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(Circulation. 1996;94:1291-1297.)
© 1996 American Heart Association, Inc.
Articles |
Prognostic Significance of Admission Troponin T Concentrations in Patients With Myocardial Infarction
Charing Cross Hospital (P.S., M.N.), Mayday University Hospital (P.C.), and West Middlesex University Hospital (D.M., T.G.), London, UK.
Correspondence to Dr Peter John Stubbs, Academic Unit of Cardiovascular Medicine, Charing Cross and Westminster Medical School, Fifth Floor South Wing, Charing Cross Hospital, Fulham Palace Rd, London W6 8RF, UK.
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Abstract |
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Background New, highly specific cardiac structural proteins can now be measured. The early presence of one of these proteins, troponin T, has been found to have important prognostic significance in patients with unstable angina pectoris. The prognostic significance of its presence on admission was assessed in patients with myocardial infarction.
Methods and Results Two hundred forty patients admitted with myocardial infarction were studied and followed prospectively for a median of 3 years. The prognostic significance of an admission troponin T concentration 
0.2 ng/mL for subsequent cardiac death and/or reinfarction was assessed and compared with other variables in a regression model. Any detectable troponin T on admission was associated with a worse prognosis on follow-up. An admission concentration of 0.2 ng/mL was associated with a higher risk of subsequent cardiac death (
2, 13.3; P=.0002) and death or nonfatal reinfarction (2, 16; P=.00006). The excess risk was seen primarily in patients with admission ECG ST-segment elevation (cardiac death 2, 9.7; P=.001; death or nonfatal reinfarction 2, 10.3; P=.001). In a stepwise regression model for cardiac death or nonfatal reinfarction, troponin T was superior to most of the other variables entered in both myocardial infarction subgroups.
Conclusions The presence of admission troponin T in patients with myocardial infarction defines a subgroup, particularly those with ST-segment elevation, at increased risk of subsequent cardiac events and identifies a group that may benefit from alternative early management strategies.
Key Words: myocardial infarction • prognosis • troponin T • risk factors
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Introduction |
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The classic role of biochemical markers of myocyte damage in patients admitted with acute coronary syndromes has been retrospective confirmation of myocardial infarction. Studies of biochemical markers have concentrated on their role for early diagnosis, which, although possible,1 2 3 4 5 6 7 8 is not considered diagnostically useful.8 9 Early clinical management decisions for patients admitted with acute coronary syndromes are based on the clinical history and the admission ECG, despite known limitations.10 11 12 13 14 ST-segment elevation, if present, occurs very shortly after coronary artery occlusion,15 16 is highly specific for myocardial infarction,11 and identifies the only group that unequivocally benefits from the use of thrombolytic agents.17 18 19 Routine early measurement of biochemical markers has been deemed unnecessary in this patient group.9 Measurement of myocardial damage by newer, highly specific markers of myocardial damage is now possible, including cardiac structural proteins such as TnT.20 This marker is not detectable in the normal population, is highly cardiac specific, and in the setting of myocardial injury is released into the circulation slightly earlier than CK.20 21 22 23 24 25 26 In the acute coronary syndrome of unstable angina pectoris, the presence of this marker in the plasma is diagnostically superior, because it identifies minor myocardial damage missed by other biochemical markers.27 28 29 30 31 It also has prognostic significance, because if present, it identifies a subgroup of patients who are at high risk for early cardiac events.24 27 28 29 30 31
The purpose of the present study was to examine the prognostic value of admission TnT concentration measurement in patients with myocardial infarction defined according to WHO criteria.32
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Methods |
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This was a single-center study of patients admitted with chest pain to a hospital CCU. Patients remained under the care of their admitting physician, who decided management in terms of need for referral for both cardiological opinion and investigation. Management decisions were based on clinical, ECG, and routine biochemical marker results. Patients who were referred for invasive investigation underwent coronary angiography at a number of different centers. The need for and timing of revascularization was decided by the receiving interventional cardiologists independent of the referring physician. All patients with a final diagnosis of myocardial infarction within the first 48 hours of admission according to WHO criteria, based on chest pain history, daily ECG, and enzyme measurements, were followed prospectively for outcome. Patients admitted to the CCU underwent daily sampling for 3 days for the routine cardiac enzyme protocol in the hospital, and the daily CK, AST, and HBD estimations were used for the final WHO biochemical diagnostic coding of the admissions.
