Authors:
M. Kalovoulos, A. Papagianni, D. Kirmizis, D. Daravingas, A. Vainas, A.-M. Belechri, E. Alexopoulos, D. Memmos; Thessaloniki/GR
DOI:
10.1594/ECR03/C-1052
Purpose
Atherosclerotic cardiovascular disease (CVD) is a significant cause of morbidity and mortality for patients with end-stage renal disease(ESRD) [1]. Undoubtedly, ESRD is associated with a higher prevalence of several traditional and uraemia-related risk factors for atherogenesis, such as hypertension, hyperlipidaemia, diabetes mellitus, anaemia and increased oxidative stress. However, the combination of the known risk factors accounts only partly for the particularly increased burden of atherosclerotic disease in haemodialysis (HD) patients, indicating that other factors yet to be defined are also probably triggered in this patient population. Recently, emerging evidence suggests a central contribution of endothelial cell adhesion molecules in the pathogenesis and progression of atherosclerosis through their effects on leukocyte activation, cell migration and smooth-muscle cell proliferation [2]. We have previously demonstrated that the dialysis procedure itself induces a striking increase in soluble endothelial cell adhesion molecules ICAM-1 and VCAM-1 concentrations independently of the type of dialysis membrane used. Moreover, a significant increase of serum ICAM-1 was observed in patients with established CVD such as a history of myocardial infarction, coronary artery bypass, angina pectoris, stroke or peripheral vascular disease [3]. Since no data were available concerning their levels in patients with subclinical atherosclerosis, we undertook an investigation of the probable association of circulating endothelial cell adhesion molecules with atherosclerotic disease as assessed by high-resolution ultrasonography of the common carotid arteries.