Aim. Carotid atherosclerosis one of the main risk factors for ischemic stroke. Acute thrombosis after atherosclerotic plaque disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. PAI-1 is the most important and most rapidly acting physiological inhibitor of tissue-type (t-PA) and urokinase type (u-PA) plasminogen activators. Active PAI-1 form spontaneously converts to the latent with a half-life of similar to 1 h. Complex formation with vitronectin increases half life of PAI-1 by two- to four-folds. Thus, this inhibitor function of PAI-1 facilitated by Vn that binds the inhibitor and may regulate its activity by the stabilizing the active PAI-1 conformation. In addition, PAI-1/VN complexes may effect vascular structure and function. However, the exact role of these complexes in vascular remodelling are not completely clear. The aim of the present study was determining, correlating and comparing the plasma vitronectin, t-PA and PAI-1 activity levels in asymptomatic and symptomatic patients with carotid artery plaque.