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(Circulation. 2000;102:1611.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Elevated Troponin I Level on Admission Is Associated With Adverse Outcome of Primary Angioplasty in Acute Myocardial Infarction
From the Division of Cardiology, Cedars-Sinai Medical Center/UCLA School of Medicine, Los Angeles, Calif.
Correspondence to Bojan Cercek, Division of Cardiology, Cedars-Sinai Medical Center, Room 5314, 8700 Beverly Blvd, PO Box 48750, Los Angeles, CA 90048-1865. E-mail cercek{at}cshs.org
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Abstract |
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Background—In patients with acute myocardial infarction (AMI) undergoing thrombolytic therapy, an elevated troponin level on admission is associated with a lower reperfusion rate and a complicated clinical course. Whether an elevated troponin level on admission similarly predicts an adverse outcome in patients undergoing primary angioplasty is currently unknown and was investigated in the present study.
Methods and Results—Cardiac troponin I (cTnI) was determined on
admission in 110 consecutive patients with AMI associated with
ST-segment elevation or left bundle branch block who underwent primary
angioplasty. Fifty-four patients (49%) had an elevated cTnI (
0.4
ng/mL) on admission. In patients with elevated cTnI, primary
angioplasty was less likely to achieve TIMI 3 flow (as classified by
the Thrombolysis in Myocardial Infarction trial) in
univariate (76% versus 96%, P=0.03) or in
multivariate (odds ratio 0.1, 95% CI 0.02 to 0.54)
analysis. Patients with elevated cTnI were more likely to
develop congestive heart failure (23% versus 9%,
P<0.05) and death, heart failure, or shock (30% versus
9%, P=0.006). Elevated cTnI remained a significant
predictor of the composite end point after controlling for other
clinical data that were available early in the course, including time
to presentation and angiographic results (relative risk
5.2, 95% CI 1.03 to 26.3). During a follow-up of 426±50 days,
elevated admission cTnI was a predictor of cardiac mortality (11%
versus 0%, P=0.012), adverse cardiac events (cardiac
mortality or nonfatal reinfarction; 19% versus 5.4%,
P=0.04), and adverse cardiac events plus target vessel
revascularization (32% versus 14%,
P=0.054).
Conclusions—In patients with ST-segment elevation AMI, an elevated cTnI on admission is associated with an increased risk of primary angioplasty failure and a more complicated clinical course.
Key Words: angioplasty • myocardial infarction • reperfusion • proteins
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Plasma levels of cardiac troponin (cTn) provide important prognostic information that is useful for the risk stratification of patients with acute coronary syndromes.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 In patients with acute myocardial infarction (AMI), elevated levels of cTnT on admission predict a higher incidence of congestive heart failure (CHF), shock, and death.3 5 10 15 Although primary angioplasty has been suggested to be the preferred reperfusion strategy in AMI patients with elevated cTn,5 15 the prognostic value of early cTn assessment in these patients has not been reported. In the present study, we examined the prognostic value of an elevated cTnI on admission in patients with ST-elevation AMI undergoing primary angioplasty.
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Methods |
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Study Population
The study population consisted of 110 consecutive patients with AMI associated with ST-segment elevation or left bundle branch block (LBBB) who were treated with primary angioplasty at Cedars-Sinai Medical Center from June 1, 1997, to December 31, 1998. Blood was sampled for cTnI routinely on admission in each patient who presented with clinical manifestations consistent with acute coronary syndrome. The diagnosis of AMI was based on the presence of ischemic chest pain of >30-minute duration and ST-segment elevation of at least 1 mm in
2 contiguous ECG leads
or LBBB. Patients were referred for primary angioplasty if they had
been admitted within 12 hours of the onset of symptoms with evidence of
ongoing ischemia (persistent pain with ST-segment elevation or
LBBB). Myocardial necrosis was confirmed by an increase in cTnI.
cTnI Determination
Venous blood for cTnI levels was collected in EDTA-coated tubes
immediately after the patient arrived at the emergency department
(admission cTnI). Two-sided immunoassay with 2 monoclonal antibodies
specific for the cardiac isotype of cTnI was used (Dade Behring). The
minimal detection concentration of this assay is <0.35 ng/mL, which is
higher than the 97th percentile of the distribution of cTnI levels in
the healthy population. As per hospital protocol, the second cTnI level
was determined 12 hours later.
