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

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Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure. / Adam, Matti; Meyer, Sven; Knors, Henning; Klinke, Anna; Radunski, Ulf K; Rudolph, Tanja K; Rudolph, Volker; Spin, Joshua M; Tsao, Philip S; Costard-Jäckle, Angelika; Baldus, Stephan.

In: SCI REP-UK, Vol. 5, 13.04.2015, p. 9704.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Adam, M, Meyer, S, Knors, H, Klinke, A, Radunski, UK, Rudolph, TK, Rudolph, V, Spin, JM, Tsao, PS, Costard-Jäckle, A & Baldus, S 2015, 'Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure', SCI REP-UK, vol. 5, pp. 9704. https://doi.org/10.1038/srep09704

APA

Adam, M., Meyer, S., Knors, H., Klinke, A., Radunski, U. K., Rudolph, T. K., Rudolph, V., Spin, J. M., Tsao, P. S., Costard-Jäckle, A., & Baldus, S. (2015). Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure. SCI REP-UK, 5, 9704. https://doi.org/10.1038/srep09704

Vancouver

Adam M, Meyer S, Knors H, Klinke A, Radunski UK, Rudolph TK et al. Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure. SCI REP-UK. 2015 Apr 13;5:9704. https://doi.org/10.1038/srep09704

Bibtex

@article{b9ba8cc174434842b480d0abb718fd84,
title = "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. ",
keywords = "Anti-Inflammatory Agents/pharmacology, Biomarkers, Blood Pressure/drug effects, Cardiotonic Agents/pharmacology, Cell Degranulation/drug effects, Female, Heart Failure/diagnosis, Humans, Hydrazones/pharmacology, Inflammation/metabolism, Leukocytes/drug effects, Male, Middle Aged, Neutrophils/drug effects, Nitric Oxide/metabolism, Peroxidase/metabolism, Pyridazines/pharmacology, Severity of Illness Index, Simendan, Time Factors",
author = "Matti Adam and Sven Meyer and Henning Knors and Anna Klinke and Radunski, {Ulf K} and Rudolph, {Tanja K} and Volker Rudolph and Spin, {Joshua M} and Tsao, {Philip S} and Angelika Costard-J{\"a}ckle and Stephan Baldus",
year = "2015",
month = apr,
day = "13",
doi = "10.1038/srep09704",
language = "English",
volume = "5",
pages = "9704",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Levosimendan displays anti-inflammatory effects and decreases MPO bioavailability in patients with severe heart failure

AU - Adam, Matti

AU - Meyer, Sven

AU - Knors, Henning

AU - Klinke, Anna

AU - Radunski, Ulf K

AU - Rudolph, Tanja K

AU - Rudolph, Volker

AU - Spin, Joshua M

AU - Tsao, Philip S

AU - Costard-Jäckle, Angelika

AU - Baldus, Stephan

PY - 2015/4/13

Y1 - 2015/4/13

N2 - 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.

AB - 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.

KW - Anti-Inflammatory Agents/pharmacology

KW - Biomarkers

KW - Blood Pressure/drug effects

KW - Cardiotonic Agents/pharmacology

KW - Cell Degranulation/drug effects

KW - Female

KW - Heart Failure/diagnosis

KW - Humans

KW - Hydrazones/pharmacology

KW - Inflammation/metabolism

KW - Leukocytes/drug effects

KW - Male

KW - Middle Aged

KW - Neutrophils/drug effects

KW - Nitric Oxide/metabolism

KW - Peroxidase/metabolism

KW - Pyridazines/pharmacology

KW - Severity of Illness Index

KW - Simendan

KW - Time Factors

U2 - 10.1038/srep09704

DO - 10.1038/srep09704

M3 - SCORING: Journal article

C2 - 25867530

VL - 5

SP - 9704

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

ER -