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Ye H., He F., Fei X., Lou Y., Wang S., Yang R., Hu Y., Chen X. High-dose atorvastatin reloading before percutaneous coronary intervention increased circulating endothelial progenitor cells and reduced inflammatory cytokine expression during the perioperative period. J Cardiovasc Pharmacol Ther. 2014. 19(3): 290-295.

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Article

Effect of Different Doses of Atorvastatin Therapy on Endothelial Progenitor Cells and Angiogenic Factors in Patients with Ischemic Heart Disease

1Department of atherosclerosis, Russian Cardiology Research Center, Moscow, Russian Federation

2Department of nuclear diagnostics, Russian Cardiology Research Center, Moscow, Russian Federation

3National Research Center for Preventive Medicine, Moscow, Russian Federation


American Journal of Clinical Medicine Research. 2015, Vol. 3 No. 4, 70-76
DOI: 10.12691/ajcmr-3-4-3
Copyright © 2015 Science and Education Publishing

Cite this paper:
Igor V. Sergienko, Alexey A. Ansheles, Oxana M. Drapkina. Effect of Different Doses of Atorvastatin Therapy on Endothelial Progenitor Cells and Angiogenic Factors in Patients with Ischemic Heart Disease. American Journal of Clinical Medicine Research. 2015; 3(4):70-76. doi: 10.12691/ajcmr-3-4-3.

Correspondence to: Igor  V. Sergienko, Department of atherosclerosis, Russian Cardiology Research Center, Moscow, Russian Federation. Email: igorcardio@mail.ru

Abstract

Aim. The purpose of current research was to assess changes in endothelial progenitor cells (EPC) counts and angiogenic factors levels during atorvastatin therapy in different doses in patients with ischemic heart disease (IHD) as an independent predictor of cardiovascular morbidity and mortality. Methods and Results. The main group included 58 patients with IHD during atorvastatin therapy. EPC quantity (CD34+/CD133+/CD309+ phenotype) was measured by flow cytometry two times – before treatment and 3 months after. Vascular endothelial growth factor (VEGF), C-reactive protein (CRP), monocyte chemoattractant protein-1 (MCP-1), endostatin levels and lipid profile were also measured twice. The control group consisted of 15 healthy volunteers with the same analyzes performed once. Atorvastatin therapy in IHD patients within three months of treatment caused a significant (72% on average) increase of EPC counts (p<0.05). Dependence of EPC gain on statin dose was not reliable (p=0.10), but it was higher when initial EPC counts were low (p=0.01). The therapy showed reliable reduction of VEGF level (by 11%, p<0.01), CRP – by 26% (p<0.01), total cholesterol (TCh) – by 30% (p<0.01), low density lipoprotein (LDL-C) – by 35% (p<0.01), triglycerides (TG) – by 18% (p<0.01), while endostatin, MCP-1 and high density lipoprotein (HDL-C) levels did not change. Correlations between the EPC, TCh and LDL-C changes during therapy were revealed: higher EPC counts gain was associated with higher TCh (p=-0.37, r<0.01) and LDL-C (p=-0.41, r<0.01) levels decrease. Conclusion. We found a significant increase of EPC counts in IHD patients when treated with atorvastatin for 3 months, without statistically reliable difference depending on dosage.

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