framingham heart study research design

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

• View all journals
• Explore content
• About the journal
• Publish with us
• Sign up for alerts
• Perspective
• Published: 07 May 2019

70-year legacy of the Framingham Heart Study

• Charlotte Andersson 1 , 2 ,
• Andrew D. Johnson 1 , 3 ,
• Emelia J. Benjamin   ORCID: orcid.org/0000-0003-4076-2336 1 , 4 , 5 ,
• Daniel Levy 1 , 3 , 4 &
• Ramachandran S. Vasan   ORCID: orcid.org/0000-0001-7357-5970 1 , 4 , 5  

Nature Reviews Cardiology volume  16 ,  pages 687–698 ( 2019 ) Cite this article

9216 Accesses

138 Citations

49 Altmetric

Metrics details

• Cardiovascular diseases
• Epidemiology
• Medical research
• Risk factors

The Framingham Heart Study (FHS) was established in 1948 to improve understanding of the epidemiology of coronary heart disease (CHD) in the USA. In 1961, seminal work identified major risk factors for CHD (high blood pressure, high cholesterol levels and evidence on the electrocardiogram of left ventricular hypertrophy), which later formed the basis for multivariable 10-year and 30-year risk-prediction algorithms. The FHS cohorts now comprise three generations of participants ( n  ≈ 15,000) and two minority cohorts. The FHS cohorts are densely phenotyped, with recurring follow-up examinations and surveillance for cardiovascular and non-cardiovascular end points. Assessment of subclinical disease and physiological profiling of these cohorts (with the use of echocardiography, ambulatory electrocardiographic monitoring, exercise stress testing, cardiac CT, heart and brain MRI, serial vascular tonometry and accelerometry) have been performed repeatedly. Over the past decade, the FHS cohorts have undergone deep ‘omics’ profiling (including whole-genome sequencing, DNA methylation analysis, transcriptomics, high-throughput proteomics and metabolomics, and microbiome studies). The FHS is a rich, longitudinal, transgenerational and deeply phenotyped cohort study with a sustained focus on state-of-the-art epidemiological methods and technological advances to facilitate scientific discoveries.

This is a preview of subscription content, access via your institution

Access options

Access Nature and 54 other Nature Portfolio journals

Get Nature+, our best-value online-access subscription

24,99 € / 30 days

cancel any time

Subscribe to this journal

Receive 12 print issues and online access

195,33 € per year

only 16,28 € per issue

Buy this article

• Purchase on Springer Link
• Instant access to full article PDF

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others

Genome-wide association and multi-trait analyses characterize the common genetic architecture of heart failure

Large-scale genome-wide association study of coronary artery disease in genetically diverse populations

The Project Baseline Health Study: a step towards a broader mission to map human health

Oppenheimer, G. M. Becoming the Framingham Study 1947–1950. Am. J. Public Health 95 , 602–610 (2005).

Article   PubMed   PubMed Central   Google Scholar  

Mahmood, S. S., Levy, D., Vasan, R. S. & Wang, T. J. The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective. Lancet 383 , 999–1008 (2014).

Article   PubMed   Google Scholar  

Dawber, T. R., Meadors, G. F. & Moore, F. E. Jr. Epidemiological approaches to heart disease: the Framingham Study. Am. J. Public Health Nations Health 41 , 279–281 (1951).

Article   CAS   PubMed   PubMed Central   Google Scholar  

Feinleib, M., Kannel, W. B., Garrison, R. J., McNamara, P. M. & Castelli, W. P. The Framingham Offspring Study. Design and preliminary data. Prev. Med. 4 , 518–525 (1975).

Article   CAS   PubMed   Google Scholar  

Splansky, G. L. et al. The Third Generation Cohort of the National Heart, Lung, and Blood Institute’s Framingham Heart Study: design, recruitment, and initial examination. Am. J. Epidemiol. 165 , 1328–1335 (2007).

Dawber, T. R., Moore, F. E. & Mann, G. V. Coronary heart disease in the Framingham Study. Am. J. Public Health Nations Health 47 , 4–24 (1957).

Kannel, W. B., Dawber, T. R., Kagan, A., Revotskie, N. & Stokes, J. 3rd. Factors of risk in the development of coronary heart disease—six year follow-up experience. The Framingham Study. Ann. Intern. Med. 55 , 33–50 (1961).

Doyle, J. T., Dawber, T. R., Kannel, W. B., Heslin, A. S. & Kahn, H. A. Cigarette smoking and coronary heart disease. Combined experience of the Albany and Framingham studies. N. Engl. J. Med. 266 , 796–801 (1962).

Doyle, J. T., Dawber, T. R., Kannel, W. B., Kinch, S. H. & Kahn, H. A. The relationship of cigarette smoking to coronary heart disease: the second report of the combined experience of the Albany, NY, and Framingham, mass, studies. JAMA 190 , 886–890 (1964).

CAS   PubMed   Google Scholar  

Moser, M. Historical perspectives on the management of hypertension. J. Clin. Hypertens. (Greenwich) 8 , 15–20 (2006).

Article   Google Scholar  

Kannel, W. B., Wolf, P. A., Verter, J. & McNamara, P. M. Epidemiologic assessment of the role of blood pressure in stroke. The Framingham Study. JAMA 214 , 301–310 (1970).

Kannel, W. B., Castelli, W. P., McNamara, P. M., McKee, P. A. & Feinleib, M. Role of blood pressure in the development of congestive heart failure. The Framingham Study. N. Engl. J. Med. 287 , 781–787 (1972).

McKee, P. A., Castelli, W. P., McNamara, P. M. & Kannel, W. B. The natural history of congestive heart failure: the Framingham Study. N. Engl. J. Med. 285 , 1441–1446 (1971).

Wolf, P. A., Dawber, T. R., Thomas, H. E. Jr & Kannel, W. B. Epidemiologic assessment of chronic atrial fibrillation and risk of stroke: the Framingham Study. Neurology 28 , 973–977 (1978).

Kannel, W. B., Hjortland, M. & Castelli, W. P. Role of diabetes in congestive heart failure: the Framingham Study. Am. J. Cardiol. 34 , 29–34 (1974).