Coronary Angiography and Angioplasty
Coronary angiography followed by primary angioplasty was
performed with standard techniques. Adjunctive therapy, intra-aortic
balloon counterpulsation, and temporary pacing were used as indicated.
After the procedure, all patients were treated with aspirin (325 mg/d).
Patients that received an intracoronary stent were also treated
with ticlopidine (250 mg BID) or clopidogrel (75 mg/d) for 4 weeks. The
angiograms were reviewed by 2 expert observers who did not perform the
angioplasty and were blinded to clinical and laboratory data. The
initial and final flow in the infarct-related artery (IRA) was assessed
according to the classification of the Thrombolysis in
Myocardial Infarction (TIMI) trial.16 Collateral flow to
the IRA was assessed as previously reported.17 Significant
stenosis of the coronary artery was defined as
narrowing in excess of 50% compared with the uninvolved segment of the
artery. The angioplasty was defined as successful with the
establishment of TIMI 3 flow and residual stenosis of
<30%.
Clinical Follow-Up
In-Hospital Follow-Up
The patients were followed up during the hospital stay for a
prespecified combined end point composed of 3 adverse events related to
the extent of myocardial damage: CHF, shock, and/or death after the
initial angiography. A standard 2D echo-Doppler study was performed
before hospital discharge, and the left ventricular
ejection fraction (LVEF) was determined by using Simpson’s
biplane method.
Long-Term Follow-Up
Patients were followed for 426±50 days. Information was
obtained by telephone questionnaire, review of hospital and primary
physician records, and death certificates. Complete follow-up data
were obtained in all patients. The data were analyzed for the
following end points: cardiac mortality, cardiac events (cardiac
mortality and nonfatal reinfarction), cardiac event, and target-vessel
revascularization.
Statistical Analysis
Comparisons between groups were performed by using t
tests for continuous variables and 
2 tests
or Fisher exact tests for categorical variables. Stepwise
multivariate logistic regression was applied to
identify independent predictors of primary angioplasty success and the
occurrence of the prespecified end point of death, CHF, and shock
during hospital stay. Stepwise multivariate hazard Cox
regression was used to identify the independent predictors of the
occurrence of cardiac events during the follow-up period. Kaplan-Meier
curves for event-free survival according to admission cTnI were
compared with log-rank statistics.
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Results |
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Of the 110 consecutive patients included in the present study, admission cTnI level was elevated (
0.4 ng/mL) in 54 patients (49%),
with a value of 17±54 (range 0.4 to 313) ng/mL. In the other 56
patients (51%), the cTnI level on admission was within the normal
range (<0.4 ng/mL), with a value of 0.13±0.07 ng/mL. All patients
underwent angioplasty, except for 1 patient with elevated cTnI who
underwent emergency CABG for severe 3-vessel coronary artery
disease (CAD).
As shown in Table 1
, there were no
significant differences in the baseline characteristics and clinical
features at presentation before the primary angioplasty
between patients with elevated cTnI and those with normal cTnI on
admission.
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Time to Presentation and cTnI Levels
There was no correlation between the time from the onset of
symptoms to presentation and the admission cTnI level. The
mean time to presentation was 212±186 minutes for patients
with elevated cTnI and 179±171 minutes for patients with normal cTnI
on admission (P=0.38). The proportion of patients with
elevated cTnI among patients who were admitted within 2, 4, 6 or >6
hours after the onset of symptoms was 39%, 41%, 64%, and 59%,
respectively (P for trend 0.4). In linear regression
analysis, there was no correlation between the time from the
onset of symptoms and the admission cTnI levels, either in the entire
study population or among the patients with elevated cTnI on admission
(r2=0.005, P=1).
