HomeCirculationVol. 126, No. 16Third Universal Definition of Myocardial Infarction Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBThird Universal Definition of Myocardial Infarction Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman and Harvey D. Whitethe Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction Kristian ThygesenKristian Thygesen Search for more papers by this author , Joseph S. AlpertJoseph S. Alpert Search for more papers by this author , Allan S. JaffeAllan S. Jaffe Search for more papers by this author , Maarten L. SimoonsMaarten L. Simoons Search for more papers by this author , Bernard R. ChaitmanBernard R. Chaitman Search for more papers by this author and Harvey D. WhiteHarvey D. White Search for more papers by this author and the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction Originally published24 Aug 2012https://doi.org/10.1161/CIR.0b013e31826e1058Circulation. 2012;126:2020–2035Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 Table of ContentsAbbreviations and Acronyms. . . . . . . . . . . . . . . . . . . .2021Definition of Myocardial Infarction. . . . . . . . . . . . . . .2022Criteria for Acute Myocardial Infarction. . . . . . . . . . . .2022Criteria for Prior Myocardial Infarction. . . . . . . . . . . .2022Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2022Pathological Characteristics of Myocardial Ischaemia and Infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2023Biomarker Detection of Myocardial Injury With Necrosis. . .2023Clinical Features of Myocardial Ischaemia and Infarction. . .2024Clinical Classification of Myocardial Infarction. . . .2024 Spontaneous Myocardial Infarction (MI Type 1). . . .2024Myocardial Infarction Secondary to an Ischaemic Imbalance (MI Type 2). . . . . . . . . . . . . . . . . . . . . . . .2024Cardiac Death Due to Myocardial Infarction (MI Type 3). .2025Myocardial Infarction Associated With Revascularization Procedures (MI Types 4 and 5). . . . . . . . . . . . . . . . . . .2026Electrocardiographic Detection of Myocardial Infarction. .2026Prior Myocardial Infarction. . . . . . . . . . . . . . . . . . . . . .2027Silent Myocardial Infarction. . . . . . . . . . . . . . . . . . . . .2027Conditions that Confound the ECG Diagnosis of Myocardial Infarction. . . . . . . . . . . . . . . . . . . . . . . . . .2027Imaging Techniques. . . . . . . . . . . . . . . . . . . . . . . . . . .2027 Echocardiography. . . . . . . . . . . . . . . . . . . . . . . . . . .2028Radionuclide Imaging. . . . . . . . . . . . . . . . . . . . . . . .2028Magnetic Resonance Imaging. . . . . . . . . . . . . . . . . .2028Computed Tomography. . . . . . . . . . . . . . . . . . . . . . .2028Applying Imaging in Acute Myocardial Infarction. .2028Applying Imaging in Late Presentation of Myocardial Infarction. . . . . . . . . . . . . . . . . . . . . . .2029Diagnostic Criteria for Myocardial Infarction With PCI (MI Type 4). . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2029Diagnostic Criteria for Myocardial Infarction With CABG (MI Type 5). . . . . . . . . . . . . . . . . . . . . . . . . . .2029Assessment of MI in Patients Undergoing Other Cardiac Procedures. . . . . . . . . . . . . . . . . . . . . . . . . . . .2030Myocardial Infarction Associated With Non-Cardiac Procedures. . . . . . . . . . . . . . . . . . . . . . . .2030Myocardial Infarction in the Intensive Care Unit. . . . .2030Recurrent Myocardial Infarction. . . . . . . . . . . . . . . . . .2030Reinfarction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2030Myocardial Injury or Infarction Associated With Heart Failure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2031Application of MI in Clinical Trials and Quality Assurance Programmes. . . . . . . . . . . . . . . . . . . . . . . . .2031Public Policy Implications of the Adjustment of the MI Definition. . . . . . . . . . . . . . . . . . . . . . . . . . . . .2031Global Perspectives of the Definition of Myocardial Infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2032Conflicts of Interest. . . . . . . . . . . . . . . . . . . . . . . . . . . .2032Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . .2033References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2033Download figureDownload PowerPointIntroductionMyocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that distinguishes between incident and recurrent events. From the epidemiological point of view, the incidence of MI in a population can be used as a proxy for the prevalence of CAD in that population. The term ‘myocardial infarction’ may have major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world and it is an outcome measure in clinical trials, observational studies and quality assurance programmes. These