AbstractThe designation of atherosclerosis as a chronic inflammatory process represents an exciting and logical paradigm shift for cardiologists. Monocyte chemoattractant protein‐1 (MCP‐1) plays an important role in the recruitment and activation of monocytes and thus in the development of atherosclerosis. Enhanced MCP‐1 expression has been detected in macrophages, endothelial cells, and vascular smooth muscle cells in the atheromatous plaque. Activation of macrophages by MCP‐1 also appears to be involved in the vulnerability of the plaque. Indeed, circulating MCP‐1 levels are elevated in patients with acute myocardial infarction and in those with unstable angina, but not in patients with stable angina. Production of MCP‐1 and macrophage accumulation are also observed after coronary angioplasty or grafting, indicating that MCP‐1 expression may be related not only to instability of atheromatous plaques, but also to the formation of restenotic lesions. The development of therapeutic drugs for atherosclerosis targeted specially against MCP‐1 may be useful in the prevention of plaque formation and future myocardial infarction.