(Circulation. 2000;102:2038.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Risk Stratification in Patients With Inferior Acute Myocardial Infarction Treated by Percutaneous Coronary Interventions
The Role of Admission Troponin T
From the Medizinische Klinik II, Medizinische Universität zu Lübeck, Lübeck, Germany.
Correspondence to Professor Hugo A. Katus, Medizinische Klinik II, Medizinische Universität zu Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. E-mail Katus{at}medinf.mu-luebeck.de
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Abstract |
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Background—Cardiac troponin T (cTnT) elevations on admission indicate a high-risk subgroup of patients with ST-segment elevation acute myocardial infarction (AMI). This finding has been attributed to less effective reperfusion after thrombolytic therapy. The aim of this study was to determine the role of admission cTnT on the efficacy of percutaneous coronary interventions (PCIs) in inferior AMI.
Methods and Results—One hundred fifty-nine consecutive patients
with inferior ST-segment AMI were enrolled and followed up
for a mean of 448 days. Patients were stratified by cTnT on admission.
A cTnT 
0.1 µg/L was found in 58% of patients. These patients had
longer time intervals from onset of symptoms to therapy
(P<0.001) and higher 30-day (10.8% versus 1.5%,
P=0.027) and long-term (17.2% versus 4.5%,
P=0.023) cardiac mortalities. Rates of the combined end
point of death, nonfatal reinfarction, and need for repeated target
vessel revascularization procedures were not
different in cTnT groups (log rank, 0.69; P=0.41). PCI
was attempted in 93.3% of cTnT-positive and 98.5% cTnT-negative
patients (P=0.24) but was less frequently successful in
patients with cTnT 0.1 µg/L (77.9% versus 96.9%,
P<0.001). Coronary stenting reduced 30-day and
long-term cardiac mortality, particularly among cTnT-positive patients.
In a multivariate analysis, cTnT indicated an
5-fold-higher risk (adjusted OR, 4.6; 95% CI, 0.79 to 27.11;
P=0.089) and was a strong albeit not independent risk
predictor.
Conclusions—In inferior AMI, a positive admission cTnT is associated with lower success rates of direct PCI and higher rates of cardiac events over the short and long term. These patients benefit from coronary stenting.
Key Words: myocardial infarction • risk factors • troponin T
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The prognosis of inferior acute myocardial infarction (AMI) is generally considered to be better than that of anterior AMI.1 However, patients with inferior AMI represent a heterogeneous risk group that includes cardiogenic shock, older age, concomitant left precordial ST-segment depression, third-degree AV block, and right ventricular infarction.2 3 4 5
Cardiac troponins (cTnTs) have improved AMI detection and allow risk stratification in acute coronary syndromes.6 7 8 9 10 Recently, large-scaled clinical studies revealed an important prognostic role of the admission cTnT value in patients with ST-elevation AMI.10 11 12 In the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO)-IIa study, 30-day mortality was 13.0% among patients with ST-segment elevation and a positive admission cTnT compared with 4.7% among those with a negative test result.10 Concordantly, the GUSTO-III troponin T substudy, which enrolled 12 806 patients, and a single-center study of 240 patients found that positive admission cTnT values were associated with worse early and long-term prognosis.11 12 In the GUSTO substudy, excess mortality did not relate to the duration of symptoms and was independent of the thrombolytic agent used.11 Interestingly, the Fragmin During Instability in Coronary Artery Disease (FRISC) study group and others have attributed this excess mortality to lower rates of complete reperfusion (TIMI grade 3 flow) after thrombolysis in patients with a positive cTnT.13 14
The present study focused on the clinical significance of admission cTnT and its impact on efficacy of percutaneous coronary interventions (PCI) in a well-defined subset of patients with inferior AMI.
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Methods |
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Patients
Between May 1996 and February 1999, 159 consecutive patients with a confirmed diagnosis of inferior or true posterior AMI who were admitted within 24 hours of onset of symptoms were enrolled in this single-center study. Diagnosis of AMI was based on chest pain history, enzyme measurements, and ECG according to World Health Organization criteria.15 Only AMI with characteristic ascending limbs of creatine kinase (CK) and CK-MB activities as disclosed by serial measurements was defined as an acute event. Data on chest pain history just before the episode leading to admission were not collected. Standard 12-lead and right precordial ECGs were obtained immediately after admission. Inferior AMI was defined by the presence of ST-segment elevation of
0.1 mV in
2 of the leads II, III, and aVF. Diagnosis of true posterior AMI was
based on the presence of an R/S ratio of >1 in lead
V1 or V2 with R waves of
>40 ms. Right ventricular involvement was defined as
ST-segment elevation of >0.1 mV in lead V4R.
