Cardiac-Specific Troponin I Levels to Predict the Risk of Mortality in Patients with Acute Coronary Syndromes
Elliott M. Antman, M.D., Milenko J. Tanasijevic, M.D., Bruce Thompson, Ph.D., Mark Schactman, M.S., Carolyn H. McCabe, B.S., Christopher P. Cannon, M.D., George A. Fischer, Ph.D., Anthony Y. Fung, M.B., B.S., Christopher Thompson, M.D., Donald Wybenga, M.D., and Eugene Braunwald, M.D.
Background In patients with acute coronary syndromes, it isdesirable to identify a sensitive serum marker that is closelyrelated to the degree of myocardial damage, provides prognosticinformation, and can be measured rapidly. We studied the prognosticvalue of cardiac troponin I levels in patients with unstableangina or non–Q-wave myocardial infarction.
Methods In a multicenter study, blood specimens from 1404 symptomaticpatients were analyzed for cardiac troponin I, a serum markernot detected in the blood of healthy persons. The relation betweenmortality at 42 days and the level of cardiac troponin I inthe specimen obtained on enrollment was determined both beforeand after adjustment for base-line characteristics.
Results The mortality rate at 42 days was significantly higherin the 573 patients with cardiac troponin I levels of at least0.4 ng per milliliter (21 deaths, or 3.7 percent) than in the831 patients with cardiac troponin I levels below 0.4 ng permilliliter (8 deaths, or 1.0 percent; P<0.001). There werestatistically significant increases in mortality with increasinglevels of cardiac troponin I ( P<0.001). Each increase of1 ng per milliliter in the cardiac troponin I level was associatedwith a significant increase (P = 0.03) in the risk ratio fordeath after adjustment for the base-line characteristics thatwere independently predictive of mortality (ST-segment depressionand age >65 years).
Conclusions In patients with acute coronary syndromes, cardiactroponin I levels provide useful prognostic information andpermit the early identificati on of patients with an increasedrisk of death.
In patients with chest pain at rest but no ST-segment elevationon the electrocardiogram, the diagnoses of unstable angina andnon–Q-wave myocardial infarction are usually consideredtogether because they cannot be distinguished clinically orangiographically.1,2,3,4 The discrimination between these conditionsis usually made by testing for elevated levels of a serum cardiacmarker that indicates myocardial necrosis when non–Q-wavemyocardial infarction is present.5 The extent of myocardialnecrosis is an important determinant of the risk of death.6,7It is therefore desirable to identify a serum marker whose releasebears a close relation to the degree of myocardial damage. Sucha marker should be more sensitive than current markers, shouldprovide prognostic information, and should be measurable ina time frame that permits treatment to minimize further necrosis.5,8
Since the conventional serum cardiac marker, creatine kinase,and its MB isoenzyme (CK-MB) lack sufficient sensitivity andspecificity, there is a need for more sensitive and cardiac-specificmarkers of myocardial necrosis.9,10,11 Troponin I, one of thesubunits of the troponin regulatory complex, binds to actinand inhibits interactions between actin and myosin. It is encodedby three different genes that are expressed to different degreesin different types of muscle.12,13,14 Cardiac troponin I isnot expressed in human skeletal muscle during fetal development,after trauma to skeletal muscle, or during the regenerationof skeletal muscle.16 Unlike CK-MB, cardiac troponin I is highlyspecific for myocardial tissue,17 is not detectable in the bloodof healthy persons, shows a greater proportional increase abovethe upper limit of the reference interval in patients with myocardialinfarction,18,19 and may remain elevated for 7 to 10 days afteran episode of myocardial necrosis.5
Given these features of cardiac troponin I as a marker of myocardialnecrosis, we designed the present study to evaluate the potentialprognostic value of this marker in patients with unstable anginaor non–Q-wave myocardial infarction. The data base weused was that of the Thrombolysis in Myocardial Ischemia PhaseIIIB (TIMI IIIB) trial.20
Methods
Study Patients
The TIMI IIIB trial, a prospective, randomized, multicenterstudy of patients with unstable angina or non–Q-wave myocardialinfarction, was conducted in the United States and Canada fromOctober 1989 through June 1992. It used a two-by-two factorialdesign to compare tissue plasminogen activator with placebo(in a double-blind analysis) and to compare an early, invasivemanagement strategy with an early, conservative strategy.20All the patients received intravenous heparin and aspirin andother standard medical therapy.
