| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1995;92:409-414.)
© 1995 American Heart Association, Inc.
Articles |
Circulating Cardiac Troponin T in Potential Heart Transplant Donors
Presented in part at the seventh Meeting of the International Trauma Anesthesia and Critical Society, Paris, May 23-25, 1994.
From the Département d'Anesthésie-Réanimation (B.R., S.R., J.-P.G., P.L., M.S., P.V.) and Laboratoire de Biologie des Urgences (S.D., M.A.), Groupe Hospitalier Pitié-Salpêtrière, Paris VI University, Paris, France.
Correspondence to Dr Bruno Riou, Département d'Anesthésie-Réanimation, Groupe Hospitalier Pitié-Salpêtrière, 47 boulevard de l'hôpital, 75651 Paris Cedex 13, Paris, France.
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background Brain death may induce myocardial dysfunction, the mechanisms of which are not yet fully understood. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury.
Methods and Results We prospectively measured circulating cardiac
troponin T in 100 brain-dead patients and measured the left
ventricular ejection fraction area (LVEFa), using
transesophageal echocardiography.
Sixty-one patients had normal LVEFa, 25 had moderate decrease in LVEFa
(30% to 50%), and 14 had severe decrease in LVEFa (
30%).
Circulating cardiac troponin T concentrations were significantly higher
(1.68±1.03 µg/L-1, P<.01) in
patients with a severe decrease in LVEFa than in the two other groups
(0.42±0.43 and 0.12±0.16 µg/L-1,
respectively),
and there was a significant correlation between LVEFa and cardiac
troponin T concentration (
=-0.59, P<.0001). An
elevated
circulating cardiac troponin T concentration (
0.5
µg/L-1) was more accurate (sensitivity, 1.00;
specificity, 0.84) in predicting a severe decrease in LVEFa than an
elevated CKMB value or an increased CKMB/CK ratio.
Conclusions An elevated circulating cardiac troponin T was associated with a severe decrease in LVEFa in brain-dead patients, suggesting that severe and potentially irreversible myocardial cell damage occurred. In contrast, CKMB determination was not useful. Since the quality of the donor's heart is considered an important prognosis factor in heart transplantation, the determination of circulating cardiac troponin T concentration could be useful to the heart transplantation team.
Key Words: troponin T • brain death • transplantation
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Numerous experimental and clinical studies have suggested that brain death may induce segmental or global myocardial dysfunction.1 2 3 The mechanism involved in this myocardial dysfunction is not yet fully understood and could be related to (1) a high level of catecholamines in the phase preceding brain death,4 associated with a prolonged release of norepinephrine from cardiac sympathetic nerve endings5 and leading to direct myocardial injury and/or coronary vasospasm; (2) hemodynamic deterioration with low perfusion pressure, which occurs immediately after brain death, leading to stunned myocardium5 ; and (3) reduction in circulating free triiodothyronine, resulting in a reduction in oxidative metabolism.6 Some authors have suggested that brain death–induced myocardial dysfunction is reversible after transplantation.3 7 In contrast, the cardiac function of brain-dead organ donors has been shown to be an important prognostic factor in the clinical outcome of cardiac transplantation.8 9
Troponin T is one of the tropomyosin-binding proteins of the troponin complex located on the actin filament of the myocyte contractile apparatus. After myocardial cell injury, proteins of the contractile apparatus, such as troponin T, are released into the circulation.10 11 Cardiac troponin T is not present in skeletal muscle and can be differentiated from its isoforms in skeletal muscle by immunologic techniques. In the absence of myocardial cell injury, circulating cardiac troponin T is not detectable. Recently, a specific and sensitive assay of cardiac troponin T has been developed.12 At present, circulating cardiac troponin T is considered to be a highly sensitive and specific marker of myocardial cell injury.13
We prospectively measured circulating cardiac troponin T in brain-dead patients and assessed their cardiac function by use of transesophageal echocardiography. We wanted to see whether an elevated level of circulating cardiac troponin T is associated with myocardial dysfunction in brain-dead patients, suggesting that myocardial cell damage occurred, and, if so, whether the dosage of circulating cardiac troponin T might be a useful predictor of severe cardiac dysfunction in brain-dead patients.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
After ethical approval (CCPPRB, GH Pitié-Salpêtrière, Paris) had been obtained, this study was conducted according to the French legislation concerning multiple organ procurement.