All patients were scheduled for immediate (within 30 minutes)
coronary angiography and direct PCI unless adequate
hemodynamic stabilization for transportation to the
catheterization laboratory could be achieved. Treatment
decisions were left to the discretion of the interventionalists who
were unaware of the cTnT result during the procedure. On admission, all
patients received a parenteral loading dose of 500 mg
acetylsalicylic acid and 5000 IU unfractionated
heparin. Other standard medications, including nitrates and
ß-adrenoreceptor blockers, were given at the
discretion of the physician on duty. Therapy with
glycoprotein (GP) IIb/IIIa antagonists was
based on the presence of large intraluminal filling defects on
coronary angiography or incomplete reperfusion, ie, less than
TIMI grade 3 flow after recanalization despite
coronary stenting. When coronary stenting was required,
patients received an oral loading of 500 mg ticlopidin followed by 250
mg twice daily for another 4 weeks. After removal of the
arterial sheath, patients received a subcutaneous dose of
low-molecular-weight heparin (7500 U dalteparin) daily for 48 hours.
An oral dose of 100 mg acetylsalicylic acid was
continued indefinitely.
The study protocol was approved by the local ethics committee of the University of Luebeck.
Clinical Data
Clinical variables were recorded on admission.
Occurrence of complete AV block, sustained ventricular
tachyarrhythmias, and cardiogenic shock and the need
for atropine or temporary pacing were registered prospectively.
Blood for measurement of cTnT was collected immediately on admission and was determined by either qualitative test (Trop T, Roche Diagnostics) or quantitative immunoassay (Elecsys Troponin T, Roche Diagnostics). A cutoff level of 0.1 µg/L was used to discriminate cTnT results. Total CK and CK-MB activities were measured with commercially available kits. The upper limit of normal CK was 80 IU/L for men and 70 IU/L for women.
Angiographic Data
Data were collected on the infarct-related artery, site of
infarction (proximal or distal to the origin of the first marginal
branch of the right coronary), extent of coronary
artery disease, left ventricular performance, TIMI
flow before and after coronary intervention, and rate of distal
thrombus dislocation during PCI. Coronary angiograms underwent
offline quantitative analysis (Medis Medical, QCA-CMS).
Procedural success was defined as residual stenosis of <50%
and TIMI grade 3 flow after PCI. Target vessel reintervention (TVR) was
defined as repeated PCI of the target vessel or CABG involving the
target vessel.
ECG Analysis
Patients with bundle-branch block, paced rhythm, or an
uninterpretable ECG were excluded. Quantitative measurements were made
in all 12 leads and lead V4R of the admission ECG
on a digitizer board (Sigma Scan, Summasketch). Anterior ST-segment
depression was defined as ST-segment depression of 0.5 mV in 2
precordial leads.
Follow-Up
Follow-up was 6 months. Data on vital status and follow-up
events, including cardiac and noncardiac death, nonfatal reinfarction,
and need for TVR (PTCA, CABG), were obtained from hospital records,
death certificates, and general practitioner questionnaire.
Statistical Analysis
Means and SDs were calculated for continuous variables, and
absolute and relative frequencies were measured for discrete
variables. Differences between groups were tested by the
2 test or Fisher’s exact test in the case of
discrete variables and by a 2-sample t test in the case
of continuous variables. Multiple logistic regression was used to
test the independent contribution of univariate risk
predictors. Cumulative hazard function plots were generated with the
Kaplan-Meier method. Differences were examined by the log-rank
statistical test. For subgroup analysis, patients were split
into cTnT-positive and cTnT-negative groups. The end points studied
were 30-day mortality, long-term all-cause mortality, long-term cardiac
mortality, and the combined end point of death, nonfatal reinfarction,
and TVR (PTCA, CABG). For all statistical evaluations, a 2-sided
P<0.05 was considered statistically significant. For all
statistical analyses, a commercially available statistical
package (SPSS system 8.0) was used.
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Results |
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Clinical Characteristics on Admission
Of the 159 patients included, 93 patients (58%) were cTnT-positive. Admission characteristics are displayed in Table 1
. Both groups compared favorably
with respect to most clinical, hemodynamic, and ECG
variables.
