Objective: To evaluate the use of video-assisted thoracoscopy in the surgical treatment of chylothorax developed after the surgical correction of congenital heart disease in children. Methods: We reviewed the medical charts of 3,092 children who underwent surgery for congenital heart disease between February of 2002 and February of 2007 at the Heart Institute of the University of São Paulo School of Medicine Hospital das Clínicas, in São Paulo, Brazil. Results: Of the 3,092 children, 64 (2.2%) presented with chylothorax as a postoperative complication. In 50 (78.1%) of those patients, the clinical management was successful, whereas it failed in 14 (21.9%), all of whom were then submitted to thoracic duct ligation by video-assisted thoracoscopy. The thoracic duct ligation was successful in 12 patients (86%) but failed in 2. In the postoperative period, additional clinical measures, such as a low-fat diet and parenteral nutrition, were required in order to resolve those 2 cases. There was no surgical morbidity or mortality. Of the 14 patients who underwent thoracic duct ligation, 5 (35%) died due to cardiac or infectious complications. Conclusions: Video-assisted thoracic duct ligation can be safely performed in patients with severe heart disease, and the outcomes are favorable.

Keywords: Chylothorax; Heart defects, congenital; Thoracic duct.

Background: Structural alterations to the pulmonary circulation characterize the vascular remodeling process and are likely correlated with local variations in flow and ischemia. Objective: To define the histological alterations to the pulmonary circulation seen after experimentally-induced ischemia of the pulmonary artery and to correlate those alterations with known patterns of blood redistribution and vascular remodeling. Method: Wistar rats (n = 48) were randomized into two groups with ligation of the pulmonary artery and without (controls) and were sacrificed on post-ischemia days 1, 7, 30 and 60. Lungs were removed and inspected for signs of parenchymal injury. External diameters, as well as wall thicknesses in the pulmonary, alveolar and bronchial end arterioles, were measured. Internal diameter and wall thickness percentage were calculated. Results: Infarction, necrosis and hemorrhage occurred only in ischemic lungs. In nonischemic lungs, there was a sustained increase in the internal and external arteriolar diameters, with an initial reduction in wall thickness on day 1, and day-60 values were similar to those seen in controls. In ischemic lungs, there was a transitory reduction in the internal and external diameters of the pulmonary and bronchial end arterioles, together with an initial, equally transitory, increase in their wall thickness. The alveolar arterioles presented sustained and progressive increases in external diameter and wall thickness, with concomitant reductions in internal diameter. Conclusion: This model mimics distal arterial disease in patients with chronic pulmonary thromboembolism. The vascular response in nonischemic lungs was consistent with a pattern of flow remodeling, whereas that seen in ischemic lungs was more consistent with flow and ischemia. In the pulmonary and bronchial end arterioles, the response was transitory, in contrast to the sustained and progressive response seen in the alveolar arterioles, which was probably caused by delayed local flow.

Keywords: Key-words: Pulmonary embolism. Pulmonary circulation. Vascular remodelling. Pulmonary artery.