Coronary stents were developed to overcome the two main limitations of balloon angioplasty, acute occlusion and long term restenosis. Coronary stents can tack back intimal flaps and seal the dissected vessel wall and thereby treat acute or threatened vessel closure after unsuccessful balloon angioplasty. Following successful balloon angioplasty stents can prevent late vessel remodeling (chronic vessel recoil) by mechanically enforcing the vessel wall and resetting the vessel size resulting in a low incidence of restenosis. All currently available stents are composed of metal and the long-term effects of their implantation in the coronary arteries are still not clear. Because of the metallic surface they are also thrombogenic, therefore rigorous antiplatelet or anticoagulant therapy is theoretically required. Furthermore, they have an imperfect compromise between scaffolding properties and flexibility, resulting in an unfavourable interaction between stents and unstable or thrombus laded plaque. Finally, they still induce substantial intimal hyperplasia which may result in restenosis. Future stent can be made less thrombogenic by modifying the metallic surface, or coating it with an antithrombotic agent or a membrane eluting an antithrombotic drug. The unfavourable interaction with the unstable plaque and the thrombus burden can be overcome by covering the stent with a biological conduit such as a vein, or a biodegradable material which can be endogenous such as fibrin or exogenous such as a polymer. Finally the problem of persisting induction of intimal hyperplasia may be overcome with the use of either a radioactive stent or a stent eluting an antiproliferative drug.