Patients
One hundred consecutive brain-dead patients
scheduled for
multiple organ harvesting were prospectively included in the study over
a 2-year period. Patients with a primary cardiac cause of brain death
(myocardial infarction or previous cardiac disease) were excluded.
Nevertheless, patients whose cardiac arrest was related to a noncardiac
cause (hypoxia, hanging, drowning, or cervical spine trauma)
were not excluded. Brain death was certified by (1) a neurological
examination demonstrating the absence of brainstem reflexes; (2) an
apnea test performed after 15 minutes of mechanical ventilation under
an FIO2 of 100% and with intratracheal
continuous high flow of oxygen (15 L · min-1); (3) the
absence of spontaneous ventilation movement after 15 minutes of apnea,
associated with an arterial PCO2
>60 mm Hg; (4) no electrical activity over a 20-minute period of
electroencephalographic recording; and (5) absence of
hypothermia (<35°C) and drugs known to depress the central nervous
system.14
In all patients, the following parameters were recorded during cardiac assessment using transesophageal echocardiography: age, sex, duration of mechanical ventilation, time lapse between brain death and cardiac assessment, mean arterial pressure measured using an indwelling radial artery catheter, heart rate, amount of fluid loading (crystalloids and colloids) administered since brain death, dose of dopamine administered, and body temperature. The following biological parameters were measured: plasma lactate concentration (Dimension apparatus, Du Pont de Nemours), arterial pH, PO2 and PCO2 (BGElectrolytes, Instrumentation Laboratories), and hematocrit levels (Cobas Argos Apparatus, Roche). Moreover, serum creatine kinase (CK) activity and its myocardial isoform (CKMB) activity were measured using immunologic inhibition of CK M-subunit activity (Dimension apparatus, Du Pont de Nemours), as previously described.15 16 In these assays, the reagents and protocols of the manufacturer were used. The upper limit of normal for total CK activity was 210 IU · L-1 and 6 IU · L-1 for CKMB. The ratio CKMB/CK was calculated, and a value of <5% was considered normal. If total serum CK activity exceeded 1000 IU · L-1, serum samples were diluted before CK determination.
Measurement of Circulating Cardiac Troponin T
Circulating
cardiac troponin T concentration was measured by an
enzyme immunoassay (ELISA troponin T, Boehringer Mannheim
GmbH). The method was based on a single-step sandwich principle, with
streptavidin-coated tubes as the solid phase and two monoclonal
anti–human cardiac troponin T antibodies, as previously
described.12 The dosage was administered by technicians
unaware of the patients' histories. Arterial blood samples
were withdrawn on dry tubes and immediately centrifuged, and
serum was stored at -40°C. Troponin T measurements were performed in
duplicate by a batch ELISA analyzer (Enzymun Test System ES
300, Boehringer Mannheim). The coefficient of variation of the
measurement was 5%, and the limit of quantitation was 0.04
µg · L-1. Circulating cardiac troponin T
concentrations <0.5 µg · L-1 were considered
normal. We assigned a value of 0.04 µg · L-1 to
samples that had troponin concentrations below the quantitation
threshold.
Assessment of Cardiac Function
Cardiac function was assessed
by transesophageal
echocardiography (HP Sonos 1500, Hewlett-Packard),
which was performed by a highly trained echocardiographist.
According to our resuscitation protocol of brain-dead patients,
dopamine dose was adjusted to obtain a mean arterial
pressure of between 60 and 100 mm Hg and a diuresis >300
mL · h-1. All assessments of cardiac function were
performed in stable hemodynamic conditions, ie, at
least 1 hour after brain death and with a mean arterial
pressure of >60 mm Hg without changes in dopamine dose over a
15-minute period. Moreover, when brain-dead patients were hypovolemic,
fluid loading was performed before measuring the left
ventricular ejection fraction area (LVEFa). Hypovolemia was
diagnosed when the left ventricular
end-diastolic area (LVEDa) was <5.5
cm2 · m-2, as previously
reported.17 We also performed fluid loading in patients
with a normal LVEDa but a virtual obliteration of the left ventricle
cavity at end systole, resulting in a supranormal value of LVEFa (ie,
of >75%), which could be considered to reflect mild hypovolemia. The
short-axis view of the left ventricle at the mid papillary muscle level
was recorded on videotape and retrospectively analyzed by a
blinded observer. LVEDa and left ventricular end-systolic
area (LVESa) areas were manually traced using the light pen system, as
previously reported.18 Three measures of left
ventricular areas at three consecutive beats were
performed, and the mean was retained. The LVEFa was calculated by means
of Equation 1
:
 | (1) |
Brain-dead
patients were divided into three groups: group 1,
with a normal LVEFa (50%); group 2, with a moderate decrease in
LVEFa (30% to 50%); and group 3, with a severe decrease in LVEFa
(30%). Echocardiographic diffuse wall motion
abnormalities have been shown to independently increase the risk of
early death in the cardiac recipient.9
In a random sample of 25 brain-dead patients, we assessed the intraobserver and interobserver variabilities in the LVEFa measurement by determining the coefficient of variation of the measure. The intraobserver variability was 4.7±3.6% and the interobserver variability was 6.0±4.2%.
