A new model for the development of atherosclerosis is emerging (1,2). The development process, called atherogenesis, is now thought to begin with metabolic dysfunction of the endothelial cells that line the innermost portion of the arterial wall. Endothelial dysfunction precedes visible changes in endothelial structure. Dysfunctional endothelium loses its ability to maintain vascular smooth muscle relaxation and instead promotes vasospasm, chemotaxis and inflammation, platelet aggregation, and diminished clot lysis.

Endothelial dysfunction appears to occur di, ffusely, rather than discretely, in affected vessels. Accordingly, local anatomical interventions, such as bypass surgery or angioplasty, can be expected to have only limited success in the treatment of patients with atherosclerotic disease. More definitive treatments must be directed at the risk factors initiating or enhancing atherogenesis. Such interventions are more likely to be medical than surgical or mechanical. With appropriate understanding of the underlying process of atherogenesis and its clinical manifestations, such medical interventions can be carried out within the boundaries of everyday practice.