screening Selected for raised blood cholesterol Randomisation by individual | |
| Participants | Men only, mean age 45.2 (40 to 49) N = 1232 | |
| Interventions | Diet and smoking Duration 5 years | |
| Outcomes | Total mortality, CHD mortality, smoking prevalence, blood cholesterol | |
| Notes | Reduction in smoking rates and blood cholesterol Significant reduction in cardiovascular disease events Concluded that advice to stop smoking and change eating habits reduces first myocardial infarctions and sudden deaths ITT used At 20‐year follow up large loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Oslo Diet Exercise.
| Methods | Open, randomised 2 x 2 factorial design | |
| Participants | Men and women, mean age 40 years N = 219 | |
| Interventions | Diet advice and supervised endurance exercise programme Duration 1 year | |
| Outcomes | No clinical event outcomes reported Systolic blood pressure, diastolic blood pressure, blood cholesterol Also measured haemostatic factors, BMI, body weight, waist‐hip ratio, aerobic capacity, thiocyanate, triglycerides, HDL/LDL cholesterol | |
| Notes | Comparison used in this review is between the control group (N = 43) and the diet + exercise group (N = 65) Diet only and exercise only groups were not considered as single interventions | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
OXCHECK 1994.
| Methods | Primary care practices in urban area Randomisation by household | |
| Participants | Men and women, mean age 49 years (35 to 64) No risk screening N = 11,090 | |
| Interventions | Diet, smoking advice, weight control, alcohol advice, exercise, protocols for management of high blood pressure and raised blood cholesterol versus usual care Duration 3 years | |
| Outcomes | Total mortality and CHD mortality Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence, BMI | |
| Notes | Changes in diet and small changes in blood cholesterol, blood pressure and body mass index No effect on smoking prevalence Concluded that primary prevention programmes were able to achieve benefits which were real but must be weighted against the costs in relation to other priorities Study was not designed to examine mortality effects but those randomised to health checks in years 1 to 3 were considered to be intervention group and those randomised to checks in year 4 were the control group Deaths up to year 4 were compared ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Perez‐Stable 1995 no prop.
| Methods | Volunteers screened Randomised by individual stratified for sex, diastolic blood pressure and weight | |
| Participants | Men and women aged 18 to 59 (mean age 45) Mild hypertension N = 156 | |
| Interventions | Nutritionist, health educator, behavioural psychologist, general internist supervised Aerobic exercise, diet, relaxation 8 weekly meetings, subsequent meeting at 3 months | |
| Outcomes | No clinical event outcomes Systolic and diastolic BP, cholesterol, physical activity, self‐reported adverse effects dietary intake, weight, 24‐hour urine test (sodium, potassium) Follow up at 1 year | |
| Notes | 4 treatment arms; other 2 had propanolol Intervention did not promote persistent behaviour change ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Perez‐Stable 1995 prop.
| Methods | Volunteers screened Randomised by individual stratified for sex, diastolic blood pressure and weight | |
| Participants | Men and women aged 18 to 59 (mean age 46) Mild hypertension on propanolol N = 156 | |
| Interventions | Nutritionist, health educator, behavioural psychologist, general internist supervised Aerobic exercise, diet, relaxation 8 weekly meetings, subsequent meeting at 3 months | |
| Outcomes | No clinical event outcomes Systolic BP diastolic BP pressure, cholesterol, physical activity, self‐reported adverse effects, dietary intake, weight, 24‐hour urine test (sodium, potassium) Follow up at 1 year | |
| Notes | 4 treatment arms; other 2 did not have propanolol Intervention did not promote persistent behaviour change | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Proper 2003.
| Methods | Block randomisation of municipal workplace units Individual randomisation within each unit | |
| Participants | Male and female employees with mean age of 44 N = 299 | |
| Interventions | Trans‐theoretical model used by physiotherapist who provided individual counselling sessions on diet, exercise, stress, smoking Individualised plans were drawn up and applied accordingly over a 9‐month period | |
| Outcomes | Physical activity, BMI, BP and cholesterol at 9 months | |
| Notes | 20% loss to follow up ITT not used Significant results observed with increased energy expenditure, reductions in BMI, cholesterol and diastolic BP | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Rachmani 2005.
| Methods | Diabetic outpatient clinic Individual randomisation | |
| Participants | Men and women with type 2 diabetes, hypertension and hyperlipidaemia Mean age 59 (45 to 69) N = 165 | |
| Interventions | Primary care physician delivered initial teaching sessions and individual consultations on the importance of maintaining desired levels of BP, cholesterol and of drug compliance Patient‐centred goals were defined Intervention group was encouraged to exercise Treatment length of 7 years | |
| Outcomes | Clinical events, BP, cholesterol, urinary albumin, BMI, triglycerides and medications at 4 and 7.7 years follow up | |
| Notes | ITT not used Significantly fewer patients in the intervention group had non‐fatal CVD events at 7.7 years Improvements were also seen in BP and in cholesterol | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Sartorelli 2005.
| Methods | Primary care Randomised by individual | |
| Participants | Overweight men and women aged 36 to 65 (mean age 45 to 46) n = 104 | |
| Interventions | 3 individual counselling sessions by nutritionist on diet and exercise in 6 months | |
| Outcomes | No clinical event outcomes Systolic and diastolic BP and total cholesterol at 1‐year follow up | |
| Notes | 29% lost to follow up ITT used Significant reduction in diastolic BP at 1 year among intervention group | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Sone (JDCS) 2002.
| Methods | Diabetic centres Individuals randomised | |
| Participants | Men and women with type 2 diabetes with a mean age of 59 N = 2205 | |
| Interventions | Nurse educators and physicians delivered programme of counselling, educational materials and patient‐centred goal‐setting over 3 years | |
| Outcomes | No clinical event outcomes Systolic and diastolic BP, cholesterol, glycaemic control, diastolic BP at 3 years | |
| Notes | ITT not used Small but significant improvements in glycaemic control | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Stamler 1989.
| Methods | Work site screening Randomisation of individuals | |
| Participants | Volunteers from work sites, raised body weight, high pulse rate and diastolic BP 80 to 89 mmHg Men and women, mean age 37.5 (30 to 44) N = 201 | |
| Interventions | Diet, weight control, exercise, alcohol Duration 5 years | |
| Outcomes | No clinical event outcomes Systolic BP, diastolic BP | |
| Notes | Small but significant reduction in blood pressure; other risk factors not reported Volunteers who were thought unlikely to comply with intervention (e.g. heavy drinkers, very obese) were excluded from the trial | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Stefanick 1998 F.
| Methods | Volunteers screened for HDL and LDL cholesterol Randomisation by individual | |
| Participants | Post‐menopausal women aged 45 to 64 (mean age 57), HDL < 60 mg/dl, LDL N = 89 | |
| Interventions | Individual diet counselling and group education Weight loss groups Supervised and home‐based exercise Duration 1 year | |
| Outcomes | No clinical event outcomes Diet assessment, body weight, exercise tests, CHD risk factors | |
| Notes | Concluded that diet and aerobic exercise was effective in reducing LDL cholesterol ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Stefanick 1998 M.
| Methods | Volunteers screened for HDL and LDL cholesterol Randomisation by individual | |
| Participants | Men aged 30 to 64, (mean age 48) HDL < 45 mg/dl, LDL 126 to 189 mg/dl 126 to 209 mg/dl N = 98 | |
| Interventions | Individual diet counselling and group education Weight loss groups Supervised and home‐based exercise Duration 1 year | |
| Outcomes | No clinical event outcomes Diet assessment, body weight, exercise tests, CHD risk factors | |
| Notes | Concluded that diet and aerobic exercise was effective in reducing LDL cholesterol ITT used | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Low risk | A ‐ Adequate |
Swedish RIS 1994.
| Methods | Clinic‐attending hypertensives Randomisation by individual after stratification by serum cholesterol, smoking habit and target organ damage | |
| Participants | All men, age 50 to 72 years (mean age 66) N = 508 | |
| Interventions | Smoking advice + nicotine gum, dietary habits, weight control, spouse involved Lipid‐lowering drugs used in needed versus usual care All patients on antihypertensive medication Duration 6 years | |
| Outcomes | Total mortality, CHD and stroke mortality Non‐fatal myocardial infarction, stroke, new onsets of claudication and angina Systolic blood pressure, diastolic blood pressure, blood cholesterol, (HDL, LDL), smoking prevalence, body weight, BMI, blood glucose, heart rate, gGT, HbA1c | |
| Notes | Significant reductions in blood cholesterol and smoking were achieved No changes in diastolic blood pressure and HbA1c Stroke incidence reduced in intervention group 31% loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Take Heart 1995.
| Methods | Workplace screening Matched pairs of work sites randomised Unit of analysis was work site | |
| Participants | Men and women mean age 40 (17 to 73) N = 1977 | |
| Interventions | Stage of Change model used: motivational, educational, workplace environment and community reinforcement; focus on smoking and food choices Duration 18 months | |
| Outcomes | Smoking, blood cholesterol, dietary intake | |
| Notes | Despite documented implementation of interventions no evidence that changes in smoking, cholesterol concentration of dietary intakes were greater than improvements associated with secular trends observed in control sites Large variation in rates of stopping smoking between sites suggested variable use and uptake of interventions | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Toobert (MLP) 2005.
| Methods | Primary care setting, individual randomisation | |
| Participants | Post‐menopausal women with type 2 diabetes Mean age 61 N = 297 | |
| Interventions | Social cognitive, goal and ecological theory applied Dietician and physiologist delivered programme on diet, exercise, stress management and social support | |
| Outcomes | BMI, blood pressure, diet and exercise modification, stress management, quality of life | |
| Notes | ITT used Improvements seen in BMI and quality of life outcomes | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Tromso 1991 F.
| Methods | Wives of the men randomised in the Tromso trial are considered to be a separate trial Randomisation therefore by husband | |
| Participants | Women aged 30 to 45 (mean age 40) N = 809 | |
| Interventions | Physician and dietician counselling on diet, smoking, exercise Duration 6 years | |
| Outcomes | No clinical event data Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | Mortality data may be available in the future 23% loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Tromso 1991 M.
| Methods | Randomisation of individuals at high risk detected by primary care screening | |
| Participants | Men and women, age 30 to 45 years (mean age 40) N = 1373 | |
| Interventions | Physician and dietician counselling of family, diet, smoking advice, exercise Duration 6 years | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, blood cholesterol, smoking prevalence | |
| Notes | Participants showed little interest in group meetings Small significant reductions in blood cholesterol but no effects on smoking or blood pressure Mortality and clinical event follow up is proceeding in the trial and lead author has not yet published data | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
Uusitupa 1993.
| Methods | Diabetes clinic Randomisation by individual | |
| Participants | Newly diagnosed NIDDM, men and women aged 40 to 64 years (mean age 53 to 54) N = 86 | |
| Interventions | Education on weight reduction, diet, physical activity Goals and regular monitoring Duration 12 months | |
| Outcomes | No clinical event data Weight reduction, normocalcaemia, correction of dislipidaemias, blood pressure | |
| Notes | Intervention and control received 3 months basic diabetes education before randomisation | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
WHLP 1998.
| Methods | Volunteers recruited Randomisation of individuals | |
| Participants | Women aged 44 to 50 (mean age 47) N = 535 | |
| Interventions | Cognitive‐behavioural programme with intensive group and individual guidance on diet, exercise and prevention of weight gain Duration 4.5 years | |
| Outcomes | No clinical event outcomes Systolic blood pressure, diastolic blood pressure, blood LDL and HDL cholesterol reported at 5 years | |
| Notes | 1 accidental death Participants were receptive to preventive approach and were successful in making long‐term lifestyle changes | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | High risk | C ‐ Inadequate |
WHO Factories 1986.
| Methods | Work sites in Belgium, Italy, Poland, Spain, UK Randomisation by factory Unit of analysis was factory | |
| Participants | Men only, mean age 48.5 (40 to 59) N = 63,732 | |
| Interventions | Diet, smoking, weight, exercise, antihypertensive drugs, mass media Control factories had usual occupational health service Duration 6 years | |
| Outcomes | Mortality: cause‐specific Blood pressure, blood cholesterol, smoking rates | |
| Notes | Only small reductions in risk factors found Spanish arm not included in event ascertainment Belgium arm showed significant reduction in mortality and was written up separately Concluded that advice on risk factor reduction is effective to the extent that it is taken up and seems to be safe | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
Wing 1998.
