Eur J Cardiothorac Surg 1998;13:57-65
© 1998 Elsevier Science NL
Cardiac troponin I plasma levels for diagnosis and quantitation of perioperative myocardial damage in patients undergoing coronary artery bypass surgery1
Volker Sadonya,
Michael Körbera,
Guido Albesa,
Volker Podtschaskea,
Thorleif Etgena,
Thomas Tröskena,
Ursula Ravensb,
Max Ernst Scheulenc
a Department of Thoracic and Cardiovascular Surgery, University of Essen, Hufelandstr. 55, D-45122 Essen, Germany
b Pharmacological Institute, University of Essen, Hufelandstr. 55, D-45122 Essen, Germany
c Diagnostic Laboratories of the Department of Internal Medicine (Cancer Research), University of Essen, Hufelandstr. 55, D-45122 Essen, Germany
Received 25 August 1997;
received in revised form 18 November 1997;
accepted 19 November 1997.
Corresponding author. Tel.: +49 201 7233596; fax: +49 201 7235931.
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Abstract
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Objective: The definition of a reliable and generally accepted diagnostic standard for perioperative myocardial damage is desirable. Cardiac troponin I (cTnI) is highly specific for myocardial tissue and can be measured rapidly. The aim of our study was to evaluate the diagnostic potential of cTnI for myocardial lesions in patients undergoing coronary artery bypass surgery (CABG). Methods: A total of 119 patients with diffuse coronary artery disease were operated on using blood cardioplegia. Serial blood samples drawn before and after surgery were analyzed for the activity of creatine kinase MB isoenzyme (CKMB) and the concentrations of CKMB mass, cardiac troponins T and I. On the basis of the biochemical results (except cTnI) and the findings of electrocardiography/echocardiography, patients were classified and cTnI was studied for each group separately: group I, minor myocardial damage; group II, non-transmural infarction; group III, transmural infarction; and group IV, preoperative non-transmural infarction. Results: In 87 patients of group I (73.1%) cTnI levels remained low; 19 patients (16.0%) were assigned to group II, 8 patients (6.7%) to group III, and 5 patients (4.2%) to group IV. For discrimination of patients without and with perioperative myocardial infarction (PMI) by one cTnI determination, the use of cutoff values of 6.5 ng/ml at 8 h, 9.8 ng/ml at 12 h, and 11.6 ng/ml at 24 h after aortic unclamping resulted in a diagnostic efficiency of 88, 94 and 98%. Especially, a cTnI value at 24 h had a sensitivity of 100% and a specificity of 97%. Cardiac troponin levels at 24 h were found to correlate closely with the well-recognized 2–48 h area-under-the-curve (P<0.0001; R=0.993), making serial determinations unnecessary. Conclusions: cTnI qualifies as a marker for diagnosis of PMI and quantitation of the amount of myocardial damage, because of the availability of a quick diagnostic test with high specificity, the high diagnostic efficiency, and especially the sufficient information gained by a single determination 24 h after aortic unclamping.
Key Words: Perioperative myocardial damage • Cardiac troponin I • Cardiac troponin T • Creatine kinase MB isoenzyme • Blood cardioplegia • Coronary artery surgery
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Introduction
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Significant perioperative myocardial infarction (PMI) in coronary artery bypass surgery (CABG) patients is associated with negative prognostic implications
[1]
[2]. Until now, the definition of a reliable and generally accepted diagnostic standard has failed. For prognostic reasons in the individual patient and for quality control of the surgical work, however, such a standard is highly desirable. Lack of sufficient sensitivity and specificity of current PMI criteria
[3]
[4]
[5]
[6]
[7] characterize the diagnostic dilemma
[8]. The reliability of newer myocardial markers remains to be proven in larger patient series.
Troponin I, one of the subunits of the troponin regulatory complex, has two skeletal muscle isoforms and one cardiac, that are encoded by three distinct genes, presenting a dissimilarity of 
40% in the amino acid sequence
[9]. Moreover, human cardiac troponin I (cTnI) has 31 additional residues on its N-terminal end that are not present in skeletal forms, thus providing a high potential for obtaining cardiac-specific antibodies
[10]. cTnI is not expressed in human skeletal muscle at any developmental stage or after trauma and regeneration
[11]. Unlike creatine kinase MB isoenzyme (CKMB), cTnI is highly specific for myocardial tissue
[12]
[13]
[14], is not detectable in healthy persons, shows a greater proportional increase above the upper limit of the reference interval in patients with myocardial infarction
[15]
[16], is released fairly rapidly because of its molecular mass of 24 kDa after an episode of myocardial necrosis, and may remain elevated for 7–10 days
[14].
