doi: 10.1161/CIRCULATIONAHA.104.503995
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2005;112:924-934.)
© 2005 American Heart Association, Inc.
Special Report |
Effect Size Estimates of Lifestyle and Dietary Changes on All-Cause Mortality in Coronary Artery Disease Patients
A Systematic Review
From the Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht (J.A.I., Y.T.v.d.S., D.E.G., W.A.v.S.); Nutrition and Consumer Safety Division, RIVM, Bilthoven (D.K.); Division of Nutrition, Wageningen University Research Center, Wageningen (D.K., W.A.v.S.); and Public Health Division, RIVM, Bilthoven (H.C.B.), the Netherlands.
Correspondence to J.A. Iestra, Julius Center for Health Sciences and Primary Care, Department of Nutritional Sciences, University Medical Center Utrecht, PO Box 85500, Room G01.111, 3508 GA Utrecht, The Netherlands. E-mail j.iestra{at}umcutrecht.nl
Received September 1, 2004; revision received February 10, 2005; accepted April 11, 2005.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background— Guidelines for lifestyle and dietary modification in patients with coronary artery disease (CAD) are mainly supported by evidence from general population studies. CAD patients, however, differ from the general population in age (older) and treatment with preventive drugs. This review seeks to provide evidence for a prognostic benefit of lifestyle and dietary recommendations from studies in CAD patients.
Methods and Results— A literature search was performed on the effect of lifestyle and dietary changes on mortality in CAD patients. Prospective cohort studies and randomized controlled trials of patients with established CAD were included if they reported all-causes mortality and had at least 6 months of follow-up. The effect estimates of smoking cessation (relative risk [RR], 0.64; 95% CI, 0.58 to 0.71), increased physical activity (RR, 0.76; 95% CI, 0.59 to 0.98), and moderate alcohol use (RR, 0.80; 95% CI, 0.78 to 0.83) were studied most extensively. For the 6 dietary goals, data were too limited to provide reliable effect size estimates. Combinations of dietary changes were associated with reduced mortality (RR, 0.56; 95% CI, 0.42 to 0.74).
Conclusions— Available studies show convincingly the health benefits of lifestyle changes in CAD patients. Effect estimates of combined dietary changes look promising. Future studies should confirm these findings and assess the contribution of the individual dietary factors.
Key Words: coronary disease • diet • lifestyle • mortality • patients
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
More than 40 years ago, Ancel Keys1 was the first to explore the relationship between coronary artery disease (CAD) and environmental factors. Since then, several lifestyle and dietary factors have been found to be associated with the risk of cardiovascular morbidity and mortality.2 This knowledge has been translated into recommendations for the general population (primary prevention) and clinical guidelines for those with manifest cardiovascular diseases (secondary prevention).
Patients with CAD, ie, myocardial infarction (MI) or angina pectoris (AP), are the largest of the secondary prevention groups. This group is characterized by older age (80% are older than 50 years) and a minority of women (30%).3 Although the prognosis of CAD patients has improved considerably during the last decades,4 they still carry a high absolute risk for future CAD events (10-year absolute risk from 20% to 80%).5 International guidelines6 defined this patient group as top priority for preventive strategies.
Guidelines for CAD prevention6–10 agree more or less on the 9 lifestyle and dietary recommendations shown in Table 1. These recommendations are supported largely by evidence from population-based cohort studies and trials with surrogate end points. The effects on life expectancy in patients with CAD are unclear. These patients differ from the general population not only by their older age and compromised vasculature but also by the drugs they take to prevent secondary events. Patients contemplating behavioral changes, as well as professionals designing preventive strategies, want to be able to make choices and rationally prioritize one goal before another. Information on the magnitude of the effect that can be expected of each of the recommended lifestyle and dietary changes is therefore needed.
|
This study seeks to summarize the evidence that the individual lifestyle and dietary goals formulated in Table 1 can improve prognosis in CAD patients. Second, we want to provide estimates of the magnitude of the effects on survival for each individual lifestyle and dietary goal based on the available studies in CAD patients.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
We conducted a systematic review of the literature on benefits of the recommended lifestyle and dietary changes in CAD patients applying the following selection criteria.
Study Population
Studies had to investigate a population of at least 50% patients diagnosed with CAD. CAD patients were defined as patients with a history of MI or AP or who underwent coronary artery bypass graft (CABG) or percutaneous transluminal coronary angioplasty (PTCA).
Determinants and Interventions
We excluded studies on nutrient supplements if the dosage of the nutrient they provide goes beyond the amount that can reasonably be achieved by changing food habits without the use of supplements. For each lifestyle and dietary recommendation (Table 1), we defined the following determinants or interventions to be accepted in our study.
Smoking Cessation
Studies reporting smoking cessation after the diagnosis of CAD were accepted.
Physical Activity
Time spent on moderate intensive activity is the best example of operationalization of the current recommendations.11 Moderately intensive activities are those with an absolute intensity of 4 to 6 METs or a relative intensity of 40% to 60% of 
O2max.12 We also accepted studies on total energy expenditure, habitual daily activity scores, time spent in vigorous intensive physical activity, physical fitness, or participation in structured exercise programs.
Alcohol Consumption
Alcohol consumption had to be reported in the number of units or grams of alcohol per day. Studies reporting only alcohol intake as a percentage of total energy intake were excluded.
Energy Balance
The recommendation to maintain or attain a healthy body weight refers to both the actual as well as the previous history of the balance between energy intake and energy expenditure (physical activity). Accepted were studies on body weight maintenance after the first manifestation of CAD and studies on intentional body weight reduction in overweight or obese CAD patients in relation to survival. Studies on the association between body weight status (body mass index [BMI]) at time of event and survival were excluded because BMI at time of diagnosis does not reflect lifestyle and dietary habits after the first manifestation of CAD.
Saturated Fat and Trans–Fatty Acids
We accepted all studies investigating a reduced intake of saturated fat and/or trans–fatty acids without a substantial restriction of total fat intake. Interventions on total fat intake restrictions beyond 25 energy% were excluded because of supposed detrimental effects on HDL and triglyceride levels.13 Given the mean intake of saturated fat in most Western countries at 
15 energy%, we defined a reduction of 5 energy% as a relevant difference.
Regular Fish (Oil) Consumption
The recommended 2 portions (400 g) of oily fish per week are equivalent to a daily dose of 500 to 1000 mg 
-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]).14 We accepted all studies on fish consumption and on fish oil supplements to a maximum increase of 1000 mg -3 fatty acids per day. We excluded studies with higher doses because it is unlikely that these levels can be achieved by increasing fish consumption alone.
Fruits and Vegetables
We included studies that examined the effect of the daily intake of fruits and vegetables in all available forms (fresh, canned, frozen, dried, or as juice).
Whole Grains, Legumes, and Nuts
We included studies on the effect of the daily intake of whole grains, legumes, and nuts or that studied the effect of intake of fiber from these products.