studies and programmes require a precise and consistent definition of MI.In the past, a general consensus existed for the clinical syndrome designated as MI. In studies of disease prevalence, the World Health Organization (WHO) defined MI from symptoms, ECG abnormalities and cardiac enzymes. However, the development of ever more sensitive and myocardial tissue-specific cardiac biomarkers and more sensitive imaging techniques now allows for detection of very small amounts of myocardial injury or necrosis. Additionally, the management of patients with MI has significantly improved, resulting in less myocardial injury and necrosis, in spite of a similar clinical presentation. Moreover, it appears necessary to distinguish the various conditions which may cause MI, such as ‘spontaneous’ and ‘procedure-related’ MI. Accordingly, physicians, other healthcare providers and patients require an up-to-date definition of MI.In 2000, the First Global MI Task Force presented a new definition of MI, which implied that any necrosis in the setting of myocardial ischaemia should be labelled as MI.1 These principles were further refined by the Second Global MI Task Force, leading to the Universal Definition of Myocardial Infarction Consensus Document in 2007, which emphasized the different conditions which might lead to an MI.2 This document, endorsed by the European Society of Cardiology (ESC), the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the World Heart Federation (WHF), has been well accepted by the medical community and adopted by the WHO.3 However, the development of even more sensitive assays for markers of myocardial necrosis mandates further revision, particularly when such necrosis occurs in the setting of the critically ill, after percutaneous coronary procedures or after cardiac surgery. The Third Global MI Task Force has continued the Joint ESC/ACCF/AHA/WHF efforts by integrating these insights and new data into the current document, which now recognizes that very small amounts of myocardial injury or necrosis can be detected by biochemical markers and/or imaging.Pathological Characteristics of Myocardial Ischaemia and InfarctionMI is defined in pathology as myocardial cell death due to prolonged ischaemia. After the onset of myocardial ischaemia, histological cell death is not immediate, but takes a finite period of time to develop—as little as 20 min, or less in some animal models.4 It takes several hours before myocardial necrosis can be identified by macroscopic or microscopic post-mortem examination. Complete necrosis of myocardial cells at risk requires at least 2–4 h, or longer, depending on the presence of collateral circulation to the ischaemic zone, persistent or intermittent coronary arterial occlusion, the sensitivity of the myocytes to ischaemia, pre-conditioning, and individual demand for oxygen and nutrients.2 The entire process leading to a healed infarction usually takes at least 5–6 weeks. Reperfusion may alter the macroscopic and microscopic appearance.Biomarker Detection of Myocardial Injury With NecrosisMyocardial injury is detected when blood levels of sensitive and specific biomarkers such as cTn or the MB fraction of creatine kinase (CKMB) are increased.2 Cardiac troponin I and T are components of the contractile apparatus of myocardial cells and are expressed almost exclusively in the heart. Although elevations of these biomarkers in the blood reflect injury leading to necrosis of myocardial cells, they do not indicate the underlying mechanism.5 Various possibilities have been suggested for release of structural proteins from the myocardium, including normal turnover of myocardial cells, apoptosis, cellular release of troponin degradation products, increased cellular wall permeability, formation and release of membranous blebs, and myocyte necrosis.6 Regardless of the pathobiology, myocardial necrosis due to myocardial ischaemia is designated as MI.Also, histological evidence of myocardial injury with necrosis may be detectable in clinical conditions associated with predominantly non-ischaemic myocardial injury. Small amounts of myocardial injury with necrosis may be detected, which are associated with heart failure (HF), renal failure, myocarditis, arrhythmias, pulmonary embolism or otherwise uneventful percutaneous or surgical coronary procedures. These should not be labelled as MI or a complication of the procedures, but rather as myocardial injury, as illustrated in Figure 1. It is recognized that the complexity of clinical circumstances may sometimes render it difficult to determine where individual cases may lie within the ovals of Figure 1. In this setting, it is important to distinguish acute causes of cTn