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CTnT-positive patients had significantly longer time intervals from symptom onset to therapy than cTnT-negative patients (7.26 versus 4.11 hours, P<0.001), developed higher peak levels of C-reactive protein (77.4 versus 42.8 mg/L, P<0.001), and tended to stay longer (56.6 versus 39.1 hours, P=0.082) in the intensive care unit.
Angiographic Characteristics and Procedural Success After
Direct PCI
CTnT groups were comparable for baseline angiographic
characteristics, as listed in Table 2. In
2 patients (1.3%), severe hemodynamic compromise
prohibited transportation to the catheterization
laboratory.
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Although the rates of patients who received early angiography (98.9% versus 98.5%, P=1.0) and attempted direct PCI (93.3% versus 98.5%, P=0.241) were comparable between cTnT-positive and cTnT-negative patients, significantly more patients with a positive cTnT on admission (22.1% versus 3.1%, P<0.001) had unsuccessful direct PCI.
In the entire group, the rate of coronary stenting was 55.3%; 22% received GP IIb/IIIa antagonists (abciximab). An intra-aortic balloon pump was inserted in 4.4% for cardiogenic shock. There was a tendency for more frequent use of abciximab (26.9% versus 15.1%, P=0.085) and more frequent embolization of thrombi (8.6% versus 1.5%, P=0.082) during angioplasty among cTnT-positive versus cTnT-negative patients.
ECG Analyses According to Admission cTnT
ECG recordings useful for quantitative analysis of
ST-segment deviations were available in 149 of the 159 patients.
Detailed results are displayed in Table 1
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Short-Term and Long-Term Outcome of Patients According to
Admission cTnT
cTnT-positive patients had higher in-hospital cardiac mortality
rates (10.8% versus 1.5%, P=0.027) and tended to have
higher rates of reinfarction (4 of 93 versus 0 of 66,
P=0.088). The rates of other major prehospital and
in-hospital complications, including ventricular
fibrillation, complete AV block, development of cardiogenic shock
during follow-up, and the need for catecholamines,
atropine, or temporary pacemaker therapy, were comparable in both
groups (Table 3).
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Long-term all-cause mortality (18.3% versus 6.1%, P=0.032)
and cardiac mortality (17.2% versus 4.5%, P=0.023) were
significantly higher in patients with elevated cTnT (Figure 1, top). In contrast, rates of the
combined end point were not different (Figure 1, bottom) because
of a high rate of CABG procedures in the cTnT-negative patients (Table 4).
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The final multivariate regression model testing the
contribution of univariate risk predictors is displayed in
Table 5. After adjustment, only
cardiogenic shock and older age remained independent predictors of
long-term prognosis, whereas cTnT was a strong albeit not independent
predictor indicating an 5-fold-higher mortality risk
(P=0.089).
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Impact of Coronary Stenting
The rate of coronary stenting was significantly lower
among cTnT-positive versus cTnT-negative patients (48.4% versus
65.2%, P=0.043). In the former, stenting reduced cardiac
mortality rates at 30 days (17.2% versus 2.2%, P=0.03).
This effect tended to persist until the end of follow-up (23.4% versus
8.9%, P=0.089; Figure 2, top). In contrast, survival rates in the cTnT-negative patients were
not affected by stenting (0% versus 4.3%, P=0.35, at 30
days; 2.3% versus 8.7%, P=0.28, at the end of
follow-up).
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Stenting also reduced the rates of the combined end point in both the
cTnT-positive (4.4% versus 36.2%, P<0.001, at 30 days;
6.9% versus 26.1%, P=0.055, at end of follow-up) and
cTnT-negative patients (11.1% versus 46.8%, P<0.0005, at
30 days; 16.3% versus 39.1%, P=0.08, at the end of
follow-up). The effect of stenting was driven by lower rates of TVR.
However, even for the combined end point, benefits of stenting tended
to be more prominent in the cTnT-positive patients (Figure 2, bottom).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients with inferior AMI are considered to have a better prognosis than anterior AMI patients, probably because of smaller infarct size,1 16 although pooled analysis reveals beneficial effects of thrombolytic therapy in inferior AMI. Although its value has been questioned in uncomplicated inferior AMI, the benefits of thrombolytic therapy are established in particular high-risk categories.1 17 Thus, risk assessment in inferior AMI is paramount for the appropriate selection of treatment modalities.
