PuSH - Publikationsserver des Helmholtz Zentrums München

Karakas, M.* ; Koenig, W.* ; Zierer, A. ; Herder, C.* ; Rottbauer, W.* ; Baumert, J.J. ; Meisinger, C. ; Thorand, B.

Myeloperoxidase is associated with incident coronary heart disease independently of traditional risk factors: Results from the MONICA/KORA Augsburg study.

J. Intern. Med. 271, 43-50 (2012)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Aims.  Oxidative stress plays a critical role in the initiation and progression of atherosclerosis. Myeloperoxidase (MPO) is a marker of oxidative stress. We prospectively investigated whether an increased serum concentration of MPO is associated with an increased risk of incident coronary heart disease (CHD). Methods.  We conducted a population-based case-cohort study in middle-aged, healthy men and women within the MONICA/KORA Augsburg studies. Serum levels of MPO were measured in 333 subjects with (cases) and 1727 without (noncases) incident CHD. Mean follow-up time was 10.8 ± 4.6 years. Results.  Baseline concentrations of MPO were higher in cases compared with noncases (P ≤ 0.001 in men; P = 0.131 in women). After adjustment for major cardiovascular risk factors, the hazard ratio (HR) with 95% confidence interval (CI) comparing the top with the two lower tertiles was 1.70 (95% CI, 1.25-2.30). After additional adjustment for markers of inflammation and endothelial dysfunction, the association was attenuated (HR 1.50; 95% CI, 1.08-2.09). There were no significant interactions of MPO with sex or increased weight on CHD risk. Conclusions.  Elevated concentrations of the oxidative stress marker MPO were independently associated with increased risk of incident CHD. This finding deserves detailed evaluation in further studies.
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter case-cohort study; coronary heart disease; MONICA/KORA; myeloperoxidase
ISSN (print) / ISBN 0954-6820
e-ISSN 1365-2796
Quellenangaben Band: 271, Heft: 1, Seiten: 43-50 Artikelnummer: , Supplement: ,
Verlag Wiley
Begutachtungsstatus Peer reviewed