elevation, which require a rise and/or fall of cTn values, from chronic elevations that tend not to change acutely. A list of such clinical circumstances associated with elevated values of cTn is presented in Table 1. The multifactorial contributions resulting in the myocardial injury should be described in the patient record.Download figureDownload PowerPointFigure 1. This illustration shows various clinical entities: for example, renal failure, heart failure, tachy- or bradyarrhythmia, cardiac or non-cardiac procedures that can be associated with myocardial injury with cell death marked by cardiac troponin elevation. However, these entities can also be associated with myocardial infarction in case of clinical evidence of acute myocardial ischaemia with rise and/or fall of cardiac troponin.Table 1. Elevations of Cardiac Troponin Values Because of Myocardial InjuryTable 1. Elevations of Cardiac Troponin Values Because of Myocardial InjuryThe preferred biomarker—overall and for each specific category of MI—is cTn (I or T), which has high myocardial tissue specificity as well as high clinical sensitivity. Detection of a rise and/or fall of the measurements is essential to the diagnosis of acute MI.7 An increased cTn concentration is defined as a value exceeding the 99th percentile of a normal reference population [upper reference limit (URL)]. This discriminatory 99th percentile is designated as the decision level for the diagnosis of MI and must be determined for each specific assay with appropriate quality control in each laboratory.8,9 The values for the 99th percentile URL defined by manufacturers, including those for many of the high-sensitivity assays in development, can be found in the package inserts for the assays or in recent publications.10,11,12Values should be presented as nanograms per litre (ng/L) or picograms per millilitre (pg/mL) to make whole numbers. Criteria for the rise of cTn values are assay-dependent but can be defined from the precision profile of each individual assay, including high-sensitivity assays.10,11 Optimal precision, as described by coefficient of variation (CV) at the 99th percentile URL for each assay, should be defined as ≤10%. Better precision (CV ≤10%) allows for more sensitive assays and facilitates the detection of changing values.13 The use of assays that do not have optimal precision (CV >10% at the 99th percentile URL) makes determination of a significant change more difficult but does not cause false positive results. Assays with CV >20% at the 99th percentile URL should not be used.13 It is acknowledged that pre-analytic and analytic problems can induce elevated and reduced values of cTn.10,11Blood samples for the measurement of cTn should be drawn on first assessment and repeated 3–6 h later. Later samples are required if further ischaemic episodes occur, or when the timing of the initial symptoms is unclear.14 To establish the diagnosis of MI, a rise and/or fall in values with at least one value above the decision level is required, coupled with a strong pre-test likelihood. The demonstration of a rising and/or falling pattern is needed to distinguish acute-from chronic elevations in cTn concentrations that are associated with structural heart disease.10,11,15–19 For example, patients with renal failure or HF can have significant chronic elevations in cTn. These elevations can be marked, as seen in many patients with MI, but do not change acutely.7 However, a rising or falling pattern is not absolutely necessary to make the diagnosis of MI if a patient with a high pre-test risk of MI presents late after symptom onset; for example, near the peak of the cTn time-concentration curve or on the slow-declining portion of that curve, when detecting a changing pattern can be problematic. Values may remain elevated for 2 weeks or more following the onset of myocyte necrosis.10Sex-dependent values may be recommended for high-sensitivity troponin assays.20,21 An elevated cTn value (>99th percentile URL), with or without a dynamic pattern of values or in the absence of clinical evidence of ischaemia, should prompt a search for other diagnoses associated with myocardial injury, such as myocarditis, aortic dissection, pulmonary embolism, or HF. Renal failure and other more non-ischaemic chronic disease states, that can be associated with elevated cTn levels, are listed in Table 1.10,11If a cTn assay is not available, the best alternative is CKMB (measured by mass assay). As with troponin, an increased CKMB value is defined as a measurement above the 99th percentile URL, which is designated as the decision level for the diagnosis of MI.22 Sex-specific values should be employed.22Clinical Features of Myocardial Ischaemia