Salt
We included all studies examining the effect of sodium restriction. Because the recommended maximal salt intake is 6 g/d15 (2400 mg or 100 mmol sodium) and current intake in Western societies is 9 g, a restriction was defined as a reduction of at least 30% or 50 mmol sodium.
Combined Lifestyle and Dietary Interventions or Combined Determinant Scores
We also included studies that examined a combination of 
2 of the aforementioned individual factors.
Outcome Measures
We only included studies that reported an effect on all-causes mortality.
Study Design and Follow-Up Period
Studies had to have a prospective design, being either a cohort study or a randomized controlled trial, and the follow-up period had to be at least 6 months. If available, meta-analyses of prospective studies were preferred and replaced the individual studies that they described.
Search Strategy
Data for this review were identified by searches in PubMed (1966 to May 2004) with the Medical Subject Heading (MeSH) terms coronary artery disease and patients in combination with the MeSH terms or text words lifestyle, smoking, physical activity, physical fitness, exercise, alcohol drinking, body weight, weight control, diet, saturated fat, trans–fatty acids, cholesterol, fish, fruit, vegetables, whole grains, cereals, legumes, nuts, fiber, salt, sodium, mortality, survival, and death. There was a restriction on English language. Relevant articles not identified by this strategy, but referenced in the bibliographies of these selected articles, were also included.
Data Extraction and Standardization
Details of the included studies were systematically described as shown in Table 2
. The relative risk (RR) was used as a measure of strength of the relationship between exposure to the lifestyle or dietary factor and all-causes mortality or other end points. The RR should compare the risk in the group practicing the desired healthy behavior (exposed group) with the group not showing the healthy behavior (reference group). For studies that reported the RR from the unhealthy lifestyle or dietary factor (eg, BMI >30 kg/m2) compared with the healthy lifestyle or dietary factor (eg, BMI <25 kg/m2), the RR from the exposed group was calculated as 1 divided by the RR in the nonexposed group. If the RR or the 95% CI of the RR was not reported in the original studies, they were calculated from the study data with the use of the number of subjects (N) and the number of cases (A) in both the exposed (1) and the unexposed (0) groups: RR=(A1/N1 divided by A0/N0) and 95% CI=EXP[lnRR±1.96
(1/A1+1/A0)] if incidence is sufficiently rare.
|
|
Summary Effect Estimates
We decided that an effect estimate per lifestyle or dietary goal could only be provided if a meta-analysis was available or if at least 2 randomized controlled trials or 2 cohort studies were available meeting the following quality criteria: in case of cohort studies, the effect estimate should be based on findings that were adjusted for confounders, at least for age and gender; in case of randomized trials, information should be given that compliance with the intervention under study was checked and considered satisfactory; and the effect estimate of each study should be based on at least 20 mortality cases to guarantee that the power of the study allowed meaningful effect estimation.
Results for the lifestyle or dietary goals that fulfilled these criteria are shown in Table 3. Before we pooled the data, heterogeneity between the studies was tested with the 
2 statistic. We used the random effects model for calculating a pooled estimate for the RR if the probability value for heterogeneity was 
0.5. In case the probability value for heterogeneity was >0.5, a fixed effects model was used.
|
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
A total of 3 meta-analyses, 10 randomized controlled trials (studying 13 interventions), and 9 cohort studies fulfilled the inclusion criteria. Details of the available studies per lifestyle or dietary goal are shown in Table 2
. For 5 goals (3 on lifestyle and 2 on dietary changes), the available studies fulfilled our additional criteria for calculating pooled effect size estimates (Table 3). For the combined interventions, only studies on combined dietary changes were available, and their pooled effect estimate is shown in Table 3.
Goals With Sufficient Studies to Calculate a Pooled Effect Estimate
Smoking Cessation
Two meta-analyses of cohort studies were found on smoking cessation. Duration of follow-up ranged from 2 to 20 years. All included studies consistently showed a protective effect of smoking cessation. Wilson et al16 performed a meta-analyses of 12 studies in patients with MI and found a pooled RR for all-causes mortality of 0.54 (95% CI, 0.46 to 0.62) for those who had quit smoking. Critchley and Capewell17 published a meta-analysis of 20 studies in patients with previous MI or AP and reported a pooled RR of 0.64 (95% CI, 0.58 to 0.71). Half of the studies were the same as in the first analysis. On the basis of these 2 meta-analyses, we conservatively estimate the effect size of smoking cessation in CAD patients as a 35% mortality risk reduction.
Habitual Physical Activity
We found no studies on the effect of increased physical activity on mortality in CAD patients. The effect of participation in a structured exercise program after a cardiac event (MI, AP, CABG, or PTCA) on morbidity and mortality has been evaluated in several meta-analyses.18–22 Reported effect size estimates of mortality reduction varied between 20% and 25%. Here we review the analysis by Brown et al,21 which is a 2003 update from earlier meta-analyses and which studied exercise-based rehabilitation programs separately from the comprehensive rehabilitation programs that also included educational and psychosocial interventions. In this study mortality data were available of 2585 patients in 12 randomized controlled trials. The interventions varied widely from gym-based aerobic exercise twice a week for 4 weeks to interventions lasting for 30 months with inpatient stays. Mean follow-up time was 24 months (range, 6 to 60 months). The study showed a significant beneficial effect of an exercise program. The effect on all-causes mortality was estimated as 25% risk reduction (RR, 0.76; 95% CI, 0.59 to 0.98).
Moderate Alcohol Consumption
We found 5 cohort studies23–27 examining the effect of moderate drinking versus rare drinkers or nondrinkers in CAD patients. All studies, except for 1,24 found a statistically significant reduction of all-causes mortality between 15% and 25% for moderate drinking. Duration of follow-up varied between 3 and 13 years. Effect estimates are shown in Table 3. The pooled effect estimate for the RR for all-causes mortality in the 5 studies was 0.80 (P for heterogeneity 0.53; 95% CI, 0.78 to 0.83), summarized in an effect estimate of 20% reduction of all-causes mortality.
Saturated Fat Reduction
Four28–31 randomized controlled trials and 1 cohort study32 met our criteria for fat modification. They all concerned saturated fat intake reduction. No studies were detected on the relation between trans–fatty acid intake and mortality in CAD patients. The randomized controlled trials were performed between 1960 and 1988 and intended to study a reduction of 5 energy% in saturated fat intake during 2 to 5 years of follow-up. The resulting reduction in serum cholesterol was 15% in 2 studies28,29 and only 5% in the other 2,31 raising doubts on adherence to the regimen in the latter 2 studies.30 Only in the 2 studies with the largest serum cholesterol reductions was total mortality reduced (12% and 25%), but the power of the studies was too limited to show statistically significant reductions. The probability value for heterogeneity was 0.18 for the 4 studies and 0.63 when the 2 studies with unsatisfying serum cholesterol reductions were excluded. The pooled effect estimates were not statistically significant for either the 4 or the 2 studies (Table 3). The cohort study32 in 400 Finnish CAD patients was supportive of a beneficial effect of a lower saturated fat intake. For every 4 energy% reduction in saturated fat, intake RR for all-causes mortality was 0.64 (95% CI, 0.46 to 0.88). However, this study on its own is not sufficient to be conclusive. Because the pooled effects are not statistically significant, we provide no summary effect estimate for saturated fat restriction.
