Plasma osteoprotegerin, its correlates, and risk of heart failure: a prospective cohort study.

Romina di Giuseppe, Ronald Biemann, Janine Wirth, Juliane Menzel, Berend Isermann, Gabriele I Stangl, Andreas Fritsche, Heiner Boeing, Matthias B Schulze, Cornelia Weikert

Journal: European journal of epidemiology 2018;32(2):113-123

PMID: 27307249

Abstract

Heart failure (HF) is a disabling condition involving complex vascular, neurohormonal and immune systems' interactions. Osteoprotegerin (OPG), a bone-regulatory cytokine, has been suggested to play a key role in skeletal, vascular, and immune biology, with elevated levels observed in both experimental and clinical HF. In the present study we aimed to identify clinical OPG correlates and investigated whether elevated OPG, as a marker of HF vascular and immune activation, may interact with N-terminal pro-brain natriuretic peptide (NT-proBNP), a marker of HF neurohormonal activation, thus synergistically increasing HF risk. We used a case-cohort study, nested within the European Prospective Investigation into Cancer and Nutrition-Potsdam, comprising 2647 participants including 252 incident HF cases identified during a mean follow-up of 8.2 ± 1.6 years. In both men and women significant positive associations were observed between OPG and age, smoking, prevalent diabetes, C-reactive protein, sex hormone-binding globulin, and additionally prevalent coronary heart disease and uric acid in men only. In women, OPG was furthermore positively related to hypertension and fetuin-A. After multivariable adjustment each doubling of OPG was associated with a 3.01-fold increased HF risk (95 % CI 1.49-6.06) in men. A significant interaction was observed between OPG and NT-proBNP. In men, a combination of high levels of both OPG and NT-proBNP, compared to a combination of low levels, was associated with an approximately fivefold increased HF risk. In women, no associations were observed. These findings suggest that, in men, the activation of different immune, neurohormonal, and vascular pathophysiological pathways may confer increased HF risk.

Address: Research Group Cardiovascular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Arthur-Scheunert-Allee, 114-116, 14558, Nuthetal, Germany. [email protected].; Institute of Epidemiology, Christian-Albrechts University Kiel, University Hospital Schleswig-Holstein (UK-SH), Campus Kiel, Niemannsweg 11, 24105, Kiel, Germany. [email protected].; Institute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Leipziger Str. 44, Building 26, 39120, Magdeburg, Germany.; Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Arthur-Scheunert-Allee, 114-116, 14558, Nuthetal, Germany.; Research Group Cardiovascular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Arthur-Scheunert-Allee, 114-116, 14558, Nuthetal, Germany.; Department of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Arthur-Scheunert-Allee, 114-116, 14558, Nuthetal, Germany.; German Center for Diabetes Research (DZD), Neuherberg, Germany.; Human Nutrition Group, Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), Von-Danckelmann-Platz 2, 06120, Halle (Saale), Germany.; Division of Endocrinology, Diabetology, Nephrology, Vascular Disease and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Otfried-Müller-Str. 10, 72076, Tübingen, Germany.; Department of Food Safety, Federal Institute of Risk Assessment, Berlin, Germany.

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