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(Circulation. 1997;95:2053-2059.)
© 1997 American Heart Association, Inc.

Articles

Prognostic Influence of Elevated Values of Cardiac Troponin I in Patients With Unstable Angina

Marcello Galvani, MD; Filippo Ottani, MD; Donatella Ferrini, MD; Jack H. Ladenson, PhD; Antonio Destro, MD; Daniele Baccos, MD; Franco Rusticali, MD; Allan S. Jaffe, MD

the Fondazione Cardiologica "Myriam Zito Sacco," Forlì (M.G., F.O., D.F., F.R.), Divisione di Cardiologia, Forlì (M.G., D.F., F.R.), Divisione di Cardiologia, Ravenna (F.O.), Divisione di Cardiologia, Rimini (A.D.), and Divisione di Cardiologia, Riccione (D.B.), Italy, and Washington University, St Louis, Mo (J.H.L., A.S.J.). Dr Jaffe is now at SUNY Health Science Center at Syracuse, NY.

Correspondence to Dr Marcello Galvani, Fondazione Cardiologica Myriam Zito Sacco, P.zza F.lli Ruffini, 6, 47100 Forlì, Italy. E-mail sacco{at}mbox.queen.it

	Abstract

Top Abstract Introduction Methods Results Discussion Appendix References

 
Background Elevations of the MB isoform of creatine kinase (CK) and cardiac troponin T seem to confer an adverse prognosis in unstable angina. We examined whether this prognostic influence is also present for cardiac troponin I (cTnI), a new and even more specific marker of myocardial injury.

Methods and Results We studied 106 patients with the clinical diagnosis of unstable angina showing chest discomfort at rest within 48 hours of admission, ECG evidence of myocardial ischemia, and normal values of total CK over the initial 16 hours of observation. The primary end point was death or nonfatal myocardial infarction (MI) at 30 days; the secondary end point was the incidence of cardiac events at 1 year. Blood was drawn every 8 hours for 3 days. Thirteen patients were excluded because of increased CK-MB mass concentrations within 16 hours of admission (non–Q-wave MI) and 2 because of inadequate blood sampling. Of the remaining 91 patients, 22 had cTnI elevations on admission (n=7) or after 8 hours (n=15). At 30 days, no deaths (0%) and 4 MIs (5.8%) occurred in the 69 patients with normal cTnI compared with 2 deaths (9.1%) and 4 MIs (18.2%) in the 22 patients with elevated cTnI. The combined incidence of death and nonfatal MI was 5.8% and 27.3%, respectively (P=.02). At 1 year, only 68% of patients with elevated cTnI were free of cardiac events, compared with 90% of those without elevations (P=.01).

Conclusions These data indicate that cTnI is an important prognostic variable in patients with unstable angina. Elevations of cTnI predict an adverse short- and long-term prognosis.

Key Words: prognosis • angina • myocardial infarction

	Introduction

Top Abstract Introduction Methods Results Discussion Appendix References

 
Patients with unstable angina are a heterogeneous group who present in diverse ways and who manifest prognoses that vary from high to low risk.¹ Unfortunately, facile noninvasive techniques with which to predict prognosis are not available.

In a significant subset of patients with unstable angina, minor elevations of CK-MB are present in the absence of marked increases in total CK. However, the prognostic implications of such a finding have never been totally elucidated.^{2 3 4 5} Recently, similar findings have been observed with the newer novel biochemical markers of myocardial injury that have enhanced sensitivity and specificity for the detection of myocardial damage. For example, the presence of elevated levels of cTnT in patients with unstable angina has been associated with a substantially higher occurrence of cardiac events over time.^{6 7}

Recently, it has been suggested that the specificity of cTnI to detect myocardial injury may be greater than that of cTnT.⁸ No false-positive elevations were found in patients with skeletal muscle damage or renal failure or after severe exertion.⁹ However, at present there are no systematic studies of the prognostic value of elevations of cTnI in patients with unstable angina. The present study was designed to examine this issue prospectively in a large cohort of patients with severe unstable angina in whom acute non–Q-wave infarction was rigorously excluded.

	Methods

Top Abstract Introduction Methods Results Discussion Appendix References

 
The study was conducted in four cardiological centers in Italy, supported by a core laboratory in the United States and a central unit for data collection and analysis, as described in the "Appendix."

