Coronary restenosis is the direct result of arterial trauma caused by angioplasty and therefore affects all patients to different degrees. Fracture of the plaque extending to the media is the principal mechanism of increase of the arterial lumen after balloon angioplasty, wall stretching concerning mainly excentric lesions. Atherectomy causes pulverisation of excision of the plaque without fracture. Stents reduce the amount of debris and the torn appearances of the plaque often observed after angioplasty. Four mechanisms are involved in the induction of restenosis: neointimal hyperplasia, proportional to the amount of trauma (damage to the internal elastic layer), related to proliferation of smooth muscle cells migrating from the media to the intima nad stimulated by many growth factors: defective remodelling or chronic elastic recoil, characterised by a reduction of the arterial lumen at the angioplasty site; acute elastic recoil in the first minutes or hours after angioplasty, mainly observed in excentric lesions; thrombosis, whose role is secondary except in certain clinical situations such as unstable angina, angioplasty of saphenous vein grafts or long dissections. The classical theories of restensosis attribute a major role to initial hyperplasia but more recent experimental and clinical data, obtained largely from endocoronary ultrasonography, suggest that defective remodelling may be more important. Although endocoronary stents prevent acute and chronic elastic recoil effectively, they do not prevent restenosis which remains a complex, multifactorial phenomenon.