Recently, it was observed that an elevated admission cTnT is associated with a higher risk for cardiac events in patients with ST-segment elevation AMI.10 11 12 First, the GUSTO-IIa study group found that in-hospital event rates were higher in cTnT-positive than in cTnT-negative patients with ST-segment elevation AMI (13.0% versus 4.7%).10 Consistently, Stubbs et al12 reported higher mortality rates at 30 days (11% versus 4%) and at 3 years (28.2% versus 7.5%) in cTnT-positive patients. Those authors speculated that cTnT-positive patients were admitted significantly later after onset of symptoms than cTnT-negative and thus benefited less from thrombolytic treatment. In the GUSTO-III troponin substudy, 12 806 patients were studied prospectively for cardiac events according to their cTnT status on admission.11 Again, cTnT positivity was found to indicate a subgroup with a 3-fold-higher cardiac event rate than cTnT-negative patients. Two aspects were particularly interesting in this trial. First, with respect to cardiac mortality, the admission cTnT value discriminated between high- and low-risk subgroups in both anterior (18.7% versus 8.5%) and inferior (14.5% versus 3.9%) AMI. Second, the duration from onset of symptoms to admission did not correlate with mortality in cTnT-positive patients. Mortality rates for patients presenting between 0 and 2 hours, 2 and 4 hours, 4 and 6 hours, and beyond 6 hours were 14.5%, 15.0%, 17.1%, and 16.7%, respectively. These findings imply that duration of myocardial ischemia before recanalization therapy is not the main cause of excess mortality in cTnT-positive patients. Furthermore, excess mortality was comparable in the patients treated by recombinant tissue plasminogen activator (15.2% versus 6.2%, P=0.0001) or tissue plasminogen activator (16.4% versus 6.1%, P=0.0001). The authors argued that higher rates of reperfusion failures may have accounted for differences in mortality. The FRISC trialists14 and Ramanathan and coworkers14 reported lower rates of TIMI grade 3 flow after thrombolytic therapy in patients with a positive admission cTnT, providing indirect support for the hypothesis of the GUSTO-III investigators. A possible alternative explanation has recently been added by the FRISC trialists, who found that repeated episodes of chest pain shortly before the onset of AMI were more often present among cTnT-positive patients and were independent indicators of long-term mortality.13
In our study, a positive cTnT indicated a significantly higher 30-day (10.8% versus 1.5%, P=0.027) and long-term (17.2% versus 4.5%) cardiac mortality. Even after adjustment, a positive cTnT result was associated with a 5-fold-higher risk of subsequent cardiac death. cTnT was superior to ECG risk predictors, including right ventricular involvement, concomitant anterior ST-segment depressions, or complete AV block, and proved a strong albeit not independent predictor when corrected for older age and cardiogenic shock.
The reason for the observed hazard is unclear but may involve longer time intervals to reperfusion therapy, less effective reperfusion, and previous myocardial damage from repeated episodes of unstable angina before the definite onset of AMI. Although our data do not allow comment on the latter, we found that reperfusion therapy was less effective in cTnT-positive patients. Direct PCI was attempted in a comparable proportion of cTnT-positive and cTnT-negative patients. However, lower rates of successful reperfusion (77.9% versus 96.9%, P<0.001) were achieved in the cTnT-positive patients.
There is a strong interrelationship between appearance of cTnT in blood and elapsed time to admission. Although mean time intervals from onset of symptoms to reperfusion were significantly longer in cTnT-positive than in cTnT-negative patients (7.26±5.99 versus 4.11±2.73 hours, P=0.001), time intervals between nonsurvivors and survivors were comparable (5.99±5.17 versus 5.64±5.03 hours, P=0.562). In multivariate analysis, the prognostic role of cTnT did not change after correction for elapsed time risk (OR, 4.4; 95% CI, 0.74 to 25.7; P=0.10), nor did time intervals per se indicate an adverse prognosis (OR,1.03; 95% CI, 0.9 to 1.2; P=0.68).
Coronary stenting has been reported to improve coronary flow reserve and to reduce rates of death, nonfatal AMI, and TVR in ST-segment elevation AMI.18 Consistently, our study disclosed a risk reduction for the composite end point in both cTnT groups that was more prominent in cTnT-positive patients. With respect to cardiac mortality, risk reduction was almost exclusively confined to cTnT-positive patients. Thus, stenting reduced the cardiac mortality rates to the rates observed in cTnT-negative patients. Our findings comply with results observed in patients with refractory unstable angina and non–Q-wave AMI.19 In these trials, beneficial effects of GP IIb/IIIa receptor antagonists were nearly exclusively restricted to the cTnT-positive patients, whereas cTnT-negative patients did not benefit.
