Atherosclerosis and its thrombotic complications are responsible for o
ver one half million deaths annually and countless other complications
. The mechanism responsible for the conversion of a stable atheroscler
otic lesion to a life-threatening condition is plaque rupture. The ris
k of plaque rupture is a function of both plaque vulnerability and ext
rinsic triggers. Atherosclerotic plaques tend to develop in lesion pro
ne areas with the participation of vascular and bloodborne cells, cyto
kines, lipids and proteins that interact simultaneously and/or sequent
ially to progress into advanced plaques. Plaque disruption can be prev
ented by the stabilization of vulnerable plaques and by avoiding or re
ducing potential trigger mechanisms.