Background-Atrial fibrillation (AF) is common after thoracic surgery. Limited data exist concerning the incidence of AF, its impact on mortality, the effectiveness of therapy, and the risk factors of AF after pulmonary transplantation. Methods and Results-We reviewed the medical files of 224 consecutive lung transplant recipients who underwent surgery over a 10-year period at a large Canadian center. We collected patient characteristics, in-hospital treatments, and outcomes. Time-to-event analysis was used to account for in-hospital follow-up and models generated to assess the impact of AF on mortality and independent risk factors of AF after transplantation. Postoperative AF occurred in 65 patients (29%). AF was more likely to occur with complications such as pneumonia, mediastinitis, and bronchial dehiscence and was not an independent risk factor of mortality (hazard ratioϭ1.56; 95% confidence interval, 0.52-4.63). Pharmacological or electric therapy for rhythm or rate control of AF was administered to 97% of patients. Intravenous amiodarone was used in 46%, electric cardioversion in 28%, and heparin in 26%. Only 1 patient remained in AF at discharge. Age (hazard ratioϭ1.08 by year; 95% confidence interval, 1.05-1.12), bilateral transplantation (hazard ratioϭ1.87; 95% confidence interval, 1.03-3.42), and a history of AF before the transplantation (hazard ratioϭ4.48; 95% confidence interval, 1.05-19.11) were found to be independently associated with an increased incidence of postoperative AF. Conclusions-AF is fairly common after pulmonary transplantation, transient, and relatively benign. It is not independently associated with increased in-hospital mortality. Most patients return to sinus rhythm before discharge. Age, prior AF, and bilateral transplantation increase the risk of postoperative AF. (Circ Arrhythm Electrophysiol. 2012;5:61-67.)
Wilson's disease (WD), caused by a mutation in the P-type copper transporting ATPase (Atp7b) gene, results in excessive accumulation of copper in the liver. Long Evans Cinnamon rats (LEC) bear a mutation in the atp7b gene and share clinical characteristics of human WD. To explore hepatocyte transplantation (HT) as therapy for metabolic liver diseases, 8-week-old LEC rats (n = 12) were transplanted by intrasplenic injection of hepatocytes from donor Long Evans (LE) rats. Immunosuppression was maintained with intraperitoneal tacrolimus. The success of HT was monitored at 24 weeks of life. Serum aminotransferases and bilirubin peaked at 14-21 weeks in both HT rats and nontransplanted controls, but at 24 weeks, survival was 97% in LEC-HT versus 63% in controls. All transplanted rats showed restored biliary copper excretion and reduced liver iron concentration associated with increased ceruloplasmin oxidase activity. Liver tissue expressed atp7b mRNA (11.9 ± 13.6%) indicative of engraftment of normal cells in 7 of 12 HT rats, associated with a reduced liver copper concentration compared to untreated LEC rats. Periportal islets of normal appearing hepatocytes, recognized by atp7b antibody, were observed in transplanted livers while lobular host cells showed persistent pleomorphic changes and inflammatory infiltrates. In conclusion, transplantation of normal hepatocytes prevented fulminant hepatitis, reduces chronic inflammation, and improved 6-month survival in LEC rats. Engraftment of transplanted cells, which express atp7b mRNA, repopulated the recipient liver with normal functional capacity.Key words: Hepatocyte transplantation; LEC rat; Wilson's disease INTRODUCTIONtathione, metallothionein, copper chaperones, or to cellular enzymes or is incorporated into ceruloplasmin for release to the circulation (4). In WD, a failure of copper Wilson's disease is an autosomal recessively inherited disorder characterized by a defect in copper incorincorporation into apoceruloplasmin results in the secretion of an enzymatically inactive form of ceruloplasmin poration into ceruloplasmin and a lack of excretion of hepatic copper into the bile, which results in copper re-(26). Ceruloplasmin oxidase is the principal ferroxidase enzyme of the liver whose activity is required for iron tention in the liver, kidneys, eye, and brain. Clinical manifestations include acute, fulminant, or chronic hepmobilization (12). The Long Evans Cinnamon LEC rat has a 900 bp atitis leading to cirrhosis and, in some patients, neurological or psychiatric symptoms (3). The Wilson's disdeletion of the C-terminal of the atp7b gene. This gene shares 87% homology with the human WD gene (34). ease gene (WD) has been localized to chromosome 13 and codes for a P-type copper transporting ATPaseThe LEC rat lacks plasma ceruloplasmin oxidase activity, which results in reduced biliary copper excretion and (ATP7B), which is expressed in the liver, kidney, and placenta (2). Copper transporting ATPase is a member accumulation of both copper and iron in the liver. Many ...
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