| Methods | Volunteers Randomisation by individual | |
| Participants | Overweight men and women aged 40 to 55 (mean age 45 to 46) Non‐diabetic but with 1 or 2 parents with type 2 diabetes N = 80 | |
| Interventions | Multidisciplinary led behavioural strategies Group and individual education Low calorie, low fat diet Supervised walking and other activities Duration 2 years | |
| Outcomes | No clinical events outcomes Eating and exercise behaviours, weight, incidence of diabetes, systolic blood pressure, diastolic blood pressure, cholesterol | |
| Notes | BMI, BP, cholesterol reductions and long‐term behaviour changes were not achieved 26% loss to follow up | |
| Risk of bias | ||
| Bias | Authors' judgement | Support for judgement |
| Allocation concealment (selection bias) | Unclear risk | B ‐ Unclear |
AMI: acute myocardial infarction
BMI: body mass index BP: blood pressure
CABG: coronary artery bypass surgery CHD: coronary heart disease CVD: cardiovascular disease HDL: high‐density lipoprotein ITT: intention‐to‐treat LDL: low‐density lipoprotein
NIDDM: non‐insulin dependent diabetes mellitus
OGTT: oral glucose tolerance test
PTCA: percutaneous transluminal coronary angioplasty VLDL: very low‐density lipoprotein
Characteristics of excluded studies [ordered by study ID]
| Study | Reason for exclusion |
|---|---|
| Aldana (DPS) 2005 | Both groups received an intervention |
| Andersen 1999 | Both groups received an intervention |
| Bakx 1997 | No multiple risk factor intervention |
| Basler 1985 | Non‐random allocation |
| Becker 2005 | No comparable control group |
| Berg 2005 | All groups received an intervention |
| Blake 1987 | No risk factor change measured or reported |
| Boylan 2003 | Relevant results not published. Data requested from author but nothing received. |
| Brekke 2005b | Follow up was less than 6 months |
| Bruckert 1999 | Study was stopped prematurely |
| Bruno 1983 | 6‐month data not available |
| Burke 2003 | Participants were younger adults |
| Burke 1999 | Participants were younger adults |
| Burke 2005 | Inadequate randomisation |
| Cambien 1981 | Participants were younger adults |
| Carlberg 1992 | No risk factor data measured or reported |
| Cicek 2004 | Inadequate randomisation |
| Crouch 1986 | Control group received some elements of intervention |
| Da Qing 1997 | No risk factor changes reported |
| Davey‐Smith 2005 | Follow up of MRFIT with no new relevant data |
| Domarkene 1990 | Non‐random allocation |
| DPP 1999 | Control group received some elements of intervention |
| DPPRG 2002 | No control group |
| Dunn 1997 | Both groups received an exercise only intervention |
| Eberle 2003 | Follow up of MRFIT with no new relevant data |
| Edye 1989 | Non‐random allocation |
| Elliot 2007 | Relevant results not published. Data requested from author but nothing received. |
| Esposito 2003 | Participants were young women |
| Ferro 2001 | Not a randomised trial |
| Fielding 1994 | Control group received some elements of intervention |
| Fox 1996 | Non‐random allocation |
| Frommer 1990 | Inadequate randomisation |
| Fuchs 1993 | Both groups received an intervention |
| Fullard 1987 | Non‐random allocation |
| Gaede 2003 | More that 25% of patients recruited had CVD |
| Gemson 1990 | Control group received some elements of intervention |
| Gemson 1995 | Control group received some elements of intervention |
| German 1994 | Control group received some elements of intervention |
| Goldhaber‐Fiebert 2003 | Follow up was less than 6 months |
| Gomel 1993 | Inadequate randomisation |
| Gordon 1997 | Control group received some elements of intervention |
| Gordon 2002 | More that 25% of patients recruited had CVD |
| Gump 2003 | Follow up of MRFIT with no new relevant data |
| Gysan 2004 | Cohort study |
| Hanlon 1995 | 6‐month data not available |
| Haskell 1988 | Secondary prevention |
| Hedberg 1998 | Non‐randomised allocation |
| Hopman‐Rock | Drop‐out replaced by recruits on reserve during the study |
| Huang 2001 | Incomplete randomisation |
| Inter99 2003 | Ongoing trial using quasi‐randomised method |
| Jiang 2004 | Community study |
| Jula 1990 | Inadequate randomisation |
| Kamioka 2006 | Control group received some elements of intervention |
| Karlehagen 2003 | No comparable control group |
| Kawakami 1999 | Participants were younger adults |
| Ketola 2001 | Mixed primary and secondary prevention |
| Kisioglu 2004 | Relevant results not published. Data requested from author but nothing received. |
| Knappe 1982 | Inadequate randomisation |
| Ko 2004 | Unclear if recruited patients had CVD. No response from author. |
| Kreuter 1996 | Outcome is contemplation of quitting smoking |
| Lasater 1986 | No risk factor changes measured or reported |
| Lauritzen 1995 | Intervention was determined by patient choice |
| Leighton 1990 | Control group received some elements of intervention |
| Lindahl 1998 | Uncontrolled study |
| Little 2004 | No results given for control group |
| Lovibond 1986 | Control group received some elements of intervention |
| Macdonald 1990 | RCT assessing simvastatin |
| Martinez‐Amenos 1990 | No risk factor changes measured or reported |
| McCance 1985 | 2‐month follow up |
| McCann 1997 | Control group received some element of the intervention |
| McMahon 2002 | No control group |
| Meimanaliev 1991 | Non‐random allocation |
| Miemanaliev 1993 | Non‐random allocation |
| Miller 2002 | Follow up was less than 6 months |
| Murray 1986 | No control group baseline data available |
| Nieman 2002 | Follow up was less than 6 months |
| Nikitin 1991 | Non‐random allocation |
| Nisbeth 2000 | Participants were younger adults |
| Nolte 1997 | 2‐month follow up |
| Olivarius 2001 | More that 25% of patients recruited had CVD |
| Ostwald 1989 | Control group received some element of the intervention |
| OXCHECK 2003 | Follow‐up data on patients that were not randomised |
| Parker 2005 | Objective to test intraclass correlations ‐ no relevant outcome data |
| Patterson 1988 | No risk factor changes measured or reported |
| Persson 1996 | No 6‐month follow up data available. After 6 months pharmacological treatment was provided to intervention group patients (67% on lipid‐lowering drugs and 13% on antihypertensives at 1 year) |
| Pierce 1984 | No risk factor change measured or reported |
| Pora 2005 | Not a randomised trial |
| PREMIER 2006 | No comparable control group |
| Pritchard 2002 | No comparable control group |
| Reid 1995 | Control group received some element of the intervention |
| Robson 1989 | No risk factor changes measured or reported |
| Rosamond 2000 | Non‐random allocation |
| Rothman 2004 | No multiple risk factor intervention |
| Rowland 1994 | Non‐random allocation |
| S‐E London 1977 | Intervention not characterised |
| Sarraf‐Zadegan 2003 | Ongoing community study |
| Schwandt 1999 | Children and families |
| Schwedes 2002 | More that 25% of patients recruited had CVD |
| Smith 1991 | Non‐random allocation |
| Steinbach 1982 | Non‐random allocation |
| Strandberg 2001 | 82% of patients recruited had CVD |
| TOMHS 1991 | All participants received intervention |
| TONE 1998 | 3‐month blood pressure follow up |
| Tonstad 2005 | Patients recruited were less than 40 years of age |
| Tsuyuki 1999 | Secondary prevention |
| Van Elderen 2001 | Patients recruited had CVD |
| Velonakis 1999 | Non‐random allocation |
| Volozh 1991 | Non‐random allocation |
| Wang 2002 | Follow up was less than 6 months |
| WHP 1999 | Numbers in intervention and control group not reported |
| Wisewoman 1999 | Control group received some element of the intervention |
| Witmer 2004 | Follow up was less than 6 months |
| Woollard 2003 | Patients recruited had CVD |
| Working Well Trial | Baseline data only, no follow up |
| Wu 1999 | Non‐random allocation |
| Zimmerman 1996 | A pilot study with no relevant results reported |
CVD: cardiovascular disease RCT: randomised controlled trial
Characteristics of ongoing studies [ordered by study ID]
Roderigues 2005.
| Trial name or title | — |
| Methods | Randomised clinical trial of an intensive intervention into lifestyle of patients with hyperfibrinogaenemia in primary prevention of cardiovascular pathology in primary health care |
| Participants | 436 men and women aged 35 to 75 |
| Interventions | Intensive counselling for lifestyle changes (smoking, diet, weight) |
| Outcomes | Quality of life, CVD events, modification of risk factors, plasm fibrinogen at 2 years |
| Starting date | 2005 |
| Contact information | — |
| Notes | — |
Contributions of authors
G. Davey Smith and S. Ebrahim wrote the original review.
For the first update:
A. Beswick selected studies, extracted data, performed analysis and co‐wrote the review. M. Burke ran searches, selected studies and extracted data. S. Ebrahim selected studies, analysed data and co‐wrote the review.
For the second update:
K. Ward selected studies, extracted data, performed analysis and co‐wrote the review. F. Taylor selected studies, extracted data, performed analysis and co‐wrote the review. M. Burke ran searches and selected studies. S. Ebrahim selected studies and co‐wrote the review.
Sources of support
Internal sources
MRC Health Services Research Collaboration, UK.
Systematic Reviews Training Unit, University of London, UK.
Department of Social Medicine, University of Bristol, UK.
Department of Epidemiology & Population Health, London School of Hygeine & Tropical Medicine, UK.
External sources
NHS Centre for Reviews & Dissemination, University of York, UK.
Health Education Authority, London, UK.
Declarations of interest
None known.
Stable (no update expected for reasons given in 'What's new')
References
References to studies included in this review
Aberg 1989 F {published data only}
- Aberg H, Tibblin G. Addition of non‐pharmacological methods of treatment in patients on antihypertensive drugs: results of previous medication, laboratory tests and life quality. Journal of Internal Medicine 1989;226:39‐46. [DOI] [PubMed] [Google Scholar]
Aberg 1989 M {published data only}
- Aberg H, Tibblin G. Addition of non‐pharmacological methods of treatment in patients on antihypertensive drugs: results of previous medication, laboratory tests and life quality. Journal of Internal Medicine 1989;226:39‐46. [DOI] [PubMed] [Google Scholar]
Abingdon 1990 {published data only}
- Baron J, Gleason R, Crowe B, Mann J. Preliminary trial of the effect of general practice based nutritional advice. British Journal of General Practice 1990;40:137‐41. [MEDLINE: ] [PMC free article] [PubMed] [Google Scholar]
ADAPT 2005 {published data only}
- Burke V, Beilin L, Cutt H, Mansour J, Wilson A, Mori TA. Effects of a lifestyle programme on ambulatory blood pressure and drug dosage in treated hypertensive patients: a randomised trial. Journal of Hypertension 2005;23:1241‐9. [DOI] [PubMed] [Google Scholar]
- Burke V, Mansour J, Beilin L, Mori T. Long‐term follow‐up of participants in a health promotion program for treated hypertensives (ADAPT). Nutrition, Metabolism & Cardiovascular Diseases 2006;December:1‐9. [DOI] [PubMed] [Google Scholar]
Aldana (CHIP) 2005 {published data only}
- Aldana SG, Greenlaw R, Diehl H, Salberg A, Merrill R, Ohmine S. The effects of a worksite chronic disease prevention program. Journal of Occupational Environmental Medicine 2005;47:558‐64. [DOI] [PubMed] [Google Scholar]
Applegate 1992 {published data only}
- Applegate WB, Miller ST, Elam JT, Cushman WC, Derwi D, Brewer A, et al. Nonpharmacologic intervention to reduce blood pressure in older patients with mild hypertension. Archives of Internal Medicine 1992;152:1162‐6. [PubMed] [Google Scholar]
Blumenthal 2000 {published data only}
- Blumenthal JA, Sherwood A, Gullette ECD, Babyak M, Waugh R, Georgiades A, et al. Exercise and weight loss reduce blood pressure in men and women with mild hypertension. Archives of Internal Medicine 2000;160(13):1947‐58. [DOI] [PubMed] [Google Scholar]
- Steffen PR, Sherwood A, Gullette EC, Georgiades A, Hinderliter A, Blumenthal JA. Effects of exercise and weight loss on blood pressure during daily life. Medicine & Science in Sports & Exercise 2001;33(10):1635‐40. [DOI] [PubMed] [Google Scholar]
Brekke 2005a {published data only}
- Brekke HK, Jansson PA, Lenner R. Long‐term (1‐and 2‐year) effects of lifestyle intervention in type 2 diabetes relatives. Diabetes Research and Clinical Practice 2005;70:225‐40. [DOI] [PubMed] [Google Scholar]
Cakir 2006 {published data only}
- Cakir H, Pinar R. Randomised controlled trial on lifestyle modification in hypertensive patients. Western Journal of Nursing Research 2006;28(2):190‐209. [DOI] [PubMed] [Google Scholar]
CELL Study 1995 {published data only}