Patients also underwent multiple timed sampling for research purposes approved by the local ethical committee within their admission period, which included samples taken on admission to the CCU before the initiation of antithrombotic therapy and at 12 to 24 hours from admission, the time point when cardiac TnT is most efficient for diagnosing myocardial damage in this population.25 These coded samples were centrifuged and separated in the CCU, and the serum was immediately frozen in liquid nitrogen before storage in a -80°C freezer. All management decisions were made without knowledge of the patients' TnT results.
Clinical Data
Full clinical details on all patients were recorded pro forma. Particular attention was paid to previous cardiac history, classification of chest pain before entry, admission clinical findings, inpatient clinical course and management, discharge drug management, and subsequent investigations and treatment. Follow-up for survival, interventions, and mortality was by examination of hospital records, postmortem results if available, death certificates, general practitioner questionnaire, and patient or next of kin questionnaire, with follow-up telephone contact if required. Survival status and cause of death were established for all patients. Cause of death was classified according to American Heart Association criteria.33
ECG Criteria
ST-segment elevation was judged to be present if raised 0.1 mV at the J-point in 1 extremity lead or 0.2 mV in 1 precordial lead. The sum of the ST-segment elevation was recorded at baseline and at 2 hours after thrombolysis. A 50% reduction in the sum of the ST-segment score between the baseline and 2-hour ECGs was taken to indicate successful reperfusion.34 35 36
Analytical Techniques
AST and HBD were measured at 37°C by optimized methods on a Perspective analyzer (American Monitor) by the manufacturer's recommended methods. The manufacturer's reagents were used for AST (reference interval, 11 to 55 U/L) and commercially supplied reagents for HBD (reference interval, 90 to 180 U/L) (Merckotest HBDH, BDH Diagnostics). Total CK was measured at 30°C by optimized methods with commercially supplied reagents (CK NAC opt., BCL) (reference interval, <120 U/L). All determinations were made with an RA 1000 analyzer (Bayer Technicon). TnT was determined by an ELISA on an ES-300 Immunoassay analyzer (Boehringer Mannheim) as previously described.25 The detection limit for the assay is 0.05 ng/mL. For the purposes of this study, admission TnT values of 0.2 ng/mL were taken to be positive, since this had been established by previous studies as being the optimal discriminant for significant myocardial damage.25 29 Interassay imprecision (coefficient of variation) was 12.3%, 7.7%, and 4.2% at mean TnT levels of 0.13, 1.6, and 7.1 ng/mL, respectively. Intra-assay imprecision was 2.0% and 1.9% at mean TnT values of 1.7 and 7.0 ng/mL, respectively. All of the samples for TnT measurement were batch assayed by a single operator unaware of the final diagnostic classification.
Statistical Analyses
Baseline demographics were expressed as percentages or medians, with UQs and LQs where appropriate. Differences in the baseline demographics and outcome measures between the two TnT groups were tested by nonparametric 2 statistics. Correlations were tested by the Spearman rank correlation test (rs). Cumulative hazard function plots were generated by the Kaplan-Meier method, with differences examined by the log rank statistical test. Multiple regression for survival used the Cox stepwise forward conditional regression statistical model, with entry and removal at the .05 and .1 significance levels, respectively. For all statistical evaluations, a two-sided value of P
.05 was considered to be statistically significant. For subgroup analysis, patients were divided into those with and those without ST-segment elevation on their admission ECGs and then split into TnT-positive and TnT-negative groups. The end points studied were cardiac death, readmission with fatal or nonfatal myocardial infarction, and the combined end point of cardiac death or nonfatal myocardial infarction as first events.