The study patients were from 21 to 76 years of age, had episodesof pain at rest that were presumed to be ischemic in originand had lasted for at least 5 minutes (but less than 6 hours)within the preceding 24 hours, and had documented evidence ofcoronary artery disease. Patients were excluded from the studyif left bundle-branch block was noted on presentation, a documentedmyocardial infarction had occurred within the previous 21 days,a treatable cause of angina was present, thrombolytic therapyhad been administered within the previous 72 hours, or angioplastyhad been performed in the previous 6 months. Patients were consideredto have unstable angina or non–Q-wave myocardial infarctionon the basis of serial electrocardiograms and determinationsof creatine kinase or CK-MB obtained locally at each enrollingcenter. A non–Q-wave myocardial infarction was consideredto have been present at the time of randomization if enzymeelevations were noted at the enrolling site (a CK-MB value inexcess of the normal value or, when no CK-MB value was available,a total creatine kinase value more than twice the normal value)at entry into the study or at any time up to 12 hours thereafter.
Blood Specimens
For 1404 of the 1473 patients enrolled in the main TIMI IIIBtrial, plasma specimens were available from the time of enrollment.Because it may take several hours from the onset of myocardialnecrosis for cardiac troponin I to be detectable in the blood,21we studied the specimens obtained at enrollment from the entirecohort of 1404 patients, as well as from the subgroup of 845patients who presented at least six hours after the onset ofthe episode of chest pain qualifying them for the study.
Measurement of Cardiac Troponin I
The blood specimens analyzed in the current study were originallyobtained in the main trial to measure various markers of activityof the coagulation system. They were therefore collected intubes containing aprotinin (200 kallikrein inhibitory unitsper milliliter of blood), 4.5 mM EDTA, and 40 µM d-phenylalanyl-l-prolyl-l-arginine(SCAT-I tubes, Haematologic Technologies, Essex Junction, Vt.).After centrifugation at each site, the plasma samples were storedlocally at 4°C and then mailed on dry ice to the HematologyCore Laboratory, where they were stored at -70°C.
Before the current study, the specimens were subjected to asingle cycle of freezing and thawing (for hematologic analyses),after which they were refrozen and stored at -70°C untiltheir shipment in 1995 to the Cardiac Serum Marker Core Laboratoryat the Clinical Chemistry Laboratory of Brigham and Women'sHospital in Boston. Studies have shown that in serum specimenswith cardiac troponin I levels between 4.2 and 20.0 ng per milliliter,measurements of cardiac troponin I remain stable, without evidenceof either time- or concentration-dependent deterioration, forup to 16 months when they are stored at -70°C (Bauer R,Dade International, Miami: personal communication).
Cardiac troponin I was measured by the Stratus II fluorometricenzyme immunoassay (Dade) for cardiac troponin I by technologistsunaware of the clinical data. This assay uses two monoclonalantibodies that recognize two different epitopes on the cardiactroponin I molecule.21 No cross-reactivity is seen with troponinI found in human skeletal muscle.21 In serum specimens fromhealthy persons without evidence of cardiac disease, the cardiactroponin I concentration is below the minimal concentrationdetectable by the assay (i.e., the smallest concentration thatcan be distinguished from zero), or 0.35 ng of cardiac troponinI per milliliter (Bauer R: personal communication). The within-runcoefficient of variation around the discriminator value is 13.3percent, and the between-run coefficient of variation is 16.0percent. Therefore, for the purposes of this study, we chosea cutoff value of 0.4 ng per milliliter as the minimal detectableconcentration of cardiac troponin I. All the measured levelsof cardiac troponin I that fell below this cutoff value werecollectively expressed as less than 0.4 ng per milliliter.
