At an early stage after stroke onset, the vascular endothelium becomes dysfunctional. The basal lamina is degraded by matrix metalloproteinases and cellular-fibronectin is released. The elevation of asymmetric dimethylarginine leads to endothelial NO synthase inhibition and decreased nitric oxide release. In addition, endothelin-1 is released by dysfunctional endothelium leading to vasoconstriction and reduction of blood flow. Thrombosis in vessels leads to the activation of both coagulation (PAI-1) and fibriolytic system (tPA). Increased von Willebrand factor (vWF) corresponds to injured endothelium. Thus, MMPs, c-Fn, ADMA, ET-1, NO, tPA, PAI-1 and vWF are potential biomarker of vascular injury in stroke.