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.

Tanshinone IIA attenuates paraquat‑induced acute lung injury by modulating angiotensin‑converting enzyme 2/angiotensin‑(1‑7) in rats

“…MPO activity analysis. MPO is predominantly secreted by neutrophils and can be used to determine neutrophil infiltration as an index of inflammation (20). Left lungs were obtained from rats, and the MPO activity was determined.…”

Brain–Heart Axis and Biomarkers of Cardiac Damage and Dysfunction after Stroke: A Systematic Review and Meta-Analysis

“…Compared with the control group, the level of NT-proBNP in the acute ischemic stroke group was higher (WMD = 1600.92, 95% CI = 607.00-2594. 84, p = 0.002, I 2 = 99%, p-value of heterogeneity <0.00001). Additionally, a significant difference in NT-proBNP was found between patients in the A maximum of two stars can be allotted in this category, one for study controls for the experimental 99 and control groups, the other for a blood collection time of <24 h. A maximum of two stars can be allotted in this category, one for study controls for the experimental 99 and control groups, the other for a blood collection time of <24 h. A maximum of two stars can be allotted in this category, one for study controls for the experimental 99 and control groups, the other for a blood collection time of <24 h. A maximum of two stars can be allotted in this category, one for study controls for the experimental 99 and control groups, the other for a blood collection time of <24 h. A maximum of two stars can be allotted in this category, one for study controls for the experimental and control groups, the other for a blood collection time of <24 h.…”

“…Compared with the control group, the level of NT-proBNP in the acute ischemic stroke group was 114 higher (WMD = 1600.92, 95% CI = 607.00-2594. 84, p = 0.002, I 2 = 99%, p-value of heterogeneity 115 <0.00001). Additionally, a significant difference in NT-proBNP was found between patients in the 116 hemorrhage.…”

Levosimendan as a new force in the treatment of sepsis-induced cardiomyopathy: mechanism and clinical application

“…The results showed that levosimendan inhibits cardiomyocyte cytokine production and downregulates the TNF-α receptor superfamily and Fas/Fas ligand apoptotic signalling pathway. 23,24…”