Izzo, J. L. Jr., Levy, D. & Black, H. R. Clinical Advisory Statement. Importance of systolic blood pressure in older Americans. Hypertension 35 , 1021–1024 (2000).

Kannel, W. B. & McGee, D. L. Diabetes and cardiovascular disease. The Framingham Study. JAMA 241 , 2035–2038 (1979).

Benjamin, E. J. et al. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. JAMA 271 , 840–844 (1994).

Ho, K. K., Pinsky, J. L., Kannel, W. B. & Levy, D. The epidemiology of heart failure: the Framingham Study. J. Am. Coll. Cardiol. 22 , 6A–13A (1993).

Kannel, W. B. & Shurtleff, D. The Framingham Study. Cigarettes and the development of intermittent claudication. Geriatrics 28 , 61–68 (1973).

Wolf, P. A., D’Agostino, R. B., Kannel, W. B., Bonita, R. & Belanger, A. J. Cigarette smoking as a risk factor for stroke. The Framingham Study. JAMA 259 , 1025–1029 (1988).

Castelli, W. P., Abbott, R. D. & McNamara, P. M. Summary estimates of cholesterol used to predict coronary heart disease. Circulation 67 , 730–734 (1983).

Kannel, W. B. Habitual level of physical activity and risk of coronary heart disease: the Framingham Study. Can. Med. Assoc. J. 96 , 811–812 (1967).

CAS   PubMed   PubMed Central   Google Scholar  

Hubert, H. B., Feinleib, M., McNamara, P. M. & Castelli, W. P. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation 67 , 968–977 (1983).

Sagie, A., Larson, M. G. & Levy, D. The natural history of borderline isolated systolic hypertension. N. Engl. J. Med. 329 , 1912–1917 (1993).

Vasan, R. S. et al. Residual lifetime risk for developing hypertension in middle-aged women and men: the Framingham Heart Study. JAMA 287 , 1003–1010 (2002).

Lloyd-Jones, D. M. et al. Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation 110 , 1042–1046 (2004).

Lloyd-Jones, D. M. et al. Lifetime risk of coronary heart disease by cholesterol levels at selected ages. Arch. Intern. Med. 163 , 1966–1972 (2003).

Staerk, L. et al. Lifetime risk of atrial fibrillation according to optimal, borderline, or elevated levels of risk factors: cohort study based on longitudinal data from the Framingham Heart Study. BMJ 361 , k1453 (2018).

Weng, L. C. et al. Genetic predisposition, clinical risk factor burden, and lifetime risk of atrial fibrillation. Circulation 137 , 1027–1038 (2018).

Wilson, P. W. et al. Prediction of coronary heart disease using risk factor categories. Circulation 97 , 1837–1847 (1998).

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the 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). JAMA 285 , 2486–2497 (2001).

Pencina, M. J. et al. Predicting the 30-year risk of cardiovascular disease: the Framingham Heart Study. Circulation 119 , 3078–3084 (2009).

Kannel, W. B. et al. Profile for estimating risk of heart failure. Arch. Intern. Med. 159 , 1197–1204 (1999).

Schnabel, R. B. et al. Development of a risk score for atrial fibrillation (Framingham Heart Study): a community-based cohort study. Lancet 373 , 739–745 (2009).

D’Agostino, R. B., Wolf, P. A., Belanger, A. J. & Kannel, W. B. Stroke risk profile: adjustment for antihypertensive medication. The Framingham Study. Stroke 25 , 40–43 (1994).

D’Agostino, R. B. et al. Primary and subsequent coronary risk appraisal: new results from the Framingham Study. Am. Heart J. 139 , 272–281 (2000).

Parikh, N. I. et al. A risk score for predicting near-term incidence of hypertension: the Framingham Heart Study. Ann. Intern. Med. 148 , 102–110 (2008).

Levy, D. et al. Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors. The Framingham Heart Study. Ann. Intern. Med. 108 , 7–13 (1988).

Levy, D. et al. Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study. Am. J. Cardiol. 59 , 956–960 (1987).

Vasan, R. S., Larson, M. G., Levy, D., Evans, J. C. & Benjamin, E. J. Distribution and categorization of echocardiographic measurements in relation to reference limits: the Framingham Heart Study: formulation of a height- and sex-specific classification and its prospective validation. Circulation 96 , 1863–1873 (1997).

Vasan, R. S., Larson, M. G., Benjamin, E. J. & Levy, D. Echocardiographic reference values for aortic root size: the Framingham Heart Study. J. Am. Soc. Echocardiogr. 8 , 793–800 (1995).

Lieb, W. et al. Longitudinal tracking of left ventricular mass over the adult life course: clinical correlates of short- and long-term change in the Framingham Offspring Study. Circulation 119 , 3085–3092 (2009).

Levy, D., Garrison, R. J., Savage, D. D., Kannel, W. B. & Castelli, W. P. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N. Engl. J. Med. 322 , 1561–1566 (1990).

Vasan, R. S., Larson, M. G., Benjamin, E. J., Evans, J. C. & Levy, D. Left ventricular dilatation and the risk of congestive heart failure in people without myocardial infarction. N. Engl. J. Med. 336 , 1350–1355 (1997).

Wang, T. J. et al. Natural history of asymptomatic left ventricular systolic dysfunction in the community. Circulation 108 , 977–982 (2003).

Cheng, S. et al. Correlates of echocardiographic indices of cardiac remodeling over the adult life course: longitudinal observations from the Framingham Heart Study. Circulation 122 , 570–578 (2010).

Vasan, R. S. et al. Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort. J. Am. Coll. Cardiol. 33 , 1948–1955 (1999).

Vasan, R. S. et al. Epidemiology of left ventricular systolic dysfunction and heart failure in the Framingham study: an echocardiographic study over 3 decades. JACC Cardiovasc. Imaging 11 , 1–11 (2018).

Lauer, M. S., Larson, M. G., Evans, J. C. & Levy, D. Association of left ventricular dilatation and hypertrophy with chronotropic incompetence in the Framingham Heart Study. Am. Heart J. 137 , 903–909 (1999).

Lauer, M. S., Okin, P. M., Larson, M. G., Evans, J. C. & Levy, D. Impaired heart rate response to graded exercise. Prognostic implications of chronotropic incompetence in the Framingham Heart Study. Circulation 93 , 1520–1526 (1996).

