Coronary angioplasty imposes injury on the coronary artery during the procedure to achieve adequate revascularization. The arterial response to that injury is critical to both the acute and long-term success or failure of the procedure. As newer technologies become clinically available, it is increasingly evident that a final common response to angioplasty is neointimal formation, and adventitial contraction known as remodelling. Both procedures appear to occur to varying degrees, and similarly appear dependent on the degree of injury. Neointimal hyperplasia is a major factor in the restenosis problem, although others are clearly important. Additional factors include thrombus, intimal and medial dissections and elastic recoil of the arterial wall. The proportion of the restenosis problem caused by each is unclear, but current efforts to solve restenosis centre on limiting neointimal hyperplasia, the primary response to injury of the vessel. This paper will review arterial injury during revascularization in both patients and animal models, with special emphasis of the nature and formation of neointimal hyperplasia.