It is tempting to speculate that besides differences in the efficiency of restoring coronary blood flow in epicardial arteries, more severe microvascular damage and reduced microvascular reflow may have contributed to the excess mortality rates in cTnT-positive patients.20 21 In addition, larger thrombus burden or higher rates of rethrombosis may have contributed. Because of the small number of patients treated, the effects of GP IIb/IIIa receptor antagonists could not be explored in our study. Although there is some preliminary evidence for a therapeutic benefit of GP IIb/IIIa antagonists in patients treated with direct PCI or in conjunction with thrombolytics22 23 for ST-segment elevation AMI, future randomized trials are mandatory to test whether addition of GP IIb/IIIa antagonists or thrombolytic agents may result in further reduction in the cardiac event rate in cTnT-positive patients treated by stent placement.
Study Limitations
Several points must be stressed when our findings are
extrapolated. First, results in this study were obtained in patients
who underwent PCI and may not relate to patients treated by
thrombolytics. Second, although admission cTnT remained
a powerful predictor of adverse outcome after adjustment for longer
time intervals from onset of symptoms to therapy, it must be
acknowledged that the study may have been underpowered to fully exclude
a potential relationship between duration of ischemia and cTnT
admission status because of small sample size and low event rates.
Third, patients in this cohort study were not randomly allocated to
coronary stenting or treatment with GP IIb/IIIa
antagonists. Therefore, unforeseen bias cannot be ruled
out. In addition, although left ventricular ejection
fractions and peak CK-MB activities were comparable in both cTnT
groups, it cannot be excluded with certainty that cTnT-positive
patients may have experienced larger infarcts. Finally, the mechanism
by which a positive admission cTnT is linked to a higher cardiac event
rate remains speculative. To test for the hypothesis of a higher
microcirculatory resistance and poorer reflow in nonstented
cTnT-positive patients, further studies with velocity probe
measurements are warranted.
Conclusions
Inferior AMI patients with a negative cTnT have very
low cardiac event rates and high success rates of mechanical
recanalization. In these patients, additional stent
implantation does not translate into an improved overall survival rate
but reduces only the long-term composite event rate, which is largely
driven by TVR. In contrast, patients with a positive cTnT seem to
behave differently. These subjects have a higher failure rate of direct
PCI and remain a high-risk group even when PCI is deemed successful as
determined by visual assessment of TIMI flow. These patients benefit
from coronary stenting with respect to cardiac mortality and
rates of death, nonfatal AMI, and TVR. Our study using PCI in
inferior AMI in aggregate with previous studies leaves
little doubt that the cTnT admission value is a valuable risk indicator
in ST-segment elevation AMI and may aid in the selection of patients in
whom stenting may be beneficial.
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Footnotes |
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Dr Katus developed and patented the troponin T assay in cooperation with Roche Co, Germany.
Received May 4, 2000; revision received June 6, 2000; accepted June 6, 2000.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and morbidity results from all randomized trials of more than 1000 patients. Lancet. 1994;343:311–322.[Medline] [Order article via Infotrieve]
2.
Berger PB, Ryan TJ. Inferior
myocardial infarction: high-risk subgroups. Circulation. 1990;81:401–411.
3.
Zehender M, Kasper W, Kauder E, et al. Right
ventricular infarction as an independent predictor of
prognosis after acute inferior myocardial infarction.
N Engl J Med. 1993;328:981–988.
4. Peterson ED, Hathaway WR, Zabel M, et al. Prognostic significance of precordial ST segment depression during inferior myocardial infarction in the thrombolytic era: results in 16,521 patients. J Am Coll Cardiol. 1996;28:305–312.[Abstract]
5. Goldberg RJ, Zervallos JC, Yarzebski J, et al. Prognosis of acute myocardial infarction complicated by complete heart block (the Worcester Heart Attack Study). Am J Cardiol. 1992;69:1135–1141.[Medline] [Order article via Infotrieve]
6.
Katus HA, Remppis A, Neumann FJ, et al. The
diagnostic efficiency of troponin T measurements in acute
myocardial infarction. Circulation. 1991;83:902–912.
7. Hamm CW, Ravkilde J, Gerhardt W, et al. The prognostic value of serum troponin T in unstable angina. N Engl J Med. 1992;327:146–150.[Abstract]
8.
Antman E, Milenko M, Tanasijevic J, et al.
Cardiac-specific troponin I levels to predict the risk of mortality in
patients with acute coronary syndromes. N Engl
J Med. 1996;335:1342–1349.
9.
Lindahl B, Venge P, Wallentin L, for the FRISC Study
Group. Relation between troponin T and the risk of subsequent cardiac
events in unstable coronary artery disease.
