title: Do changes in traditional coronary heart disease risk factors over time explain the association between socio-economic status and coronary heart disease?
abstract: BACKGROUND
  Socioeconomic status (SES) predicts coronary heart disease independently of the traditional risk factors included in the Framingham risk score. However, it is unknown whether changes in Framingham risk score variables over time explain the association between SES and coronary heart disease. We examined this question given its relevance to risk assessment in clinical decision making.
  
  
  METHODS
  The Atherosclerosis Risk in Communities study data (initiated in 1987 with 10-years follow-up of 15,495 adults aged 45-64 years in four Southern and Mid-Western communities) were used. SES was assessed at baseline, dichotomized as low SES (defined as low education and/or low income) or not. The time dependent variables - smoking, total and high density lipoprotein cholesterol, systolic blood pressure and use of blood pressure lowering medication - were assessed every three years. Ten-year incidence of coronary heart disease was based on EKG and cardiac enzyme criteria, or adjudicated death certificate data. Cox survival analyses examined the contribution of SES to heart disease risk independent of baseline Framingham risk score, without and with further adjustment for the time dependent variables.
  
  
  RESULTS
  Adjusting for baseline Framingham risk score, low SES was associated with an increased coronary heart disease risk (hazard ratio [HR] = 1.53; 95% Confidence Interval [CI], 1.27 to 1.85). After further adjustment for the time dependent variables, the SES effect remained significant (HR = 1.44; 95% CI, 1.19 to 1.74).
  
  
  CONCLUSIONS
  Using Framingham Risk Score alone under estimated the coronary heart disease risk in low SES persons. This bias was not eliminated by subsequent changes in Framingham risk score variables.
authors.affiliation: Center for Healthcare Policy and Research, University of California at Davis, University of California, Davis, 4860 Y Street, Suite 2300, Sacramento, California 95817, USA. pfranks@ucdavis.edu
authors.forename: Peter
authors.initials: P
authors.lastname: Franks
authors.forename: Paul C
authors.initials: PC
authors.lastname: Winters
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Tancredi
authors.forename: Kevin A
authors.initials: KA
authors.lastname: Fiscella
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology / Q000517:prevention & control; D050171:Dyslipidemias / Q000097:blood / Q000150:complications; D004522:Educational Status; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D015994:Incidence; D007182:Income; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D018570:Risk Assessment; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D012923:Social Class; D016019:Survival Analysis; D015996:Survival Rate; D013997:Time Factors; D014481:United States / Q000453:epidemiology
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers; D002784:Cholesterol