Given these features of cTnI, recently commercially available assays for measuring cTnI in serum and/or plasma focus the interest on this marker as a promising candidate for the solution of the diagnostic problems. The aim of our study was to evaluate the potential of cTnI for diagnosis and quantitation of perioperative myocardial damage in CABG patients.
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Material and methods
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Patients, anesthesia, surgical and cardioplegic techniques
After approval by the local ethic committee and written informed consent, a selected group of 119 patients at higher risk with severe diffuse three-vessel disease undergoing CABG was studied. The preoperative clinical data are summarized in Table 1. The definition of urgent operation was surgery within one to several days after the definitive cardiologic diagnosis without interruption of the hospitalization phase.
A standard anesthesiological regimen was applied. Premedication was with flunitrazepam (Rohypnol®, Hoffmann-La Roche, Grenzach-Wyhlen, Germany), 2 mg p.o., on the eve and 90 min before the transfer of the patient to the operating room. Anesthesia was induced with flunitrazepam, 0.02 mg/kg of body weight, fentanyl (Fentanyl-Janssen®, Janssen, Neuss, Germany), 0.01 mg/kg, and pancuronium (Pancuronium Organon®, Organon Teknika, Oberschleißheim, Germany), 0.1 mg/kg. After intubation, anesthesia was maintained by controlled ventilation (AV1 Dräger, Lübeck, Germany) with oxygen and nitrous oxide in a ratio of 1:1 and isoflurane (Forene®, Deutsche Abbott, Delkenheim, Germany) with an inspiratory concentration of 0.5–0.8 vol%. Additional doses of fentanyl, 0.01 mg/kg, and pancuronium, 0.025 mg/kg, were given if necessary.
Cardiopulmonary bypass was established with an ascending aortic and a two-stage venous cannula using a membrane oxygenator (Cobe Excel, Cobe Laboratories). The perfusion temperature was maintained at 33°C or above, the hematocrit was between 20 and 25%, pump flows were between 1.8 and 2.2 l/min per m2, and mean arterial pressures were kept between 50 and 60 mmHg. In all patients cardioprotection was achieved by combined antegrade and retrograde (coronary sinus) multidose cold blood cardioplegia without/with warm induction and with warm terminal reperfusion
[17]. All distal and proximal anastomoses were carried out during one period of aortic cross clamping
[18]. Cardiopulmonary bypass was terminated without or with inotropic/mechanical support.
Protocol of investigation, blood specimens
In all patients perioperative hemodynamic measurements including the routine use of a Swan-Ganz catheter were made following a standardized scheme. In each patient the amount of postoperative inotropic support required was registered and the postoperative hemodynamic state was roughly calculated according to the recommendations of the German Society for Thoracic and Cardiovascular Surgery. A 12-lead electrocardiogram was recorded before surgery, immediately after the arrival in the intensive care unit, 12 h later, and every day thereafter until discharge. All ECGs were reviewed using criteria recently published
[19].
Perioperatively serial blood samples for measuring CKMB activity and the concentrations of CKMB mass, cardiac troponin T (cTnT), and cTnI were obtained via a central venous line shortly before induction of anesthesia and at (2), 3, 6, (8), 12, 24 and 48 h after release of the aortic clamp. In selected patients blood sampling for analysis of cTnI levels was continued once a day up to 144 h.
From each patient the records of transthoracic and/or transesophageal echocardiography carried out by the respective cardiologist 4–6 weeks after surgery were reviewed and compared with the preoperative echocardiographic and levocardiographic findings.
Laboratory analysis
Handling of blood samples
Following centrifugation, all serum/plasma samples were frozen in aliquots and stored at -70°C. After thawing, the samples were analyzed as a batch.
CKMB activities
CKMB catalytic concentrations in heparin-plasma were measured after immunoinhibition at 25°C by means of a N-acetylcysteine-activated, optimized ultraviolet test from Merck (Darmstadt, Germany). The normal range of CKMB activity measured by this method is <10 U/l.
