Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure.

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.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Adam M,Meyer S,Knors H,Klinke A,Radunski UK,Rudolph TK,Rudolph V,Spin JM,Tsao PS,Costard-Jäckle A,Baldus S

doi

10.1038/srep09704

subject

Has Abstract

pub_date

2015-04-13 00:00:00

pages

9704

issn

2045-2322

pii

srep09704

journal_volume

5

pub_type

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