International Journal of Cardiology 173 (2014) 216–221

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Weak diagnostic performance of troponin, creatine kinase and creatine kinase-MB to diagnose or exclude myocardial infarction after successful resuscitation☆ Jan M. Kruse a,⁎,1,2, Philipp Enghard a,1,2, Tim Schröder a,1, Dietrich Hasper a,1, York Kühnle b,1, Achim Jörres a,1, Christian Storm a,1 a b

Abteilung für Nephrologie und Internistische Intensivemdizin, Charité Universitätsmedizin Berlin, Germany Abteilung für Kardiologie, Charité Universitätsmedizin Berlin, Germany

a r t i c l e

i n f o

Article history: Received 13 September 2013 Accepted 19 February 2014 Available online 28 February 2014 Keywords: Cardiac arrest Myocardial infarction Coronary angiography Creatine kinase Troponin Cardiopulmonary resuscitation

a b s t r a c t Background: The aim of this study is to evaluate the diagnostic accuracy of the cardiac injury markers troponin (TNT), creatine kinase (CK) and creatine kinase-MB (CK-MB) to diagnose or exclude acute myocardial infarction after cardiac arrest. Methods: 226 patients who underwent diagnostic coronary angiography after sudden cardiac arrest were analyzed retrospectively. Levels of TNT, CK and CK-MB on admission and 6 h, 24 h and 36 h later were retrieved from the files and compared with the results of coronary angiography. Results: Acute myocardial infarction (AMI) as well as non-AMI patients showed increasing levels of TNT and CK after resuscitation, although the AMI group showed significantly higher TNT and CK levels. Receiver operator curves were calculated to determine the diagnostic precision of TNT, CK and CK-MB to differentiate AMI and non-AMI patients. All analyzed markers yielded mediocre diagnostic precision with an area under the ROC curve of 0.7020, 0.6802 and 0.6508 for 6 h TNT, CK and CK-MB, respectively. Applying a modified cut-off of 1 μg/l the 6 h TNT measurement had a sensitivity of 70.9% and specificity of 61.2% to diagnose AMI after cardiac arrest. Using CK 800 U/l as cut-off level resulted in a sensitivity of 62.5% and specificity of 73.7%, CK-MB levels higher than 100 U/l yielded a sensitivity of 58.8% and specificity of 72.7%. Conclusion: Cardiac injury markers cannot be used to reliably diagnose or rule out AMI after resuscitation. Consequently we propose that indication for coronary angiography should be extended to all patients without a certain alternative diagnosis explaining the occurrence of cardiac arrest. © 2014 Elsevier Ireland Ltd. All rights reserved.

1. Introduction Sudden cardiac arrest (SCA) is a frequent event and a leading cause of death in western countries [1,2]. Acute myocardial infarction (AMI) is one of the most frequent causes of SCA [1]. Patients who survive to hospital admission should receive a standardized postresuscitation care to improve the probability of survival and favorable neurological outcome [3,4]. Initiation of therapeutic hypothermia as early as possible not only leads to better neurologic outcome [5,6] but may also improve cardiac function [7,8]. Moreover, recent studies suggested a survival benefit for patients who underwent urgent percutaneous coronary

☆ No financial support was used for the study. ⁎ Corresponding author at: Spiegelweg 2, 14057 Berlin, Germany. Tel.: +49 3012029552. E-mail address: [email protected] (J.M. Kruse). 1 This author takes responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation. 2 Shared authorship.

http://dx.doi.org/10.1016/j.ijcard.2014.02.033 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

intervention (PCI) after successful resuscitation [9–13]. Accordingly, current guidelines advocate the use of PCI in all patients after successful resuscitation in whom coronary artery disease and cardiac ischemia are suspected [14]. (See Table 1.) The diagnostic hallmark of acute myocardial ischemia and -infarction is the ECG. For patients after cardiac arrest however the ECG was reported a poor predictor of coronary artery occlusion [13]. Alternative cardiac markers such as troponin T and I, creatine kinase and its isoenzymes can be used to diagnose myocardial infarction [15–17]. Whether and in which way the blood levels of cardiac markers are influenced by cardiopulmonary resuscitation is still a matter of debate. Most publications reported good diagnostic performance of troponin and CK to detect AMI in patients after resuscitation [18–20]. In contradiction a recent publication demonstrated only weak sensitivity and specificity of cardiac troponin to detect AMI after resuscitation [21]. Furthermore several groups reported various resuscitation specific confounders of cardiac marker levels. Thus, the diagnostic accuracy of cardiac injury markers upon cardiopulmonary resuscitation is still uncertain [19,20,22–24].

