BACKGROUND AND PURPOSE: Activation of endothelial cells is a consequence of cerebral ischemia and leads to the expression of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, which can be released into the blood. This study aimed to define the kinetics of soluble adhesion molecule serum levels after cerebral ischemia and their correlation with the extent of neurological deficits, clinical outcome, and infarct volume as measured on CT scans. Methods-Plasma levels of soluble (s) ICAM-1, sVCAM-1, and sE-selectin were repeatedly determined by ELISA in 38 patients during a period of 14 days after acute cerebral ischemia. RESULTS: Soluble adhesion molecule levels demonstrated considerable variability. Overall, concentrations revealed characteristic and significant changes after completed strokes but not after transient ischemic attacks. In patients with completed stroke (n=26) but not in patients with transient ischemic attacks (n=12), sICAM-1 peaked within 24 hours (P=0.04), sVCAM-1 reached a maximum after 5 days (P=0.02), and sE-selectin levels decreased after 5 days (P=0.002). There was no clear-cut correlation of soluble adhesion molecule levels with infarct volume or clinical disability. The initial increase of sE-selectin levels was higher in more disabled patients (P=0.02). sICAM-1 levels were higher in patients with signs of infection (n=9; P=0.03). CONCLUSIONS: As a result of large interindividual variability influenced by ischemia-independent factors, soluble adhesion molecules are not reliable candidates as surrogate markers in acute cerebral ischemia. The characteristic profile of individual soluble adhesion molecules after completed stroke supports prior hypotheses of their involvement in the pathogenesis of acute cerebral ischemia, but this needs to be clarified in detail.
BACKGROUND AND PURPOSE: Activation of endothelial cells is a consequence of cerebral ischemia and leads to the expression of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, which can be released into the blood. This study aimed to define the kinetics of soluble adhesion molecule serum levels after cerebral ischemia and their correlation with the extent of neurological deficits, clinical outcome, and infarct volume as measured on CT scans. Methods-Plasma levels of soluble (s) ICAM-1, sVCAM-1, and sE-selectin were repeatedly determined by ELISA in 38 patients during a period of 14 days after acute cerebral ischemia. RESULTS: Soluble adhesion molecule levels demonstrated considerable variability. Overall, concentrations revealed characteristic and significant changes after completed strokes but not after transient ischemic attacks. In patients with completed stroke (n=26) but not in patients with transient ischemic attacks (n=12), sICAM-1 peaked within 24 hours (P=0.04), sVCAM-1 reached a maximum after 5 days (P=0.02), and sE-selectin levels decreased after 5 days (P=0.002). There was no clear-cut correlation of soluble adhesion molecule levels with infarct volume or clinical disability. The initial increase of sE-selectin levels was higher in more disabled patients (P=0.02). sICAM-1 levels were higher in patients with signs of infection (n=9; P=0.03). CONCLUSIONS: As a result of large interindividual variability influenced by ischemia-independent factors, soluble adhesion molecules are not reliable candidates as surrogate markers in acute cerebral ischemia. The characteristic profile of individual soluble adhesion molecules after completed stroke supports prior hypotheses of their involvement in the pathogenesis of acute cerebral ischemia, but this needs to be clarified in detail.