Related Experiment Video

Updated: Aug 9, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

Levosimendan reduces plasma B-type natriuretic peptide and interleukin 6, and improves central hemodynamics in severe

Stamos Kyrzopoulos1, Stamatis Adamopoulos, John T Parissis

  • 1Second Department of Cardiovascular Medicine and Laboratory of Molecular Immunology and Histocompatibility, Onassis Cardiac Surgery Center, Maroussi, Athens 15122, Greece.

International Journal of Cardiology
|March 18, 2005
PubMed

Insights

Levosimendan treatment significantly reduced NT-proBNP and IL-6 levels in chronic heart failure (CHF) patients. These neurohormonal markers correlate with improved hemodynamics, suggesting their utility in assessing CHF treatment efficacy.

Area of Science:

  • Cardiology
  • Biochemistry
  • Pharmacology

Background:

  • Plasma B-type natriuretic peptide (BNP) and interleukin 6 (IL-6) are key neurohormonal markers in chronic heart failure (CHF) progression.
  • Levosimendan, a calcium sensitizer, demonstrates beneficial effects on CHF hemodynamics and prognosis.

Purpose of the Study:

  • To investigate the relationship between levosimendan-induced hemodynamic improvements and changes in NT-proBNP and IL-6 levels in CHF patients.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) measured NT-proBNP and IL-6 levels in 12 advanced CHF patients.
  • Hemodynamic parameters including pulmonary pressures, vascular resistance, cardiac output, and stroke volume were monitored over 72 hours during levosimendan infusion.

Main Results:

  • NT-proBNP and IL-6 levels significantly decreased within 72 hours of levosimendan treatment (p<0.01 and p<0.05, respectively).
  • Pulmonary wedge and artery pressures also showed significant reductions (p<0.01 and p<0.05).
  • A strong correlation was observed between reduced NT-proBNP levels and decreased pulmonary wedge pressure (r(s)=0.65, p<0.05).

Conclusions:

  • Changes in NT-proBNP and IL-6 levels serve as valuable biochemical markers.
  • These markers are associated with levosimendan-induced improvements in central hemodynamics and clinical status in decompensated advanced CHF.
Abstract

More Related Videos

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing12:45

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure Drugs: &#946;-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...