PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
 
JAMA Intern Med. Author manuscript; available in PMC 2014 April 28.
Published in final edited form as:
PMCID: PMC3874045
NIHMSID: NIHMS529223

Dietary quality and mortality among myocardial infarction survivors

Shanshan Li, MD., Msc., ScD.,1 Stephanie E. Chiuve, ScD.,2,4 Alan Flint, MD., DrPH.,1,2 Jennifer Pai, ScD.,1,3 John P. Forman, MD., Msc.,3 Frank B. Hu, MD., PhD.,1,2,3 Walter C. Willett, MD., DrPH.,1,2,3 Kenneth J. Mukamal, MD., MPH,5 and Eric B. Rimm, ScD.1,2,3

Abstract

Importance

Information on diet after myocardial infarction (MI) and mortality is limited, despite the growing number of MI survivors in the United States.

Objective

To examine the association of post-MI dietary quality, and changes from pre- to post-MI, with all-cause and cardiovascular mortality among MI survivors.

Design, Setting, and Participants

We included 2,258 women from the Nurses’ Health Study and 1,840 men from the Health Professional Follow-Up Study. Participants survived an initial MI during study follow up and provided both pre- and post-MI food frequency questionnaire (FFQ). Diet quality was measured using Alternative Healthy Eating Index 2010 (AHEI2010), which consists of food and nutrients associated with risk of chronic disease in the literature. We adjusted for medication use, medical history, and lifestyle risk factors using Cox proportional hazards models.

Main Outcome Measures

all-cause and cardiovascular mortality.

Results

During follow-up, we confirmed 682 all-cause deaths for women, and 451 for men. The median survival time after initial MI onset was 8.7 years for women and 9.0 years for men. After pooling results together, the adjusted HR was 0.76 (95% CI: 0.60–0.96) for all-cause and 0.73 (95% CI: 0.51–1.04) for cardiovascular mortality, comparing extreme quintiles of post-MI AHEI2010. A greater increase in the AHEI2010 score from pre- to post-MI was significantly associated with lower all-cause (pooled HR= 0.71, 95% CI: 0.56–0.91) and cardiovascular mortality (pooled HR= 0.60, 95% CI: 0.41–0.86), comparing extreme quintiles. The adjusted HR associated with post-MI AHEI2010 were 0.73 (95% CI: 0.58–0.93) for all-cause mortality and 0.81 (95% CI: 0.64–1.04) for cardiovascular mortality when the alcohol component was excluded.

Conclusions and Relevance

MI survivors who consume a higher quality diet, which has been associated with lower risk of CHD in primary prevention, have lower subsequent all-cause mortality.

Keywords: Diet quality, myocardial infarction, secondary prevention

Introduction

Patients with coronary heart disease (CHD) have substantially greater risk of cardiovascular events and risk of death compared with the general population1. Lifestyle changes in myocardial infarction (MI) survivors that include smoking cessation, regular physical activity, and dietary improvements may reduce mortality by 20% to 35%13. In the US alone, approximately 80,000 lives per year could be saved through optimizing secondary prevention strategies1.

In epidemiological studies and clinical trials, a Mediterranean-style diet was beneficial in both primary and secondary prevention47. Despite these potential benefits, post-MI patients report poor dietary quality 1 year after the initial event8. Worldwide, 43.4% of CHD patients in high income countries eat a healthy diet, and only 25.8% do so in low income countries9. Even though patients often receive information about a balanced diet, some perceive it as simply to “cut things out” of their diet8. Likewise, the American College of Cardiology and American Heart Association updated their guidelines for clinicians on secondary prevention of MIs in 201210,11, but continued to use diet recommendations from 2007 that focus on reducing saturated and trans fat intake and do not address unsaturated fats, the quality of carbohydrates, sugar-sweetened beverages, and red and processed meat. The traditional low-fat diet has failed to improve cardiovascular risk profiles and MI prognosis1214.

Use of a composite score to reflect overall diet quality is easy for clinicians and dietitians to use and communicate with patients. The Alternative Healthy Eating Index 2010 (AHEI2010) was defined a priori based upon previous knowledge, through a comprehensive review of studies of foods and nutrients most consistently associated with lower chronic disease risk in recent literatures15. In the general population, a higher AHEI2010 score is associated with 16% lower risk of chronic disease and 23% lower risk of cardiovascular disease15. It includes 11 components, many of which are known to be associated with CHD risk among healthy population: vegetables, fruits, nuts and legumes, red meat and processed meats, sugar-sweetened beverages, alcohol, polyunsaturated fat, trans fat, omega-3 fat (EPA and DHA), whole grains and sodium intake15.

