Current views on the pathophysiology of atherosclerosis

Atherosclerosis and its thrombotic complications are responsible for over one half million deaths annually and countless other complications. The mechanism responsible for the conversion of a stable atherosclerotic lesion to a life-threatening condition is plaque rupture. The risk of plaque rupture is a function of both plaque vulnerability and extrinsic triggers. Atherosclerotic plaques tend to develop in lesion prone areas with the participation of vascular and blood-borne cells, cytokines, lipids and proteins that interact simultaneously and/or sequentially to progress into advanced plaques. Plaque disruption can be prevented by the stabilization of vulnerable plaques and by avoiding or reducing potential trigger mechanisms.