title: Remodeling of human transplanted myocardium in ten-year follow-up: a clinical pathology study.
abstract: Remodeling taking place in transplanted myocardium leads to a change in the number of cardiocytes. Ultrasound measurements and biopsy evaluation should reflect their loss and compensation. We sought to evaluate the morphology of the transplanted heart upon long-term follow-up.
  
  
  METHODS
  Myocardial biopsies were obtained in the first week, first month, and then annually for 10 years from transplantation that did not show rejection (grade "0" ISHLT, 122 biopsies). The control group encompassed 7 donor heart fragments. Proliferation in biopsies was evaluated with Ki67 (M7240, DAKO), cardiocyte hypertrophy by measuring their diameter, the surface area of the nuclei, nuclear-sarcoplasmic index, and stromal fibrosis evaluated as the surface area fraction. Ultrasound measurements included diastolic thickness of the interventricular septum, posterior wall of the left ventricle, and left ventricular mass. The correlation of measurements with time from transplantation was evaluated using Spearman's test.
  
  
  RESULTS
  A positive Ki67 reaction was observed in fibroblasts and endothelial cells. The increased cardiocyte nuclear area correlated with the time elapsed since transplantation (r = 0.2; P < .05) with a simultaneous decrease in cardiocyte thickness (r = -0.3; P < .05), without changes in the nuclear-cytoplasmic index (r = 0.02; P > .05). Stromal fibrosis also increased (r = 0.1; P < .05). Ultrasound measurements of the left ventricle showed a decreased tendency with the passage of time (r = -0.2 to -0.3; P < .05).
  
  
  CONCLUSIONS
  A transplanted heart does not undergo hypertrophy but rather fibrous atrophy with apparent compensatory hypertrophy of the cardiomyocytes.
authors.affiliation: Department of Cardiac Surgery & Transplantation, Silesian Center for Heart Disease, Zabrze, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Nozyński
authors.forename: M
authors.initials: M
authors.lastname: Zakliczyński
authors.forename: E
authors.initials: E
authors.lastname: Zembala-Nozyńska
authors.forename: D
authors.initials: D
authors.lastname: Konecka-Mrówka
authors.forename: R
authors.initials: R
authors.lastname: Przybylski
authors.forename: B
authors.initials: B
authors.lastname: Nikiel
authors.forename: D
authors.initials: D
authors.lastname: Lange
authors.forename: A
authors.initials: A
authors.lastname: Mrówka
authors.forename: J
authors.initials: J
authors.lastname: Przybylski
authors.forename: M
authors.initials: M
authors.lastname: Maruszewski
authors.forename: M
authors.initials: M
authors.lastname: Zembala
mesh_terms: D001706:Biopsy; D002455:Cell Division; D002467:Cell Nucleus / Q000648:ultrastructure; D003971:Diastole; D005500:Follow-Up Studies; D006085:Graft Survival; D016027:Heart Transplantation / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D009206:Myocardium / Q000276:immunology / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000473:pathology; D012189:Retrospective Studies; D012519:Sarcoplasmic Reticulum / Q000648:ultrastructure; D013997:Time Factors; D016276:Ventricular Function; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D007166:Immunosuppressive Agents