Regular Fish (Oil) Consumption
We found 3 randomized controlled trials31,33–35 and 2 cohort studies32,36 fulfilling our selection criteria. The trials tested either the effect of advice to increase fatty fish consumption up to 200 to 400 g/wk31,33 or the effect of a fish oil supplement containing 900 mg EPA and DHA per day.34,35 Two of them31,34,35 showed a significant mortality reduction, but the trial in AP patients33 found a nonsignificant mortality increase in the intervention group.
Both cohort studies were supportive of a protective effect of a higher fish intake. The study by Barzi et al36 (n=11 246) was performed in the participants of the GISSI-Prevenzione trial studying the effects of fish oil (900 mg EPA and DHA) and/or vitamin E (300 mg) supplements. Irrespective of their assignment to the study intervention, most patients increased their fish consumption subsequent to the MI, as was advised by the hospital. Fish intake was assessed 4 times during the intervention period of 3.5 years, and duration of follow-up was 6.5 years. In the small cohort study by Erkkila et al,32 fish consumption was assessed at baseline only, and patients were followed up for 5 years. Both cohort studies fulfilled our quality criteria on adjustment for confounding and the number of cases. Table 3 shows the effect estimates of the presented studies. Before the data were pooled, heterogeneity tests were performed. Heterogeneity existed (P=0.002) for the 3 fish trials but disappeared when the AP patients’ trial was excluded (P=0.56). Pooled effect estimates for both the 3 and the 2 trials as well as for the 2 cohort studies are shown in Table 3. Because of the unexplained heterogeneity in the results, no summary effect estimate is provided for regular fish (oil) consumption.
Remaining Goals
For the remaining dietary goals, the available studies (Table 2 ) were insufficient to provide a reliable effect estimate on life expectancy in CAD patients. For body weight control, we found only 1 study37 on the effect of weight reduction after MI, but this study was considered of low quality because the results were not adjusted for confounding, not even for age and gender. For fruits and vegetables, the available randomized controlled trial33 was not a good test for the effect of increased fruit and vegetable consumption because compliance with the intervention was doubted as a result of a lack of any rise in serum concentrations of folate or carotenoids. The cohort study by Barzi et al36 supported a beneficial effect of the recommendations on both fruit (RR, 0.73; 95% CI, 0.54 to 0.98) and vegetables (raw vegetables: RR, 0.67; 95% CI, 0.56 to 0.79; cooked vegetables: RR, 0.84; 95% CI, 0.71 to 1.00) but was insufficient on its own to be included in Table 3. For dietary fiber and whole grain products, available studies were not consistent. The only trial31 showed no effect (because compliance was not measured, it is unclear whether this is due to a lack of effect or a lack of compliance), and the cohort study32 on total fiber intake was too small (n=400; 34 mortality cases) to show a statistically significant difference (RR, 0.81; 95% CI, 0.55 to 1.19). No studies were found relating the intake of trans–fatty acids, legumes, nuts, or salt to mortality in CAD patients.
Combined Interventions
We found no studies on the mortality effects of combinations of both lifestyle and dietary changes. On combined dietary changes alone, 3 randomized controlled trials37–40 and 1 cohort study36 met our inclusion criteria for the summary effect estimate. The interventions consisted of an increased intake of fiber-rich foods (fruits, vegetables, nuts, legumes) and fish and eventually an enhanced intake of unsaturated fatty acid intake through the use of oils or special margarines. Average duration of follow-up varied between 1 and 4 years. Mortality reduction was statistically significant in 2 of the 3 trials.37,39 Both the individual and the pooled effect estimates on mortality are shown in Table 3. The pooled RR for all-causes mortality was 0.56 (P for heterogeneity=0.73; 95% CI, 0.42 to 0.74). The effect estimate in the cohort study36 was based on a combined score on the consumption of fish, fruit, cooked vegetables, raw vegetables, and olive oil. All-causes mortality was 49% lower in patients in the highest quartile of the dietary score compared with the lowest quartile. We estimate the mortality risk reduction potential for combinations of individual dietary goals (as formulated in Table 1) to be 45%.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Although many of the commonly provided lifestyle and dietary recommendations (Table 1) are supported with evidence from surrogate end point studies and studies in the general population, there is only limited evidence from studies in CAD patients that these recommendations indeed improve their life expectancy. The available studies show significant effects for 3 lifestyle recommendations on prognosis of CAD patients. Effects for smoking cessation, increased physical activity, and moderate alcohol consumption vary from a 20% to 35% reduction in all-causes mortality. For individual dietary goals, evidence from studies in CAD patients was not available or was too limited to provide reliable effect estimates. A few studies on combinations of dietary changes show promising results, with mortality reductions of
45%. In this review we included both experimental and observational studies. Randomized controlled trials are generally rated as a higher level of evidence than prospective cohort studies because they exclude self-selection and confounding by indication as a source of bias. Randomized clinical trials, however, have their own drawbacks: their inclusion criteria often limit generalization to the average patient population in routine care, their costs often limit the duration of the study, in the case of lifestyle or dietary interventions double blinding is often impossible, or the intervention itself is unethical (eg, smoking or alcohol consumption). Prospective cohort studies, on the other hand, may be confounded by unknown prognostic factors associated with lifestyle or dietary habits, but they have the advantage of giving a better reflection of the "real-life" situation with long-term exposure and mostly a mixed patient population. The advantages and disadvantages of each design do not outweigh those of the other. In this review we reported effect sizes of both study designs (if available) separately and did not make an attempt to rank one above the other.
This review has several potential limitations. Most evidence was available for studies on lifestyle changes in CAD patients. Studies on dietary changes are scarce, and several are of poor methodological quality. Confounding due to clustering of lifestyle and dietary factors as well as bias because of unblinding or poor compliance with the intervention or changes in habits of the control group is more common in lifestyle and dietary studies than in drugs trials. Many of the studies included in this review were underpowered to assess effects on total mortality. This problem may be solved by pooling the results of individual studies, but, even if tests for heterogeneity are not significant, this operation may be problematic because of the heterogeneity of studies with respect to background habits, intervention characteristics, exposure (time and dose), and length of follow-up. Sometimes the point estimates are impressive, but the wide CIs indicate a high degree of uncertainty. Therefore, caution is needed in interpreting the results and particularly in translating the effect size estimates to the individual patient.