Morshedi-Meibodi, A., Larson, M. G., Levy, D., O’Donnell, C. J. & Vasan, R. S. Heart rate recovery after treadmill exercise testing and risk of cardiovascular disease events (the Framingham Heart Study). Am. J. Cardiol. 90 , 848–852 (2002).

Ivan, C. S. et al. Dementia after stroke: the Framingham Study. Stroke 35 , 1264–1268 (2004).

Seshadri, S. et al. Stroke risk profile, brain volume, and cognitive function: the Framingham Offspring Study. Neurology 63 , 1591–1599 (2004).

Seshadri, S. et al. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. N. Engl. J. Med. 346 , 476–483 (2002).

Elias, M. F., Elias, P. K., Sullivan, L. M., Wolf, P. A. & D’Agostino, R. B. Lower cognitive function in the presence of obesity and hypertension: the Framingham Heart Study. Int. J. Obes. Relat. Metab. Disord. 27 , 260–268 (2003).

Debette, S. et al. Midlife vascular risk factor exposure accelerates structural brain aging and cognitive decline. Neurology 77 , 461–468 (2011).

Myers, R. H. et al. Apolipoprotein E epsilon4 association with dementia in a population-based study: the Framingham Study. Neurology 46 , 673–677 (1996).

Elias, M. F. et al. Atrial fibrillation is associated with lower cognitive performance in the Framingham offspring men. J. Stroke Cerebrovasc. Dis. 15 , 214–222 (2006).

Nishtala, A. et al. Atrial fibrillation and cognitive decline in the Framingham Heart Study. Heart Rhythm 15 , 166–172 (2018).

Lieb, W. et al. Association of plasma leptin levels with incident Alzheimer disease and MRI measures of brain aging. JAMA 302 , 2565–2572 (2009).

Satizabal, C. L. et al. Incidence of dementia over three decades in the Framingham Heart Study. N. Engl. J. Med. 374 , 523–532 (2016).

Wang, T. J. et al. Multiple biomarkers and the risk of incident hypertension. Hypertension 49 , 432–438 (2007).

Freitag, M. H. et al. Plasma brain natriuretic peptide levels and blood pressure tracking in the Framingham Heart Study. Hypertension 41 , 978–983 (2003).

Kathiresan, S. et al. Cross-sectional relations of multiple biomarkers from distinct biological pathways to brachial artery endothelial function. Circulation 113 , 938–945 (2006).

Adlin, E. V., Braitman, L. E. & Vasan, R. S. Bimodal aldosterone distribution in low-renin hypertension. Am. J. Hypertens. 26 , 1076–1085 (2013).

Shoamanesh, A. et al. Circulating biomarkers and incident ischemic stroke in the Framingham Offspring Study. Neurology 87 , 1206–1211 (2016).

Andersson, C. et al. Relations of circulating GDF-15, soluble ST2, and troponin-I concentrations with vascular function in the community: the Framingham Heart Study. Atherosclerosis 248 , 245–251 (2016).

Schnabel, R. B. et al. Relations of biomarkers of distinct pathophysiological pathways and atrial fibrillation incidence in the community. Circulation 121 , 200–207 (2010).

Schnabel, R. B. et al. Relation of multiple inflammatory biomarkers to incident atrial fibrillation. Am. J. Cardiol. 104 , 92–96 (2009).

de Boer, R. A. et al. Association of cardiovascular biomarkers with incident heart failure with preserved and reduced ejection fraction. JAMA Cardiol. 3 , 215–224 (2018).

Xanthakis, V. et al. Prevalence, neurohormonal correlates, and prognosis of heart failure stages in the community. JACC Heart Fail 4 , 808–815 (2016).

Velagaleti, R. S. et al. Multimarker approach for the prediction of heart failure incidence in the community. Circulation 122 , 1700–1706 (2010).

Xanthakis, V. et al. Association of novel biomarkers of cardiovascular stress with left ventricular hypertrophy and dysfunction: implications for screening. J. Am. Heart Assoc. 2 , e000399 (2013).

Article   PubMed   PubMed Central   CAS   Google Scholar  

Fox, C. S. et al. A multi-marker approach to predict incident CKD and microalbuminuria. J. Am. Soc. Nephrol. 21 , 2143–2149 (2010).

O’Seaghdha, C. M. et al. Analysis of a urinary biomarker panel for incident kidney disease and clinical outcomes. J. Am. Soc. Nephrol. 24 , 1880–1888 (2013).

Puurunen, M. K. et al. Biomarkers for the prediction of venous thromboembolism in the community. Thromb. Res. 145 , 34–39 (2016).

Pikula, A. et al. Multiple biomarkers and risk of clinical and subclinical vascular brain injury: the Framingham Offspring Study. Circulation 125 , 2100–2107 (2012).

Andersson, C. et al. Associations of circulating growth differentiation factor-15 and ST2 concentrations with subclinical vascular brain injury and incident stroke. Stroke 46 , 2568–2575 (2015).

Shoamanesh, A. et al. Inflammatory biomarkers, cerebral microbleeds, and small vessel disease: Framingham Heart Study. Neurology 84 , 825–832 (2015).

Puurunen, M. K. et al. ADP platelet hyperreactivity predicts cardiovascular disease in the FHS (Framingham Heart Study). J. Am. Heart Assoc. 7 , e008522 (2018).

Chouraki, V. et al. Plasma amyloid-beta and risk of Alzheimer’s disease in the Framingham Heart Study. Alzheimers Dement. 11 , 249–257 (2015).

Tan, Z. S. et al. Inflammatory markers and the risk of Alzheimer disease: the Framingham Study. Neurology 68 , 1902–1908 (2007).

Wang, T. J. et al. Multiple biomarkers for the prediction of first major cardiovascular events and death. N. Engl. J. Med. 355 , 2631–2639 (2006).

Fradley, M. G. et al. Reference limits for N-terminal-pro-B-type natriuretic peptide in healthy individuals (from the Framingham Heart Study). Am. J. Cardiol. 108 , 1341–1345 (2011).

Cheng, S. et al. Relation of visceral adiposity to circulating natriuretic peptides in ambulatory individuals. Am. J. Cardiol. 108 , 979–984 (2011).

