Inflammation is a crucial feature of atherosclerosis and a potential target to reduce cardiovascular events.

Contrary to popular opinion, atherosclerosis is not a disease unique to modern civilization. In fact, atherosclerotic lesions have been found in the arteries of mummies dating back to 1,500 B.C., and yet our understanding of this complex process is still evolving. A fusion of basic science advances and clinical research findings has radically altered our traditional concepts about the pathogenesis and treatment of the clinical complications of atherosclerosis. Most physicians previously regarded the artery as a being merely a blood conduit that became encrusted with lipid detritus as part of the aging process. Modern-day treatment of atherosclerosis has arisen primarily from an understanding of the epidemiology of the disease rather than its pathophysiology, in that risk factors have traditionally been targeted. Our concepts of atherogenesis have evolved from vague ideas of inevitable degeneration to a much better defined scenario of molecular and cellular events. As we enhance our understanding of its fundamental mechanism, we can begin to approach atherogenesis as a modifiable rather than ineluctable process. Indeed, as we recognize now that inflammation plays a pivotal role in the process of atherosclerosis, it is noteworthy to evaluate the effect of modern therapies on this facet of the disease.