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Results |
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Admission TnT results were available for 513 admissions with chest pain; 259 admissions were classified according to the criteria defined above as myocardial infarction. Only the first admission was included in the analysis; thus, 240 patients were finally studied. The patients were followed for a median of 1032 days (LQ, 858 days; UQ, 1307 days). Overall, there were 60 deaths (25%) in the cohort, 52 (22%) cardiac and 8 (3%) noncardiac (6 deaths of malignancy, 1 fatal stroke after thrombolysis, and 1 septic shock and renal failure). Of the 25 deaths in the ST-segment elevation group, 19 were cardiac, versus 33 of the 35 deaths in the non-ST-segment elevation group. The noncardiac deaths were treated as censored observations in the statistical analyses.
All Myocardial Infarction Patients
The baseline demographics and differences in outcomes in patients with a final diagnosis of myocardial infarction according to admission TnT status are shown in Table 1
. Admission TnT was 0.2 ng/mL in 45% of patients (108/240) with a median admission concentration of 0.67 ng/mL (LQ, 0.3; UQ, 1.65) in this group. Patients considered TnT positive on admission were significantly more likely to have a more atypical cardiac history, to have intermittent rather than continuous chest pain, to present later, and to have a nondiagnostic ECG on admission (Table 1). They also appeared to sustain a significantly larger amount of myocardial damage, to require antifailure treatment at discharge more frequently, and to have an adverse prognosis in terms of cardiac death or readmission with nonfatal infarction on long-term follow-up compared with those patients whose admission TnT was considered negative. There were no differences between the frequencies of subsequent revascularization (Table 1).
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Significant positive correlations were seen between admission TnT and admission CK concentrations (rs=.51, P.00001), admission TnT concentration and time from onset of symptoms to sampling (rs=.36, P.00001), and a weak correlation between admission TnT concentration and age (rs=.16, P=.02). Admission TnT did not correlate with admission Killip score (rs=-.08, P=.21), although Killip score did correlate with age (rs=.20, P=.004). Although it was significantly higher in the TnT-positive group, admission CK concentration 120 U/L was not associated with an adverse prognosis (P=.89 for cardiac death).
Subgroup Analyses
Myocardial Infarction With ST-Segment Elevation on Admission
Admission TnT concentration was 0.2 ng/mL in 36.5% of patients (46/126) with ST-segment elevation on their admission ECG. The differences in demographics for this group are shown in Table 2. The median admission TnT concentration was 0.55 ng/mL (LQ, 0.2; UQ, 1.4) in the TnT-positive group. Again, patients who were TnT positive were more likely to present with an atypical history and to present slightly later. The most significant difference between the groups early in their admission course was the significantly lower reperfusion rate after thrombolysis in the TnT-positive group (Table 2) when assessed noninvasively. Not surprisingly, then, there was a higher TnT concentration at 12 to 24 hours and an increased need for antifailure treatment on discharge in this group.
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In the whole ST-segment elevation group, the admission TnT concentration correlated positively with admission CK concentration (rs=.49, P.00001), although neither admission CK concentration nor an admission CK 120 U/L was associated with an increased risk of cardiac death (P=.75 and P=.86, respectively). Admission TnT also correlated positively with the time from the onset of the worst pain to first sampling (rs=.33, P=.00018). There was no correlation between the admission TnT concentration and the admission sum of the ST-segment score (rs=.10, P=.27), although a positive correlation was found between the sum of the ST-segment score and admission Killip score (rs=.33, P=.00018). Significant negative correlations were seen between time from pain onset to sampling and the admission Killip score (rs=-.37, P=.00003) and sum of the ST-segment score (rs=-.24, P=.008). There was a threefold difference in the 30-day cardiac death event rate in the admission TnT-positive group compared with the admission TnT-negative group, which had increased to nearly a fourfold difference by 3 years of follow-up, with a doubling of the further reinfarction rate (Table 2
). The Kaplan-Meier cumulative hazard function curves with the log-rank statistics according to the admission TnT status are shown in Fig 1A for cardiac death and Fig 1B for cardiac death or nonfatal reinfarction as first events.