and InfarctionOnset of myocardial ischaemia is the initial step in the development of MI and results from an imbalance between oxygen supply and demand. Myocardial ischaemia in a clinical setting can usually be identified from the patient's history and from the ECG. Possible ischaemic symptoms include various combinations of chest, upper extremity, mandibular or epigastric discomfort (with exertion or at rest) or an ischaemic equivalent such as dyspnoea or fatigue. The discomfort associated with acute MI usually lasts >20 min. Often, the discomfort is diffuse—not localized, nor positional, nor affected by movement of the region—and it may be accompanied by diaphoresis, nausea or syncope. However, these symptoms are not specific for myocardial ischaemia. Accordingly, they may be misdiagnosed and attributed to gastrointestinal, neurological, pulmonary or musculoskeletal disorders. MI may occur with atypical symptoms—such as palpitations or cardiac arrest—or even without symptoms; for example in women, the elderly, diabetics, or post-operative and critically ill patients.2 Careful evaluation of these patients is advised, especially when there is a rising and/or falling pattern of cardiac biomarkers.Clinical Classification of Myocardial InfarctionFor the sake of immediate treatment strategies, such as reperfusion therapy, it is usual practice to designate MI in patients with chest discomfort, or other ischaemic symptoms that develop ST elevation in two contiguous leads (see ECG section), as an ‘ST elevation MI’ (STEMI). In contrast, patients without ST elevation at presentation are usually designated as having a ‘non-ST elevation MI’ (NSTEMI). Many patients with MI develop Q waves (Q wave MI), but others do not (non-Q MI). Patients without elevated biomarker values can be diagnosed as having unstable angina. In addition to these categories, MI is classified into various types, based on pathological, clinical and prognostic differences, along with different treatment strategies (Table 2).Table 2. Universal Classification of Myocardial InfarctionTable 2. Universal Classification of Myocardial InfarctionSpontaneous Myocardial Infarction (MI Type 1)This is an event related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries, leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD but, on occasion (5 to 20%), non-obstructive or no CAD may be found at angiography, particularly in women.23–25Myocardial Infarction Secondary to an Ischaemic Imbalance (MI Type 2)In instances of myocardial injury with necrosis, where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, the term ‘MI type 2’ is employed (Figure 2). In critically ill patients, or in patients undergoing major (non-cardiac) surgery, elevated values of cardiac biomarkers may appear, due to the direct toxic effects of endogenous or exogenous high circulating catecholamine levels. Also coronary vasospasm and/or endothelial dysfunction have the potential to cause MI.26–28Download figureDownload PowerPointFigure 2. Differentiation between myocardial infarction (MI) types 1 and 2 according to the condition of the coronary arteries.Cardiac Death Due to Myocardial Infarction (MI Type 3)Patients who suffer cardiac death, with symptoms suggestive of myocardial ischaemia accompanied by presumed new ischaemic ECG changes or new LBBB—but without available biomarker values—represent a challenging diagnostic group. These individuals may die before blood samples for biomarkers can be obtained, or before elevated cardiac biomarkers can be identified. If patients present with clinical features of myocardial ischaemia, or with presumed newischaemic ECG changes, they should be classified as having had a fatal MI, even if cardiac biomarker evidence of MI is lacking.Myocardial Infarction Associated With Revascularization Procedures (MI Types 4 and 5)Periprocedural myocardial injury or infarction may occur at some stages in the instrumentation of the heart that is required during mechanical revascularization procedures, either by PCI or by coronary artery bypass grafting (CABG). Elevated cTn values may be detected following these procedures, since various insults may occur that can lead to myocardial injury with necrosis.29–32 It is likely that limitation of such injury is beneficial to the patient: however, a threshold for a worsening prognosis, related to an asymptomatic increase of cardiac biomarker values in the absence of procedural complications, is not well defined.33–35 Subcategories of PCI-related MI are connected to stent thrombosis and restenosis that may happen after the primary procedure.Electrocardiographic Detection of Myocardial InfarctionThe ECG is an integral part of the diagnostic work-up of patients