Statistical Analysis
The results are expressed as
mean±SD. Nonparametric
tests were used because of the nongaussian distribution
(Kolmogorov-Smirnov test) of many variables studied, including
troponin T, CK, CKMB, and CKMB/CK. Comparison of several means was
performed using the Kruskall-Wallis test, then the Mann-Whitney
U test with the Bonferroni correction. Comparison of several
percentages was performed using the 
2 test with
the Bonferroni correction. Correlation between two variables was
performed using the Spearman rank method. To analyze the
accuracy of troponin T in predicting a low LVEFa, sensitivity,
specificity, and negative and positive predictive values were
calculated.19 Moreover, the receiver operating
characteristic (ROC) curve was obtained, and the area under the ROC
curve (A) and its standard error were calculated, as previously
reported.20 A is thought to be a precise and valid measure
of diagnostic accuracy in that it is not influenced by
decision biases and prior probabilities.20 All tests were
two-tailed, and P values of .05 were considered
significant. The statistical analysis was performed on a
computer using PCSM software (Deltasoft).
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
One hundred consecutive brain-dead patients were included in the study (mean age, 39±13 years; range, 16 to 68 years; 66 men and 34 women). During the study period, only 1 brain-dead patient was excluded, since cardiac arrest was related to myocardial infarction. The cause of brain death was head trauma in 52, cerebrovascular disease in 40, and cerebral anoxia related to cardiac arrest in 8 patients. In these last 8 patients, cardiac arrest was not related to a primary cardiac cause. In the 100 brain-dead patients, 61 had normal LVEFa (60±7%), 25 had moderate decrease in LVEFa (42±5%), and 14 had severe decrease in LEVFa (22±6%). The comparison between these three groups is shown in Table 1
. There were no significant
differences in LVEFa in patients whose brain death was related to head
trauma (51±12%), cerebrovascular disease (48±19%), or cardiac
arrest (53±13%). Severe left ventricular dysfunction
occurred in 4 patients (8%) with head trauma, in 10 patients (25%)
with cerebrovascular disease, and in no patients with cardiac
arrest.
|
As shown in Table 2, there were no significant
differences in CK, CKMB, and CKMB/CK between the three groups. The
percentages of patients with elevated CKMB or CKMB/CK were not
significantly different between the three groups. In contrast,
circulating cardiac troponin T was significantly higher in patients
with a severe decrease in LVEFa (Table 2). There was no
significant
correlation between LVEFa and CK (=-0.05,
P=.31) or
between LVEFa and CKMB/CK (=-0.13, P=.10).
In contrast,
there was a significant correlation between LVEFa and CKMB
(=-0.17,
P=.048) and a highly significant correlation between LVEFa
and circulating cardiac troponin T concentration (=-0.59,
P<.0001) (Fig 1).
|
|
As shown in Table 3, an elevated circulating cardiac
troponin T concentration was more accurate than an elevated CKMB value
or an elevated CKMB/CK ratio in predicting a severe decrease in LVEFa.
An ROC curve illustrates the relation between sensitivity and
specificity in determining the predictive value of circulating cardiac
troponin T concentration for severe decrease in LVEFa (Fig 2).
The area under the ROC curve was A=0.980±0.027,
indicating a very accurate diagnostic tool.19
In comparison, the areas under the ROC curve were not significantly
different from 0.50 for CKMB (A=0.565±0.09) and CKMB/CK
(A=0.423±0.105), indicating the lack of accuracy of these two
parameters in predicting a low LVEFa (Fig 3).