J.M. Kruse et al. / International Journal of Cardiology 173 (2014) 216–221 Table 1 Baseline characteristics of the analyzed patients. Values are given as absolute numbers and percent or median and percentiles (25–75). Data on adrenalin dose and time to ROSC was missing in 5 patients, ventilator time in 3 and the APACHE score in 16 patients. Variable

All 226

AMI 117

Non AMI 109

p-value

Adrenalin (mg) ROSC (min) Age (years) Gender male APACHE Ventilator time (h) Shockable rhythm Location OHCA Good outcome Poor outcome

3 (1–5) 20 (13–30) 63 (54–70) 177 (78) 28 (22–33) 232 (118–433) 167 (74) 185 (82) 94 (42) 132 (58)

3 (1–5) 22 (14–30) 61 (51–69) 98 (84) 27 (21–33) 237 (135–452) 95 (82) 99 (85) 45 (38) 71 (61)

3 (1–5) 20 (13–29) 65 (57–71) 79 (72) 28 (23–34) 214 (105–426) 72 (66) 86 (79) 49 (45) 61 (56)

n.s. n.s. n.s. 0.02 n.s. n.s. b0.01 n.s. n.s. n.s.

Here we report the results of a single-center retrospective trial to evaluate troponin T (TNT), creatine kinase (CK) and creatine kinaseMB (CK-MB) in patients with successful cardiopulmonary resuscitation to later invasive diagnosis of AMI by comparing measured concentrations of these cardiac markers to the results of coronary angiography as the current gold standard for AMI diagnosis. 2. Methods 2.1. Patients We enrolled all patients N18 years of age who suffered an event of sudden cardiac arrest (SCA), were primarily successfully resuscitated, received a diagnostic coronary angiography and were admitted to one of our Intensive Care Units in the years 2001 to 2010. The decision, whether a patient received angiography or not, was left to the discretion of the cardiologist and/or intensivist in charge. All forms of cardiac arrest, shockable as well as non-shockable rhythms, out of hospital as well as in hospital cardiac arrests were included. Patients were included regardless, whether they had a history of CAD respectively AMI or not. All patients were treated according to the current ESC-guidelines for postresuscitation care. Patients treated in 2005 and later underwent therapeutic hypothermia according to our local protocol. The supportive therapy was left to the discretion of the attending physician. In this study 226 patients who underwent diagnostic coronary angiography after sudden cardiac arrest (SCA) were analyzed retrospectively. CK values were available in 213, 132, 174 and 170 patients for the time points “initial”, 6 h, day 2 and day 3, respectively. CK-MB values for the respective time points were available in 126, 100, 138 and 158 patients, and TNT values in 205, 112, 113 and 93 patients. The Pittsburgh cerebral performance category was used to analyze the global outcome at discharge from ICU. The study was conducted according to the principles of the Declaration of Helsinki (World Medical Association 2008).

2.2. Data collection The data were collected retrospectively from the protocols of the rescue service and the electronic patient files. Data collected included the initial time of alarming the rescue service, arrival of the rescue team, initial heart rhythm, time to return of spontaneous circulation (ROSC), dose of adrenalin, angiographic diagnosis, survival and neurologic outcome. The levels of troponin T, CK and CK-MB were recorded on admission, after 6 h and on day 2 (=24 h) and 3 (=36 h).

2.3. Angiographic diagnosis We analyzed the angiography reports of the patients included. Acute myocardial infarction was defined as occlusion of a coronary vessel that was assumed to be recent and interpreted as the culprit lesion by the cardiologist in charge. Coronary artery disease (CAD) was defined as at least one significant stenosis of 50% or more in the coronary angiography report. Patients who had no coronary artery stenosis of at least 50% were classified as having no CAD.

