ADHESION MOLECULE (ICAM-1) SERUM LEVELS ARE RELATED TO SPONTANEOUS RECANALIZATION IN HUMAN ISCHEMIC STROKE.
Background: There is active migration of leukocytes into the brains of patients with cerebral infarctions directed by several classes of cell surface glycoproteins. Among the most studied adhesion molecules is ICAM-1 (intercellular adhesion molecule-1) which is located on the endothelial surface. As the extent of the infarction and timing of recanalization largely vary between patients these may be some of the reasons for the differences found in the soluble adhesion molecule field in previous human studies. Transcranial Doppler (TCD) offers a continous means of monitoring vessel patency, therefore we have chosen this tool to correlate the development of adhesion molecules mediated injury with the recanalization after middle cerebral artery stroke Objectives: To study adhesion molecules temporal profile in the acute phase of an homogeneus sample of stroke patients. To correlate adhesion molecule levels with the time-to-spontaneous-recanalization. Methods: From all consecutive stroke patients attended during a year period we selected and prospectively studied those presenting as a cardioembolic stroke involving the MCA territory. In 45 patients, serum levels of soluble ICAM-1 were repeatedly determined by ELISA in the acute phase. Serial TCD studies were performed to determine the time course of spontaneous recanalization, at study entry and at 12, 24 and 48 hours of the symptoms onset, when the blood sample for adhesion molecules determination was obtained. Results: ICAM-1 levels peaked at baseline determination (414,44 ng/ml) and decreased by the following determinations (12h=401,25 ng/ml; 24h=392,08 ng/ml; 48h=379,34 ng/ml). ICAM-1 levels at 12h of stroke onset were closely related with the MCA recanalization (p=0,032). Low ICAM-1 levels at 12h (356,81 ng/ml) are associated with the finding of a patent MCA at the 48h TCD, conversely high ICAM-1 levels (459,97 ng/ml) are associated with a persistent MCA occlussion. Conclusions: Patients who develop postischemic adhesion molecules upregulation are less prone to spontaneous recanalization. Antiadhesion therapies could facilitate reperfusion strategies.