Pan-aortic hybrid treatment of mega-aorta syndrome

Hybrid procedures combining traditional open and newer endovascular techniques are increasingly used to treat complex aortic disease. We present a novel approach for total aortic replacement, including hybrid repair of the arch and thoracoabdominal aorta, in a patient with “mega-aorta syndrome.” A two-stage approach using a valve-sparing aortic root replacement, total arch replacement (stage I elephant trunk), and left carotid-axillary bypass was used to treat the root, proximal-mid arch, and left subclavian aneurysmal pathology. This was followed by a hybrid distal arch/Extent II thoracoabdominal aneurysm repair 3 months later. After 15 months follow-up, the patient remains asymptomatic with an intact repair, no endoleak, and normal ventricular and aortic valve function. This case demonstrates a novel “pan-aortic” hybrid approach for repair of extensive thoracic aortic disease

Retrocardiac mediastinal foregut duplication cyst

AbstractForegut duplications occur at various locations throughout the upper gastrointestinal tract, including the thoracic cavity. Thoracic foregut duplications are typically intimately associated with the esophagus and therefore are located in either the posterior mediastinum or in pleural cavity. Here we report a case of foregut duplication of the middle mediastinum, intimately associated with the pericardium and great vessels that contained gastric mucosa, ciliated respiratory epithelium, bronchial-type epithelium, pancreatic tissue and hepatocytes. The literature of mediastinal foregut duplications is also reviewed

Risk factors for 1-year mortality after thoracic endovascular aortic repair

ObjectiveThoracic endovascular aortic repair, although physiologically well tolerated, may fail to confer significant survival benefit in some high-risk patients. In an effort to identify patients most likely to benefit from intervention, the present study sought to determine the risk factors for 1-year mortality after thoracic endovascular aortic repair.MethodsA retrospective review was performed on prospectively collected data from all patients undergoing thoracic endovascular aortic repair from 2002 to 2010 at a single institution. Univariate analysis and multivariate Cox proportional hazards regression analysis were used to identify risk factors associated with mortality within 1 year after thoracic endovascular aortic repair.ResultsDuring the study period, 282 patients underwent at least 1 thoracic endovascular aortic repair; index procedures included descending aortic repair (n = 189), hybrid arch repair (n = 55), and hybrid thoracoabdominal repair (n = 38). The 30-day/in-hospital mortality was 7.4% (n = 21) and the overall 1-year mortality was 19% (n = 54). Cardiopulmonary pathologies were the most common cause of nonperioperative 1-year mortality (22%, n = 12). Multivariate modeling demonstrated 3 variables independently associated with 1-year mortality: age older than 75 years (hazard ratio, 2.26; P = .005), aortic diameter greater than 6.5 cm (hazard ratio, 2.20; P = .007), and American Society of Anesthesiologists class 4 (hazard ratio, 1.85; P = .049). A baseline creatinine greater than 1.5 mg/dL (hazard ratio, 1.79; P = .05) and congestive heart failure (hazard ratio, 1.87; P = .08) were also retained in the final model. These 5 variables explained a large proportion of the risk of 1-year mortality (C statistic = 0.74).ConclusionsAge older than 75 years, aortic diameter greater than 6.5 cm, and American Society of Anesthesiologists class 4 are independently associated with 1-year mortality after thoracic endovascular aortic repair. These clinical characteristics may help risk-stratify patients undergoing thoracic endovascular aortic repair and identify those unlikely to derive a long-term survival benefit from the procedure

Mitochondrial Role in Oncogenesis and Potential Chemotherapeutic Strategy of Mitochondrial Infusion in Breast Cancer

Triple negative breast cancer (TNBC) is one of the most aggressive cancers diagnosed amongst women with a high rate of treatment failure and a poor prognosis. Mitochondria have been found to be key players in oncogenesis and tumor progression by mechanisms such as altered metabolism, reactive oxygen species (ROS) production and evasion of apoptosis. Therefore, mitochondrial infusion is an area of interest for cancer treatment. Studies in vitro and in vivo demonstrate mitochondrial-mediated reduction in glycolysis, enhancement of oxidative phosphorylation (OXPHOS), reduction in proliferation, and an enhancement of apoptosis as effective anti-tumor therapies. This review focuses on mitochondrial dysregulation and infusion in malignancies, such as TNBC