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Ladwig, K.-H. ; Marten-Mittag, B.* ; Löwel, H. ; Döring, A. ; König, W.*

C-reactive protein, depressed mood, and the prediction of coronary heart disease in initially healthy men: Results from the MONICA-KORA Augsburg Cohort Study 1984-1998.

Eur. Heart J. 26, 2537-2542 (2005)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Aims C-reactive protein and depressive mood (DM) are novel risk factors for coronary heart disease (CHD). The goal of the present study was to assess possible combined effects of these factors on the prediction of a future fatal and non-fatal coronary event. Methods and results Baseline highly sensitive (hs) C-reactive protein and DM were analysed in 3021 apparently healthy male subjects aged 45–74 from three subsequent population based surveys (1984–95) of the MONICA–KORA Augsburg Cohort Study. During a median follow-up period of 7.7 years (IQR=6.9 years), 165 CHD events occurred. Risks of CHD were estimated from Cox proportional hazard models adjusted for age and survey and multiple risk factors. The age and survey adjusted interaction term of continuous hs-C-reactive protein by DM disclosed a significant effect (HR 1.03; 95% CI 1.00–1.06; P=0.037). A stratified analysis of subpopulations with (n=986) and without (n=2035) DM revealed that high hs-C-reactive protein (>3 mg/L) was predictive in the group with DM (HR 2.69; 95% CI 1.32–5.47) but was not significant in the low-level depression group (HR 1.55; 95% CI 0.89–2.69). Relative to the low C-reactive protein/no depression subgroup (n=712), high C-reactive protein/no depression (n=565) did not significantly predict a future CHD event. However, combined high C-reactive protein and DM (n=282) significantly predicted future CHD events (HR 2.91; 95% CI 1.25–2.18; P>0.0001). Conclusion In apparently healthy men, a DM substantially increases the power of elevated C-reactive protein to predict a subsequent myocardial infarction. Both conditions may share a common underlying mechanism.  
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 0195-668X
e-ISSN 1522-9645
Quellenangaben Band: 26, Heft: , Seiten: 2537-2542 Artikelnummer: , Supplement: ,
Verlag Oxford University Press
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)