Wang, T. J. et al. Impact of obesity on plasma natriuretic peptide levels. Circulation 109 , 594–600 (2004).

Sinner, M. F. et al. B-Type natriuretic peptide and C-reactive protein in the prediction of atrial fibrillation risk: the CHARGE-AF Consortium of community-based cohort studies. Europace 16 , 1426–1433 (2014).

Wang, T. J. et al. Plasma natriuretic peptide levels and the risk of cardiovascular events and death. N. Engl. J. Med. 350 , 655–663 (2004).

Vasan, R. S. et al. Plasma natriuretic peptides for community screening for left ventricular hypertrophy and systolic dysfunction: the Framingham Heart Study. JAMA 288 , 1252–1259 (2002).

Tsuji, H. et al. Reduced heart rate variability and mortality risk in an elderly cohort. The Framingham Heart Study. Circulation 90 , 878–883 (1994).

Ho, K. K. et al. Predicting survival in heart failure case and control subjects by use of fully automated methods for deriving nonlinear and conventional indices of heart rate dynamics. Circulation 96 , 842–848 (1997).

Tsuji, H. et al. Impact of reduced heart rate variability on risk for cardiac events. The Framingham Heart Study. Circulation 94 , 2850–2855 (1996).

Benjamin, E. J. et al. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 98 , 946–952 (1998).

Wang, T. J. et al. Temporal relations of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Circulation 107 , 2920–2925 (2003).

Santhanakrishnan, R. et al. Atrial fibrillation begets heart failure and vice versa: temporal associations and differences in preserved versus reduced ejection fraction. Circulation 133 , 484–492 (2016).

Mitchell, G. F. et al. Arterial stiffness and cardiovascular events: the Framingham Heart Study. Circulation 121 , 505–511 (2010).

Andersson, C. et al. Association of parental hypertension with arterial stiffness in nonhypertensive offspring: the Framingham Heart Study. Hypertension 68 , 584–589 (2016).

Kaess, B. M. et al. Aortic stiffness, blood pressure progression, and incident hypertension. JAMA 308 , 875–881 (2012).

Niiranen, T. J. et al. Relative contributions of arterial stiffness and hypertension to cardiovascular disease: the Framingham Heart Study. J. Am. Heart Assoc. 5 , e004271 (2016).

Maillard, P. et al. Aortic stiffness, increased white matter free water, and altered microstructural integrity: a continuum of injury. Stroke 48 , 1567–1573 (2017).

Maillard, P. et al. Effects of arterial stiffness on brain integrity in young adults from the Framingham Heart Study. Stroke 47 , 1030–1036 (2016).

Pase, M. P. et al. Association of aortic stiffness with cognition and brain aging in young and middle-aged adults: the Framingham Third Generation Cohort Study. Hypertension 67 , 513–519 (2016).

Pase, M. P. et al. Aortic stiffness and the risk of incident mild cognitive impairment and dementia. Stroke 47 , 2256–2261 (2016).

Shaikh, A. Y. et al. Relations of arterial stiffness and brachial flow-mediated dilation with new-onset atrial fibrillation: the Framingham Heart Study. Hypertension 68 , 590–596 (2016).

Kaess, B. M. et al. Relations of central hemodynamics and aortic stiffness with left ventricular structure and function: the Framingham Heart Study. J. Am. Heart Assoc. 5 , e002693 (2016).

Tsao, C. W. et al. Relation of central arterial stiffness to incident heart failure in the community. J. Am. Heart Assoc. 4 , e002189 (2015).

Zachariah, J. P. et al. Circulating adipokines and vascular function: cross-sectional associations in a community-based cohort. Hypertension 67 , 294–300 (2016).

Chami, H. A. et al. The association between sleep-disordered breathing and aortic stiffness in a community cohort. Sleep Med. 19 , 69–74 (2016).

Zachariah, J. P. et al. Metabolic predictors of change in vascular function: prospective associations from a community-based cohort. Hypertension 71 , 237–242 (2018).

Andersson, C. et al. Physical activity measured by accelerometry and its associations with cardiac structure and vascular function in young and middle-aged adults. J. Am. Heart Assoc. 4 , e001528 (2015).

Benjamin, E. J. et al. Clinical correlates and heritability of flow-mediated dilation in the community: the Framingham Heart Study. Circulation 109 , 613–619 (2004).

Widlansky, M. E. et al. Relation of season and temperature to endothelium-dependent flow-mediated vasodilation in subjects without clinical evidence of cardiovascular disease (from the Framingham Heart Study). Am. J. Cardiol. 100 , 518–523 (2007).

Mitchell, G. F. et al. Local shear stress and brachial artery flow-mediated dilation: the Framingham Heart Study. Hypertension 44 , 134–139 (2004).

Lee, J. J. et al. Cross-sectional associations of computed tomography (CT)-derived adipose tissue density and adipokines: the Framingham Heart Study. J. Am. Heart Assoc. 5 , e002545 (2016).

Murabito, J. M. et al. Moderate-to-vigorous physical activity with accelerometry is associated with visceral adipose tissue in adults. J. Am. Heart Assoc. 4 , e001379 (2015).

Lee, J. J., Pedley, A., Hoffmann, U., Massaro, J. M. & Fox, C. S. Association of changes in abdominal fat quantity and quality with incident cardiovascular disease risk factors. J. Am. Coll. Cardiol. 68 , 1509–1521 (2016).

Rosenquist, K. J. et al. Fat quality and incident cardiovascular disease, all-cause mortality, and cancer mortality. J. Clin. Endocrinol. Metab. 100 , 227–234 (2015).

Rosenquist, K. J. et al. Visceral and subcutaneous fat quality and cardiometabolic risk. JACC Cardiovasc. Imaging 6 , 762–771 (2013).

Kaess, B. M. et al. The ratio of visceral to subcutaneous fat, a metric of body fat distribution, is a unique correlate of cardiometabolic risk. Diabetologia 55 , 2622–2630 (2012).

Mahabadi, A. A. et al. Association of pericardial fat, intrathoracic fat, and visceral abdominal fat with cardiovascular disease burden: the Framingham Heart Study. Eur. Heart J. 30 , 850–856 (2009).

