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COPD Rehabilitation PostersSESSION TYPE: Poster PresentationsPRESENTED ON: Saturday, March 22, 2014 at 01:15 PM - 02:15 PMPURPOSE: Acute exacerbation is a common cause of hospital admission in patients with chronic obstructive pulmonary disease (COPD). COPD also involves non-pulmonary manifestations including exercise intolerance and skeletal muscle dysfunction. These manifestations added to the hospitalization stay have been associated to a loss of muscle mass partially recovered 3 months after discharge. The aims of this study were to examine the effects of a physical therapy (PT) program in hospitalized patients due to an acute exacerbation of COPD (AE-COPD). ⋯ The following authors have nothing to disclose: Irene Torres-Sánchez, Marie Carmen Valenza, Gerald Valenza-Demet, Irene Cabrera-Martos, María José Flores-Barba, Sonia Rodríguez-MoralesNo Product/Research Disclosure Information.
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Slide PresentationsPRESENTED ON: Sunday, March 23, 2014 at 04:15 PM - 05:15 PMPURPOSE: QVA149 is a once-daily dual bronchodilator containing a fixed-dose combination of the long-acting β2-agonist (indacaterol) and long-acting muscarinic antagonist glycopyrronium, for the treatment of COPD. We evaluated the overall rate of exacerbations and the health status with QVA149 in comparison with glycopyrronium and tiotropium. ⋯ Jadwiga Wedzicha: Consultant fee, speaker bureau, advisory committee, etc.: JW has received speaking fee and/or for advisory boards from GlaxoSmithKline, AstraZeneca, Novartis, Bayer, Boehringer Ingelheim, Nycomed. Chiesi and Respifor as well as travel reimbursements from Boehringer Ingelheim. JW has received research grants from GlaxoSmithKline, AstraZeneca, Chiesi and Novartis. Joachim Ficker: Consultant fee, speaker bureau, advisory committee, etc.: Dr. Ficker has received speaker fees from AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Pfizer, Nycomed, Almirall, Berlin-C hemie, Takeda and Novartis, consulting fees from AstraZeneca, Boehringer Ingelheim, and Novartis. Angel FowlerTaylor: Employee: The author is an employee of Novartis Pharmaceuticals Corporation Peter D'Andrea: Employee: The author is an employee of Novartis Pharmaceuticals Corporation Christie Arrasate: Employee: The author is an employee of Novartis Pharmaceuticals Corporation Hungta Chen: Employee: The author is an employee of Novartis Pharmaceuticals Corporation Donald Banerji: Employee: The author is an employee of Novartis Pharmaceuticals CorporationClinical trial results of QVA149, combination of two approved products indacaterol and glycopyrronium, will be presented, QVA149 is in the late stage phase 3 trials prior to approval.
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DVT/PE PostersSESSION TYPE: Poster PresentationsPRESENTED ON: Saturday, March 22, 2014 at 01:15 PM - 02:15 PMPURPOSE: Although fondaparinux is recommended by experts for the treatment of heparin- induced thrombocytopenia (HIT), recent guidelines from the American College of Chest Physicians do not support its use. In light of the aforementioned uncertainties, we conducted a systematic review to assess outcomes in HIT patients treated with fondaparinux. ⋯ The following authors have nothing to disclose: Catherine Ivory, Gregoire Le Gal, Marc Carrier, Marc Rodger, Catherine Code, Esteban GandaraNo Product/Research Disclosure Information.
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Surgery Case Report Posters ISESSION TYPE: Case Report PosterPRESENTED ON: Sunday, March 23, 2014 at 01:15 PM - 02:15 PMINTRODUCTION: Bronchogenic cysts are developmental anomalies of the ventral foregut arising from abnormal budding of the primitive tracheobronchial tree. Usually they acquire an intra-thoracic location primarily mediastinal or intraparenchymal, though atypical locations including cervical, intradiaphragmatic, interatrial septum and retroperitoneal have been reported. We present an extremely rare, aberrant location of a bronchogenic cyst within the thymic tissue that was minimally resected with robotic assistance. ⋯ The following authors have nothing to disclose: Maria Siddiqui, Adnan Al-Ayoubi, Sadiq Rehmani, Faiz BhoraNo Product/Research Disclosure Information.
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Nocturnal hypoxia, the hallmark of OSA, is a potential contributing factor for nonalcoholic fatty liver disease (NAFLD). NAFLD severity and its implication in OSA-related endothelial dysfunction have not been investigated in a large, unselected OSA population, including nonobese subjects. ⋯ In a large, unselected OSA population, the severity of nocturnal hypoxia was independently associated with steatosis. Preexisting obesity exacerbated the effects of nocturnal hypoxemia. NAFLD is a potential mechanism of endothelial dysfunction in OSA.