ABSTRACT
Radiotherapy as one of the four pillars of cancer therapy plays a critical role in the multimodal treatment of thoracic cancers. Due to significant improvements in overall cancer survival, radiotherapy-induced heart disease (RIHD) has become an increasingly recognized adverse reaction which contributes to major radiation-associated toxicities including non-malignant death. This is especially relevant for patients suffering from diseases with excellent prognosis such as breast cancer or Hodgkin's lymphoma, since RIHD may occur decades after radiotherapy. Preclinical studies have enriched our knowledge of many potential mechanisms by which thoracic radiotherapy induces heart injury. Epidemiological findings in humans reveal that irradiation might increase the risk of cardiac disease at even lower doses than previously assumed. Recent preclinical studies have identified non-invasive methods for evaluation of RIHD. Furthermore, potential options preventing or at least attenuating RIHD have been developed. Ongoing research may enrich our limited knowledge about biological mechanisms of RIHD, identify non-invasive early detection biomarkers and investigate potential treatment options that might attenuate or prevent these unwanted side effects. Here, we present a comprehensive review about the published literature regarding clinical manifestation and pathological alterations in RIHD. Biological mechanisms and treatment options are outlined, and challenges in RIHD treatment are summarized.
ABSTRACT
At present,the heart has become an important organ at risk during radiotherapy for thoracic,mediastinal and breast carcinoma.Heart is relatively sensitive to radiation because of its anatomical location and structure.Long-term survival of patients have been affected by cardiac adverse effect postradiotherapy.In this paper,the progress of clinical manifestations,risk factors,screening methods,prevention and treatment of radiation-induced cardiac damage were reviewed as follows.
ABSTRACT
Objective To establish and investigate C57 BL/6 mice model of radiation induced heart injury and ser-um marker. Methods Twenty eight female C57BL/6 mice were randomly divided into 3 groups:normal group (n=4 ) , 18 Gy radiation therapy group ( n=12 ) , 25 Gy radiation therapy group ( n=12 ) . The mice were weighed every week. Respectively, 0, 8 and 16 weeks after irradiation, the pathological changes of myocardial tissue were observed by hemetoxylin-eosin( HE) staining and made pathological score. Inferior vena cava blood was collected to take cardiac troponin I ( cTnI) test. Results Compared with the normal group,the weight of radiation group went down first then went up slowly. The myocardial tissue from mice had obvious histopathological changes. Acute in-flammation was the main change in the early days. At the late stage, progressive fibrosis was the main characteris-tic. With the increase of the dose, the inflammatory reaction and fibrosis degree had aggravated, pathological chan-ges had occurred earlier. cTnI showed a trend of higher performance over time, and had a correlation with patholo-gy. Conclusion We successfully established radiation induced myocaridal injury model. As a noninvasive serum marker, cTnI can be used as the evaluation standard of radiation induced myocardial injury animal model.
ABSTRACT
Objective To investigate the effect of radiation-induced heart injury on cardiac troponin I (cTnI)and endothelin-1(ET-1) and observe the preventive and therapeutic effect of fluvastatin. Methods Healthy female SD rats were randomly divided into three groups: control group(c), irradiation alone group(R) and fluvastatin therapeutic group (F). Rats of F group had been gastrogavaged with fluvastatin at dose of 20mg?kg -1?d -1 from 1week before irradiation to the end of the experiment. In C group and R group, rats were gastrogavaged with the same volume isotonic sodium chloride. The rats of R and F group were irradiated with accelerator linear at a dose of 20Gy thoracically. Rats were executed at 5,15,30d and 60d after irradiation, then cTnI in serum and ET-1 in blood plasma were detected. Results On 5d, the content of cTnI in R group increased significantly than that in C group(P
