[Investigation of von Willebrand-factor as a marker of endothelial dysfunction in atherosclerotic patients].

Autor: Horváth B; Pécsi Tudományegyetem, Altalános Orvostudományi Kar, I. Belgyógyászati Klinika., Hegedüs D, Szapáry L, Márton Z, Alexy T, Koltai K, Gyevnár Z, Juricskay I, Tóth K, Késmárky G
Jazyk: maďarština
Zdroj: Orvosi hetilap [Orv Hetil] 2003 Dec 14; Vol. 144 (50), pp. 2471-6.
Abstrakt: Objective: To determine von Willebrand-factor activity as the marker of endothelium dysfunction in vascular diseases and to compare it to healthy controls.
Methods: von Willebrand-factor activity was determined by enzyme-linked immunosorbant assay (ELISA) in patients with acute coronary syndromes (29 patients, 67 +/- 13 years), acute stroke (15 pts, 67 +/- 12 years) on admission, 2nd and 6th day; and chronic vascular diseases (56 pts, 67 +/- 10 years) and was compared to the values of healthy controls (23 persons, 36 +/- 12 years).
Results: von Willebrand-factor activity was significantly (p < 0.001) higher in all the measured vascular patients than in the control group. The values of acute patients were significantly (p < 0.05-0.001) higher than those of patients with chronic vascular diseases. In the hospital phase von Willebrand-factor activity in acute patients increased continuously and on day 6 was significantly (p < 0.05-0.01) higher than on admission. von Willebrand-factor activity was significantly (p < 0.05) higher in troponin positive patients with acute coronary syndromes compared to the troponin negative subjects.
Conclusions: von Willebrand-factor was found to be a suitable marker of endothelial dysfunction. The higher von Willebrand-factor activity in patients with vascular diseases compared to the control group can be caused by the endothelial dysfunction and extensive atherosclerosis. The significantly higher von Willebrand-factor activity in acute disorders suggests the more severe endothelium dysfunction and could be related to the development of acute event through increased platelet adhesion and aggregation.
Databáze: MEDLINE