2.4. Analysis of cardiac injury markers The UV based kinetic assay was used to measure CK activity on admission, at 6 h and the second and third days after admission. The cut-off value according to the manufacturer for creatine kinase (CK) was 170 U/l for men and 145 U/l for women respectively. Creatine kinase-MB (CK-MB) was measured using a UV based assay with inhibition of CK-M with the recommended cut-off of 24 U/l.

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Cardiac troponin T was measured on admission, after 6 h, and on the second and third days after admission using an immunologic assay. The cut-off value according to the manufacturer was b0.05 μg/l. The assays used were not changed by the laboratory during the period of the study. 2.5. Statistical analysis Continuous data are reported as the median and the interquartile range (IQR) and comparison was made using the two tailed Mann–Whitney test. The Spearman coefficient was used to determine correlations. For categorical variables we used frequencies and percentages and the chi-square test or Fisher's exact test. Statistical analysis was performed using SPSS (Version 19, IBM), and graphs were generated using GraphPad prism 3.0.

3. Results 3.1. Cardiac injury markers after resuscitation peak 6–24 h after admission 226 patients who underwent diagnostic coronary angiography after sudden cardiac arrest (SCA) were analyzed retrospectively. 117 patients were angiographically classified as having acute myocardial infarction (AMI), 86 patients showed coronary artery disease without signs of acute vascular occlusion and 23 patients showed no signs of coronary artery disease (all patients without signs of acute coronary occlusion were termed non-AMI). As expected, patients with AMI showed increasing levels of CK and TNT, with peak values at 6–24 h after admission. TNT values at 6 h, 2 d and 3 d after admission were significantly higher than the level on admission (p b 0.0001 for 6 h and 2 d, p = 0.0003 for d3). Likewise CK values were higher at all time points after admission (compared to 6 h CK p = 0.0007, 2 d p b 0.0001, 3 d p = 0.0001). There was no significant difference between the 6 h and 2 d CK or TNT. There was no significant increase of CK-MB until d3 (p0.0097) (Fig. 1). In the non-AMI group there also was a significant increase of TNT and CK levels over time. In the values obtained 6 h after admission there was a significant increase of TNT (p b 0.001), but not of CK. On day 2 changes for both CK and TNT levels were highly significant (p b 0.0001). In the non-AMI group no significant changes of CK-MBconcentrations could be found over time (Fig. 1). 3.2. Patients with sudden cardiac arrest due to AMI demonstrate higher cardiac markers than patients with cardiac arrest without AMI On admission the AMI patient group showed significantly higher TNT and CK levels than the non-AMI group (median TNT values 0.60 and 0.11 respectively, p = 0.0030; median CK values 361 and 202 U/l respectively, p for CK 0.0002). In the analysis 6 h after admission the difference between AMI and non-AMI patients was even more obvious for TNT (median TNT 2.86 and 0.64 respectively, p = 0.0002) and stayed significant for CK (median CK 1403 U/l and 265.5 U/l respectively, p =0.0002). Likewise the TNT and CK values obtained 1 and 2 days after admission were significantly higher in the AMI than the non-AMI group (Fig. 2). For CK-MB we observed a significant difference between both groups 6 h after admission (median CK-MB 151 and 64 respectively, p = 0.0074). Likewise 1 and 2 days after admission significantly higher CKMB levels were seen in AMI patients (Fig. 2). 3.3. Weak correlation of coronary artery stenosis with cardiac markers In the non-AMI group, 86 of 109 patients showed coronary artery disease, defined as stenosis of at least one coronary vessel graded N50%, while 23 patients showed no detectable stenosis. The TNT levels acquired on admission did not show a significant correlation with the grade of stenosis, but values obtained 6 h and 1 day after admission both significantly correlated (Spearman p = 0.0483, r = 0.1932 and p = 0.0163, r = 0.2296 respectively). For CK the values obtained on admission (p = 0.0164, r = 0.1658) and on day 2 (p = 0.0068, r = 0.2088) correlated significantly with the extent of stenosis, for CK-MB only the day 2 and day 3 levels (p = 0.0418. r = 0.1774 and p = 0.0417, r = 0.1654).

