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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1398-1406
Published online before print April 24, 2008, doi: 10.1161/ATVBAHA.108.167239
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1398.)
© 2008 American Heart Association, Inc.


Clinical and Population Studies

Do Psychological Factors Affect Inflammation and Incident Coronary Heart Disease

The Whitehall II Study

Hermann Nabi; Archana Singh-Manoux; Martin Shipley; David Gimeno; Michael G. Marmot; Mika Kivimaki

From the Department of Epidemiology and Public Health (H.N., A.S.-M., M.S., D.G., M.G.M., M.K.), University College London, United Kingdom; INSERM U687-IFR69 (H.N., A.S.-M.), Hôpital Paul Brousse, Villejuif Cedex, France; Hôpital Ste Périne (A.S.-M.), Centre de Gérontologie, Paris, France; Finnish Institute of Occupational Health (M.K.), Helsinki, Finland.

Correspondence to Hermann Nabi Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, UK. E-mail H.Nabi{at}public-health.ucl.ac.uk

Objectives— The purpose of this study was to test whether psychological factors affect inflammation processes to an extent that increases the risk of coronary heart disease (CHD).

Methods and Results— We used data from 6396 civil servants (4453 men, 1943 women) from the Whitehall II Study, aged 35 to 55 years and free from clinically validated CHD at the start of the follow-up period. Two psychological factors were assessed at phase 1 (1985 to 1988) and phase 2 (1989 to 1990): negative affect and psychological distress. Inflammatory biomarkers (fibrinogen, high-sensitivity C-reactive- protein, interleukin-6) and 12 baseline covariates including biological and behavioral CHD risk factors, sociodemographic variables, and work stress were measured at phase 3 (1991 to 1993). Follow-up for CHD death, first nonfatal myocardial infarction, or definite angina occurring between phase 3 and phase 7 (2003 to 2004) was based on clinical records. Higher levels of inflammatory markers were associated with higher CHD incidence, with hazard ratios (HR) ranging from 1.31 to 2.37 in age-and sex-adjusted models. Higher levels of negative affectivity and psychological distress were not associated with greater concentrations of inflammatory markers. Negative affectivity (relative index of inequality=1.68, 95% confidence interval [CI] 1.20 to 2.36) and higher psychological distress exposure (HR=1.66, 95% CI 1.28 to 2.14) were associated with higher CHD incidence and these associations remained unchanged after adjustment for inflammatory markers.

Conclusions— Our findings suggest that psychological factors do not affect inflammation although they predict incident CHD.


Key Words: inflammation • psychological factors • coronary heart disease




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