with suspected MI and should be acquired and interpreted promptly (i.e. target within 10 min) after clinical presentation.2 Dynamic changes in the ECG waveforms during acute myocardial ischaemic episodes often require acquisition of multiple ECGs, particularly if the ECG at initial presentation is non-diagnostic. Serial recordings in symptomatic patients with an initial non-diagnostic ECG should be performed at 15–30 min intervals or, if available, continuous computer-assisted 12-lead ECG recording. Recurrence of symptoms after an asymptomatic interval are an indication for a repeat tracing and, in patients with evolving ECG abnormalities, a pre-discharge ECG should be acquired as a baseline for future comparison. Acute or evolving changes in the ST-T waveforms and Q waves, when present, potentially allow the clinician to time the event, to identify the infarct-related artery, to estimate the amount of myocardium at risk as well as prognosis, and to determine therapeutic strategy. More profound ST-segment shift or T wave inversion involving multiple leads/territories is associated with a greater degree of myocardial ischaemia and a worse prognosis. Other ECG signs associated with acute myocardial ischaemia include cardiac arrhythmias, intraventricular and atrioventricular conduction delays, and loss of pre-cordial R wave amplitude. Coronary artery size and distribution of arterial segments, collateral vessels, location, extent and severity of coronary stenosis, and prior myocardial necrosis can all impact ECG manifestations of myocardial ischae-mia.36 Therefore the ECG at presentation should always be compared to prior ECG tracings, when available. The ECG by itself is often insufficient to diagnose acute myocardial ischaemia or infarction, since ST deviation may be observed in other conditions, such as acute pericarditis, left ventricular hypertrophy (LVH), left bundle branch block (LBBB), Brugada syndrome, stress cardiomyopathy, and early repolarization patterns.37 Prolonged new ST-segment elevation (e.g. >20 min), particularly when associated with reciprocal ST-segment depression, usually reflects acute coronary occlusion and results in myocardial injury with necrosis. As in cardiomyopathy, Q waves may also occur due to myocardial fibrosis in the absence of CAD.ECG abnormalities of myocardial ischaemia or infarction may be inscribed in the PR segment, the QRS complex, the ST-segment or the T wave. The earliest manifestations of myocardial ischaemia are typically T wave and ST-segment changes. Increased hyperacute T wave amplitude, with prominent symmetrical T waves in at least two contiguous leads, is an early sign that may precede the elevation of the ST-segment. Transient Q waves may be observed during an episode of acute ischaemia or (rarely) during acute MI with successful reperfusion. Table 3 lists ST-T wave criteria for the diagnosis of acute myocardial ischaemia that may or may not lead to MI. The J point is used to determine the magnitude of the ST-segment shift. New, or presumed new, J point elevation ≥0.1 mV is required in all leads other than V2 and V3. In healthy men under age 40, J-point elevation can be as much as 0.25 mV in leads V2 or V3, but it decreases with increasing age. Sex differences require different cut-points for women, since J point elevation in healthy women in leads V2 and V3 is less than in men.38 ‘Contiguous leads’ refers to lead groups such as anterior leads (V1–V6), inferior leads (II, III, aVF) or lateral/apical leads (I, aVL). Supplemental leads such as V3R and V4R reflect the free wall of the right ventricle and V7–V9 the infero-basal wall.Table 3. ECG Manifestations of Acute Myocardial IschaemiaTable 3. ECG Manifestations of Acute Myocardial IschaemiaThe criteria in Table 3 require that the ST shift be present in two or more contiguous leads. For example, ≥0.2 mV of ST elevation in lead V2, and ≥0.1 mV in lead V1, would meet the criteria of two abnormal contiguous leads in a man >40 years old. However, ≥0.1 mV and <0.2 mV of ST elevation, seen only in leads V2–V3 in men (or <0.15 mV in women), may represent a normal finding. It should be noted that, occasionally, acute myocardial ischaemia may create sufficient ST-segment shift to meet the criteria in one lead but have slightly less than the required ST shift in a contiguous lead. Lesser degrees of ST displacement or T wave inversion do not exclude acute myocardial ischaemia or evolving MI, since a single static recording may miss the more dynamic ECG changes that might be detected with serial recordings. ST elevation or diagnostic Q waves in contiguous lead groups are more specific than ST depression in localizing the site of myocardial ischaemia or necrosis.39,40 