Survey of brachytherapy training experience among radiation oncology trainees and fellows in the Royal Australian and New Zealand College of Radiologists (RANZCR).

INTRODUCTION: To evaluate brachytherapy training experience among trainees and fellows trained through the Royal Australian and New Zealand College of Radiologists (RANZCR). METHODS: All current trainees and fellows (who obtained fellowship from 2015 onwards) were sent an online anonymous questionnaire on various aspects of brachytherapy training, including number of cases observed/ performed, opinions on brachytherapy assessment during training, barriers to brachytherapy training and future role of brachytherapy. RESULTS: The overall survey response rate was 24% (40/161 trainees, 30/126 fellows). Of the 70 respondents, 50 (71%), 38 (54%) and 43 (61%) reported to have received formal brachytherapy teaching from radiation oncologists, radiation therapists and medical physicists respectively. Most respondents had exposure to gynaecology brachytherapy - two-thirds of trainees and all fellows have performed at least one gynaecology brachytherapy procedure. Prostate brachytherapy exposure was more limited - by the end of training, 27% and 13% of fellows did not have exposure to LDR and HDR prostate brachytherapy. More than two-thirds indicated there should be a minimum number of brachytherapy case requirements during training, and half indicated that trainees should be involved in ≥6 gynaecology brachytherapy procedures. Barriers affecting training include lack of caseload (70%) and perceived decreasing role of brachytherapy (66%). Forty-three percent of respondents were concerned about the decline in brachytherapy utilisation. CONCLUSION: This is the first survey on brachytherapy training experience among RANZCR trainees and fellows. It highlighted limited brachytherapy exposure during RANZCR training, and the need to revisit brachytherapy training requirement in the current training programme, along with long-term brachytherapy workforce planning.

Pattern and Outcome of Heart Failure-Related Hospitalization Over 5 Years in a Remote Australian Population: A Retrospective Administrative Data Cohort of 617 Indigenous and non-Indigenous Cases.

OBJECTIVE: The aim of this work was to understand the pattern and outcomes for heart failure (HF)-related hospitalization among Indigenous and non-Indigenous patients living in Central Australia. METHODS AND RESULTS: A retrospective analysis of administrative data for patients presenting with a primary or secondary diagnosis of HF to Central Australia's Alice Springs Hospital during 2008-2012 was performed. The population rate of admission and subsequent outcomes (including mortality and readmission) during the 5-year study period were examined. A total of 617 patients, aged 55.8 ± 17.5 years and 302 (49%) female constituted the study cohort. The 446 Indigenous patients (72%) were significantly younger (50.8 ± 15.9 vs 68.7 ± 14.9; P < .001) and clinically more complex compared with the non-Indigenous patients. Annual prevalence of any HF hospitalization was markedly higher in the Indigenous population (1.9%, 95% CI 1.7-2.1) compared with the non-Indigenous population (0.5%, 95% CI 0.4-0.6); the greatest difference being for women. Overall, non-Indigenous patients had poorer outcomes and were significantly more likely to die (P < .0001), but this was largely driven by age differences. Alternatively, Indigenous patients were significantly more likely to have a higher number of hospitalizations, although indigeneity was not a predictor for 30- or 365-day rehospitalization from the index admission. CONCLUSION: The pattern of HF among Indigenous Australians in Central Australia is characterized by a younger population with more clinically complex cases and greater health care utilization.

Endocardial fibroelastosis is caused by aberrant endothelial to mesenchymal transition.

RATIONALE: Endocardial fibroelastosis (EFE) is a unique form of fibrosis, which forms a de novo subendocardial tissue layer encapsulating the myocardium and stunting its growth, and which is typically associated with congenital heart diseases of heterogeneous origin, such as hypoplastic left heart syndrome. Relevance of EFE was only recently highlighted through the establishment of staged biventricular repair surgery in infant patients with hypoplastic left heart syndrome, where surgical removal of EFE tissue has resulted in improvement in the restrictive physiology leading to the growth of the left ventricle in parallel with somatic growth. However, pathomechanisms underlying EFE formation are still scarce, and specific therapeutic targets are not yet known. OBJECTIVE: Here, we aimed to investigate the cellular origins of EFE tissue and to gain insights into the underlying molecular mechanisms to ultimately develop novel therapeutic strategies. METHODS AND RESULTS: By utilizing a novel EFE model of heterotopic transplantation of hearts from newborn reporter mice and by analyzing human EFE tissue, we demonstrate for the first time that fibrogenic cells within EFE tissue originate from endocardial endothelial cells via aberrant endothelial to mesenchymal transition. We further demonstrate that such aberrant endothelial to mesenchymal transition involving endocardial endothelial cells is caused by dysregulated transforming growth factor beta/bone morphogenetic proteins signaling and that this imbalance is at least in part caused by aberrant promoter methylation and subsequent transcriptional suppression of bone morphogenetic proteins 5 and 7. Finally, we provide evidence that supplementation of exogenous recombinant bone morphogenetic proteins 7 effectively ameliorates endothelial to mesenchymal transition and experimental EFE in rats. CONCLUSIONS: In summary, our data point to aberrant endothelial to mesenchymal transition as a common denominator of infant EFE development in heterogeneous, congenital heart diseases, and to bone morphogenetic proteins 7 as an effective treatment for EFE and its restriction of heart growth.

An animal model of endocardial fibroelastosis.

BACKGROUND: Hypoplastic left heart syndrome (HLHS) is one of the most common severe congenital cardiac anomalies, characterized by a marked hypoplasia of left-sided structures of the heart, which is commonly accompanied by a thick layer of fibroelastic tissue, termed endocardial fibroelastosis (EFE). Because human EFE develops only in fetal or neonatal hearts, and often in association with reduced blood flow, we sought to mimic these conditions by subjecting neonatal and 2-wk-old rat hearts to variations of the heterotopically transplanted heart model with either no intracavitary or normal flow and compare endocardium with human EFE tissue. MATERIALS AND METHODS: Hearts obtained from neonatal and 2-wk-old rats were heterotopically transplanted in young adult Lewis rats in a working (loaded) or nonworking (unloaded) mode. After 2-wk survival, hearts were explanted for histologic analysis by staining for collagen, elastin, and cellular elements. These sections were compared with human EFE tissue from HLHS. RESULTS: EFE, consisting of collagen and elastin with scarce cellular and vascular components, developed only in neonatal unloaded transplanted hearts and displayed the same histopathologic findings as EFE from patients with HLHS. Loaded hearts and 2-wk-old hearts did not show these alterations. CONCLUSIONS: This animal model for EFE will serve as a tool to study the mechanisms of EFE formation, such as fluid forces, in HLHS in a systematic manner. A better understanding of the underlying cause of the EFE formation in HLHS will help to develop novel treatment strategies to better preserve growth of the hypoplastic left ventricle.