Abstract
Almost two decades after the first percutaneous transluminal coronary angioplasty (PTCA) was performed, restenosis remains the major unmet clinical need in modern interventional cardiology. The identification of clinical candidates has been based, primarily, on data obtained in animal models of restenosis, and has met with frustrating results. Although the failure to identify efficacious agents can, in part, be accounted for by poor experimental design, such a shortfall underlines the paucity of knowledge concerning the precise cellular/molecular mechanisms which drive restenosis. However, recent advances in molecular medicine have facilitated the identification of novel mechanisms involved in the aetiology of restenosis following balloon angioplasty. As a consequence, these discoveries have led to the development of novel therapeutic adjuncts to PTCA which may prove to be of significant clinical utility.