Abstract
Percutaneous transluminal angioplasty (PTA) and percutaneous transluminal coronary angioplasty (PTCA) are generally accepted and used as a minimal invasive therapeutic intervention for treatment of symptomatic stenoses of the central, peripheral, and coronary arteries. Clinical success and vessel patencies after PTCA are dependent on the pathology and type of lesion and the anatomic location.1–3 Several mechanisms are responsible for the success after PTA. Recoil, remodeling, and restenosis are factors responsible for reocclusions, but it is not known which factor is most influential. Recoil and remodeling might be prevented or reduced by the use of stents. Many attempts to prevent restenosis have failed.4–12 An important factor in restenosis is neointimal hyperplasia (NIH). As with other vascular interventions the vessel wall becomes traumatized after PTA. This trauma initiates a cascade of reactions in the vessel wall, the mechanism of which is not completely understood. In addition to smooth muscle cell proliferation with migration of cells from media across the internal elastic lamina and formation of an intimal mass of actively proliferating cells,13–18 there seems to be an important role for adventitial responses as well.19–27 Radiation therapy has been used successfully in several benign hyperproliferative diseases to prevent a proliferative response,28–34 so it was conjectured to be beneficial in reducing NIH as well.
Published Version
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