title: Cardiac-specific troponin I levels and risk of coronary artery disease and graft failure following heart transplantation.
abstract: BACKGROUND
  Previous studies have yielded conflicting data regarding whether a relationship exists between elevated cardiac troponin levels and acute allograft rejection in patients who have received heart transplants.
  
  
  OBJECTIVE
  To determine whether cardiac troponin I levels after heart transplantation were associated with a procoagulant microvasculature and long-term allograft outcome.
  
  
  METHODS
  Prospective cohort study with a mean (SE) follow-up of 45.1 (2.5) months. Serum troponin I levels were measured 9.9 (0.2) times per patient during the first 12 months after heart transplantation.
  
  
  METHODS
  Heart transplant center in the United States.
  
  
  METHODS
  A total of 110 consecutive patients who received a heart transplant between 1989 and 1997 and survived at least 1 year after transplantation.
  
  
  METHODS
  Histological and immunohistochemical biopsy findings, development of coronary artery disease (CAD), and graft failure in patients with vs without elevated serum cardiac troponin I levels.
  
  
  RESULTS
  All recipients had elevated troponin I levels during the first month after transplantation. Troponin I levels remained persistently elevated during the first 12 months in 56 patients (51%) and became undetectable in 54 patients (49%). Persistently elevated troponin I levels were associated with increasing fibrin deposits in microvasculature and cardiomyocytes (P<.001). Patients with persistently elevated levels of troponin I had significantly increased risk for subsequent development of CAD (odds ratio [OR], 4. 3; 95% confidence interval [CI], 1.8-10.1; P<.001) and graft failure (OR, 3.4; 95% CI, 1.2-9.7; P =.02), and also developed more severe CAD (OR, 4.2; 95% CI, 1.9-9.3; P<.001) and showed more disease progression (OR, 3.7; 95% CI, 1.3-10.4; P =.009).
  
  
  CONCLUSIONS
  In this study, elevated cardiac troponin I levels, which are considered to be a noninvasive surrogate marker of a procoagulant microvasculature, identified a subgroup of patients with high risk for developing CAD and graft failure after cardiac transplantation. JAMA. 2000;284:457-464
authors.affiliation: Methodist Research Institute, Clarian Health, 1812 N Capitol Ave, Indianapolis, IN 46202, USA. Clabarrere@clarian.com
authors.forename: C A
authors.initials: CA
authors.lastname: Labarrere
authors.forename: D R
authors.initials: DR
authors.lastname: Nelson
authors.forename: C J
authors.initials: CJ
authors.lastname: Cox
authors.forename: D
authors.initials: D
authors.lastname: Pitts
authors.forename: P
authors.initials: P
authors.lastname: Kirlin
authors.forename: H
authors.initials: H
authors.lastname: Halbrook
mesh_terms: D000328:Adult; D003327:Coronary Disease / Q000175:diagnosis / Q000209:etiology*; D005337:Fibrin / Q000032:analysis; D006084:Graft Rejection; D016027:Heart Transplantation / Q000276:immunology / Q000473:pathology* / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008833:Microcirculation / Q000473:pathology; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D011379:Prognosis; D011446:Prospective Studies; D012044:Regression Analysis; D012306:Risk; D019210:Troponin I / Q000097:blood*
chemical_list: D019210:Troponin I; D005337:Fibrin