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Coronary artery disease
The effect of granulocyte-colony stimulating factor on endothelial function in patients with myocardial infarction
  1. Y-J Kim1,
  2. J-I Shin1,
  3. K-W Park1,
  4. H-Y Lee1,
  5. H-J Kang1,
  6. B-K Koo1,
  7. B-J Park2,
  8. D-W Sohn1,
  9. B-H Oh1,
  10. Y-B Park1,
  11. H-S Kim1
  1. 1
    Department of Internal Medicine, Seoul National University College of Medicine: Innovative Research Institute for Cell Therapy, Seoul National University Hospital, Seoul, Republic of Korea
  2. 2
    Department of Preventive Medicine, Medical Research Collaborating Center, Seoul National University Hospital, Seoul, Republic of Korea
  1. Professor Hyo-Soo Kim, Department of Internal Medicine, Seoul National University College of Medicine, 28 Yongon-dong Chongno-gu, Seoul 110-744, Korea; hyosoo{at}snu.ac.kr

Abstract

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 μg/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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Footnotes

  • See Editorial, p 1301

  • ClinicalTrival.gov Identifier: NCT00291629. Name: Myocardial Regeneration and Angiogenesis in Myocardial Infarction With G-CSF and Intra-Coronary Stem Cell Infusion-3-DES (MAGIC Cell-DES). http://www.clinicaltrial.gov/ct/show/NCT00291629?order = 1

  • Funding: This study was supported by grants from the Innovative Research Institute for Cell Therapy (IRICT) and the Clinical Research Center for Ischemic Heart Disease (0412-CR02-0704-0001).

  • Competing interests: None.

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