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Introduction: Endobronchial ultrasound-guided transbronchial needle aspiration(EBUS-TBNA) is utilized for the diagnosis and staging of mediastinal lesions. However, currently no consensus identifies the quantity of tissue or the number of immunhisotchemical (IHC) staining required for the processing of common molecular mutation profiles. In collaboration with out cytopathology department we developed and implemented a two-step protocol to optimize tissue sampling. First, we mandated two additional passes after a tissue specimen has been deemed diagnostic by rapid on-site cytopathologic examinations (ROSE). Second, the cytology department implemented a tissue-sparing algorithm proposed by Mukhopadhyay and Katzenstein to further characterize non-small cell lung cancer (NSCLC). The purpose of this study is to evaluate the effectiveness of the algorithm to yield adequate tissue for molecular mutation profiling. Methods: This retrospective study reviewed all patients who had undergone EBUS-TBNA at NYU Langone Medical Center from January 2009 to July 2012. The study identified patients with a diagnosis of lung adenocarcinoma or unclassifiable NSCLC. Excluded from this study were adenocarcinoma of non-lung origin and negative lymph nodes. For Each EBUS-TBNA sampling we documented patient's baseline characteristics, size and location of lymph nodes, number of needle passes, and the number of IHC stains. Analyses were also made to compare data before and after July 2011, when a new implemented two-step protocol took place. Results: 293 patients underwent EBUS-TBNA, and thirty-four patients were diagnosed with lung adenocarcinoma or NSCLC-NOS. Thirteen patients had molecular mutation testing completed. Prior to July 2011, 1/19 patients had molecular mutation profiles compared to 12/14 patients after July 2011. Several factors increased the success of the protocol, such as lymph node size and number of IHC stains. Average lymph node size for adequate tissue sampling was 25.1mm compared to 18.0mm (p value <0.05). Minimization of IHC staining was also significant. Specimens that yielded molecular profiles involved IHC staining limited to mean of 3.0 slides vs 5.4 slides (p value <0.05). Conclusion: The results of this study shows that utility of EBUS-TBNA to obtain molecular mutation profile is associated with lymph node size and IHC staining. The implementation of our algorithm significantly increased the number of patients with adequate tissue to complete molecular mutation profiles

Introduction Complications of radiofrequency ablation (RFA) for atrial fibrillation (AF) include tamponade, atrio-esophageal fistulas, vagal nerve injury, and pulmonary vein stenosis (PVS). PVS may present without symptoms or with dyspnea, cough, chest pain, hemoptysis, or rarely with X-ray infiltrates.7 We present a case of man with ground-glass opacities (GGOs) and left hilar soft tissue lesion masquerading as lymphadenopathy in a patient with recurrent PVS. Case Presentation The patient is a 44-year old man with AF, refractory to pharmacologic treatment, who required left atrial RFA x 2. Two months later, he developed a cough and dyspnea. Cardiac MRI and VQ scan showed severe narrowing/sub-total occlusion of the left inferior pulmonary vein (LIPV), as well as left lung hypoperfusion but normal ventilation. He underwent balloon dilatation and stenting of the left superior pulmonary vein (LSPV). The LIPV was not amenable to stenting or dilatation due to near-total occlusion. Venous drainage of the left lower lung field was thought to occur via collateral circulation from the LSPV. Three months later, the patient's symptoms recurred. Cardiopulmonary exercise stress testing demonstrated increased pulmonary vascular resistance. Scattered GGOs and a left infrahilar soft tissue density were seen on Chest CT. PFTs revealed a restrictive defect with decreased DLCO. These findings were suggestive of sarcoidosis, hypersensitivity pneumonitis, and connective tissue-related pneumonitis. EBUS-FNA of the infrahilar lesion failed to show lymphatic tissue. Transbronchial biopsy revealed benign bronchial mucosa and mild chronic inflammation without granuloma or neoplasia. Repeat chest CT showed in-stent severe restenosis of the LSPV and no change in the soft tissue density. Discussion Symptoms of PVS include cough, chest pain, hemoptysis, and dyspnea. Patients may develop symptoms immediately, though most develop symptoms 1-3 months after RFA. Single PVS usually causes mild symptoms, which often subside due to collateral vessel formation.1 Though treatment with pulmonary vein balloon dilatation is associated with immediate symptomatic relief, restenoses recur with a 47% restenosis rate by 11 months after the intervention, likely as a result of neointimal hyperplasia and fibrosis.3 The mediastinal soft tissue densities seen on imaging may reflect extension of inflammation and fibrosis caused by thermal injury. Conclusion Pulmonary vein stenosis is a complication of RFA for AF. Long-term effects of pulmonary vein occlusion on adjacent structures in the mediastinum and lung are unknown. We recommend serial PFTs and as needed Chest CT imaging to exclude findings that may masquerade as connective tissue or neoplastic disorders