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Admission Killip score, TnT status, the sum of the ST-segment score, thrombolysis, an admission CK >120 IU/L, and the time from the onset of the worst pain to admission sampling were entered into a forward conditional stepwise Cox regression model of event-free survival for the end point cardiac death or nonfatal reinfarction as first event.
An admission TnT concentration of 0.2 ng/mL was the most significant predictor for this end point (2, 6.9; P=.0086; RR, 2.9; 95% CI, 1.31 to 6.43), followed by the time from the onset of the worst pain to admission sampling (2, 5.6; P=.017; RR, 1.04; 95% CI, 1.0 to 1.07). The other variables entered did not achieve significance in this analysis.
Myocardial Infarction Without ST-Segment Elevation on Admission
Admission TnT concentration was 0.2 ng/mL in 54% of patients (62/114) without ST-segment elevation on their admission ECG. The differences in demographics for this group are shown in Table 3. The median admission TnT concentration was 0.9 ng/mL (LQ, 0.36; UQ, 1.9) in the TnT-positive group. Patients who were TnT positive in this group had intermittent rather than continuous pain more frequently and presented later. Although the total median Killip scores were not significantly different between the two groups, frank pulmonary edema was present more frequently in the TnT-positive group, and this group required antifailure treatment more frequently on discharge. Admission TnT concentrations correlated positively with admission CK concentrations (rs=.55, P.00001), although again, neither admission CK concentration nor an admission CK 120 U/L was associated with an increased risk of cardiac death (P=.15 and P=.80, respectively). Admission TnT also correlated positively with the time from the onset of the worst pain to first sampling (rs=.34, P=.00024) and with age (rs=.24, P=.01) but did not correlate with admission Killip score (P=.75). There was, however, a significant negative correlation between admission Killip score and the time from the onset of the worst pain to first sampling (rs=-.37, P=.00007). Both groups had a high mortality at 30 days, and the survival differences appear to slowly separate over time. The TnT-positive group were more likely, however, to suffer a further reinfarction than the TnT-negative group (Table 3). The Kaplan-Meier cumulative hazard function curves with the log-rank statistics according to the admission TnT status are shown in Fig 2A for cardiac death and Fig 2B for cardiac death or nonfatal reinfarction as first events.
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Admission Killip score, TnT status, previous angina, chest pain on admission, an admission CK >120 IU/L, and the time from the onset of the worst pain to admission sampling were entered into a forward conditional stepwise Cox regression model of event-free survival for the end point cardiac death or nonfatal reinfarction as first event. The time from the onset of the worst pain to admission sampling was the most significant predictor for this end point (2, 7.56; P=.006; RR, 1.04; 95% CI, 1.0 to 1.08), followed by an admission TnT concentration of 0.2 ng/mL (2, 4.8; P=.028; RR, 2.49; 95% CI, 1.1 to 5.6). The other variables entered did not achieve significance in this analysis.
Analysis of Discriminant Level
This question was addressed by examination of variations in significance and 2 values of changing the admission TnT discriminant level (ie, 0.1, 0.2, 0.3 ng/mL) against the main end points, the results of which are shown in Table 4. As can be seen, any detectable TnT is associated with a worse prognosis. A diagnostic cutoff for admission TnT of 0.2 ng/mL, however, had the highest 2 value and significance across all the patient groups, although in terms of total numbers of events identified, a cutoff of 0.1 ng/mL was superior.
