The in vivo detection of early atherosclerosis remains a problem. First, atherogenesis is a process with an insidious onset and course. Once clinical signs and symptoms have developed the lesion usually is in an advanced stage. Second, the detection of early atherosclerotic lesions creates the problem of distinguishing between almost natural, age-related intimal changes and intimal thickening as a precursor lesion of atherosclerosis. The hallmark of atherosclerosis is the abnormal deposition of lipids within the intima. This process is accompanied by a cellular response, composed of macrophages, lymphocytes and proliferating vascular smooth muscle cells. An increasing quantity of collagen and elastin fibers eventually will replace the cellular constituents. In other words, a changing histological picture with respect to component make up in time. Third, an adequate interpretation of intimal thickening may be complicated further by tissue characteristics of the arterial media. The elastin units of an elastic type artery produce an echo-dense image, whereas a muscular media is hypoechoic. All in all it seems fair to state that ultrasound imaging techniques, at least for the time being, will be inadequate to distinguish between 'early' atherosclerotic lesions and intimal thickenings which will not necessarily progress to the full blown lesion.