title: Aortic valve replacement with autologous pericardium: long-term follow-up of 15 patients and in vivo histopathological changes of autologous pericardium.
abstract: OBJECTIVE
  The study aimed to assess the long-term follow-up of patients with an autologous pericardial aortic valve (APAV) replacement and to analyse in vivo histopathological changes in implanted APAVs.
  
  
  METHODS
  From 1996 to 1997, 15 patients (mean age, 34 years) underwent aortic valve replacement with the glutaraldehyde-treated autologous pericardium. All patients were followed up after discharge. The excised APAVs were processed for haematoxylin-eosin, Victoria blue-van Gieson and immunohistochemical staining.
  
  
  RESULTS
  The mean clinical follow-up was 11.43 ± 4.50 years. APAV-related in-hospital and late mortalities were both 0%. Five (33%) patients required reoperation because of a prolapse of the right coronary cusp (n = 1), infective endocarditis (n = 1) or fibrocalcific degeneration (n = 3). Freedom from endocarditis, fibrocalcific degeneration and reoperation at the end of follow-up was 93, 80 and 67%, respectively. The remaining 10 patients were alive and well with a mean New York Heart Association class of 1.10 ± 0.32 and normally functioning aortic valves (peak pressure gradient: 7.70 ± 3.41 mmHg; mean pressure gradient: 1.79 ± 0.64 mmHg). Histopathology revealed that (i) a thin factor VIII-positive layer (endothelialization) was found on all non-endocarditis APAVs; (ii) pericardial cells in all APAVs were positive for α-smooth muscle actin (myofibroblast phenotype) and some cells in the fibrocalcific APAVs were positive for alkaline phosphatase (osteoblast phenotype) and (iii) an elastic band was found in 3 cases (in vivo >9 years).
  
  
  CONCLUSIONS
  APAV replacement is a procedure with a low mortality. APAVs adapt to new environmental demands by producing an elastic band and by endothelialization, whereas myofibroblast/osteoblast transdifferentiation seems to be responsible for the fibrocalcification of APAVs.
authors.affiliation: Institute of Cardiothoracic Surgery,  Changhai Hospital, Second Military Medical University, Shanghai,  China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Liu
authors.forename: Lin
authors.initials: L
authors.lastname: Han
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Song
authors.forename: Mengwei
authors.initials: M
authors.lastname: Tan
authors.forename: Dejun
authors.initials: D
authors.lastname: Gong
authors.forename: Zhiyun
authors.initials: Z
authors.lastname: Xu
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000469:Alkaline Phosphatase / Q000378:metabolism; D001021:Aortic Valve / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D015415:Biomarkers / Q000378:metabolism; D001705:Bioprosthesis; D002114:Calcinosis; D054338:Cell Transdifferentiation; D004547:Elastic Tissue / Q000473:pathology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D005500:Follow-Up Studies; D006350:Heart Valve Prosthesis; D019918:Heart Valve Prosthesis Implantation / Q000009:adverse effects / Q000295:instrumentation*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D058628:Myofibroblasts / Q000378:metabolism / Q000473:pathology; D010006:Osteoblasts / Q000378:metabolism / Q000473:pathology; D010496:Pericardium / Q000378:metabolism / Q000473:pathology / Q000637:transplantation*; D010641:Phenotype; D011446:Prospective Studies; D011474:Prosthesis Design; D012086:Reoperation; D013194:Staining and Labeling; D013997:Time Factors; D014182:Transplantation, Autologous; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D015415:Biomarkers; C078147:F8 protein, human; D005169:Factor VIII; D000469:Alkaline Phosphatase