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Criteria for the diagnosis of acute m ocardial infarction

Official reprint from UpToDate www.uptodate.com

2012 UpToDate

Criteria for the diagnosis of acute m ocardial infarction

Authors
Guy S Reeder, MD
Harold L Kennedy, MD, MPH

Section Editors
Christopher P Cannon, MD
James Hoekstra, MD
Allan S Jaffe, MD

Deput Editor
Gordon M Saperia, MD, FACC

Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: ene 2012. | This topic last updated: jun 14, 2011.
INTRODUCTION Myocardial infarction (MI) is defined as a clinical (or pathologic) event caused
by myocardial ischemia in which there is evidence of myocardial injury or necrosis [1,2]. Criteria are
met when there is a rise and/or fall of cardiac biomarkers, along with supportive evidence in the
form of typical symptoms, suggestive electrocardiographic changes, or imaging evidence of new
loss of viable myocardium or new regional wall motion abnormality.
Initial care of the patient with suspected acute myocardial infarction (MI) should include the early
and simultaneous achievement of four goals:
Confirmation of the diagnosis by electrocardiogram (ECG) and biomarker measurement
Relief of ischemic pain
Assessment of the hemodynamic state and correction of abnormalities that may be present
Initiation of antithrombotic and reperfusion therapy if indicated
The management of patients with an ST segment elevation (Q wave) MI or non-ST segment
elevation acute coronary syndrome (ACS) is discussed elsewhere. (See "Overview of the acute
management of acute ST elevation myocardial infarction" and "Overview of the acute management
of unstable angina and acute non-ST elevation myocardial infarction".)
A related issue is the evaluation of a patient who presents with chest pain suggestive of an ACS in
whom the initial evaluation (ECG, cardiac enzymes) is not diagnostic. This issue is discussed
separately. (See "Initial evaluation and management of suspected acute coronary syndrome in the
emergency department", section on 'Observation'.)
DEFINITIONS
Acute coronar s ndrome The term acute coronary syndrome (ACS) is applied to patients in
whom there is a suspicion of myocardial ischemia. There are three types of ACS: ST elevation
(formerly Q-wave) MI (STEMI), non-ST elevation (formerly non-Q wave) MI (NSTEMI), and unstable
angina (UA). The first two are characterized by a typical rise and/or fall in biomarkers of myocyte
injury [3].
Two multicenter, international surveys published in 2002 - the Euro Heart Survey and the GRACE
registry - determined the relative frequency of these disorders in approximately 22,000 patients
admitted with an ACS [4,5]. STEMI occurred in 30 to 33 percent, NSTEMI in 25 percent, and UA in
38 to 42 percent.
Acute MI For many years, the diagnosis of acute MI relied on the revised criteria established
by the World Health Organization (WHO) in 1979 [6]. These criteria were epidemiological and aimed
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at specificity. A joint European Society of Cardiology (ESC) and American College of Cardiology
(ACC) committee proposed a more clinically based definition of an acute, evolving, or recent MI in
2000 [1]. In 2007 the Joint Task Force of the European Society of Cardiology, American College of
Cardiology Foundation, the American Heart Association, and the World Health Federation
(ESC/ACCF/AHA/WHF) refined the 2000 criteria and defined acute MI as a clinical event consequent
to the death of cardiac myocytes (myocardial necrosis) that is caused by ischemia (as opposed to
other etiologies such as myocarditis or trauma) [2].
The criteria used to define MI differ somewhat depending upon the particular clinical circumstance
of the patient: those suspected of acute MI based upon their presentation, those undergoing either
coronary artery bypass graft surgery or percutaneous intervention, or those who have sustained
sudden unexpected, cardiac arrest with or without death [2]. (See 'After revascularization' below.)
For patients who have undergone recent revascularization or who have sustained cardiac arrest or
death, the criteria for the diagnosis of MI are given in detail in the table (table 1).
For all other patients in whom there is a suspicion of MI, a typical rise and/or gradual fall (troponin)
or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis, with at least one
of the following is required:
Ischemic symptoms
Development of pathologic Q waves on the ECG
ECG changes indicative of ischemia (ST segment elevation or depression)
Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality.
In addition, pathologic findings (generally at autopsy) of an acute MI are accepted criteria.
The joint task force further refined the definition of MI by developing a clinical classification
according to the assumed proximate cause of the myocardial ischemia:
Type 1: MI consequent to a pathologic process in the wall of the coronary artery (e.g. plaque
erosion/rupture, fissuring, or dissection)
Type 2: MI consequent to increased oxygen demand or decreased supply (e.g. coronary
artery spasm, coronary artery embolus, anemia, arrhythmias, hypertension or hypotension)
Type 3: Sudden unexpected cardiac death before blood samples for biomarkers could be
drawn or before their appearance in the blood
Type 4a: MI associated with percutaneous coronary intervention
Type 4b: MI associated with stent thrombosis
Type 5: MI associated with coronary artery bypass graft surgery
Unstable angina Unstable angina (UA) is considered to be present in patients with ischemic
symptoms suggestive of an ACS without elevation in biomarkers with or without ECG changes
indicative of ischemia. Due to the insensitivity of CK-MB compared to troponin, one must be
circumspect if that is the only biomarker available. Elevations of troponin with contemporary assays
probably take two to three hours, while elevations for CK-MB take longer. (See 'Cardiac
biomarkers' below.)
UA and NSTEMI are frequently indistinguishable at initial evaluation. ST segment and/or T wave
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changes are often persistent in NSTEMI while, if they occur in UA, they are usually transient.
Regardless, of the category, ST segment change defines a higher-risk group [7].
After revasculari ation Following revascularization with either coronary artery bypass graft
surgery (CABG) or percutaneous coronary intervention (PCI) cardiac biomarkers may rise. Transient
elevations in troponins may represent necrosis, although the mechanism is unknown. Higher
elevations are associated with worse prognosis after CABG. A discussion of MI following PCI is found
elsewhere. (See "Periprocedural myocardial infarction following percutaneous coronary
intervention".)
The Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction addressed
the issue of biomarker rise after revascularization procedures [2]. They state that for patients
undergoing PCI who have normal baseline troponin value (99th percentile URL) is mandatory in order
to use the definition below. If the baseline value is elevated or rising, it is impossible to tell if
elevations postprocedure are related to the initial insult or to additional injury. However, they also
state that if the troponin values are stable or falling before revascularization, the use of the
reinfarction criteria may be reasonable. We also believe it is reasonable to obtain a troponin prior
and proximate (within six hours at the outside) to PCI (baseline value). (See 'Recommended
approach' below.)
No criteria have been established to separate expected rises (such as needle trauma to the
myocardium at CABG) from those that represent a complication of the procedure (such as
unexpected coronary artery dissection due to wire trauma at PCI) [8]. In addition, the cut points
given below are controversial.
The definition of (periprocedural) myocardial infarction after revascularization requires a normal
baseline troponin (99th percentile URL) and is as follows below [2]:
Type 4a (associated with PCI): Increases of biomarkers greater than three times the 99th
percentile URL.
Type 4b: Increases of biomarkers associated with stent thrombosis as documented by
angiography or at autopsy.
Type 5 (associated with CABG): Increases of biomarkers greater than five times the
99th percentile URL plus either new pathological Q waves or new LBBB, or angiographically
documented new graft or native coronary artery occlusion, or imaging evidence of new loss of
viable myocardium.
Prior MI
Any one of the following three criteria satisfies the diagnosis for a prior (established) MI (table
1) [2]:
Development of pathologic Q waves (0.04 sec) on serial ECGs. The patient may or may not
remember previous symptoms. Biochemical markers of myocardial necrosis may have
normalized, depending upon the length of time that has passed since the MI occurred.
Pathologic findings of a healed or healing MI.
Evidence from an imaging study of a region of loss of viable myocardium that is thinned and
fails to contract, in the absence of a nonischemic cause. (See "Role of echocardiography in
acute myocardial infarction", section on 'Diagnosis of MI'.)

