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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
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.