The clinical ischaemic events resulting from progressive atherosclerosis include angina pectoris, transient ischemic brain attacks, and intermittent claudication, which cause significant morbidity but are not in themselves life threatening. Potentially fatal myocardial infarctions and strokes are precipitated by acute atherosclerotic plaque instability, either surface erosion or rupture of the fibrous cap. There is an urgent need to identify the genes that mediate plaque instability in humans, to design diagnostic tests to identify high-risk individuals and develop drugs to decrease risk of rupture. Determining differential gene expression in stable and unstable plaques, in association with animal models of atherosclerosis, will allow identification of novel genes involved in plaque instability.

Atherosclerosis has been identified as an arterial immuno-inflammatory disease, and its severe clinical manifestations, including sudden death, myocardial infarction and stroke, are mainly the consequences of atherosclerotic plaque rupture or erosion, which trigger thrombus formation leading to the vessel lumen occlusion.