Abstract
Treatment of decompensated heart failure often includes administration of levosimendan. Myeloperoxidase (MPO) is released during polymorphonuclear neutrophil (PMN) degranulation, and mediates dysregulation of vascular tone in heart failure. We evaluated the effects of levosimendan-treatment on MPO in patients with acute decompensation of chronic heart failure over a one week course. Plasma MPO levels were significantly decreased after levosimendan treatment (from 252.1 ± 31.1 pmol/l at baseline to 215.02 ± 27.96 pmol/l at 6 h, p < 0.05). Ex vivo incubation of whole blood with levosimendan decreased MPO release after PMN-stimulation (8.2 ± 1.4-fold increase at baseline vs. 6.0 ± 1.1-fold increase with levosimendan). MPO levels also significantly correlated with diastolic blood pressure over the time course. In a multivariate linear model, the main contributor to systolic, diastolic and mean blood pressure was level of PMN elastase. MPO contributed only in heparin-treated patients, suggesting a more significant role for endothelial-bound MPO than for circulating MPO or elastase with respect to blood pressure regulation. We here provide the first evidence that levosimendan treatment inhibits MPO release by PMNs in decompensated heart failure patients. This mechanism may regulate endothelial function and vascular tone in heart failure patients.
Highlights
Treatment of decompensated heart failure often includes administration of levosimendan
Endothelial nitric oxide (NO) bioavailability is reduced by active MPO8, and outcomes in Heart failure (HF) patients are adversely affected by decreased endothelial NO bioavailability[10,11]
As we were interested in the association between polymorphonuclear neutrophil (PMN) activation and vascular tone, we evaluated the correlations between systolic, diastolic, and mean blood pressure, and nitrite levels and markers of leukocyte activity as well as inflammation (CRP, interleukin-6) in our patients
Summary
Matti Adam[1], Sven Meyer[2,3], Henning Knors[4], Anna Klinke[5], Ulf K. Myeloperoxidase (MPO) is released during polymorphonuclear neutrophil (PMN) degranulation, and mediates dysregulation of vascular tone in heart failure. We evaluated the effects of levosimendan-treatment on MPO in patients with acute decompensation of chronic heart failure over a one week course. We here provide the first evidence that levosimendan treatment inhibits MPO release by PMNs in decompensated heart failure patients. This mechanism may regulate endothelial function and vascular tone in heart failure patients. The present study assessed the effects of levosimendan on PMN function and activation by analysis of MPO and elastase levels as indicators of neutrophil degranulation in patients with acute heart failure. We analyzed the correlation of PMN activation with blood pressure regulation and vascular tone in these patients
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