Published online before print April 6, 2009, doi: 10.1161/CIRCULATIONAHA.108.809491
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(Circulation. 2009;119:2026-2031.)
© 2009 American Heart Association, Inc.
Coronary Heart Disease |
Lifestyle Interventions Reduce Coronary Heart Disease Risk
Results From the PREMIER Trial
From the Division of General Internal Medicine (N.M.M., L.J.A.) and the Welch Center for Prevention, Epidemiology, and Clinical Research (N.M.M., N.-Y.W., L.J.A.), The Johns Hopkins University School of Medicine, Baltimore, Md; and Department of Epidemiology (L.J.A.), The Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md.
Reprint requests to Lawrence J. Appel, MD, MPH, 2024 E Monument St, Suite 2-618, Baltimore, MD 21287. E-mail lappel1{at}jhmi.edu
Received July 23, 2008; accepted February 2, 2009.
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Abstract |
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Background— Although trials of lifestyle interventions generally focus on cardiovascular disease risk factors rather than hard clinical outcomes, 10-year coronary heart disease (CHD) risk can be estimated from the Framingham risk equations. Our objectives were to study the effect of 2 multicomponent lifestyle interventions on estimated CHD risk relative to advice alone and to evaluate whether differences can be observed in the effects of the lifestyle interventions among subgroups defined by baseline variables.
Methods and Results— A total of 810 healthy adults with untreated prehypertension or stage I hypertension were randomized to 1 of 3 intervention groups: An "advice-only" group, an "established" group that used established lifestyle recommendations for blood pressure control (sodium reduction, weight loss, and increased physical activity), or an "established-plus-DASH" group that combined established lifestyle recommendations with the DASH (Dietary Approaches to Stop Hypertension) diet. The primary outcome was 10-year CHD risk, estimated from follow-up data collected at 6 months. A secondary outcome was 10-year CHD risk at 18 months. Of the 810 participants, 62% were women and 34% were black. Mean age was 50 years, mean systolic/diastolic blood pressure was 135/85 mm Hg, and median baseline Framingham risk was 1.9%. The relative risk ratio comparing 6-month to baseline Framingham risk was 0.86 (95% confidence interval 0.81 to 0.91, P<0.001) in the established group and 0.88 (95% confidence interval 0.83 to 0.94, P<0.001) in the established-plus-DASH group relative to advice alone. Results were virtually identical in sensitivity analyses, in each major subgroup, and at 18 months.
Conclusions— The observed reductions of 12% to 14% in estimated CHD risk are substantial and, if achieved, should have important public health benefits.
Key Words: coronary disease • lifestyle • prevention • risk factors
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Introduction |
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Adverse lifestyles have a major impact on the burden of coronary heart disease (CHD). Physical inactivity,1 smoking,2 obesity,3 and several aspects of diet are the underlying causative factors for CHD and its risk factors. Blood pressure (BP), a major risk factor for CHD,4 is strongly associated with obesity,5 physical inactivity,6 sodium intake,7 and alcohol intake.8 Obesity,9 physical inactivity,10 and smoking11 are the major modifiable risk factors for diabetes mellitus, another important cause of CHD.12 Serum cholesterol, an established risk factor for CHD,13 is also influenced by diet and physical activity.14
Clinical Perspective p 2031
Lifestyle modification is a critical component of population-based strategies to prevent CHD. Because of logistic considerations, trials of lifestyle modification rarely have sufficient power to detect intervention effects on clinical outcomes such as CHD events. Instead, the outcome variables of such trials are often CHD risk factors. Trials of single15,16 and multiple17 lifestyle interventions reveal that lifestyle change can have substantial effects on CHD risk factors such as BP.
CHD risk prediction equations, such as the Framingham Heart Study equations,14,18 provide an opportunity to estimate the effect of lifestyle modification on CHD risk. The current Framingham risk equation estimates 10-year CHD risk from a series of nonmodifiable (sex and age) and modifiable (BP, serum lipids, and smoking) risk factors.14
We conducted an analysis of data from the PREMIER trial that tested the effects of 2 multicomponent lifestyle interventions on BP relative to a control group.17 We hypothesized that relative to the control group, both lifestyle interventions would reduce the estimated 10-year CHD risk.
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Methods |
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PREMIER was a National Heart, Lung, and Blood Institute–sponsored, multicenter, 3-group, parallel-arm randomized trial conducted in the United States.17 The methods and main results have been published.17,19 Participants provided written informed consent, and institutional review boards at each center reviewed and approved the protocol.
