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

Matti Adam1, Sven Meyer2, Henning Knors3

  • 1Stanford University, Division of Cardiovascular Medicine, Stanford, CA, USA.

Scientific Reports
|April 14, 2015
PubMed

Insights

Levosimendan treatment significantly reduces myeloperoxidase (MPO) release in patients with decompensated heart failure. This finding suggests a novel mechanism involving MPO inhibition that may improve vascular tone and endothelial function.

Area of Science:

  • Cardiology
  • Biochemistry
  • Pharmacology

Background:

  • Decompensated heart failure involves vascular tone dysregulation mediated by myeloperoxidase (MPO) released from neutrophils.
  • Levosimendan is a common treatment for acute decompensated heart failure.

Purpose of the Study:

  • To investigate the effect of levosimendan on MPO levels in patients with acute decompensation of chronic heart failure.
  • To explore the relationship between MPO, neutrophil activity, and blood pressure regulation during levosimendan treatment.

Main Methods:

  • Plasma MPO levels were measured in patients over a one-week course of levosimendan treatment.
  • Ex vivo whole blood assays assessed levosimendan's effect on MPO release after neutrophil stimulation.
  • Multivariate linear regression analyzed the association between MPO, PMN elastase, and blood pressure parameters.

Main Results:

  • Levosimendan treatment led to a significant decrease in plasma MPO levels.
  • Ex vivo, levosimendan inhibited MPO release from stimulated neutrophils.
  • MPO levels correlated with diastolic blood pressure, particularly in heparin-treated patients.

Conclusions:

  • Levosimendan treatment inhibits MPO release by neutrophils in heart failure patients.
  • This MPO inhibition may contribute to improved endothelial function and vascular tone regulation.
  • Endothelial-bound MPO appears to play a role in blood pressure regulation in this context.

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