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
In the present study, we measured circulating cardiac troponin T in brain-dead patients who underwent cardiac function assessment by transesophageal echocardiography. We observed that an elevated circulating cardiac troponin T concentration was correlated to a severe decrease in LVEFa (Fig 1
) and
was an accurate diagnostic tool in predicting such a severe
decrease in LVEFa (Fig 2). Brain death may induce severe myocardial dysfunction. Goarin et al21 observed that a severe decrease in LVEFa occurred in 18% of brain-dead patients. In the present study, we observed that 39% of brain-dead patients had an abnormal LVEFa and that 14% had a severe decrease in LVEFa that would have precluded heart harvesting for transplantation.9 21 22 The precise mechanisms involved in this myocardial dysfunction remain unknown. Consequently, the reversibility of this myocardial dysfunction is also a matter for debate. Indeed, Galinanes et al3 have recently performed an experimental study suggesting that brain death–induced myocardial dysfunction is reversible after explantation. Nevertheless, in their study, myocardial dysfunction after brain death was only assessed by the measurement of dP/dt, which is considered an unreliable index of cardiac function, especially when a dramatic decrease in afterload is observed. Thus, the possibility that these authors failed to induce myocardial dysfunction after brain death cannot be ruled out.3 In contrast, other studies have shown a relation between myocardial dysfunction in the heart donor and a poor clinical outcome in the heart transplant recipient.8 9 Our study demonstrated that high levels of circulating cardiac troponin T occurred in brain-dead patients with severe myocardial dysfunction. Circulating cardiac troponin T has been shown to be associated with cardiac ischemic damage during unstable angina13 and myocardial infarction.10 11 Thus, our results suggest that brain death–induced myocardial dysfunction is associated to some degree with irreversible myocardial cell damage, even if other mechanisms (potentially reversible or not) may also participate in this myocardial dysfunction. Our results are compatible with the hypothesis that the enormous sympathetic activity that occurs just before brain death-and the prolonged release of endogenous catecholamines from cardiac sympathetic nerve endings that occurs after brain death-may be responsible for this myocardial dysfunction.4 5
Precise assessment of the heart donor is essential, since it is an
important prognosis factor in heart transplantation
outcome8 9 and 18% of brain-dead patients have a
severe
decrease in LVEFa.21 However, this assessment is not easy
because most brain-dead patients receiving dopamine and/or
vasoconstrictors have elevated heart rate, low arterial
pressure, and low oxygen consumption. Cardiac assessment with a
Swan-Ganz catheter has been shown to be an unreliable
diagnostic tool in these patients.21 As shown
in Table 1, no significant differences in mean arterial
pressure and plasma lactates were observed in patients with or without
myocardial dysfunction. Only 3 of the 14 patients with a severe
decrease in LVEFa required the administration of epinephrine
and/or dobutamine (Table 1). Thus, only
echocardiography can precisely assess cardiac
function in brain-dead patients.21 22 Moreover,
because
brain-dead patients are mechanically ventilated and may require
positive end-expiratory pressure administration,
transesophageal echocardiography is
often necessary to obtain high-quality imaging. However, not all
centers are able to perform transesophageal
echocardiography in potential heart donors, and
many transplantation teams perform heart harvesting in small centers
with few facilities. When the brain-dead patient has an unstable
hemodynamic status, requiring high doses of
catecholamines, it is well known that cardiac function
sometimes may be preserved, but, in these conditions, the heart
transplantation team would not select such donors without further
cardiac assessment. Therefore, transplantation teams may be interested
in a simple diagnostic procedure that could enable them to
precisely diagnose severe myocardial dysfunction in heart donors.
We showed that CKMB and CKMB/CK determinations could not indicate
myocardial dysfunction in brain-dead patients. These results are not
surprising because the variable normal values of CKMB and the brief
elevation of CKMB after myocardial necrosis are known to limit the
diagnostic value.23 24 Moreover, CKMB is not
totally specific to myocardial cells and is also present in
skeletal muscle.25 In our patients, brain injury was an
obvious source of CK, and in patients whose brain death was related to
trauma, skeletal muscle was probably another important source of CK and
CKMB release. In patients with both skeletal and cardiac muscle damage,
the determination of the ratio of CKMB/CK has been shown to improve
specificity but with an unacceptable loss of sensitivity in predicting
myocardial infarction.26 In the present study, CKMB
and CKMB/CK had a very poor diagnostic value in predicting
a severe decrease in LVEFa (Table 3 and Fig 2).
