(A) High plasma monocyte chemoattractant protein (MCP)-1 levels may reflect increased synthesis of the chemokine by vascular cells leading to more extensive atherosclerotic disease. Monocyte chemoattractant protein-1 is immobilized on the luminal surface of the endothelium through binding with proteoglycans and mediates mononuclear cell (M) recruitment into the subendothelial space. Monocytes differentiate into macrophages (Ma) and ingest lipids to form foam cells (FCs). Monocyte chemoattractant protein-1 is involved in FC formation, one of the earliest manifestations of atherosclerosis. (B) Enhanced expression of MCP-1 in the vascular wall may contribute to progression of atherosclerotic disease through FC activation, stimulation of smooth muscle cell (SMC) proliferation, and induction of plaque neovascularization (V, neovessel). Also, MCP-1 may induce matrix metalloproteinase (MMP) synthesis, promoting matrix degradation and plaque disruption, and may up-regulate tissue factor (TF) expression exerting procoagulant effects. (C) Prolonged increase of plasma MCP-1 levels after an acute coronary syndrome event may identify patients showing an enhanced inflammatory response in the healing myocardium. The induction of MCP-1 in the infarcted myocardium during the inflammatory phase of healing mediates macrophage recruitment resulting in clearance of the infarct from dead cells and matrix debris, but also seems to play a role in the pathogenesis of adverse remodeling. Timely repression of MCP-1 synthesis is crucial for optimal healing; sustained inflammation results in adverse remodeling of the infarcted ventricle.