At the end of the 1970s balloon angioplasty emerged as a new hope in the treatment of coronary atherosclerosis.1 A decade later, the implantation of endovascular stents2 did not only reduce the number of acute complications of percutaneous coronary interventions, but also the incidence of restenosis.3 Now, as we begin the new millennium, intravascular radiotherapy promises to lower the restenosis rate further and has been shown to be especially effective in treatment of in-stent restenosis.4

Restenosis develops as a response to injury, mediated by a complex interaction of an inflammatory process, thrombus formation, proliferation and migration of smooth muscle cells (SMCs), expression of growth factors, matrix synthesis, and finally vascular remodelling.5 The antiproliferative effects of ionising radiation, which are widely used in treating various benign and malignant proliferative diseases, are based on the interaction of primary (β radiation) or secondary (γ radiation) electrons with biochemical bonds in cellular DNA,6 and on subsequent changes in gene expression that finally lead to a reduction of cell growth. In cell culture and …