Atherosclerosis is now recognized to be an inflammatory disease, and several inflammatory markers have been shown to be associated with both the presence and future risk of symptomatic cardiovascular disease. Cellular adhesion molecules, particularly members of the selectin family and immunoglobulin superfamily, are intimately involved in the recruitment of leucocytes to sites of inflammation, including developing atherosclerotic lesions. Their role in the pathogenesis of atherosclerosis has been clearly demonstrated using knockout mice models. Plasma levels of adhesion molecules, which have been shed from the cell surface, have been associated with the presence of clinical atherosclerotic disease, although published studies differ in their findings. This limited consensus in the literature may be explained either by unrecognized confounding factors, or perhaps by the unpredictable relationship between cell surface expression and activity of cellular adhesion molecules and their shedding into the plasma. While cell surface activity of adhesion molecules appears critical in the development of atherosclerotic lesions, the measurement of plasma levels of soluble adhesion molecules may offer little additional benefit for individual patients in the prediction of the extent of atherosclerotic disease above the assessment of conventional cardiovascular risk factors.