Hoffmann, U., Massaro, J. M., Fox, C. S., Manders, E. & O’Donnell, C. J. Defining normal distributions of coronary artery calcium in women and men (from the Framingham Heart Study). Am. J. Cardiol. 102 , 1136–1141 (2008).

Tsao, C. W. et al. Relations of long-term and contemporary lipid levels and lipid genetic risk scores with coronary artery calcium in the framingham heart study. J. Am. Coll. Cardiol. 60 , 2364–2371 (2012).

Hwang, S. J. et al. Maintenance of ideal cardiovascular health and coronary artery calcium progression in low-risk men and women in the Framingham Heart Study. Circ. Cardiovasc. Imaging 11 , e006209 (2018).

Moselewski, F. et al. Calcium concentration of individual coronary calcified plaques as measured by multidetector row computed tomography. Circulation 111 , 3236–3241 (2005).

Preis, S. R. et al. Eligibility of individuals with subclinical coronary artery calcium and intermediate coronary heart disease risk for reclassification (from the Framingham Heart Study). Am. J. Cardiol. 103 , 1710–1715 (2009).

Ferencik, M. et al. Coronary artery calcium distribution is an independent predictor of incident major coronary heart disease events: results from the Framingham Heart Study. Circ. Cardiovasc. Imaging 10 , e006592 (2017).

Hoffmann, U. et al. Cardiovascular event prediction and risk reclassification by coronary, aortic, and valvular calcification in the Framingham Heart Study. J. Am. Heart Assoc. 5 , e003144 (2016).

Chuang, M. L. et al. CMR reference values for left ventricular volumes, mass, and ejection fraction using computer-aided analysis: the Framingham Heart Study. J. Magn. Reson. Imaging 39 , 895–900 (2014).

Yeon, S. B. et al. Impact of age, sex, and indexation method on MR left ventricular reference values in the Framingham Heart Study offspring cohort. J. Magn. Reson. Imaging 41 , 1038–1045 (2015).

Foppa, M. et al. Right ventricular volumes and systolic function by cardiac magnetic resonance and the impact of sex, age, and obesity in a longitudinally followed cohort free of pulmonary and cardiovascular disease: the Framingham Heart Study. Circ. Cardiovasc. Imaging 9 , e003810 (2016).

Tsao, C. W. et al. Subclinical and clinical correlates of left ventricular wall motion abnormalities in the community. Am. J. Cardiol. 107 , 949–955 (2011).

Tsao, C. W. et al. Left ventricular structure and risk of cardiovascular events: a Framingham Heart Study Cardiac Magnetic Resonance Study. J. Am. Heart Assoc. 4 , e002188 (2015).

Jeerakathil, T. et al. Stroke risk profile predicts white matter hyperintensity volume: the Framingham Study. Stroke 35 , 1857–1861 (2004).

Debette, S. et al. Association of MRI markers of vascular brain injury with incident stroke, mild cognitive impairment, dementia, and mortality: the Framingham Offspring Study. Stroke 41 , 600–606 (2010).

Williams, L. R. et al. Clinical correlates of cerebral white matter hyperintensities in cognitively normal older adults. Arch. Gerontol. Geriatr. 50 , 127–131 (2010).

DeCarli, C. et al. Measures of brain morphology and infarction in the framingham heart study: establishing what is normal. Neurobiol. Aging 26 , 491–510 (2005).

Au, R. et al. Association of white matter hyperintensity volume with decreased cognitive functioning: the Framingham Heart Study. Arch. Neurol. 63 , 246–250 (2006).

Tan, Z. S. et al. Association of metabolic dysregulation with volumetric brain magnetic resonance imaging and cognitive markers of subclinical brain aging in middle-aged adults: the Framingham Offspring Study. Diabetes Care 34 , 1766–1770 (2011).

Christakis, N. A. & Fowler, J. H. The collective dynamics of smoking in a large social network. N. Engl. J. Med. 358 , 2249–2258 (2008).

Christakis, N. A. & Fowler, J. H. The spread of obesity in a large social network over 32 years. N. Engl. J. Med. 357 , 370–379 (2007).

Pachucki, M. A., Jacques, P. F. & Christakis, N. A. Social network concordance in food choice among spouses, friends, and siblings. Am. J. Public Health 101 , 2170–2177 (2011).

Fowler, J. H., Settle, J. E. & Christakis, N. A. Correlated genotypes in friendship networks. Proc. Natl Acad. Sci. USA 108 , 1993–1997 (2011).

Cupples, L. A. et al. The Framingham Heart Study 100K SNP genome-wide association study resource: overview of 17 phenotype working group reports. BMC Med. Genet. 8 (Suppl. 1), 1 (2007).

Article   CAS   Google Scholar  

Tennessen, J. A. et al. Evolution and functional impact of rare coding variation from deep sequencing of human exomes. Science 337 , 64–69 (2012).

Eicher, J. D. et al. Whole exome sequencing in the Framingham Heart Study identifies rare variation in HYAL2 that influences platelet aggregation. Thromb. Haemost. 117 , 1083–1092 (2017).

Peloso, G. M. et al. Association of low-frequency and rare coding-sequence variants with blood lipids and coronary heart disease in 56,000 whites and blacks. Am. J. Hum. Genet. 94 , 223–232 (2014).

Gordon, A. S. et al. Quantifying rare, deleterious variation in 12 human cytochrome P450 drug-metabolism genes in a large-scale exome dataset. Hum. Mol. Genet. 23 , 1957–1963 (2014).

Norton, N. et al. Exome sequencing and genome-wide linkage analysis in 17 families illustrate the complex contribution of TTN truncating variants to dilated cardiomyopathy. Circ. Cardiovasc. Genet. 6 , 144–153 (2013).

Lubitz, S. A. et al. Whole exome sequencing in atrial fibrillation. PLOS Genet. 12 , e1006284 (2016).

Psaty, B. M. et al. Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium: design of prospective meta-analyses of genome-wide association studies from 5 cohorts. Circ. Cardiovasc. Genet. 2 , 73–80 (2009).

The International Consortium for Blood Pressure Genome-Wide Association Studies. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Nature 478 , 103–109 (2011).

Article   PubMed Central   CAS   Google Scholar  

Dehghan, A. et al. Genome-wide association study for incident myocardial infarction and coronary heart disease in prospective cohort studies: the CHARGE Consortium. PLOS ONE 11 , e0144997 (2016).

