Donor cardiac troponin-I: a biochemical surrogate of heart function§,§§
Rajamiyer V. Venkateswarana, Jegatheesan Saravana Ganesha,
Joyce Thekkudana, Richard Steedsb, Ian C. Wilsona, Jorge Mascaroa,
Richard Thompsona, Robert Stuart Bonsera,c,*
aDepartment of Heart and Lung Transplantation, University Hospital Birmingham NHS Trust, Birmingham, UK
bDepartment of Cardiology, University Hospital Birmingham NHS Trust, Birmingham, UK
cUniversity of Birmingham, Birmingham, UK
Received 20 September 2008; received in revised form 14 February 2009; accepted 20 February 2009; Available online 25 April 2009
Objective: Cardiac troponin-I (cTnI) levels in the potential heart transplant donor may be a marker of heart dysfunction and predictive of
performed at initial assessment in 79 potential heart donors (mean age 43 ? 13.1 years). All donors were then managed according to a strict
algorithm tooptimisecardiacfunction,some receivinghormonaltherapyas part of a randomised trial. Donorheart suitability fortransplantation
was assessed after 7 h of management. The association of cTnI with initial functional indices was assessed and outcome compared for donors
categorised according to cTnI level ?1 mg l?1or >1 mg l?1. Results: Serum cTnI levels negatively correlated with initial cardiac index (CI)
(p = 0.003), right (p < 0.001) and left ventricular ejection fraction (p = 0.001) and positively with LV Tei index (p = 0.003). Serum cTnI was
>1 mg l?1in 29/79 donors. Higher CVP (10 ? 5.1 vs 7.9 ? 2.9; p = 0.026) and PAWP (12 ? 5.4 vs 8.1 ? 3.1; p = 0.002), lower cardiac index
(2.7 ? 1.1 vs 3.6 ? 0.9; p = 0.001) and fractional shortening (p < 0.01) and worse wall motion score index (p < 0.01) were observed in the cTnI
>1 mg l?1group. CTnI and functional markers correlated with the time duration from coning. Conclusion: The donor cTnI level represents a
biochemical surrogate of functional donor heart assessment. High cTnI is associated with worse donor heart function and may act as a prompt for
detailed assessment and optimisation.
# 2009 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
Keywords: Cardiac troponin-I; Heart transplantation; Donor management
Heart transplantation (HTx) is an established treatment
option for patients with end-stage heart failure but, as HTx
numbers have been declining, there is a need to explore the
existing donor pool to maximise activity . Although donor
heart assessment remains a critical factor in determining
post-transplant outcome, the criteria for donor heart
selection are ill defined and some hearts that appear
unacceptable on initial data may in fact become satisfactory
for transplantation. Brain-stem death (BSD) may cause
myocardial injury through various mechanisms, which if
undetected may lead to primary graft dysfunction (PGD) and
death of the recipient . Despite best attempts to match
the donor to the recipient, PGD remains the major cause for
30-day mortality . In an attempt to stratify the suitability
of donor hearts for transplantation a number of biomarkers
have been studied [3,4]. Among these are cardiac troponins,
markers of myocardial injury or infarction and an important
prognostic index in ischaemic heart disease and advanced
heart failure . Elevated troponins have been correlated
with donor heart dysfunction and may predict adverse
recipient outcome, being associated in some studies with
increased risk of early graft failure and increased rates of
inotrope requirement post-transplantation and post-trans-
plant rejection [6—10] However, this association remains
controversial as equivalent outcomes have been achieved in
other studies with noincreasedrisk ofrejection [11—13].The
objectives of this study were to evaluate the prevalence of
cardiac troponin-I (cTnI) elevation in heart donors, its
relationship to donor heart function and time from coning,
its predictive value of donor heart suitability and post-
transplant recipient outcome in a prospective study.
European Journal of Cardio-thoracic Surgery 36 (2009) 286—292
§Presented at the 22nd Annual Meeting of the European Association for
Cardio-thoracic Surgery, Lisbon, Portugal, September 14—17, 2008.
§§This study was funded by the British Heart Foundation.
* Corresponding author. Address: Department of Cardiothoracic Surgery,
University Hospital Birmingham NHS Foundation Trust, Edgbaston, Birmingham
B15 2TH, UK. Tel.: +44 121 627 2543; fax: +44 121 627 2542.