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INITIAL EVALUATION For a patient presenting with a suspected acute MI, the characteristics
of the chest pain and the ECG findings permit initial risk stratification. An ECG and an abbreviated
history and physical examination should be obtained within 10 minutes of patient arrival [9]. Other
steps in the immediate management of patients suspected of an acute MI are discussed separately
(see "Initial evaluation and management of suspected acute coronary syndrome in the emergency
department", section on 'Immediate ED interventions').
The history should be targeted toward pain duration, character, similarity to possible previous
episodes, provoking factors, and past history of coronary disease risk factors. The physical
examination (including auscultation of the heart and lungs, measurement of blood pressure in both
arms, and assessment for heart failure or circulatory compromise, which are associated with a high
early mortality).
Patients with a strong clinical history and ST segment elevation or new left bundle branch block
should be assumed to have an acute MI and undergo immediate reperfusion therapy. (See
"Selecting a reperfusion strategy for acute ST elevation myocardial infarction".)
"Ruling in" an acute MI with newer troponin assays occurs in 80 percent of patients by two to three
hours after presentation; "ruling out" may take longer (up to six hours) (see 'Cardiac
biomarkers' below).
CHEST PAIN While chest pain is not required for the diagnosis of MI, its presence, particularly if
characteristic for myocardial ischemia, may influence decision making about the likelihood of the
presence of MI (table 2). A discussion of the characteristic of ischemic chest pain is found
elsewhere. (See "Diagnostic approach to chest pain in adults", section on 'Description of chest
pain'.)
Present Among patients with chest pain characteristic of myocardial ischemia (angina pectoris),
there are three primary presentations that suggest a change in the anginal pattern as ACS as
opposed to stable or exertional angina [3]:
Rest angina, which is usually more than 20 minutes in duration
New onset angina that markedly limits physical activity
Increasing angina that is more frequent, longer in duration, or occurs with less exertion than
previous angina
Absent Patients without features of typical angina are more likely to have another cause of
chest pain. Common causes include other cardiovascular, pulmonary, and gastrointestinal disorders
(table 3). (See "Diagnostic approach to chest pain in adults" and "Differential diagnosis of chest
pain in adults".)
In a review of over 430,000 patients with confirmed acute MI from the National Registry of
Myocardial Infarction 2, one-third had no chest pain on presentation to the hospital [10]. These
patients may present with dyspnea alone, nausea and/or vomiting, palpitations, syncope, or cardiac
arrest. They are more likely to be older, diabetic, and women. (See "Clinical features and diagnosis
of coronary heart disease in women".)
The absence of chest pain has important implications for therapy and prognosis. In the Registry
report, patients without chest pain were much less likely to be diagnosed with a confirmed MI on
admission (22 versus 50 percent in those with chest pain) and were less likely to be treated with
appropriate medical therapy and to receive fibrinolytic therapy or primary angioplasty (25 versus 74
percent) [10]. Not surprisingly, these differences were associated with an increase in in-hospital
mortality (23.3 versus 9.3 percent, adjusted odds ratio 2.21, 95 percent confidence interval 2.17 to
2.26).
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ECG The electrocardiogram (ECG) is a mainstay in the initial diagnosis of patients with suspected
ACS. It allows initial categorization of the patient with a suspected MI into one of three groups
based on the pattern:
ST elevation MI (ST elevation or new left bundle branch block)
non-ST elevation ACS, with either NSTEMI or UA (ST-depression, T wave inversions, or
transient ST-elevation)
Undifferentiated chest pain syndrome (nondiagnostic ECG)
The 2004 ACC/AHA guideline on ST myocardial infarction (and the 2007 focused update) concluded
that it is reasonable for emergency medical service (EMS) personnel with advanced cardiac life
support training to perform and evaluate a 12-lead ECG on a patient suspected of having an acute
MI [9,11]. (See "Overview of the acute management of acute ST elevation myocardial infarction".)
ST elevation MI In patients with acute ST elevation MI, the electrocardiogram evolves through
a typical sequence. (See "Electrocardiogram in the diagnosis of myocardial ischemia and
infarction" and "ECG tutorial: Myocardial infarction".)
Although not frequently seen, the earliest change in an STEMI is the development of a hyperacute
or peaked T wave that reflects localized hyperkalemia. Thereafter, the ST segment elevates in the
leads recording electrical activity of the involved region of the myocardium; it has the following
appearance:
Initially, there is elevation of the J point and the ST segment retains its concave
configuration.
Over time, the ST segment elevation becomes more pronounced and the ST segment
becomes more convex or rounded upward.
The ST segment may eventually become indistinguishable from the T wave; the QRS-T
complex can actually resemble a monophasic action potential.
The joint ESC/ACCF/AHA/WHF committee for the definition of MI established specific ECG criteria for
the diagnosis of ST elevation MI, which include 2 mm of ST segment elevation the precordial leads
