Akademik Veri Yönetim Sistemi
NUKLEARMEDIZIN-NUCLEAR MEDICINE, cilt.49, sa.6, ss.209-215, 2010 (SCI-Expanded)
Aim Myocardial perfusion scintigraphy (MPS) is one of the widely used tools to follow developing radiation induced heart disease (RIHD) But the clinical significance of MPS defects has not been fully understood We have investigated the biodistribution alterations related to perfusion defects following radiotherapy (RI) and showed coexisting morphologic changes Animals, methods A total of 18 Wistar rats were divided into three groups (1 con trol and 2 irradiated groups) A single cardiac 20 Gy radiation dose was used to induce long term cardiac defects Biodistribution studies with technetium ((99m)Tc) sestamibi and histo logical evaluations were performed 4 and 6 months all er irradiation The percent radio activity (%ID/g) was calculated for each heart For determination of the myocardial damage positive apoptotic cardiomyocytes, myocardial cell degeneration, myocardial fibrosis vascular damage and ultrastructural structures were evaluated Results Six months after treatment, a significant drop of myocardial uptake was observed (p <0 05) Irradiation induced apoptosi, rose within the first 4 months after radiation treatment and were stayed elevated until the end of the observation period (p < 0 05) Also the iiradiation has induced myocardial degeneration perivascular and interstitial fibrosis in the heart at the end of six and four months (p <0 01) The severity and extent of myocardial injury has became more evident at the end of six month (p < 0 05) At ultrastructural level prominent changes have been observed in the capillary endothelial and myocardial cells Conclusion Our findings suggest that the reduced rest myocardial per fusion occuring months after the radiation indicates a serious myocard tissue damage which is characterized by myocardial degeneration and fibrosis