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Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
Macrophage-modulating cytokines predict adverse outcome in heart failure
P J Hohensinner1, K Rychli, G Zorn
1Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
Thrombosis and Haemostasis
|January 16, 2010
Summary
Macrophage colony-stimulating factor (M-CSF) and monocyte chemoattractant protein 1 (MCP-1) are linked to worse outcomes in advanced heart failure patients. Granulocyte colony-stimulating factor (G-CSF) showed no significant association.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biochemistry
Background:
- Mononuclear cell regulation is crucial in heart failure progression.
- Specific cytokines like G-CSF, MCP-1, and M-CSF may influence heart failure outcomes.
Purpose of the Study:
- To investigate the role of G-CSF, MCP-1, and M-CSF in advanced heart failure.
- To determine if these cytokines predict adverse outcomes like rehospitalization and mortality.
Main Methods:
- Plasma levels of G-CSF, MCP-1, and M-CSF were measured in 351 advanced heart failure patients using ELISAs.
- Patients were followed for a median of 16 months for rehospitalization and all-cause mortality.
- Multivariable Cox regression analysis was used to assess associations with outcomes, adjusting for known risk factors.
Main Results:
- Elevated M-CSF levels were significantly associated with increased risk of the composite endpoint (rehospitalization/mortality) and all-cause mortality.
- High MCP-1 concentrations correlated with a higher risk of all-cause mortality.
- G-CSF levels did not show a significant association with adverse outcomes.
Conclusions:
- M-CSF and MCP-1 are independent predictors of adverse outcomes in advanced heart failure.
- These macrophage-modulating cytokines play a significant pathophysiological role in heart failure progression.
- Targeting these cytokines may offer new therapeutic strategies for heart failure.
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