for men and 1.5 mm for women (who tend to have less ST elevation) and greater than 1mm in other
leads (table 4) [12]. An initial Q wave or abnormal R wave develops over a period of several hours
to days. Specific ECG criteria were also established for the diagnosis of a prior myocardial infarction
(table 5).
Over time there is further evolution of these ECG changes; the ST segment gradually returns to the
isoelectric baseline, the R wave amplitude becomes markedly reduced, and the Q wave deepens. In
addition, the T wave becomes inverted. These changes generally occur within the first two weeks
after the event, but may progress more rapidly, within several hours of presentation.
In addition to patients with ST elevation on the ECG, two other groups of patients with an acute
coronary syndrome are considered to have an STEMI: those with new or presumably new left
bundle branch block and those with a true posterior MI. (See 'Bundle branch block or paced
rhythm' below and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction",
section on 'Posterior wall MI'.)
A separate issue, the assessment of patients with a suspected acute MI who have known left
bundle branch block or a paced rhythm, is discussed below. (See 'Bundle branch block or paced
rhythm' below.)
Absence of Q waves A subset of patients who present with initial ST segment elevation, do
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not develop Q waves. These patients are treated for an ST elevation MI. Such patients have a
better prognosis than those who develop Q waves because of more frequent reperfusion, a less
severe infarction, and, at follow-up, better left ventricular function and improved survival. (See
"Electrocardiogram in the prognosis of myocardial infarction or unstable angina", section on
'Presence or absence of new Q waves'.)
Locali ation The electrocardiogram can be used to localize the MI, and at times, predict the
infarct-related artery. These issues are discussed separately. (See "Electrocardiogram in the
diagnosis of myocardial ischemia and infarction".)
If there is electrocardiographic evidence of inferior wall ischemia (ST or T wave changes in leads II,
III, and aVF), the right-sided leads V4R, V5R, and V6R should also be obtained to evaluate the
possibility of right ventricular infarction. The recording of right-sided leads in this setting was given
a class I recommendation by the 2004 ACC/AHA task force [9]. No changes to this approach were
made in the 2007 focused update of the 2004 ACC/AHA guidelines for the management of patients
with ST-elevation MI [11]. Posterior leads (V7-9) are also indicated for those who present with ST
segment depression in the inferior leads to evaluate the possibility of posterior infarction [13].
Other causes of ST elevation and Q waves Although ST segment elevation and Q waves
are consistent with acute MI (particularly if new), each alone can be seen in other disorders (table
6 and table 7). As examples, ST segment elevation can occur in myocarditis, acute pericarditis,
patients with old MI and persistent ST segment elevation often associated with wall motion
abnormalities, and with the early repolarization variant, and Q waves can be seen in hypertrophic
cardiomyopathy. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and
"Pathogenesis and diagnosis of Q waves on the electrocardiogram" and "Clinical manifestations and
diagnosis of myocarditis in adults".)
Non-ST elevation ACS A non-ST elevation ACS is manifested by ST depressions and/or T wave
inversions without ST segment elevations or pathologic Q waves. These ST-T wave abnormalities
may be present diffusely in many leads; more commonly they are localized to the leads associated
with the region of ischemic myocardium. (See "Electrocardiogram in the diagnosis of myocardial
ischemia and infarction".)
As noted above, the two forms of non-ST elevation ACS (UA and NSTEMI) are frequently
indistinguishable at initial evaluation (prior to biomarker elevation). In a patient with an NSTEMI, ST
segment depressions usually evolve over the subsequent few days to result in residual ST segment
depression and T wave inversions, but not to the formation of pathologic Q waves. In a patient
with UA, ST segment and T wave changes usually resolve completely.
Nondiagnostic initial ECG The initial ECG is often not diagnostic in patients with MI. In two
series, for example, the initial ECG was not diagnostic in 45 percent and normal in 20 percent of
patients subsequently shown to have an acute MI [14,15]. In patients clinically suspected of
having an acute MI in whom the ECG is nondiagnostic, it is recommended that the ECG should be
repeated at 20 to 30 minute intervals for any patient with ongoing pain in whom the suspicion of
ACS remains high. In some patients, initially nondiagnostic electrocardiographic changes will evolve
into ST elevation or ST depression [14,16].
The efficacy of repeated ECGs was addressed in a study of 1000 patients presenting to the
emergency department with chest pain in whom serial ECGs were obtained every 20 minutes for an
average of two hours. Serial ECGs were equally specific (95 percent) but more sensitive than an
initial single ECG for detecting an acute MI (68 versus 55 percent) [14].
Bundle branch block or paced rh thm Both left bundle branch block (LBBB), which is present
in approximately 7 percent of patients with an acute MI [17], and pacing can interfere with the
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electrocardiographic diagnosis of MI or coronary ischemia. Of note, approximately one-half of