Measurement of Creatine Kinase and CK-MB
The plasma specimens that were analyzed for cardiac troponinI were also studied for CK-MB in the Cardiac Serum Marker CoreLaboratory by a mass assay to permit the consistent comparisonwith cardiac troponin I levels in a single reference laboratory.The mass assay for CK-MB, using monoclonal antibodies, was performedwith the Stratus instrument (Dade).
Statistical Analysis
The results of the cardiac troponin I and CK-MB assays weremerged with the data base of the main study at the MarylandMedical Research Institute, where the statistical analyses wereperformed. With regard to base-line characteristics, patientswith cardiac troponin I levels of at least 0.4 ng per milliliterwere compared with patients who had lower levels by Student'sunpaired t-test in the case of continuous variables and by thechi-square test in the case of dichotomous variables. The relationbetween mortality at 42 days and the presence or absence ofat least 0.4 ng of cardiac troponin I per milliliter at enrollmentwas analyzed by constructing contingency tables. Multivariateanalysis of predictors of the risk of death was performed withCox proportional-hazard regression models that included termsfor cardiac troponin I and CK-MB (as measured in the core laboratory).The Cox models were used to estimate the risk ratio for mortalityat 42 days that was associated with each increase of 1 ng permilliliter in the level of cardiac troponin I. The statisticalcomparisons were two-tailed, and P values of less than 0.05were considered to indicate statistical significance.
Results
Base-Line Characteristics
Only patients who were enrolled in the original study aftermeeting its criteria for inclusion and from whom plasma specimenswere available were included in the analysis. Of 1404 such patients,573 (41 percent) had cardiac troponin I levels of at least 0.4ng per milliliter at the time of enrollment, and 831 (59 percent)had levels below 0.4 ng per milliliter. The base-line characteristicsof these two groups of patients are compared in Table 1. Patientswith at least 0.4 ng of cardiac troponin I per milliliter atenrollment were less likely to have a history of angina, hypertension,or myocardial infarction; to have a prior coronary angiogramshowing at least one epicardial vessel with 70 percent or morestenosis; or to have received nitrates, beta-blockers, calciumantagonists, or aspirin before the qualifying episode of ischemicdiscomfort. However, they had qualifying episodes of pain thatlasted significantly longer than those of the patients whosecardiac troponin I levels were below 0.4 ng per milliliter atenrollment (2.3 vs. 1.6 hours, P = 0.001), and they were significantlymore likely to present with ST-segment deviation (either depressionor transient elevation).
Table 1. Selected Base-line Characteristics of the Study Patients.
The angiographic findings in 1150 patients who underwent coronaryarteriography are shown in Table 2. There were no significantdifferences between patients with cardiac troponin I levelsof 0.4 ng per milliliter or higher and those with lower levels.
Table 2. Angiographic Findings in 1150 Study Patients.
Classification of the Qualifying Episode of Ischemic Discomfort
On the basis of the CK-MB values measured at the enrolling centersin the specimens obtained at base line or within 12 hours afterenrollment, the presenting episodes were classified as unstableangina in 948 patients (68 percent) and non–Q-wave myocardialinfarction in 453 patients (32 percent) (Table 3). In 3 of the1404 patients in whom cardiac troponin I was measured, CK-MBdata from the enrolling sites were not available. Thus, datafrom a total of 1401 patients were used to compare CK-MB measurementsat the enrolling site with cardiac troponin I measurements atthe core laboratory. The diagnosis of non–Q-wave myocardialinfarction or unstable angina was only moderately correlatedwith the presence or absence of a cardiac troponin I level ofat least 0.4 ng per milliliter measured subsequently (Spearmanrho, 0.465). Among the 948 patients without CK-MB elevationsat enrollment or within 12 hours thereafter, 238 (25 percent)had cardiac troponin I levels of at least 0.4 ng per milliliterat enrollment, whereas among the 453 with such elevations, 335(74 percent) had cardiac troponin I levels of at least 0.4 ngper milliliter at enrollment.