Long-term effects of overall diet quality among MI survivors are not well studied. Previous studies measured post-MI diet only at one single point in time and could not assess changes in diet from pre- to post-MI5,6,16. At an advanced stage of the atherosclerotic process, whether and to what degree dietary changes from pre- to post-MI improve prognosis is unclear. Two large prospective cohort studies, the Nurses’ Health Study and the Health Professional Follow-up Study, have repeated dietary, lifestyle and medication use measurements with long duration of follow-up. This provides a unique opportunity to investigate dietary changes pre- to post- MI. We therefore examined post-MI AHEI2010, and changes in AHEI2010 from pre- to post-MI in relation to all-cause and cardiovascular (CVD) mortality.

Methods

Study population

The Nurses’ Health Study (NHS) is a prospective cohort of 121,700 registered female nurses, 30–55 years of age at baseline in 197617. The Health Professional Follow-up Study (HPFS) is a prospective cohort of 51,529 U.S. male health professionals, 40–75 years old at baseline in 198618. Information on lifestyle and medical history was assessed through questionnaires biennially.

We included 2,258 women and 1,840 men who were free of cardiovascular disease, stroke or cancer at the time of enrollment, survived a first myocardial infarction (MI) during follow up, and were free of stroke at the time of initial MI onset. They all provided a pre-MI and at least one post-MI food frequency questionnaire (FFQ). The median time from initial MI onset to the first post-MI FFQ return date was 2 years.

Exposure assessment

Diet was assessed using a validated FFQ every 4 years1921. Nutrient intake was calculated by multiplying nutrient content for each food (obtained from the Harvard University Food Composition Database) with the frequency of consumption, and then summing across all food items. A valid FFQ was defined as within a preset estimated caloric range (600 – 3500 Kcals/day for women and 800–4200 Kcals/day for men) and have less than 70 food items with missing data22.

Diet quality was measured using the AHEI2010 score, which was developed based upon a comprehensive review of the relevant literature to determine score for foods and nutrients most consistently associated with lower chronic disease risk a priori15. The score for each of the 11 components ranged from 0 (worst) to 10 (best), and the total AHEI2010 score ranged from 0 (minimal adherence) to 110 (maximum adherence)15.

Identification of incident MI

Medical records were reviewed by study physicians blinded to participants’ exposure status23. MI was defined based upon symptoms plus either diagnostic electrocardiographic changes or elevated cardiac-specific enzyme levels24.

Outcome assessment

Our outcomes were all-cause and cardiovascular mortality. Deaths occurring during follow up were identified from vital records, the National Death Index, reports by the participant’s next of kin, or the postal system25. Cardiovascular mortality consisted of fatal coronary heart disease and fatal stroke confirmed through medical records review or autopsy reports.

Covariate assessment

Covariates were chosen a priori based upon the literature. We considered medication use, medical history, and lifestyle factors previously associated with MI risk. All covariates were updated with each subsequent questionnaire cycle. We kept only the key predictors of MI survival and confounders (more than 10% change in regression coefficients for main effects). Physical activity was measured using a self-administered questionnaire every 2 years. Time spent per week in each of the activity reported (walking, jogging, running, bicycling, lap swimming, tennis, squash or racquetball, other aerobic exercise) and total MET-hrs/wk was calculated. Questions on physical activity have been shown in previous studies to have good reproducibility and validity2628.

Statistical analysis

We defined post-MI period as the time from the return of the first post-MI FFQ until death or the end of the study period (June 30, 2008), whichever came first. Pre-MI dietary intake was estimated from the most recent FFQ before initial MI onset. Post-MI dietary intake was modeled first as a simple time varying exposure and then secondly as a running cumulative average exposure of all post-MI FFQs. The cumulative average is calculated as the average of all available data post-MI up to the current questionnaire cycle. The results were similar between the simple time varying post-MI diet and the cumulative average post-MI diet, so we used the former for simplicity29. We defined change from the pre-MI to post-MI as quintiles of the absolute difference of the AHEI2010 (post-MI AHEI2010 – pre-MI AHEI2010). We categorized AHEI2010 (post-MI and changes from pre- to post-) into quintiles. For missing covariate data, we used the value reported on the previous post-MI questionnaire.