patients with LBBB and an acute MI do not have chest pain [18]. New right bundle branch block,
while generally not interfering with the electrocardiographic diagnosis of STEMI, connotes an
adverse prognosis similar in degree to LBBB.
Patients with LBBB, compared to those without bundle branch block, are much less likely to receive
aspirin, beta blockers, and reperfusion therapy [17,18], particularly if they present without chest
pain [18]. Similar observations have been made in patients with a paced rhythm [19].
Careful evaluation of the ECG may show some evidence of coronary ischemia in patients with LBBB
or a paced rhythm. However, the clinical history and cardiac enzymes are of primary importance in
diagnosing MI in this setting. (See "Electrocardiographic diagnosis of myocardial infarction in the
presence of bundle branch block or a paced rhythm".)
CARDIAC BIOMARKERS A variety of biomarkers have been used to evaluate patients with a
suspected acute MI. The cardiac troponins I and T as well as the MB isoenzyme of creatine kinase
(CK-MB) are the most frequently used.
The use of these tests is discussed in detail elsewhere, but the general principles will be briefly
reviewed here. Values 99 percentile of the upper reference limit (URL) should be considered
abnormal [2]. This value for troponin and CK-MB will vary depending on the assay used. (See
"Troponins and creatine kinase as biomarkers of cardiac injury".)
The following discussion will emphasize the diagnostic role of cardiac markers. These markers as
well as many other factors are important for risk stratification. These issues for both ST elevation
and non-ST elevation MI are discussed separately. (See "Risk stratification for cardiac events after
acute ST elevation myocardial infarction" and "Risk stratification after unstable angina or non-ST
elevation myocardial infarction" and "Risk factors for adverse outcomes after unstable angina or
non-ST elevation myocardial infarction".)
An elevation in the concentration of troponin or CK-MB is required for the diagnosis of acute MI
[1,2]. If both are measured and the troponin value is normal but the CK-MB is elevated, MB is likely
due to release from noncardiac tissue. Follow-up on such individuals reveals that they do extremely
well without subsequent events [20].
Troponin is the preferred marker for the diagnosis of myocardial injury because of their increased
specificity and better sensitivity compared to CK-MB [1,2,9]. The preferential use of cTnI or cTnT
for AMI diagnosis was recommended by 2007 joint ESC/ACCF/AHA/WHF task force for the definition
of myocardial infarction (table 1) [20]. (See "Troponins and creatine kinase as biomarkers of cardiac
injury".)
An elevation in cardiac troponins must be interpreted in the context of the clinical history and ECG
findings since it can be seen in a variety of clinical settings and is therefore not specific for an
acute coronary syndrome. (See 'Other causes of biomarker elevation' below and "Elevated cardiac
troponin concentration in the absence of an acute coronary syndrome".)
As there can be chronic elevations of troponin in patients who do not have acute events, the
guidelines emphasize the need for a changing pattern of values [1,2,21]. The magnitude of change
needed to operationalize this recommendation varies from assay to assay, so it is optimal when the
clinical laboratory helps to make these distinctions [22].
Three points should be kept in mind when using troponin to diagnose AMI:
With contemporary troponin assays, most patients can be diagnosed within two to three
hours of presentation [23].
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A negative test at the time of presentation, especially if the patient presents early after the
onset of symptoms, does not exclude myocardial injury.
AMI can be excluded in most patients by six hours, but the guidelines suggest that, if there is
a high degree of suspicion of an ACS, a 12-hour sample be obtained. [1,2,9]. However, very
few patients become positive after eight hours [24].
Other causes of biomarker elevation Elevations of biochemical markers diagnose cardiac
injury, not infarction due to coronary artery obstruction [25]. If an ischemic mechanism of injury is
present, for example, as indicated by ischemic ECG changes, then an ACS is diagnosed.
Otherwise, other mechanisms for cardiac injury must be considered (eg, heart failure, rapid atrial
fibrillation, myocarditis, anthracycline cardiotoxicity, subendocardial wall stress, myopericarditis,
sepsis, etc). As an example, small amounts of cardiac injury can occur in critically ill patients, which
may or may not represent an AMI [26,27]. Troponin elevations also occur in chronic kidney disease.
(See "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".)
In the emergency department setting, life-threatening causes of chest pain with troponin elevation
not due to coronary artery disease are acute pulmonary embolism, in which troponin release may
result from acute right heart overload, myocarditis [25], and stress-induced cardiomyopathy. (See
