Recurrence of stenosis occurs in 15% to 45% of patients who have undergone successful percutaneous transluminal coronary angioplasty. Restenosis is believed to represent an accelerated form of atherosclerosis. It is recognized that the human coronary artery response to balloon dilatation reflects complex interactions among mediators of tissue injury and inflammation. Prominent among these are monocytes/macrophages, neutrophils, platelets, smooth muscle cells and endothelial cells. Certain changes suggest the potential for immunologically mediated inflammatory responses. It is therefore considered that restenosis, at least in part, reflects perturbations of cellular mediators of tissue injury leading to accelerated atherosclerosis, and that modulation of these processes by glucocorticoids might be therapeutically beneficial.