A Cox proportional hazards model was used with time since the return of the first post-MI FFQ as the underlying time scale. For analyses of trends, we fit a continuous variable assigning each individual the median level of their respective quintile. We constructed adjusted survival curves using an inverse probability weighting method30. To identify key components of the AHEI2010 that associated with post-MI prognosis, we modeled the 11 individual components simultaneously. When assessing the association of changes in AHEI2010 from pre- to post- with mortality, we adjusted for changes in covariates pre- to post-MI to better capture the fact that dietary changes and other healthy behaviors are correlated. We evaluated heterogeneity of HRs from men and women using Cochrane Q statistics and meta-analyzed results using fixed-effect models31,32.

As moderate alcohol consumption is inversely associated with total mortality among MI survivors33,34, but may not be an appropriate recommendation for some patients, we performed secondary analyses in which we removed the alcohol component to evaluate the contribution of a healthy diet independent of alcohol intake.

We evaluated whether the associations differed by lipid lowering medication use, aspirin use, and age of MI onset, using the likelihood ratio test. To avoid possible misclassification of diet pre- and post-MI, we further excluded FFQs returned within 12 months of initial MI onset (remaining sample size 1,689 for men and 2,059 for women). In addition, physical activity level could be an indicator of underlying disease severity, and MI survivors may avoid certain activity due to symptoms. To reduce this potential bias, in sensitivity analysis, we adjusted for physical activity level pre-MI, with a 2-year lag for post-MI physical activity level and also after further excluding participants in the lowest quintile of physical activity.

We did not have information on acute characteristics of the index MI in women, but we collected this information from hospital discharge records for men. We compared the results in men with and without adjusting for heart failure, left ventricular ejection fraction, acute therapy received during hospitalization, and self-reported beta-blocker medication in the sensitivity analyses. We tested for proportional hazard assumption by adding an interaction term between the AHEI2010 score and time since entry into study, and used the likelihood ratio test to test for the significance.

Results

During follow-up, we confirmed 682 all-cause and 336 cardiovascular deaths for women, and 451 all-cause and 222 cardiovascular deaths for men. Participants on average improved diet quality from pre- to post-MI, with a greater increase of AHEI2010 in men (median change =5.5) compared with women (median change =2.1). For both men and women, the greatest improvement of diet quality pre- to post- was an increase in whole grain intake, and a reduction of trans fat, and red and processed meat consumption. The lowest score for a diet component in the post-MI period was sugar-sweetened beverage consumption (Figure 1). The median survival time after initial MI onset was 8.7 years for women and 9.0 years for men.

Figure 1
Legend: Components of the Alternative Healthy Eating Index 2010 score post-MI and changes from pre- to post-MI period among MI survivors

Post MI Diet Quality and Prognosis

Comparing the highest vs. lowest quintile, the AHEI2010 was highly significantly associated with lower all-cause mortality in women (HR=0.66, 95% CI: 0.49–0.88, p trend=0.0007, Table 2) but not in men (HR=0.98, 95% CI: 0.66–1.44, p trend=0.72). After pooling the results from men and women together (p for heterogenenity= 0.11), overall, the AHEI2010 was inversely associated with all-cause mortality (Pooled HR=0.76, 95% CI: 0.60–0.96, p trend=0.02, for the fifth vs. first quintile). Physical activity appeared to be the strongest confounder for both men and women. During the post-MI period, MI survivors who were in the 5th quintile of the AHEI2010 had a better prognosis (p<0.0001) compared with those in the 1st quintile for both men and women (Figure 2). Higher whole grain consumption (p<0.0001) was associated with better post-MI survival in women; for men, none of the individual components alone were associated with all-cause mortality.

Figure 2
Legend: Adjusted survival curve comparing MI survivors in the highest quintile of Alternative Healthy Eating Index 2010 score vs. those in the lowest quintile. (Quintile 5th vs. 1st)
Table 2
Multivariate adjusted hazard ratios for all-cause and cardiovascular mortality according to simple-updated post-MI Alternative Healthy Eating Index 2010 after initial Myocardial Infarction

The AHEI2010 was marginally significantly inversely associated with cardiovascular mortality (Pooled HR between extreme quintiles of post-MI diet quality=0.73, 95% CI: 0.51–1.04, p trend=0.08). The post-MI AHEI2010 was associated with lower cardiovascular mortality for women (p trend=0.03), with whole grain consumption (p=0.002) the strongest individual contributor to post-MI survival; the post-MI AHEI2010 score was not associated with lower cardiovascular mortality for men (p trend=0.84, Table 2) and none of the 11 individual components were significant.

