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.
Circulation is available at http://www.circulationaha.org
I-192
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