"Diagnosis of acute pulmonary embolism" and "Clinical manifestations and diagnosis of myocarditis in
adults", section on 'Cardiac enzymes'.)
Absence of biomarker elevation Using older assays, some patients with STEMI who were
rapidly reperfused did not develop a cardiac biomarker elevation. These patients were called
"aborted MIs." With contemporary troponin assays, this does not occur or is extremely rare. For
example, in an analysis of 767 patients with STEMI, the frequency of patients who had elevations
of troponin above the 99th percent value was 100 percent [28]. For patients with ST elevation on
the electrocardiogram and no biomarker elevation one of the other causes of ST elevation should be
considered (table 6). (See 'Other causes of ST elevation and Q waves' above and "Fibrinolytic
(thrombolytic) agents in acute ST elevation myocardial infarction: Therapeutic use", section on
'Introduction'.)
Discordant cardiac en mes biomarkers At least one third of patients with an ACS have
elevated troponins but normal CK-MB [20,29-31]. The frequency and prognostic significance of
discordant troponin and CK-MB were illustrated in a review of almost 30,000 such patients from the
multicenter CRUSADE initiative in the United States [31]. The following findings were noted:
The results were discordant in 28 percent of patients despite the fact that many centers
were still using either high cut-off values or inadequately sensitive troponin assays. Troponin
was more sensitive, as 18 percent had elevated troponin but normal CK-MB values. In
addition, 10 percent had false positive CK-MB elevations, as defined by normal troponin
values.
Compared to patients who were negative for both biomarkers, in-hospital mortality was not
increased in patients who were Tn-negative and CK-MB-positive (ie, false positives; 3.0
versus 2.7 percent, adjusted odds ratio 1.02, 95% CI 0.75-1.38).
Compared to patients who were negative for both biomarkers, there was a nonsignificant
trend toward increased mortality in patients who were Tn-positive/CK-MB-negative (4.5
versus 2.7 percent, adjusted odds ratio 1.15, 95 percent CI 0.86-1.54) and a significant
increase in mortality in patients who were positive for both biomarkers (5.9 versus 2.7
percent, adjusted odds ratio 1.53, 95 percent CI 1.18-1.98). The latter finding reflects the
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fact that patients with larger insults do worse [32]. The two discordant groups were treated
similarly with antithrombotic agents and percutaneous coronary intervention so differences in
outcomes are less likely to be explained by differences in therapy. Thus, an isolated CK-MB
elevation has limited prognostic value in patients with a non-ST elevation ACS. Several metaanalyses suggest that patients with isolated troponin elevations do much worse than those
without elevations [33,34]. If high cut-off values are used, these effects are obfuscated by
the admixture of patients with and without real troponin elevations.
Similar findings were noted among 1825 patients with a non-ST elevation ACS in the TACTICS-TIMI
18 trial in whom troponin T was measured; 668 (37 percent) had elevated CK-MB, almost all of
whom had elevated troponin T, while 361 patients (20 percent) had an elevated troponin T with
normal CK-MB [30]. The latter patients the greatest benefit from an early invasive strategy. (See
"Coronary arteriography and revascularization for unstable angina or non-ST elevation acute
myocardial infarction".)
Recommended approach The following general statements apply to the biochemical diagnosis
of an acute MI [2].
Troponins are the markers of choice and should be used instead of CK-MB except when postprocedural MI, where CK-MB may be more useful [1,2]. (See "Troponins and creatine kinase as
biomarkers of cardiac injury", section on 'Late diagnosis and reinfarction'.)
We recommend the following approach [20]:
Measure serum troponin-I or troponin-T at first presentation.
If the troponin is not elevated, repeat at six to nine hours. It is not uncommon to measure a
second troponin earlier than six hours in patients who are highly suspected of having ongoing
NSTEMI, since 80 percent of patients who rule in will do so in two to three hours [23]. In an
occasional patient in whom the index of suspicion for acute MI is high, but the first two
troponin measurements are not elevated, a repeat measurement at 12 to 24 hours may be
necessary.
CK-MB is measured when a troponin assay is not available. Previously, CK-MB was advocated
to help diagnose reinfarction, but now troponin has subsumed that role [2]. Reinfarction is
diagnosed if there is a 20 percent increase of the value in the second sample [2].
Troponin elevations persist for one to two weeks after AMI, but values are usually not rising
or falling rapidly at this time, allowing one to distinguish acute from more chronic events
[2,21].
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Beyond the Basics topic (see "Patient information: Heart attack (Beyond the Basics)")
SUMMARY Myocardial infarction (MI) is defined as a clinical (or pathologic) event caused by
