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The New Definition of Myocardial Infarction
Diagnostic and Prognostic Implications in Patients With Acute Coronary Syndromes
Mark A. Meier, MD;
Wisam H. Al-Badr, MD;
Jeanna V. Cooper, MS;
Eva M. Kline-Rogers, MS;
Dean E. Smith, PhD;
Kim A. Eagle, MD;
Rajendra H. Mehta, MD, MS
Arch Intern Med. 2002;162:1585-1589.
ABSTRACT
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Background The clinical implications of the recently revised criteria for diagnosis
of acute myocardial infarction (AMI) in patients with suspected acute coronary
syndromes are unknown.
Methods To evaluate the prognostic implications of the new diagnostic criteria
for AMI, we studied 493 consecutive patients with suspected acute coronary
syndromes admitted to University of Michigan, Ann Arbor, between May 1, 1999,
and January 1, 2000. Patients with positive cardiac enzymes and symptoms suggestive
of coronary ischemia (n = 275) were divided into 2 groups: group A, with elevated
peak creatine kinase–MB fraction and/or new electrocardiographic changes
suggestive of AMI regardless of troponin status (diagnosed as AMI by old criteria),
and group B, with normal peak creatine kinase–MB fraction but elevated
troponin I level (additional patients diagnosed as having AMI by new criteria).
Results As compared with group A (n = 224), patients in group B (n = 51) were
older women, with increased comorbidities such as previous stroke or aortic
stenosis, and had fewer in-hospital procedures. In-hospital adverse events
(reinfarction, heart failure, shock, and mortality) were similar between the
groups, whereas 6-month mortality was higher among group B patients (16.3%
vs 5.8%; P = .03). This difference was not statistically
significant after adjustment for differences in baseline characteristics between
the groups (odds ratio, 1.6; 95% confidence interval, 0.5-5.9).
Conclusions The new criteria result in a substantial increase in the diagnosis of
AMI. Furthermore, they help to identify patients with acute coronary syndromes
who have greater comorbidities and worse 6-month outcomes who are otherwise
missed by the old criteria. Additional studies are needed to confirm these
preliminary findings and to determine the financial implications of the new
criteria.
INTRODUCTION
ACUTE MYOCARDIAL infarction (AMI) is a clinical and pathological entity
that has been independently defined in the past by various organizations by
means of a combination of clinical, laboratory, and electrocardiographic (ECG)
criteria.1-5
Until recently, diagnosis of AMI was based on the revised World Health Organization
(WHO) criteria that require 2 of the following 3 conditions for diagnosis:
ischemic symptoms, ECG changes consistent with ischemia, and elevated enzyme
levels, usually creatine kinase–MB (CK-MB).6
Although the use of troponins to diagnose AMI has been previously proposed,7-10 in September
2000, a joint committee of the European Society of Cardiology and the American
College of Cardiology (ESC/ACC) published a new definition of AMI that for
the first time officially included troponins.11
According to these criteria, elevated levels of enzymes (including CK-MB or
troponin I or T) with either symptoms or ECG changes suggestive of ischemia
constitute an AMI. The inclusion of troponins was based on a large body of
evidence showing that an elevated troponin level correlates with pathologically
proved myocardial necrosis12 and carries poor
prognosis in patients with suspected acute coronary syndromes.13-21
The clinical implications of applying the new criteria with troponins
in terms of their diagnostic and prognostic impact in patients with suspected
acute coronary syndromes have not yet been defined. The objectives of this
study were to address the following issues: (1) Does the new definition influence
the number of patients diagnosed as having AMI in those with suspected acute
coronary syndromes? (2) Is there a difference in the in-hospital and 6-month
clinical outcomes between patients diagnosed as having AMI by the WHO criteria
vs those diagnosed only by the new criteria? We hypothesized that more AMI
would be detected by means of the new definition and, further, that the prognosis
of patients with AMI diagnosed with the 2 criteria may be significantly different.
