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Atorvastatin decreases vascular endothelial growth factor in patients with coronary artery disease
Hannes Franz Alber1, Jozef Dulak, Matthias Frick
1Division of Cardiology, Department of Internal Medicine, University of Innsbruck, Innsbruck, Austria.
Insights
Atorvastatin therapy significantly reduced vascular endothelial growth factor (VEGF) levels in patients with coronary artery disease. This suggests a novel beneficial effect of statins beyond lipid lowering.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Vascular Endothelial Growth Factor (VEGF) is implicated in atherosclerotic plaque neovascularization.
- Statins, like atorvastatin, offer atheroprotective benefits beyond lipid reduction.
Purpose of the Study:
- To investigate the effect of atorvastatin on VEGF production in coronary artery disease (CAD) patients.
- To evaluate atorvastatin's direct impact on VEGF synthesis in vitro.
Main Methods:
- Plasma VEGF levels were measured in CAD patients before and after atorvastatin treatment.
- Human coronary artery smooth muscle cells (HCASMC) were exposed to patient plasma and atorvastatin in vitro.
- VEGF concentration was quantified using enzyme-linked immunosorbent assay.
Main Results:
- Atorvastatin therapy reduced plasma VEGF levels in CAD patients (p < 0.05).
- Pre-treatment plasma induced higher VEGF production in HCASMC compared to post-treatment plasma.
- In vitro, atorvastatin decreased both basal and IL-1β-induced VEGF release from HCASMC.
Conclusions:
- Atorvastatin may lower plasma VEGF levels in CAD patients.
- This reduction in VEGF could represent a novel beneficial mechanism of statin therapy.
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 microM). 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-1beta-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.