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Clin Chem. 2019 Jul;65(7):849-861. doi: 10.1373/clinchem.2018.297242. Epub 2019 Mar 27.

Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study).

Author information

1
Mannheim Institute of Public Health, Social and Preventive Medicine, Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany; Tanja.Grammer@medma.uni-heidelberg.de.
2
Department of Internal Medicine V (Nephrology, Hypertensiology, Endocrinology, Diabetolgy, and Rheumatology), Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany.
3
Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria.
4
DACH Society for the Prevention of Cardiovascular Diseases, Hamburg, Germany.
5
Division of Angiology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
6
Department of Cardiology, Charité Berlin, Berlin Institute of Health and German Research Centre for Cardiovascular Research, Berlin, Germany.
7
Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
8
Clinic Bad Gleichenberg, Bad Gleichenberg, Austria.
9
Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.
10
DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany.
11
Max Planck Institute of Psychiatry, Munich, Germany.
12
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
13
Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
14
Synlab Academy, Synlab Holding Deutschland GmbH, Augsburg and Mannheim, Germany.
15
Department of Internal Medicine III and IZKF, University Hospital Aaachen, Aachen, Germany.

Abstract

BACKGROUND:

Anemia has been shown to be a risk factor for coronary artery disease (CAD) and mortality, whereas the role of iron metabolism remains controversial.

METHODS:

We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a median follow-up of 9.9 years. Hemoglobin and iron status were determined in 1480 patients with stable CAD and in 682 individuals in whom significant CAD had been excluded by angiography.

RESULTS:

Multivariate-adjusted hazard ratios (HRs) for total mortality in the lowest quartiles of iron, transferrin saturation, ferritin, soluble transferrin receptor (sTfR), and hemoglobin were 1.22 (95% CI, 0.96-1.60), 1.23 (95% CI, 0.97-1.56), 1.27 (95% CI, 1.02-1.58), 1.26 (95% CI, 0.97-1.65), and 0.99 (95% CI, 0.79-1.24), respectively, compared to the second or third quartile, which served as reference (1.00) because of a J-shaped association. The corresponding HRs for total mortality in the highest quartiles were 1.44 (95% CI, 1.10-1.87), 1.37 (95% CI, 1.05-1.77), 1.17 (95% CI, 0.92-1.50), 1.76 (95% CI, 1.39-2.22), and 0.83 (95% CI, 0.63-1.09). HRs for cardiovascular death were similar. For hepcidin, the adjusted HRs for total mortality and cardiovascular deaths were 0.62 (95% CI, 0.49-0.78) and 0.70 (95% CI, 0.52-0.90) in the highest quartile compared to the lowest one.

CONCLUSIONS:

In stable patients undergoing angiography, serum iron, transferrin saturation, sTfR, and ferritin had J-shaped associations and hemoglobin only a marginal association with cardiovascular and total mortality. Hepcidin was continuously and inversely related to mortality.

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