ABSTRACT

The importance of inflammation in atherosclerosis, including carotid artery disease, has been increasingly appreciated in recent years. According to the current theory developed by Sir Russell Ross1 and others,2 athero - sclerosis is predominantly an inflammatory condition produced by a ‘response to injury.’ Many different toxic stimuli can cause endothelial injury, with the final result being a cascade of immunologically mediated events: adhesion of monocytes and lymphocytes to the

endothelial surface, migration of these leukocytes beneath the endothelial surface, and subsequent subendothelial localization. Macrophages then take up lipid, forming foam cells, these and other macrophages are activated, and cytokines and growth factors are released. This leads to smooth muscle cell proliferation and plaque formation. The potential causes of the underlying endothelial injury include oxidized low-density lipoprotein (LDL), high shear force as is present in hypertension, homocysteine, toxic constituents of cigarette smoke, and possibly even infections. Inflammation also plays a role in plaque rupture, potentially precipitating a clinical event.2