- Lindholm LH, Ekbom T, Dash C, Eriksson M, Tibblin G, Schersten B. The impact of health care advice given in primary care on cardiovascular risk. BMJ 1995;310:1105‐9. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
- Lindholm LH, Ekbom T, Dash C, Isacsson A, Schersten B. Changes in cardiovascular risk factors by combined pharmacological and nonpharmacological strategies: the main results of the CELL Study. Journal of Internal Medicine 1996;240(1):13‐22. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Change of Heart 1999 {published data only}
- Hilton S, Doherty S, Kendrick T, Kerry S, Rink E, Steptoe A. Promotion of healthy behaviour among adults at increased risk of coronary heart disease in general practice: methodology and baseline data from the Change of Heart study. Health Education Journal 1999;58:3‐16. [Google Scholar]
- Steptoe A, Doherty S, Rink E, Kerry S, Kendrick T, Hilton S. Behavioural counselling in general practice for the promotion of healthy behaviour among adults at increased risk of coronary heart disease: randomised trial. BMJ 1999;319:943‐8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Steptoe A, Kerry S, Rink E, Hilton S. The impact of behavioral counseling on stage of change in fat intake, physical activity, and cigarette smoking in adults at increased risk of coronary heart disease. American Journal of Public Health 2001;91(2):265‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Steptoe A, Rink E, Kerry S. Psychosocial predictors of changes in physical activity in overweight sedentary adults following counseling in primary care. Preventive Medicine 2000;31(2 Pt 1):183‐94. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Connell 1995 {published data only}
- Connell CM, Sharpe PA, Gallabt MP. Effect of health risk appraisal on health outcomes in a university worksite health promotion trial. Health Education Research 1995;10:199‐209. [Google Scholar]
Esposito 2004 {published data only}
- Esposito K, Giugliano F, Palo C, Giugliano G, Marfella R, D'Andrea F, et al. Effect of lifestyle changes on erectile dysfunction in obese men. JAMA 2004;291:2978‐84. [DOI] [PubMed] [Google Scholar]
Family Heart 1994 F {published and unpublished data}
- Family Heart Study Group. Randomised controlled trial evaluating cardiovascular screening and intervention in general practice: principal results of British family heart study. BMJ 1994;308:313‐20. [PMC free article] [PubMed] [Google Scholar]
Family Heart 1994 M {published and unpublished data}
- Family Heart Study Group. Randomised controlled trial evaluating cardiovascular screening and intervention in general practice: principal results of British family heart study. BMJ 1994;308:313‐20. [MEDLINE: ] [PMC free article] [PubMed] [Google Scholar]
FARIS 1997 F {published data only}
- Goble A, Jackson B, Phillips P, Race E, Oliver RG, Worcester MC. The Family Atherosclerosis Risk Intervention Study (FARIS): risk factor profiles of patients and their relatives following an acute cardiac event. Australian and New Zealand Journal of Medicine 1997;27(5):568‐77. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
FARIS 1997 M {published data only}
- Goble A, Jackson B, Phillips P, Race E, Oliver RG, Worcester MC. The Family Atherosclerosis Risk Intervention Study (FARIS): risk factor profiles of patients and their relatives following an acute cardiac event. Australian and New Zealand Journal of Medicine 1997;27(5):568‐77. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Finnish DPS 2001 {published data only}
- Eriksson J, Lindström J, Valle T, Aunola S, Hamalainen H, Ilanne‐Parikka P, et al. Prevention of type II diabetes in subjects with impaired glucose tolerance: the Diabetes Prevention Study (DPS) in Finland. Study design and 1‐year interim report on the feasibility of the lifestyle intervention programme. Diabetologia 1999;42(7):793‐801. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Lindström J, Louheranta A, Mannelin M, Rastas M, Salminen V, Eriksson J, et al. The Finnish Diabetes Prevention Study: lifestyle intervention and 3 year results on diet and physical activity. Diabetes Care 2003;26(12):3230‐6. [DOI] [PubMed] [Google Scholar]
- Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hamalainen H, Ilanne‐Parikka P, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine 2001;344:1343‐50. [DOI] [PubMed] [Google Scholar]
- Uusitupa M, Louheranta A, Lindström J, Valle T, Sundvall J, Eriksson J, et al. The Finnish Diabetes Prevention Study. British Journal of Nutrition 2000;83(Suppl 1):S137‐42. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Finnish men 1985 {published and unpublished data}
- Miettinen T, Huttunen J, Naukkarinen V, Strandberg T, Mattila S, Kundin T, et al. Multifactorial primary prevention of cardiovascular diseases in middle‐aged men. Risk factor changes, incidence, and mortality. JAMA 1985;254:2097‐102. [MEDLINE: ] [PubMed] [Google Scholar]
- Strandberg T, Salomaa V, Naukkarinen V, Vanhanen, Sarna S, Miettinen T. Long‐term mortality after 5‐year multifactorial primary prevention of cardiovascular diseases in middle‐aged men. JAMA 1991;266:1225‐9. [MEDLINE: ] [PubMed] [Google Scholar]
- Strandberg TE, Salomaa VV, Vanhanen, HT, Naukkarinen VA, Sarna SJ, Miettinen TA. Mortality in participants and non‐participants of a multifactorial prevention study of cardiovascular diseases: a 28 year follow up of the Helsinki Businessmen Study. British Heart Journal 1995;74:449‐54. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Garcia‐Pena 2001 {published data only}
- Garcia‐Pena C, Thorogood M, Armstrong B, Reyes‐Frausto S, et al. Pragmatic randomised trial of home visits by a nurse to elderly people with hypertension in Mexico. International Journal of Epidemiology 2001;30:1485‐91. [DOI] [PubMed] [Google Scholar]
Given 1984 {published data only}
- Given CW, Given BA, Coyle BW. The effects of patient characteristics and beliefs on responses to behavioral interventions for control of chronic diseases. Patient Education and Counseling 1984;6:131‐140. [DOI] [PubMed] [Google Scholar]
Gothenberg Study 1986 {published and unpublished data}
- Wilhelmsen L, Berglund G, Elmfeldt D, Tibblin G, Wedel H, Pennert K, et al. The multifactor primary prevention trial in Goteborg, Sweden. European Heart Journal 1986;7:279‐88. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
HDFP trial 1970 {published data only}
- Hypertension Detection and Follow‐up Program Cooperative Group. Five‐year findings of the Hypertension Detection and Follow‐up Program. 1. Reduction in mortality of persons with high blood pressure, including mild hypertension. JAMA 1979;242:2562‐71. [MEDLINE: ] [PubMed] [Google Scholar]
Hellenius 1993 {published data only}
- Hellenius M‐L, Faire U, Berglund B, Hamsten A, Krakau I. Diet and exercise are equally effective in reducing risk for cardiovascular disease. Results of a randomized controlled study in men with slightly to moderately raised cardiovascular risk factors. Atherosclerosis 1993;103:81‐91. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Iso 1994 {published data only}
- Iso H, Shimamato T, Yokota K, Sankai T, Jacobs DR, Komachi Y. Community‐based education classes for hypertension control. Hypertension 1996;27:968‐74. [DOI] [PubMed] [Google Scholar]
- Iso H, Shimamoto T, Sankai T, Imano H, Koike K, Yokota K, et al. A randomized controlled trail of intensive and usual community‐based education for blood pressure control [Japanese]. Nippon Koshu Eisei Zasshi [Japanese Journal of Public Health] 1994;41(10):1015‐26. [MEDLINE: ] [PubMed] [Google Scholar]
Iso 2002 {published data only}
- Iso H, Imano H, Nakagawa Y, Kiyama M, Kitamura A, Sato S, et al. One year community‐based education program for hypercholesterolemia in middle aged Japanese: a long‐term outcome at 8 years follow‐up. Atherosclerosis 2002;164:195‐202. [DOI] [PubMed] [Google Scholar]
Jalkanen 1991 {published data only}
- Jalkanen L. The effect of a weight reduction program on cardiovascular risk factors among overweight hypertensives in primary health care. Scandinavian Journal of Social Medicine 1991;19:66‐71. [DOI] [PubMed] [Google Scholar]
Johns Hopkins {published data only}
- Morisky D, Levine D, Green L, Shapiro S, Russell R, Smith C. Five‐year blood pressure control and mortality following health education for hypertensive patients. American Journal of Public Health 1983;73:153‐62. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Kastarinen 2002 {published data only}
- Kastarinen M, Puska P, Korhonen M, Mustonen J, Salomaa VV, Sundvall JE, et al. Non‐pharmacological treatment of hypertension in primary health care: a 2 year open randomised controlled trial of lifestyle intervention against hypertension in eastern Finland. Journal of Hypertension 2002;20:2505‐12. [DOI] [PubMed] [Google Scholar]
Lin 1996 {published data only}
- Lin T, Chen C‐H, Chou P. A hypertension control program in Yu‐Chi, Taiwan: preliminary results. Journal of the Formosan Medical Association 1997;96:613‐20. [PubMed] [Google Scholar]
Lindahl 1999 {published data only}
- Lindahl B, Nilsson TK, Jansson J‐H, Asplund K, Hallmans G. Improved fibrinolysis by intense lifestyle intervention. A randomized trial in subjects with impaired glucose tolerance. Journal of Internal Medicine 1999;246:105‐12. [DOI] [PubMed] [Google Scholar]
Look AHEAD 2003 {published data only}
- The Look AHEAD Research Group. Baseline characteristics of the randomised cohort from the Look AHEAD study. Diabetes and Vascular Disease Research 2006;3:202‐15. [DOI] [PMC free article] [PubMed] [Google Scholar]
- The Look AHEAD Research Group. Look AHEAD (Action for Health in Diabetes): design and methods for a clinical trial of weight loss for the prevention of cardiovascular disease in type 2 diabetes. Controlled Clinical Trials 2003;24:610‐28. [DOI] [PubMed] [Google Scholar]
- The Look AHEAD Research Group. Reduction in weight and cardiovascular disease risk factors in individuals with type 2 diabetes. One year results of the Look AHEAD trial. Diabetes Care 2007;30(6):1374‐83. [DOI] [PMC free article] [PubMed] [Google Scholar]
- The Look AHEAD Research Group. The Look AHEAD Study: a description of the lifestyle intervention and evidence supporting it. Obesity 2006;14(5):737‐52. [DOI] [PMC free article] [PubMed] [Google Scholar]
Mattila 2003 {published data only}
- Mattila R, Malmivaara A, Kastarinen M, Kivelä SL, Nissinen A. Effectiveness of multidisciplinary lifestyle intervention for hypertension: a randomised controlled trial. Journal of Human Hypertension 2003;17:199‐205. [DOI] [PubMed] [Google Scholar]
Meland 1997 {published data only}
- Meland E, Laerum E, Ulvik RJ. Effectiveness of two preventive interventions for coronary heart disease in primary care. Scandinavian Journal of Primary Health Care 1997;15:57‐64. [DOI] [PubMed] [Google Scholar]
- Meland E, Maeland JG, Laerum E. The importance of self‐efficacy in cardiovascular risk factor change. Scandinavian Journal of Public Health 1999;27(1):11‐17. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
MRFIT Study 1982 {published and unpublished data}
- Multiple Risk Factor Intervention Trial Research Group. Mortality rates after 10.5 years for participants in the multiple risk factor intervention trial. Findings related to a priori hypotheses of the trial. JAMA 1990;263:1795‐801. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Multiple Risk Factor Intervention Trial Research Group. Multiple Risk Factor Intervention Trial. Risk factor changes and mortality results. JAMA 1982;248:1465‐77. [MEDLINE: ] [PubMed] [Google Scholar]
Muto 2001 {published data only}
- Muto T, Yamauchi K. Evaluation of a multicomponent workplace health promotion program conducted in Japan for improving employees' cardiovascular disease risk factors. Preventative Medicine 2001;33:571‐7. [DOI] [PubMed] [Google Scholar]
Nilsson 1992 {published data only}
- Nilsson PM, Lindholm LH, Schersten BF. Life style changes improve insulin resistance in hyperinsulinaemic subjects: a one‐year intervention study of hypertensives and normotensives in Dalby. Journal of Hypertension 1992;10(9):1071‐8. [MEDLINE: ] [PubMed] [Google Scholar]
Nilsson 2001 {published data only}
- Nilsson PM, Klasson E‐B, Nyberg P. Life‐style intervention at the worksite ‐ reduction of cardiovascular risk factors in a randomized study. Scandinavian Journal of Work and Environmental Health 2001;27:57‐62. [DOI] [PubMed] [Google Scholar]
Okayama 2004 {published data only}
- Okayama A, Chiba N, Ueshima H. Non‐pharmacological intervention study of hypercholesterolemia among middle‐aged people. Environmental Health and Preventative Medicine 2004;9:165‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
