This scientific statement presents considerations for clinical management regarding the assessment and risk reduction of select pediatric populations at high risk for premature cardiovascular disease, including acquired arteriosclerosis or atherosclerosis. For each topic, the evidence for accelerated acquired coronary artery disease and stroke in childhood and adolescence and the evidence for benefit of interventions in youth will be reviewed. Children and adolescents may be at higher risk for cardiovascular disease because of significant atherosclerotic or arteriosclerotic risk factors, high-risk conditions that promote atherosclerosis, or coronary artery or other cardiac or vascular abnormalities that make the individual more vulnerable to the adverse effects of traditional cardiovascular risk factors. Existing scientific statements and guidelines will be referenced when applicable, and suggestions for risk identification and reduction specific to each setting will be described. This statement is directed toward pediatric cardiologists, primary care providers, and subspecialists who provide clinical care for these young patients. The focus will be on management and justification for management, minimizing information on pathophysiology and epidemiology.

Many risk factors for breast cancer are associated with hormonally regulated events. Although numerous mouse models of mammary cancer exist, few address the roles of hormones in spontaneous tumor formation. Here we report that transgenic mice that overexpress LH, resulting in ovarian hyperstimulation, undergo precocious mammary gland development. A significant increase in proliferation leads to ovary-dependent mammary gland hyperplasia. Transgenic glands morphologically mimic those of wild-type pregnant mice and expression levels of multiple milk protein genes are comparable with what is observed at d 14 of pregnancy. In addition to sustained hyperplasia, spontaneous mammary tumors were observed with a mean latency of 41 wk, indicating that chronic hormonal stimulation causes mammary cancer. Although hormonally induced, these tumors lack expression of progesterone receptor, suggesting that following initiating events, the tumors may become hormone independent. This mouse model likely holds great potential as a tool for discovery of hormone-mediated mechanisms of breast cancer and identification of future targets for breast cancer prevention and treatment.

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The risk factors for superior vena cava (SVC) obstruction after pediatric orthotopic heart transplantation (OHT) have not been identified. This study tested the hypothesis that pretransplant superior cavopulmonary anastomosis (CPA) predisposes patients to SVC obstruction. A retrospective review of file Pediatric Cardiac Care Consortium registry from 1982 through 2007 was performed. Previous CPA, other cardiac surgeries, gender, age at transplantation, and weight at transplantation were assessed for the risk of developing SVC obstruction. Death, subsequent OHT, or reoperation involving the SVC were treated as competing risks. Of the 894 pediatric OHT patients identified, 3.1% (n = 28) developed SVC obstruction during median follow-up of 1.0 year (range: 0 to 19.5 years). Among patients who developed SVC obstruction, 32% (n = 9) had pretransplant CPA. SVC surgery before OHT was associated with posttransplant development of SVC obstruction (p <0.001) after adjustment for gender, age, and weight at OHT and year of OHT. Patients with previous CPA had increased risk for SVC obstruction compared with patients with no history of previous cardiac surgery (hazard ratio 10.6,95% confidence interval: 3.5 to 31.7) and to patients with history of non-CPA cardiac surgery (hazard ratio 4.7,95% confidence interval: 1.8 to 12.5). In conclusion, previous CPA is a significant risk factor for the development of post—heart transplant SVC obstruction. Published by Elsevier Inc. (Am J Cardiol 2013;112:286–291)