PMID- 25027585 OWN - NLM STAT- MEDLINE DCOM- 20150330 LR - 20220311 IS - 1475-2840 (Electronic) IS - 1475-2840 (Linking) VI - 13 DP - 2014 Jul 16 TI - Effects of pitavastatin versus atorvastatin on the peripheral endothelial progenitor cells and vascular endothelial growth factor in high-risk patients: a pilot prospective, double-blind, randomized study. PG - 111 LID - 10.1186/s12933-014-0111-1 [doi] AB - BACKGROUND: Circulating endothelial progenitor cells (EPCs) reflect endothelial repair capacity and may be a significant marker for the clinical outcomes of cardiovascular disease. While some high-dose statin treatments may improve endothelial function, it is not known whether different statins may have similar effects on EPCs.This study aimed to investigate the potential class effects of different statin treatment including pitavastatin and atorvastatin on circulating EPCs in clinical setting. METHODS: A pilot prospective, double-blind, randomized study was conducted to evaluate the ordinary dose of pitavastatin (2 mg daily) or atorvastatin (10 mg daily) treatment for 12 weeks on circulating EPCs in patients with cardiovascular risk such as hypercholesterolemia and type 2 diabetes mellitus (T2DM). Additional in vitro study was conducted to clarify the direct effects of both statins on EPCs from the patients. RESULTS: A total of 26 patients (19 with T2DM) completed the study. While the lipid-lowering effects were similar in both treatments, the counts of circulating CD34+KDR+EPCs were significantly increased (from 0.021 +/- 0.015 to 0.054 +/- 0.044% of gated mononuclear cells, P < 0.05) only by pitavastatin treatment. Besides, plasma asymmetric dimethylarginine level was reduced (from 0.68 +/- 0.10 to 0.53 +/- 0.12 mumol/L, P < 0.05) by atorvastatin, and plasma vascular endothelial growth factor (VEGF) level was increased (from 74.33 +/- 32.26 to 98.65 +/- 46.64 pg/mL, P < 0.05) by pitavastatin. In the in vitro study, while both statins increased endothelial nitric oxide synthase (eNOS) expression, only pitavastatin increased the phosphorylation of eNOS in EPCs. Pitavastatin but not atorvastatin ameliorated the adhesion ability of early EPCs and the migration and tube formation capacities of late EPCs. CONCLUSIONS: While both statins similarly reduced plasma lipids, only pitavastatin increased plasma VEGF level and circulating EPCs in high-risk patients, which is probably related to the differential pleiotropic effects of different statins. TRIAL REGISTRATION: This trial is registered at ClinicalTrials.gov, NCT01386853. FAU - Lin, Liang-Yu AU - Lin LY FAU - Huang, Chin-Chou AU - Huang CC FAU - Chen, Jia-Shiong AU - Chen JS FAU - Wu, Tao-Cheng AU - Wu TC FAU - Leu, Hsin-Bang AU - Leu HB FAU - Huang, Po-Hsun AU - Huang PH FAU - Chang, Ting-Ting AU - Chang TT FAU - Lin, Shing-Jong AU - Lin SJ FAU - Chen, Jaw-Wen AU - Chen JW LA - eng SI - ClinicalTrials.gov/NCT01386853 PT - Comparative Study PT - Journal Article PT - Randomized Controlled Trial PT - Research Support, Non-U.S. Gov't DEP - 20140716 PL - England TA - Cardiovasc Diabetol JT - Cardiovascular diabetology JID - 101147637 RN - 0 (Biomarkers) RN - 0 (Heptanoic Acids) RN - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors) RN - 0 (Pyrroles) RN - 0 (Quinolines) RN - 0 (VEGFA protein, human) RN - 0 (Vascular Endothelial Growth Factor A) RN - A0JWA85V8F (Atorvastatin) RN - M5681Q5F9P (pitavastatin) SB - IM MH - Aged MH - Atorvastatin MH - Biomarkers/blood MH - Diabetes Mellitus, Type 2/blood/drug therapy MH - Double-Blind Method MH - Endothelial Progenitor Cells/drug effects/*metabolism MH - Female MH - Follow-Up Studies MH - Heptanoic Acids/pharmacology/*therapeutic use MH - Humans MH - Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology/*therapeutic use MH - Hypercholesterolemia/blood/drug therapy MH - Male MH - Middle Aged MH - Pilot Projects MH - Prospective Studies MH - Pyrroles/pharmacology/*therapeutic use MH - Quinolines/pharmacology/*therapeutic use MH - Risk Factors MH - Treatment Outcome MH - Vascular Endothelial Growth Factor A/*blood PMC - PMC4223413 EDAT- 2014/07/17 06:00 MHDA- 2015/03/31 06:00 PMCR- 2014/07/16 CRDT- 2014/07/17 06:00 PHST- 2014/04/26 00:00 [received] PHST- 2014/07/07 00:00 [accepted] PHST- 2014/07/17 06:00 [entrez] PHST- 2014/07/17 06:00 [pubmed] PHST- 2015/03/31 06:00 [medline] PHST- 2014/07/16 00:00 [pmc-release] AID - s12933-014-0111-1 [pii] AID - 10.1186/s12933-014-0111-1 [doi] PST - epublish SO - Cardiovasc Diabetol. 2014 Jul 16;13:111. doi: 10.1186/s12933-014-0111-1.