The effect of granulocyte-colony stimulating factor on endothelial function in patients with myocardial infarction
1Department of Internal Medicine, Seoul National University College of Medicine: Innovative Research Institute for Cell Therapy, Seoul National University Hospital, Chongno-gu, Seoul, Korea.
Insights
Granulocyte-colony stimulating factor (G-CSF) treatment did not impair endothelial function in patients with myocardial infarction or healthy individuals. G-CSF did increase systemic inflammation markers, but flow-mediated dilation remained unaffected.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Immunology
Background:
- Endothelial dysfunction is a key factor in cardiovascular disease.
- Granulocyte-colony stimulating factor (G-CSF) is used to stimulate white blood cell production.
- The impact of G-CSF on endothelial function is not well understood.
Purpose of the Study:
- To investigate the effects of G-CSF on endothelial function.
- To assess G-CSF's impact in patients with acute myocardial infarction (AMI) and old myocardial infarction (OMI), as well as in healthy subjects.
Main Methods:
- A randomized controlled trial (MAGIC-Cell-3-DES) involving 76 patients (AMI or OMI) post-percutaneous coronary intervention (PCI) and 20 healthy volunteers.
- Participants were assigned to G-CSF treatment or control groups.
- Flow-mediated dilation (FMD) of the brachial artery and serum inflammatory biomarkers (hsCRP) were measured before and after G-CSF administration.
Main Results:
- G-CSF significantly increased high-sensitivity C-reactive protein (hsCRP) levels in healthy and OMI groups, indicating increased systemic inflammation.
- In the AMI group, G-CSF prevented the natural decline of hsCRP during recovery.
- Despite increased inflammation, G-CSF did not significantly alter brachial artery FMD in any group.
Conclusions:
- G-CSF treatment does not acutely impair endothelial function in healthy individuals or patients with myocardial infarction.
- G-CSF administration is associated with increased systemic inflammation.
- These findings suggest a dissociation between systemic inflammation and acute endothelial function changes induced by G-CSF.
Objective:
The effects of granulocyte-colony stimulating factor (G-CSF) on endothelial function are unknown. Therefore, we investigated the effects of G-CSF on endothelial function.
Methods:
76 patients participating in the MAGIC-Cell-3-DES trial were enrolled. These were patients with acute myocardial infarction (AMI) or old MI (OMI) who underwent percutaneous coronary intervention (PCI), and were prospectively randomised into a G-CSF group (G-CSF (10 microg/kg/day) injection for 3 days after PCI) or a control group. Additionally, 20 healthy volunteers were also enrolled. These subjects were categorised into five groups: AMI-control (n = 18), AMI-G-CSF (18), OMI-control (20), OMI-G-CSF (20) and healthy-G-CSF (20). Baseline flow-mediated dilation (FMD) of the brachial artery and serum inflammatory biomarkers were performed on day 1, and repeated on day 4 in all groups. G-CSF was injected for 3 days between days 1 and 4 in the AMI-G-CSF, OMI-G-CSF and healthy-G-CSF groups.
Results:
In both the healthy-G-CSF and OMI-G-CSF groups, G-CSF increased serum high sensitivity C-reactive protein (hsCRP) (0.3 (0.5) mg/l vs 6.1 (3.5) mg/l and 5.6 (3.8) mg/l vs 13.0 (7.7) mg/l, baseline vs post-G-CSF in the healthy and OMI-G-CSF groups, respectively, p<0.001). In the AMI-G-CSF group, G-CSF hindered the decline of hsCRP during the recovery phase, resulting in a relative increase in hsCRP. However, in all three groups, G-CSF did not significantly alter FMD.
Conclusion:
Despite an associated increase in systemic inflammation, G-CSF treatment does not lead to acute impairment of brachial artery endothelial function in either healthy subjects or patients with MI.
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