Coronary Angiography and Angioplasty Results
The distribution of IRA and the proportion of patients with
3-vessel CAD were similar in both groups. The proportion of patients
with TIMI 2 or TIMI 3 flow in the IRA on the initial angiogram was also
similar (Table 2).
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Of the 56 patients with normal cTnI on admission, primary angioplasty
was successful in 54 (96%). Two patients had TIMI 2 flow despite
successful dilatation of the culprit lesion. In contrast, in patients
with an elevated cTnI on admission, angioplasty was successful in only
40 patients (76%) (P=0.003 compared with patients with
normal cTnI, Figure 1). The failure of
angioplasty was due to the inability to cross the culprit lesion in 5
patients (9%), and in 8 patients (15%), the postangioplasty TIMI flow
was 
2 despite the successful dilatation of the culprit lesion. There
were no significant differences between the 2 study groups in the use
of platelet glycoprotein IIb/IIIa
inhibitors (79% versus 89%, P=0.19).
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By multivariate analysis, the cTnI level on
admission was an independent predictor of the success of the primary
angioplasty after controlling for age, sex, risk factors for CAD, and
clinical features on admission, including time to
presentation, initial angiographic findings, and use of
adjunctive therapy during the procedure. The final model for prediction
of angioplasty success included elevated cTnI on admission (relative
risk [RR] 0.10, 95% CI 0.02 to 0.54), the LAD as the IRA (RR 0.18,
95% CI 0.04 to 0.73), and TIMI flow before angioplasty (RR 2.5, 95%
CI 1.1 to 5.7). This model had a global 2
value of 14, with P=0.0009.
Indices of Myocardial Damage
Despite the similar extent of ST-segment elevation on admission
ECG in the 2 groups of patients (number of leads with ST elevation
2.5±2.7 versus 3.2±2.3, P=0.11), Q-wave MI pattern
on predischarge ECG tended to be more common in patients with elevated
cTnI compared with patients with normal cTnI (47% versus 30%,
P=0.09). The predischarge LVEF was significantly lower in
patients with elevated admission cTnI (46±10% versus 51±11%,
P=0.04).
In-Hospital Clinical Course
Patients with elevated cTnI on admission had a significantly
higher incidence of CHF (22% versus 9%, P<0.05) and a
significantly higher incidence of the combined end point of CHF, shock,
and/or death (30% versus 9%, P=0.006). All 3 patients who
died during the initial hospital stay had elevated admission cTnI
(Table 3).
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Elevated cTnI on admission was an independent predictor of the combined
end point (RR 5.2, 95% CI 1.03 to 26.26) even after adjustments for
demographic and clinical characteristics (Table 1
), angiographic
findings (Table 2), and success of angioplasty. The other
independent predictors of the composite end point were Killip
class (RR 12.6, 95% CI 3.4 to 46.6) and angiographic success of
angioplasty (RR 0.12, 95% CI 0.02 to 0.62). When only the 94 patients
with successful angioplasty were analyzed, elevated cTnI on
admission was still associated with a greater incidence of CHF, shock,
and/or death during the hospital stay (22% versus 6%,
P=0.026). Failed angioplasty was associated with worse
overall prognosis, with 53% incidence of CHF, shock, and/or death. Six
of the 13 patients with failed angioplasty and elevated cTnI had an
adverse event, and 2 died. The 2 patients with failed angioplasty and
normal admission cTnI had adverse events, but none of them died.
Long-Term Follow-Up
During a mean follow-up of 426±50 days, patients with elevated
admission cTnI had a significantly higher incidence of cardiac
mortality and of cardiac events (Table 3, Figure 2). The Kaplan-Meier curves for
event-free survival in the 2 groups were statistically different
(Figure 3, P<0.04 by log-rank
statistics). The 2 curves diverged early and were separated further
over the first few months. Admission cTnI elevation remained a
significant predictor of the occurrence of cardiac events after
adjustment for differences in age, sex, risk factors for CAD,
angiographic extent of CAD, success of primary angioplasty, and time to
presentation in stepwise Cox regression analysis.