Table 3. Classification of the Study Patients, as Determined by Measuring CK-MB and Cardiac Troponin I.
The cardiac troponin I values obtained at enrollment in thepatients with diagnoses of non–Q-wave myocardial infarctionor unstable angina are shown in Figure 1. As compared with thepatients without CK-MB elevations measured at the enrollinghospitals, the patients with elevated CK-MB levels had highercardiac troponin I values; in 47 percent of the latter, thesevalues were above 2.0 ng per milliliter.
Figure 1. Cardiac Troponin I Measurements at Base Line in 1401 Study Patients.
The cardiac troponin I levels at enrollment are shown for patients with and those without abnormal elevations in CK-MB, as measured at the enrolling centers. The distribution of cardiac troponin I levels was shifted toward higher values in the patients with elevated levels of CK-MB.
Mortality at 42 Days
Among the 1404 patients with cardiac troponin I measurements,29 (2.1 percent) died by day 42 after study enrollment. Therewere 21 deaths among the 573 patients with troponin I levelsof at least 0.4 ng per milliliter and 8 deaths among the 831patients with troponin I levels below 0.4 ng per milliliter.The relation between the presence of a cardiac troponin I measurementof at least 0.4 ng per milliliter at enrollment and mortalityby 42 days is shown in Figure 2 for several groups of patientsaccording to the number of hours since the onset of chest painand the presence of elevated CK-MB measurements. In all theanalyses shown, the mortality rate was consistently higher amongthe patients with cardiac troponin I levels of at least 0.4ng per milliliter (mortality, 2.4 to 4.0 percent) than amongthose with values below that level (mortality, 0.5 to 1.7 percent).The difference in the mortality rate between the patients withlevels of cardiac-specific troponin I of at least 0.4 ng permilliliter and those with lower levels was greatest for patientswho presented at least six hours after the onset of their chestpain, as evidenced by the much higher risk ratio for mortalityin that subgroup.
Figure 2. Mortality Rates at 42 Days According to the Time from the Onset of Pain to Study Enrollment and the Base-Line Cardiac Troponin I Levels.
Mortality rates (without adjustment for base-line characteristics) are shown for the study patients according to the time from the onset of chest pain to enrollment (0 to 6, >6 to 24, and 0 to 24 hours). For each subgroup the findings are shown for all patients and those in whom no elevation of CK-MB was found at the enrolling center. The numbers at the bottom of each bar are the numbers of patients in each category, and the numbers above the bars are percentages. For each comparison, the mortality rate was higher in the patients with cardiac troponin I levels of at least 0.4 ng per milliliter. Risk ratios and 95 percent confidence intervals for mortality are shown at the bottom of the figure for the group with cardiac troponin I levels of at least 0.4 ng per milliliter as compared with the group with lower levels. The asterisks indicate p<0.05, and the daggers p<0.001.
The correlation between mortality at 42 days (without adjustmentfor base-line characteristics) and the cardiac troponin I levelin the plasma specimen obtained at enrollment is shown in Figure 3.There were statistically significant increases in mortalitywith increasing levels of cardiac troponin I (P<0.001 bythe chi-square test for trend). The risk ratio for mortalityin the patients with troponin I levels of 0.4 ng per milliliteror more (as compared with those with lower levels) rose progressivelywith increasing troponin I levels (Figure 3).
Figure 3. Mortality Rates at 42 Days According to the Level of Cardiac Troponin I Measured at Enrollment.
Mortality rates at 42 days (without adjustment for base-line characteristics) are shown for ranges of cardiac troponin I levels measured at base line. The numbers at the bottom of each bar are the numbers of patients with cardiac troponin I levels in each range, and the numbers above the bars are percentages. P<0.001 for the increase in the mortality rate (and the risk ratio for mortality) with increasing levels of cardiac troponin I at enrollment.