CKMB mass concentrations
Serum concentrations were determined by the Tandem Icon QSR CKMB test, a two-site enzyme immunoassay from Hybritech (Cologne, Germany). In presumably healthy subjects the upper reference limit for CKMB mass concentrations was 6.1 ng/ml
[20].
cTnT
Serum concentrations were determined by a commercial one-step sandwich immunoassay (Enzymun-Test® Troponin T, second-generation) on an ES 300 automated analyzer (both from Boehringer Mannheim, Mannheim, Germany). By this assay, in apparently healthy individuals cTnT values <0.1 ng/ml have been found
[21].
cTnI
Concentrations in heparin-plasma were measured by the Stratus II automated two-site fluorometric enzyme immunoassay (Dade Diagnostika, Munich, Germany) which uses dual mouse monoclonal antibodies that recognize two different epitopes on the cTnI molecule. From assay initiation, time to first result is 10 min. In serum specimens from healthy persons without evidence of cardiac disease, cTnI concentration is below the minimal concentration detectable by the assay (i.e. the smallest concentration that can be distinguished from zero), or 0.35 ng/ml
[22].
Data analysis
Patients were assigned to four groups according to the criteria of patient classification shown in Table 2. cTnI levels were studied for each group separately.
Statistical analysis
Statistical analysis was done with the SAS programs (SAS Institute, Cary, NC). Mean values±S.D. were calculated to describe continuous variables. Integration of the time–concentration curves of the biochemical myocardial markers within the first 48 h after unclamping the aorta was used for calculation of the total amount of CKMB (U/lxh), CKMB mass (ng/mlxh), cTnT (ng/mlxh), and cTnI (ng/mlxh) released. The two-tailed Wilcoxon rank-sum test and the Mann–Whitney U-test were used for group comparison. When multiple comparisons were carried out, P-values were adjusted according to the Tippett–Holm procedure. P-values of less than 0.05 were considered to indicate statistical significance. Special statistical tests are indicated in the text.
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Results
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Patient classification
On the basis of the criteria outlined in Table 2, 113 out of 119 patients (95.0%) could be classified without any problem. In 6 patients there was a discrepancy between the results of cTnT and CKMB measurements. In 4 of these patients cTnT values were confirmed by the results of serial cTnI measurements. Another 2 patients with known compensated chronic renal failure demonstrated cTnT concentrations >1.0 ng/ml in the presence of low CKMB values. In both cases cTnI levels were low, excluding PMI.
In summary, the strict criteria of group I were fulfilled by 87 patients (73.1%), 19 patients (16.0%) were classified to be in group II and 8 patients (6.7%) to be in group III, respectively. Group IV comprised 5 patients (4.2%).
Overall clinical results
Intra- and postoperative surgical data are summarized in Table 3. Postoperatively 1 patient out of each group (I–IV) died resulting in a 30-day mortality rate of 3.4%.
Biochemical results
Time courses of cTnT, CKMB catalytic and mass concentrations in serum/plasma and total release
All 6 patients demonstrating discrepancies between the results of serial cTnT and CKMB determinations were excluded from the following statistics.
Group I
cTnT levels remained consistently low (<1.0 ng/ml) with an integrated area of 16.7±9.7 ng/mlxh (
Fig. 1
). Time courses of CKMB catalytic and mass concentrations were characterized by an early peak at 3 h with 19.2±5.7 U/l and 24.6±10.4 ng/ml and a monoexponential decline with mean values at 24 h of 9.7±4.1 U/l and 13.7±8.0 ng/ml, respectively. The mean integrated areas were 453.4±147.8 U/lxh and 621.8±302.7 ng/mlxh, respectively (
Fig. 2
).
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Fig. 2. Integrated areas-under-the-curve (time-frame 3–48 h after aortic unclamping; mean±S.D.) of CKMB catalytic and mass concentrations of groups I-III (n=108). Statistical symbols as in
Fig. 1.
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Groups II and III
In both groups cTnT levels and the respective integrated areas-under-the-curve were significantly higher than those of group I (P<0.001). Time courses of CKMB catalytic and mass concentrations revealed a biphasic peak pattern resulting in significantly higher integrated areas than those of group I (P<0.001).
Group IV
cTnT levels and CKMB values indicated Q-wave PMI in 3 patients and no additional significant perioperative myocardial damage in 2 patients (data not shown).
Time course of cTnI plasma levels and total release
Group I
cTnI levels remained low reaching peak values of 4.8±2.5 ng/ml at 12 h and 5.2±3.2 ng/ml at 24 h after aortic unclamping with an integrated area of 194.4±103.6 ng/mlxh (
Fig. 3
). The relative increase in cTnI concentrations was 16.2±9.0 times the smallest concentration that can be distinguished from zero. Thereafter, cTnI levels declined and, on the average, could be detected up to postoperative day 4.