Patient Selection
One hundred six patients with the clinical diagnosis of unstable angina admitted to the coronary care units of four Italian hospitals between March 1994 and October 1994 were included in the present study. To facilitate enrollment of high-risk patients, we required that patients have chest discomfort at rest thought to be due to myocardial ischemia during the 48 hours before admission (the III B class of Braunwald's classification) accompanied by objective evidence of ischemia on the qualifying ECG (either transient ST-segment elevation >0.5 mm, transient or persistent ST-segment depression >0.5 mm, or definite T-wave inversion >1 mm). Additionally, total CK activity had to remain 200 IU/L (the upper reference limit) on serial determinations performed during the first 16 hours at the clinical centers to exclude most of the patients with acute MI. Furthermore, we excluded patients with elevations of CK-MB isoenzyme mass concentration determined at the core laboratory during the same 16-hour time period. Exclusion of patients with elevations of CK-MB was done at the core laboratory by investigators unaware of the clinical characteristics of the patients. Patients with MI documented in the 2 weeks before hospitalization, those with valvular heart disease, and those with known cardiomyopathy were also excluded.

Management
The protocol-defined conventional medical therapy for unstable angina included bed rest, oxygen, aspirin 325 mg orally at admission and continued thereafter at half the initial dose, intravenous heparin (a 5000-U bolus followed by a continuous infusion adjusted to keep the activated partial thromboplastin time at 1.5 to 2.0 times laboratory control value), and intravenous nitrates (mainly isosorbide dinitrate, starting at a dose of 1 mg/h and adjusted until there was a 15% drop in blood pressure from baseline values). Other therapy for ischemia (eg, ß-blockers and calcium antagonists) was used at the discretion of the attending physician.

Clinical Evaluation and Follow-up
On admission, a complete medical and chest pain history was obtained from each patient along with a 12-lead ECG. Additional 12-lead ECGs were performed for recurrent chest pain. Coronary angiography was performed when clinically indicated. All therapeutic decisions were made without knowledge of the cTnI values.

Patients were followed up for 30 days after admission to record cardiac events (death or nonfatal MI) and the need for interventions (coronary angioplasty or bypass surgery). During this period, the categorization of cardiac events was based on a review of all the pertinent clinical documentation, including ECGs and locally obtained enzyme data, by clinicians unaware of the cTnI values. The patients or their relatives were subsequently contacted by phone call for a 1-year follow-up interview. Since patients who experienced cardiac events during follow-up generally were rehospitalized in the same coronary care units in which they had been admitted previously, we were able to review the clinical charts in every patient with a potential cardiac event.

Blood Sampling
After informed consent was obtained from each patient, 7 mL of blood was collected on admission (within 1 hour) and every 8 hours thereafter for the following 3 days. The samples were kept at room temperature for 20 minutes to allow clotting, centrifuged, and then stored at -70°C until they were shipped on dry ice to Washington University School of Medicine, where the assays were performed. The samples remained frozen during transfer.

Analytic Methods
Biochemical analyses were performed by individuals unaware of the clinical status of the patients. cTnI was assayed by an immunoassay in a preliminary research application on the Baxter Stratus analyzer. The method uses two cTnI-specific antibodies, each of which recognizes different epitopes.¹⁰ Values of cTnI in healthy volunteers are undetectable by this method. Studies performed with this assay on samples of hospitalized patients without known cardiac disease have defined the upper limit of the reference range to be 3.1 ng/mL based on a 95% cutoff value by nonparametric analysis; the lower limit of detection is 1.5 ng/mL. The cTnI immunoassay has no detectable cross-reactivity with human skeletal muscle cTnI.¹⁰ There is excellent correlation between this research procedure and the recently released commercial assay (r=.982). A value of 3.1 ng/mL with the old assay extrapolates to a value of 0.6 µg/mL with the newer procedure.¹¹

CK-MB (upper reference limit, 6.7 ng/mL; lower limit of detection, 2.2 ng/mL) was measured with a commercially available immunosorbent assay (Stratus CK-MB; Baxter Dade), in which a monoclonal antibody recognizes CK-MB but neither CK-BB nor CK-MM isoenzymes.¹²

