title: Hostility and physiological risk in the National Heart, Lung, and Blood Institute Family Heart Study.
abstract: BACKGROUND
  The present analyses investigated possible pathways for earlier reported associations in the National Heart, Lung, and Blood Institute Family Heart Study between hostility and coronary and carotid end points.
  
  
  METHODS
  The cross-sectional design recruited 535 women and 491 men with average familial risk for coronary heart disease and 1950 women and 1667 men with high familial coronary risk from 3 prospective ongoing studies at 4 sites. Recruitment of high-risk participants was based on family risk score. Average-risk participants came from a randomly selected group. Outcome measures were plasminogen activator inhibitor type 1 (PAI-1), homocysteine, fibrinogen, fasting glucose, blood pressure, high-density lipoprotein cholesterol, triglycerides, low-density lipoprotein cholesterol, and "lipid metabolic disorder" (LMD) (defined as systolic blood pressure >/=140 mm Hg or diastolic blood pressure >/=90 mm Hg); fasting glucose >/=126 mg/dL (>/=7.0 mmol/L) or the use of diabetes medications; body mass index (calculated as weight in kilograms divided by the square of height in meters) >/=30; triglycerides >/=250 mg/dL (>/=2.8 mmol/L), high-density lipoprotein cholesterol <40 mg/dL (<1.0 mmol/L) in men and <50 mg/dL (<1.3 mmol/L) in women; and low-density lipoprotein cholesterol level >/=130 mg/dL (>/=3.4 mmol/L).
  
  
  RESULTS
  After adjustment for age and risk-related behaviors, hostility was significantly associated with glucose level and LMD in high-risk women, with LMD in average-risk women, with PAI-1 and LMD in high-risk men, and with fibrinogen level in average-risk men.
  
  
  CONCLUSIONS
  Associations between hostility and physiological risk were only partially accounted for by health behaviors, suggesting that further investigation of mechanistic pathways is warranted.
authors.affiliation: Division of Epidemiology, Statistics, and Prevention Research, National Institute of Child Health & Human Development, National Institutes of Health, Bethesda, MD, USA. knoxss@mail.nih.gov
authors.forename: Sarah S
authors.initials: SS
authors.lastname: Knox
authors.forename: Gerdi
authors.initials: G
authors.lastname: Weidner
authors.forename: Avril
authors.initials: A
authors.lastname: Adelman
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Stoney
authors.forename: R Curtis
authors.initials: RC
authors.lastname: Ellison
mesh_terms: D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology*; D008076:Cholesterol, HDL / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006710:Homocysteine / Q000097:blood; D006791:Hostility; D006801:Humans; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D006710:Homocysteine; D005340:Fibrinogen