The Role of Atorvastatin on Monocyte Function in Patients With Coronary Artery Disease and Hypercholesterolemia

Coronary Artery Disease, Hypercholesterolemia, Monocyte Function

statin, atorvastatin, hypercholesterolemia, coronary artery disease, monocyte, collateral formation, arteriogenesis, chemotaxis, migration, growth factors, vascular endothelial growth factor A, placenta growth factor 1, hepatocyte growth factor, monocyte chemotactic protein 1

The aim of this study is to determine, whether an intensified atorvastatin therapy can improve monocyte function in patients with coronary artery disease and hypercholesterolemia.

Hypercholesterolemia is one of the most important cardiovascular risk factors that significantly elevates the risk for the development and progression of arteriosclerotic diseases. Statins such as atorvastatin have been shown to reduce atherogenic lipoprotein levels as well as cardiovascular morbidity and mortality in a large number of clinical trials. It is suggested that statins have- apart from their lipid-lowering properties- other pleiotropic effects that are responsible for their anti-atheroslerotic and and cardioprotective potential. Monocytes are crucially involved in the process of arteriogenesis (i.e. the growth of preexisting arterioles). Monocyte chemotaxis can be stimulated with arteriogenic molecules such as vascular endothelial growth factor A (VEGF-A). In previous studies we could demonstrate that the VEGF-A- induced monocyte chemotaxis is severely impaired in hypercholesterolemic patients. This reduced response to VEGF seems to be associated with a decreased ability to form functional collaterals. Therefore we hypothesize that an intensified therapy with atorvastatin 40 mg once a day can significantly improve monocyte function in patients with coronary artery disease and hypercholesterolemia compared to patients who are only treated with a placebo.

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