Oldroyd 2001 {published data only}
- Oldroyd JC, Unwin NC, White M, Imrie K, Mathers JC, Alberti KGMM. Randomised controlled trial evaluating the effectiveness of behavioural interventions to modify cardiovascular risk factors in men and women with impaired glucose tolerance: outcomes at 6 months. Diabetes Research and Clinical Practice 2001;52:29‐43. [DOI] [PubMed] [Google Scholar]
Oslo Diet Antismoking {published data only}
- Ellingsen I, Hjerkinn E, Arnesen H, Seljeflot I, Hjermann I, Tonstad S. Follow‐up of diet and cardiovascular risk factors 20 years after cessation of the intervention in the Oslo Diet and Antismoking Study. European Journal of Clinical Nutrition 2006;60:378‐85. [DOI] [PubMed] [Google Scholar]
- Hjermann I, Holme I, Leren P. Oslo Study Diet and Antismoking Trial. American Journal of Medicine 1986;80(Suppl 2A):7‐11. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Hjermann I, Holme I, Velve Byre K, Leren P. Effect of diet and smoking on the incidence of coronary heart disease. Report from the Oslo Study Group of a randomised trial in healthy men. Lancet 1981;ii:1303‐10. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Holme I, Hjermann I, Helgeland A, Leren P. The Oslo Study; diet and antismoking advice. Additional results from a 5‐year primary preventive trial in middle‐aged men. Preventive Medicine 1985;14:279‐92. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Oslo Diet Exercise {published data only}
- Anderssen SA, Haaland A, Hjerman I, Urdal P, Gjesdal K, Holme I. Oslo diet and exercise study: a one year randomized intervention trial. Effect on haemostatic variables and other coronary risk factors. Nutrition Metabolism & Cardiovascular Diseases 1995;5:189‐200. [Google Scholar]
OXCHECK 1994 {published and unpublished data}
- Imperial Cancer Research Fund OXCHECK Study Group. Effectiveness of health checks conducted by nurses in primary care: results of the OXCHECK study after one year. BMJ 1994;308:308‐12. [MEDLINE: ] [PMC free article] [PubMed] [Google Scholar]
Perez‐Stable 1995 no prop {published data only}
- Perez‐Stable EJ, Coates TJ, Baron RB, Biro BS, Hauck WW, McHenry KS, et al. Comparison of a lifestyle modification program with propanolol use in the management of diastolic hypertension. Journal of General Internal Medicine 1995;10:419‐28. [DOI] [PubMed] [Google Scholar]
Perez‐Stable 1995 prop {published data only}
- Perez‐Stable EJ, Coates TJ, Baron RB, Biro BS, Hauck WH, McHenry KS, et al. Comparison of a lifestyle modification program with propanolol use in the management of diastolic hypertension. Journal of General Internal Medicine 1995;10:419‐28. [DOI] [PubMed] [Google Scholar]
Proper 2003 {published data only}
- Proper K, Hildebrandt V, Beek A, Twisk J, Mechelen W. Effect of individual counselling on physical activity fitness and health. A randomised controlled trial in a workplace setting. American Journal of Preventative Medicine 2003;24(3):218‐26. [DOI] [PubMed] [Google Scholar]
Rachmani 2005 {published data only}
- Rachmani R, Levi Z, Slavachevski I, Avin M, Ravid M. Teaching patients to monitor their risk factors retards the progression of vascular complications in high risk patients with type 2 diabetes ‐ a randomised prospective study. Diabetic Medicine 2002;19:385‐92. [DOI] [PubMed] [Google Scholar]
- Rachmani R, Slavachevski I, Berla M, Frommer‐Shapira, Ravid M. Teaching and motivating patients to control their risk factors retards progression of cardiovascular as well as microvascular sequelae of type 2 diabetes mellitus ‐ a randomised prospective 8 year follow‐up. Diabetic Medicine 2005;22:410‐14. [DOI] [PubMed] [Google Scholar]
Sartorelli 2005 {published data only}
- Sartorelli D, Sciarra E, Franco LJ, Cardoso MA. Beneficial effects of short‐term nutritional counselling at primary health care level among Brazilian adults. Public Health Nutrition Journal 2005;8(7):820‐5. [DOI] [PubMed] [Google Scholar]
Sone (JDCS) 2002 {published data only}
- Sone H, Katagiri A, Ishibashi S, Abe R, Saito Y, Murase T, et al. Effects of lifestyle modifications on patients with type 2 diabetes: the Japan diabetes complications study (JDCS) study design, baseline analysis and three year interim report. Hormone and Metabolic Research 2002;34:509‐15. [DOI] [PubMed] [Google Scholar]
Stamler 1989 {published data only}
- Stamler R, Stamler J, Gosch F, Civinelli J, Fishman J, McKeever P, et al. Primary prevention of hypertension by nutritional hygienic means: final report of a randomized controlled trial. JAMA 1989;262:1801‐7. [MEDLINE: ] [PubMed] [Google Scholar]
Stefanick 1998 F {published data only}
- Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD. Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. New England Journal of Medicine 1998;339:12‐20. [DOI] [PubMed] [Google Scholar]
Stefanick 1998 M {published data only}
- Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD. Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. New England Journal of Medicine 1998;339:12‐20. [DOI] [PubMed] [Google Scholar]
Swedish RIS 1994 {published data only}
- Agewall S, Wikstrand J, Samuelsson O, Persson B, Andersson OK, Fagerberg B. The efficacy of multiple risk factor intervention in treated hypertensive men during long‐term follow up. Journal of Internal Medicine 1994;236:651‐9. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Agewell S, Fagerberg B, Berglund G, Schmidt C, Wendelhag I, Wikstrand J, et al. Multiple risk factor intervention trial in high risk hypertensive men: comparison of ultrasound intima‐media thickness and clinical outcome during 6 years follow‐up. Journal of Internal Medicine 2001;249:305‐14. [DOI] [PubMed] [Google Scholar]
- Fagerberg B, Wikstrand J, Berglund G, Samuelsson O, Agewall S. Mortality rates in treated hypertensive men with additional risk factors are high but can be reduced. A randomized intervention study. American Journal of Hypertension 1998;11:14‐22. [DOI] [PubMed] [Google Scholar]
- Schmidt C, Fagerberg B, Wikstrand J, Hulthe J. Multiple risk factor intervention reduces cardiovascular risk in hypertensive patients with echolucent plaques in the carotid artery. Journal of Internal Medicine 2003;253:430‐8. [DOI] [PubMed] [Google Scholar]
- Suurkula M, Agewell S, Fagerberg B, Wendelhag, et al. Multiple risk factor intervention in high risk hypertensive patients. Arteriosclerosis, Thrombosis and Vascular Biology 1996;16:462‐70. [DOI] [PubMed] [Google Scholar]
Take Heart 1995 {published data only}
- Glasgow RE, Terborg JR, Hollis JF, Severson HH, Boles SM. Take heart: results from the initial phase of a work‐site wellness program. American Journal of Public Health 1995;85(2):209‐16. [DOI] [PMC free article] [PubMed] [Google Scholar]
Toobert (MLP) 2005 {published data only}
- Toobert D, Glasgow R, Strycker L, Barrera M, Ritzwoller DP, Weidner G. Long‐term effects of the Mediterranean lifestyle program: a randomised clinical trial for post menopausal women with type 2 diabetes. International Journal of Behavioural Nutritional and Physical Activity 2007;4(1):1‐12. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Toobert DJ, Glasgow RE, Strycker LA, Barrera M, Radcliffe JL, Wander RC, et al. Biologic and quality of life outcomes from the Mediterranean lifestyle program. Diabetes Care 2003;26(8):2288‐93. [DOI] [PubMed] [Google Scholar]
- Toobert DJ, Strycker LA, Glasgow RE, Barrera M, Bagdade JD. Enhancing support for health behaviour change among women at risk for heart disease: the Mediterranean lifestyle program. Health Education Research 2002;17(5):574‐85. [DOI] [PubMed] [Google Scholar]
- Toobert DJ, Strycker LA, Glasgow RE, Barrera M, Bagdade JD, et al. Effects of the Mediterranean lifestyle program on multiple risk behaviours and psychosocial outcomes among women at risk for heart disease. Annals of Behavioural Medicine 2005;29(2):128‐37. [DOI] [PMC free article] [PubMed] [Google Scholar]
Tromso 1991 F {published and unpublished data}
- Knutsen S, Knutsen R. The Tromso Survey: The Family Intervention Study ‐ The effect of intervention on some coronary risk factors and dietary habits, a 6‐year follow‐up. Preventive Medicine 1991;20:197‐212. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Tromso 1991 M {published and unpublished data}
- Knutsen S, Knutsen R. The Tromso Survey: The Family Intervention Study ‐ The effect of intervention on some coronary risk factors and dietary habits, a 6‐year follow‐up. Preventive Medicine 1991;20:197‐212. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Uusitupa 1993 {published data only}
- Laitinen JH, Ahola IE, Sarkkinen ES, Winberg RL, Harmaakorpi‐Iivonen PA, Uusitupa MI. Impact of intensified dietary therapy on energy and nutrient intakes and fatty acid composition of serum lipids in patients with recently diagnosed non‐insulin‐dependent diabetes mellitus. Journal of the American Dietetic Association 1993;93(3):276‐83. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Uusitupa M, Laitinen J, Siitonen O, Vanninen E, Pyorala K. The maintenance of improved metabolic control after intensified diet therapy in recent type 2 diabetes. Diabetes Research & Clinical Practice 1993;19(3):227‐38. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Uusitupa MIJ. Early lifestyle intervention in patients with non‐insulin‐dependent diabetes mellitus and impaired glucose tolerance. Annals of Internal Medicine 1996;28:445‐9. [DOI] [PubMed] [Google Scholar]
- Vanninen E, Uusitupa M, Siitonen O, Laitinen J, Lansimies E. Habitual physical activity, aerobic capacity and metabolic control in patients with newly‐diagnosed type 2 (non‐insulin‐dependent) diabetes mellitus: effect of 1‐year diet and exercise intervention. Diabetologia 1992;35(4):340‐6. [EMBASE: 92117529] [DOI] [PubMed] [Google Scholar]
WHLP 1998 {published data only}
- Kuller LH, Simkin‐Silverman LR, Wing RR, Meilahn EN, Ives DG. Women's healthy lifestyle project: a randomized clinical trial. Circulation 2001;103:32‐7. [DOI] [PubMed] [Google Scholar]
- Simkin‐Silverman L, Wing R, Boraz M, Kuller L. Lifestyle intervention can prevent wight gain during menopause: results from a 5‐year randomised clinical trial. Annals of Behavioral Medicine 2003;26(3):212‐20. [DOI] [PubMed] [Google Scholar]
- Simkin‐Silverman L, Wing RR, Hansen DH, Klem ML, Pasagian‐Macaulay AP, Meilahn EN, et al. Prevention of cardiovascular risk factor elevations in healthy premenopausal women. Preventive Medicine 1995;24(5):509‐17. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
- Simkin‐Silverman LR, Wing RR, Boraz MA, Meilahn EN, Kuller LH. Maintenance of cardiovascular risk factor changes among middle‐aged women in a lifestyle intervention trial. Women's Health 1998;4(3):255‐71. [MEDLINE: ] [PubMed] [Google Scholar]
WHO Factories 1986 {published and unpublished data}
- World Health Organization European Collaborative Group. WHO European collaborative trial in the multifactorial prevention of coronary heart disease. Copenhagen: World Health Organization, 1989. [MEDLINE: ] [PubMed] [Google Scholar]
- World Health Organization European Collaborative Group. European collaborative trial of multifactorial prevention of coronary heart disease: final report on the 6‐year results. Lancet 1986;i:869‐75. [MEDLINE: ] [PubMed] [Google Scholar]
- World Health Organization European Collaborative Group. Multifactorial trial in the prevention of coronary heart disease: 2. Risk factor changes at two and four years. European Heart Journal 1982;3:184‐90. [MEDLINE: ] [PubMed] [Google Scholar]
Wing 1998 {published data only}
- Wing RR, Polley BA, Venditti E, Lang W, Jakicic JM. Lifestyle intervention in overweight individuals with a family history of diabetes. Diabetes Care 1998;21:350‐9. [DOI] [PubMed] [Google Scholar]
References to studies excluded from this review
Aldana (DPS) 2005 {published data only}
- Aldana SG, Barlow M, Smith R, Yanowitz FG, Adams T, Loveday L, et al. The Diabetes Prevention Program. AAOHN Journal 2005;53(11):499‐505. [PubMed] [Google Scholar]
Andersen 1999 {published data only}
- Andersen RE, Wadden TA, Bartlett SJ, Zemel B, Verde TJ, Franckowiak SC. Effects of lifestyle activity vs structured aerobic exercise in obese women: a randomized trial [see comments]. JAMA 1999;281(4):335‐40. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Bakx 1997 {published data only}
- Bakx JC, Stafleu A, Staveren WA, Hoogen HJ, Weel C. Long‐term effect of nutritional counseling; a study in family medicine. American Journal of Nutrition 1997;65(Suppl):1946S‐50S. [DOI] [PubMed] [Google Scholar]
Basler 1985 {published data only}
