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CLINICAL STUDY

Atorvastatin decreases vascular endothelial growth factor in patients with coronary artery disease

Hannes Franz Alber, MD^*, Jozef Dulak, PhD^*, 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
Department of Cell Biochemistry, Institute of Molecular Biology, Jagiellonian University, Krakow, Poland

Manuscript received October 31, 2001; revised manuscript received March 4, 2002, accepted March 15, 2002.

^* Reprint requests and correspondence: Dr. Franz Weidinger, Division of Cardiology, Department of Internal Medicine, University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.

OBJECTIVES: The aim of this study was to test a possible influence of atorvastatin on the production of vascular endothelial growth factor (VEGF) in patients with coronary artery disease (CAD) and in vitro.

BACKGROUND: Vascular endothelial growth factor is suggested to be involved in the growth of atherosclerotic plaque by inducing its neovascularization. Hepatic hydroxymethyl glutaryl-coenzyme A reductase inhibitors (statins) are known to have atheroprotective effects beyond lipid lowering.

METHODS: Blood was collected from 14 male hypercholesterolemic patients with angiographically confirmed CAD at baseline and after two months of atorvastatin therapy (20 mg/d) and from eight male control patients. In an ex vivo assay, human coronary artery smooth muscle cells (HCASMC) were incubated with the patient plasma collected before and after atorvastatin therapy. To test the direct effect of atorvastatin on VEGF synthesis in vitro, HCASMC were treated with atorvastatin (1, 3 and 10 µM). The VEGF concentration was measured by enzyme-linked immunosorbent assay.

RESULTS: Atorvastatin therapy reduced VEGF plasma levels in CAD patients (from 31.1 ± 6.1 to 19.0 ± 3.6 pg/ml; p < 0.05). The VEGF plasma concentration tended to be higher in CAD patients before treatment compared to control patients (31.1 ± 6.1 vs. 23.4 ± 3.6 pg/ml; p = NS). Plasma collected before therapy induced significantly more VEGF in HCASMC compared to the plasma collected after treatment and compared to control cells. In vitro, atorvastatin decreased both the basal and the interleukin-1ß-induced VEGF release in HCASMC.

CONCLUSIONS: These data suggest that atorvastatin may lower the plasma level of VEGF in CAD patients, which could represent a novel beneficial effect of this and perhaps other statins.

Abbreviations and Acronyms   CAD   coronary artery disease   DMSO   dimethyl sulfoxide   EDTA   ethylenediamine-tetraacetic acid   ELISA   enzyme-linked immunosorbent assay   FCS   fetal calf serum   HCASMC   human coronary artery smooth muscle cells   IL   interleukin   LDH   lactate dehydrogenase   LDL   low-density lipoprotein   VEGF   vascular endothelial growth factor

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