Healthy endothelium plays a central role in cardiovascular control. Therefore endothelial dysfunction (ED), which is characterized by an imbalance between relaxing and contracting factors, procoagulant and anticoagulant substances, and between proinflammatory and antiinflammatory mediators, may play a particularly significant role in the pathogenesis of atherosclerosis and cardiovascular disease. ED is thought to be an early physiologic event in the development of atherosclerosis, occurring before morphologic changes in the vessel wall can be detected. It is closely related to different risk factors of atherosclerosis, to their intensity and their duration. The involvement of risk factors in ED is also supported by results of intervention studies that showed regression of ED with treatment of risk factors. Further, it was shown that ED is significantly and directly correlated with the occurrence of cardiac events. The common denominator whereby different risk factors cause ED is most probably increased oxidative stress and consequently decreased bioavailability of nitrogen oxide. Endothelial dysfunction promotes atherosclerosis and probably plays an important role in the development of thrombotic complications in late stages of the disease. As ED is a key underlying factor in the atherosclerotic process, markers of endothelial abnormalities have been proposed, but loss of endothelium-dependent vasodilation has became a broadly accepted indicator of endothelial dysfunction. Using these non-invasive tests it is possible to follow the dose-response of harmful effects or risk factors, and the effects of preventive procedures on vessel wall function.