Prognostic Value of Myeloperoxidase in Patients With Chest Pain

The entire process of arterial plaque formation has been linked with inflammation, and extensive infiltration of neutrophils and monocytes is observed in thrombosed plaque in patients with acute coronary disease. One possible means by which leukocytes could influence the stability of plaque is myeloperoxidase, a leukocyte enzyme that is present in elevated amounts in patients with cardiovascular disease. This study examined the possibility that plasma levels of myeloperoxidase might serve as a marker of plaque vulnerability in patients seen in the emergency department with chest pain. The study group included 604 such patients, seen sequentially, whose most frequent final diagnoses were suspected coronary syndrome and myocardial infarction (MI). Control subjects were healthy and had no historic or clinical evidence of coronary artery disease. Enzyme levels were estimated by an enzyme-linked immunosorbent assay. Patients were seen an average of 4 hours after the onset of chest pain. Plasma myeloperoxidase levels were significantly higher in the study group than in control subjects. They correlated weakly with peak levels of troponin T, C-reactive protein, and age, but not with white cell count. Patients having MI within 16 hours before presentation had especially high myeloperoxidase levels, and the incidence of MI increased with increasing quartiles of myeloperoxidase. Baseline levels were higher in patients who later required revascularization or had a major adverse cardiac event in the next 30 days or 6 months. Multivariate logistic regression analyses confirmed that elevated plasma myeloperoxidase independently predicted an increased risk of MI, the need for revascularization, and major coronary events. Baseline levels helped to identify patients at risk even if troponin T was absent. Plasma myeloperoxidase concentration appears to be a marker of vulnerable coronary artery plaque. It helps to identify patients at risk for major adverse cardiac events independently of evidence that myocardial necrosis is present.