Change in Diet Quality and Prognosis

The Spearman correlations between pre- and post-MI AHEI2010 were 0.49 for women and 0.56 for men. A greater increase in AHEI2010 from pre- to post-MI was significantly associated with lower all-cause and cardiovascular mortality (Table 3).

Table 3
Multivariate adjusted hazard ratios for all-cause and cardiovascular mortality according to changes from pre- to post-MI period of Alternative Healthy Eating Index 2010

Secondary Analyses

After removing the alcohol component, the pooled HR was 0.73 (95% CI: 0.58–0.93, p trend= 0.01, comparing extreme quintiles) for all-cause mortality. Association with changes from pre- to post- attenuated but remained inverse (pooled HR=0.81, 95% CI: 0.64–1.04, p trend=0.12 for all-cause mortality comparing extreme quintiles, supplementary table). Associations with cardiovascular mortality were attenuated without alcohol component in the AHEI2010 score (supplementary table).

Results were similar after excluding FFQs returned within 12 months of the initial MI. We adjusted for physical activity level pre-MI, included a 2-year lag after the first post-MI dietary assessment, and excluded participants in the lowest quintile of physical activity; in these analyses we found similar, albeit slightly stronger inverse associations for the AHEI2010 with all-cause mortality. Results were very similar after further adjustment for beta-blocker use, antihypertension medication use and clinical characteristics. We did not observe significant effect modification by lipid lowering medication, aspirin or age of MI onset (data not shown). No significant violation of proportional hazard assumption was detected.

Discussion

In our prospective study of diet quality among MI survivors, we found that AHEI2010 post-MI, was associated with 24% lower all-cause and 26% lower cardiovascular mortality, comparing extreme quintiles. Greater improvement of diet quality from pre- to post-MI was associated with 30% lower all-cause and 40% lower cardiovascular mortality. Sugar-sweetened beverages and fruit juice had the lowest component score on the post-MI diet. In addition to reducing saturated and trans fat intake, MI patients also tended to reduce polyunsaturated fat intake.

Previous studies of diet and secondary prevention were mostly based on Mediterranean-style diet7,35,36. The Lyon Diet Heart Study reported a 70% reduction in CHD deaths among MI survivors randomized to a Mediterranean-type diet, which was rich in fruit, vegetables, and alpha-linolenic acid7,35. The trial was stopped after an average of 4 years because of the significant difference in recurrence rates7,35. Additionally, the association between a modified Mediterranean diet and post-MI survival was evaluated in two prospective cohort studies, which reported a 27% lower all-cause and 31% lower cardiovascular mortality in Greece, and 18% lower all-cause mortality in a European study (per two-unit increment based a 10-unit Mediterranean diet score)5,6. Dehghan et al. reported that higher score for diet quality was associated with 35% reduction of cardiovascular death among participants with cardiovascular disease16. However, this study had limited details on many aspects of diet, and information of specific fatty acids including trans isomers was not available. Most importantly, previous studies did not have dietary information both before and after MI. Finally, the average follow-up time in these studies was relatively short (3.78 years24, 6.7 years23 and 4.6 years16).

Nonetheless, the results from our study are consistent with those from the Lyon Diet-Heart Study and previous observational studies. The AHEI2010 shares some components with the Mediterranean diet but has the specific components more relevant to Western diets, such as trans fat, sugar-sweetened beverages, and red and processed meat. The stronger association of the AHEI2010 with all-cause and cardiovascular mortality than those for individual components suggests that the AHEI2010 captures the synergistic or interactive effects of dietary components. To our knowledge, our study provides the first evidence that a substantial improvement in diet quality from pre- to post-MI markedly associated with a significant lower all-cause and cardiovascular mortality.

The etiology of atherosclerotic disease is complicated and likely has origins in lipids, inflammation, coagulation and endothelial reactivity3741. Although not all of the mechanisms are fully understood, it is likely that many of the underlying etiologic pathways are similar in the pre- and post-MI periods. Consumption of a Mediterranean-style diet improved endothelial function and reduced systemic inflammation markers among patients with metabolic syndrome42,43. Panagiotakos et al. found that among post-MI patients in various European countries, higher adherence to a Mediterranean diet was independently associated with lower level of CRP and IL-6 level44. The PREDIMED study, thus far the largest clinical trial investigating the effects of the Mediterranean diet for CHD primary prevention4,45,46, showed that among high cardiovascular risk participants, those who followed a Mediterranean diet supplemented with extra-virgin olive oil or nuts had reduced the incidence of major cardiovascular events, had better lipid profiles, better antioxidant capacity, lower insulin resistance, lower inflammatory markers and blood pressure4,46.

