vlog

Object moved to here.

Contributions of the Framingham Heart Study to the Epidemiology of Coronary Heart Disease | Cardiology | JAMA Cardiology | vlog

vlog

[Skip to Navigation]
Sign In
1.
Dawber  TR, Meadors  GF, Moore  FE  Jr.  Epidemiological approaches to heart disease: the Framingham Study.  Am J Public Health Nations Health. 1951;41(3):279-281.
2.
Feinleib  M, Kannel  WB, Garrison  RJ, McNamara  PM, Castelli  WP.  The Framingham Offspring Study: design and preliminary data.  Prev Med. 1975;4(4):518-525.
3.
Splansky  GL, Corey  D, Yang  Q,  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. 2007;165(11):1328-1335.
4.
Cupples  LA, Arruda  HT, Benjamin  EJ,  et al.  The Framingham Heart Study 100K SNP genome-wide association study resource: overview of 17 phenotype working group reports.  BMC Med Genet. 2007;8(suppl 1):S1.
5.
National Heart, Lung, and Blood Institute. SHARe: SNP Health Association Resource. . Updated September 2011. Accessed March 1, 2016.
6.
Oppenheimer  GM.  Becoming the Framingham Study 1947-1950.  Am J Public Health. 2005;95(4):602-610.
7.
Minutes  MF. October 14-15, 1949. Located at: Records of the National Institutes of Health, National Advisory Heart Council, Box 21, National Archives, College Park, MD.
8.
Wong  ND, Levy  D.  Legacy of the Framingham Heart Study: rationale, design, initial findings, and implications.  Glob Heart. 2013;8(1):3-9.
9.
Dawber  TR, Moore  FE, Mann  GV.  Coronary heart disease in the Framingham Study.  Am J Public Health Nations Health. 1957;47(4, pt 2):4-24.
10.
Dawber  TR, Kannel  WB, Revotskie  N, Stokes  J  III, Kagan  A, Gordon  T.  Some factors associated with the development of coronary heart disease: six years’ follow-up experience in the Framingham Study.  Am J Public Health Nations Health. 1959;49:1349-1356.
11.
Kannel  WB, Dawber  TR, Kagan  A, Revotskie  N, Stokes  J  III.  Factors of risk in the development of coronary heart disease—six-year follow-up experience: the Framingham Study.  Ann Intern Med. 1961;55:33-50.
12.
 Effects of treatment on morbidity in hypertension. Results in patients with diastolic blood pressures averaging 115 through 129 mm Hg. Ѵ. 1967;202(11):1028-1034.
13.
 The Lipid Research Clinics Coronary Primary Prevention Trial results, I: reduction in incidence of coronary heart disease. Ѵ. 1984;251(3):351-364.
14.
James  PA, Oparil  S, Carter  BL,  et al.  2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). Ѵ. 2014;311(5):507-520.
15.
Stone  NJ, Robinson  JG, Lichtenstein  AH,  et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines.  2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 侱ܱپDz. 2014;129(25)(suppl 2):S1-S45.
16.
Kannel  WB, McGee  D, Gordon  T.  A general cardiovascular risk profile: the Framingham Study.  Am J Cardiol. 1976;38(1):46-51.
17.
Anderson  KM, Odell  PM, Wilson  PWF, Kannel  WB.  Cardiovascular disease risk profiles.  Am Heart J. 1991;121(1, pt 2):293-298.
18.
Wilson  PW, D’Agostino  RB, Levy  D, Belanger  AM, Silbershatz  H, Kannel  WB.  Prediction of coronary heart disease using risk factor categories. 侱ܱپDz. 1998;97(18):1837-1847.
19.
 The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V).  Arch Intern Med. 1993;153(2):154-183.
20.
National Cholesterol Education Program.  National Cholesterol Education Program. Second Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). 侱ܱپDz. 1994;89(3):1333-1445.
21.
