ABSTRACT
For years, emphasis on the pathophysiology and management of atherosclerosis had focused on the deposition of cholesterol in the subintimal ground space of the large arteries. Treatment of elevated LDL levels, hypertension, diabetes and smoking had led to a reduction in strokes and heart attacks from the 1960s through the mid-1990s. However, since the mid-1990s the incidence of stroke has been on the rise in the USA1. This trend is believed to be due in part to the aging of the population and suboptimal management of the major stroke risk factors2. However, data are now emerging that demonstrate that atherosclerosis is not just a cholesterol disease but is more accurately characterized as a chronic inflammatory disease3,4. In addition to the aggressive modification of the major conventional risk factors, further understanding of the pathophysiologic mechanisms that are dependent upon the inflammatory and immune pathways in atherosclerosis is necessary to make advances in the reduction of atherothrombotic stroke. Attention is now focused on the inflammatory factors that lead to the development of ‘unstable’ or ‘vulnerable’ plaque, which is believed to be linked to acute coronary syndromes and thrombo-embolic stroke.