We found the associations between post-MI diet quality and changes from pre- to post-MI with mortality were stronger for women than for men, which is different from our previous studies of diet and primary prevention of CHD15,47. Although the test for heterogeneity between genders was not significant, the weaker results among men may be due to a limited number of events in the extreme categories. The observed gender difference for diet in secondary prevention could also be due to greater case fatality rate among women4850, differences in MI pathophysiology51,52, clinical presentation, or initial management and prognosis53. Younger women have lower risk of MI but worse short-term and long-term prognosis after MI onset compared with men or older women48. Men usually have more advanced and worse composition of coronary atherosclerotic plaques, more plaque vulnerability, and extensive coronary calcium compared with women51,52. Overall, our study found a gender difference for diet among MI survivors. Future studies are needed to investigate this gender difference to confirm the results.

In our study of men, the association between change in AHEI from pre- to post-MI period and all cause and cardiovascular mortality was attenuated after removing the alcohol component. This is consistent with our previous finding from this cohort that moderate alcohol intake is an important contributor to the AHEI and post-MI, and is associated with lower all-cause and cardiovascular mortality33.

Our study has several limitations. First, the validity and reproducibility of the AHEI2010 as assessed by our FFQ are unknown among post-MI patients. However, the components of the AHEI2010 have been validated in previous studies1921,54,55 and it is highly likely that AHEI2010 has a high degree of validity and reproducibility for our study populations. Even though we adjusted for major confounders, residual and unmeasured confounding may impact results. For example, we do not have detailed information on medication adherence or underlying severity of the disease, although these are unlikely to be strongly associated with the AHEI2010. Physical activity level may be an indication of underlying disease severity. In sensitivity analyses, we adjusted for activity level pre-MI, included a 2-year lag for post-MI reporting of physical activity and also further excluded participants in the lowest quintile of physical activity to reduce this potential bias. The inverse association between AHEI2010 score and mortality became stronger although the qualitative conclusions remained the same. Finally, our cohorts consist of female and male health professionals, and thus substantial unmeasured confounding by socioeconomic status is unlikely to explain our results. While this is strength of our findings, we recognize that our results are not necessarily generalizable to all post-MI patients. In addition, our study population was mainly non-Hispanic white, which might limit generalizability of our results to other ethnic populations. Further studies in other ethnicities and with greater numbers of men in particular are necessary to confirm our findings.

In our study, diet was assessed using a self-reported food frequency questionnaire, which has modest measurement error. However, our diet information was collected prospectively and thus any error is likely to be non-differential with respect to mortality. We modeled AHEI2010 using both simple-updated and cumulative average and the results were similar. We were concerned that FFQs returned within one year post-MI may not reflect their post-MI diet accurately, because the time frame bridged the pre- and post-MI period. However, the results were similar after excluding post-MI FFQs that were returned within one year of initial MI onset.

Finally, we did not have enough power to examine associations between post-MI AHEI2010 score, or changes from pre- to post- MI among patients with specific clinical characteristics. Previously, Ma et al. reported lower adherence to a healthy diet among smokers, and more obese patients8. Future studies are needed regarding targeted or personalized dietary recommendations for post-MI patients. The use of lipid-lowering medication may reduce patients’ efforts at dietary control8, and few studies have investigated the interaction between diet and medication. We did not observe a significant interaction between the post-MI AHEI2010 score and use of lipid lowering medication, although we had limited power to explore this issue in detail.

In conclusion, our results suggest that post-MI patients who consume a higher quality diet have lower all-cause mortality. Greater improvements from the pre- to post-MI period were strongly associated with lower all-cause and cardiovascular mortality. Future studies on the effects of dietary changes from pre- to post-MI are needed because of the direct clinical relevance of the findings. Dietary recommendations for secondary prevention need to pay more emphasis on polyunsaturated fat intake, and reduce sugar-sweetened beverages and fruit juice consumption.

Table 1
Age-standardized baseline characteristics of 2,258 post-MI women in the Nurses’ Health Study and 1,840 post-MI men in the Health Professional Follow-up Study by quintiles of Alternative Healthy Eating Index 2010

Supplementary Material

Acknowledgments

We thank Lydia Liu, Dr. Donna Spiegelman, Ellen Hertzmark for their help with programming for this study. We thank the staff and participants in the NHS and the HPFS studies, Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School.