myocardial ischemia in which there is evidence of myocardial injury or necrosis. Criteria are met
when there is a rise and/or fall of cardiac biomarkers, along with supportive evidence in the form of
typical symptoms, suggestive electrocardiographic changes, or imaging evidence of new loss of
viable myocardium or new regional wall motion abnormality. (See 'Introduction' above.)
The criteria used to define MI differ somewhat depending upon the particular clinical circumstance
of the patient: those suspected of acute MI based upon their presentation; those undergoing either
coronary artery bypass graft surgery or percutaneous intervention; or those who have sustained
sudden, unexpected cardiac arrest with or without death (table 1). (See 'Definitions' above.)
We recommend the following approach to diagnose an acute MI (excluding patients who have just
undergone revascularization):
An ECG, an abbreviated history (which focuses on the chest pain), and physical examination
should be obtained within 10 minutes of patient arrival. (See 'ECG' above and 'Chest
pain' above.)
Measure serum troponin-I or troponin-T at first presentation. (See 'Cardiac
biomarkers' above.)
If the serum troponin is not elevated, repeat at six to nine hours. It is not uncommon to
measure a second troponin earlier than six hours in patients who are highly suspected of
having ongoing NSTEMI. In an occasional patient in whom the index of suspicion for acute MI
is high but the first two troponin measurements are not elevated, a repeat measurement at
12 to 24 hours may be necessary. (See 'Cardiac biomarkers' above.)
Measure serum creatine kinase-MB (CK-MB) when a troponin assay is not available. (See
'Cardiac biomarkers' above.)
For patients who have undergone recent revascularization with either percutaneous coronary
intervention (PCI) or coronary artery bypass graft surgery (CABG), we suggest measurement of
troponin after the procedure. In order to diagnose myocardial infarction resulting from either PCI or
CABG, the baseline troponin has to have been normal, and thus a troponin should be ordered prior
to all revascularization procedures. (See 'After revascularization' above.)
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20. Goodman SG, Steg PG, Eagle KA, et al. The diagnostic and prognostic impact of the
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measurement in acute cardiac care. Eur Heart J 2010; 31:2197.
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between specimens in the American Heart Association Classification of Myocardial Infarction in
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24. Newby LK, Christenson RH, Ohman EM, et al. Value of serial troponin T measures for early and
late risk stratification in patients with acute coronary syndromes. The GUSTO-IIa
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27. Babuin L, Vasile VC, Rio Perez JA, et al. Elevated cardiac troponin is an independent risk factor
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28. Vasile VC, Babuin L, Ting HH, et al. Aborted myocardial infarction: is it real in the troponin era?
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29. Meier MA, Al-Badr WH, Cooper JV, et al. The new definition of myocardial infarction: diagnostic
and prognostic implications in patients with acute coronary syndromes. Arch Intern Med 2002;
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30. Kleiman NS, Lakkis N, Cannon CP, et al. Prospective analysis of creatine kinase muscle-brain
fraction and comparison with troponin T to predict cardiac risk and benefit of an invasive
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40:1044.
31. Newby LK, Roe MT, Chen AY, et al. Frequency and clinical implications of discordant creatine
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32. 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.
33. Ottani F, Galvani M, Nicolini FA, et al. Elevated cardiac troponin levels predict the risk of
adverse outcome in patients with acute coronary syndromes. Am Heart J 2000; 140:917.
34. Heidenreich PA, Alloggiamento T, Melsop K, et al. The prognostic value of troponin in patients
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38:478.
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GRAPHICS
Definition of m ocardial infarction
Criteria for acute m ocardial infarction
The term myocardial infarction should be used when there is evidence of myocardial necrosis
in a clinical setting consistent with myocardial ischaemia. Under these conditions any one of
the following criteria meets the diagnosis for myocardial infarction:
Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one
value above the 99th percentile of the upper reference limit (URL) together with evidence
of myocardial ischaemia with at least one of the following:
Symptoms of ischaemia
EC G changes indicative of new ischaemia (new ST-T changes or new left bundle branch block
[LBBB])
Development of pathological Q waves in the EC G
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