Multivariate Models of Mortality
Under the assumption that there was an exponential relationbetween the cardiac troponin I concentration and mortality,we evaluated the effect of each increase of 1 ng per milliliterin cardiac troponin I on the risk ratio for mortality by day42, after adjusting for the base-line variables in Table 1 thatwere found to be statistically significant independent predictorsof death. As Table 4 shows, in the overall study populationof 1404 patients there was a significant increase in the riskratio for mortality for each increase of 1 ng per milliliterin cardiac troponin I (P=0.03). Among the 845 patients presentingmore than six hours after the onset of chest pain, there wasan even stronger correlation between cardiac troponin I andthe risk of mortality. Again, for each increase of 1 ng permilliliter in cardiac troponin I, the risk ratio for mortalityincreased significantly (P=0.02), an even more significant increasethan was found for an age of 65 years or older (chi-square,5.47 vs. 1.37).
Table 4. Risk Ratios for Mortality after Adjustment for Base-line Variables.
Because of possible variation in the measurement of CK-MB amongthe hospital laboratories at the centers where the patientswere enrolled in the study, CK-MB was measured again in theCardiac Serum Marker Core Laboratory by a mass assay. For eachincrease of 1 ng per milliliter in CK-MB, the risk ratio formortality increased significantly in both the overall cohortof 1404 patients and the cohort of 845 patients who presentedmore than six hours after the onset of symptoms (risk ratioin both cohorts, 1.01; P=0.03) when we adjusted the analysisfor the base-line characteristics shown in Table 4. However,among the 838 patients with base-line CK-MB levels below theupper limit of the reference interval (5 ng per milliliter),as detected by the mass assay, those with simultaneously measuredcardiac troponin I levels of at least 0.4 ng per milliliterhad a higher mortality rate than those with cardiac troponinI levels below 0.4 ng per milliliter (2.6 percent vs. 0.4 percent;risk ratio, 3.1 [95 percent confidence interval, 0.8 to 12.2]).
Discussion
The development of unstable angina or non–Q-wave myocardialinfarction indicates that a patient has entered a phase of ischemicheart disease associated with an increased risk of death, oneintermediate between the risk in chronic stable exertional anginaand the risk in Q-wave myocardial infarction. Postmortem examinationsin patients who die suddenly of ischemic causes after presentingwith unstable angina often reveal layers of thrombus materialof varying ages in the culprit coronary vessel and evidenceof the embolic occlusion of small intramyocardial arteries withmicroinfarcts.23,24 It is therefore of interest to determinewhether the detection of even minimally elevated levels of serummarkers of cardiac necrosis correlates with an increased riskof mortality.
Identifying Patients at Increased Risk of Mortality
Our study indicates that the detection of the highly specificmarker cardiac troponin I17 in blood is an independent riskfactor that identifies patients presenting with unstable anginaor non–Q-wave myocardial infarction who are at increasedrisk of death. The prognostic value of cardiac troponin I wasgreater among patients who presented more than six hours afterthe onset of chest discomfort. The likely explanation for thepotential of cardiac troponin I to indicate an adverse prognosisis the high sensitivity and specificity of this marker in identifyingpatients with recent episodes of myocardial necrosis. The patientsin this study who had cardiac troponin I levels of at least0.4 ng per milliliter were less likely than patients with lowerlevels of the marker to be receiving antianginal medicationsbefore enrollment, they had significantly longer qualifyingepisodes of chest pain, and they were significantly more likelyto present with ST-segment deviation on the electrocardiogram.It is also less likely that they had collateral vessels to theischemic zone, because their incidence of prior angina was lowerand their angiograms were less likely to show substantial stenosis.
The prognostic information conveyed by elevated levels of cardiactroponin I at presentation was evident even in a group of patientswith a low overall mortality rate (2.1 percent at 42 days).The prognostic potential of cardiac troponin I persisted evenafter adjustment for independent base-line variables known tobe significantly associated with an increased risk of cardiacevents, such as an age of 65 years or older and ST-segment depressionon the electrocardiogram.