Nevertheless, most of the presented effect estimates are in accord with results from studies performed in the general population. Table 4 compares the effect estimates in CAD patients with results from cohort studies in the general population.
|
Smoking Cessation
Our effect estimate of 35% risk reduction is similar to findings from population-based cohort studies indicating that quitters before age 50 have a 50% lower risk of dying than continuing smokers.41,42
Physical Activity Level
An effect estimate of 25% mortality risk reduction for an increased level of physical activity was obtained from a meta-analysis on the effect of exercise-based revalidation. Although the best available, this is not a good estimate for adherence to the guideline11 to increase habitual physical activity level to a daily amount of at least 30 minutes of moderately intensive activity. Participation in a program is not necessarily related to a higher physical activity level in the long run.43,44 However, the estimated 25% mortality risk reduction compares well with estimates from other populations. A review45 of 44 population-based cohort studies reported that adherence to the guideline was associated with a 20% to 30% reduction in all-causes mortality. Further reductions were observed at higher volumes of energy expenditure. Not only high baseline levels but also increments in physical activity level later in life are shown to be associated with lower mortality.46,47
Alcohol
Although the protective effect of moderate alcohol consumption on cardiovascular risk has been sufficiently demonstrated in the general population cohorts,48 for CAD patients there was concern about the adverse effects on the cardiovascular system, such as hypertension, arrhythmias, hemorrhagic stroke, and cardiomyopathy.49 The presented studies are consistent in their finding that moderate alcohol consumption can improve the prognosis in CAD patients, even in patients with associated heart failure,23 as long as the alcohol intake is moderate (2 to 3 U/d). The estimate of 20% mortality risk reduction in CAD patients is in range with a pooled estimate of 15% mortality reduction in cohort studies in middle-aged populations.50 Of course, the benefits of moderate alcohol consumption should always be mentioned in relation to the potential risks of excessive alcohol consumption because there are still more deaths caused by alcohol than prevented.51
Saturated Fat
Reliable effect estimates could be provided for none of the individual dietary factors.
The pooled effect estimates for saturated fat reduction were not statistically significant (for the 4 studies: RR, 0.98; 95% CI, 0.81 to 1.18) but agreed with the findings of 2 meta-analyses on fat modification combining the results of both primary and secondary prevention trials: RR, 0.94 (95% CI, 0.89 to 0.99; 17 trials)52 and RR, 0.98 (95% CI, 0.86 to 1.12; 11 trials).53 In contrast to our study, these meta-analyses also included studies on total fat restriction, which might have attenuated the effect. They confirm our finding that a trend was seen toward a greater risk reduction in trials in which better adherence to the intervention is shown by a greater reduction in serum cholesterol.
Regular Fish (Oil) Consumption
There was heterogeneity between the studies, but the calculated pooled effect estimates for the trials (12% to 23% mortality risk reduction) are in agreement with an estimate of 20% all-causes mortality reduction in a meta-analysis by Bucher et al54 based on 9 trials in CAD patients on the effects of dietary fish or fish oil supplementation in doses up to 10 g of -3 fatty acids per day. The pooled effect estimate from the cohort studies in CAD patients was also 20%. Data on fish and all-causes mortality from population-based cohorts are inconsistent and vary from 0% to 30%.55–60 Null findings in some of the studies can possibly be explained by the adverse effects of the high mercury content of fish in some geographic areas56,61 or by the fact that the protective effect is specific for fatty fish and not for total fish consumption.62 The association with CAD mortality is more frequently studied than all-causes mortality, and significant risk reductions are reported.63–65
For the remaining individual goals, studies on mortality were too few to provide effect estimates. This should not be interpreted as a lack of scientific support for these recommendations. The evidence from surrogate end point or clinical end point studies is reviewed elsewhere.66–77 Studies on all-causes mortality, however, are scarce, not only in CAD patients but also in other populations. Given the alarming signals78,79 on a high prevalence (80%) of overweight and obesity in CAD patients, it is surprising that no studies were found on the effect of intentional weight loss on mortality in CAD patients. Weight loss might be one of the mechanisms through which other lifestyle or dietary changes (eg, regular exercise or increased intake of whole grains and vegetables) might exert their protective effect, but few authors report on body weight changes.40 Cohort studies in the general population have shown that mortality is 30% to 50% lower in normal-weight individuals than in their obese peers,80 although this difference decreases with age.81 The effect that can be expected from weight reduction in patients already treated with preventive drugs is unclear. Some studies in CAD patients82–86 (not meeting our inclusion criteria) even suggest a prognostic benefit of obesity. These studies, however, are inconclusive because they often lack appropriate adjustments for confounding (eg, confounding by age because obese persons are generally 7 years younger at time of their first MI than normal-weight individuals), but they stress the need for high-quality additional research. Finally, population-based cohort studies that study all-causes mortality in relation to the intake of fruits and vegetables,87–90 whole grains,87,91,92 legumes,93 nuts,94,95 or salt96–98 are scarce but are generally supportive of a protective effect of the recommendations.
The trials on combined dietary interventions showed impressive results, varying from 35% to 55% mortality reduction. Other intervention studies in CAD patients showed benefits of combined lifestyle and dietary changes on surrogate end points and cardiac events.99,100 The cohort study in 11 000 CAD patients by Barzi et al36 showed an almost 50% lower mortality risk for those with the highest dietary quality score. Mortality risk reductions associated with dietary quality reported from other populations were generally smaller (15% to 25%), but a significant benefit was demonstrated in many studies.101–110 Two studies in elderly people101,104 showed a 60% to 70% lower mortality associated with a higher quality score for a combination of both lifestyle and dietary habits. Although the studies on combined changes are promising, they shed no light on the dominant mechanism and on the contribution of the individual lifestyle and dietary factors. More knowledge on the benefits of the 6 individual dietary goals in particular is necessary for designing effective preventive strategies.
If the effect sizes of lifestyle and dietary changes in Table 4 reflect the true value, they compare favorably with effect size estimates for cardiopreventive drugs as shown in Table 5. 111–114 In contrast to these pharmacological interventions, the prognostic effects of lifestyle and dietary changes are, however, less rigorously studied. For the future, well-designed and powered studies are needed to test the effect of dietary changes on prognosis. Second, because compliance with the recommendations is crucial, research is needed on strategies to enhance adaptation and maintenance of healthy lifestyle and dietary habits in CAD patients.
|
In conclusion, there is evidence from mortality studies in CAD patients that smoking cessation, physical activity, moderate alcohol consumption, and combined dietary changes improve prognosis. Effect size estimates for the lifestyle goals vary between 20% and 35% mortality reductions. Data on the benefits of individual dietary goals are limited. For the future, more and better-quality studies are needed to reduce the uncertainty that surrounds these effect size estimates.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Keys A, Aravanis C, Blackburn HW, Van Buchem FS, Buzina R, Djordjevic BD, Dontas AS, Fidanza F, Karvonen MJ, Kimura N, Lekos D, Monti M, Puddu V, Taylor HL. Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries. Acta Med Scand Suppl. 1966; 460: 1–392.[Medline] [Order article via Infotrieve]
2. Kromhout D, Menotti A, Kesteloot H, Sans S. Prevention of coronary heart disease by diet and lifestyle: evidence from prospective cross-cultural, cohort, and intervention studies. Circulation. 2002; 105: 893–898.