Sources of funding and support: This study was supported by National Institute of Health grants AA11181, HL35464, HL34594, HL60712, CA55075, CA87969, and CA055075.

Role of the sponsors: None.

Footnotes

Results were presented in the moderate poster session at the American Heart Association Epidemiology and Prevention| Nutrition, Physical activity and metabolism 2013 scientific sessions on March 19th, 2013 in New Orleans, La., USA.

Authors’ contributions: Study concept and design (Drs. Li, Hu, Willett, Mukamal and Rimm); acquisition of data (Drs. Hu, Willett, Mukamal and Rimm); analysis and interpretation of data (Drs. Li, Hu, Willett, Mukamal and Rimm); drafting of the manuscript (Dr. Li); and critical revision of the manuscript for important intellectual content (Drs. Li, Chiuve, Flint, Pai, Forman, Hu, Willett, Mukamal and Rimm).

Access to the data: Drs. Li and Rimm had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Disclosure of potential conflicts of interest: None.

Duplicate submissions: None.

Previous presentation of the data: None.

References

1. Weiner S, Rabbani L. Secondary prevention strategies for coronary heart disease. J Thromb Thrombolysis. 2010;29(1):8–24. [PubMed]
2. Scrutinio D. The potential of lifestyle changes for improving the clinical outcome of patients with coronary heart disease: mechanisms of benefit and clinical results. Rev Recent Clin Trials. 2010;5(1):1–13. [PubMed]
3. Iestra JA, Kromhout D, van der Schouw YT, Grobbee DE, Boshuizen HC, van Staveren WA. Effect size estimates of lifestyle and dietary changes on all-cause mortality in coronary artery disease patients. Circulation. 2005;112(6):924–34. [PubMed]
4. Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368(14):1279–90. [PubMed]
5. Trichopoulou A, Bamia C, Norat T, et al. Modified Mediterranean diet and survival after myocardial infarction: the EPIC-Elderly study. Eur J epidemiol. 2007;22(12):871–81. [PubMed]
6. Trichopoulou A, Bamia C, Trichopoulos D. Mediterranean diet and survival among patients with coronary heart disease in Greece. Arch Intern Med. 2005;165(8):929–35. [PubMed]
7. de Lorgeril M, Salen P, Martin J-L, 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(6):779–85. [PubMed]
8. Ma Y, Li W, Olendzki BC, et al. Dietary quality 1 year after diagnosis of coronary heart disease. J Am Diet Assoc. 2008;108(2):240–6. discussion 6–7. [PMC free article] [PubMed]
9. Teo K, Lear S, Islam S, et al. PURE Investigators. Prevalence of a healthy lifestyle among individuals with cardiovascular disease in high-, middle- and low-income countries: The prospective urban rural epidemiology (pure) study. JAMA. 2013;309(15):1613–21. [PubMed]
10. Jneid H, Anderson JL, Wright RS, et al. 2012 Writing committee members; American college of cardiology foundation; American heart association task force on practice guidelines. 2012 ACCF/AHA focused update of the guideline for the management of patients with unstable angina/Non-ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update): a report of the American college of cardiology foundation/American heart association task force on practice guidelines. Circulation. 2012;126(7):875–910. [PubMed]
11. Anderson JL, Adams CD, Antman EM, et al. American college of cardiology; American Heart Association task force on practice guidelines (Writing committee to revise the 2002 guidelines for the management of patients with unstable angina/Non-ST-elevation myocardial infarction); American college of emergency physicians; Society for cardiovascular angiography and interventions; Society of thoracic surgeons; American association of cardiovascular and pulmonary rehabilitation; Society for academic emergency medicine. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American college of cardiology/American heart association task force on practice guidelines (Writing committee to revise the 2002 guidelines for the management of patients with unstable angina/Non-ST-elevation myocardial infarction) developed in collaboration with the American college of emergency physicians, the Society for cardiovascular angiography and interventions, and the Society of thoracic surgeons endorsed by the American association of cardiovascular and pulmonary rehabilitation and the society for academic emergency medicine. J Am Coll Cardiol. 2007;50(7):e1–e157. [PubMed]