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Fig. 3. Doubly logarithmic diagram of cTnI plasma concentration time courses (mean±S.D.) in CABG patients (n=114). Insert: integrated areas-under-the-curve (time-frame 2–48 h after aortic unclamping; mean±S.D.). Statistical symbols as in
Fig. 1.
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Groups II and III
In both groups cTnI levels increased significantly, reaching peak values at 24 h after aortic clamp release. From 8 h after the beginning of reperfusion all three groups could be separated from each other with statistical significance (P<0.001). The further time course was characterized by a monoexponential decline and detectable concentrations were still noted on day 6 after the operation. Likewise calculated areas differed significantly from each other and those of group I (P<0.001).
Group IV
Preoperative subacute non-Q-wave infarction was verified in all 5 patients by increased cTnI levels before induction of anesthesia. The diagnosis of Q-wave PMI in 3 patients and of no additional significant perioperative myocardial damage in 2 patients as established by cTnT and CKMB measurements was confirmed by the results of serial cTnI determination (data not shown).
Cutoff values/sensitivity and specificity of cTnI
For the discrimination between patients without and with PMI by one cTnI determination, cutoff values for different time points after aortic unclamping were calculated on the basis of cTnI concentrations measured in patients of group I (mean+2 S.D.). Using cutoff values of 6.5 ng/ml at 8 h, 9.8 ng/ml at 12 h, and 11.6 ng/ml at 24 h resulted in a diagnostic efficiency of 87.9, 94.4, and 97.8%, respectively. Especially, one cTnI value at 24 h had a sensitivity of 100% and a specificity of 96.6%. The percental prediction for diagnosing PMI was 93.9%, whereas the predictive value for excluding myocardial infarction was 100%.
Correlations between cTnI values at 12 and 24 h after aortic unclamping and total cTnI release
cTnI levels in patients of groups I–III at 12 and 24 h after aortic unclamping were found to correlate with the respected calculated area-under-the-curve of the time frame 2–48 h. Spearman rank order coefficients were r=0.956 and r=0.990, respectively (in both cases P<0.0001). The estimated linear regression equations for both time points were: (cTnI 2–48 h) ng/mlxh=-180.191+75.725x(cTnI 12 h) ng/ml, and (cTnI 2–48 h) ng/mlxh=22.458+32.671x(cTnI 24 h) ng/ml. The calculated coefficients of determination for 12 h with R=0.830 and especially for 24 h with R=0.993 (
Fig. 4
) were high.
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Fig. 4. Correlation between cTnI concentrations in patients of groups I-III at 24 h after aortic unclamping and the respected calculated area-under-the-curve of the time-frame 2–48 h (n=114); (P<0.0001, R=0.993).
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Discussion
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Patient classification
Despite substantial refinements in the methods of perioperative myocardial management, it is still a fact that all patients undergoing CABG suffer some sort of myocardial damage. Traditionally, distinctions were made between minor damage usually seen in the majority of patients with uneventful cardiac recovery (no PMI) and significant damage defined either as non-Q-wave PMI or Q-wave PMI. Current PMI criteria are mainly based on CKMB catalytic concentrations with activity limits, evaluated in large cohorts of CABG patients
[3]
[4]
[5]
[6]
[7]
[8]. Cutoff values for CKMB mass concentration in PMI have not yet been defined in comparably large CABG patient series. Recently, cTnT proved to be a reliable marker of PMI
[19].
In our study decisive criteria excluding PMI were cTnT levels strictly <1.0 ng/ml and an early peak pattern of CKMB catalytic concentrations (and CKMB mass concentrations as well) with a CKMB activity <20 U/l on the first postoperative day. These values fitted rather well both the standard definition of patients without PMI on the basis of CKMB activity
[6]
[7] and the results of serial measurements of cTnT by Hake and co-workers
[19]. The electrocardiogram was mainly used for differentiation between non-transmural and transmural necrosis. Late echocardiography served to confirm the diagnosis of PMI in the presence of increased levels of cTnT and catalytic concentrations of CKMB. Otherwise, in patients with a newly reduced wall motion but borderline biochemical findings echocardiography proved less useful because of its limited power to differentiate between myocardial necrosis and myocardial stunning.
