Procalcitonin, A Donor-Specific Predictor of Early Graft Failure–Related Mortality After Heart Transplantation Frank D. Wagner, MD; Britta Jonitz, MD; Evgenij V. Potapov, MD; Naser Qedra, MD; Karl Wegscheider, MD, PhD; Klaus Abraham, MD; Ekaterina A. Ivanitskaia, MD; Matthias Loebe, MD, PhD; Roland Hetzer, MD, PhD Background—To date, donor-specific markers to predict outcome after heart transplantation (HTx) are unknown. Increased procalcitonin (PCT) levels have been found in infectious inflammation with systemic reactions and/or poor organ perfusion but have not been studied in heart donors. We evaluated PCT as a predictor of early graft failure–related mortality after HTx. Methods and Results—PCT and C-reactive protein (CRP) serum concentrations were measured in samples collected immediately before pericardium opening from 81 consecutive brain-dead multiple-organ donors. Donors for high- urgency-status recipients (n=2) were excluded from analysis. The remaining donors were retrospectively divided into 2 groups: donors for recipients who died within 30 days after HTx, after an early graft failure (group II, n=8), and all other donors (group I, n=71). No differences in donor and recipient demographic characteristics were found between groups. Areas under the receiver operating characteristic curves for graft failure–related mortality were 0.71 for PCT and 0.64 for CRP. A PCT value 2 ng/mL as a predictor of graft failure–related mortality had a specificity of 95.8% and sensitivity of 50.0%. The odds ratio for graft failure–related mortality for recipients of hearts from donors with PCT levels 2 ng/mL was 22.7 (unadjusted, 95% CI 3.7 to 137.8, P=0.0007) and 43.8 (after adjustment for prespecified potential confounders, 95% CI 1.4 to 1361.0, P=0.031). Conclusions—A PCT level 2 ng/mL in a cardiac donor at the time of explantation appears to predict early graft failure–related mortality. (Circulation. 2001;104[suppl I]:I-192-I-196.) Key Words: transplantation mortality heart failure infection procalcitonin T he donor pool for heart transplantation (HTx) worldwide has plateaued in recent years. Expansion of the donor pool by inclusion of donors who previously would not have been accepted for HTx is the only way to increase the number of heart transplantations. 1 However, data on donor-specific parameters to predict success or failure of HTx and thus prevent a higher risk to the recipient are limited. 2 Moreover, donor-specific biochemical markers to predict outcome after HTx are currently unknown, with the exception of a recent report on troponins as indicators of myocardial damage. 3 Myocardial dysfunction occurs to various degrees in all brain-dead donors, and in up to 20% of cases, it precludes the use of these hearts for HTx. 4 Experimental and clinical studies have suggested that brain death may induce irrevers- ible myocardial damage. 5 In clinical practice, the potential donors are mechanically ventilated and may develop systemic infections before brain death and subsequent donation. How- ever, brain death–associated physiological changes and anti- biotic therapy may conceal the symptoms. After the first reports that calcitonin precursor molecules were found to be elevated in patients with bacterial infection and sepsis, 6 procalcitonin (PCT) was proposed as a marker of severe infection and systemic inflammatory response. 7 Recent stud- ies indicated that an acute infection or inflammation may impair myocardial function, 8 which affects outcome after HTx. Therefore, knowledge of a specific and sensitive marker of systemic inflammation in heart donors would help to avoid early graft failure, which causes up to one third of early postoperative mortality. 9 Moreover, such knowledge could prevent transmission of an unrecognized infection to the recipient. 10 The objective of the present study was to evaluate PCT for selection of heart donors in relation to clinical outcome and as a predictor of early graft failure–related mortality after HTx. C-reactive protein (CRP) was used as a reference parameter because it is the most widely used marker for assessing the severity of the inflammatory response to infection or tissue injury. 11 Methods From November 1998 to May 2000, 81 consecutive potential multiorgan donors above the age of 10 years who were accepted for From the Department of Cardiothoracic and Vascular Surgery (F.D.W., B.J., E.V.P., N.Q., K.A., E.A.I., R.H.), Deutsches Herzzentrum Berlin, Berlin, Germany; the Department of Biometrics and Statistics (K.W.), University of Hamburg, Hamburg, Germany; and Michael E. DeBakey Department of Surgery (M.L.), Division of Transplantation and Assist Devices, Baylor College of Medicine, Houston, Tex. Correspondence to Frank D. Wagner, MD, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. E-mail wagner@dhzb.de © 2001 American Heart Association, Inc. 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