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Hostility and Physiological Risk in the National Heart, Lung, and Blood Institute Family Heart Study
Sarah S. Knox, PhD;
Gerdi Weidner, PhD;
Avril Adelman, MA;
Catherine M. Stoney, PhD;
R. Curtis Ellison, MD; for the Investigators of the National Heart, Lung, and Blood Institute Family Heart Study
Arch Intern Med. 2004;164:2442-2447.
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.
Author Affiliations: Division of Epidemiology, Statistics, and Prevention Research, National Institute of Child Health & Human Development, National Institutes of Health, Bethesda, Md (Dr Knox); Preventive Medicine Research Institute, Sausalito, Calif (Dr Weidner); Division of Biostatistics, Washington University School of Medicine, St Louis, Mo (Ms Adelman); Department of Psychology, The Ohio State University, Columbus (Dr Stoney); and Section of Preventive Medicine and Epidemiology, Boston University School of Medicine, Boston, Mass (Dr Ellison).
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