Secondary prevention with fluvastatin decreases levels of adhesion molecules, neopterin and C-reactive protein

• Published in: European journal of internal medicine 2001-12, Vol.12 (6), p.503-509
• Main Authors: van Haelst, P.L, van Doormaal, J.J, May, J.F, Gans, R.O.B, Crijns, H.J.G.M, Cohen Tervaert, J.W
• Format: Article
• Language: English
• Subjects: Adhesion molecules; Atherosclerosis; Endothelial dysfunction; HMG-CoA reductase inhibitor; Hypercholesterolaemia; Neopterin
• ISSN: 0953-6205; 1879-0828
• DOI: 10.1016/S0953-6205(01)00172-8

Background: Treatment of hypercholesterolaemia with HMG-CoA reductase inhibitors results in an earlier reduction of morbidity and mortality than expected from trials using conventional cholesterol-lowering therapies. Possible explanations for this effect include stimulation of angiogenesis, improvement of endothelial function, plaque stabilisation, inhibition of coagulation and/or thrombocyte aggregation and inhibition of the inflammatory response associated with atherosclerosis. Methods: We investigated whether statins exert their effects by inhibition of endothelial activation, inflammation and/or monocyte/macrophage activation by measuring plasma levels of soluble cell adhesion molecules, neopterin and C-reactive protein upon treatment with fluvastatin for a period of 12 months in patients with established atherosclerosis and hypercholesterolaemia. Results: Blood samples were taken at baseline and at 3 and 12 months after starting treatment with fluvastatin 80 mg daily. Upon treatment, a reduction of s-ICAM-1 (956.3±123.6 vs. 745.4±127.4 vs. 674.9±70.8 ng/ml, P