ABSTRACT

Introduction Percutaneous transluminal coronary angioplasty (PTCA) is an accepted treatment for coronary artery disease.1 However, angiographical restenosis is reported in 30-60% of patients after a successful PTCA.1-3 The main mechanisms of restenosis include acute elastic recoil of the vessel, late constriction of the arterial wall (negative remodeling), and neointimal hyperplasia.4-8 Neointimal hyperplasia develops by migration and proliferation of smooth muscle cells and myofibroblasts after balloon-induced trauma of the arterial wall and by deposition of an extracellular matrix by the smooth muscle cells.7,9-11 The restenosis rate has been reduced to 15-20% by stent implantation,3,12 by preventing elastic recoil and negative remodeling.13

However, the occurrence of restenosis after stent implantation remains unresolved, especially in small vessels and long lesions, where it may take place in more than 30% of the cases.14 It is primarily caused by neointimal hyperplasia, which occurs due to trauma of the arterial wall by the stent struts.6 The treatment of in-stent restenosis with conventional techniques (balloon angioplasty or debulking) is rather disappointing, with restenosis rates of 27-63%, which increase with the number of re-interventions.15-19 The term brachytherapy is used to describe intracavitary or interstitial radiation therapy.20 Recently, the term vascular brachytherapy has been introduced to describe endovascular radiation therapy. Vascular brachytherapy with a radio-