12. Appel LJ, Sacks FM, Carey VJ, et al. OmniHeart Collaborative Research Group. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA. 2005;294(19):2455–64. [PubMed]
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. [PubMed]
14. Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: The women’s health initiative randomized controlled dietary modification trial. JAMA. 2006;295(6):655–66. [PubMed]
15. Chiuve SE, Fung TT, Rimm EB, et al. Alternative dietary indices both strongly predict risk of chronic disease. J Nutr. 2012;142(6):1009–18. [PubMed]
16. Dehghan M, Mente A, Teo KK, et al. Ongoing telmisartan alone and in combination with ramipril global end point trial (ONTARGET)/Telmisartan randomized assessment study in ACEI intolerant subjects with cardiovascular disease (TRANSCEND) trial investigators. Relationship between healthy diet and risk of cardiovascular disease among patients on drug therapies for secondary prevention: a prospective cohort study of 31 546 high-risk individuals from 40 countries. Circulation. 2012;126(23):2705–12. [PubMed]
17. Willett WC, Green A, Stampfer MJ, et al. Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. N Engl J Med. 1987;317(21):1303–9. [PubMed]
18. Colditz GA, Rimm EB, Giovannucci E, Stampfer MJ, Rosner B, Willett WC. A prospective study of parental history of myocardial infarction and coronary artery disease in men. Am J Cardiol. 1991;67(11):933–8. [PubMed]
19. Rimm EB, Giovannucci EL, Stampfer MJ, Colditz GA, Litin LB, Willett WC. Reproducibility and validity of an expanded self-administered semiquantitative food frequency questionnaire among male health professionals. Am J Epidemiol. 1992;135(10):1114–26. [PubMed]
20. Feskanich D, Rimm EB, Giovannucci EL, et al. Reproducibility and validity of food intake measurements from a semiquantitative food frequency questionnaire. J Am Diet Assoc. 1993;93(7):790–6. [PubMed]
21. Willett WC, Sampson L, Stampfer MJ, et al. Reproducibility and validity of a semiquantitative food frequency questionnaire. Am J Epidemiol. 1985;122(1):51–65. [PubMed]
22. Willett WC. Nutritional Epidemiology. 2. New York: Oxford University Press; 1998.
23. Mendis S, Thygesen K, Kuulasmaa K, et al. Writing group on behalf of the participating experts of the WHO consultation for revision of WHO definition of myocardial infarction. World Health Organization definition of myocardial infarction: 2008–09 revision. Int J Epidemiol. 2011;40(1):139–46. [PubMed]
24. Luepker RV, Apple FS, Christenson RH, et al. AHA council on epidemiology and prevention; AHA statistics committee; World heart federation council on epidemiology and prevention; European society of cardiology working group on epidemiology and prevention; Centers for disease control and prevention; National heart, lung, and blood institute. Case definitions for acute coronary heart disease in epidemiology and clinical research studies: a statement from the AHA Council on epidemiology and prevention. Circulation. 2003;108(20):2543–9. [PubMed]
25. Rich-Edwards JW, Corsano KA, Stampfer MJ. Test of the national death index and equifax nationwide death search. Am J Epidemiol. 1994;140(11):1016–9. [PubMed]
26. Wolf AM, Hunter DJ, Colditz GA, et al. Reproducibility and validity of a self-administered physical activity questionnaire. Int J Epidemiol. 1994;23(5):991–9. [PubMed]
27. Chasan-Taber S, Rimm EB, Stampfer MJ, et al. Reproducibility and validity of a self-administered physical activity questionnaire for male health professionals. Epidemiology. 1996;7(1):81–6. [PubMed]
28. Ainsworth BE, Haskell WL, Leon AS, et al. Compendium of physical activities: classification of energy costs of human physical activities. Med Sci Sports Exerc. 1993;25(1):71–80. [PubMed]
29. Hu FB, Stampfer MJ, Rimm E, et al. Dietary fat and coronary heart disease: a comparison of approaches for adjusting for total energy intake and modeling repeated dietary measurements. Am J Epidemiol. 1999;149(6):531–40. [PubMed]
30. Cole SR, Hernán MA. Constructing inverse probability weights for marginal structural models. Am J Epidemiol. 2008;168(6):656–64. [PMC free article] [PubMed]
31. Higgins JP, Thompson SG. Quantifying heterogeneity in a meta-analysis. Stat Med. 2002;21(11):1539–58. [PubMed]
32. DerSimonian R, Laird N. Meta-analysis in clinical trials. Control Clin Trials. 1986;7(3):177–88. [PubMed]