- Basler H‐D, Brinkmeier U, Buser K, Haehn K‐D, Molders‐Kober R. Psychological group treatment of obese essential hypertensives by lay therapists in rural general practice settings. Journal of Psychosomatic Research 1985;29(4):383‐91. [DOI] [PubMed] [Google Scholar]
Becker 2005 {published data only}
- Becker D, Yanek L, Johnson W, Garrett D, Moy TF, Reynolds SS, et al. Impact of a community‐based multiple risk factor intervention on cardio vascular risk in black families with a history of premature coronary disease. Circulation 2005;111:1298‐304. [DOI] [PubMed] [Google Scholar]
Berg 2005 {published data only}
- Berg A, Frey I, Landmann U, Deibert P, et al. Weight reduction is feasible‐preliminary results of a controlled, randomised intervention study in overweight adults. [Gewichtsreduktion ist machbar. Halbjahresergebnisse einer klinisch kontrolierten, randomisierten Interventionstudie mit übergewichtigen Erwachsenen]. Ernährungs Umschau 2003;50(10):386‐93. [Google Scholar]
Blake 1987 {published data only}
- Blake R, Doyle M, Straub V, Zweig S, Brent E, Ingman S, et al. A randomized controlled evaluation of an educational program in adults with high psychosocial risk of morbidity. Journal of Family Practice 1987;24:369‐76. [MEDLINE: ] [PubMed] [Google Scholar]
Boylan 2003 {published data only}
- Boylan M, Renier C, Knuths J, Haller I. Preventing cardiovascular disease in women. Minnesota Medicine 2003;86(5):52‐6. [PubMed] [Google Scholar]
Brekke 2005b {published data only}
- Brekke H, Lenner L, Taskinen M, Mansson J, et al. Lifestyle modification improves risk factors in type 2 diabetes relatives. Diabetes Research and Clinical Practice 2005;68:18‐28. [DOI] [PubMed] [Google Scholar]
Bruckert 1999 {published data only}
- Bruckert E, Lievre M. Primary prevention of cardiovascular disease in the elderly. Atherosclerosis 1999;144:182. [Google Scholar]
Bruno 1983 {published data only}
- Bruno R, Arnold C, Jacobson L, Winick M, Wynder E. Randomized controlled trial of a nonpharmacologic cholesterol reduction program at the worksite. Preventive Medicine 1983;12:523‐32. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Burke 1999 {published data only}
- Burke V, Giangiulio N, Gillam HF, Beilin LJ, Houghton S, Houghton S, et al. Health promotion in couples adapting to a shared lifestyle. Health Education Research 1999;14:269‐88. [DOI] [PubMed] [Google Scholar]
Burke 2003 {published data only}
- Burke V, Gianguilio N, Gillam H, Beilin L, et al. Physical activity and nutrition programmes for couples: a randomise controlled trial. Journal of Clinical Epidemiology 2003;56:421‐32. [DOI] [PubMed] [Google Scholar]
- Dzator JA, Hendrie D, Burke V, Gianguilio N, Gillam HF, Beilin LJ, et al. A randomized trial of interactive group sessions achieved greater improvements in nutrition and physical activity at a tiny increase at cost. Journal of Clinical Epidemiology 2004;57:610‐9. [DOI] [PubMed] [Google Scholar]
Burke 2005 {published data only}
- Burke V, Beilin L, Cutt H, Mansour J, Wilson A, Mori TA, et al. Effects of a lifestyle programme on ambulatory blood pressure and drug dosage in treated hypertensive patients: a randomised controlled trial. Journal of Hypertension 2005;23:1241‐9. [DOI] [PubMed] [Google Scholar]
Cambien 1981 {published data only}
- Cambien F, Richard JL, Ducimetiere P, Warnet JM, Kahn J. The Paris Cardiovascular Risk Factor Prevention Trial. Effects of two years of intervention in a population of young men. Journal of Epidemiology & Community Health 1981;35:91‐7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Cambien F, Richard JL, Jaqueson A, Ducimetiere P. Analysis of the results of a trial where groups have been randomized. The Paris cardiovascular‐prevention trial. Revue d Epidemiologie et de Sante Publique. 1981;29(3):281‐8. [EMBASE: 82013888] [PubMed] [Google Scholar]
Carlberg 1992 {published data only}
- Carlberg A, Tibblin G. Patient satisfaction in primary health care. A comparative study of two modes of treatment for hypertension. Family Practice 1992;9:304‐10. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Cicek 2004 {published data only}
- Cisek MM, Brzostek T, Gorkiewicz, M. Influence of health education on the occurrence of risk factors for coronary heart disease. Wiadomosci Lekarskie 2004;57(Suppl 1):38‐42. [PubMed] [Google Scholar]
Crouch 1986 {published data only}
- Crouch M, Sallis J, Farquhar JW, Haskell W, Ellsworth N, King A, et al. Personal and mediated health counseling for sustained dietary reduction of hypercholesterolaemia. Preventive Medicine 1986;15:282‐91. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Da Qing 1997 {published data only}
- Pan XR, Li GW, Hu YH, Wang JX, Yang WY, An ZX, et al. The effect of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 1997;20:537‐544. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Davey‐Smith 2005 {published data only}
- Davey Smith G, Bracha Y, Svendsen KH, Neaton JD, Haffner SM, Kuller LH, et al. Incidence of type 2 diabetes in the randomised multiple risk factor intervention trial. Annals of Internal Medicine 2005;142:313‐22. [DOI] [PubMed] [Google Scholar]
Domarkene 1990 {published data only}
- Domarkene S, Baubinene A, Chazova L, Kalinina A, Meimanaliev T, Shleifer E, et al. Efficiency of a cooperative program on multifactor prevention of coronary heart disease. Results of a 3 year follow up. Kardiologiia 1990;30:95‐8. [MEDLINE: ] [PubMed] [Google Scholar]
DPP 1999 {published data only}
- The Diabetes Prevention Program. Design and methods for a clinical trial in the prevention of type 2 diabetes. Diabetes Care 1999;22(4):623‐34. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
- The Diabetes Prevention Program: baseline characteristics of the randomized cohort. The Diabetes Prevention Program Research Group. Diabetes Care 2000;23(11):1619‐29. [DOI] [PMC free article] [PubMed] [Google Scholar]
DPPRG 2002 {published data only}
- Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine 2002;346(6):393‐403. [DOI] [PMC free article] [PubMed] [Google Scholar]
Dunn 1997 {published data only}
- Dunn AL, Marcus BH, Kampert JB, Garcia ME, Kohl HW 3rd, Blair SN. Reduction in cardiovascular disease risk factors: 6‐month results from Project Active. Preventive Medicine 1997;26(6):883‐92. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Eberle 2003 {published data only}
- Eberly L, Cohen J, Prineas R, Yang l, Intervention Trial Research group. Impact of incident diabetes and incident nonfatal cardiovascular disease on 18 year mortality. Diabetes Care 2003;26(3):848‐54. [DOI] [PubMed] [Google Scholar]
Edye 1989 {published data only}
- Edye B, Mandryk J, Frommer M, Healey S, Ferguson D. Evaluation of a worksite programme for the modification of cardiovascular risk factors. Medical Journal of Australia 1989;150:574‐81. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Elliot 2007 {published data only}
- Elliot D, Goldberg L. Kuehl K, Moe E, Breger RK, Pickering MA. The PHLAME (Promoting Healthy Lifestyles: Alternative Models Effect) firefighter study. Outcomes of two models of behaviour change. Journal of Occupational Environmental Medicine 2007;49:204‐13. [DOI] [PubMed] [Google Scholar]
Esposito 2003 {published data only}
- Esposito K, Pontillo A, Palo C, Giugliano G, Masella M, Marfella R, et al. Effect on weight loss and life style changes on vascular inflammatory markers in obese women. JAMA 2003;289(14):1799‐804. [DOI] [PubMed] [Google Scholar]
Ferro 2001 {published data only}
- Ferro A, Walton R. Racial differences in the effectiveness of non‐pharmacologic treatment of hypertension. Hypertension 2001;38:24. [PubMed] [Google Scholar]
Fielding 1994 {published data only}
- Fielding JE, Knight K, Mason T, Klesges RC, Pelletier KR. Evaluation of the IMPACT blood pressure program. Journal of Occupational Medicine 1994;36(7):743‐6. [MEDLINE: ] [PubMed] [Google Scholar]
- Fielding JE, Mason T, Kinght K, Klesges R, Pelletier KR. A randomized trial of the IMPACT worksite cholesterol reduction program. American Journal of Preventive Medicine 1995;11(2):120‐3. [PubMed] [Google Scholar]
Fox 1996 {published data only}
- Fox AA, Thompson JL, Butterfield GE, Gylfadottir U, Moynihan S, Spiller G. Effects of diet and exercise on common cardiovascular disease risk factors in moderately obese older women. American Journal of Clinical Nutrition 1996;63(2):225‐33. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Frommer 1990 {published data only}
- Frommer MS, Mandryk JA, Edye BV, Healey S, Berry G, Ferguson DA. A randomised controlled trial of counseling in a workplace setting for coronary heart disease risk factor modification: effects on blood pressure. Asia‐Pacific Journal of Public Health 1990;4(1):25‐33. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Fuchs 1993 {published data only}
- Fuchs Z, Viskoper JR, Drexler I, Nitzan H, Lubin F, Berlin S, et al. Comprehensive individualised nonpharmacological treatment programme for hypertension in physician‐nurse clinics: two year follow‐up. Journal of Human Hypertension 1993;7(6):585‐91. [MEDLINE: ] [PubMed] [Google Scholar]
Fullard 1987 {published data only}
- Fullard E, Fowler G, Gray M. Promoting prevention in primary care: controlled trial of low technology, low cost approach. BMJ 1987;294:1080‐2. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Gaede 2003 {published data only}
- Gaede P, Vedel P, Larsen N, Jensen GV, Parving HH, Pedersen O. Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. New England Journal of Medicine 2003;348(5):383‐93. [DOI] [PubMed] [Google Scholar]
- Gaede P, Vedel P, Parving H, Pederen O. Intensified multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: the Steno type 2 randomised study. Lancet 1999;353:617‐22. [DOI] [PubMed] [Google Scholar]
- Pedersen O, Gaede P. Intensified multifactorial intervention and cardiovascular outcome in type 2: the Steno type 2 randomised study. Metabolism 2003;52(8):19‐23. [DOI] [PubMed] [Google Scholar]
Gemson 1990 {published data only}
- Gemson DH, Sloan RP, Messeri P, Goldberg IJ. A public health model for cardiovascular risk reduction. Impact of cholesterol screening with brief nonphysician counseling. Archives of Internal Medicine 1990;150:985‐9. [MEDLINE: ] [PubMed] [Google Scholar]
Gemson 1995 {published data only}
- Gemson DH, Sloan RP. Efficacy of computerized health risk appraisal as part of a periodic health examination at the worksite. American Journal of Health Promotion 1995;9:462‐6. [DOI] [PubMed] [Google Scholar]
German 1994 {published data only}
- German C, Heierle C, Zunzunegui MV, Contreras E, Blanco P, Ruiz E, et al. The control of arterial hypertension in primary care: the evaluation of a program of self‐care [El control de la hipertension arterial en atencion primaria: evaluacion de un programa de autocuidados]. Atencion Primaria 1994;13(1):3‐7. [MEDLINE: ] [PubMed] [Google Scholar]
Goldhaber‐Fiebert 2003 {published data only}
- Goldhaber‐Fiebert J, Goldhaber‐Fiebert S, Tristran M, Nathan D. Randomised controlled community based nutrition and exercise intervention improves glycemia and cardiovascular risk factors in type 2 diabetic patients in rural Costa Rica. Diabetes Care 2003;26(1):24‐9. [DOI] [PubMed] [Google Scholar]
Gomel 1993 {published data only}
- Gomel M, Oldenburg B, Simpson JM, Owen N. Work‐site cardiovascular risk reduction: a randomized trial of health risk assessment, education, counseling, and incentives. American Journal of Public Health 1993;83:1231‐8. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
- Gomel MK, Oldenburg B, Simpson JM, Chilvers M, Owen N. Composite cardiovascular risk outcomes of a work‐site intervention trial. American Journal of Public Health 1997;87(4):673‐6. [DOI] [PMC free article] [PubMed] [Google Scholar]
Gordon 1997 {published data only}
- Gordon NF, Scott CB, Levine BD. Comparison of single versus multiple lifestyle interventions: are the antihypertensive effects of exercise training and diet‐induced weight loss additive?. American Journal of Cardiology 1997;79(6):763‐7. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Gordon 2002 {published data only}
- Gordon N, English C, Contractor A, Salmon R, Leighton RF, Franklin BA, et al. Effectiveness of three models for comprehensive cardiovascular disease risk reduction. American Journal of Cardiology 2002;89(1):1263‐8. [DOI] [PubMed] [Google Scholar]
Gump 2003 {published data only}
- Gump B, Matthews K. Special intervention reduces CVD mortality for adherent participants in the multiple risk factor intervention trial. Annals of Behavioural Medicine 2003;26(1):61‐8. [DOI] [PubMed] [Google Scholar]
Gysan 2004 {published data only}