Natarajan, P. et al. Multiethnic exome-wide association study of subclinical atherosclerosis. Circ. Cardiovasc. Genet. 9 , 511–520 (2016).

Broer, L. et al. GWAS of longevity in CHARGE consortium confirms APOE and FOXO3 candidacy. J. Gerontol. A Biol. Sci. Med. Sci. 70 , 110–118 (2015).

Thanassoulis, G. et al. Genetic associations with valvular calcification and aortic stenosis. N. Engl. J. Med. 368 , 503–512 (2013).

Seshadri, S. et al. Genome-wide analysis of genetic loci associated with Alzheimer disease. JAMA 303 , 1832–1840 (2010).

Roselli, C. et al. Multi-ethnic genome-wide association study for atrial fibrillation. Nat. Genet. 50 , 1225–1233 (2018).

Johnson, A. D. et al. Genome-wide meta-analyses identifies seven loci associated with platelet aggregation in response to agonists. Nat. Genet. 42 , 608–613 (2010).

Richard, M. A. et al. DNA methylation analysis identifies loci for blood pressure regulation. Am. J. Hum. Genet. 101 , 888–902 (2017).

Chu, A. Y. et al. Epigenome-wide association studies identify DNA methylation associated with kidney function. Nat. Commun. 8 , 1286 (2017).

Huan, T. et al. A whole-blood transcriptome meta-analysis identifies gene expression signatures of cigarette smoking. Hum. Mol. Genet. 25 , 4611–4623 (2016).

Mendelson, M. M. et al. Association of body mass index with DNA methylation and gene expression in blood cells and relations to cardiometabolic disease: a mendelian randomization approach. PLOS Med. 14 , e1002215 (2017).

Lin, H. et al. Methylome-wide association study of atrial fibrillation in Framingham Heart Study. Sci. Rep. 7 , 40377 (2017).

Ligthart, S. et al. DNA methylation signatures of chronic low-grade inflammation are associated with complex diseases. Genome Biol. 17 , 255 (2016).

Liu, C. et al. A DNA methylation biomarker of alcohol consumption. Mol. Psychiatry 23 , 422–433 (2018).

Joehanes, R. et al. Epigenetic signatures of cigarette smoking. Circ. Cardiovasc. Genet. 9 , 436–447 (2016).

Huan, T. et al. Genome-wide identification of microRNA expression quantitative trait loci. Nat. Commun. 6 , 6601 (2015).

Huan, T. et al. Dissecting the roles of microRNAs in coronary heart disease via integrative genomic analyses. Arterioscler. Thromb. Vasc. Biol. 35 , 1011–1021 (2015).

Joehanes, R. et al. Integrated genome-wide analysis of expression quantitative trait loci aids interpretation of genomic association studies. Genome Biol. 18 , 16 (2017).

Merino, J. et al. Metabolomics insights into early type 2 diabetes pathogenesis and detection in individuals with normal fasting glucose. Diabetologia 61 , 1315–1324 (2018).

Yin, X. et al. Metabolite signatures of metabolic risk factors and their longitudinal changes. J. Clin. Endocrinol. Metab. 101 , 1779–1789 (2016).

Rhee, E. P. et al. An exome array study of the plasma metabolome. Nat. Commun. 7 , 12360 (2016).

Benson, M. D. et al. Genetic architecture of the cardiovascular risk proteome. Circulation 137 , 1158–1172 (2018).

Ho, J. E. et al. Metabolomic profiles of body mass index in the Framingham Heart Study reveal distinct cardiometabolic phenotypes. PLOS ONE 11 , e0148361 (2016).

Cheng, S. et al. Distinct metabolomic signatures are associated with longevity in humans. Nat. Commun. 6 , 6791 (2015).

Ho, J. E. et al. Effect of phosphodiesterase inhibition on insulin resistance in obese individuals. J. Am. Heart Assoc. 3 , e001001 (2014).

Rhee, E. P. et al. A genome-wide association study of the human metabolome in a community-based cohort. Cell Metab. 18 , 130–143 (2013).

Yao, C. et al. Genome-wide mapping of plasma protein QTLs identifies putatively causal genes and pathways for cardiovascular disease. Nat. Commun. 9 , 3268 (2018).

Bookman, E. B. et al. Reporting genetic results in research studies: summary and recommendations of an NHLBI working group. Am. J. Med. Genet. A 140A , 1033–1040 (2006).

Johnson, A. D. et al. CLIA-tested genetic variants on commercial SNP arrays: potential for incidental findings in genome-wide association studies. Genet. Med. 12 , 355–363 (2010).

Levy, D. et al. Consent for genetic research in the Framingham Heart Study. Am. J. Med. Genet. A 152A , 1250–1256 (2010).

Natarajan, P. et al. Aggregate penetrance of genomic variants for actionable disorders in European and African Americans. Sci. Transl Med. 8 , 364ra151 (2016).

Patel, M. S. et al. Effect of a game-based intervention designed to enhance social incentives to increase physical activity among families: the BE FIT randomized clinical trial. JAMA Intern. Med. 177 , 1586–1593 (2017).

Fox, C. S. et al. Digital connectedness in the Framingham Heart Study. J. Am. Heart Assoc. 5 , e003193 (2016).

Ford, E. S. et al. Explaining the decrease in U. S. deaths from coronary disease, 1980–2000. N. Engl. J. Med. 356 , 2388–2398 (2007).

Andersson, C. & Vasan, R. S. Epidemiology of cardiovascular disease in young individuals. Nat. Rev. Cardiol. 15 , 230–240 (2018).

Myers, R. H., Kiely, D. K., Cupples, L. A. & Kannel, W. B. Parental history is an independent risk factor for coronary artery disease: the Framingham Study. Am. Heart J. 120 , 963–969 (1990).

Levy, D., Larson, M. G., Vasan, R. S., Kannel, W. B. & Ho, K. K. The progression from hypertension to congestive heart failure. JAMA 275 , 1557–1562 (1996).

Vasan, R. S., Larson, M. G., Leip, E. P., Kannel, W. B. & Levy, D. Assessment of frequency of progression to hypertension in non-hypertensive participants in the Framingham Heart Study: a cohort study. Lancet 358 , 1682–1686 (2001).