End Points
The prospectively determined primary end point for the comparison between patients with and without elevated cTnI values was a composite of death from cardiac causes and nonfatal MI within 30 days after admission. Acute MI was considered to have occurred in the presence of recurrent severe ischemic pain at rest 30 minutes, accompanied by new or recurrent ST-segment shifts (0.1 mV in at least two contiguous leads) that also persisted for 30 minutes and total CK elevation twice the upper limit of normal. After an intervention such as coronary angioplasty or bypass surgery, a threefold increase in total CK was required for diagnosis. The presence of new Q waves (>30 ms) in two contiguous leads was required to diagnose infarction after bypass surgery. The diagnostic criteria for MI were reviewed in all instances and confirmed by two independent evaluators (F.O. and D.F.) unaware of the cTnI results.

Secondary end points also tabulated included (1) the frequency of myocardial ischemia (defined as any episode of typical chest pain associated with ECG changes occurring during hospital stay); (2) the need for revascularization procedures (coronary angioplasty or bypass surgery) within 30 days of hospitalization; and (3) the 1-year rates for cardiac mortality and nonfatal MI.

Statistical Methods
On the basis of the incidence of events in the study by Hamm et al,⁶ we calculated the need for a sample size of 48 patients, given a reported rate of death and nonfatal MI of 33% in patients with elevated troponin values and 2.5% in patients with normal levels of troponin. If a lower event rate of 25% were used for the group with elevated values of cTnI and 5% for the group without elevations (equivalent to the event rate in unstable angina patients belonging to the placebo arm of the TIMI IIIB trial),¹³ the sample size required would be 90 patients to detect a significant difference between populations (two-sided level of =.05 and a power of 80%).

All results are expressed as mean±SD except as stated otherwise. Continuous variables were analyzed with unpaired t tests and Mann-Whitney U tests where appropriate. Categorical variables were compared by ² tests. The relative risk of events and 95% CIs for those variables were also calculated. Independent determinants of prognosis were identified by multivariate logistic regression analysis. We included in the logistic regression model all variables with a value of P<.1 by univariate comparison. Wald statistics were used to test the differences. Event-free survival curves were computed according to the Kaplan-Meier method. Comparison of survival between subgroups was performed by the log-rank test. Differences were considered significant if the null hypothesis could be rejected with >95% confidence. The SPSS 6.0 statistical software package was used for all calculations.

	Results

Top Abstract Introduction Methods Results Discussion Appendix References

 
From the initial population of 106 consecutive patients with prolonged chest pain within 48 hours of admission, ECG evidence of myocardial ischemia, and total CK activity 200 IU/L, 2 patients were excluded because inadequate blood supplies were obtained for analysis. Nine patients had increased levels of CK-MB mass concentration at baseline, and 4 additional patients developed elevations at 8 hours. Concurrently, all also had serum values of cTnI >3.1 ng/mL. These 13 patients were therefore designated as having non–Q-wave MIs and were excluded from further analysis, leaving a final study cohort of 91 patients with unstable angina. Among these patients, 22 (24%) had increased levels of cTnI with normal values of CK-MB: 7 (32%) on admission, 14 (64%) after 8 hours, and 1 (4%) only after 16 hours of hospital admission. No patient had detectable cTnI levels not exceeding the upper reference limit, ie, >1.5 and <3.1 ng/mL, in the absence of clear-cut elevations at different times.

Patients with values of cTnI normal and >3.1 ng/mL did not differ with respect to baseline clinical characteristics and treatment approach (Table 1). Conversely, patients with cTnI levels >3.1 ng/mL had a significantly longer duration (median, 60 versus 30 minutes; P=.01) of chest discomfort before admission, more ST-segment shifts (77% versus 55%; P=.06), and fewer T-wave inversions (23% versus 45%; P=.05) on their qualifying ECGs. Coronary angiography was performed in 74% of patients. The extent and severity of coronary artery disease were similar between the two groups except for 9 patients who had angiographically normal coronary arteries. No patient with normal coronary arteries had a value of cTnI >3.1 ng/mL.

View this table: [in this window] [in a new window]   Table 1.