Only the cTnI level on admission (OR 3.57, 95% CI 0.99 to 13.0) and
age (OR 1.05 95% CI 1.0 to 1.09) were independent predictors of the
occurrence of cardiac events.
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cTnI Threshold
To determine the best discriminant level in predicting primary
angioplasty success and in-hospital course, we examined the OR and
2 values of different admission cTnI
discriminant levels (0.2, 0.4, 0.6, 1.0, 1.5, and 3.0 µg/mL). Any
elevation of cTnI on admission was associated with a lower success rate
for primary angioplasty and a more complicated in-hospital course.
However, a cutoff point of 0.4 µg/mL gained the highest
2 value (9.87) and OR (9.45) for primary
angioplasty success as well as for the occurrence of CHF, shock, and/or
death (2 7.9, OR 4.3).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study demonstrated that in patients with AMI who present with ST-segment elevation or LBBB, an elevated cTnI level at admission is associated with a lower success rate for primary angioplasty, a higher risk for in-hospital death, CHF, or shock, and higher long-term cardiac mortality and nonfatal reinfarction.
Admission cTn and Duration of Symptoms
In the present study, no correlation was found between the
duration of the pain and the cTnI levels on admission. In
multivariate analysis, the time to
presentation did not provide incremental prognostic
information over admission cTnI. These findings are in agreement with
the results of the troponin substudy of the Global Utilization of
Streptokinase and TPA for Occluded Arteries (GUSTO) IIa trial, in which
58% of the patients presented with ST
elevation.3 10 On the other hand, in a larger study of
patients with ST elevation, Ohman et al15 found a
significant correlation between symptom duration and the likelihood of
a positive qualitative cTnT test on admission. This difference may be
due to the larger patient population that was enrolled within 6 hours
of symptoms in the later study as well as the use of a different assay
for troponin. Furthermore, 30% of the patients in that study who had a
positive troponin test were admitted within the first 2 hours of
symptoms, and the relation between 30-day mortality and pain duration
was much stronger in those with negative cTnT on
admission.15 Hamm et al8 reported a shorter
duration of pain (3.1 hours, on average, compared with 5.4 hours after
the beginning of chest pain) in patients with negative compared with
positive cTn tests. However, in their study, only half of the patients
with elevated cTn levels had elevated levels at admission; the other
half had elevated levels at 4 hours after arrival. These findings
suggest that admission cTn levels correlate poorly with the duration of
symptoms. Symptoms are only a crude marker of the onset of
ischemia,15 and elevated cTn levels may reflect
more accurately the extent and duration of the myocardial
ischemia.
Success of Reperfusion Therapy
In a study by Stubbs et al,5 noninvasive signs of
reperfusion were noted after thrombolytic therapy in
50% of patients with elevated admission cTnT compared with 72% of
patients with normal admission cTnT. In the TIMI 10B study, admission
cTnI levels were significantly lower in the patients that achieved TIMI
3 flow in the 60-minute angiogram after thrombolytic
therapy,18 and in a study by Stewart et al,19
these levels were lower in patients that achieved TIMI 3 flow in the
90-minute angiogram.