Circulation. 1996;93:1651–1657.
10.
Ohman EM, Armstrong PW, Christenson RH, et al, for the
GUSTO IIa Investigators. Cardiac troponin T levels for risk
stratification in acute myocardial ischemia. N Engl
J Med. 1996;335:1333–1341.
11. Stubbs P. The cardiac troponins: uses in routine clinical practice: experiences from GUSTO and other clinical trials. Eur Heart J. 1998;19(suppl N):59–63.
12.
Stubbs P, Collinson P, Moseley D, et al. The prognostic
significance of admission troponin T concentrations in myocardial
infarction. Circulation. 1996;94:1291–1297.
13. Frostfeldt G, Lindahl B, Nygren A, et al. Possible reasons for the prognostic value of troponin T on admission in patients with ST-segment elevation myocardial infarction. Eur Heart J. 1999;20(suppl P):P-2110.
14. Ramanathan K, Stewart T. Admission Troponin T level may predict 90 minute TIMI flow after thrombolysis. Circulation. 1997;96(suppl I):I-270.
15.
Report on the Joint International Society and
Federation of Cardiology/World Health Organization Task
Force and Standardization of Clinical Nomenclature. Nomenclature and
criteria for diagnosis of ischemic heart disease.
Circulation. 1979;59:607–608.
16.
Lee KL, WoodliefLH, Topol EJ, et al. Predictors of
30-day mortality in the era of reperfusion for acute myocardial
infarction: results from an international trial of 41,021 patients.
Circulation. 1995;91:1659–1668.
17. Bates ER. Revisiting reperfusion therapy in inferior myocardial infarction. J Am Coll Cardiol. 1997; 30: 334–342.
18. Antoniucci D, Valenti R, Trapani M, et al. Current role of stenting in acute myocardial infarction. Am Heart J. 1999;138:147–152.
19.
Hamm CW, Heeschen C, Goldmann B, et al, for the CAPTURE
Study Investigators. Benefit of abciximab in patients with refractory
unstable angina in relation to serum troponin T levels. N
Engl J Med. 1999;340:1623–1629.
20.
Sakuma T, Hayashi Y, Sumii K, et al. Prediction of
short-and intermediate-term prognoses of patients with acute myocardial
infarction using myocardial contrast
echocardiography one day after
recanalization. J Am Coll Cardiol. 1998;32:890–897.
21.
Kondo M, Nakano A, Saito D, et al. Assessment of
microvascular no-reflow phenomenon using technetium-99m
macroaggregated albumin scintigraphy in patients
with acute myocardial infarction. J Am Coll Cardiol. 1998;32:898–903.
22.
Ohman EM, Kleiman NS, Gacioch G, et al. Combined
accelerated tissue-plasminogen activator and
platelet glycoprotein IIb/IIIa integrin receptor
blockade with integrelin in acute myocardial infarction: results of a
randomized, placebo-controlled, dose-ranging trial: IMPACT-AMI
Investigators. Circulation. 1997;95:846–854.
23.
Antman EM, Giugliano RP, Gibson CM, et al, for the TIMI
14 Investigators. Abciximab facilitates the rate and extent of
thrombolysis: results of the
thrombolysis in myocardial infarction (TIMI) 14 trial.
Circulation. 1999;99:2720–2732.
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 E. Bjorklund, B. Lindahl, P. Johanson, T. Jernberg, A.-M. Svensson, P. Venge, L. Wallentin, M. Dellborg, and the ASSENT-2 and ASSENT-PLUS study groups Admission Troponin T and measurement of ST-segment resolution at 60 min improve early risk stratification in ST-elevation myocardial infarction Eur. Heart J., January 2, 2004; 25(2): 113 - 120. [Abstract] [Full Text] [PDF]
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M. Panteghini Acute Coronary Syndrome: Biochemical Strategies in the Troponin Era Chest, October 1, 2002; 122(4): 1428 - 1435. [Abstract] [Full Text] [PDF]
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E. Giannitsis, M. Muller-Bardorff, S. Lehrke, U. Wiegand, R. Tolg, B. Weidtmann, F. Hartmann, G. Richardt, and H. A. Katus Admission Troponin T Level Predicts Clinical Outcomes, TIMI Flow, and Myocardial Tissue Perfusion After Primary Percutaneous Intervention for Acute ST-Segment Elevation Myocardial Infarction Circulation, August 7, 2001; 104(6): 630 - 635. [Abstract] [Full Text] [PDF]
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