Intimal hyperplasia is extensively studied in order to improve arterial reconstruction outcome. The mechanisms leading to stenosis or restenosis may vary according to the technique used for arterial reconstruction. Lesions are mostly made of an accumulation of smooth muscle cells and fibroblasts, with only sparse inflammatory cells. The accumulated material reduces the graft lumen and ultimately induces thrombosis. Intimal hyperplasia with smooth muscle cell and matrix accumulation is the prominent feature in all these situations with evidences of intense cell proliferation and cell death. The purpose of this review is to present the biology of intimal hyperplastic response based on the recently published data. Experiments in the rabbits have shown that the vein wall thickening is mainly regulated by the tangential wall stress which is applied transversely to the vein wall as a blood pressure. Experiments in the rat carotid artery balloon injury suggested that heparin could be used as a treatment to prevent intimal hyperplasia. Treatments for preventing restenosis after angioplasty or stenoses development in bypasses have been disappointing clinical evaluation suffers from insufficient prospective randomized studies. Intimal hyperplasia is the major cause of failure after arterial reconstruction. The biology of intimal hyperplasia is complex, and treatment disappointing. Some types of hyperplasia may need to be preserved in order to prevent functional atrophy and aneurysmal dilatation of vein grafts.