Participants
Participants were 810 adults with prehypertension or stage 1 hypertension who met Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure criteria for a 6-month trial of nonpharmacological BP treatment.20 Other inclusion criteria were age 
25 years; a body mass index of 18.5 to 45.0 kg/m2; systolic BP of 120 to 159 mm Hg; and diastolic BP of 80 to 90 mm Hg.17,19 Main exclusion criteria were use of antihypertensive medications or weight-loss drugs; diabetes mellitus (glucose 126 mg/dL); BP-related target-organ damage (cardiovascular event, congestive heart failure, or angina); cancer or treatment for cancer in the last 2 years; consumption of >21 alcoholic drinks/week; and pregnancy or lactation.17,19
Randomization and Masking
Randomization was stratified by site and hypertension status with a block size of 24 to promote balance of treatment assignment.17,19 Intervention staff were masked to follow-up data, and staff collecting follow-up data were masked to intervention assignment.19 Participants received their BP measurement results at baseline and 6 months.19
Interventions
Over 6 months, the "advice-only" control group received printed educational information and brief advice on lifestyle modifications at 1 individual, 30-minute session at randomization.21 Participants in the established interventions group (EST) and the established interventions plus DASH (Dietary Approaches to Stop Hypertension) diet group (EST+DASH) received an intensive behavioral intervention and had in-person contacts with an interventionist at 4 individual and 14 group sessions.21 The EST component consisted of individualized advice on established recommendations,22 including physical activity (180 min/wk), weight loss, and caloric, alcohol, sodium (
2400 mg/d), and total (30% of calories) and saturated (10% of calories) fat intake.21 In addition to the EST recommendations, the EST+DASH group also received advice on the DASH diet, which focused on the intake of less total (25% of calories) and saturated (7% of calories) fat and the consumption of 9 to 12 servings of fruits and vegetables per day and 2 to 3 servings of low-fat dairy products per day.16,21
The effects of the interventions on the primary outcome variable of the trial (ie, systolic BP change from randomization to 6 months) have been published.17 Relative to the advice-only group, mean systolic BP was 3.7 mm Hg (P<0.001) lower in the EST group and 4.3 mm Hg (P<0.001) lower in the EST+DASH group.17 No statistically significant systolic BP difference was found between EST and EST+DASH.17
Measurements
BP and weight were measured in a standardized fashion by trained, certified observers using a random-zero sphygmomanometer.19 From fasting blood specimens, glucose, total cholesterol, and high-density lipoprotein (HDL) cholesterol were measured directly.19 Smoking status, medication use, and demographic variables were obtained by questionnaire.19 We defined diabetes mellitus as a fasting glucose of 140 mg/dL because the Framingham risk equations were developed with this cut point.18
Our primary outcome was the change in estimated 10-year CHD risk at 6 months compared with baseline using the sex-specific Framingham risk equations.14 The current equation estimates CHD risk from age, total cholesterol, HDL cholesterol, and BP (each entered as continuous variables) and from antihypertensive medication use and smoking status (each entered as binary variables).14
Consistent with the main results of the PREMIER trial, we chose the 6-month follow-up visit as the time of primary outcome assessment, because clinical guidelines20 recommended consideration of pharmacological therapy for those with a BP of 140/90 mm Hg after 6 months of lifestyle therapy.19 Adherence to lifestyle interventions is also optimized at 6 months.19
Statistical Analysis
We analyzed the present data using STATA version 9.2 (StataCorp, College Station, Tex). The distributions of baseline characteristics of the PREMIER participants were examined for each intervention group. Means and SDs were calculated for continuous variables, and proportions were calculated for categorical variables. Median estimated 10-year CHD risk at baseline and 6 months was calculated for each intervention group. In regression analysis, the difference between the logarithm of estimated 10-year CHD risk at the 6-month visit and the logarithm of 10-year CHD risk at the baseline visit, as the response variable, was regressed on indicators of the 2 behavioral interventions and on indicators of the clinical sites to evaluate the effect of the intervention groups while adjusting for site. For ease of interpretation, we used the ratio of 6-month to baseline 10-year CHD risk to compare the intervention groups (EST and EST+DASH) with the reference group (advice only) and refer to this as the "relative risk ratio."