- Gysan DB, Latsch J, Bjarnason‐Wehrens B, Albus C, Falkowski G, Herold G, et al. The PreFord Study. A prospective cohort study to evaluate the risk of a cardiovascular event (overall‐collective) as well as a prospective, randomized, controlled, multicentre clinical intervention study (high‐risk‐collective) on primary prevention of cardiovascular diseases in the Ford Motor Company employees in Germany [Die PraeFord Studie]. Zeitschrift für Kardiologie 2004;93(2):131‐6. [DOI] [PubMed] [Google Scholar]
Hanlon 1995 {published data only}
- Hanlon P, McEwan J, Gilmour H, Tannahill C, Tannahill A, Kelly M. Health checks and coronary risk: further evidence from a randomized controlled trial. BMJ 1995;311:1609‐13. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Haskell 1988 {published data only}
- Haskell WL, Fair J, Sanders W, Alderman EL. New methodologies for studying the prevention of atherosclerosis. Annals of Clinical Research 1988;20(1‐2):39‐45. [MEDLINE: ] [PubMed] [Google Scholar]
Hedberg 1998 {published data only}
- Hedberg GE, Wikstrom‐Frisen L, Janlert U. Comparison between two programmes for reducing the levels of risk indicators of heart diseases among male professional drivers. Occupational & Environmental Medicine 1998;55(8):554‐61. [DOI] [PMC free article] [PubMed] [Google Scholar]
Hopman‐Rock {published data only}
- Hopman‐Rock M, Westhoff M. Health education and exercise stimulation for older people: development and evaluation of the program "Healthy and Vital" [Gezondheidsvoorlichting en bewegingsstimulering voor ouderen: ontwikkeling en evaluatie van het programma "Gezond & Vitaal"]. Tijdschrift Voor Gerontologie En Geriatrie 2002;33:56‐63. [PubMed] [Google Scholar]
Huang 2001 {published data only}
- Huang E, Meigs J, Singer D. The effects of intervention to prevent cardiovascular disease in patients with type 2 diabetes mellitus. American Journal of Medicine 2001;111(8):633‐42. [DOI] [PubMed] [Google Scholar]
Inter99 2003 {published data only}
- Jorgensen T, Borch‐Johnsen K, Thomsen T, Ibsen H, Glümer C, Pisinger C, et al. A randomised non‐pharmacological intervention study for the prevention of Ischaemic heart disease: baseline results Inter99. European Journal of Cardiovascular Prevention Rehabilitation 2003;10:377‐86. [DOI] [PubMed] [Google Scholar]
- Toft U, Kristoffersen L, Aadahl M, Huth Smith L, et al. Diet and exercise intervention in a general population‐mediators of participation and adherence: the Inter99 study. European Journal of Public Health 2006;12:1‐9. [DOI] [PubMed] [Google Scholar]
Jiang 2004 {published data only}
- Jiang B, Wang W, Wu S, Hong Z. Control effect of health education on body mass index of community population. Wei Sheng Yan Jui 2004;33(1):98‐100. [PubMed] [Google Scholar]
Jula 1990 {published data only}
- Jula A, Ronnemaa J, Rastas A, Karvetti R‐L, Muki J. Long‐term nonpharmacological treatment for mild to moderate hypertension. Journal of Internal Medicine 1990;227:413‐21. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Kamioka 2006 {published data only}
- Kamioka H, Nakamura Y, Yazaki T, Uebaba K, Mutoh Y, Okada S, et al. Comprehensive heath eduction combining hot sap bathing and lifestyle education in middle‐aged and elderly women: one year follow‐up on randomised control trial of three and six month interventions. Journal of Epidemiology 2006;16(1):35‐44. [DOI] [PMC free article] [PubMed] [Google Scholar]
Karlehagen 2003 {published data only}
- Karlehagen S, Ohlson C. Primary prevention of cardiovascular disease by an occupational health service. Preventative Medicine 2003;37:219‐25. [DOI] [PubMed] [Google Scholar]
Kawakami 1999 {published data only}
- Kawakami N, Haratani T, Iwata N, Imanaka Y, Murata K, Araki S. Effects of mailed advice on stress reduction among employees in Japan: a randomized controlled trial. Industrial Health 1999;37(2):237‐42. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Ketola 2001 {published data only}
- Ketola E, Makela M, Klockars M. Individualised multifactorial lifestyle intervention trial for high‐risk cardiovascular patients in primary care. British Journal of General Practice 2001;51:291‐4. [PMC free article] [PubMed] [Google Scholar]
Kisioglu 2004 {published data only}
- Kisioglu A, Aslan B, Ozturk M, Aykut M, Ilhan I. Improving control of high blood pressure among middle‐aged Turkish women of low socio‐economic status through public health training. Croatian Medical Journal 2004;45(4):477‐82. [PubMed] [Google Scholar]
Knappe 1982 {published data only}
- Knappe J, Heinrich J, Duck KD. On the efficacy of a programme of the prevention of cardio‐vascular diseases [Zur Wirksamkeit eines Präventionsprogramms gegen Herz‐Kreislauf‐Krankheiten]. Zeitschrift für die Gesamte Innere Medizin und Ihre Grenzgebiete 1982;37(19):633‐41. [EMBASE: 83029552] [PubMed] [Google Scholar]
Ko 2004 {published data only}
- Ko G. Effects of structured health education programme by a diabetic education nurse on cardiovascular risk factors in Chinese Type 2 diabetic patients: a 1 year prospective randomised trial. Diabetic Medicine 2004;21:1274‐9. [DOI] [PubMed] [Google Scholar]
Kreuter 1996 {published data only}
- Kreuter MW, Strecher VJ. Do tailored behavior change messages enhance the effectiveness of health risk appraisal. Health Education Research 1996;11:97‐105. [DOI] [PubMed] [Google Scholar]
Lasater 1986 {published data only}
- Lasater TM, Wells BL, Carleton RA, Elder JP. The role of churches in disease prevention research studies. Public Health Reports 1986;101(2):125‐31. [MEDLINE: ] [PMC free article] [PubMed] [Google Scholar]
Lauritzen 1995 {published data only}
- Engberg MD, Christensen B, Karlsmose B, Lous J, Lauritzen T. General health screenings to improve cardiovascular risk profiles: a randomized controlled trial in general practice with 5 year follow‐up. Journal of Family Practice 2002;51(6):546‐52. [PubMed] [Google Scholar]
- Lauritzen T, Leboeuf‐Yde C, Lunde IM, Nielsen KD. Ebeltoft project: baseline data from a five‐year randomized, controlled, prospective health promotion study in a Danish population. British Journal of General Practice 1995;45(399):542‐7. [MEDLINE: ] [PMC free article] [PubMed] [Google Scholar]
Leighton 1990 {published data only}
- Leighton RF, Repka FJ, Birk TJ, Lynch DJ, Bingle JF, Gohara AF, et al. The Toledo Exercise and Diet Study. Results at 26 weeks. Archives of Internal Medicine 1990;150(5):1016‐20. [MEDLINE: ] [PubMed] [Google Scholar]
Lindahl 1998 {published data only}
- Lindahl B, Nilsson TK, Asplund K, Hallmans G. Intense nonpharmacological intervention in subjects with multiple cardiovascular risk factors: decreased fasting insulin levels but only a minor effect on plasma plasminogen activator inhibitor activity. Metabolism: Clinical & Experimental 1998;47(4):384‐90. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Little 2004 {published data only}
- Little P, Kelly J, Barnett J, Dorward M, Margetts B, Warm D. Randomised controlled trial of dietary advice for patients with single high blood pressure reading in primary care. BMJ 2004;328:1054‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
Lovibond 1986 {published data only}
- Lovibond S, Birrell P, Langeluddecke P. Changing coronary heart disease risk‐factor status: the effects of three behavioural programs. Journal of Behavioural Medicine 1986;9:414‐36. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Macdonald 1990 {published data only}
- Macdonald NJ, Stark S, et al. Multiple risk factor intervention in the prevention of coronary heart disease [abstract]. Clinical Science 1990;78(Suppl 22):6P. [Google Scholar]
Martinez‐Amenos 1990 {published data only}
- Martínez‐Amenós A, Fernández Ferré ML, Mota Vidal C, Alsina Rocasalbas J. Evaluation of two educative models in a primary care hypertension programme. Journal of Human Hypertension 1990;4:362‐4. [MEDLINE: ; CN‐00060437] [PubMed] [Google Scholar]
McCance 1985 {published data only}
- McCance KL, Eutropius L, Jacobs MK, Williams RR. Preventing coronary heart disease in high‐risk families. Research in Nursing & Health 1985;8(4):413‐20. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
McCann 1997 {published data only}
- McCann TJ, Criqui MH, Kashani IA, Sallis JF, Calfas KJ, Langer RD, et al. A randomized trial of cardiovascular risk factor reduction: patterns of attrition after randomization and during follow‐up. Journal of Cardiovascular Risk 1997;4(1):41‐6. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
McMahon 2002 {published data only}
- McMahon A, Hodgins M, Kelleher C. Feasibility of a men's health promotion programme in Irish primary care. Irish Journal of Medical Science 2002;171(1):20‐3. [DOI] [PubMed] [Google Scholar]
Meimanaliev 1991 {published data only}
- Meimanaliev T, Shleifer E, Aitbaev K, Aitmurzaeva G, Gilfanova V, Podgurskaya L, et al. Prevalence of ischaemic heart disease risk factors among the male population in Frunze aged 40‐59 years and results of a five‐year prevention programme. Cor et Vasa 1991;33:451‐7. [MEDLINE: ] [PubMed] [Google Scholar]
Miemanaliev 1993 {published data only}
- Meimanaliev T, Oteva E, Aitbaev K, Maslennikov A, Nikolaeva A, Shterental I, et al. Prevalence of main risk factors among probands with a history of early myocardial infarction and their relatives. Terapevticheskii Arkhiv 1993;65:28‐30. [MEDLINE: ] [PubMed] [Google Scholar]
Miller 2002 {published data only}
- Miller E, Erlinger T, Young D, Jehn M, Charleston J, Rhodes D, et al. Results of diet, exercise, and weight loss intervention trial (DEW‐IT). Hypertension 2002;40:612‐18. [DOI] [PubMed] [Google Scholar]
Murray 1986 {published data only}
- Murray DM, Luepker RV, Pirie PL, Grimm RH Jr, Bloom E, Davis MA, et al. Systematic risk factor screening and education: a community‐wide approach to prevention of coronary heart disease. Preventive Medicine 1986;15(6):661‐72. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Nieman 2002 {published data only}
- Nieman D, Brock D, Butterworth D, Utter A, Nieman CC. Reducing diet and/or exercise training decreases the lipid and lipoprotein risk factors of moderately obese women. Journal of the American College of Nutrition 2002;21(4):344‐50. [DOI] [PubMed] [Google Scholar]
Nikitin 1991 {published data only}
- Nikitin Y, Bondareva Z, Oteva E, Filimonova T. Serum lipid composition in healthy subjects and patients of senile age and long livers. Klinicheskaya Meditsina 1991;69:32‐5. [PubMed] [Google Scholar]
Nisbeth 2000 {published data only}
- Andersen L, Klausen K, Nisbeth O. One‐year effect of health counselling on life‐style and risk factors for heart disease [Et ars effekt af sundhedsvejledning pa livsstil og risikofaktorer for hjertesygdom]. Ugeskfrift For Laeger 2002;164(13):1814‐9. [PubMed] [Google Scholar]
- Nisbeth O, Klausen K, Andersen LB. Effectiveness of counselling over 1 year on changes in lifestyle and coronary heart disease risk factors. Patient Education and Counseling 2000;40:121‐31. [DOI] [PubMed] [Google Scholar]
Nolte 1997 {published data only}
- Nolte LJ, Nowson CA, Dyke AC. Effect of dietary fat reduction and increased aerobic exercise on cardiovascular risk factors. Clinical and Experimental Pharmacology and Physiology 1997;24(11):901‐3. [EMBASE: 97321842] [DOI] [PubMed] [Google Scholar]
Olivarius 2001 {published data only}
- Olivarius NF, Beck‐Nielsen H, Andreasen AH, Hørder M, Pedersen PA. Randomised trial of structured personal care of type 2 diabetes mellitus. BMJ 2001;232:1‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
Ostwald 1989 {published data only}
- Ostwald SK. Changing employees' dietary and exercise practices: an experimental study in a small company. Journal of Occupational Medicine 1989;31:90‐7. [MEDLINE: ] [PubMed] [Google Scholar]
OXCHECK 2003 {published data only}
- Hillsdon M, Thorogood M, Murphy M, Jones L. Can a simple measure of vigorous physical activity predict future mortality? Results from the OXCHECK study. Public Health Nutrition 2003;7(4):557‐62. [DOI] [PubMed] [Google Scholar]
Parker 2005 {published data only}
- Parker D, Evangelou E, Eaton C. Intraclass correlation co‐efficients for cluster randomised trials in primary care: the cholesterol education and research trial. Contemporary Clinical Trials 2005;26:260‐7. [DOI] [PubMed] [Google Scholar]
Patterson 1988 {published data only}
- Patterson T, Sallis J, Nader P, Rupp J, McKenzie T, Roppe B, et al. Direct observation of physical activity and dietary behaviours in a structured environment: effects of a family‐based health promotion program. Journal of Behavioural Medicine 1988;11:447‐58. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Persson 1996 {published data only}
