Abstract

Purpose: Previous studies have demonstrated that stem cell mobilization by granulocyte-colony stimulating factor (G-CSF) attenuates the endothelial dysfunction in mechanically disrupted animal artery models. However, some clinical studies have shown increased neointimal hyperplasia in patients who underwent bare metal stent implantation. Furthermore, the effect of stem cell mobilization on non-culprit plaques is unknown. The purpose of this study was to evaluate the effects of stem cell mobilization by G-CSF on non-culprit coronary plaques after sirolimus-eluting stent (SES) implantation. Methods: This double-blinded randomized placebo-control study (primarily designed to evaluate the effect of stem cell mobilization by G-CSF on endothelial function after SES implantation) assigned patients to the G-CSF group (n=50) or the placebo group (n=50). After successful SES implantation, the patients received subcutaneous injection of G-CSF (300 mg daily) or saline for 5 days. Follow-up angiography and intravascular ultrasound (IVUS) was performed 9 months after SES implantation. Plaque volume was measured by IVUS at non-culprit segments which were defined as more than 5mm proximal or distal from the stent. Percent change in plaque volume (ΔPV) of non-culprit segments between post-procedure and follow-up was evaluated. Results: Plasma CD34+ cell level did not differ between the 2 groups at baseline (0.94±0.55 vs. 0.93±0.68/μL, p = 0.96). It significantly increased after G-CSF injection (0.94±0.55 vs. 18.39±13.55/μL, p <0.001) but did not in the placebo group (0.93±0.68/μL vs. 1.35±2.36/μL, p = 0.22). No death or myocardial infarction was observed during follow-up. Follow-up IVUS was available in 39 G-CSF patients (78%) and 43 placebo patients (86%) (p = 0.30). There was no significant difference in ΔPV between both groups at proximal (-11.0±16.4% vs. -14.7±9.8%, p = 0.35) and distal (-5.1±28.6% vs. -4.9±17.3%, p = 0.97) non-culprit segments. Conclusion: Stem cell mobilization by G-CSF does not increase plaque volume at non-culprit coronary plaques after SES implantation.

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