Supplemental leads, as well as serial ECG recordings, should always be considered in patients that present with ischaemic chest pain and a non-diagnostic initial ECG.41,42 Electrocardiographic evidence of myocardial ischaemia in the distribution of a left circumflex artery is often overlooked and is best captured using posterior leads at the fifth intercostal space (V7 at the left posterior axillary line, V8 at the left mid-scapular line, and V9 at the left paraspinal border). Recording of these leads is strongly recommended in patients with high clinical suspicion for acute circumflex occlusion (for example, initial ECG non-diagnostic, or ST-segment depression in leads V1–3).41 A cut-point of 0.05 mV ST elevation is recommended in leads V7–V9; specificity is increased at a cut-point ≥0.1 mV ST elevation and this cut-point should be used in men <40 years old. ST depression in leads V1–V3 may be suggestive of infero-basal myocardial ischaemia (posterior infarction), especially when the terminal T wave is positive (ST elevation equivalent), however this is non-specific.41–43 In patients with inferior and suspected right ventricular infarction, right pre-cordial leads V3R and V4R should be recorded, since ST elevation ≥0.05 mV (≥0.1 mV in men <30 years old) provides supportive criteria for the diagnosis.42During an episode of acute chest discomfort, pseudo-normalization of previously inverted T waves may indicate acute myocardial ischaemia. Pulmonary embolism, intracranial processes, electrolyte abnormalities, hypothermia, or peri-/myocarditis may also result in ST-T abnormalities and should be considered in the differential diagnosis. The diagnosis of MI is more difficult in the presence of LBBB.44,45 However, concordant ST-segment elevation or a previous ECG may be helpful to determine the presence of acute MI in this setting. In patients with right bundle branch block (RBBB), ST-T abnormalities in leads V1–V3 are common, making it difficult to assess the presence of ischaemia in these leads: however, when new ST elevation or Q waves are found, myocardial ischaemia or infarction should be considered.Prior Myocardial InfarctionAs shown in Table 4, Q waves or QS complexes in the absence of QRS confounders are pathognomonic of a prior MI in patients with ischaemic heart disease, regardless of symptoms.46,47 The specificity of the ECG diagnosis for MI is greatest when Q waves occur in several leads or lead groupings. When the Q waves are associated with ST deviations or T wave changes in the same leads, the likelihood of MI is increased; for example, minor Q waves ≥0.02 sec and <0.03 sec that are ≧0.1 mV deep are suggestive of prior MI if accompanied by inverted T waves in the same lead group. Other validated MI coding algorithms, such as the Minnesota Code and WHO MONICA, have been used in epidemiological studies and clinical trials.3Table 4. ECG Changes Associated With Prior Myocardial Infarction (in Absence of LVH and LBBB)Table 4. ECG Changes Associated With Prior Myocardial Infarction (in Absence of LVH and LBBB)aThe same criteria are used for supplemental leads V7–V9.Silent Myocardial InfarctionAsymptomatic patients who develop new pathologic Q wave criteria for MI detected during routine ECG follow-up, or reveal evidence of MI by cardiac imaging, that cannot be directly attributed to a coronary revascularization procedure, should be termed ‘si lent MI.’48–51 In studies, silent Q wave MI accounted for 9–37% of all non-fatal MI events and were associated with a significantly increased mortality risk.48,49 Improper lead placement or QRS confounders may result in what appear to be new Q waves or QS complexes, as compared to a prior tracing. Thus, the diagnosis of a new silent Q wave MI should be confirmed by a repeat ECG with correct lead placement, or by an imaging study, and by focussed questioning about potential interim ischaemic symptoms.Conditions That Confound the ECG Diagnosis of Myocardial InfarctionA QS complex in lead V1 is normal. A Q wave <0.03 sec and <25% of the R wave amplitude in lead III is normal if the frontal QRS axis is between −30° and 0°. A Q wave may also be normal in aVL if the frontal QRS axis is between 60° and 90°. Septal Q waves are small, non-pathological Q waves <0.03 sec and <25% of the R-wave amplitude in leads I, aVL, aVF, and V4–V6. Pre-excitation, obstructive, dilated or stress cardiomyopathy, cardiac amyloidosis, LBBB, left anterior hemiblock, LVH, right ventricular hypertrophy, myocarditis, acute cor pulmonale, or hyperkalaemia may be associated with Q waves or QS complexes in the absence of MI. ECG abnormalities that mimic myocardial ischaemia or MI are presented in Table 5.Table 5. Common ECG Pitfalls in Diagnos