- Persson J, Israelsson B, Stavenow L, Holmstrom E, Berglund G. Progression of atherosclerosis in middle‐aged men: effects of multifactorial intervention. Journal of Internal Medicine 1996;239:425‐33. [DOI] [PubMed] [Google Scholar]
Pierce 1984 {published data only}
- Pierce J, Watson D, Knightsm S, Gliddon T, Williams S, Watson R. A controlled trial of health education in the physician's office. Preventive Medicine 1984;13:185‐4. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Pora 2005 {published data only}
- Pora V, Farrell B, Dolovich L, Kaczorowski J. Promoting cardiovascular health among older adults. CPJ/RCP 2005;138(7):50‐5. [Google Scholar]
PREMIER 2006 {published data only}
- Elmer P, Obarzanek E, Vollmer W, Simons‐Morton D, Stevens VJ, Young DR, et al. Effects of comprehensive lifestyle modification on diet, weight, physical fitness, and blood pressure control: 18 month results of a randomised trial. Annals of Internal Medicine 2006;144:485‐95. [DOI] [PubMed] [Google Scholar]
- Svetkey L, Erlinger T, Vollmer W, Feldstein A, Cooper LS, Appel LJ, et al. Effect of lifestyle modifications on blood pressure by race, sex, hypertension status and age. Journal of Human Hypertension 2005;19:21‐31. [DOI] [PubMed] [Google Scholar]
- Svetkey L, Harsha D, Vollmer W, Stevens V, Obarzanek E, Elmer PJ, et al. PREMIER: a clinical trial of comprehensive lifestyle modification for blood pressure control: rational, design and baseline characteristics. Annals of Epidemiology 2003;13:462‐71. [DOI] [PubMed] [Google Scholar]
Pritchard 2002 {published data only}
- Pritchard J, Nowson C, Billington T, Wark J. Benefits of a year long workplace weight loss program on cardiovascular risk factors. Nutrition and Diet 2002;59:87‐96. [Google Scholar]
Reid 1995 {published data only}
- Reid C, McNeil JJ, Williams F, Powles J. Cardiovascular risk reduction: a randomized trial of two health promotion strategies for lowering risk in a community with low socioeconomic status. Journal of Cardiovascular Risk 1995;2(2):155‐63. [MEDLINE: ] [PubMed] [Google Scholar]
Robson 1989 {published data only}
- Robson J, Boomla K, Fitzpatrick S, Jewell A, Taylor J, Self J, et al. Using nurses for preventive activities with computer assisted follow‐up: a randomised controlled trial. BMJ 1989;298:433‐6. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Rosamond 2000 {published data only}
- Rosamond WD, Ammerman AS, Holliday JL, Tawney KW, Hunt KJ, Keyserling TC, et al. Cardiovascular disease risk factor intervention in low‐income women: the North Carolina WISEWOMAN project. Preventive Medicine 2000;31(4):370‐9. [DOI] [PubMed] [Google Scholar]
Rothman 2004 {published data only}
- Rothman R, DeWalt D, Malone R, et al. Diabetes disease management program is more effective for patients with low literacy. JAMA 2004;11(12):752‐3. [Google Scholar]
- Rothman R, Malone R, Bryant B, Shintani A, et al. A randomised trial of a primary care‐based disease management program to improve cardiovascular risk factors and glycated hemoglobin level in patients with diabetes. American Journal of Medicine 2005;118:279‐84. [DOI] [PubMed] [Google Scholar]
Rowland 1994 {published data only}
- Rowland L, Dickinson EJ, Newman P, Ford D, Ebrahim S. Look After Your Heart programme: impact on health status, exercise knowledge, attitudes, and behaviour of retired women in England. Journal of Epidemiology & Community Health 1994;48:123‐8. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Sarraf‐Zadegan 2003 {published data only}
- Sarraf‐Zadegan N, Sadri G, Malek‐Afzali H, Baghaei M, Mohammadi Fard N, Shahrokhi S, et al. Isfahan healthy heart programme:a comprehensive integrated community based programme for cardiovascular disease prevention and control. Acta Cardiology 2003;58(4):309‐20. [DOI] [PubMed] [Google Scholar]
Schwandt 1999 {published data only}
- Ohrig E, Geib HC, Haas G‐M, Schwandt P. The Prevention Education Program (PEP) Nuremberg: design and baseline data of a family oriented intervention study. International Journal of Obesity 2001;25(Suppl 1):S89‐S92. [DOI] [PubMed] [Google Scholar]
- Schwandt P, Geiss HC, Ritter MM, Ublacker C, Parhofer KG, Otto C, et al. The prevention education program (PEP). A prospective study of the efficacy of family‐oriented life style modification in the reduction of cardiovascular risk and disease: design and baseline data. Journal of Clinical Epidemiology 1999;52(8):791‐800. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Schwedes 2002 {published data only}
- Schwedes U, Siebolds M, Mertes G. Meal related structured self monitoring of blood glucose. Diabetes Care 2002;25(11):1928‐32. [DOI] [PubMed] [Google Scholar]
S‐E London 1977 {published data only}
- South East London Screening Study Group. A controlled trial of multiphasic screening in middle‐age: results of the South‐East London Screening Study. International Journal of Epidemiology 1977;6:357‐63. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Smith 1991 {published data only}
- Smith K, McKinlay S. The validity of health risk appraisals for coronary heart disease: results from a randomized field trial. American Journal of Public Health 1991;81:466‐70. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Steinbach 1982 {published data only}
- Steinbach M, Constantineanu M, Harnagea P, Theodorini S, Georgescu M, Mitu S, et al. The Bucharest Multifactorial Prevention Trial. The changes of morbidity and of general and specific mortality. Revue Roumaine de Medecine ‐ Medicine Interne 1982;20:197‐208. [MEDLINE: ] [PubMed] [Google Scholar]
Strandberg 2001 {published data only}
- Strandberg T, Pitkala K, Berglind S, Nieminen M, Tilvis RS, et al. Multi‐factorial cardiovascular disease prevention in patients aged 75 and older: a randomised controlled trial. American Heart Journal 2001;142:945‐51. [DOI] [PubMed] [Google Scholar]
TOMHS 1991 {published data only}
- No authors listed. The treatment of mild hypertension study. A randomized, placebo‐controlled trial of a nutritional‐hygienic regimen along with various drug monotherapies. The Treatment of Mild Hypertension Research Group. Archives of Internal Medicine 1991;151(7):1413‐23. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
TONE 1998 {published data only}
- Whelton PK, Appel LJ, Espeland MA, Applegate WB, Ettinger WH Jr, Kostis JB. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomized controlled trial of nonpharmacologic interventions in the elderly (TONE). TONE Collaborative Research Group. JAMA 1998;279(11):839‐46. [DOI] [PubMed] [Google Scholar]
Tonstad 2005 {published data only}
- Tonstad S, Sundfar T, Seljeflot I. Effect of lifestyle changes on atherogenic lipids and endothelial cell adhesion molecules in young adults with familial premature coronary heart disease. American Journal of Cardiology 2005;95:1187‐91. [DOI] [PubMed] [Google Scholar]
Tsuyuki 1999 {published data only}
- Tsuyuki RT, Johnson JA, Teo KK, Ackman ML, Biggs RS, Cave A, et al. Study of Cardiovascular Risk Intervention by Pharmacists (SCRIP): a randomized trial design of the effect of a community pharmacist intervention program on serum cholesterol risk. Annals of Pharmacotherapy 1999;33(9):910‐19. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Van Elderen 2001 {published data only}
- Elderen T, Dusseldorp E. Lifestyle effects of group health education for patients with coronary heart disease. Psychology and Health 2001;16:327‐41. [Google Scholar]
Velonakis 1999 {published data only}
- Velonakis E, Sourtzi P, Komitopoulos N, Ioannides J, Varsamis E. A health promotion programme for the prevention of cardiovascular diseases in the elderly. International Journal of Health Promotion & Education 1999;37(1):26‐9. [Google Scholar]
Volozh 1991 {published data only}
- Volozh O, Saava M, Tur I, Neilinn K, Solodkaia E, Taggerluk H. Risk factors of coronary heart disease and atherosclerosis in Tallin inhabitants ‐ relation of age, sex and ethnic origin. A population study. Kardiologiia 1991;31:20‐4. [MEDLINE: ] [PubMed] [Google Scholar]
Wang 2002 {published data only}
- Wang A, Seng C. Effect of non‐pharmacologic treatments on early stage of primary hypertension. Anhiu Medical Journal 2002;23(6):7‐9. [Google Scholar]
WHP 1999 {published data only}
- Emmons KM, Linnan LA, Shadel WG, Marcus B, Abrams DB. The working healthy project: a worksite health‐promotion trial targeting physical activity, diet and smoking. Journal of Occupational and Environmental Medicine 1999;41:545‐55. [DOI] [PubMed] [Google Scholar]
- Emmons KM, Shadel WG, Linnan L, Marcus BH, Abrams DB. A prospective analysis of change in multiple risk factors for cancer. Cancer Research Therapy & Control 1999;8(1‐2):15‐23. [Google Scholar]
Wisewoman 1999 {published data only}
- The Wisewoman Group. Cardiovascular disease prevention for women attending breast and cervical cancer screening programs: the WISEWOMAN projects. Preventive Medicine 1999;28(5):496‐502. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Witmer 2004 {published data only}
- Witmer J, Hensel M, Holck P, Ammerman A, Will JC. Heart disease prevention for Alaska native women: a review of pilot findings. Journal of Women's Health 2004;13(5):569‐77. [DOI] [PubMed] [Google Scholar]
Woollard 2003 {published data only}
- Woollard J, Burke V, Beilin L, Verheijden M, Bulsara MK. Effects of general practice based intervention on diet body mass index and blood lipids in patients at cardiovascular risk. Journal of Cardiovascular Risk 2003;10:31‐40. [DOI] [PubMed] [Google Scholar]
Working Well Trial {published data only}
- Abrams DB, Boutwell WB, Grizzle J, Heimendinger J, Sorensen G, Varnes J. Cancer control at the workplace: the Working Well Trial. Preventive Medicine 1994;23:15‐27. [DOI] [PubMed] [Google Scholar]
Wu 1999 {published data only}
- Wu X, Cao T, Zhu Y. Effects of dietary pattern modification on blood pressure over in a work site intervention program. Chinese Journal of Cardiology 1999;27(1):22‐5. [Google Scholar]
Zimmerman 1996 {published data only}
- Zimmerman E, Horton La Forge B. Detection and prevention of cardiac risk factors: health risk assessment and target follow‐up in a managed care population. Journal of Cardiovascular Nursing 1996;11(1):27‐38. [DOI] [PubMed] [Google Scholar]
References to ongoing studies
Roderigues 2005 {published data only}
- Rodriguez CJJ, Benavides M F, Villaverde GC, Pena SE, Flor SF, Trave MP, et al. Randomised clinical trial of an intensive intervention into life‐styles of patients with hyperfibrinogenaemia in primary prevention of cardiovascular pathology in primary health care [Ensayo clínico aleatorizado de una intervención intensiva sobre los estilos de vida de pacientes con hiperfibrinogenemia en prevención primaria de las enfermedades cardiovasculares en el ámbito de la atención primaria de salud]. Atencion Primaria 2005;25(5):260‐4. [DOI] [PMC free article] [PubMed] [Google Scholar]
Additional references
AHA 2002
- Pearson TA, Blair SN, Daniels SR, Eckel RH, Fair JM, Fortmann SP, et al. AHA Guidelines for primary prevention of cardiovascular disease and stroke: 2002 Update: Consensus Panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases. American Heart Association Science Advisory and Coordinating Committee. Circulation 2002;106:388‐91. [DOI] [PubMed] [Google Scholar]
Appel 2004
- Appel LJ. Lifestyle modification: is it achievable and durable?. Journal of Clinical Hypertension 2004;6(10):578‐81. [DOI] [PMC free article] [PubMed] [Google Scholar]
Asaria 2007
- Asaria P, Chisholm D, Mathers C, Ezzati M, Beaglehole R. Chronic disease prevention: health effects and financial costs of strategies to reduce salt intake and control tobacco use. Lancet 2007;370(9604):2044‐53. [DOI] [PubMed] [Google Scholar]
Bejot 2007
- Bejot Y, Giroud M, Rouaud O, Benatru I, Moreau T, Freycz M, et al. Trends in stroke incidence and case‐fatality rates over a 20‐year period (1985‐2004) in Dijon, France. Bulletin de l'Académie Nationale de Médecine 2007;191(2):305‐22. [PubMed] [Google Scholar]
Ben‐Shlomo 1994
- Ben‐Shlomo Y, Davey Smith G, Shipley M, Marmot MG. What determines mortality risk in male former cigarette smokers?. American Journal of Public Health 1994;84:1235‐42. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Berglund 2000
- Berglund G, Nilsson P, Eriksson KF, Nilsson JA, Hedblad B, Kristenson H, et al. Long‐term outcome of the Malmo preventive project: mortality and cardiovascular morbidity. Journal of Internal Medicine 2000;247:19‐29. [DOI] [PubMed] [Google Scholar]
Brunner 1997
- Brunner E, White I, Thorogood M, Bristow A, Curle D, Marmot MG. Can dietary interventions in the population change diet and cardiovascular risk factors? An assessment of effectiveness utilising a meta‐analysis of randomized controlled trials. American Journal of Public Health 1997;87:1451‐22. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Callow 2006
