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Ann Thorac Surg 1996;61:277-278
© 1996 The Society of Thoracic Surgeons
The Analytical Unit, Department of Cardiological Sciences, St George's Hospital Medical School, London SW17 0RE, UK
Department of Cardiothoracic Surgery, St George's Hospital, London SW17 0QT, UK
To the Editor:
We were interested to read the article ``Use of Cardiac Troponin I as a Marker of Perioperative Myocardial Ischemia'' by Dr Etievent and associates [1]; in the discussion they mentioned the evaluation of this marker in heart transplantation.
We have been investigating the potential value of several soluble markers of ischemic myocardial injury as indicators of acute allograft rejection after cardiac transplantation. The markers studied have included creatine kinase (CK) MB isoforms (MB2 = cardiac tissue form and MB1 = plasma modified form), cardiac troponin T (CTnT), and cardiac troponin I (CTnI). In 50 orthotopic heart transplant recipients, an increased MB2/MB1 ratio was shown to be associated with acute rejection [2]. However, this ratio failed to diagnose acute rejection with the required sensitivity and specificity to replace endomyocardial biopsy. The MB2/MB1 ratio was shown to return to baseline values by a median of 24 hours after transplantation [3]. In a subgroup of these patients (n = 29), the measurement of CTnT concentration (Boehringer Mannheim UK Ltd, Lewes, UK) did not appear to possess sufficient sensitivity to detect acute rejection [4]. In contrast to CK-MB isoforms, CTnT concentration did not return to baseline values for a mean of 47 18 days after transplantation. In 17 of these patients, serum samples (n = 214) for CTnI analysis (Sanofi Diagnostic Pasteur Ltd, Guildford, UK) were obtained before biopsy, during hospital stay, and at out-patient visits.
Patients were followed up for a mean of 61 16 days after transplantation. The median peak CTnI concentration was 0.994 µg/L (range, 0.452 to 9.880 µg/L) at the time of the first sample collection (3 2 days), and returned to baseline values of 0.061 µg/L (range, <0.030 to 0.097 µg/L) at 14 5 days after transplantation. Eight patients each had an episode of significant acute rejection (grades 2 and 3), with myocytolysis. At the time of endomyocardial biopsy, there was no significant difference in CTnI concentration between patients with grades 2 and 3 rejection and those with grades 0 and 1 rejection (0.015 0.025 versus 0.036 0.073 µg/L, respectively). In addition, CTnI did not have any predictive value in the diagnosis of acute rejection.
We agree with Etievent and associates that CTnI is a reliable marker of ischemic damage during cardiac operations. However, as with CTnT, its measurement does not seem to be useful in the diagnosis of acute rejection after cardiac transplantation. In addition, there appears to be a difference in the release kinetics of CTnT and CTnI after transplantation: CTnI returns to baseline values sooner than CTnT. Further work is needed to investigate the underlying mechanism of the release of these two cardiac proteins after heart transplantation.
References
Departement of Thoracic and Cardiovascular Surgery, Hopital Saint-Jacques, 25030 Besançon, France
To the Editor:
We thank Dr Hossein-Nia and associates for their comments concerning our article, the only conclusion of which was that CTn I is a reliable marker of cardiac ischemia during open heart operations. We did, nevertheless, hope to be able to demonstrate the usefulness of CTnI in two fields: (1) in comparing the efficiency of several methods of cardioplegia, a study we are currently conducting, and (2) in evaluating ischemia in heart transplantation.
Concerning the second point, two situations must be distinguished. First is the diagnosis of acute allograft rejection, where neither CTnI nor CTnT seems to be an efficient indicator, as mentioned by Dr Hossein-Nia and associates. The La Pitie group demonstrated that for these two proteins the specificity and the sensitivity were insufficient [1]. The second situation is the quality of donor hearts in cardiac transplantation. To assess the usefulness of CTnI in this field, we designed an experimental study (submitted for publication) on isolated rat hearts that had undergone different durations of cold ischemia. Our results showed a highly significant linear correlation between CTnI release and ischemia duration. In addition, Riou and associates [2] demonstrated a correlation between the left ventricular ejection fraction and CTnI release in 100 brain-dead patients who were potential heart donors; thus, there is a possibility of predicting a severe decrease in left ventricular ejection fraction (sensitivity, 1.00; specificity, 0.84). Accordingly, in this series, the hearts of most patients with a low left ventricular ejection fraction and a high concentration of circulating troponin were not transplanted.
Conversely, Riou and associates suggest that hemodynamically unstable brain-dead patients with normal values of troponin may be considered for heart donation. Further studies of CTnI are necessary to determine the level of release that would signify irreversible cell damage and thus be a contraindication for heart donation.
References
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