Nevertheless, the
significant correlation between LVEFa and CKMB indicated that part of
CKMB came from the myocardium and therefore also suggests
that myocardial cell injury was associated with brain death–induced
myocardial dysfunction.
Our results suggest that circulating cardiac troponin T determination
might fulfill the criteria of a simple diagnostic procedure
indicating severe myocardial dysfunction in brain-dead patients (Table
3 and Fig 2). Of course, this factor should be
included in the
perspective of heart donor shortage and with the risk of excluding too
many heart donors from transplantation. Because of the high sensitivity
and negative predictive value, elevated cardiac troponin T
concentrations might indicate that further donor heart assessment is
mandatory. We suggest that hemodynamically unstable
brain-dead patients who require high doses of
catecholamines but who have a normal concentration of
circulating cardiac troponin T may be considered for heart donation.
The results concerning the prognostic value of an elevated
concentration of cardiac circulating troponin T in brain-dead patients
should be interpreted with great caution. Indeed, because elevated
cardiac troponin T concentrations were associated with a decreased
LVEFa (Fig 1), most of the hearts in brain-dead patients with a
high
concentration of cardiac troponin T were not transplanted. Thus, the
number of heart donors with a high concentration of cardiac troponin T
(n=6) was too small to draw any conclusion, and only a large,
multicenter, prospective study could determine the precise consequence
of an elevated concentration of cardiac troponin T on the heart
recipient outcome. Nevertheless, it should be pointed out that first,
echocardiographic diffuse wall motion abnormalities
independently increase the risk of early death in the adult cardiac
recipient9 and that an elevated circulating cardiac
troponin T concentration is associated with such severe
echocardiographic abnormalities; second, two recent
reports support the hypothesis that an elevated cardiac troponin
concentration in the donor can modify the heart recipient
outcome.27 28 Grant et al27 have noted
that
elevated donor cardiac troponin I appears to be a marker of acute graft
failure in infant heart recipients, and Anderson et al28
have observed that elevated donor cardiac troponin T is associated with
a significant increase in the incidence of catecholamine
support in the heart recipient.
Some remarks must be included to assess the relevance of our
results. First, the threshold for normal cardiac troponin T
concentration was set at 0.5 µg · L-1 before
initiating the study, as previously reported.11 13
Recent
studies have suggested that the threshold for myocardial infarction
should be lower. Nevertheless, our results showed that a lower
threshold would have resulted in an unacceptable loss of specificity in
predicting a severe decrease in LVEFa (Fig 2). On the contrary,
our
results suggest that the threshold value of cardiac troponin T
concentration might be slightly increased to more accurately predict a
severe decrease in LVEFa in brain-dead patients (Fig 2). It
should be
pointed out that in the present study, cardiac troponin T was not
used to diagnose myocardial cell damage that probably occurred to a
lesser degree in some patients with a moderate decrease in LVEFa (Fig
1
and Table 2) but was used to diagnose a severe decrease in
myocardial
function. Moreover, there are data to indicate that there may not be a
perfect cardiac specificity with troponin
T,11 12 13 which
also may argue for a higher threshold value. Second, LVEFa is not
considered a reliable parameter of myocardial
contractility because it is both preload and afterload
dependent, and a precise assessment of myocardial
contractility would have required more sophisticated
methods, such as determination of the end-systolic pressure-volume
relation.29 Nevertheless, LVEFa is considered to be an
efficient and integrated measure of the heart's ability to cope with
abnormalities in the three variables that determine
ventricular function, that is, preload, afterload, and
contractility.30 Moreover, hypovolemia was
corrected before cardiac assessment, and no significant differences in
mean arterial pressure were observed between groups (Table 1),
suggesting that afterload was similar in all groups. Third, we
measured fractional ventricular area changes and not volume
changes by use of transesophageal
echocardiography. However, LVEFa measured by use of
transesophageal echocardiography
has been shown to accurately correlate with LVEF measured by use of
radionuclide angiography.18
Conclusions
We demonstrated that an elevated circulating
cardiac troponin T
concentration was associated with a severe decrease in cardiac function
in brain-dead patients, suggesting that severe and potentially
irreversible myocardial cell damage occurred. In contrast, CKMB
determination was not useful in brain-dead patients. Circulating
cardiac troponin T concentration determination was an interesting
diagnostic tool in predicting a severe decrease in LVEFa in
brain-dead patients (sensitivity, 1.00; specificity, 0.84). Since the
quality of the donor's heart is considered an important prognosis
factor in heart transplantation, the determination of circulating
cardiac troponin T concentration could be useful to heart
transplantation teams. Nevertheless, the precise relation between an
elevated circulating cardiac troponin T concentration and heart
transplantation outcome remains to be determined and requires a large,
prospective, multicenter study.
|
Acknowledgments |
|---|
Thanks to Boehringer Mannheim for kindly providing all facilities to administer the dosage of cardiac troponin T.