E-mail address: email@example.com (R.S. Bonser).
1010-7940/$ — see front matter # 2009 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
acute myocardial infarction in patients. J Mol Cell Cardiol 1989;21:1349—
 Darracott-CankovicS,StovinPG,Wheeldon D,WallworkJ,WellsF,English
TA. Effect of donor heart damage on survival after transplantation. Eur J
Cardiothorac Surg 1989;3:525—32.
 Naidech AM, Kreiter KT, Janjua N, Ostapkovich ND, Parra A, Commichau
C, Fitzsimmons BF, Connolly ES, Mayer SA. Cardiac troponin elevation,
cardiovascular morbidity, and outcome after subarachnoid hemorrhage.
 Zaroff JG, Rordorf GA, Ogilvy CS, Picard MH. Regional patterns of left
ventricular systolic dysfunction after subarachnoid hemorrhage: evi-
dence for neurally mediated cardiac injury. J Am Soc Echocardiogr
 Zaroff JG, Babcock WD, Shiboski SC, Solinger LL, Rosengard BR. Temporal
changes in left ventricular systolic function in heart donors: results of
serial echocardiography. J Heart Lung Transplant 2003;22:383—8.
 Deibert E, Barzilai B, Braverman AC, Edwards DF, Aiyagari V, Dacey R,
Diringer M. Clinical significance of elevated troponin I levels in patients
with nontraumatic subarachnoid hemorrhage. J Neurosurg 2003;98:741—
 Banki NM, Kopelnik A, Dae MW, Miss J, Tung P, Lawton MT, Drew BJ, Foster
E, Smith W, Parmley WW, Zaroff JG. Acute neurocardiogenic injury after
subarachnoid hemorrhage. Circulation 2005;112:3314—9.
 Mertes PM, Carteaux JP, Jaboin Y, Pinelli G, el Abassi K, Dopff C, Atkinson
J, Villemot JP, Burlet C, Boulange M. Estimation of myocardial interstitial
norepinephrine release after brain death using cardiac microdialysis.
Appendix A. Conference discussion
Dr H. Reichenspurner (Hamburg, Germany): Do you include that now in
your daily practice? Do you measure the levels at the donor site, and does it
have any consequence on your clinical practice?
Dr Venkateswaran: No, we do not at the moment. It is not on the schedule
routinely. I think the study actually reiterates the fact it should be done. It is a
very noninvasive available tool. We should measure it, and it could probably
guide us to identify the donor with the worst heart function and target the
donor management to increase the retrieval rate without affecting the
So maybe larger studies are needed to find out whether the findings shown
in this small study group actually are possible.
Dr Reichenspurner: Yes.
Dr D. Jenkins (Cambridge, UK): One comment and one question. It is a
beautiful study, andit all correlates nicely apart from the final step, which just
doesn’t make sense. You must have thought about the reasons for it. Is it just
that you’re very good at optimising the worst donors, and is it to do with the
timing of the original measurements and the time of actual procurement?
Dr Venkateswaran: As I showed you in the slide, there is a significant
inverse correlation between the cardiac troponin-I level and the coning time.
And it definitely looks like in all the donors with an elevated cTnI we probably
went to retrieve the heart soon after they were brain dead from the time of
coning. They were probably in the stage of catecholamine-induced myocardial
stunning. The hearts were probably just recovering from that phase, so we
went in and noted the indices were worse.
If the retrieval was delayed for logistical reasons of getting the brain stem
testing, in some of the donors it was more than 24 h from the time of coning,
we found that their cTnI was going down. We know that the half-life of serum
cardiac troponin-I is around 24 h.
So whatever was released at the time of coning is probably tapering down,
and the heart is recovering from the stunning phenomena.
Dr M. Zembala (Zabrze, Poland): Our policy is to ask for troponin-I always
when we go to the older donor. When we have a young donor who has good
haemodynamic stability, we carry on.
With the older donor, we always go as a mobile group. We echo our expert
site and reinvestigate using Swann—Ganz catheter contractility of the heart
and haemodynamic parameters, and if they are good, we go through.
R.V. Venkateswaran et al./European Journal of Cardio-thoracic Surgery 36 (2009) 286—292