D’Agostino  RB  Sr, Grundy  S, Sullivan  LM, Wilson  P; CHD Risk Prediction Group.  Validation of the Framingham coronary heart disease prediction scores: results of a multiple ethnic groups investigation. Ѵ. 2001;286(2):180-187.
22.
Goff  DC  Jr, Lloyd-Jones  DM, Bennett  G,  et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines.  2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 侱ܱپDz. 2014;129(25)(suppl 2):S49-S73.
23.
Lloyd-Jones  DM, Wilson  PW, Larson  MG,  et al.  Framingham risk score and prediction of lifetime risk for coronary heart disease.  Am J Cardiol. 2004;94(1):20-24.
24.
Pencina  MJ, D’Agostino  RB  Sr, Larson  MG, Massaro  JM, Vasan  RS.  Predicting the 30-year risk of cardiovascular disease: the Framingham Heart Study. 侱ܱپDz. 2009;119(24):3078-3084.
25.
Cupples  LA, D’Agostino  RB, Anderson  K, Kannel  WB.  Comparison of baseline and repeated measure covariate techniques in the Framingham Heart Study.  Stat Med. 1988;7(1-2):205-222.
26.
Kannel  WB, Wolf  PA, Garrison  RJ.  Monograph Section 34: Some Risk Factors Related to the Annual Incidence of Cardiovascular Disease and Death Using Pooled Repeated Biennial Measurements: Framingham Heart Study, 30-Year Follow-Up. Springfield, MA: National Technical Information Service; 1987:1-459.
27.
D’Agostino  RB, Russell  MW, Huse  DM,  et al.  Primary and subsequent coronary risk appraisal: new results from the Framingham study.  Am Heart J. 2000;139(2, pt 1):272-281.
28.
Kannel  WB, Gordon  T, Offutt  D.  Left ventricular hypertrophy by electrocardiogram: prevalence, incidence, and mortality in the Framingham Study.  Ann Intern Med. 1969;71(1):89-105.
29.
Kannel  WB, Gordon  T, Castelli  WP, Margolis  JR.  Electrocardiographic left ventricular hypertrophy and risk of coronary heart disease: the Framingham Study.  Ann Intern Med. 1970;72(6):813-822.
30.
Kannel  WB.  Prevalence and natural history of electrocardiographic left ventricular hypertrophy.  Am J Med. 1983;75(3A):4-11.
31.
Levy  D, Labib  SB, Anderson  KM, Christiansen  JC, Kannel  WB, Castelli  WP.  Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. 侱ܱپDz. 1990;81(3):815-820.
32.
Feigenbaum  H.  Evolution of echocardiography. 侱ܱپDz. 1996;93(7):1321-1327.
33.
Levy  D, Savage  DD, Garrison  RJ, Anderson  KM, Kannel  WB, Castelli  WP.  Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study.  Am J Cardiol. 1987;59(9):956-960.
34.
Levy  D, Garrison  RJ, Savage  DD, Kannel  WB, Castelli  WP.  Left ventricular mass and incidence of coronary heart disease in an elderly cohort: the Framingham Heart Study.  Ann Intern Med. 1989;110(2):101-107.
35.
Levy  D, Garrison  RJ, Savage  DD, Kannel  WB, Castelli  WP.  Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study.  N Engl J Med. 1990;322(22):1561-1566.
36.
Havlik  RJ, Garrison  RJ, Feinleib  M, Kannel  WB, Castelli  WP, McNamara  PM.  Blood pressure aggregation in families.  Am J Epidemiol. 1979;110(3):304-312.
37.
Garrison  RJ, Castelli  WP, Feinleib  M,  et al.  The association of total cholesterol, triglycerides and plasma lipoprotein cholesterol levels in first degree relatives and spouse pairs.  Am J Epidemiol. 1979;110(3):313-321.
38.
Chesebro  JH, Fuster  V, Elveback  LR, Frye  RL.  Strong family history and cigarette smoking as risk factors of coronary artery disease in young adults.  Br Heart J. 1982;47(1):78-83.
39.
Schildkraut  JM, Myers  RH, Cupples  LA, Kiely  DK, Kannel  WB.  Coronary risk associated with age and sex of parental heart disease in the Framingham Study.  Am J Cardiol. 1989;64(10):555-559.
40.