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Fig. 1. Patients after succesful cardiopulmonary reanimation show increasing TNT and CK levels. A, B and C: Cardiac markers in patients after resuscitation and AMI. Significant increase of TNT (A) and CK (B) levels peaking 6–24 h after the event. No significant increase of CK-MB (C) levels comparing initial values with the 6 h and 24 h follow up measurements. C, D and E: Cardiac markers in patients after resuscitation without AMI. Significant increase of TNT (D) and CK (E) levels with peak values achieved 6–24 h after resuscitation. No significant increase in CK-MB (F).

Furthermore we observed no significant difference in the CK and TNT levels between patients with subcritical coronary artery disease (nonAMI) and patients with absence of coronary artery disease (Fig. 3). 3.4. Impact of time to ROSC and defibrillation on CK and TNT levels In the non-AMI group the 6 h, day 1 and day 3 levels for CK correlated with the duration of CPR (low-flow-time) (p = 0.0142 and r = 0.3232 for 6 h, p b 0.0001 and r = 0.4610 for d1 and p = 0.0004 and r =

0.4238 for d3). Similarly CK-M levels on admission and 6 h later also correlated with time to ROSC (p = 0.0048 and r = 0.3220 and p = 0.0180 and r = 0.3401 respectively). No such correlation was observed for TNT. In contrast in AMI patients no correlation was observed for any of the analysis markers and time points (Fig. 4). No difference was observed in the levels of cardiac injury markers between patients that had undergone cardiac defibrillation or not, regardless whether they were diagnosed as having AMI or no-AMI.

Fig. 2. Patients with cardiac arrest due to AMI present higher levels of cardiac injury markers than non-AMI patients after successful reanimation. A, B and C: Levels of TNT, CK and CK-MB drawn immediately after resuscitation. Patients with AMI show significantly higher values of TNT (A) and CK (B). No significant difference in the levels of CK-MB (C). D, E and F: Analysis 6 h after cardiopulmonary reanimation. Patients with AMI present significantly higher levels of TNT (D), CK (E) and CK-MB (F).

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Fig. 3. Weak correlation of the grade of coronary artery stenosis with cardiac injury markers. A. No significant correlation of initial TNT levels with the grade of coronary artery stenosis (Spearman p = 0.2272, r = 0.0864). B. Significant correlation of initial CK values with the grade of stenosis (Spearman p = 0.0164, r = 0.1658). C. Positive correlation between 6 h TNT levels with the grade of coronary artery stenosis (Spearman p = 0.0483, r = 0.1932). D. No correlation between 6 h CK measurements and coronary artery stenosis (Spearman p = 0.1719, r = 0.1225).

3.5. Diagnostic performance of CK, TNT and CK-MB to differentiate patients with and without AMI after resuscitation ROC curves were generated to determine the diagnostic precision of cardiac injury markers to diagnose AMI after resuscitation. Using the manufacturer's cut-off of 0.5 μg/l for TNT yielded for the 6 h values a sensitivity of 83.6% and specificity of 49.0%. For the 6 h CK (cut-off 170 U/l) a sensitivity of 82.8% and specificity of 33.3% were observed, for the 6 h CK-MB (cut-off 25 U/l) the sensitivity was 92.2% and the specificity 13.6% (Fig. 5).

In order to increase the specificity higher cut-off values were tested. Applying a cut-off of 1 μg/l for 6 h TNT yielded a sensitivity of 70.9% and specificity of 61.2%. For the 6 h CK using 800 U/l as cutoff resulted in a sensitivity of 62.5% and specificity of 73.7%, and for CK-MB a cut-off of 100 U/l gave a sensitivity of 58.8 and specificity of 72.7%. Subgrouping the patients according to the time to ROSC (b25 min or over) and rhythm (shockable or non-shockable) did not relevantly increase the diagnostic accuracy of cardiac injury markers to diagnose AMI after resuscitation.

Fig. 4. Influence of time to ROSC on 6 h TNT and CK levels. A. No significant correlation of tROSC with 6 h TNT values in AMI patients (Spearman p = 0.1715, r = 0.1925) B. No significant correlation between 6 h CK levels and tROSC in AMI patients (Spearman p = 0.6746, r = 0.0544). C. No correlation of 6 h TNT levels in non-AMI patients with tROSC (Spearman p = 0.1076, r = 0.2403). D. Significant correlation of 6 h CK values with tROSC in non-AMI patients (Spearman p = 0.0142, r = 0.3232).

