The major limitation of the long term success of percutaneous coronary interventions is the development of restenosis, which occurs in 30–50% of patients within six months.1 2 Restenosis is the result of a complex pathophysiological process in the arterial wall in response to balloon dilatation or stent insertion. For many years the hallmark of this response to injury was considered to be the development of intimal hyperplasia resulting from the proliferation and migration of smooth muscle cells from the arterial media.3More recently, it has become clear that this is not the only factor involved. Other key aspects in the development of the restenotic lesion are the extracellular matrix, elastic vessel recoil, and arterial remodelling.4 While our understanding of the processes induced by balloon injury has improved, treatment strategies to limit this have been disappointing in clinical practice.5Stenting, which is now used in up to 80% of all coronary interventional procedures, has almost eliminated problems from elastic recoil and has reduced restenosis rates, but neointimal hyperplasia around stent struts can still lead to in-stent restenosis.6

Intracoronary brachytherapy is one technique that has proved promising in the prevention of restenosis using either catheter based systems for radiation delivery or radioactive stents.7 Concerns have been expressed about late thrombotic occlusion after brachytherapy.8 However, the prolonged use of antiplatelet drugs may control this problem. Brachytherapy is probably the best option for treating restenosis currently available. Nevertheless, it would be attractive to find a method of preventing restenosis after percutaneous intervention that does not involve ionising radiation or prolonged drug treatment. Photodynamic therapy (PDT), which in contrast to brachytherapy uses non-ionising radiation, is emerging as another possible strategy.