Furthermore, levels of cardiac troponin I of at least 0.4 ngper milliliter in a single plasma specimen at presentation appearto be associated with an increased risk of mortality even inpatients whose CK-MB measurements are not considered abnormallyelevated. This is probably due to a reduced sensitivity andspecificity of CK-MB in detecting microinfarction.25,26,27 SinceCK-MB is found in the skeletal muscle and blood of healthy persons,diagnostic cutoff values for myocardial infarction are typicallyset above the upper limit of the reference range for the assay.Because cardiac troponin I does not normally circulate in theblood and is 13 times more abundant in the myocardium than CK-MBon a weight basis,19 the signal-to-noise ratio associated withcardiac troponin I is much more favorable for the detectionof minor amounts of cardiac necrosis. The interpretation ofminimally elevated CK-MB levels is also confounded by coexistingillnesses that may produce hypoperfusion and injury of skeletalmuscles, with re-expression of the B subunit of creatine kinase.19,26,28
Comparison with Previous Studies
Previous investigators have suggested that the measurement ofcardiac troponin T is useful in predicting risk in patientswith unstable angina and that it appears to be superior to CK-MBin its predictive potential.29,30,31 It is noteworthy that previousstudies of troponin T in patients with unstable angina usedblood specimens obtained serially 24 to 48 hours after presentationin order to screen for elevated levels of that serum cardiacmarker in the evaluation of risk. Our study not only providesdata on cardiac troponin I, another cardiac-specific markermeasurable in blood, but also emphasizes the use of a singlemeasurement at presentation and describes the quantitative relationbetween measurements of cardiac troponin I and the risk of mortality.
Clinical Implications
In the context of other reports documenting the usefulness ofcardiac troponin I for the diagnosis of myocardial infarctionin patients with ST-segment elevation, Q waves, or both, ourfindings extend the observations on the benefits of measuringthis marker to the entire range of acute coronary syndromes.5,17,18,19A cardiac troponin I level of at least 0.4 ng per milliliterwhen a patient with unstable angina is first evaluated predictsan increased risk of short-term mortality, probably becauseit permits the diagnosis of non–Q-wave myocardial infarctionthat one might otherwise have overlooked by sampling only forCK-MB. With progressively higher levels of cardiac troponinI, the risk of mortality increases, presumably because the amountof myocardial necrosis increases. Measuring cardiac troponinI is therefore useful in evaluating patients with unstable angina.Elevated levels of this marker provide prognostic informationbeyond that supplied by the demographic characteristics of thepatient or the electrocardiogram at presentation. This permitsthe early identification of patients at increased risk of death.
Supported by grants (R01-HL-42311 and R01-HL-42428) from theNational Heart, Lung, and Blood Institute and by Dade International,Miami.
Source Information
From the Department of Medicine (E.M.A., C.H.M., C.P.C., E.B.) and the Clinical Laboratories (M.J.T., G.A.F., D.W.), Brigham and Women's Hospital, Boston; the Maryland Medical Research Institute, Baltimore (B.T., M.S.); and the University of British Columbia, Vancouver (A.Y.F., C.T.).
Address reprint requests to Dr. Antman at the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115.
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Cardiac Troponins in Acute Coronary Syndromes
Haft J. I., Saadeh S. A., Stubbs P., Collinson P., Brogan G. X., Hollander J. E., Thode H., Carbajal E. V., Ohman E. M., Califf R. M., Topol E. J., Antman E. M., Tanasijevic M. J., Cannon C. P., Van de Werf F.
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Missed Diagnoses of Acute Cardiac Ischemia
Davidson S. J., Murphy D. G., Barbaro G., Giancaspro G., Soldini M., Kohn M. A., Gruber T., Potts J. L., Jordan D., Selker H. P., Feldman J. A., Pope J. H., Aufderheide T. P.
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