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Fig. 5. ROC curves for 6 h cardiac injury markers. A. ROC curve for 6 h value of TNT (AUC 0.7020). B. ROC curve for 6 h CK levels (AUC 0.6802) C. ROC curve for 6 h CK-MB values (AUC 0.6508).

Of note, the sensitivity and specificity of the feature “shockable rhythm” for later detection of acute myocardial infarction in the coronary angiography were 82.9% and 57.0% respectively. 3.6. No correlation peak cardiac markers with prognosis Neurological outcome was assessed by the Pittsburgh cerebral performance category at discharge from ICU. In 45.7% (n = 96/210) a good neurological outcome was achieved (CPC 1–2) whereas 54.3% (n = 114/210) had a poor outcome including 33.3% (n = 70/210) of the patients who died. There was no statistically significant correlation between neurological outcome and TNT or CK levels at admission and after 6 h (CK at admission Spearman p = 0.7936, r = − 0.0189, CK 6 h Spearman p = 0.5708, r = 0.0520, TNT at admission Spearman p = 0.3942, r = 0.0638, THT 6 h Spearman p = 0.0731, r = 0.1765). Furthermore there was no significant correlation between neurological outcome and PCI diagnosis (patients grouped as having either AMI, coronary heart disease but no AMI or absence of coronary heart disease and AMI, Spearman p = 0.983, r = 0.068). 4. Discussion Cardiac injury markers are the cornerstone in the diagnosis of myocardial infarction. Whether cardiac arrest and cardiopulmonary resuscitation influence sensitivity and specificity of these parameters is still a matter of debate. To this aim our study evaluated three main cardiac markers troponin T, creatine kinase and isoenzyme creatine kinaseMB in the diagnosis of AMI that was secured by coronary angiography after successful cardiopulmonary resuscitation. We found an initial elevation above the recommended cut-off for diagnosis of myocardial infarction of each of the three markers in a high percentage of patients. As expected, patients with diagnosis of AMI showed increasing values of the cardiac injury markers TNT and CK, peaking 6–24 h after the event. Observed TNT and CK levels were significantly higher than in non-AMI patients. Somehow surprisingly we found an only moderate increase over time of CK-MB levels and a weak statistical difference comparing the respective CK-MB levels of AMI and non-AMI patients. Earlier reports suggested that time to ROSC and the cumulative amount of electric shock given for defibrillation influence levels of cardiac injury markers after resuscitation [18,19,22]. In our cohort we observed a close correlation between cardiac markers and time to ROSC in the non-AMI group, but not in patients with AMI. We suppose that in patients with AMI the effect of prolonged CPR is overruled by the impact of acute infarction on cardiac marker release. Moreover, in our study initial presence of a shockable rhythm was not associated with higher cardiac injury markers. Interestingly we only found a weak correlation between grade of coronary artery stenosis and levels of cardiac injury markers at all time points. This implies that hypoperfusion after subcritical stenosis during CPR only mildly contributes to the systemic elevated levels of TNT and CK. Interestingly also patients without any