Primary and Secondary End Points
Clinical outcomes during the first 30 days of follow-up were significantly different between patients with and without elevations of cTnI (Table 2). The overall cardiac event rate (death or nonfatal MI) for patients with cTnI >3.1 ng/mL was 27.3%, compared with 5.8% for those without elevations (P=.02). This result was mainly due to a difference in the incidence of death from cardiac causes (P=.05).

View this table: [in this window] [in a new window]   Table 2.

The incidence of in-hospital recurrent ischemia was similar in the two patient groups, as was the overall 30-day revascularization rate. When the prospectively defined primary study end point was analyzed with the inclusion of the 13 patients with increased CK-MB mass concentrations, there still was a difference in the rate of cardiac events between the two groups of patients (20% for those with elevations of cTnI compared with 5.8% for those without; relative risk, 2.1 [95% CI, 1.2 to 3.6]; P=.04). Furthermore, we were also interested to know whether the 7 patients with cTnI levels >3.1 ng/mL on admission had a worse outcome than the remaining study population. However, the 30-day event rate was not significantly different, being 14.3% among patients with cTnI >3.1 ng/mL in the baseline sample compared with 8.8% among those with normal values at the time of hospital admission.

Table 3 tabulates the major cardiac events and their timing during follow-up. Both deaths (one sudden and one complicating acute MI) occurred in patients with cTnI >3.1 ng/mL. In addition, 4 of the 8 patients who developed clear-cut, clinically apparent acute MIs had increased cTnI levels at the time of their initial evaluation. Three infarctions occurred during the perioperative period (two in patients with cTnI >3.1 ng/mL and one in a patient with normal levels of cTnI) and were associated with the occurrence of new pathological Q waves in the leads that had shown ischemic changes on the admission ECG. Among the 5 patients with cardiac events associated with cTnI elevations, 2 had increased levels on admission and the remaining 3 on the 8-hour sample.

View this table: [in this window] [in a new window]   Table 3.

Relation Between ECG Findings, cTnI Elevations, and Clinical Outcome
The qualifying ECGs showed transient ST-segment elevation in 22 patients, ST-segment depression in 32, and T-wave inversion in the remaining 37 patients. Patients with ST-segment shifts (ST-segment depression or elevation) were more likely to have ongoing anginal pain at the time of ECG recording than those presenting with T-wave inversion (56% versus 16%, P=.0002). Only 14% (5/36) of patients presenting with T-wave inversion had cTnI levels >3.1 ng/mL, as opposed to 31% (17/54) of those with ST-segment shifts (P=.05). However, more of the cardiac events occurred in patients with T-wave inversion and cTnI >3.1 ng/mL (3/5, 60%) than in those with ST-segment shifts (2/17, 12%) (relative risk, 5.1; 95% CI, 1.2 to 22.5; P=.05).

Independent Prognostic Value of Elevated cTnI
Table 4 shows the univariate comparisons between patients with and without cardiac events within 30 days. Only variables available early after admission were selected for analysis. Compared with patients who had a favorable outcome, patients with cardiac events were older, more frequently showed T-wave inversion on the qualifying ECG, and had cTnI levels >3.1 ng/mL. When these univariate predictors of 30-day cardiac events were included in the multivariate logistic regression analysis, a model was elaborated (model ²=14.298; P=.0025) that identified cTnI levels >3.1 ng/mL (Z value, 5.3; P=.02) and the presence of T-wave inversion (Z value, 5.5; P=.02) as independent predictors of cardiac events. Age did not reach formal statistical significance (Z value, 3.4; P=.07). The relative risk of cardiac events at 30 days among patients with cTnI levels >3.1 ng/mL and T-wave inversion was 8.6 (95% CI, 3.0 to 24.6; P=.006) compared with the remaining study population.

View this table: [in this window] [in a new window]   Table 4.

Long-term Prognostic Value of Elevated cTnI
The prognostic value of cTnI >3.1 ng/mL levels was also maintained at 1-year follow-up, as illustrated in the Figure. After the initial 30-day follow-up, two additional MIs occurred in patients with cTnI >3.1 ng/mL and three in the group with normal levels. At 1 year, only 68% of patients with cTnI elevations were free of cardiac events, compared with 90% of those without elevation of cTnI (P=.01). The relative risk of death or MI at 1 year in patients with cTnI >3.1 ng/mL was 2.6 (95% CI, 1.3 to 5.1).