Sudden, unexpected cardiac death, involving cardiac arrest, often with symptoms
suggestive of myocardial ischaemia, and accompanied by presumably new ST elevation, or
new LBBB, and/or evidence of fresh thrombus by coronary angiography and/or at autopsy,
but death occurring before blood samples could be obtained, or at a time before the
appearance of cardiac biomarkers in the blood.
For percutaneous coronary interventions (PCI) in patients with normal baseline troponin
values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of
peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 3
x 99th percentile URL have been designated as defining PCI-related myocardial infarction.
A subtype related to a documented stent thrombosis is recognized.
For coronary artery bypass grafting (CABG) in patients with normal baseline troponin
values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of
peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 5
x 99th percentile URL plus either new pathological Q waves or new LBBB, or
angiographically documented new graft or native coronary artery occlusion, or imaging
evidence of new loss of viable myocardium have been designated as defining CABG-related
myocardial infarction.
Pathological findings of an acute myocardial infarction.

Criteria for prior m ocardial infarction

Any one of the following criteria meets the diagnosis for prior myocardial infarction:
Development of new pathological Q waves with or without symptoms.
Imaging evidence of a region of loss of viable myocardium that is thinned and fails to
contract, in the absence of a non-ischaemic cause.
Pathological findings of a healed or healing myocardial infarction.
Reproduced with permission from: Thygesen, K, Alpert, JS, White, HD, et al. Universal definition of
myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf of the Joint
ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Eur Heart J 2007;
28:2525. Copyright 2007 Oxford University Press.

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Coronar arter surger stud definitions of angina

Definite angina
Substernal discomfort precipitated by exertion, with a typical radiation to the shoulder, jaw
or inner aspect of the arm relieved by rest or nitroglycerin in less than 10 minutes

Probable angina
Has most of the features of definite angina but may not be entirely typical in some aspects

"Probabl not" angina

Defined as an atypical overall pattern of chest pain that does not fit the description of
definite angina

"Definitel not" angina

Chest pain is unrelated to activity, appears to be clearly of non-cardiac origin and is not
relieved by nitroglycerin
Adapted from CASS Investigators. National Heart Lung and Blood Institute Coronary Artery Study,
Circulation 1981; 63(Suppl I):I-81.