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Discussion |
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This study shows that the presence of TnT concentrations of
0.2 ng/mL on admission in patients who have sustained a myocardial infarction identifies a group at significant risk for cardiac events on subsequent follow-up. For subsequent cardiac events, its presence on admission appears to be most hazardous for those patients with ST-segment elevation on their admission ECG (Table 2, Fig 1). Compared with the ST-segment elevation group with admission TnT concentrations <0.2 ng/mL, the increased mortality in the TnT-positive group appears early and continues to gain significance on long-term follow-up (Table 2, Fig 1). There were no significant correlations between admission TnT concentrations and either Killip score or the sum of the ST-segment elevation score on admission. The significant negative correlation between Killip score and time to presentation and the positive correlation between Killip score and the sum of the ST-segment score on admission suggest that patients with large infarcts and significant cardiac decompensation present early, before significant release of TnT into the circulation has occurred. Patients with a high sum of ST-segment scores on admission reflect either patients who are presenting early with hyperacute large-amplitude ST-segment changes in the infarcting area or patients who have a large area of jeopardized myocardium.37 38 These groups have the most to gain from thrombolytic therapy in terms of mortality reduction,17 18 19 20 37 38 and this is the explanation offered for the stepwise regression analysis results for the ST-segment group. The group without ST-segment elevation had a high mortality whether TnT was positive or negative on admission, confirming that an ideal management strategy for this group remains elusive, which continues to justify trials examining alternative strategies.39
There was some evidence of more cardiac damage in the TnT-positive than the TnT-negative group, and the cardiac event rates were separating over time (Fig 2, Table 3). The time from the worst chest pain to sampling, however, was the most powerful predictor of an adverse outcome in this group as a whole in the stepwise regression model. In both the groups with and, in particular, without ST-segment elevation myocardial infarction, the presence of TnT on admission was associated with a much higher subsequent reinfarction rate than in those whose admission TnT was considered negative, and it was usually fatal. Reinfarction, both early and late, has been documented in most series examining outcome after myocardial infarction,17 18 19 20 38 40 41 but the substrate for reinfarction and the pathophysiological processes involved remain poorly defined.
In the group with ST-segment elevation, our overall impression is that the TnT-positive patients are presenting later and that the thrombolytic therapy they received was less effective in restoring patency or perhaps in achieving TIMI 3 flow.40 41 42 Limitations of noninvasive assessments of reperfusion and grade of reperfusion have been documented43 ; thus, this finding requires confirmation by a formal angiographic patency study. Our view is consistent, however, with the findings of the large thrombolytic trials and angiographic patency and subsequent outcome studies. If our findings are confirmed, the question then arises as to whether this group, if identified soon after admission, might do better with a more aggressive strategy, such as direct PTCA.44 45 Early rapid identification of TnT presence will depend on what TnT concentration is used as the discriminant to define positivity. The most appropriate cutoff level of TnT concentration on admission is addressed in Table 4. As can be seen, if present, there is no lower level of TnT that is not associated with a poorer prognosis. A practical problem exists, however.
To measure TnT at the 0.1-ng/mL level requires a quantitative measurement with the ELISA method, which currently takes about 2 hours to complete and requires a dedicated immunoassay analyzer. If prospective testing of other, more interventional strategies, such as direct PTCA, in this group were contemplated, then these procedures should be carried out as soon as possible after admission.45 The only way to achieve this currently would be by measurement of TnT with the rapid assay (Cardiac T, Boehringer Mannheim).46 This bedside assay takes a maximum of 20 minutes to give a result and has a detection limit of 0.2 ng/mL.47 We believe, therefore, that the current cutoff for admission TnT concentrations should be 0.2 ng/mL but that this should be lowered to <0.1 ng/mL as the assay technology advances.
Conclusions
The presence of TnT in patients admitted with myocardial infarction at a concentration of 0.2 ng/mL identifies a subgroup at significantly higher risk of subsequent cardiac events on follow-up. Its presence is a more powerful predictor of a poor prognosis in patients with ST-segment elevation on the admission ECG than in those without ST-segment elevation and identifies a group that may benefit from alternative early management strategies.
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Selected Abbreviations and Acronyms |
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Received January 22, 1996; revision received April 2, 1996; accepted April 7, 1996.
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References |
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