PATIENTS AND METHODS
PATIENT POPULATION
For this study, we included all patients admitted to the University
of Michigan Medical Center, Ann Arbor, between May 1, 1999, and January 1,
2000, with suspected acute coronary syndromes. To be admitted, these patients
were at least at intermediate to high risk for their symptoms to represent
a coronary event by the criteria established per the ACC–American Heart
Association guidelines.22 The project was approved
by the institutional review board at our institution. Four hundred ninety-three
consecutive symptomatic patients met the inclusion criteria within the study
period, although 1 patient with insufficient laboratory data was excluded
from analysis. Twenty-one patients were readmitted within the study period,
and only their index admission was included in our analysis. Thus, 471 patients
were available for the final data analysis.
Patients with elevated cardiac enzyme levels (peak values rather than
initial values were used) were stratified into 2 groups. Group A consisted
of patients who would have been diagnosed as having AMI by the old (WHO) criteria.
These patients had an elevated peak CK-MB level and/or new ECG changes or
symptoms suggestive of AMI regardless of troponin (I or T) status. Although
patients with chest pain and ECG evidence of new ST-segment elevation or left
bundle-branch block in the absence of an elevated CK-MB level would additionally
have met the requirement for AMI by the WHO criteria, we did not have any
patients in this subgroup. Hence, all patients diagnosed as having an AMI
by the WHO criteria had an elevation of CK-MB level (regardless of cardiac
troponins). Group B contained symptomatic patients with a negative CK-MB finding
but an elevated troponin I level, and without ECG evidence of new ST-segment
elevation or left bundle-branch block. Thus, group B consisted of patients
who would have been diagnosed as having an AMI by the ESC/ACC, but not by
WHO criteria. Patients with enzyme elevations noted only after percutaneous
coronary intervention (9 patients with elevated CK-MB level and 9 patients
with normal CK-MB level but elevated troponin I level) were excluded from
further analysis.
DATA COLLECTION
Although patients with acute coronary syndromes were prospectively identified,
assistants with no knowledge of the present study collected data on patient
demographics, medical history and comorbid conditions, admission signs and
symptoms (including ECG interpretations), in-hospital management and events,
and mortality by means of retrospective chart reviews and computerized records.
A standard data collection form and standard definitions were used. Similar
information collection techniques in addition to telephone calls were used
to conduct a 6-month follow-up with respect to death status and further hospitalizations
for suspected acute coronary syndromes, heart failure, and arrhythmia. Verbal
consent was obtained at each follow-up telephone call. All primary data were
entered into a spreadsheet manually by individuals unaware of the study design
or preliminary results.
LABORATORY DATA
The CK-MB and troponin I analyses were performed with a microparticle
enzyme immunoassay (Abbott AxSym System; Abbott Diagnostics Division, Abbott
Park, Ill). As determined by our laboratory, the CK-MB assay was performed
for all creatine kinase values greater than 100 IU/L and was considered positive
for values greater than 6 IU/L or 2.5% of total creatine kinase. The CK-MB
level was assumed to be normal for creatine kinase values less than 100 IU/L.
Troponin I level was considered to be elevated and consistent with an AMI
at levels greater than 2.0 x 10-6 mg/mL according to
the standards set forth by our laboratory.
DATA ANALYSIS
Summary statistics were presented as frequencies and percentages or
as mean ± SD unless stated otherwise. The 2 groups were compared by
means of a  2 test or Fisher exact test, when appropriate,
for categorical variables and a 2-sample 2-tailed t
test for continuous variables. P values less than
.05 were considered indicative of a significant difference between the 2 groups.
Multivariable logistic regression analysis was performed with variables suggestive
of marginal significance on univariate analysis (P<.20)
to assess independent predictors of in-hospital and 6-month mortality. All
statistical analyses were performed with SAS 8.1 for Windows (SAS Institute
Inc, Cary, NC).