3. Lifestyle and risk factor management and use of drug therapies in coronary patients from 15 countries: principal results from EUROASPIRE II Euro Heart Survey Programme. Eur Heart J. 2001; 22: 554–572.
4. Heidenreich PA, McClellan M. Trends in treatment and outcomes for acute myocardial infarction: 1975–1995. Am J Med. 2001; 110: 165–174.[CrossRef][Medline] [Order article via Infotrieve]
5. D’Agostino RB, Russell MW, Huse DM, Ellison RC, Silbershatz H, Wilson PW, Hartz SC. Primary and subsequent coronary risk appraisal: new results from the Framingham Study. Am Heart J. 2000; 139: 272–281.[Medline] [Order article via Infotrieve]
6. De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J, Ebrahim S, Faergeman O, Graham I, Mancia G, Cats VM, Orth-Gomer K, Perk J, Pyorala K, Rodicio JL, Sans S, Sansoy V, Sechtem U, Silber S, Thomsen T, Wood D. European guidelines on cardiovascular disease prevention in clinical practice: third joint task force of European and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of eight societies and by invited experts). Eur J Cardiovasc Prev Rehabil. 2003; 10: S1–S10.[CrossRef][Medline] [Order article via Infotrieve]
7. Working Group on Cardiac Rehabilitation of the Dutch Association of Cardiology and the Dutch Heart Association. Dutch Guideline for Cardiac Rehabilitation. The Hague, the Netherlands: Dutch Heart Association; 2004.
8. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): final report. Circulation. 2002; 106: 3143–3421.
9. Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman JW Jr, Kris-Etherton P, Goldberg IJ, Kotchen TA, Lichtenstein AH, Mitch WE, Mullis R, Robinson K, Wylie-Rosett J, St Jeor S, Suttie J, Tribble DL, Bazzarre TL. AHA dietary guidelines: revision 2000: a statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation. 2000; 102: 2284–2299.
10. Kromhout D, Menotti A, Kesteloot H, Sans S. Prevention of coronary heart disease by diet and lifestyle: evidence from prospective cross-cultural, cohort, and intervention studies. Circulation. 2002; 105: 893–898.
11. Blair SN, LaMonte MJ, Nichaman MZ. The evolution of physical activity recommendations: how much is enough? Am J Clin Nutr. 2004; 79: 913S–920S.
12. Thompson PD, Buchner D, Pina IL, Balady GJ, Williams MA, Marcus BH, Berra K, Blair SN, Costa F, Franklin B, Fletcher GF, Gordon NF, Pate RR, Rodriguez BL, Yancey AK, Wenger NK. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity). Circulation. 2003; 107: 3109–3116.
13. Sacks FM, Katan M. Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease. Am J Med. 2002; 113 (suppl 9B): 13S–24S.[CrossRef][Medline] [Order article via Infotrieve]
14. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002; 106: 2747–2757.
15. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003; 289: 2560–2572.
16. Wilson K, Gibson N, Willan A, Cook D. Effect of smoking cessation on mortality after myocardial infarction: meta-analysis of cohort studies. Arch Intern Med. 2000; 160: 939–944.
17. Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA. 2003; 290: 86–97.
18. Oldridge NB, Guyatt GH, Fischer ME, Rimm AA. Cardiac rehabilitation after myocardial infarction: combined experience of randomized clinical trials. JAMA. 1988; 260: 945–950.
19. O’Connor GT, Buring JE, Yusuf S, Goldhaber SZ, Olmstead EM, Paffenbarger RS Jr, Hennekens CH. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation. 1989; 80: 234–244.
20. Jolliffe JA, Rees K, Taylor RS, Thompson D, Oldridge N, Ebrahim S. Exercise-based rehabilitation for coronary heart disease. Cochrane Database Syst Rev. 2001; CD001800.
21. Brown A, Taylor R, Noorani H, Stone J, Skidmore B. Exercise-Based Cardiac Rehabilitation Programs for Coronary Artery Disease: A Systematic Clinical and Economic Review. Ottawa, Canada: Canadian Coordinating Office for Health Technology Assessment (CCOHTA); 2003. Technology report.
22. Taylor RS, Brown A, Ebrahim S, Jolliffe J, Noorani H, Rees K, Skidmore B, Stone JA, Thompson DR, Oldridge N. Exercise-based rehabilitation for patients with coronary heart disease: systematic review and meta-analysis of randomized controlled trials. Am J Med. 2004; 116: 682–692.[CrossRef][Medline] [Order article via Infotrieve]
23. Cooper HA, Exner DV, Domanski MJ. Light-to-moderate alcohol consumption and prognosis in patients with left ventricular systolic dysfunction. J Am Coll Cardiol. 2000; 35: 1753–1759.
24. Shaper AG, Wannamethee SG. Alcohol intake and mortality in middle aged men with diagnosed coronary heart disease. Heart. 2000; 83: 394–399.
25. Muntwyler J, Hennekens CH, Buring JE, Gaziano JM. Mortality and light to moderate alcohol consumption after myocardial infarction. Lancet. 1998; 352: 1882–1885.[CrossRef][Medline] [Order article via Infotrieve]
26. Thun MJ, Peto R, Lopez AD, Monaco JH, Henley SJ, Heath CW Jr, Doll R. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med. 1997; 337: 1705–1714.
27. Doll R, Peto R, Hall E, Wheatley K, Gray R. Mortality in relation to consumption of alcohol: 13 years’ observations on male British doctors. BMJ. 1994; 309: 911–918.
28. Leren P. The effect of plasma cholesterol lowering diet in male survivors of myocardial infarction: a controlled clinical trial. Acta Med Scand Suppl. 1966; 466: 1–92.[Medline] [Order article via Infotrieve]
29. Research Committee to the MRC. Controlled trial of soya-bean oil in myocardial infarction. Lancet. 1968; 2: 693–700.[Medline] [Order article via Infotrieve]
30. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB. Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Adv Exp Med Biol. 1978; 109: 317–330.[Medline] [Order article via Infotrieve]
31. Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Sweetnam PM, Elwood PC, Deadman NM. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: Diet and Reinfarction Trial (DART). Lancet. 1989; 2: 757–761.[Medline] [Order article via Infotrieve]
32. Erkkila AT, Lehto S, Pyorala K, Uusitupa MI. n-3 Fatty acids and 5-y risks of death and cardiovascular disease events in patients with coronary artery disease. Am J Clin Nutr. 2003; 78: 65–71.
33. Burr ML, Ashfield-Watt PA, Dunstan FD, Fehily AM, Breay P, Ashton T, Zotos PC, Haboubi NA, Elwood PC. Lack of benefit of dietary advice to men with angina: results of a controlled trial. Eur J Clin Nutr. 2003; 57: 193–200.[CrossRef][Medline] [Order article via Infotrieve]
34. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet. 1999; 354: 447–455.[CrossRef][Medline] [Order article via Infotrieve]
35. Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R, Franzosi MG, Geraci E, Levantesi G, Maggioni AP, Mantini L, Marfisi RM, Mastrogiuseppe G, Mininni N, Nicolosi GL, Santini M, Schweiger C, Tavazzi L, Tognoni G, Tucci C, Valagussa F. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002; 105: 1897–1903.