The present study extends this observation to patients treated with primary angioplasty. Elevated cTnI levels were an independent predictor of the lower success rate of primary angioplasty. These results are particularly striking in light of the high utilization of platelet glycoprotein IIb/IIIa inhibitors and stents in patients with and without elevated cTnI. The lower rate of successful reperfusion in patients with elevated admission cTnI was primarily due to slow blood flow (TIMI flow <3) in the IRA in spite of successful dilatation of the culprit lesion. This angiographic finding is the hallmark of the "no-reflow" phenomenon20 21 22 23 24 and is associated with extensive microvascular damage within the jeopardized myocardium. As previously suggested,15 elevated cTnI on admission appears to be an independent marker of an early and extensive myocardial damage that is associated with extensive microvascular damage.25
Admission cTn Levels and Prognosis
Recent reports suggest that in patients with acute
coronary syndrome, the cTn level on admission is an independent
predictor of death or AMI.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 In a prospective
analysis of 855 patients with unstable angina or AMI who
presented within 12 hours of the onset of symptoms enrolled in
the GUSTO IIa study,3 elevated cTnT on admission was
associated with a 3-fold higher 30-day mortality. The predictive value
of elevated cTnT remained strong even after adjustment for ECG changes
and creatine kinase MB levels.3 Similar were the findings
from retrospective analysis of 2 large trials, TIMI
IIIB4 and the Fragmin During Instability in
Coronary Artery Disease (FRISC) study.6
Fewer data regarding the prognostic value of admission troponin levels in patients with ST-elevation AMI exist, and there are no data regarding the prognostic significance in patients treated with primary angioplasty. In the study by Stubbs et al,5 the differences in early mortality (11% versus 4%) were not statistically significant (P=0.11) in patients with elevated compared with normal admission cTnT levels, respectively. The differences, however, were significant at the 1- and 3-year follow-ups.5 In the GUSTO IIa trial,3 patients with ST-elevation AMI and elevated levels of cTnI on admission compared with patients with normal levels had higher rates of death in a 30-day follow-up (13% versus 4.7%). Recently, in the 12 666 patients treated with thrombolytic therapy in the GUSTO III trial, elevated cTnT on admission was shown to be independent predictor of a higher 30-day mortality.15
In the present study, the more extensive damage in patients with elevated cTnI at admission was reflected in the higher incidence of CHF, shock, in-hospital death, and a decreased predischarge LVEF. In the analysis of the GUSTO IIa study, the findings were similar; the incidence of shock was 7%, and CHF was 13% in patients with elevated cTnT on admission, but these values were only 1% and 6%, respectively, in patients with normal admission cTnI.3 Similarly, the GUSTO III patients with elevated cTnT had a higher incidence of CHF and of cardiogenic shock despite the administration of thrombolytic therapy.15
The follow-up in the present study demonstrated that elevated cTnI was also a strong independent predictor of higher long-term cardiac death and nonfatal reinfarction. The higher failure rate of the primary angioplasty in patients with elevated cTnI contributed to the worse early and late outcomes. However, cTnI elevation remained a significant predictor of the clinical outcomes even after controlling for the differences in the angioplasty results.
Discriminant cTnI Level
The predictive value of admission cTnI was strongest with the
discriminant level of cTnI, 0.4 ng/mL. In a previous
study,5 a discriminant level of 0.2 ng/mL cTnT was found
to have higher 2 values compared with a
borderline elevated cTnT level of 0.1 ng/mL. However, further increase
of the threshold beyond this level compromises the negative prognostic
value of the test for predicting reperfusion therapy success and
clinical outcome in patients with evolving AMI. These data suggest that
most of the information derived from early cTn levels can be obtained
by the use of bedside kits in patients with AMI, as recently
demonstrated with a kit for cTnT.15
Study Limitations
We recognized several limitations of the present study. The
relatively small number of patients included in the study mandates
caution in the interpretation of the results, especially because this
is the first study that addressed the prognostic value of troponin
levels in patients undergoing primary angioplasty. The present
study reports the experience of a single center in which primary
angioplasty is the principal reperfusion strategy. Therefore, the
results may not be reproduced in other settings. In the present
study, we used cTnI as determined by quantitative method. Our
conclusions should not be extended to cTnT or other methods of troponin
determination without further validation.
Conclusions
An elevated cTnI level (>0.4 ng/mL) in patients admitted with
chest pain and ST-segment elevation identifies a subgroup of patients
with lower success of primary angioplasty and worse short- and
long-term prognosis.
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Acknowledgments |
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Drs Matetzky and Sharir were supported by the Save-A-Heart Foundation, Los Angeles, Calif; Dr Noc, by the Slovenian Science Foundation and University Medical Center, Ljubljana, Slovenia.
Received March 6, 2000; revision received April 20, 2000; accepted May 8, 2000.
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