Abstract

Objective: The effects of G-CSF on endothelial function are unknown. Therefore, we investigated the effects of G-CSF on endothelial function.

Methods: Seventy-six 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 randomized into G-CSF group {G-CSF(10 μg/kg/day) injection for 3 days after PCI} or control group. Additionally, 20 healthy volunteers were also enrolled. These subjects were categorized into 5 groups; AMI-control (n=18), AMI-G-CSF (18), OMI-control (20), OMI-G-CSF (20), healthy-G-CSF (20). Baseline flow-mediated dilation (FMD) of brachial artery and serum inflammatory biomarkers were performed at day 1, and repeated at day 4 in all groups. G-CSF was injected for 3 days between day 1 and 4 in AMI-, OMI-, and healthy-G-CSF groups.

Results: In both healthy-G-CSF and OMI-G-CSF group, G-CSF increased serum high sensitivity C-reactive protein (hsCRP) (0.3±0.5 vs. 6.1±3.5 and 5.6±3.8 vs 13.0±7.7 mg/l, baseline vs. post-G-CSF in the healthy and OMI-G-CSF group, 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 of hsCRP. However, in all three groups alike, 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.