36. Barzi F, Woodward M, Marfisi RM, Tavazzi L, Valagussa F, Marchioli R. Mediterranean diet and all-causes mortality after myocardial infarction: results from the GISSI-Prevenzione trial. Eur J Clin Nutr. 2003; 57: 604–611.[CrossRef][Medline] [Order article via Infotrieve]
37. Singh RB, Rastogi SS, Verma R, Laxmi B, Singh R, Ghosh S, Niaz MA. Randomised controlled trial of cardioprotective diet in patients with recent acute myocardial infarction: results of one year follow up. BMJ. 1992; 304: 1015–1019.
38. De Lorgeril M, Renaud S, Mamelle N, Salen P, Martin JL, Monjaud I, Guidollet J, Touboul P, Delaye J. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet. 1994; 343: 1454–1459.[CrossRef][Medline] [Order article via Infotrieve]
39. De Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation. 1999; 99: 779–785.
40. Singh RB, Dubnov G, Niaz MA, Ghosh S, Singh R, Rastogi SS, Manor O, Pella D, Berry EM. Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk patients (Indo-Mediterranean Diet Heart Study): a randomised single-blind trial. Lancet. 2002; 360: 1455–1461.[CrossRef][Medline] [Order article via Infotrieve]
41. US Department of Health and Human Services. The Health Benefits of Smoking Cessation. Washington, DC: US Dept of Health and Human Services, Centers for Disease Control, Office of Smoking and Health; 1990: 75–100.DHHS publication (CDC) 90-8416; a report of the Surgeon General.
42. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ. 2004; 328: 1519.
43. Dorn J, Naughton J, Imamura D, Trevisan M. Results of a multicenter randomized clinical trial of exercise and long-term survival in myocardial infarction patients: the National Exercise and Heart Disease Project (NEHDP). Circulation. 1999; 100: 1764–1769.
44. Bethell HJN, Turner SC, Mullee MA. Cardiac rehabilitation in the community: 11 year follow-up after a randomized controlled trial. Coron Health Care. 1999; 3: 183–188.[CrossRef]
45. Lee IM, Skerrett PJ. Physical activity and all-cause mortality: what is the dose-response relation? Med Sci Sports Exerc. 2001; 33: S459–S471.[CrossRef][Medline] [Order article via Infotrieve]
46. Bijnen FC, Feskens EJ, Caspersen CJ, Nagelkerke N, Mosterd WL, Kromhout D. Baseline and previous physical activity in relation to mortality in elderly men: the Zutphen Elderly Study. Am J Epidemiol. 1999; 150: 1289–1296.
47. Schnohr P, Scharling H, Jensen JS. Changes in leisure-time physical activity and risk of death: an observational study of 7,000 men and women. Am J Epidemiol. 2003; 158: 639–644.
48. Corrao G, Rubbiati L, Bagnardi V, Zambon A, Poikolainen K. Alcohol and coronary heart disease: a meta-analysis. Addiction. 2000; 95: 1505–1523.[CrossRef][Medline] [Order article via Infotrieve]
49. Klatsky AL. Should patients with heart disease drink alcohol? JAMA. 2001; 285: 2004–2006.
50. Gmel G, Gutjahr E, Rehm J. How stable is the risk curve between alcohol and all-cause mortality and what factors influence the shape? A precision-weighted hierarchical meta-analysis. Eur J Epidemiol. 2003; 18: 631–642.[Medline] [Order article via Infotrieve]
51. Britton A, Nolte E, White IR, Gronbaek M, Powles J, Cavallo F, McPherson K. A comparison of the alcohol-attributable mortality in four European countries. Eur J Epidemiol. 2003; 18: 643–651.[Medline] [Order article via Infotrieve]
52. Truswell AS. Review of dietary intervention studies: effect on coronary events and on total mortality. Aust NZ J Med. 1994; 24: 98–106.[Medline] [Order article via Infotrieve]
53. Hooper L, Summerbell CD, Higgins JP, Thompson RL, Capps NE, Smith GD, Riemersma RA, Ebrahim S. Dietary fat intake and prevention of cardiovascular disease: systematic review. BMJ. 2001; 322: 757–763.
54. Bucher HC, Hengstler P, Schindler C, Meier G. N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials. Am J Med. 2002; 112: 298–304.[CrossRef][Medline] [Order article via Infotrieve]
55. Dolecek TA, Granditis G. Dietary polyunsaturated fatty acids and mortality in the Multiple Risk Factor Intervention Trial (MRFIT). World Rev Nutr Diet. 1991; 66: 205–16.: 205–216.[Medline] [Order article via Infotrieve]
56. Salonen JT, Seppanen K, Nyyssonen K, Korpela H, Kauhanen J, Kantola M, Tuomilehto J, Esterbauer H, Tatzber F, Salonen R. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men. Circulation. 1995; 91: 645–655.
57. Daviglus ML, Stamler J, Orencia AJ, Dyer AR, Liu K, Greenland P, Walsh MK, Morris D, Shekelle RB. Fish consumption and the 30-year risk of fatal myocardial infarction. N Engl J Med. 1997; 336: 1046–1053.
58. Albert CM, Hennekens CH, O’Donnell CJ, Ajani UA, Carey VJ, Willett WC, Ruskin JN, Manson JE. Fish consumption and risk of sudden cardiac death. JAMA. 1998; 279: 23–28.
59. Gillum RF, Mussolino ME, Madans JH. The relationship between fish consumption and stroke incidence: the NHANES I Epidemiologic Follow-up Study (National Health and Nutrition Examination Survey). Arch Intern Med. 1996; 156: 537–542.
60. Osler M, Andreasen AH, Hoidrup S. No inverse association between fish consumption and risk of death from all-causes, and incidence of coronary heart disease in middle-aged, Danish adults. J Clin Epidemiol. 2003; 56: 274–279.[CrossRef][Medline] [Order article via Infotrieve]
61. Guallar E, Sanz-Gallardo MI, van’t Veer P, Bode P, Aro A, Gomez-Aracena J, Kark JD, Riemersma RA, Martin-Moreno JM, Kok FJ. Mercury, fish oils, and the risk of myocardial infarction. N Engl J Med. 2002; 347: 1747–1754.
62. Oomen CM, Feskens EJ, Rasanen L, Fidanza F, Nissinen AM, Menotti A, Kok FJ, Kromhout D. Fish consumption and coronary heart disease mortality in Finland, Italy, and the Netherlands. Am J Epidemiol. 2000; 151: 999–1006.
63. Whelton SP, He J, Whelton PK, Muntner P. Meta-analysis of observational studies on fish intake and coronary heart disease. Am J Cardiol. 2004; 93: 1119–1123.[CrossRef][Medline] [Order article via Infotrieve]
64. Marckmann P, Gronbaek M. Fish consumption and coronary heart disease mortality: a systematic review of prospective cohort studies. Eur J Clin Nutr. 1999; 53: 585–590.[CrossRef][Medline] [Order article via Infotrieve]
65. He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR, Greenland P. Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies. Circulation. 2004; 109: 2705–2711.
66. Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S, Kris-Etherton PM. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr. 1999; 69: 632–646.
67. Ascherio A. Epidemiologic studies on dietary fats and coronary heart disease. Am J Med. 2002; 113 (suppl 9B): 9S–12S.[CrossRef][Medline] [Order article via Infotrieve]
68. Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr. 1992; 56: 320–328.
69. Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2003; 42: 878–884.
70. Law MR, Morris JK. By how much does fruit and vegetable consumption reduce the risk of ischaemic heart disease? Eur J Clin Nutr. 1998; 52: 549–556.[CrossRef][Medline] [Order article via Infotrieve]
71. Bazzano LA, Serdula MK, Liu S. Dietary intake of fruits and vegetables and risk of cardiovascular disease. Curr Atheroscler Rep. 2003; 5: 492–499.[Medline] [Order article via Infotrieve]
72. Pereira MA, O’Reilly E, Augustsson K, Fraser GE, Goldbourt U, Heitmann BL, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies. Arch Intern Med. 2004; 164: 370–376.
73. Anderson JW. Whole grains protect against atherosclerotic cardiovascular disease. Proc Nutr Soc. 2003; 62: 135–142.[CrossRef][Medline] [Order article via Infotrieve]
74. Anderson JW, Major AW. Pulses and lipaemia, short- and long-term effect: potential in the prevention of cardiovascular disease. Br J Nutr. 2002; 88 (suppl 3): S263–S271.[CrossRef][Medline] [Order article via Infotrieve]
75. Kris-Etherton PM, Zhao G, Binkoski AE, Coval SM, Etherton TD. The effects of nuts on coronary heart disease risk. Nutr Rev. 2001; 59: 103–111.[Medline] [Order article via Infotrieve]
76. Geleijnse JM, Kok FJ, Grobbee DE. Blood pressure response to changes in sodium and potassium intake: a metaregression analysis of randomised trials. J Hum Hypertens. 2003; 17: 471–480.[CrossRef][Medline] [Order article via Infotrieve]
77. Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA. 2002; 288: 2569–2578.
78. Montaye M, De Bacquer D, De Backer G, Amouyel P. Overweight and obesity: a major challenge for coronary heart disease secondary prevention in clinical practice in Europe. Eur Heart J. 2000; 21: 808–813.
79. De Bacquer D, De Backer G, Cokkinos D, Keil U, Montaye M, Ostor E, Pyorala K, Sans S. Overweight and obesity in patients with established coronary heart disease: are we meeting the challenge? Eur Heart J. 2004; 25: 121–128.
80. National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the evidence report. Obes Res. 1998; 6 (suppl 2): 51S–209S.[Medline] [Order article via Infotrieve]
81. Bender R, Jockel KH, Trautner C, Spraul M, Berger M. Effect of age on excess mortality in obesity. JAMA. 1999; 281: 1498–1504.
82. Kim J, Hammar N, Jakobsson K, Luepker RV, McGovern PG. Obesity and the risk of early and late mortality after coronary artery bypass graft surgery. Am Heart J. 2003; 146: 555–560.[CrossRef][Medline] [Order article via Infotrieve]
83. Gurm HS, Whitlow PL, Kip KE. The impact of body mass index on short- and long-term outcomes in patients undergoing coronary revascularization: insights from the Bypass Angioplasty Revascularization Investigation (BARI). J Am Coll Cardiol. 2002; 39: 834–840.
84. Eisenstein EL, Shaw LK, Nelson CL, Anstrom KJ, Hakim Z, Mark DB. Obesity and long-term clinical and economic outcomes in coronary artery disease patients. Obes Res. 2002; 10: 83–91.[Medline] [Order article via Infotrieve]
85. Gruberg L, Weissman NJ, Waksman R, Fuchs S, Deible R, Pinnow EE, Ahmed LM, Kent KM, Pichard AD, Suddath WO, Satler LF, Lindsay J Jr. The impact of obesity on the short-term and long-term outcomes after percutaneous coronary intervention: the obesity paradox? J Am Coll Cardiol. 2002; 39: 578–584.
86. Hoit BD, Gilpin EA, Maisel AA, Henning H, Carlisle J, Ross J Jr. Influence of obesity on morbidity and mortality after acute myocardial infarction. Am Heart J. 1987; 114: 1334–1341.[CrossRef][Medline] [Order article via Infotrieve]
87. Steffen LM, Jacobs DR Jr, Stevens J, Shahar E, Carithers T, Folsom AR. Associations of whole-grain, refined-grain, and fruit and vegetable consumption with risks of all-cause mortality and incident coronary artery disease and ischemic stroke: the Atherosclerosis Risk in Communities (ARIC) Study. Am J Clin Nutr. 2003; 78: 383–390.
88. Rissanen TH, Voutilainen S, Virtanen JK, Venho B, Vanharanta M, Mursu J, Salonen JT. Low intake of fruits, berries and vegetables is associated with excess mortality in men: the Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study. J Nutr. 2003; 133: 199–204.
89. Strandhagen E, Hansson PO, Bosaeus I, Isaksson B, Eriksson H. High fruit intake may reduce mortality among middle-aged and elderly men: the Study of Men Born in 1913. Eur J Clin Nutr. 2000; 54: 337–341.[CrossRef][Medline] [Order article via Infotrieve]
90. Bazzano LA, He J, Ogden LG, Loria CM, Vupputuri S, Myers L, Whelton PK. Fruit and vegetable intake and risk of cardiovascular disease in US adults: the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Am J Clin Nutr. 2002; 76: 93–99.
91. Liu S, Sesso HD, Manson JE, Willett WC, Buring JE. Is intake of breakfast cereals related to total and cause-specific mortality in men? Am J Clin Nutr. 2003; 77: 594–599.
92. Jacobs DR, Pereira MA, Meyer KA, Kushi LH. Fiber from whole grains, but not refined grains, is inversely associated with all-cause mortality in older women: the Iowa Women’s Health Study. J Am Coll Nutr. 2000; 19: 326S–330S.
93. Nagata C, Takatsuka N, Shimizu H. Soy and fish oil intake and mortality in a Japanese community. Am J Epidemiol. 2002; 156: 824–831.