We used multiple imputation by chained equations (ice) and generated 10 imputations to replace missing values for systolic and diastolic BP at 6 months, total and HDL cholesterol at baseline and 6 months, and antihypertensive medication use at 6 months using the "ice" command in STATA.23 First, we evaluated the assumption of missingness at random by attempting to predict missingness with known covariates24 using multiple logistic regression and calculating the area under the receiver operating characteristic curve. We then developed regression models to predict the variables with missing data.
In exploratory analyses, we evaluated for interactions between the interventions and subgroups defined by baseline factors (sex, baseline 10-year CHD risk [<10% or 10%], age [<60 or 60 years], hypertension status [prehypertension or hypertension], and total cholesterol [<5.2 or 5.2 mmol/L]). We allowed different intervention effects among subgroups by using models that included a main effect for the subgroup and interactions between the subgroup and the interventions with adjustment for site.
In sensitivity analyses, we calculated the relative risk ratios for those with a complete set of covariates using the current14 and older18 versions of the Framingham risk equations. Compared with the older equations,18 the updated equations include antihypertensive medication use, exclude diabetes, and use continuous rather than categorical measures for BP and lipids.14 We also performed an analysis for participants with complete data at baseline and 18 months.
A P value <0.05 was considered statistically significant. No adjustment for multiple comparisons was made.
The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Participants (n=810) were randomized into 3 intervention groups, and 704 had a complete set of covariates at baseline and 6 months for Framingham risk score calculation (Figure 1). Three participants were missing total and HDL cholesterol data at baseline, whereas 77 were missing these at 6 months, and 74 participants were missing BP values at 6 months. Forty-eight of those participants with missing data were missing both BP and cholesterol measurements at 6 months. Thus, we imputed 10-year CHD risk for a total of 106 participants (13.1%). Table 1 displays baseline data of the 810 participants. Median baseline 10-year CHD risk was slightly higher in EST+DASH (2.15%) than in the advice-only group (1.91%) or the EST group (1.75%). Among the 704 participants with complete covariates, slightly more smokers were in the EST group, and systolic BP was slightly higher in the EST and EST+DASH groups than in the advice-only group.
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At 6 months, median 10-year CHD risk decreased and was similar in each of the randomized groups (Figure 2). BP, total cholesterol, and HDL cholesterol decreased in all groups. The decrease in 10-year CHD risk over 6 months was significantly greater in EST and EST+DASH than in the advice-only group, and no difference in the change in 10-year CHD risk was found between EST and EST+DASH (Table 2). The relative risk ratios comparing EST and EST+DASH to advice-only were 0.86 (95% confidence interval [CI] 0.81 to 0.91, P<0.001) and 0.88 (95% CI 0.83 to 0.94, P<0.001), respectively. Risk reductions were similar in subgroups, and interaction tests were nonsignificant (Table 2). Results were similar with the inclusion of the 704 participants with complete data by use of both the current14 and older18 Framingham risk equations.
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At 18 months, 654 participants had complete data for calculation of the 10-year CHD risk. Among these participants, baseline systolic BP was slightly higher in EST and EST+DASH than in the advice-only group. When we compared 18-month and baseline 10-year CHD risk and adjusted for site, the relative risk ratios were 0.92 (95% CI 0.86 to 0.98, P<0.001) and 0.92 (95% CI 0.87 to 0.98, P<0.001) for EST and EST+DASH, respectively, relative to the advice-only group.
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Discussion |
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In individuals with prehypertension or stage 1 hypertension, 2 multicomponent behavioral interventions, EST+DASH and EST, significantly reduced the estimated 10-year CHD risk by 12% and 14%, respectively, compared with advice only. Results were similar across subgroups defined by baseline variables, and improvements in 10-year CHD risk were maintained at 18 months.
The 2 behavioral interventions (EST and EST+DASH) had similar effects on CHD risk. One possibility is that participants received an inadequate dose of the DASH diet, as evidenced by lack of full adherence to DASH recommendations for fruit and vegetable intake.17 An alternative explanation is subadditivity25; specifically, the combined effects of 2 interventions when implemented together are less than the sum of the 2 when implemented separately. Subadditivity can occur when adherence is reduced in the combined intervention or when the interventions work through similar mechanisms to achieve improvements in CHD risk factors.