RESULTS
A total of 224 patients had an elevated CK-MB level with or without
troponin elevation (group A), while 51 patients were found to have a negative
CK-MB finding but an elevated troponin I level (group B). Patients in group
B tended to be older (67.5 vs 63.8 years; P = .05)
and less often male (Table 1).
In addition, they were significantly more likely to have a history of stroke
or transient ischemic attack (19.6% vs 9.0%; P =
.03) and aortic stenosis (7.8% vs 0.9%; P = .01).
Other comorbidities were not significantly different between the 2 groups.
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Table 1. Patient Demographics, Cardiac Risk Factors, and Comorbid Conditions*
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There was a nonsignificant trend for group B patients to present with
atypical symptoms and to have a higher heart rate and blood pressure on admission
(Table 2). The degree of heart
failure was similar among the 2 groups.
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Table 2. Clinical Signs and Symptoms on Admission*
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Procedures were used less frequently in group B than group A (intra-aortic
balloon pump [0.0% vs 10.3%; P = .01], pulmonary
artery catheter [3.9% vs 17.4%; P = .01], and percutaneous
coronary interventions [17.7% vs 54.5%, P<.001])
(Table 3). Patients in group B
also had fewer coronary artery bypass operations during their hospital course,
although this did not reach statistical significance.
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Table 3. Management in Hospital and at Discharge*
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Patients in group B were less likely to have received unfractionated
or low-molecular-weight heparin (74.5% vs 88.4%; P
= .001) and glycoprotein IIb/IIIa receptor antagonists (21.6% vs 43.1%; P = .005). The use of aspirin or  -blockers in the
early phase (within 24 hours of admission) did not differ between the 2 groups.
At discharge, patients in group B more often received -blockers,
but use of ticlopidine hydrochloride or clopidogrel bisulfate, angiotensin-converting
enzyme inhibitors, and aspirin did not differ between the 2 groups.
In-hospital events did not differ significantly between groups A and
B (Table 4). However, every outcome
measured tended to occur less frequently in group B, and the length of stay
was shorter for patients in group B (5.3 vs 6.8 days; P = .04). No patients were entirely lost to follow-up, although rehospitalization
status was unavailable for 2 patients in group A. At 6 months after discharge,
12 patients in group A and 8 patients in group B had died (5.8% vs 16.3%; P = .03; odds ratio, 3.2; 95% confidence interval, 6-8.3; P = .02) (Figure 1).
This difference remained significant after adjustment for age and sex (odds
ratio, 3.1; 95% confidence interval, 1.7-8.2; P =
.02). However, after adjustment for age, sex, and baseline differences in
patient characteristics, the 6-month mortality was not significantly different
between the groups (odds ratio, 1.6; 95% confidence interval, 0.5-5.9; P = .45). Similarly, there was no difference in the composite
end point of death plus rehospitalization for heart disease at 6-month follow-up.
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Table 4. In-Hospital and 6-Month Outcomes
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Clinical events at 6-month follow-up (death, readmission for cardiac
reasons, and combined end point of death and readmission).
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COMMENT
Our study demonstrates that, when compared with the old definition established
by the WHO for AMI diagnosis, the new criteria proposed by the joint committee
of the ESC/ACC detects more patients with AMI among those admitted with suspected
acute coronary syndromes. In fact, the additional 51 patients detected as
having AMI only by the new definition would have been missed by the WHO criteria.
Not only did the use of the new definition allow more AMI to be diagnosed,
but also it did not miss the diagnosis of AMI in a single patient who was
diagnosed as having AMI by the WHO criteria.
It is interesting that the in-hospital events and mortality of patients
in group B were similar to those in group A. However, the mortality at 6 months
was higher for group B. This was due to the dissimilarities in baseline characteristics
of the patients, since the adjusted odds ratio of death in the 2 groups was
not significant when adjusted for the differences in these baseline charateristics.