Diagnostic features of cTnI for patient classification
Out of the 119 patients, 113 (95.0%) could be classified without any problem. In 4 patients CKMB catalytic (and mass) concentrations did not concur with cTnT levels. In all these 4 cases cTnT values were confirmed by the results of serial cTnI measurements, thus reflecting lack of sufficient sensitivity and specificity of CKMB. Another 2 patients with known compensated chronic renal failure had slightly increased cTnT levels in the presence of low CKMB catalytic (and mass) concentrations. In both cases cTnI levels were low excluding PMI. Such a discordance between results for cTnT and cTnI in renal patients is well known from the literature
[23]
[24].
In patients without PMI, cTnI levels remained low, reaching peak values at 12 or 24 h after aortic unclamping. The relative increase in cTnI concentrations was 16.2±9.0 times the smallest concentration that can be distinguished from zero. This indicated a wide variation of myocardial damage being found in this group. Thus, cTnI seems to be well qualified to detect even small differences in myocardial damage in patients without PMI. This may be potentially useful in evaluating the efficacy of different techniques of perioperative myocardial management. In PMI patients, cTnI levels showed a rapid and significant increase. Peak values were reached at 24 h followed by a monoexponential decline. From 8 h after the beginning of reperfusion all three groups could be separated from each other by statistical significance. For differentiation between CABG patients without and with PMI, the acceptance of cutoff values for cTnI of 6.5 ng/ml at 8 h, 9.8 ng/ml at 12 h, and 11.6 ng/ml at 24 h resulted in a diagnostic efficiency of 88, 94, and 98%, respectively.
Comparison with previous studies
Similar first results have been reported in the literature. In a study comprising 65 CABG patients Bonnefoy and co-workers
[25] evaluated a cutoff value for cTnI of 10 ng/ml at 12 h after aortic unclamping. In a series of patients undergoing CABG or valve replacement, Alyanakian and co-workers
[26] proposed a cutoff value of 15 ng/ml. After an investigation of 117 CABG patients Jacquet and co-workers concluded, that a value of <10 ng/ml for cTnI at 8 h after surgery can exclude PMI with high probability (personal communication). All these results are based on the measurement of cTnI concentrations using the same two-site fluorometric enzyme immunoassay as in our study. However, it must be emphasized that a different method of cTnI determination resulted in lower peak values
[7].
Diagnostic features of cTnI for quantitation of perioperative myocardial damage
The negative prognostic implications of perioperative myocardial necrosis are determined by the number of myocytes irreversibly damaged. For quantitation of myocardial damage, simple integration of the time–concentration curves of CKMB catalytic concentrations, for example, has been utilized successfully mainly in research trials
[6]. Serial marker pattern assessment in the early postoperative period is not routine practice, however. In our study cTnI levels at 24 h after aortic unclamping were found to correlate closely with the respective 2–48 h area-under-the-curve (R=0.993) making serial determinations unnecessary. In this context, a previous study demonstrating a significant relationship between cTnI release and myocardial infarction size is of special interest
[27].
A single cTnI value at 24 h reflects the approximate amount of myocardial damage. This measurement may allow a more precise description of the quality of myocardial management in a patient population than the traditional documentation of the percentage of PMI patients.
Clinical implications and conclusions
In summary, we conclude that cTnI qualifies as a useful tool to check on the quality of surgical work and the adequacy of the methods of perioperative myocardial management in use. This is because of (1) the availability of a quick diagnostic test with high specificity for myocardial tissue, (2) the high diagnostic efficiency of 94% at 12 h and 98% at 24 h, and (3) especially the opportunity to gain sufficient information by a single determination 24 h after aortic unclamping for diagnosis of PMI and quantitation of the amount of myocardial damage.
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Acknowledgments
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We are very grateful for excellent technical assistance by Christel Heisters. This work was supported in part by the Elisabeth-Wagener-Foundation, Essen, Germany.
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Footnotes
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Presented in part at the 26th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery, Dresden, Germany, 5–8 February, 1997. 
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Top
Abstract
Introduction
, patients without PMI (group I); 
, patients with non-Q-wave PMI (group II); and 
, patients with Q-wave-PMI (group III). Insert: integrated areas-under-the-curve (time-frame 2–48 h after aortic unclamping; mean±S.D.). Asterisks indicate significant difference (P<0.001) between values of group I and values of groups II and III. Crosses indicate significant difference (P<0.001) between values of groups II and III.