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Updated: Apr 19, 2026

Isolation of Endothelial Progenitor Cells from Human Umbilical Cord Blood
Published on: September 14, 2017
Atorvastatin treatment improves endothelial function through endothelial progenitor cells mobilization in ischemic
Evangelos Oikonomou1, Gerasimos Siasos2, Marina Zaromitidou1
11st Cardiology Department, University of Athens Medical School, "Hippokration" Hospital, Athens, Greece.
Insights
Atorvastatin treatment improved endothelial function and increased endothelial progenitor cells (EPCs) in heart failure patients. Monitoring EPC status may help personalize atorvastatin therapy for heart failure.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Endothelial dysfunction is a key prognostic indicator in heart failure (HF).
- Statins, including atorvastatin, offer benefits beyond lipid reduction, particularly in atherosclerotic conditions.
- Understanding atorvastatin's impact on endothelial function and progenitor cells in HF is crucial for treatment optimization.
Purpose of the Study:
- To investigate the effects of low and intermediate doses of atorvastatin on endothelial function.
- To assess the impact of atorvastatin on the mobilization of bone marrow-derived endothelial progenitor cells (EPCs).
- To evaluate changes in inflammatory status in heart failure patients treated with atorvastatin.
Main Methods:
- A randomized, double-blind, cross-over study involving 26 ischemic heart failure patients.
- Administration of atorvastatin at 40 mg/day and 10 mg/day for 4 weeks each.
- Evaluation of circulating CD34(+)/CD133(+)/KDR(+) EPCs via flow cytometry, endothelial function by flow-mediated dilation (FMD), and serum TNF-α levels by ELISA.
Main Results:
- Both 40 mg/day and 10 mg/day atorvastatin significantly increased circulating EPCs and reduced TNF-α levels compared to baseline.
- Atorvastatin treatment significantly improved flow-mediated dilation (FMD) at the 40 mg/day dose.
- A greater increase in EPCs was observed in NYHA class II patients compared to NYHA class III patients with 40 mg/day atorvastatin.
Conclusions:
- Atorvastatin treatment effectively restores endothelial function through enhanced EPC mobilization in ischemic heart failure.
- The findings suggest that monitoring EPC status can aid in individualizing atorvastatin treatment strategies for HF patients.
- Atorvastatin demonstrates pleiotropic effects beneficial for cardiovascular health in HF patients.
Objective:
Endothelial function is an independent predictor of prognosis in heart failure (HF) subjects. Statins, beyond their lipid lowering role, exert beneficial effect in patients with atherosclerosis. In the present study we examined the impact of low and intermediate dose atorvastatin treatment on endothelial function, bone marrow-derived endothelial progenitor cells (EPC) mobilization and inflammatory status according to HF patient status.
Methods:
We studied the effect of 4 weeks administration of atorvastatin in 26 patients with ischemic HF. The study was carried out on two separate arms, one with atorvastatin 40 mg/d and one with atorvastatin 10 mg/d (randomized, double-blind, cross-over design). The number of circulating CD34(+)/CD133(+)/KDR(+) EPCs was evaluated by flow cytometry. Endothelial function was evaluated by flow mediated dilation (FMD) in the brachial artery. Serum levels of tumor necrosis factor alpha (TNF-α) were measured by ELISA.
Results:
Treatment with atorvastatin 40 mg/d significantly increased circulating EPC (p = 0.002), FMD (p = 0.001) and reduced TNF-α (p = 0.01) compared to baseline. Similarly, treatment with atorvastatin 10 mg/day increased circulating EPC (p = 0.01), FMD (p = 0.08) and reduced TNF-α (p = 0.01) compared to baseline. Interestingly, with 40 mg/day atorvastatin treatment the increase in EPC was higher in subjects categorized as NYHA class II compared to subjects categorized as NYHA class III (p = 0.03).
Conclusions:
Our results confirmed the distinct impact of atorvastatin treatment on the restoration of endothelial function due to EPC mobilization in ischemic HF subjects. Moreover, these findings provide the potential clinical significance of EPC status monitoring to individualize treatment in HF subjects.
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