In other words, our data suggest that the new criteria identify patients with
AMI who are likely to be missed by the previous diagnostic criteria or, at
best, labeled as having unstable angina, and who have more comorbid conditions
leading to a higher 6-month mortality as a result of their greater comorbidities.
Our findings are consistent with those from the Global Use of Strategies to
Open Occluded Coronary Arteries (GUSTO) IIa trial, which demonstrated higher
30-day all-cause mortality for patients with a normal CK-MB level and elevated
troponin T level than for patients with an elevated CK-MB level.16
Our study has important clinical implications in patients with symptoms
suggestive of acute coronary syndromes. First, a substantial proportion of
patients with suspected acute coronary syndrome (10.8%) in our study were
classified as having AMI, and not classified as having unstable angina or
being missed completely, as a result of the new criteria. Furthermore, these
additional patients diagnosed as having AMI by the new definition had more
comorbid conditions and as a result were at greater risk of adverse events.
Missed diagnosis of such a high-risk cohort has been shown to be associated
with worse outcomes.23-24 Second,
the new criteria, by facilitating the identification of patients who are at
increased risk of adverse outcomes, will allow physicians to tailor specific
treatment strategies that may help decrease mortality in this high-risk subset.
This may include the use of glycoprotein IIb/IIIa receptor antagonists, low-molecular-weight
heparin, clopidogrel, and/or an invasive strategy. Many studies have confirmed
the benefits of glycoprotein IIb/IIIa receptor antagonists25-27
and low-molecular-weight heparin28-29
in improving outcomes in patients with acute coronary syndromes who have elevated
troponin levels. Similarly, an aggressive early invasive strategy has been
shown to be particularly useful, especially in combination with the above
agents, for improving outcomes in the subset of patients with acute coronary
syndromes who have evidence of myocardial necrosis.25, 30-31
In our study, patients in group B received fewer invasive procedures (including
revascularization) and were treated less frequently with heparin and glycoprotein
IIb/IIIa antagonists. This may be because physicians considered group B patients
to have unstable angina rather than AMI without ST-segment elevation (hence
"less sick"), or this may have occurred as a result of increased comorbidities
in these patients. On the basis of current evidence, it is likely that the
use of a more aggressive approach in our patients in combination with newer
antiplatelet agents or low-molecular-weight heparin would have resulted in
better outcomes.
Finally, because the new criteria would lead to an increase in the number
of patients diagnosed as having AMI in those presenting with symptoms suggestive
of acute coronary syndromes, this would have significant financial implications
from the provider perspective. In the era of diagnosis-related group–based
payment, hospitals are reimbursed more for an AMI than for a diagnosis of
unstable angina. As the patients diagnosed as having AMI by the new criteria
would have been labeled as having unstable angina in the past by the WHO criteria,
the same patient would generate more revenue (appropriately) for health care
institutions now than before the new criteria were published. This, however,
needs to be confirmed in future studies.
One limitation of our study is that we included patients who were admitted
to the hospital for acute coronary syndromes. Therefore, these patients had
at least an intermediate, but more likely a high, probability of their symptoms
being related to a coronary event. As such, our study findings may not be
extrapolated to all patients presenting with suspected acute coronary syndromes,
particularly those with a low probability of coronary events. Furthermore,
our study enrolled a relatively small number of patients. Thus, our study
findings need to be confirmed in future large investigations in different
risk groups. Finally, elevated cardiac markers of necrosis are only one of
the many components in the risk stratification of acute coronary syndromes.
The most optimal risk stratification strategy involves the collective use
of patients' clinical presentation, physical examination, laboratory and ECG
data, and noninvasive and/or invasive tests findings. Our study did not evaluate
this strategy.
We conclude that, unlike the WHO definition, the use of the new ESC/ACC
criteria enhances identification of a high-risk subset of patients with AMI.