Vasan, R. S. et al. Impact of high-normal blood pressure on the risk of cardiovascular disease. N. Engl. J. Med. 345 , 1291–1297 (2001).

Kenchaiah, S. et al. Obesity and the risk of heart failure. N. Engl. J. Med. 347 , 305–313 (2002).

Wang, T. J. et al. Obesity and the risk of new-onset atrial fibrillation. JAMA 292 , 2471–2477 (2004).

Fox, C. S. et al. Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring. JAMA 291 , 2851–2855 (2004).

Lee, D. S. et al. Association of parental heart failure with risk of heart failure in offspring. N. Engl. J. Med. 355 , 138–147 (2006).

Lubitz, S. A. et al. Association between familial atrial fibrillation and risk of new-onset atrial fibrillation. JAMA 304 , 2263–2269 (2010).

Tsao, C. W. et al. Temporal trends in the incidence of and mortality associated with heart failure with preserved and reduced ejection fraction. JACC Heart Fail. 6 , 678–685 (2018).

Download references

Acknowledgements

The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the US National Heart, Lung, and Blood Institute (NHLBI), the NIH or the US Department of Health and Human Services. The Framingham Heart Study (FHS) acknowledges the support of contracts NO1-HC-25195 and HHSN268201500001I from the NHLBI and grant supplement R01 HL092577-06S1 for this research. The authors also acknowledge the dedication of the FHS study participants, without whom this research would not be possible. E.J.B. is supported by NIH grants R01 HL128914, 2R01 HL092577, 2U54 HL120163 and 1R01 HL141434 01A1 and AHA grant 18SFRN34110082. R.S.V. is supported in part by the Evans Medical Foundation and the Jay and Louis Coffman Endowment from the Department of Medicine, Boston University School of Medicine, USA.

Author information

Authors and affiliations.

Boston University’s and National Heart, Lung, and Blood Institute’s Framingham Heart Study, Framingham, MA, USA

Charlotte Andersson, Andrew D. Johnson, Emelia J. Benjamin, Daniel Levy & Ramachandran S. Vasan

Department of Cardiology, Gentofte and Herlev Hospital, Herlev, Denmark

Charlotte Andersson

Population Sciences Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, USA

Andrew D. Johnson & Daniel Levy

Preventive Medicine and Cardiology Sections, Evans Department of Medicine, Boston University School of Medicine, Boston, MA, USA

Emelia J. Benjamin, Daniel Levy & Ramachandran S. Vasan

Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA

Emelia J. Benjamin & Ramachandran S. Vasan

You can also search for this author in PubMed   Google Scholar

Contributions

All the authors researched data for the article. C.A. and R.S.V. discussed its content. C.A. wrote the initial version of the manuscript, and the other authors reviewed and edited the manuscript before submission.

Corresponding authors

Correspondence to Charlotte Andersson or Ramachandran S. Vasan .

Ethics declarations

Competing interests.

The authors declare no competing interests.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Reviewer information

Nature Reviews Cardiology thanks B. Psaty, C. Torp-Pedersen, and the other anonymous reviewer(s), for their contribution to the peer review of this work.

Related links

Biologic Specimen and Data Repository Information Coordinating Center: https://biolincc.nhlbi.nih.gov/studies/framcohort/

Cross-Cohort Collaboration Consortium: https://chs-nhlbi.org/node/6539

Database of Genotypes and Phenotypes: https://www.ncbi.nlm.nih.gov/gap

Grand Opportunity Exome Sequencing Project: https://esp.gs.washington.edu/

Rights and permissions

Reprints and permissions

About this article

Cite this article.

Andersson, C., Johnson, A.D., Benjamin, E.J. et al. 70-year legacy of the Framingham Heart Study. Nat Rev Cardiol 16 , 687–698 (2019). https://doi.org/10.1038/s41569-019-0202-5

Download citation

Published : 07 May 2019

Issue Date : November 2019

DOI : https://doi.org/10.1038/s41569-019-0202-5

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

This article is cited by

Alcohol consumption as a socially contagious phenomenon in the framingham heart study social network.

• Maarten W. J. van den Ende
• Han L. J. van der Maas
• Mike H. Lees

Scientific Reports (2024)

Cardiovascular Disease in Anti-neutrophil Cytoplasm Antibody-Associated Vasculitis

• Matthew Sayer
• Gavin B. Chapman
• Neeraj Dhaun

Current Rheumatology Reports (2024)

Cardiovascular disease incidence prediction by machine learning and statistical techniques: a 16-year cohort study from eastern Mediterranean region

• Kamran Mehrabani-Zeinabad
• Nizal Sarrafzadegan

BMC Medical Informatics and Decision Making (2023)

Hypomethylation of ABCG1 in peripheral blood as a potential marker for the detection of coronary heart disease

• Xiaojing Zhao
• Rongxi Yang

Clinical Epigenetics (2023)

Integrated omics analysis of coronary artery calcifications and myocardial infarction: the Framingham Heart Study

• Amalie Lykkemark Møller
• Ramachandran S. Vasan
• Honghuang Lin

Scientific Reports (2023)

Quick links

• Explore articles by subject
• Guide to authors
• Editorial policies

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Legacy of the framingham heart study: rationale, design, initial findings, and implications

Affiliations.

• 1 Heart Disease Prevention Program, University of California, Irvine, CA, USA. Electronic address: [email protected].
• 2 Framingham Heart Study, Framingham, MA, USA; Center for Population Research of the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
• PMID: 25690260
• DOI: 10.1016/j.gheart.2012.12.001

