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International Angiology 2006 December;25(4):414-7


language: English

The effect of fluvastatin on cICAM-1 as a biomarker of endothelial dysfunction in patients with dyslipidemia

Sejda T. 1, Jedlièková V. 1, Svandová E. 2, Poledne R. 3

1 Department of Internal Medicine I, Thomayer University Hospital, Prague, CzechRepublic 2 National Health Institute, Prague, Czech Republic 3 Institute for Clinical and Experimental Medicine, Prague, Czech Republic


Aim. Upregulation of intercellular adhesion molecule-1 (ICAM-1) expression has been suggested to play an important role in the pathogenesis of atherosclerosis. Lipid-lowering therapy with 3-hydroxy-methylglutaryl-coenzyme A reductase inhibitors reduces the incidence of atherosclerosis-related cardiovascular events. The aim of this study was to establish the effect of a 3-month treatment of fluvastatin on circulating (c)ICAM-1 and standard lipid parameters.
Methods. A total of 14 patients (6 men and 8 women), 59.7±11 years old, with mean systolic and diastolic blood pressure 135±16.3 and 81±9.3 mmHg, respectively, fasting plasma cholesterol 6.2±1 mmol/L and plasma triglycerides 2.6±1 mmol/L, took part in the study. The observed parameters were measured before and after 3 months of therapy.
Results. When comparing total cholesterolemia, low-density lipoprotein (LDL) cholesterol, and apolipoprotein B, there were significant decreases after a 3-month treatment. By contrast, no significant difference was observed when we compared the values of triglycerides, high-density lipoprotein (HDL) cholesterol, apolipoprotein A1 and, especially, of cICAM-1. Our results demonstrate the well-known capacity of fluvastatin to lower LDL- and total cholesterol; however, it failed to reduce cICAM after a 3-month treatment.
Conclusions. It can be concluded that a 3-month therapy with fluvastatin does not decrease cICAM-1 levels, despite normalization of cholesterol levels. The implication is that cholesterol may not induce endothelial activation by the initial upregulation of this adhesive molecule.

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