Larson  MG, Atwood  LD, Benjamin  EJ,  et al.  Framingham Heart Study 100K project: genome-wide associations for cardiovascular disease outcomes.  BMC Med Genet. 2007;8(suppl 1):S5.
41.
Psaty  BM, O’Donnell  CJ, Gudnason  V,  et al; CHARGE Consortium.  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. 2009;2(1):73-80.
42.
Ehret  GB, Munroe  PB, Rice  KM,  et al; International Consortium for Blood Pressure Genome-Wide Association Studies; CARDIoGRAM consortium; CKDGen Consortium; KidneyGen Consortium; EchoGen consortium; CHARGE-HF consortium.  Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. ٳܰ. 2011;478(7367):103-109.
43.
Schunkert  H, König  IR, Kathiresan  S,  et al; Cardiogenics; CARDIoGRAM Consortium.  Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease.  Nat Genet. 2011;43(4):333-338.
44.
Musunuru  K, Strong  A, Frank-Kamenetsky  M,  et al.  From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locus. ٳܰ. 2010;466(7307):714-719.
45.
Huan  T, Zhang  B, Wang  Z,  et al; Coronary ARteryDIsease Genome wide Replication and Meta-analysis (CARDIoGRAM) Consortium, International Consortium for Blood Pressure GWAS (ICBP).  A systems biology framework identifies molecular underpinnings of coronary heart disease.  Arterioscler Thromb Vasc Biol. 2013;33(6):1427-1434.
46.
Joehanes  R, Ying  S, Huan  T,  et al.  Gene expression signatures of coronary heart disease.  Arterioscler Thromb Vasc Biol. 2013;33(6):1418-1426.
47.
Huan  T, Rong  J, Tanriverdi  K,  et al.  Dissecting the roles of microRNAs in coronary heart disease via integrative genomic analyses.  Arterioscler Thromb Vasc Biol. 2015;35(4):1011-1021.
48.
Yao  C, Chen  BH, Joehanes  R,  et al.  Integromic analysis of genetic variation and gene expression identifies networks for cardiovascular disease phenotypes. 侱ܱپDz. 2015;131(6):536-549.
49.
Whitman  IR, Pletcher  MJ, Vittinghoff  E,  et al.  Perceptions, information sources, and behavior regarding alcohol and heart health.  Am J Cardiol. 2015;116(4):642-646.
Views 1,959
Special Communication
ٴDz2016

Contributions of the Framingham Heart Study to the Epidemiology of Coronary Heart Disease

Author Affiliations
  • 1Framingham Heart Study, Framingham, Massachusetts
  • 2Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland
  • 3Boston University School of Medicine, Boston, Massachusetts
JAMA Cardiol. 2016;1(7):825-830. doi:10.1001/jamacardio.2016.2050
Abstract

Since its launch in 1948, the Framingham Heart Study has proved critical to shaping and enhancing our understanding of the history and root causes of coronary heart disease (CHD). A modern prototype for population-based studies, the Framingham Heart Study garnered widespread recognition in its early years for identifying risk factors for CHD and stroke and formulating CHD risk scores. Although the study remains iconic for its robust design and successes in uncovering risk factors for CHD, it has undergone transformations during the past 2 decades. The 21st century ushered in a new era in “molecular epidemiology” centered on cutting-edge genetic and “-omics technologies.” Framingham Heart Study investigators embraced these opportunities by pioneering genome-wide association studies at the population level and examining CHD through the lens of genetic variation, gene expression, and microRNA signatures. The Framingham Heart Study continues to evolve as it seeks to pinpoint new causes of disease with the hope of advancing personalized approaches to the treatment and prevention of CHD.

×