Risk markers that allow improved and individualized assessment of atheroscl
erotic disease risk and response to treatment are needed. Current candidate
markers include cell adhesion molecules, such as intercellular adhesion mo
lecule-1 and E-selectin, and inflammatory markers, such as C-reactive prote
in; advances in genomics and proteomics will suggest additional candidate m
arkers. Noninvasive imaging procedures such as electron-beam computed tomog
raphy and magnetic resonance imaging also show considerable promise for mon
itoring disease status and response to treatment, and ultimately could prov
ide surrogate endpoints for clinical trials of therapeutic interventions.