With the dramatic rise in coronary heart disease (CHD) during the first half of the 20th century, the newly formed National Heart Institute realized the significant gap in knowledge about the causes of CHD and embarked in 1947 on planning what was to become the renowned Framingham Heart Study. Dr. Thomas Royal Dawber's initial paper on the design of the project described studying up to 6,000 persons in a single geographic area and the formation of a technical advisory committee of 11 physicians in cardiology and public health to determine the hypotheses and protocol. A comprehensive physical examination and series of measurements and laboratory work were proposed and the initial examination was completed in 1952. The first paper describing 4 years of follow-up was published in 1957, and this was followed by a subsequent report in 1959 describing 6 years of follow-up. The first follow-up report described sex and age group differences in incidence of CHD and pointed out the noteworthy prominence of sudden cardiac death as the first manifestation of CHD and the initial observations regarding the significance of elevated blood pressure, cholesterol, and overweight in predicting future CHD. Importantly, the significance of a combination of risk factors for identifying those at highest risk was described as well as how the number of risk factors related to risk (the beginnings of what was decades later to become the famous risk scores from Framingham). Dr. William Kannel's 1961 publication, "Factors of Risk in the Development of Coronary Heart Disease," first highlighted the term risk factors, and it described how specific levels of cholesterol, blood pressure, as well as how electrocardiographic left ventricular hypertrophy predicted future CHD incidence. The standardized measurement of risk factors and follow-up in Framingham served as an important precedent for future observational studies designed and directed by what is now the National Heart, Lung, and Blood Institute, including the ARIC (Atherosclerosis Risk in Communities) study, the CARDIA (Coronary Artery Risk Development in Young Adults) study, the CHS (Cardiovascular Health Study), and the MESA (Multiethnic Study of Atherosclerosis). These studies and others continue the legacy that Framingham began more than 60 years ago into the investigation of the epidemiology of cardiovascular diseases.

Copyright © 2013 World Heart Federation (Geneva). All rights reserved.

Framingham Heart Study

Since its beginning in 1948, the Framingham Heart Study, under the direction of the National Heart, Lung, and Blood Institute (NHLBI), formerly known as the National Heart Institute, has been committed to identifying the common factors or characteristics that contribute to cardiovascular disease (CVD). It has followed CVD development over a long period of time in three generations of participants. Since 1971, the Boston University School of Medicine has served as NHLBI contractor and academic partner for the study.

Information For...

• Search Menu
• Advance Articles
• Editor's Choice
• Supplements
• Image Library
• ESC Journals App
• ESC Content Collections
• Author Guidelines
• Submission Site
• Open Access Options
• Read & Publish
• Author Resources
• Self-Archiving Policy
• About European Journal of Preventive Cardiology
• Editorial Board
• ESC Publications
• About European Society of Cardiology
• Advertising & Corporate Services
• Developing Countries Initiative
• Journals on Oxford Academic
• Books on Oxford Academic

Article Contents

Lay summary, modifiable risk factors and risk of myocardial infarction in offspring with parental disease.

• Article contents
• Figures & tables
• Supplementary Data

Amalie Lykkemark Møller, Martin Larson, Vanessa Xanthakis, Ramachandran S Vasan, Charlotte Andersson, Modifiable risk factors and risk of myocardial infarction in offspring with parental disease, European Journal of Preventive Cardiology , 2024;, zwae169, https://doi.org/10.1093/eurjpc/zwae169

• Permissions Icon Permissions

Children of patients with early-onset myocardial infarction (MI) are at increased risk, but the importance of concordant versus discordant parent-offspring risk factor profiles on MI risk is largely unknown. We quantified the long-term absolute risk of MI according to shared risk factors in adulthood.

We sampled data on familial predisposed offspring and their parents from the Framingham Heart Study. Early MI was defined as a history of parental MI onset before age 55 in men or 65 in women. Individuals were matched 3:1 with non-predisposed offspring. Cardiovascular risk factors included obesity, smoking, hypertension, high cholesterol, and diabetes. We estimated the absolute 20-year incidence of MI using the Aalen-Johansen estimator.

At age 40, the 20-year risk of MI varied by cholesterol level (high cholesterol 25.7% [95% confidence interval 11.2%; 40.2%] vs. non-high cholesterol 3.4% [0.5; 6.4]) among predisposed individuals and this difference was greater than in controls (high cholesterol 9.3% [1.5; 17.0] vs. non-high cholesterol 2.5% [1.1; 3.8]). Similar results were observed for prevalent hypertension (26.7% [10.8; 42.5] vs. 4.0% [0.9; 7.1] in predisposed vs. 10.8% [3.2; 18.3] and 2.1% [0.8; 3.4] in controls). Among offspring without risk factors, parental risk factors carried a residual impact on 20-year MI risk in offspring (0% [0; 11.6] for 0-1 parental risk factors versus 3.3% [0; 9.8] for ≥2 parent risk factors at age 40, versus 2.9% [0; 8.4] and 8.5% [0; 19.8] at age 50 years).

Children of patients with early-onset MI have low absolute risks of MI in the absence of midlife cardiovascular risk factors, especially if the parent also had a low risk factor burden prior to MI.

Children of patients with early-onset myocardial infarction (MI) are at a higher risk of disease themselves. Cardiovascular risk factor control is important to lower the risk of disease, but little is known about how the offspring’s risk differs based on risk factor controls.

Using multi-generational data from the Framingham Heart Study, we observed that adult children of people with early-onset MI have low absolute 20-year risk of developing an MI if they do not have any cardiovascular risk factors, especially if the parent also had low risk factor burden prior to MI, suggesting that close surveillance for risk factor development in offspring is warranted. In offspring of parents with early-onset MI who did not have any risk factors, the number of risk factors in the parent seemed to slightly impact the risk of MI.

Improved clarity of the interplay between risk factors in parents and offspring can help medical doctors provide accurate guidance in terms of preventing the development of MI. Our findings suggest that in the absence of risk factors, assessment of the parents’ risk factors burden may be helpful for further risk stratification.

• myocardial infarction
• hypercholesterolemia
• framingham heart study
• heart disease risk factors

Email alerts

Related articles in pubmed, citing articles via.

• Recommend to Your Librarian
• Advertising and Corporate Services
• Journals Career Network

Affiliations

• Online ISSN 2047-4881
• Print ISSN 2047-4873
• Copyright © 2024 European Society of Cardiology
• About Oxford Academic
• Publish journals with us
• University press partners
• What we publish
• New features  
• Open access
• Institutional account management
• Rights and permissions
• Get help with access
• Accessibility
• Advertising
• Media enquiries
• Oxford University Press
• Oxford Languages
• University of Oxford

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide

• Copyright © 2024 Oxford University Press
• Cookie settings
• Cookie policy
• Privacy policy
• Legal notice

This Feature Is Available To Subscribers Only

Sign In or Create an Account

This PDF is available to Subscribers Only

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

Research Milestones