Received November 30, 1994; revision received January 23, 1995; accepted January 28, 1995.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Novitzky D, Wicomb WN, Cooper DKC, Rose AG, Fraser RC, Barnard CN. Electrocardiographic, hemodynamic and endocrine changes occurring during experimental brain death in the Chacma baboon. J Heart Transplant. 1984;4:63-69.
2. Novitzky D, Rose AG, Cooper DKC. Injury of myocardial conduction tissue and coronary artery smooth muscle following brain death in the baboon. Transplantation. 1988;45:964-966. [Medline] [Order article via Infotrieve]
3.
Galinanes M, Hearse DJ. Brain death–induced
impairment of cardiac contractile performance can be reversed
by explantation and may not preclude the use of hearts for
transplantation. Circ Res. 1992;71:1213-1219.
4.
Pilati CF, Bosso FJ, Maron MB. Factors involved
in left ventricular dysfunction after massive sympathetic
activation. Am J Physiol. 1992;263:H784-H791.
5. 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. Transplantation. 1994;57:371-377. [Medline] [Order article via Infotrieve]
6.
Bolli R. Mechanism of myocardial `stunning.'
Circulation. 1990;82:723-738.
7. Novitzky D, Cooper DKC, Morrell D, Isaacs S. Change from aerobic to anaerobic metabolism after brain death, and reversal following triiodothyronine therapy. Transplantation. 1988;45:32-36. [Medline] [Order article via Infotrieve]
8. Darracott-Cankovic S, Stovin PGI, Wheeldon D, Wallwork J, Wells F, English TAH. Effect of donor heart damage on survival after transplantation. Eur J Cardiothorac Surg. 1989;3:525-532. [Abstract]
9. Young JB, Naftel DC, Bourge RC, Kirklin JK, Clemson BS, Porter CB, Rodeheffer RJ, Kenzora JL, Cardiac Transplant Research Database Group. Matching the heart donor and heart transplant recipient: clues for successful expansion of the donor pool: a multivariable, multiinstitutional report. J Heart Lung Transplant. 1994;13:353-365. [Medline] [Order article via Infotrieve]
10. Katus HA, Remppis A, Looser S, Hallermeier K, Scheffolf T, Küber W. Enzymed linked immunoassay of cardiac troponin T for the detection of acute myocardial infarction in patients. J Mol Cell Cardiol. 1989;21:1349-1353.[Medline] [Order article via Infotrieve]
11.
Katus HA, Remppis A, Neumann FJ, Scheffold T, Diederich
KW, Vinar K, Noe A, Matern G, Kuebler W. Diagnosis efficiency of
troponin T measurements in acute myocardial infarction.
Circulation. 1991;83:902-912.
12.
Katus HA, Looser S, Hallermayer K, Remppis A, Scheffold
T, Borgya A, Essig U, Geuss U. Development and in vitro
characterization of a new immunoassay of cardiac troponin T.
Clin Chem. 1992;38:386-393.
13. Hamm CW, Ravkilde J, Gerhardt W, Jorgensen P, Peheim E, Ljungdahl L, Goldmann B, Katus HA. The prognostic value of serum troponin T in unstable angina. N Engl J Med. 1992;327:146-150. [Abstract]
14. Kofke WA, Darby JM. Evaluation and certification of brain death. In: Grande CM, ed. Textbook of Trauma Anesthesia and Critical Care. St Louis, Mo: Mosby Year Book; 1993:994-1006.
15. Rosalski SB. An improved procedure for serum creatine phosphokinase determination. J Lab Clin Med. 1967;69:696-705.
16. Neumeier D, Prellwitz W, Würzburg U, Brundobler M, Olbermann M, Just H-J, Knedel M, Lang H. Determination of CK-MB activity in serum using immunological inhibition of CK-M subunit activity. Clin Chim Acta. 1976;73:445-551. [Medline] [Order article via Infotrieve]
17. Feigenbaum H. Echocardiographic measurements and normal values. In: Feigenbaum H, ed. Echocardiography. 4th ed. Philadelphia, Pa: Lea & Febiger; 1986:621-639.
