Clinical trials have provided increasing evidence of the value of lipi
d lowering in preventing clinical coronary events. With the advent of
more potent lipid-regulating agents, a greater degree of cholesterol l
owering - particularly of cholesterol carried in low density lipoprote
ins - is now possible. Trials monitored by angiography or ultrasound h
ave demonstrated slowed progression and even regression of atheroscler
otic lesions in subjects in whom lipid lowering was accomplished by di
et and other lifestyle modifications, drugs, and/or partial ileal bypa
ss surgery, but the changes measured in the vessel lumen or wall are o
ften modest compared with the reduction in clinical events, suggesting
that clinical benefit may be derived from mechanisms other than the a
bsolute decrease in lesion size. Possible mechanisms include lesion st
abilization, improved endothelial function, increased vascular reactiv
ity, and decreased inflammatory response. The identification of risk f
actors besides elevated blood cholesterol level, such as lipoprotein o
xidation, blood triglyceride level and insulin resistance, may provide
additional targets for intervention.