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, thereby treating acute or threatened vessel closure after unsuccessful balloon angioplasty. After 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 unfavorable interaction between stents and unstable or thrombus-laden plaque. Finally, they still induce substantial intimal hyperplasia that may result in restenosis. Future stents 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 unfavorable 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 that 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.