Criteria for diagnosis of acute myocardial infarction

Criteria for the diagnosis of acute myocardial infarction

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

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

Deputy 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: Oct 2013. | This topic last updated: Dec 12, 2012.

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 measurementRelief of ischemic painAssessment of the hemodynamic state and correction of abnormalities that may be presentInitiation 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 ST elevation myocardial infarction" and "Overview of the acute management of unstable angina and 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 coronary syndrome  — 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 ]. This definition was not fundamentally changed in the third universal definition of MI released in 2012 by the ESC/ACCF/AHA/WHF [ 7 ].

According to the third universal definition, any one of the following criteria meets the diagnosis of MI:

Detection of a rise and/or fall of cardiac biomarker values (preferably cTn with at least one value above the 99 th percentile upper reference limit [URL]) and with at least one of the following:

Symptoms of ischemiaDevelopment of pathologic Q waves in the ECGNew or presumed new significant ST-segment-T wave (ST-T) changes or new left bundle branch block (LBBB)Identification of an intracoronary thrombus by angiography or autopsyImaging evidence of new loss of viable myocardium or a new regional wall motion abnormality.

Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemia ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained, or before cardiac biomarker values would be increased.PCI related MI was defined by elevation of biomarker values (cTn is preferred) >5 x 99 th percentile upper reference limit [URL]) in patients with normal baseline values (<99 th percentile URL) or a rise of values >20 percent if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial ischemia, or (ii) new ischemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no-flow or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischemia and with a rise and/or fall of cardiac biomarkers with at least one value above the 99 th percentileCoronary artery bypass graft surgery (CABG) associated MI was defined by elevation of cardiac biomarker values >10 x 99 th percentile URL in patients with normal baseline cTn values. In addition, either (i) new pathologic Q waves or new LBBB, or (ii) angiographic documented new graft of native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

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 (spontaneous MI): MI consequent to a pathologic process in the wall of the coronary artery (eg, plaque erosion/rupture, fissuring, or dissection), resulting in intraluminal thrombusType 2 (MI secondary to an ischemic imbalance): MI consequent to increased oxygen demand or decreased supply (eg, coronary endothelial dysfunction, coronary artery spasm, coronary artery embolus, anemia, tachy-/brady-arrhythmias, anemia, respiratory failure, hypertension or hypotension)Type 3 (MI resulting in death when biomarker values are unavailable): Sudden unexpected cardiac death before blood samples for biomarkers could be drawn or before their appearance in the bloodType 4a (MI related to PCI): See criteria directly above.Type 4b (MI related to stent thrombosis): See criteria directly above.Type 5 (MI related to CABG): See criteria directly above.

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 [ 8 ].

After revascularization  — 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 [ 7 ]. They state that for patients undergoing PCI who have normal baseline troponin value (99 th 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) [ 9 ]. In addition, the cut points given below are controversial.

The specific criteria for meeting the definition of MI in the setting of PCI or CABG are presented above. (See 'Acute MI' above.)

Prior MI

According to the third universal definition of MI, any one of the following three criteria satisfies the diagnosis for a prior (established) MI [ 7 ]:

Pathologic Q waves (≥0.04 sec) with or without symptoms in the absence of non-ischemic causes.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' .)

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 [ 10 ]. 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 1 ). 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 durationNew onset angina that markedly limits physical activityIncreasing 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 2 ). (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 [ 11 ]. 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) [ 11 ]. 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 [ 10,12 ]. (See "Overview of the acute management of 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 [ 7,13 ]:

New ST segment elevation at the J point in two contiguous leads with the cut-points: >0.1 mV in all leads other than leads V2-V3;

For leads V2-V3, the following cut points apply: ≥0.2 mV in men ≥40 years, ≥0.25 mV in men <40 years, or ≥0.15 mV in women.

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' .)

Localization  — 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 2004ACC/AHA task force [ 10 ]. 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 [ 12 ]. 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 [ 14 ].

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 3 and table 4 ). 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.

The joint ESC/ACCF/AHA/WHF committee for the definition of MI established specific ECG criteria for the diagnosis of non-ST elevation MI [ 7,13 ]: new horizontal or down-sloping ST depression ≥0.05 mV in two contiguous leads and/or T inversion ≥0.1 mV in two contiguous leads with prominent R wave or R/S ratio >1.

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 [ 15,16 ]. 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 [ 15,17 ].

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) [ 15 ].

Bundle branch block or paced rhythm  — Both left bundle branch block (LBBB), which is present in approximately 7 percent of patients with an acute MI [ 18 ], 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 [ 19 ]. 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 [ 18,19 ], particularly if they present without chest pain [ 19 ]. Similar observations have been made in patients with a paced rhythm [ 20 ].

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 [21 ].

Troponin is the preferred marker for the diagnosis of myocardial injury for all diagnostic categories because of their increased specificity and better sensitivity compared to CK-MB [ 1,2,10 ]. However, 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. The new guidelines endorse the concept that if there are elevations of cTn in a situation where ischemia is not present that term cardiac injury should be used. (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 [ 1,2,22 ]. 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 [ 23 ].

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 [ 24 ].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. [ 1,2,10 ]. However, very few patients become positive after eight hours [ 25 ].

Other causes of biomarker elevation  — Elevations of biochemical markers diagnose cardiac injury, not infarction due to coronary artery obstruction [ 26 ]. 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 [27,28 ]. 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 [ 26 ], and stress-induced cardiomyopathy. (See "Diagnosis of acute pulmonary embolism" and "Clinical manifestations and diagnosis of myocarditis in adults" .)

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 [ 29 ]. For patients with ST elevation on the electrocardiogram and no biomarker elevation one of the other causes of ST elevation should be considered ( table 3 ). (See 'Other causes of ST elevation and Q waves' above and "Fibrinolytic therapy in acute ST elevation myocardial infarction: Initiation of therapy", section on 'Introduction' .)

Discordant cardiac enzymes biomarkers  — At least one third of patients with an ACS have elevated troponins but normal CK-MB [ 21,30-32 ]. 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 [ 32 ]. 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 cTn-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 [ 33 ]. 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 [34,35 ]. 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 [ 31 ]. 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 [ 21 ]:

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 [ 24 ]. 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 [ 2,22 ].

INFORMATION FOR PATIENTS  — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5 th to 6 th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

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Beyond the Basics topic (see "Patient information: Heart attack (Beyond the Basics)" )

SUMMARY AND RECOMMENDATIONS  — 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. (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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