18.
Folland ED, Parisi AF, Moynihan PF, Jones DR, Feldman
CL, Tow DE. Assessment of left ventricular ejection
fraction and volumes by real-time, two-dimensional
echocardiography: a comparison of cineangiographic
and radionuclide techniques. Circulation. 1979;60:760-766.
19.
Swets JA. Measuring the accuracy of
diagnostic systems. Science. 1988;240:1285-1293.
20.
Hanley JA, McNeil BJ. The meaning and use of the
area under a receiver operating characteristic (ROC) curve.
Radiology. 1982;143:29-36.
21. Goarin JP, Cohen S, Jacquens Y, Le Bret F, Clergue F, Viars P. Left ventricular function in brain dead donors: assessment using transesophageal echocardiography. Anesthesiology. 1990;73:A84. Abstract.
22. Gilbert EM, Krueger SK, Murray JL, Renlund DG, O'Connell JB, Gay WA, Bristow MR, the Utah Cardiac Transplant Program. Echocardiographic evaluation of potential cardiac transplant donors. J Thorac Cardiovasc Surg. 1988,95:1003-1007.
23. Shell WE, DeWood MA, Kligerman M, Ganz W, Swan HJC. Early appearance of MB-creatine kinase activity in non-transmural myocardial infarction detected by a sensitive assay for the isoenzyme. Am J Med. 1981;71:254-262. [Medline] [Order article via Infotrieve]
24.
Irvin RG, Cobb FR, Roe CR. Acute myocardial
infarction and MB creatine phosphokinase: relationship between onset of
symptoms of infarction and appearance and disappearance of
enzyme. Arch Intern Med. 1980;140:329-334.
25. Jockers-Wretou E, Pfleiderer G. Quantitation of creatine kinase in human tissues and sera by an immunological method. Clin Chim Acta. 1975;58:223-229.[Medline] [Order article via Infotrieve]
26.
Thompson WG, Mahr RG, Yohannan WS, Pincus MR.
Use of creatine kinase MB isoenzyme for diagnosing myocardial
infarction when total creatine kinase activity is high.
Clin Chem. 1988;34:2208-2210.
27.
Grant JW, Canter CE, Spray TL, Landt Y, Saffitz JE,
Ladenson JH, Jaffe AS. Elevated donor cardiac troponin I: a
marker of acute graft failure in infant heart recipients.
Circulation. 1994;90:2618-2621.
28. Anderson JR, Hossein-Nia M, Brown P, Holt DW, Murday A. Donor cardiac troponin-T predicts subsequent inotrope requirements following cardiac transplantation. Transplantation. 1994;58:1056-1057. [Medline] [Order article via Infotrieve]
29. Sasaki H, Sada M, Beppu S, Adachi R, Yokoyama Y, Kawaguchi O, Tajima K, Kawazoe K, Kito Y, Fujita T. Left ventricular pressure-volume relationships in brain-dead canine hearts: preoperative evaluation of donor hearts. Transplant Proc. 1989;21:2570-2572. [Medline] [Order article via Infotrieve]
30. Robotham JL, Takata M, Berman M, Harasawa Y. Ejection fraction revisited. Anesthesiology. 1991;74:172-183.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  D. A. Waxman, S. Hecht, J. Schappert, and G. Husk A Model for Troponin I as a Quantitative Predictor of In-Hospital Mortality J. Am. Coll. Cardiol., November 7, 2006; 48(9): 1755 - 1762. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Caus, F. Kober, A. Mouly-Bandini, A. Riberi, D. R. Metras, P. J. Cozzone, and M. Bernard 31P MRS of heart grafts provides metabolic markers of early dysfunction Eur. J. Cardiothorac. Surg., October 1, 2005; 28(4): 576 - 580. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Vijay, V. A. Scavo, R. J. Morelock, T. G. Sharp, and J. W. Brown Donor cardiac troponin T: a marker to predict heart transplant rejection Ann. Thorac. Surg., December 1, 1998; 66(6): 1934 - 1938. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Hossein-Nia, D. W. Holt, J. R. Anderson, A. J. Murday, J.-P. Etievent, and S. Chocron Cardiac troponin I release in heart transplantation. Ann. Thorac. Surg., January 1, 1996; 61(1): 277 - 278. [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||