Abstract

Myeloperoxidase (MPO)1 has been shown to play a role in the pathogenesis of coronary artery disease. It is released from activated neutrophils at sites of vascular damage and has been shown to increase in atherosclerotic plaques before the onset of myocardial injury (1). Elevations in MPO occur independently of C-reactive protein (CRP) and other markers of inflammation, and it has been suggested as a marker of risk in patients who have high as well as low cardiac troponin T concentrations and who present with acute coronary syndrome (2). We recruited 12 apparently healthy individuals, 10 women and 2 men with a mean age of 33 years (range 27–43) for estimation of the biological variation of MPO. None had a history of heart disease or any clinically apparent inflammatory processes. Serum samples were collected between 0800 and 1000 on the same day of the week, weekly for 5 weeks as described by Fraser and Harris (3). Venous blood was collected in plastic serum separator tubes. All samples were centrifuged after clotting and were stored …

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