Identification of high-risk patients with AMI allows physicians to target
more aggressive treatments in this cohort that have the potential of improving
their outcomes. Further studies are needed to confirm our findings, to understand
the mechanisms of the difference in patient risk between the 2 groups, and
to evaluate the health care cost implications of the new criteria for AMI.
AUTHOR INFORMATION
Accepted for publication November 29, 2001.
This study was presented in part at the American College of Cardiology
Scientific Sessions, Orlando, Fla, March 18, 2001.
Corresponding author and reprints: Rajendra H. Mehta, MD, MS, Department
of Internal Medicine, University of Michigan, 2215 Fuller Rd, 7E, 111A, Ann
Arbor, MI 48105 (e-mail: rmehta{at}umich.edu).
From the Division of Cardiology, Department of Internal Medicine, University
of Michigan, Ann Arbor.
REFERENCES
| |
1. Kannel WB, Gordon T. The Framingham Study: An Epidemiological Investigation
of Cardiovascular Disease. Section 8: Two-Year Incidence by Exam Interval
by Age and Sex at Exam 1. Washington, DC: US Government Printing Office; 1968.
2. Hypertension and coronary artery disease: classification and criteria
for epidemiological studies. World Health Organ Tech Rep Ser. 1959;168.
3. Arterial hypertension and ischemic heart disease. World Health Organ Tech Rep Ser. 1962:231:17-18.
4. Gillum RF, Fortmann SP, Prineas RJ, Kottke TE. International diagnostic criteria for acute myocardial infarction and
acute stroke. Am Heart J. 1984;108:150-158.
FULL TEXT
|
ISI
| PUBMED
5. WHO-MONICA Project MONICA Manual. Geneva, Switzerland: World Health Organization; 1999.
6. Nomenclature and criteria for diagnosis of ischemic heart disease:
report of the Joint International Society and Federation of Cardiology/World
Health Organization Task Force on Standardization of Clinical Nomenclature. Circulation. 1979;59:607-609.
FREE FULL TEXT
7. Falahati A, Sharkey SW, Christensen D, et al. Implementation of serum cardiac troponin I as marker for detection
of acute myocardial infarction. Am Heart J. 1999;137:332-337.
FULL TEXT
|
ISI
| PUBMED
8. Char DM, Israel E, Ladenson J. Early laboratory indicators of acute myocardial infarction. Emerg Med Clin North Am. 1998;16:519-539.
FULL TEXT
|
ISI
| PUBMED
9. Adams III JE, Sicard GA, Allen BT, et al. Diagnosis of perioperative myocardial infarction with measurement of
cardiac troponin I. N Engl J Med. 1994;330:670-674.
FREE FULL TEXT
10. Wu AHB, Apple F, Gibler B, Jesse R, Warshaw M, Valdes R. National Academy of Clinical Biochemistry standard of laboratory practice:
recommendations for the use of cardiac markers in coronary artery disease. Clin Biochem. 1999;415:1104-1121.
11. The Joint European Society of Cardiology/American College of Cardiology
Committee. Myocardial infarction redefined—a consensus document of the Joint
European Society of Cardiology/American College of Cardiology Committee for
the redefinition of myocardial infarction. Eur Heart J. 2000;21:1502-1513.
FREE FULL TEXT
12. Antman EM, Grudzien C, Mitchell RN, Sacks DB. Detection of unsuspected myocardial necrosis by rapid bedside assay
for cardiac troponin T. Am Heart J. 1997;133:596-598.
FULL TEXT
|
ISI
| PUBMED
13. Galvani M, Ottani F, Ferrini D, et al. Prognostic influence of elevated values of cardiac troponin I in patients
with unstable angina. Circulation. 1997;95:2053-2059.
FREE FULL TEXT
14. Newby KL, Christenson RH, Ohman EM, et al. Value of serial troponin T measures for early and late risk stratification
in patients with acute coronary syndromes. Circulation. 1998;98:1853-1859.
