ABSTRACT
Although extensive research in atherosclerosis has been performed for more than a century, we still fail to understand the mechanisms causing atherogenesis, and believe that the disease has a discontinuous natural course with long asymptomatic stages until all of a sudden, symptoms due to local thrombosis or distal embolism occur. Distinction from normal aging has long been difficult, but seems to be facilitated by new ultrasound (US) investigations [intima-media thickness (IMT) imaging, plaque development, and vascular remodeling] (1). On the other end of the spectrum, compensatory mechanisms may be identified in patients with few symptoms but extensive cerebrovascular occlusive disease; in contrast to what has long been believed, these patients usually do not need any surgical or interventional treatment because of an associated developing collateral capacity of complex networks from large and small arteries.