View larger version (13K): [in this window] [in a new window]   Figure 1. Cumulative percent of patients free of death or nonfatal MI according to elevation of cTnI. , Normal cTnI; , elevated cTnI.

	Discussion

Top Abstract Introduction Methods Results Discussion Appendix References

 
The results of the present study confirm that the presence of myocardial damage identified by elevations of cTnI is a potent prognostic indicator in patients with unstable angina. Elevations were associated with a 2.5-fold increase in the relative risk of death or nonfatal MI both at 30 days and at 1 year. Moreover, cTnI manifested independent prognostic value that was additive to the clinical and ECG variables associated with adverse outcomes. With the exception of one letter to the editor concerning the prognostic value of elevated cTnI in patients with chest pain but not necessarily unstable angina,¹⁴ these data are the first to be published evaluating the prognostic value of elevations of cTnI.

Our findings are consistent with those reported for cTnT in similar patient populations.^{6 7 15 16 17} Hamm et al⁶ found elevations of cTnT in 33 of 84 patients (39%) with Braunwald's class III unstable angina. Ten of the 11 cardiac events (death or nonfatal MI) in that series occurred in patients with elevated levels. In another report,¹⁵ in which 16 of 28 patients had unstable angina with abnormal cTnT levels, all (5, or 31%) of the patients who developed MI during their hospital stay belonged to this group. Furthermore, Wu et al¹⁶ found that the incidence of MI was higher (30% versus 3%) in patients with myocardial damage defined by the elevation of cTnT in a single blood sample obtained at the time of admission. Ravkilde et al¹⁷ recently extended these observations by reporting that the 2-year event rate in patients with unstable angina and elevated cTnT was 24%, compared with only 5% in patients without elevations. Even more recently, Lindahl and colleagues⁷ described a progressive increase in risk as values of cTnT rose. It should be noted that the frequency of elevations of cTnI in our study and our subsequent event rates were only slightly lower than in other series, even though we aggressively eliminated patients with elevations of CK-MB over the first 16 hours. This group with acute non–Q-wave MI has been reported to be at far greater risk than those with elevations of troponin alone.¹⁷

cTnI is a new biochemical marker of myocardial damage that is at least as sensitive as CK-MB for the detection of acute MI.¹⁸ cTnI has high specificity for cardiac injury,⁹ because it is not found in skeletal muscle during neonatal development or adulthood.^{19 20 21 22} Furthermore, it is not expressed in regenerating human skeletal muscle tissue.²³ Accordingly, elevations do not occur, even in patients with acute or chronic skeletal muscle damage, unless myocardial injury is present.⁹ This is to some extent in contrast to cTnT, which, though a sensitive marker of myocardial necrosis,²⁴ appears to be less specific.^{25 26}

The reason why detection of myocardial damage has such important prognostic implications in patients with unstable angina is still unclear. It has been reported that in patients with unstable angina who die, there are focal areas of myocardial necrosis^{27 28} that would mark vascular territories potentially at high risk. Myocardial necrosis could be due to the presence of active coronary thrombosis^{29 30 31 32 33} with subsequent distal embolization or to abnormalities in the supply-demand relationship. Therefore, increases of sensitive markers of myocardial injury, such as cTnI, in the circulation may reflect sensitive detection of minor amounts of myocardial necrosis, marking the presence of a high risk. Consistent with the concept that elevations of cTnI represent more sensitive detection of myocardial necrosis is the fact that patients with elevations of cTnI had longer durations of symptoms before admission than those without elevations. Furthermore, in two thirds of our patients, increases in cTnI were detected only after admission despite normal values of CK-MB. These data support the concept that cTnI allows more sensitive detection of myocardial injury than CK-MB. A potential explanation for the increased sensitivity of cTnI is the fact that the concentration of cTnI in the myocardium is about 13-fold higher than that of CK-MB.¹⁷ Therefore, absolute increases in plasma concentrations per unit of damaged tissue may be more pronounced. Second, the reference normal range is far more narrow for cTnI than for CK-MB, because cTnI is virtually undetectable in normal subjects. Therefore, even small increases in plasma of cTnI are reflected in elevations above the conventional reference limit. In about one third of our cases, however, cTnI was elevated in the first blood sample and decreased thereafter. It is possible that these patients had unstable angina after a clinically undetected MI, ie, early postinfarction unstable angina, a condition known to be associated with a markedly increased risk of subsequent cardiac events.^{34 35} This is an important consideration for the use of cTnI, because after acute MI, increases in cTnI often are found in plasma for at least 1 week (median, 8 days), even if the size of the infarction is modest. These persistent elevations appear to reflect degradation of structural cTnI from the contractile apparatus, because the half-life of the protein in blood is short.¹¹ Thus, increases of cTnI in patients with ischemic heart disease may represent more sensitive detection (minor necrosis) or suggest that significant numbers of patients with unstable angina have suffered cardiac injury in the week or so before presentation.

