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Ann Thorac Surg 1999;68:1121-1122
© 1999 The Society of Thoracic Surgeons


Correspondence

The role of cardiac troponin T to predict heart transplant rejection

Jonathan R. Anderson, FRCSa, David W. Holt, FRCPathb

a Dept of Cardiac Surgery, St. Mary’s Hospital, London, England, W21NY England, UK
b Analytical Unit, St. George’s Hospital Medical School, London, England, W21NY England, UK

To the Editor

We would like to question the conclusions of Vijay and associates [1] regarding the value of donor cardiac troponin T as a prognostic indicator of allograft rejection. We have investigated the role of sensitive and specific markers of myocardial injury in cardiac transplantation [2] and found that donor TnT and TnI are useful predictors of poor myocardial performance posttransplant, irrespective of brain death etiology or ischemic time. We did not find a role for the troponins in diagnosing or predicting acute rejection because of the unusual release of kinetics of troponins posttransplant [3, 4] and the fact that many of these patients have renal impairment that could affect troponin levels. Creatine kinase isoenzyme subforms were predictive of rejection, but the test was not specific enough and too unwieldy to be of use in the clinical situation [5]. During the course of our study, patients had weekly endomyocardial biopsies for 6 weeks, then every 2 weeks and then every 6 weeks for a further 6 months. We have measured donor TnT in 23 cases in which heart transplant patients went on to have this biopsy schedule. In group 1 (TnT < 0.5 ng/mL, n = 17), there were 18 episodes of rejection involving myocytolysis (grade 2 or 3a). In group 2 (TnT > 0.5 ng/mL, n = 6), there were six episodes of rejection.

Five patients in group 1 had no rejection, compared with 2 patients in group 2. There was no difference between the groups in terms of ischemic times or time to first rejection (Table 1).


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Table 1. Cardiac Troponin T and Rejection Grade

 
These data are at variance with Vijay and associates, and the likely explanation is that they have made a statistical error in rejecting the null hypothesis that donor troponin T does not predict acute cellular rejection. We believe the reason for this error is that their groups are too small and they have insufficient biopsy data to justify their conclusions.

References

  1. Vijay P., Scavo V.A., Moreluck R., Sharp T.G., Brown J.W. Donor cardiac troponin T. Ann Thorac Surg 1998;66:1934-1939.[Abstract/Free Full Text]
  2. Anderson J.R. The assessment of myocardial damage in heart transplant recipients. In: Kaski J.C., Holt D., eds. Myocardial damage. Dordrecht, the Netherlands: Kluwer Academic Publishers, 1998:159-172.
  3. Hossein-Nia M., Anderson J.R., Treasure T., Murday A., Holt D.W. Troponin T release following cardiac transplantation. Eur J Lab Med 1995;3:1-5.
  4. Zimmerman R., Baki S., Dengler T.J., et al. Troponin T release after heart transplantation. Br Heart J 1993;69:395-398.[Abstract/Free Full Text]
  5. Anderson J.R., Hossein-Nia M., Brown P., Corbishley C., Murday A., Holt D.W. Creatine kinase MB isoforms. J Heart Lung Transplant 1995;14:666-670.[Medline]

Related Article

Reply
Palaniswamy Vijay, Thomas G. Sharp, and John W. Brown
Ann. Thorac. Surg. 1999 68: 1122. [Extract] [Full Text] [PDF]




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