- Callow AD. Cardiovascular disease 2005 ‐ the global picture. Vascular Pharmacology 2006;45(5):302‐7. [DOI] [PubMed] [Google Scholar]
Collins 1994
- Collins R, MacMahon S. Blood pressure, antihypertensive drug treatment and the risks of stroke and coronary heart disease. British Medical Bulletin 1994;50:272‐98. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Cook 1986
- Cook D, Shaper AG, Pocock S, Kussick S. Giving up smoking and the risk of heart attacks. Lancet 1986;ii:1376‐80. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
CTT 2005
- Cholesterol Treatment Trialists (CTT) Collaborators. Efficacy and safety of cholesterol‐lowering treatment: prospective meta‐analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005;366:1267‐78. [DOI] [PubMed] [Google Scholar]
Davey Smith 1993
- Davey Smith G, Song S, Sheldon T. Cholesterol lowering and mortality: the importance of considering initial level of risk. BMJ 1993;306:1367‐73. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Davey Smith 1994
- Davey Smith G, Egger M. Who benefits from medical interventions?. BMJ 1994;308:72‐4. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Davey Smith 2005
- Davey Smith G, Bracha Y, Svendsen KH, Neaton JD, Haffner SM, Kuller LH for the Multiple Risk Factor Intervention Trial. Incidence of type 2 diabetes in the randomized multiple risk factor intervention trial. Annals of Internal Medicine 2005;142:313‐22. [DOI] [PubMed] [Google Scholar]
Daviglus 2006
- Daviglus ML, Lloyd‐Jones DM, Pirzada A. Preventing cardiovascular disease in the 21st Century: therapeutic and preventive implications of current evidence. American Journal of Cardiovascular Drugs 2006;6(2):87‐101. [DOI] [PubMed] [Google Scholar]
Dickersin 1994
- Dickersin K, Scherer R, Lefebvre C. Identifying relevant studies for systematic reviews. BMJ 1994;309:1286‐91. [DOI] [PMC free article] [PubMed] [Google Scholar]
DiClemente 1991
- DiClemente CC, Prochaska J, Fairhurst S, Velicer W, Velasques M, Rossi J. The process of smoking cessation: an analysis of precontemplation, contemplation and preparation stages of change. Journal of Consulting & Clinical Psychology 1991;59:295‐304. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Ebrahim 2001
- Ebrahim S, Davey Smith GD. Exporting failure? Coronary heart disease and stroke in developing countries. International Journal of Epidemiology 2001;30:201‐5. [DOI] [PubMed] [Google Scholar]
Ebrahim 2008
- Ebrahim S. Chronic diseases and calls to action. International Journal of Epidemiology 2008;37(2):225‐30. [DOI] [PubMed] [Google Scholar]
Editorial 1982a
- Editorial. Trials of coronary heart disease prevention. Lancet 1982;ii:803‐4. [MEDLINE: ] [PubMed] [Google Scholar]
Editorial 1982b
- Editorial. Coronary disease and multiple‐risk factor intervention. Lancet 1982;i:1395. [MEDLINE: ] [PubMed] [Google Scholar]
Editorial 1984
- Editorial. Double first in Wales. BMJ 1984;289:514‐15. [MEDLINE: ] [PMC free article] [PubMed] [Google Scholar]
Egger 1995
- Egger M, Davey Smith G. Risks and benefits of treating mild hypertension: a misleading meta‐analysis?. Journal of Hypertension 1995;13:813‐15. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Ellekjaer 2007
- Ellekjaer H, Selemer R. Stroke similar incidence, better prognosis. Tidsskr Nor Laegeforen 2007;127(6):740‐3. [PubMed] [Google Scholar]
European Task Force 2007
- Graham I, Atar D, Borch‐Johnsen K, Boysen G, Burell G, Cifkova R, et al. European guidelines on cardiovascular disease prevention in clinical practice: full text. Fourth Joint Task Force of the European Society of Cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts). European Journal of Cardiovascular Prevention and Rehabilitation 2007;14(Suppl 2):S1‐113. [DOI] [PubMed] [Google Scholar]
Fang 2007
- Fang J, Alderman MH, Keenan NL, Croft JB. Declining US Stroke Hospitalization since 1997: National Hospital Discharge Survey, 1988‐2004. Neuroepidemiology 2007;29:243‐9. [DOI] [PubMed] [Google Scholar]
Farquhar 1977
- Farquhar J, Wood P, Breitrose H, Haskell W, Meyer A, MacCoby N, et al. Community education for cardiovascular health. Lancet 1977;i:1192‐5. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Farquhar 1990
- Farquhar J, Fortmann S, Flora J, Taylor B, Haskell W, Williams P, et al. Effects of communitywide education on cardiovascular disease risk factors. The Stanford Five‐City Project. JAMA 1990;264:359‐65. [MEDLINE: ] [PubMed] [Google Scholar]
Fortmann 1993
- Fortmann S, Barr Taylor C, Flora J, Jatulis D. Changes in adult cigarette smoking prevalence after 5 years of community health education: the Stanford Five‐City Project. American Journal of Epidemiology 1993;137:82‐96. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Higgins 2008
- Higgins JPT, Green S (editors). Cochrane Handbook for Systematic Reviews of Interventions Version 5.0.2 [updated September 2009]. The Cochrane Collaboration, 2008. Available from www.cochrane‐handbook.org.
Kickbush 1988
- Kickbush I. Report on the Adelaide Conference. Healthy public policy. 2nd International Conference on Health Promotion. 1988.
Lefebvre 1996
- Lefebvre C, McDonald S. Development of a sensitive search strategy for reports of randomised controlled trials in EMBASE. Fourth International Cochrane Colloquium 20‐24 Oct, Adelaide, Australia. 1996.
Levi 2002
- Levi F, Lucchini F, Negri E, Vecchaia C. Trends in mortality from cardiovascular and cerebrovascular diseases in Europe and other areas of the world. Heart 2002;88:119‐24. [DOI] [PMC free article] [PubMed] [Google Scholar]
Lim 2007
- Lim SS, Gaziano TA, Gakidou E, Reddy KS, Farzadfar F, Lozano R, et al. Prevention of cardiovascular disease in high‐risk individuals in low‐income and middle‐income countries: health effects and costs. Lancet 2007;370(9604):2054‐62. [DOI] [PubMed] [Google Scholar]
Little 2004
- Little P, Kelly J, Barnett J, Dorward M, Margetts B, Warm D. Randomised controlled factorial trial of dietary advice for patients with a single high blood pressure reading in primary care. BMJ 2004;328:1054‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
Luepker 1996
- Luepker RV, Rastam L, Hanham PJ, Murray DM, Gray C. Community education for cardiovascular disease prevention: morbidity and mortality results from the Minnesota Heart Health Programme. American Journal of Epidemiology 1996;144:351‐62. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
McCormick 1988
- McCormick J, Skrabanek P. Coronary heart disease is not preventable by population interventions. Lancet 1988;ii:839‐41. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Meichenbaum 1993
- Meichenbaum D. Changing conceptions of cognitive behavior modification: retrospect and prospect. Journal of Consulting and Clinical Psychology 2001;61(2):210‐5. [DOI] [PubMed] [Google Scholar]
MRFITRG 1990
- Multiple Risk Factor Intervention Trial Research Group. Mortality rates after 10.5 years for participants in the multiple risk factor intervention trial. Findings related to a priori hypotheses of the trial. JAMA 1990;263:1795‐801. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Mullen 1992
- Mullen PD, Mains DA, Velez R. A meta analysis of controlled trials of cardiac education. Patient Education Counselling 1992;19:143‐62. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Mulrow 1995
- Mulrow CD, Cornell JA, Herrera CR, Kadri A, Farnett L, Aguilar C. Hypertension in the elderly: implications and generalizability of randomized trials. JAMA 1995;272:1932‐8. [MEDLINE: ] [PubMed] [Google Scholar]
NSF‐CHD 2000
- Department of Health. National Service Framework for coronary heart disease: modern standards and service models. London: Department of Health, 2000. [Google Scholar]
NSF‐CHD 2006
- Department of Health. The coronary heart disease national service framework: shaping the future ‐ progress report for 2006. http://www.doh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_063168 (accessed 27 October 2010).
O'Connor 1989
- O'Connor GT, Buring JE, Yusuf S, Goldhaber S, Olmstead E, Pafenbarger R, et al. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation 1989;80:234‐44. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Oldridge 1988
- Oldridge NB, Guyatt GH, Fischer ME, Rimm AA. Cardiac rehabilitation after myocardial infarction. Combined experience of randomized clinical trials. JAMA 1988;260:945‐50. [MEDLINE: ] [PubMed] [Google Scholar]
Pearson 1993
- Pearson T, Jamison D, Trejo‐Gutierrez J. Cardiovascular Disease. In: Jamison D, Mosley WH, Measham A, Bobadilla J editor(s). Disease control priorities in developing countries. Oxford: Oxford University Press, 1993:577‐94. [Google Scholar]
Pickering 2003
- Pickering T. Lifestyle modification and blood pressure control: is the glass half full or half empty?. JAMA 2003;289(16):2131‐2. [DOI] [PubMed] [Google Scholar]
Pickering 2004
- Pickering TG. Lifestyle modification: is it achievable and durable? The argument against. Journal of Clinical Hypertension 2004;6(10):581‐4. [PubMed] [Google Scholar]
Prochaska 1983
- Prochaska JO, DiClemente CC. Stages and processes of self‐change in smoking: toward an integrative model of change. Journal of Consulting and Clinical Psychology 1983;5:390‐5. [DOI] [PubMed] [Google Scholar]
Puska 1976
- Puska P, Koskela K, Pakarinen H, Puumalainen P, Soininen V, Tuomilehto J. The North Karelia Project: a programme for community control of cardiovascular diseases. Scandinavian Journal of Social Medicine 1976;4:57‐60. [MEDLINE: ] [PubMed] [Google Scholar]
Puska 1981
- Puska P, Tuomilehto J, Salonen J, Nissinen A, Koskela K, Vartiainen E, et al. Community control of cardiovascular diseases. The North Karelia Project. Copenhagen: World Health Organization, 1981:1‐351. [Google Scholar]
Puska 1985
- Puska P, Nissinen A, Tuomilehto J. The community based strategy to prevent coronary heart disease conclusions from the ten years of the North Karelia Project. Annual Review Public Health 1985;6:147‐93. [DOI] [PubMed] [Google Scholar]
Rose 1992
- Rose G. Chapter 4. Prevention for individuals and the "high risk" strategy. The Strategy of Preventive Medicine. Oxford: Oxford University Press, 1992:29‐52. [Google Scholar]
Scandinavian 1994
- Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandanavian Simvastatin Survival Study (4S). Lancet 1994;344:1383‐9. [MEDLINE: ] [PubMed] [Google Scholar]
Schoenberger 1990
- Schoenberger J. Cardiovascular risk factors: multiple interventions in man. Clinical and Experimental Hypertension. Part A, Theory and Practice. 1990;A12:931‐8. [MEDLINE: ] [DOI] [PubMed] [Google Scholar]
Svetkey 2005
- Svetkey LP, Erlinger TP, Vollmer WM, Feldstein A, Cooper LS, Appel LJ, et al. Effect of lifestyle modifications on blood pressure by race, sex, hypertension status and age. Journal of Human Hypertension 2005;19:21‐31. [DOI] [PubMed] [Google Scholar]
Tudor‐Smith 1998
- Tudor‐Smith C, Nutbeam D, Moore L, Catford J. Effects of the Heartbeat Wales programme over five years on behavioural risks for cardiovascular disease: quasi‐experimental comparison of results from Wales and a matched reference area. BMJ 1998;316:818‐22. [DOI] [PMC free article] [PubMed] [Google Scholar]
Valkonen 1992
- Valkonen T. Trends in regional and socio‐economic mortality differentials in Finland. International Journal of Health Sciences 1992;3:157‐6. [PubMed] [Google Scholar]
Vartiainen 1994
- Vartiainen E, Puska P, Pekkanen J, Tuomilehto J, Jousilahti P. Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. BMJ 1994;309:23‐7. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]
Vartiainen 2009
- Vartiainen E, Laatikainen T, Peltonen M, Juolevi A, Männistö S, Sundvall J, et al. Thirty‐five‐year trends in cardiovascular risk factors in Finland. International Journal of Epidemiology 2009;39(2):504‐18. [DOI: 10.1093/ije/dyp330] [DOI] [PubMed] [Google Scholar]
Wannamethee 1995
- Wannamethee G, Shaper AG, Whincup P, Walker M. Smoking cessation and the risk of stroke in middle‐aged men. JAMA 1995;274:155‐60. [MEDLINE: ] [PubMed] [Google Scholar]
West 2007
- West R, Zatonski W, Przewozniak K, Jarvis MJ. Can we trust national smoking prevalence figures? Discrepancies between biochemically assessed and self‐reported smoking rates in three countries. Cancer Epidemiology, Biomarkers and Prevention 2007;16:820‐2. [DOI] [PubMed] [Google Scholar]
References to other published versions of this review
Ebrahim 1997
- Ebrahim S, Davey Smith G. Systematic review of randomised controlled trials of multiple risk factor interventions for preventing coronary heart disease. BMJ 1997;314:1666‐74. [MEDLINE: ] [DOI] [PMC free article] [PubMed] [Google Scholar]