Criteria for the Diagnosis of Acute Myocardial Infarction

2/21/12 Criteria for the diagnosis of acute m\ocardial infarction

1/20www.uptodate.com/contents/criteria-for-the-diagnosis-of-acute-m\ocardial-infarction?view=print

Official reprint from UpToDate www.uptodate.com

2012 UpToDate

AuthorsGuy S Reeder, MDHarold L Kennedy, MD, MPH

Section EditorsChristopher P Cannon, MDJames Hoekstra, MDAllan S Jaffe, MD

Deput\ EditorGordon M Saperia, MD, FACC

Criteria for the diagnosis of acute m\ocardial infarction

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



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



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 (99 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 (99 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

99 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).



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



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



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].



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



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 meta-

analyses 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 post-

procedural 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].

INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The

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Here are the patient education articles that are relevant to this topic. We encourage you to print

or e-mail these topics to your patients. (You can also locate patient education articles on a variety

of subjects by searching on patient info and the keyword(s) of interest.)

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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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REFERENCES

1. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensusdocument of The Joint European Society of Cardiology/American College of CardiologyCommittee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000; 36:959.

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3. Anderson J, Adams C, Antman E, et al. ACC/AHA 2007 guidelines for the management ofpatients with unstable angina/non-ST-elevation myocardial infarction: a report of theAmerican College of Cardiology/American Heart Association Task Force on Practice Guidelines(Writing Committee to revise the 2002 Guidelines for the Management of Patients withUnstable Angina/Non-ST-Elevation Myocardial Infarction): developed in collaboration with the



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Topic 52 Version 10.0



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 necrosisin a clinical setting consistent with myocardial ischaemia. Under these conditions any one ofthe following criteria meets the diagnosis for myocardial infarction:

Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least onevalue above the 99th percentile of the upper reference limit (URL) together with evidenceof myocardial ischaemia with at least one of the following:

Symptoms of ischaemia

ECG changes indicative of new ischaemia (new ST-T changes or new left bundle branch block[LBBB])

Development of pathological Q waves in the ECG

Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

Sudden, unexpected cardiac death, involving cardiac arrest, often with symptomssuggestive of myocardial ischaemia, and accompanied by presumably new ST elevation, ornew 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 theappearance of cardiac biomarkers in the blood.

For percutaneous coronary interventions (PCI) in patients with normal baseline troponinvalues, elevations of cardiac biomarkers above the 99th percentile URL are indicative ofperi-procedural myocardial necrosis. By convention, increases of biomarkers greater than 3x 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 troponinvalues, elevations of cardiac biomarkers above the 99th percentile URL are indicative ofperi-procedural myocardial necrosis. By convention, increases of biomarkers greater than 5x 99th percentile URL plus either new pathological Q waves or new LBBB, orangiographically documented new graft or native coronary artery occlusion, or imagingevidence of new loss of viable myocardium have been designated as defining CABG-relatedmyocardial 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 tocontract, 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.



Coronar\ arter\ surger\ stud\ definitions of angina

Definite angina

Substernal discomfort precipitated by exertion, with a typical radiation to the shoulder, jawor 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 ofdefinite angina

"Definitel\ not" angina

Chest pain is unrelated to activity, appears to be clearly of non-cardiac origin and is notrelieved by nitroglycerin

Adapted from CASS Investigators. National Heart Lung and Blood Institute Coronary Artery Study,

Circulation 1981; 63(Suppl I):I-81.



Alternative diagnoses to cardiac ischemia for patients with chest pain

Non-ischemiccardiovascular

Aortic dissection*

Myocarditis

Pericarditis

Chest wall

Cervical disc disease

Costochondritis

Fibrositis

Herpes zoster (before the rash)

Neuropathic pain

Rib fracture

Sternoclavicular arthritis

Pulmonar\

Pleuritis

Pneumonia

Pulmonary embolus*

Tension pneumothorax*

Ps\chiatric

Affective disorders (eg,depression)

Anxiety disorders

Hyperventilation

Panic disorder

Primary anxiety

Somatiform disorders

Thought disorders (eg, fixeddelusions)

Gastrointestinal

Biliary

Cholangitis

Cholecystitis

Choledocholithiasis

Colic

Esophageal

Esophagitis

Spasm

Reflux

Rupture*

Pancreatitis

Peptic ulcerdisease

Nonperforating

Perforating*

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

1999 American College of Cardiology.



ECG manifestations of acute m\ocardial ischaemia (in absence of LVH andLBBB)

ST elevation

New ST elevation at the J-point in two contiguous leads with the cut-off points: 0.2 mV inmen 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 Tinversion 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.



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. Universaldefinition 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.



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 othercauses (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)



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 themid-precordial leads

Right ventricle: reversed R wave progression in which there is a progressive decrease in Rwave 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 Rwaves in the mid-precordial leads

Wolff-Parkinson-White patterns



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Criteria for the Diagnosis of Acute Myocardial Infarction

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