33. Pai JK, Mukamal KJ, Rimm EB. Long-term alcohol consumption in relation to all-cause and cardiovascular mortality among survivors of myocardial infarction: the Health Professionals Follow-up Study. Eur Heart J. 2012;33(13):1598–605. [PMC free article] [PubMed]
34. Rosenbloom JI, Mukamal KJ, Frost LE, Mittleman MA. Alcohol consumption patterns, beverage type, and long-term mortality among women survivors of acute myocardial infarction. Am J Cardiol. 2012;109(2):147–52. [PMC free article] [PubMed]
35. de Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet. 1994;343(8911):1454–9. [PubMed]
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(4):604–11. [PubMed]
37. Iwata H, Nagai R. Novel immune signals and atherosclerosis. Curr Atheroscler Rep. 2012;14(5):484–90. [PubMed]
38. Libby P. Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol. 2012;32(9):2045–51. [PMC free article] [PubMed]
39. Vaidya D, Szklo M, Cushman M, et al. Association of endothelial and oxidative stress with metabolic syndrome and subclinical atherosclerosis: multi-ethnic study of atherosclerosis. Eur J Clin Nutr. 2011;65(7):818–25. [PMC free article] [PubMed]
40. Blann AD, Lip GY, McCollum CN. Changes in von Willebrand factor and soluble ICAM, but not soluble VCAM, soluble E selectin or soluble thrombomodulin, reflect the natural history of the progression of atherosclerosis. Atherosclerosis. 2002;165(2):389–91. [PubMed]
41. Gonzalez MA, Selwyn AP. Endothelial function, inflammation, and prognosis in cardiovascular disease. Am J Med. 2003;115(Suppl 8A):99S–106S. [PubMed]
42. Esposito K, Marfella R, Ciotola M, et al. Effect of a mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: A randomized trial. JAMA. 2004;292(12):1440–6. [PubMed]
43. Urpi-Sarda M, Casas R, Chiva-Blanch G, et al. Virgin olive oil and nuts as key foods of the Mediterranean diet effects on inflammatory biomarkers related to atherosclerosis. Pharmacol Res. 2012;65(6):577–83. [PubMed]
44. Panagiotakos DB, Dimakopoulou K, Katsouyanni K, et al. Mediterranean diet and inflammatory response in myocardial infarction survivors. Int J Epidemiol. 2009;38(3):856–66. [PubMed]
45. Martínez-González MÁ, Corella D, Salas-Salvadó J, et al. Cohort Profile: Design and methods of the PREDIMED study. International Journal of Epidemiology. 2012;41(2):377–85. [PubMed]
46. Estruch R, Martínez-González MA, Corella D, et al. PREDIMED Study Investigators. Effects of a Mediterranean-style diet on cardiovascular risk factors: a randomized trial. Ann Intern Med. 2006;145(1):1–11. [PubMed]
47. Stampfer MJ, Hu FB, Manson JE, Rimm EB, Willett WC. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 2000;343(1):16–22. [PubMed]
48. Lehto HR, Lehto S, Havulinna AS, et al. Sex differences in short- and long-term case-fatality of myocardial infarction. Eur J Epidemiol. 2011;26(11):851–61. [PubMed]
49. Lundberg V, Wikstrom B, Bostrom S, Asplund K. Exploring sex differences in case fatality in acute myocardial infarction or coronary death events in the northern Sweden MONICA Project. J Intern Med. 2002;251(3):235–44. [PubMed]
50. Coppieters Y, Collart P, Leveque A. Gender differences in acute myocardial infarction, twenty-five years registration. Int J Cardiol. 2011 [PubMed]
51. Lansky AJ, Ng VG, Maehara A, et al. Gender and the extent of coronary atherosclerosis, plaque composition, and clinical outcomes in acute coronary syndromes. JACC: Cardiovascular Imaging. 2012;5(3 Supplement):S62–S72. [PubMed]
52. Pundziute G, Schuijf JD, van Velzen JE, et al. Assessment with multi-slice computed tomography and gray-scale and virtual histology intravascular ultrasound of gender-specific differences in extent and composition of coronary atherosclerotic plaques in relation to age. Am J Cardiol. 2010;105(4):480–6. [PubMed]
53. Thelle DS. Case fatality of acute myocardial infarction: an emerging gender gap. Eur J Epidemiol. 2011;26(11):829–31. [PubMed]
54. Hu FB, Rimm E, Smith-Warner SA, et al. Reproducibility and validity of dietary patterns assessed with a food-frequency questionnaire. Am J Clin Nutr. 1999;69:243–249. [PubMed]
55. Salvini S, Hunter DJ, Sampson L, et al. Food-based validation of a dietary questionnaire: the effects of week-to-week variation in food consumption. Int J Epidemiol. 1989;18:858–867. [PubMed]