Troponin T and I are not reliable markers of cardiac transplant rejection.

OBJECTIVE: Heart transplant recipients undergo a number of invasive endomyocardial biopsies to screen for rejection. Serum assays of troponin T and/or I may provide a less invasive alternative. The purpose of this study was to evaluate troponin T and I as markers of cardiac transplant rejection. METHODS: We conducted a prospective analysis comparing troponin T and I levels to biopsy results in heart transplant recipients. Plasma was assayed for troponin T and I preoperatively, on the first 3 postoperative days, and with each subsequent biopsy. RESULTS: Twenty-nine patients entered the study. A total of 173 biopsies were performed at a mean follow-up of 129+/-9 days (range: 12-564 days). There were two rejection episodes (> or = grade 3), one in each of two patients. There were no significant relationships between troponin T or I and biopsy-proven rejection (> or = grade 3; P=0.59 and 0.54, respectively). There were also no correlations between troponin T or I levels and biopsy grade (P=0.40 and 0.92, respectively). Troponin T and I levels peaked on postoperative day 1 and fell to baseline over long-term follow-up with no peak in serum markers associated with rejection episodes. Donor ischemic time was significantly correlated to troponin T on postoperative days 1-3 (r=0.58, P=0.005; r=0.61, P=0.004; and r=0.61, P=0.003, respectively). CONCLUSIONS: Troponin T and I are not useful indicators of cardiac rejection, but do correlate with donor heart ischemic injury.

Serologic responses to hepatitis C virus in solid organ transplant recipients.

BACKGROUND: Hepatitis C (HCV) infection is known to have been transmitted by both blood transfusion and donor organs. We sought to determine the historical incidence of donor- and transfusion-acquired HCV infection in kidney transplant (RTx) and heart transplant (HTx) recipients at our center and to study the kinetics of seroconversion to HCV. METHODS: A bank of sera collected from organ donors (388 RTx and 88 HTx) who received allografts between January 1984 and April 1992 was screened for anti-HCV using a third generation enzyme immunoassay. Recipient sera collected before transplant (preTx), at 1 year after transplant, and at last follow-up were tested. Fresh follow-up sera on all surviving anti-HCV-positive (+) RTx and HTx, all anti-HCV-negative (-) HTx, and a subset of 85 anti-HCV- RTx were assayed for HCV RNA using an reverse transcriptase-polymerase chain reaction assay. RESULTS: Twenty-four of 388 RTx (6.2%) and 2 of 88 HTx (2.3%) were anti-HCV+ preTx. Eight of 218 (3.7%) organ donors were anti-HCV+. Six of the seven (85.7%) anti-HCV+ donors with adequate recipient follow-up transmitted HCV infection to one or more recipients. Nineteen of 313 RTx (6.1%) and 8 of 72 HTx (11.1%) with follow-up > or =1 year seroconverted to anti-HCV. One of 85 (1.2%) anti-HCV- RTx and 3 of 44 (6.8%) anti-HCV-HTx were HCV RNA+ when tested at last follow-up. Five cases of de novo HCV infection occurred after the introduction of first generation anti-HCV screening of donors. Persistent viremia (HCV RNA+) at last follow-up was observed in 70.6% (12/17) RTx anti-HCV+ preTx. Fourteen of 15 (93.3%) RTx and 9 of 9 (100%) HTx with de novo HCV infection had persistent viremia. Seroconversion was more delayed in HTx than RTx (P=0.0572, log-rank Mantel-Cox statistic) although both groups demonstrated an impaired humoral response to HCV when compared with the immunocompetent host. CONCLUSIONS: Organ donor- and transfusion-acquired HCV infection was common in RTx and HTx transplanted before the introduction of second generation anti-HCV screening in 1992. Serologic responses to HCV are often delayed and sometimes absent in these patients. Assays for HCV RNA should be considered as a screening test for the detection of HCV infection in this population. Serologic responses to HCV were more impaired in HTx compared with RTx, which may reflect the more intensive immunosuppressive regimens given to HTx at our center.