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J Am Coll Cardiol, 2002; 39:1951-1955
© 2002 by the American College of Cardiology Foundation
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Atorvastatin decreases vascular endothelial growth factor in patients with coronary artery disease

Hannes Franz Alber, MD*, Jozef Dulak, PhD*{dagger}, Matthias Frick, MD*, Wolfgang Dichtl, MD*, Severin Paul Schwarzacher, MD, FACC*, Otmar Pachinger, MD* and Franz Weidinger, MD*,*

* Division of Cardiology, Department of Internal Medicine, University of Innsbruck, Innsbruck, Austria
{dagger} Department of Cell Biochemistry, Institute of Molecular Biology, Jagiellonian University, Krakow, Poland



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Figure 1 The effect of atorvastatin therapy on vascular endothelial growth factor (VEGF) plasma levels. Two months of atorvastatin therapy (20 mg/d) decreased VEGF plasma levels (pg/ml) in patients with coronary artery disease (CAD) (white bars, *p < 0.05). No significant difference in VEGF plasma concentration between control patients (black bar) and CAD patients after treatment with atorvastatin could be observed. The VEGF concentrations in CAD patients tended to be higher compared to those in control patients (p = NS).

 


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Figure 2 The effect of patient plasma collected before and after therapy with atorvastatin on vascular endothelial growth factor (VEGF) synthesis by human coronary artery smooth muscle cells (HCASMC). The VEGF synthesis in HCASMC (in % of untreated cells, black bar) incubated with the plasma of patients with coronary artery disease (white bars) collected before atorvastatin therapy was increased (*p < 0.003 vs. untreated cells). The plasma collected after atorvastatin treatment reversed this stimulatory effect (#p < 0.03 vs. the plasma collected before therapy).

 


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Figure 3 The effect of atorvastatin on vascular endothelial growth factor (VEGF) synthesis by human coronary artery smooth muscle cells (HCASMC) in vitro. The VEGF synthesis in HCASMC (in % of untreated cells). Atorvastatin (1, 3 and 10 µmol/l) decreased basal (*p < 0.003 vs. untreated cells) VEGF production in HCASMC. Interleukin (IL)-1ß (10 ng/ml) induced VEGF synthesis (§p < 0.003 vs. untreated cells) in these cells. Incubation of IL-1ß-treated HCASMC with atorvastatin again decreased the VEGF production (#p < 0.0001 vs. IL-1ß-treated cells).

 




 
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