Abstract
Myeloperoxidase (MPO), a heme protein abundantly expressed by neutrophils, monocytes
and macrophages, has been suggested to critically accelerate the course of vascular
inflammatory disease: Myeloperoxidase not only has been localized to atherosclerotic
plaques, it also binds to and transcytopses endothelial cells to accumulate in the
subendothelial space. Here, MPO remains catalytically active and is capable of oxidizing
lipoproteins, matrix proteins and nitric oxide, thereby adversely affecting endothelial
function.
Multiple clinical trials suggest that circulating MPO levels identify patients with
stable and unstable coronary artery disease as well as those with heart failure and
peripheral vascular disease, who are at risk for adverse cardiovascular events. Given
the powerful proinflammatory properties of this enzyme, MPO suggests to be both marker
and mediator of cardiovascular pathology and emerges as both marker and potential
target of treatment.
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PD Dr. med. Stephan Baldus
Universitäres Herzzentrum Hamburg
Abteilung für Kardiologie
Martinistraße 52
20246 Hamburg, Germany
Email: baldus@uke.uni-hamburg.de