title: Donor hepatitis-C seropositivity is an independent risk factor for the development of accelerated coronary vasculopathy and predicts outcome after cardiac transplantation.
abstract: BACKGROUND
  It is possible, but unproven, that hepatitis C (HCV) infection accelerates atherosclerosis. We evaluated the hypothesis that donor HCV seropositivity predicts mortality and the development of coronary vasculopathy in cardiac transplant recipients.
  
  
  METHODS
  Thirty-four cardiac transplant recipients who were seronegative for HCV at the time of transplantation received hearts from HCV-seropositive donors. We compared the mortality and the incidence of vasculopathy in this group of patients (study group) with a group of 183 successive heart transplant recipients (control group) with no evidence of HCV in the donor or in the recipient.
  
  
  RESULTS
  After transplantation, 75% of the HCV-seronegative patients who received hearts from HCV-seropositive donors had detectable and persistent viremia (presence of HCV-RNA by reverse-transcription polymerase chain reaction). After a mean follow-up of 4.2 +/- 1.9 years, mortality was 2.8-fold greater in the study group than in controls (95% confidence interval [CI], 1.3-5.7; p = 0.006). The risk of having any vasculopathy after a mean follow-up of 3.4 +/- 1.6 years and after adjustment for other significant risk factors was 3-fold greater (hazards ratio, 3.08; 95% CI 1.52-6.20; p = 0.001) in the HCV group compared with controls. The risk of developing advanced vasculopathy was much greater in the study group compared with controls (hazard ratio, 9.4; 97% CI, 3.3-26.6; p = < 0.0001). The risk of mortality (p = 0.005) and vasculopathy (p = < 0.0001) was greatest in patients with combined donor HCV seropositivity and the presence of antibodies against donor B cells by flow cytometry.
  
  
  CONCLUSIONS
  We conclude that donor hepatitis-C virus seropositivity is an independent risk factor for increased mortality and for the development of accelerated allograft vasculopathy after cardiac transplantation. These observations may have implications for the use of HCV-positive donors in heart transplant recipients.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
authors.forename: Showkat A
authors.initials: SA
authors.lastname: Haji
authors.forename: Randall C
authors.initials: RC
authors.lastname: Starling
authors.forename: Robin K
authors.initials: RK
authors.lastname: Avery
authors.forename: Steven
authors.initials: S
authors.lastname: Mawhorter
authors.forename: E Murat
authors.initials: EM
authors.lastname: Tuzcu
authors.forename: Paul
authors.initials: P
authors.lastname: Schoenhagen
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Cook
authors.forename: Norman B
authors.initials: NB
authors.lastname: Ratliff
authors.forename: Patrick M
authors.initials: PM
authors.lastname: McCarthy
authors.forename: James B
authors.initials: JB
authors.lastname: Young
authors.forename: Mohamad H
authors.initials: MH
authors.lastname: Yamani
mesh_terms: D016022:Case-Control Studies; D003327:Coronary Disease / Q000453:epidemiology*; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D016027:Heart Transplantation; D016174:Hepacivirus / Q000302:isolation & purification; D006526:Hepatitis C / Q000453:epidemiology*; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000453:epidemiology*; D012189:Retrospective Studies; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012307:Risk Factors; D013997:Time Factors; D014019:Tissue Donors