Author/Authors :
Gravanis، نويسنده , , Michael B and Waksman، نويسنده , , Ron، نويسنده ,
Abstract :
Although the precise pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA) remains somewhat elusive, our understanding about the reparative phenomena at the site of dilatation has been significantly improved in recent years. Thus, restenosis appears to be the result of migration, proliferation, and excessive matrix formation by smooth muscle cells plus vascular wall remodeling leading to chronic recoil (constriction). Proposed pharmacotherapies to prevent restenosis have been ineffective in humans, in spite of a relative success in certain experimental animals. The rationale for low-dose irradiation (either β or γ) in order to prevent restenosis is based on the known ability of ionizing irradiation to arrest cell division and, therefore, to reduce the number of clonal progenitors in situations like angioplasty.