FREE FULL TEXT
15. Lindahl B, Venge P, Wallentin L. Relation between troponin T and the risk of subsequent cardiac events
in unstable coronary artery disease. Circulation. 1996;93:1651-1657.
FREE FULL TEXT
16. Ohman EM, Armstrong PW, Christenson RH, et al. Cardiac troponin T levels for risk stratification in acute myocardial
ischemia. N Engl J Med. 1996;335:1333-1341.
FREE FULL TEXT
17. Antman EM, Tanasijevic MJ, Thompson B, 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.
FREE FULL TEXT
18. 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
19. Stubbs P, Collinson P, Moseley D, Greenwood T, Noble M. Prospective study of the role of cardiac troponin T in patients admitted
with unstable angina. BMJ. 1996;313:262-264.
FREE FULL TEXT
20. Fuchs S, Kornowski R, Mehran R, et al. Cardiac troponin I levels and clinical outcomes in patients with acute
coronary syndromes. J Am Coll Cardiol. 1999;34:1704-1710.
FREE FULL TEXT
21. Green GB, Beaudreau RW, Chan DW, DeLong D, Kelley CA, Kelen GD. Use of troponin T and creatine kinase-MB subunit levels for risk stratification
of emergency department patients with possible myocardial ischemia. Ann Emerg Med. 1998;31:19-29.
FULL TEXT
|
ISI
| PUBMED
22. Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA guidelines for the management of patients with unstable angina
and non–ST-segment elevation myocardial infarction: a report of the
American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol. 2000;36:970-1062.
FREE FULL TEXT
23. Mehta RH, Eagle KA. Missed diagnoses of acute coronary syndromes in the emergency room:
continuing challenges. N Engl J Med. 2000;342:1207-1210.
FREE FULL TEXT
24. Pope JH, Aufderheide TP, Rutbazer R, et al. Missed diagnoses of acute myocardial ischemia in the emergency department. N Engl J Med. 2000;342:1163-1170.
FREE FULL TEXT
25. The PURSUIT Trial Investigators. Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients
with acute coronary syndromes. N Engl J Med. 1998;339:436-443.
FREE FULL TEXT
26. PRISM Study Investigators. A comparison of aspirin plus tirofiban with aspirin plus heparin for
unstable angina. N Engl J Med. 1998;338:1498-1505.
FREE FULL TEXT
27. The CAPTURE Investigators. Randomised placebo-controlled trial of abciximab before and during
coronary intervention in refractory unstable angina: the CAPTURE study. Lancet. 1997;349:1429-1435.
FULL TEXT
|
ISI
| PUBMED
28. Cohen M, Demers C, Gurfinkel EP, et al for the Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-Wave
Coronary Events Study Group. A comparison of low-molecular-weight heparin with unfractionated heparin
for unstable coronary artery disease. N Engl J Med. 1997;337:447-452.
FREE FULL TEXT
29. Antman EM, McCabe CH, Gurfinkel EP, et al. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non–Q-wave
myocardial infarction: results of the Thrombolysis in Myocardial Infarction
(TIMI) IIB Trial. Circulation. 1999;100:1593-1601.
FREE FULL TEXT
30. Wallentin L, Lagerquist B, Husted S, Kontny F, Stahle E, Swahn E for the FRISC II Investigators (Fast Revascularization During Instability
in Coronary Artery Disease). Outcome at 1 year after an invasive compared with a non-invasive strategy
in unstable coronary artery disease: the FRISC II Invasive Randomised Trial. Lancet. 2000;356:9-16.
FULL TEXT
|
ISI
| PUBMED
31. Boersma E, Akkerhuis KM, Theroux P, Califf RM, Topol EJ, Simoons ML. Platelet glycoprotein IIb/IIIa receptor inhibition in non-ST-elevation
acute coronary syndromes: early benefit during medical treatment only, with
additional protection during percutaneous coronary intervention. Circulation. 1999;100:2045-2048.
FREE FULL TEXT
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