signs of CAD presented elevated amount of cardiac markers, indicating that cardiac arrest and/or CPR per se may lead to release of cardiac enzymes and proteins. Previous publications reported reasonably good diagnostic performance of cardiac injury markers to diagnose AMI after resuscitation. Using a cut-off of 4 ng/ml TNT one study reported a sensitivity of 88% and specificity of 95% [18]. A second study described the sensitivity and specificity of the 12 h TNT after cardiac arrest as 96% and 80% respectively, using a 0.6 g/ml TNT as cut-off [19]. Neither of these two studies, however, used coronary angiography to diagnose AMI but rather employed ECG or a combination of ECG, scintigraphy and autopsy [19]. A further paper applying the gold standard coronary angiography diagnosing AMI found a sensitivity of 84% and specificity of 84% of the 6–12 h TNT [20]. Again this study used a modified cut-off for TNT of 14.5 ng/ml. In contradiction a recent study analyzing troponin I levels in patients after cardiac arrest reported only weak sensitivity and specificity (both 66%) to detect AMI. This study also used coronary angiography to diagnose AMI and the diagnostic performance of troponin I was weak, regardless whether the conventional or modified cut off values were applied [21]. In our cohort we were not able to reproduce such favorable diagnostic performance of TNT, CK or CK-MB to diagnose or exclude AMI after cardiac arrest. Although concentrations were higher in the AMI group, sensitivity and specificity were not favorably changed using the ROC-curves to define higher cut-off values than those we used. Altogether, troponin T reached a higher sensitivity and specificity than creatine kinase but neither reached a sensitivity and specificity level of 70% or greater, leaving them rather weak criteria for diagnosis or exclusion of AMI. Interestingly, the presence of shockable initial rhythm showed a higher sensitivity and a comparable specificity compared to either of the three cardiac markers, underlining the limited value of cardiac markers in this scenario. Whether the combination of ECG criteria with cardiac markers may improve predictive value was not tested in our study. In a retrospective analysis by Sideris et al. ST-segment elevation reached a sensitivity of 88% and a specificity of 84% for diagnosis of myocardial infarction [25]. ST-segment depression, bundle-branch block or nonspecific widening of the QRS-complex did not reach comparable results. Another study by Voicu et al. reached a sensitivity of 94% but still only a specificity of 64% by combining TNT elevation of above 2.5 ng/ml with ST-elevation in the ECG, however, values for ST-elevation alone were not given and overall specificity remained rather weak [20]. Given the current data, ST-segment elevation seems to give an indication for immediate coronary angiography on its own regardless of the level of cardiac markers. Some limitations of this analysis have to be addressed. An important limitation of our study is the retrospective character and therefore no implemented standard protocol was given to decide which patients should receive a coronary angiography; this decision was left to the intensivist and cardiologist in charge. The second limitation is the small sample of patients compared to the long time period of inclusion of 9 years. 393 patients were admitted to our units after primary successful resuscitation, 226 received early coronary angiography. That means that only 57% of all patients received

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invasive cardiologic work up. Our study addresses the question whether cardiac enzymes could predict the angiographic diagnosis, so only those patients could be included, who received coronary angiography and in whom cardiac markers were assessed at the time points of interest. We think that the relatively small number of patients represents clinical practice and points out the importance of the study's main result, that indication for invasive diagnostics should not be solely made by laboratory values given the low sensitivity and specificity of the cardiac markers troponin, CK and CKMB after succesful cardiopulmonary resuscitation. Third, no significant correlation between levels of cardiac injury markers towards neurological outcome at discharge from ICU was found. Overall outcome in our study was comparable to other published data [26]. Mortality tended to be higher in the non-shockable group reflecting the non-cardiac cause of arrest in most of the patients in this subgroup. 5. Conclusion Increases in cardiac injury markers TNT, CK and CK-MB cannot be used to reliably diagnose or rule out AMI after cardiac arrest. Consequently, in the absence of other reliable means to exclude AMI after resuscitation, the indication for coronary angiography should be extended to all patients without a certain alternative explanation for the occurrence of cardiac arrest. Acknowledgments We thank our study nurse Astrid Cämmerer for her outstanding support of this project. References [1] de Vreede-Swagemakers JJ, Gorgels AP, Dubois-Arbouw WI, et al. Circumstances and causes of out-of-hospital cardiac arrest in sudden death survivors. Heart 1998;79:356–61. [2] Zipes DP, Wellens HJ. Sudden cardiac death. Circulation 1998;98:2334–51. [3] Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:S640–56. [4] Sandroni C, Nolan J, European Resuscitation C. ERC 2010 guidelines for adult and pediatric resuscitation: summary of major changes. Minerva Anestesiol 2011;77:220–6. [5] Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-ofhospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557–63.

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Weak diagnostic performance of troponin, creatine kinase and creatine kinase-MB to diagnose or exclude myocardial infarction after successful resuscitation.

The aim of this study is to evaluate the diagnostic accuracy of the cardiac injury markers troponin (TNT), creatine kinase (CK) and creatine kinase-MB...
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