Despite the intuitive appeal and public health relevance of estimated CHD risk, few studies of lifestyle interventions have used change in CHD risk as an outcome variable. In a recent randomized trial of 315 participants in Canada with 10-year CHD risk of 10%, a lifestyle intervention (health report card and telephone counseling on smoking, exercise, nutrition, and stress) reduced 10-year CHD risk at 1 year of follow-up by approximately 2% compared with a usual-care group.26 A smaller randomized trial (n=75) reported a similar but nonsignificant decrease in 10-year CHD risk at 16 weeks for a nutrition program combined with exercise relative to the nutrition program alone, but loss to follow-up was high (36%).27 On pre-post analysis, 1 observational study with a median follow-up time of 8 months found a nonsignificant increase in estimated CHD risk with dietary advice given to patients without CHD in an urban clinic in the United Kingdom.28 Another uncontrolled, longitudinal study of multiple lifestyle changes (diet, stress management, and aerobic exercise) in participants with CHD risk factors from the Windber Coronary Artery Disease Reversal (CADRe) program reported a nonsignificant 6.8% decrease in estimated CHD risk over 1 year for participants at risk for cardiovascular disease.29
A major strength of the present study is its large and diverse study population. Although the study was not powered to examine the subgroups, results were consistent across subgroups, which suggests broad applicability of trial interventions. Second, the trial has high internal validity, as evidenced by high rates of data collection during follow-up. In the present study, only 13% of participants had missing data at 6 months, and missing data were imputed by multiple imputation. Third, data collectors were trained, and BP and serum cholesterol were measured directly in a standardized fashion.19 Lastly, the Framingham risk functions have been validated in whites and blacks in the United States.30
The present study also has limitations. Our results may underestimate the magnitude of the effect of the EST and EST+DASH interventions on CHD risk because adherence was incomplete17 and because the advice-only group made lifestyle changes, perhaps because of high motivation17,31 or a Hawthorne effect related to data-collection visits.32 Second, smoking status was not available at 6 months, but the use of baseline smoking status carried forward is reasonable because the interventions did not include advice on smoking cessation. Third, the current Framingham risk equations14 do not include diabetes, but we obtained similar results when using the older equations that include diabetes status.18 Finally, the Framingham risk equations may overestimate absolute risk in some populations33; for this reason, we emphasize relative risk reductions. Of note, the baseline CHD risk was highest in the EST+DASH group, and the 6-month CHD risk was similar among the 3 randomized groups. It is possible that the smaller decrease in 10-year CHD risk in the advice-only group relative to the EST and EST+DASH groups may have occurred because of a "floor" below which the risk could not decrease; however, populations exist in which actual CHD risk is extremely low.34,35 Also, 10-year CHD risk estimated by the Framingham equations can be <1% when biologically plausible values of the variables are included in the equations.
Future research should focus on understanding the individual components of the behavioral interventions that are most effective in decreasing CHD risk. For example, an analysis of the effect of individual PREMIER lifestyle changes on BP at 6 months showed that decreased urinary sodium, improved fitness, and low total fat intake were associated with a decrease in systolic BP before controlling for weight loss; in that study, it was concluded that error in measurement of dietary and urinary sodium might account for the loss of their statistical significance after the inclusion of weight in regression models.36 Also, a comparison of CHD incidence with the change in 10-year CHD risk would be useful to validate the change in 10-year CHD risk as a surrogate outcome.
In summary, in the PREMIER trial, 2 multicomponent behavioral interventions incorporating diet and physical activity recommendations significantly lowered estimated 10-year CHD risk by 12% to 14% relative to a control condition. These estimated reductions in CHD risk are substantial and support research and translational efforts to implement counseling on lifestyle change as part of routine medical care. Given that heart disease remains the leading cause of death in the United States,37 translation of these findings into clinical practice should have a substantial public health impact.
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Acknowledgments |
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Sources of Funding
No project-specific funding was received for this study. Dr Maruthur was supported by a training grant (5 T32 HL007024-31) from the National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH). Dr Wang’s effort was supported by a grant (UL1 RR 025005) from the National Center for Research Resources, a component of the NIH and the NIH Roadmap for Medical Research. The PREMIER trial was sponsored by NHLBI, NIH grants UO1 HL60570, UO1 HL60571, UO1 HL 60573, UO1 HL60574, UO1 HL62828, and MO1 RR00052. The contents of the manuscript are solely the responsibility of the authors and do not necessarily represent the official view of National Center for Research Resources or the NIH.
Disclosures
None.
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Footnotes |
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The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.108. 809491/DC1.
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