94. Ellsworth JL, Kushi LH, Folsom AR. Frequent nut intake and risk of death from coronary heart disease and all causes in postmenopausal women: the Iowa Women’s Health Study. Nutr Metab Cardiovasc Dis. 2001; 11: 372–377.[Medline] [Order article via Infotrieve]
95. Fraser GE, Sumbureru D, Pribis P, Neil RL, Frankson MA. Association among health habits, risk factors, and all-cause mortality in a black California population. Epidemiology. 1997; 8: 168–174.[Medline] [Order article via Infotrieve]
96. Tuomilehto J, Jousilahti P, Rastenyte D, Moltchanov V, Tanskanen A, Pietinen P, Nissinen A. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet. 2001; 357: 848–851.[CrossRef][Medline] [Order article via Infotrieve]
97. He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA. 1999; 282: 2027–2034.
98. Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet. 1998; 351: 781–785.[CrossRef][Medline] [Order article via Infotrieve]
99. Dusseldorp E, van Elderen T, Maes S, Meulman J, Kraaij V. A meta-analysis of psychoeduational programs for coronary heart disease patients. Health Psychol. 1999; 18: 506–519.[CrossRef][Medline] [Order article via Infotrieve]
100. Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998; 280: 2001–2007.
101. Knoops KT, de Groot LC, Kromhout D, Perrin AE, Moreiras-Varela O, Menotti A, Van Staveren WA. Mediterranean diet, lifestyle factors, and 10-year mortality in elderly European men and women: the HALE project. JAMA. 2004; 292: 1433–1439.
102. Kant AK, Graubard BI, Schatzkin A. Dietary patterns predict mortality in a national cohort: the National Health Interview Surveys, 1987 and 1992. J Nutr. 2004; 134: 1793–1799.
103. Trichopoulou A, Costacou T, Bamia C, Trichopoulos D. Adherence to a Mediterranean diet and survival in a Greek population. N Engl J Med. 2003; 348: 2599–2608.
104. Haveman-Nies A, de Groot LP, Burema J, Cruz JA, Osler M, Van Staveren WA. Dietary quality and lifestyle factors in relation to 10-year mortality in older Europeans: the SENECA study. Am J Epidemiol. 2002; 156: 962–968.
105. Michels KB, Wolk A. A prospective study of variety of healthy foods and mortality in women. Int J Epidemiol. 2002; 31: 847–854.
106. Kant AK, Schatzkin A, Graubard BI, Schairer C. A prospective study of diet quality and mortality in women. JAMA. 2000; 283: 2109–2115.
107. Huijbregts P, Feskens E, Rasanen L, Fidanza F, Nissinen A, Menotti A, Kromhout D. Dietary pattern and 20 year mortality in elderly men in Finland, Italy, and the Netherlands: longitudinal cohort study. BMJ. 1997; 315: 13–17.
108. Osler M, Schroll M. Diet and mortality in a cohort of elderly people in a North European community. Int J Epidemiol. 1997; 26: 155–159.
109. Trichopoulou A, Kouris-Blazos A, Wahlqvist ML, Gnardellis C, Lagiou P, Polychronopoulos E, Vassilakou T, Lipworth L, Trichopoulos D. Diet and overall survival in elderly people. BMJ. 1995; 311: 1457–1460.
110. Kant AK, Schatzkin A, Harris TB, Ziegler RG, Block G. Dietary diversity and subsequent mortality in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Am J Clin Nutr. 1993; 57: 434–440.
111. Weisman SM, Graham DY. Evaluation of the benefits and risks of low-dose aspirin in the secondary prevention of cardiovascular and cerebrovascular events. Arch Intern Med. 2002; 162: 2197–2202.
112. LaRosa JC, He J, Vupputuri S. Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. JAMA. 1999; 282: 2340–2346.
113. Freemantle N, Cleland J, Young P, Mason J, Harrison J. Beta blockade after myocardial infarction: systematic review and meta regression analysis. BMJ. 1999; 318: 1730–1737.
114. Rodrigues EJ, Eisenberg MJ, Pilote L. Effects of early and late administration of angiotensin-converting enzyme inhibitors on mortality after myocardial infarction. Am J Med. 2003; 115: 473–479.[CrossRef][Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  F. Imamura, P. F Jacques, D. M Herrington, G. E Dallal, and A. H Lichtenstein Adherence to 2005 Dietary Guidelines for Americans is associated with a reduced progression of coronary artery atherosclerosis in women with established coronary artery disease Am. J. Clinical Nutrition, July 1, 2009; 90(1): 193 - 201. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Mildestvedt, E. Meland, and G. E. Eide How important are individual counselling, expectancy beliefs and autonomy for the maintenance of exercise after cardiac rehabilitation? Scand J Public Health, November 1, 2008; 36(8): 832 - 840. [Abstract] [PDF]
|
|
|
|
|
|
T. Mildestvedt, E. Meland, and G. E. Eide No difference in lifestyle changes by adding individual counselling to group-based rehabilitation RCT among coronary heart disease patients Scand J Public Health, December 1, 2007; 35(6): 591 - 598. [Abstract] [PDF]
|
|
|
|
 |
|
 R. J. Thomas, M. King, K. Lui, N. Oldridge, I. L. Pina, J. Spertus, R. O. Bonow, N.A. M. Estes III, D. C. Goff, K. L. Grady, et al. AACVPR/ACC/AHA 2007 Performance Measures on Cardiac Rehabilitation for Referral to and Delivery of Cardiac Rehabilitation/Secondary Prevention Services: Endorsed by the American College of Chest Physicians, American College of Sports Medicine, American Physical Therapy Association, Canadian Association of Cardiac Rehabilitation, European Association for Cardiovascular Prevention and Rehabilitation, Inter-American Heart Foundation, National Association of Clinical Nurse Specialists, Preventive Cardiovascular Nurses Association, and the Society of Thoracic Surgeons J. Am. Coll. Cardiol., October 2, 2007; 50(14): 1400 - 1433. [Full Text] [PDF]
|
|
|
|
 |
|
 Authors/Task Force Members, J.-P. Bassand, C. W. Hamm, D. Ardissino, E. Boersma, A. Budaj, F. Fernandez-Aviles, K. A.A. Fox, D. Hasdai, E. M. Ohman, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology Eur. Heart J., July 1, 2007; 28(13): 1598 - 1660. [Full Text] [PDF]
|
|
|
|
 |
|
 D. G. Hackam and J. D. Spence Combining Multiple Approaches for the Secondary Prevention of Vascular Events After Stroke: A Quantitative Modeling Study Stroke, June 1, 2007; 38(6): 1881 - 1885. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Colquhoun, K. Kostner, and A. Ferreira-Jardim Letter by Colquhoun et al Regarding Article "Effect Size Estimates of Lifestyle and Dietary Changes on All-Cause Mortality in Coronary Artery Disease Patients: A Systematic Review" Circulation, July 11, 2006; 114(2): e40 - e40. [Full Text] [PDF]
|
|
|
|
|
|
J. A. Iestra, PhD, Y. T. van der Schouw, D. E. Grobbee, W. A. van Staveren, D. Kromhout, and H. C. Boshuizen Response to Letter Regarding Article "Effect Size Estimates of Lifestyle and Dietary Changes on All-Cause Mortality in Coronary Artery Disease Patients: A Systematic Review" Circulation, July 11, 2006; 114(2): e41 - e41. [Full Text] [PDF]
|
|
|
|
 |
|
 Additional articles abstracted in ACP Journal Club Evid. Based Med., February 1, 2006; 11(1): 30 - 30. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||