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Alternative diagnoses to cardiac ischemia for patients with chest pain

Non-ischemic
cardiovascular
Aortic dissection*
Myocarditis
Pericarditis

Chest wall
Cervical disc disease

Pulmonar

Gastrointestinal

Pleuritis

Biliary

Pneumonia
Pulmonary embolus*
Tension pneumothorax*

Ps chiatric

C holangitis
C holecystitis
C holedocholithiasis
C olic

Esophageal
Esophagitis

Costochondritis

Affective disorders (eg,

depression)

Fibrositis

Anxiety disorders

Reflux

Herpes zoster (before the rash)

Neuropathic pain
Rib fracture
Sternoclavicular arthritis

Hyperventilation

Spasm

Rupture*

Panic disorder

Pancreatitis

Primary anxiety

Peptic ulcer
disease

Somatiform disorders
Thought disorders (eg, fixed
delusions)

Nonperforating
Perforating*

* Potentially life-threatening conditions. Adapted with permission from: ACC/AHA/ACP Guidelines for
the Management of Patients with Chronic Stable Angina. J Am Coll Cardiol 1999; 33:2092. Copyright
1999 American College of Cardiology.

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ECG manifestations of acute m ocardial ischaemia (in absence of LVH and

LBBB)
ST elevation
New ST elevation at the J-point in two contiguous leads with the cut-off points: 0.2 mV in
men or 0.15 mV in women in leads V2 -V3 and/or 0.1 mV in other leads

ST depression and T-wave changes

New horizontal or down-sloping ST depression 0.05 mV in two contiguous leads; and/or T
inversion 0.1 mVin two contiguous leads with prominent R-wave or R/S ratio >1
Reproduced with permission from: Thygesen, K, Alpert, JS, White, HD, et al. Universal definition of
myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf of the Joint
ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Eur Heart J 2007;
28:2525. Copyright 2007 Oxford University Press.

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ECG changes associated with prior m ocardial infarction

Any Q-wave in leads V2 -V3 0.02 s or QS complex in leads V2 and V3
Q-wave 0.03 s and 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4 -V6 in any two
leads of a contiguous lead grouping (I, aVL,V6 ; V4 -V6 ; II, III, and aVF)*
R-wave 0.04 s in V1 -V2 and R/S 1 with a concordant positive T-wave in the absence of a
conduction defect
* The same criteria are used for supplemental leads V7 -V9 , and for the Cabrera frontal plane lead
grouping. Reproduced with permission from: Thygesen, K, Alpert, JS, White, HD, et al. Universal
definition of myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf
of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Eur Heart J
2007; 28:2525. Copyright 2007 Oxford University Press.

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Causes of ST segment elevation

Myocardial ischemia or infarction
Noninfarction, transmural ischemia (Prinzmetal's angina pattern or acute takotsubo syndrome)
Acute myocardial infarction (MI) usually due to coronary atherosclerosis or occasionally to other
causes (eg, acute takotsubo syndrome)
Post-MI (ventricular aneurysm pattern)

Acute pericarditis
Normal variants (including benign early repolarization)
Left ventricular hypertrophy or left bundle branch block (V1-V2 or V3)
Other
Myocarditis (may look like MI or pericarditis)
Massive pulmonary embolism (leads V1-V2 in occasional cases)
Brugada-type patterns (V1-V3 with right bundle branch block-appearing morphology)
Myocardial tumor
Myocardial trauma
Hyperkalemia (only leads V1 and V2)
Hypothermia (J wave/Osborn wave)
Hypercalcemia (rarely)
Post-DC cardioversion (rarely)

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Causes of Q waves
Ph siologic or positional factors
Normal variant "septal" q waves
Normal variant Q waves in leads V1,V2, aVL, III, and aVF
Left pneumothorax or dextrocardia: loss of lateral precordial R wave progression

M ocardial injur

or infiltration

Acute processes: myocardial ischemia or infarction, myocarditis, hyperkalemia

Chronic processes: myocardial infarction, idiopathic cardiomyopathy, myocarditis,
amyloidosis, tumor, sarcoid, scleroderma, Chagas' disease, echinococcus cyst

Ventricular h pertroph

or enlargement

Left ventricle: slow R wave progression in which there are small or absent R waves in the
mid-precordial leads
Right ventricle: reversed R wave progression in which there is a progressive decrease in R
wave amplitude from V1 to the mid-lateral precordial leads, or slow R wave progression,
particularly with chronic obstructive lung disease or acute pulmonary embolism
Hypertrophic cardiomyopathy - may simulate anterior, inferior, posterior, or lateral infarcts

Conduction abnormalities
Left bundle branch block - slow R wave progression in which there are small or absent R
waves in the mid-precordial leads
Wolff-Parkinson-White patterns

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