Clinical Chemistry
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Clinical Chemistry 55: 1462-1470, 2009. First published June 25, 2009; 10.1373/clinchem.2009.126029
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(Clinical Chemistry. 2009;55:1462-1470.)
© 2009 American Association for Clinical Chemistry, Inc.

Mini-Review

Myeloperoxidase: A Useful Biomarker for Cardiovascular Disease Risk Stratification?

Roger K. Schindhelm1,a, Leonard P. van der Zwan2, Tom Teerlink2 and Peter G. Scheffer2

1 Department of Clinical Chemistry, Isala Clinics, Zwolle, the Netherlands; 2 Metabolic Laboratory, Department of Clinical Chemistry, VU University Medical Center, Amsterdam, the Netherlands.

aAddress correspondence to this author at: Department of Clinical Chemistry, Isala Clinics, P.O. Box 10400, 8000 GK Zwolle, the Netherlands. Fax +31-38-424-2676; e-mail r.k.schindhelm{at}isala.nl.


Abstract

Background: Inflammation and oxidative stress are associated with atherosclerosis. Myeloperoxidase (MPO) is linked to both inflammation and oxidative stress by its location in leukocytes and its role in catalyzing the formation of oxidizing agents. Recent evidence suggests that MPO activity precipitates atherogenesis. Measurement of MPO in plasma may therefore contribute to cardiovascular disease (CVD) risk stratification.

Content: Cross-sectional studies, case-control studies, and prospective-cohort studies investigating the relation between MPO and CVD have been evaluated. Differences in study populations, sample materials, sample handling, and assays were ascertained. Potential causal mechanisms linking MPO to accelerated atherosclerosis are discussed here. A majority of studies indicate that measurement of MPO in plasma was associated with improved CVD risk stratification above and beyond risk stratification results obtained with markers used in routine clinical practice. However, comparison of these epidemiological studies with regard to MPO and outcome is hampered because the reported MPO concentration depends on the assay method, sampling material, and preanalytical and analytical procedures. The link between MPO and CVD can, at least partly, be explained by MPO-dependent oxidation of LDL and HDL, subsequently leading to cholesterol accumulation in the arterial wall. Furthermore, MPO may reduce the bioavailability of nitric oxide, resulting in endothelial dysfunction. Finally, MPO destabilizes atherosclerotic plaques.

Summary: Increasing evidence suggests that MPO is causally linked to atherosclerosis and its measurement may improve CVD risk estimation. Before MPO can be used in routine clinical practice, however, standardization of sampling and laboratory procedures is needed.






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Copyright © 2009 by the American Association for Clinical Chemistry.