We have documented for the first time that elevations of cTnI have prognostic value independent of the information provided by the analysis of the ECG in patients with the most severe type of unstable angina despite a very aggressive approach to exclude non–Q-wave MI. The role of the ECG abnormalities in helping to define the risk of patients with unstable angina is believed to be important. However, the exact type of abnormality linked to adverse prognosis is incompletely defined, in part because the relationship between ECG changes and the presence or absence of anginal pain at the time of ECG recording has not been systematically investigated. Although in patients with ongoing anginal pain on admission, the presence of ST-segment changes on the ECG has been associated with increased coagulant activity³⁶ and an adverse prognosis by some,^{37 38} in other series, when pain-free patients are considered, those with T-wave inversion appear to be exposed to increased risks.^{39 40 41} In our study, the presence of T-wave inversion on the qualifying ECGs was a weak predictor of cardiac events. However, since we studied a relatively small number of patients with and without anginal pain on admission, we believe that our data are insufficient to delineate the prognostic significance of the qualifying ECG. Furthermore, we cannot exclude the possibility that patients with ST-segment changes (especially ST-segment elevation) received more intense management. Thus, we cannot confirm either the contention of Ravkilde et al,¹⁷ who found that the detection of myocardial damage by cTnT had no independent prognostic value when the presence of ECG abnormalities was entered into the statistical model, or that of Lindahl et al,⁷ who reported the opposite.

In conclusion, the results of our prospective study provide evidence that cTnI is an indicator of adverse outcome in patients with severe unstable angina. Our results are in keeping with the recent retrospective analysis of patients enrolled in the TIMI IIIB study.⁴² The use of cTnI in the immediate triage of patients with unstable angina appears warranted to identify those at greater risk for cardiac events.

	Appendix

Top Abstract Introduction Methods Results Discussion Appendix References

 
Coordinating center for data collection and analysis: Fondazione Cardiologica "Myriam Zito Sacco," Forlì, Italy. Chairman of the Foundation: Franco Rusticali, MD. Principal investigators: Marcello Galvani, MD; Filippo Ottani, MD; Donatella Ferrini, MD. Coinvestigators: Roberto Puggioni, MD; Jean Ellen Page, RN.

Core laboratory for cTnI and CK-MB mass assays: Washington University, St Louis, Mo. Principal investigators: Allan S. Jaffe, MD; Jack H. Ladenson, PhD. Coinvestigator: Yvonne Landt.

Clinical participating centers: Ospedale G.B. Morgagni, Forlì, Italy. Principal investigators: Marcello Galvani, MD; Donatella Ferrini, MD. Coinvestigator: Roberto Puggioni, MD. Ospedale S Maria delle Croci, Ravenna, Italy. Principal investigator: Filippo Ottani, MD. Coinvestigators: Stefano Bosi, MD; Giancarlo Bellanti, MD. Ospedale degli Infermi, Rimini, Italy. Principal investigator: Antonio Destro, MD. Coinvestigators: Antonio Pesaresi, MD; Francesco Cioppi, MD. Ospedale Ceccarini, Riccione, Italy. Principal investigator: Daniele Baccos, MD.

	Selected Abbreviations and Acronyms

 

CK = creatine kinase CK-MB = creatine kinase MB isoenzyme cTnI = cardiac troponin I cTnT = cardiac troponin T MI = myocardial infarction

Received August 5, 1996; revision received November 22, 1996; accepted November 25, 1996.

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