Intimal hyperplasia is extensively studied in order to improve arterialreconstruction outcome. The mechanisms leading to stenosis or restenosis may vary according to the techniqueused for arterial reconstruction. Lesions are mostly made of an accumulation of smooth muscle cells andfibroblasts, with only sparse inflammatory cells. The accumulated material reduces the graft lumen andultimately induces thrombosis. Intimal hyperplasia with smooth muscle cell and matrix accumulation isthe 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 recentlypublished data. Experiments in the rabbits have shown that the vein wall thickening is mainly regulatedby the tangential wall stress which is applied transversely to the vein wall as a blood pressure. Experimentsin the rat carotid artery balloon injury suggested that heparin could be used as a treatment to preventintimal hyperplasia. Treatments for preventing restenosis after angioplasty or stenoses development inbypasses have been disappointing clinical evaluation suffers from insufficient prospective randomizedstudies. Intimal hyperplasia is the major cause of failure after arterial reconstruction. The biologyof intimal hyperplasia is complex, and treatment disappointing. Some types of hyperplasia may need tobe preserved in order to prevent functional atrophy and aneurysmal dilatation of vein grafts.

Keywords: smooth muscle cells, intimal hyperplasia, vessel injury