ABSTRACT
The vascular endothelium promotes inflammation through the up-regulation of inflammatory leukocyte-endothelial cell adhesion molecules such as intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1] and E-selectin. These molecules bind to circulating leucocytes and facilitate their migration into the Central Nervous system CNS. In the CNS, these cells produce a number of cytotoxic molecules that may facilitate cell death and increase the infarct volume. To define the extent of expression of VCAM-1 in correlation to the clinical disability and outcome in stroke patients. Complete lipid profile, fibrinogen assay, lipoprotein [a] and FIM were determined in 25 recent stroke patients at the time of admission and compared with 15 matched apparently healthy control subjects. The difference between the mean total cholesterol [TC] level of patients and controls was not significant. However, high density lipoprotein [HDL] was significantly lower in patients as compared to controls but low density lipoprotein LDL was significantly higher. The concentration of Lp [a] and fibrinogen level, were significantly higher in the patients' group than controls. The concentration of VCAM-1 was significantly higher in stroke patients as compared to controls. Multiple regression analysis was performed to assign the predictors for functional independence measures [FIM] as a clinical outcome for the functional disability. The independent parameters were the duration of stroke as well as the laboratory tests [lipid profile, Lp [a], fibrinogen and VCAM-1]. The duration of stroke and VCAM-1 level negatively correlated with FIM, meaning that patients with high VCAM-1 level demonstrated more functional disability as manifested by low FIM score. The most sensitive parameters that can predict FIM were the duration of stroke and VCAM-1 level. Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies in an attempt to reduce leukocyte-induced damage in stroke