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Atorvastatin treatment mobilizes endothelial progenitor cells in early stages of ischemic heart failure

Session Poster session 3

Speaker Evangelos Oikonomou

Event : ESC Congress 2014

  • Topic : heart failure
  • Sub-topic : Chronic Heart Failure - Other
  • Session type : Poster Session

Authors : E Oikonomou (Athens,GR), D Tousoulis (Athens,GR), G Siasos (Athens,GR), S Mazaris (Athens,GR), G Hatzis (Athens,GR), E Kokkou (Athens,GR), T Konsola (Athens,GR), K Maniatis (Athens,GR), S Michalea (Athens,GR), C Stefanadis (Athens,GR)

E. Oikonomou1 , D. Tousoulis1 , G. Siasos1 , S. Mazaris1 , G. Hatzis1 , E. Kokkou1 , T. Konsola1 , K. Maniatis1 , S. Michalea1 , C. Stefanadis1 , 1University of Athens Medical School, 1st Cardiology Department, “Hippokration” Hospital - Athens - Greece ,

European Heart Journal ( 2014 ) 35 ( Abstract Supplement ), 512

Purpose: Patients with heart failure (HF) manifest endothelial dysfunction. Circulating endothelial progenitor cells (EPC) contribute to reendothelialization and repair of damaged endothelium in HF. Statins with anti-inflammatory and pleiotropic properties can restore endothelial function in HF. Aim of the present study was to examine the effects of different doses of atorvastatin treatment and clinical status, on mobilization of EPC and endothelial function in patients with ischemic HF.

Methods: We studied the effect of 4 weeks atorvastatin treatment in 23 subjects with ischemic HF at New York Heart Association (NYHA) functional class II and III. The study was carried out on two separate arms, one with atorvastatin 40mg/d and one with atorvastatin 10mg/d (randomized, double-blind, cross-over design). Endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery. Serum levels of tumor necrosis factor alpha (TNFa) were measured by ELISA. The number of circulating CD34(+)/CD133(+)/KDR(+) EPCs were evaluated by flow cytometry.

Results: From the study population, 15 subjects were categorized as NYHA II and 8 subjects as NYHA III. Compared to baseline, treatment with 40 mg/d of atorvastatin improved FMD (3.16±2.98% vs. 6.05±2.45%, p=0.001), TNFa levels [1.08 (0.79-1.35) pg/ml vs. 0.85 (0.68-1.24) pg/ml, p=0.01] and circulating EPC [362 (209-456) cells/ml vs. 175 (143-232) cells/ml, p=0.002]. Similarly, compared to baseline, treatment with atorvastatin 10mg/d also improved FMD (3.24±3.12% vs. 4.20±2.09%, p=0.08), TNFa [1.11 (0.73-1.37)pg/ml vs. 0.99 (0.64-1.12) pg/ml, p=0.01] and EPC [201 (151-309) cells/ml vs. 169 (115-228) cells/ml, p=0.01]. The increase in EPC (p=0.02) and FMD (p=0.001) was greater with the dose of 40 mg/d. Moreover, in the 40 mg/day atorvastatin treatment group we found an association between baseline FMD and increased EPC numbers (r=0.48, p=0.03). Importantly, in the 40 mg/day atorvastatin treatment group, the increase in EPC was higher in NYHA II subjects compared to NYHA III subjects (217±142 cells/ml vs. 60±150 cells/ml, p=0.03).

Conclusions: In ischemic HF subjects, both high and low dose atorvastatin treatment mobilizes EPC and improves endothelial function with a parallel anti-inflammatory effect. This improvement is more pronounced in subjects with better clinical status and better functional endothelium. These findings shed some light on the pleiotropic effects of statins in patients with ischemic HF.

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