Elevated donor cardiac troponin T and procalcitonin indicate two independent mechanisms of early graft failure after heart transplantation

• Published in: International journal of cardiology Vol. 92; no. 2; pp. 163 - 167
• Main Authors: Potapov, Evgenij V., Wagner, Frank D., Loebe, Matthias, Ivanitskaia, Ekaterina A., Müller, Christian, Sodian, Ralf, Jonitz, Britta, Hetzer, Roland
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.12.2003; Elsevier Science
• Subjects: Adult; Biological and medical sciences; Brain Death; Calcitonin - blood; Calcitonin Gene-Related Peptide; Cardiac troponin T; Cardiology. Vascular system; Case-Control Studies; Female; Glycoproteins - blood; Graft failure; Graft Survival; Heart; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Heart Transplantation - physiology; Humans; Inflammation; Ischemia; Logistic Models; Male; Medical sciences; Procalcitonin; Prognosis; Protein Precursors - blood; Sensitivity and Specificity; Systemic Inflammatory Response Syndrome - blood; Time Factors; Tissue Donors; Transplantation; Troponin T - blood; Transplantation; Inflammation; Ischemia; Procalcitonin; Cardiac troponin T; Graft failure; Heart; Heart failure; Cardiovascular disease; Homotransplantation; Mechanism; Troponin T; Treatment; Donor; Heart disease; Surgery; Graft; Early
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/S0167-5273(03)00083-4

Background: Cardiac troponin T (cTnT) >0.1 μg/l and procalcitonin (PCT) >2 μg/l in the serum of heart donors are predictors of early graft failure after heart transplantation (HTx). The current study investigates the relationship between these two markers and their prognostic value when one or both of them are elevated. Methods: Cardiac TnT and PCT were measured in serum from 92 consecutive brain-dead donors accepted for HTx. The donors were retrospectively divided into two groups: group I ( n=78) donors of hearts with good function, group II ( n=14) donors of hearts with early graft failure after transplantation. Results: There were no correlations between cTnT and PCT values ( r=0.12, P=0.27). In eight donors in group I one or both markers were elevated. In one donor both markers were above the cut-off levels. In 12 donors (86%) in group II one or both markers were elevated. In two donors both markers were above the cut-off levels and in a further two below. There was no significant interaction between the two markers in either group using a logistic regression model ( P=0.28). Conclusions: Elevated cTnT and PCT levels in the serum of heart donors were independent prognostic markers of early graft failure. This fact may suggest two different mechanisms of early graft failure: primary myocardial damage and damage related to systemic inflammatory response. The combination of both markers had a higher sensitivity than each parameter on its own. Their use as additional parameters may improve heart donor selection.