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Background: Myeloperoxidase (MPO) is a biomarker of inflammation and oxidative stress produced by neutrophils, monocytes, and endothelial cells. Concentrations of MPO predict mortality in patients with chronic heart failure. This study sought to investigate the diagnostic accuracy and prognostic value of MPO in patients with acute heart failure (AHF). Methods: We prospectively enrolled 667 patients presenting to the emergency department with dyspnea and observed them for 1 year. MPO and B-type natriuretic peptide (BNP) were measured at presentation. Two independent cardiologists adjudicated final discharge diagnoses. Results: MPO concentrations were similar in patients with AHF (n = 377, median 139 pmol/L) and patients with noncardiac causes of dyspnea (n = 290, median 150 pmol/L, P = 0.26). The diagnostic accuracy of MPO for AHF was limited [area under the ROC curve (AUC) 0.53] and inferior to that of BNP (AUC 0.95, P < 0.001). In patients with AHF, MPO concentrations above the lowest tertile (MPO >99 pmol/L) were associated with significantly increased 1-year mortality (hazard ratio 1.58, P = 0.02). The combination of MPO (≤99 vs >99 pmol/L) and BNP (median of ≤847 vs >847 ng/L) improved the prediction of 1-year mortality (hazard ratio 2.80 for both variables increased vs both low, P < 0.001). After adjustment for cardiovascular risk factors in multivariable Cox proportional hazard analysis, increases in MPO contributed significantly toward the prediction of 1-year mortality (hazard ratio 1.51, P = 0.045). Conclusions: MPO is an independent predictor of 1-year mortality in AHF, is additive to BNP, and could be helpful in identifying patients with a favorable prognosis despite increased BNP concentrations.

Copeptin (the glycosylated 39–amino acid C-terminal fragment of the arginine vasopressin (AVP)1 precursor peptide), when measured with a novel assay (1), has emerged as a promising marker for the early diagnosis of acute myocardial infarction (MI)(2) and a powerful prognostic marker in a variety of settings. The underlying mechanism is thought to be the role of copeptin as a measure of a high individual stress level(3). Interestingly, exercise seems to elicit a significant increase in circulating copeptin concentrations within minutes(4). The aim of our study was to assess the copeptin response to exercise and its determinants. We studied 414 consecutive patients undergoing myocardial perfusion scintigraphy (n = 253) or cardiopulmonary exercise testing (CPET) (n = 161) with upright symptom-limited cycle ergometer tests (increments of 10–25 W/min). In the CPET cohort, arterial samples for blood gas analysis were obtained at rest and peak exercise and were analyzed immediately. In all patients, venous blood was drawn immediately from a catheter in an antecubital vein with the patient in the seated position (rest) before the test and immediately after test termination (peak exercise). These samples were collected in EDTA-containing tubes, placed on ice, and centrifuged at 3000 g . Plasma samples were stored at …