SOLUBLE ADHESION MOLECULES REFLECT ENDOTHELIAL-CELL ACTIVATION IN ISCHEMIC STROKE AND IN CAROTID ATHEROSCLEROSIS

Background and Purpose Activation of endothelial cells and platelets p lays an important role in the development of atherosclerosis and throm botic disorders. Soluble adhesion molecules originating from these cel ls can be demonstrated in plasma. We hypothesized that elevated plasma concentrations of soluble P-selectin (sP-selectin), soluble intercell ular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion mol ecule-1 (sVCAM-1), and soluble E-selectin (sE-selectin) can reflect ac tivation of endothelial cells and/or platelets in acute ischemic strok e and in previously symptomatic internal carotid artery stenosis. Meth ods Plasma was sampled from patients within 2 days of acute ischemic s troke (n=28), from patients with a previous (>1 week) transient or per sistent ischemic neurological deficit associated with stenosis of the internal carotid artery (n=34), and from control patients without a hi story of vascular disease (n=34). Concentrations of sP-selectin, sICAM -1, sVCAM-1, and sE-selectin were measured by means of an enzyme-linke d immunosorbent assay. Results Compared with control subjects, sP-sele ctin and sE-selectin were significantly elevated in the acute stage of ischemic stroke (P<.0001 and P=.001, respectively) as well as in prev iously symptomatic carotid stenosis (P<.0001 and P=.0007). sICAM-1 and sVCAM-1 were not increased. Conclusions The elevated levels of sE-sel ectin indicate that endothelial cell activation occurs both in the acu te stage of ischemic stroke and in previously symptomatic carotid athe rosclerosis. Increased sP-selectin concentrations reflect endothelial cell activation. as well but may also be caused by platelet activation .