Universal Definition of Myocardial Infarction

HomeCirculationVol. 116, No. 22Universal Definition of Myocardial Infarction Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessReview ArticlePDF/EPUBUniversal Definition of Myocardial Infarction Kristian Thygesen, Joseph S. Alpert, Harvey D. White, , TASK FORCE MEMBERS: Chairpersons: Kristian Thygesen (Denmark), Joseph S. Alpert (USA)*, Harvey D. White (New Zealand)* Biomarker Group: Allan S. Jaffe, Coordinator (USA), Fred S. Apple (USA), Marcello Galvani (Italy), Hugo A. Katus (Germany), L. Kristin Newby (USA), Jan Ravkilde (Denmark) ECG Group: Bernard Chaitman, Co-ordinator (USA), Peter M. Clemmensen (Denmark), Mikael Dellborg (Sweden), Hanoch Hod (Israel), Pekka Porela (Finland) Imaging Group: Richard Underwood, Coordinator (UK), Jeroen J. Bax (The Netherlands), George A. Beller (USA), Robert Bonow (USA), Ernst E. Van Der Wall (The Netherlands) Intervention Group: Jean-Pierre Bassand, Co-ordinator (France), William Wijns, Coordinator (Belgium), T. Bruce Ferguson (USA), Philippe G. Steg (France), Barry F. Uretsky (USA), David O. Williams (USA) Clinical Investigation Group: Paul W. Armstrong, Coordinator (Canada), Elliott M. Antman (USA), Keith A. Fox (UK), Christian W. Hamm (Germany), E. Magnus Ohman (USA), Maarten L. Simoons (The Netherlands) Global Perspective Group: Philip A. Poole-Wilson, Coordinator (UK), Enrique P. Gurfinkel (Argentina), José-Luis Lopez-Sendon (Spain), Prem Pais (India), Shanti Mendis (Switzerland), Jun-Ren Zhu (China) Implementation Group: Lars C. Wallentin Coordinator (Sweden), Francisco Fernández-Avilés (Spain), Kim M. Fox (UK), Alexander N. Parkhomenko (Ukraine), Silvia G. Priori (Italy), Michal Tendera (Poland), Liisa-Maria Voipio-Pulkki (Finland) ESC COMMITTEE FOR PRACTICE GUIDELINES Alec Vahanian, Chair (France), A. John Camm (UK), Raffaele De Caterina (Italy), Veronica Dean (France), Kenneth Dickstein (Norway), Gerasimos Filippatos (Greece), Christian Funck-Brentano (France), Irene Hellemans (The Netherlands), Steen Dalby Kristensen (Denmark), Keith McGregor (France), Udo Sechtem (Germany), Sigmund Silber (Germany), Michal Tendera (Poland), Petr Widimsky (Czech Republic), José Luis Zamorano (Spain) DOCUMENT REVIEWERS Joao Morais, Review Coordinator (Portugal), Sorin Brener (USA), Robert Harrington (USA), David Morrow (USA), Udo Sechtem (Germany), Michael Lim (Singapore), Marco A. Martinez-Rios (Mexico), Steve Steinhubl (USA), Glen N. Levine (USA), W. Brian Gibler (USA), David Goff (USA), Marco Tubaro (Italy), Darek Dudek (Poland), Nawwar Al-Attar (France) Kristian ThygesenKristian Thygesen Search for more papers by this author , Joseph S. AlpertJoseph S. Alpert Search for more papers by this author , Harvey D. WhiteHarvey D. White Search for more papers by this author , Search for more papers by this author , TASK FORCE MEMBERS: Chairpersons: Kristian Thygesen (Denmark), Joseph S. Alpert (USA)*, Harvey D. White (New Zealand)* Search for more papers by this author , Biomarker Group: Allan S. Jaffe, Coordinator (USA), Fred S. Apple (USA), Marcello Galvani (Italy), Hugo A. Katus (Germany), L. Kristin Newby (USA), Jan Ravkilde (Denmark) Search for more papers by this author , ECG Group: Bernard Chaitman, Co-ordinator (USA), Peter M. Clemmensen (Denmark), Mikael Dellborg (Sweden), Hanoch Hod (Israel), Pekka Porela (Finland) Search for more papers by this author , Imaging Group: Richard Underwood, Coordinator (UK), Jeroen J. Bax (The Netherlands), George A. Beller (USA), Robert Bonow (USA), Ernst E. Van Der Wall (The Netherlands) Search for more papers by this author , Intervention Group: Jean-Pierre Bassand, Co-ordinator (France), William Wijns, Coordinator (Belgium), T. Bruce Ferguson (USA), Philippe G. Steg (France), Barry F. Uretsky (USA), David O. Williams (USA) Search for more papers by this author , Clinical Investigation Group: Paul W. Armstrong, Coordinator (Canada), Elliott M. Antman (USA), Keith A. Fox (UK), Christian W. Hamm (Germany), E. Magnus Ohman (USA), Maarten L. Simoons (The Netherlands) Search for more papers by this author , Global Perspective Group: Philip A. Poole-Wilson, Coordinator (UK), Enrique P. Gurfinkel (Argentina), José-Luis Lopez-Sendon (Spain), Prem Pais (India), Shanti Mendis (Switzerland), Jun-Ren Zhu (China) Search for more papers by this author , Implementation Group: Lars C. Wallentin Coordinator (Sweden), Francisco Fernández-Avilés (Spain), Kim M. Fox (UK), Alexander N. Parkhomenko (Ukraine), Silvia G. Priori (Italy), Michal Tendera (Poland), Liisa-Maria Voipio-Pulkki (Finland) Search for more papers by this author , ESC COMMITTEE FOR PRACTICE GUIDELINES Search for more papers by this author , Alec Vahanian, Chair (France), A. John Camm (UK), Raffaele De Caterina (Italy), Veronica Dean (France), Kenneth Dickstein (Norway), Gerasimos Filippatos (Greece), Christian Funck-Brentano (France), Irene Hellemans (The Netherlands), Steen Dalby Kristensen (Denmark), Keith McGregor (France), Udo Sechtem (Germany), Sigmund Silber (Germany), Michal Tendera (Poland), Petr Widimsky (Czech Republic), José Luis Zamorano (Spain) Search for more papers by this author , DOCUMENT REVIEWERS Search for more papers by this author and on behalf of Joao Morais, Review Coordinator (Portugal), Sorin Brener (USA), Robert Harrington (USA), David Morrow (USA), Udo Sechtem (Germany), Michael Lim (Singapore), Marco A. Martinez-Rios (Mexico), Steve Steinhubl (USA), Glen N. Levine (USA), W. Brian Gibler (USA), David Goff (USA), Marco Tubaro (Italy), Darek Dudek (Poland), Nawwar Al-Attar (France) Search for more papers by this author and on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction Originally published19 Oct 2007https://doi.org/10.1161/CIRCULATIONAHA.107.187397Circulation. 2007;116:2634–2653Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: October 19, 2007: Previous Version 1 Myocardial infarction is a major cause of death and disability worldwide. Coronary atherosclerosis is a chronic disease with stable and unstable periods. During unstable periods with activated inflammation in the vascular wall, patients may develop a myocardial infarction. Myocardial infarction may be a minor event in a lifelong chronic disease, it may even go undetected, but it may also be a major catastrophic event leading to sudden death or severe hemodynamic deterioration. A myocardial infarction may be the first manifestation of coronary artery disease, or it may occur, repeatedly, in patients with established disease. Information on myocardial infarction attack rates can provide useful data regarding the burden of coronary artery disease within and across populations, especially if standardized data are collected in a manner that demonstrates the distinction between incident and recurrent events. From the epidemiological point of view, the incidence of myocardial infarction in a population can be used as a proxy for the prevalence of coronary artery disease in that population. Furthermore, the term myocardial infarction has 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 and observational studies. With these perspectives, myocardial infarction may be defined from a number of different clinical, electrocardiographic, biochemical, imaging, and pathological characteristics. Download figureDownload PowerPointIn the past, a general consensus existed for the clinical syndrome designated as myocardial infarction. In studies of disease prevalence, the World Health Organization (WHO) defined myocardial infarction from symptoms, ECG abnormalities, and enzymes. However, the development of more sensitive and specific serological biomarkers and precise imaging techniques allows detection of ever smaller amounts of myocardial necrosis. Accordingly, current clinical practice, health care delivery systems, as well as epidemiology and clinical trials all require a more precise definition of myocardial infarction and a re-evaluation of previous definitions of this condition.It should be appreciated that over the years, while more specific biomarkers of myocardial necrosis became available, the accuracy of detecting myocardial infarction has changed. Such changes occurred when glutamine-oxaloacetic transaminase (GOT) was replaced by lactate dehydrogenase (LDH) and later by creatine kinase (CK) and the MB fraction of CK, i.e. CKMB activity and CKMB mass. Current, more specific, and sensitive biomarkers and imaging methods to detect myocardial infarction are further refinements in this evolution.In response to the issues posed by an alteration in our ability to identify myocardial infarction, the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) convened a consensus conference in 1999 in order to re-examine jointly the definition of myocardial infarction (published in the year 2000 in the European Heart Journal and Journal of the American College of Cardiology1). The scientific and societal implications of an altered definition for myocardial infarction were examined from seven points of view: pathological, biochemical, electro-cardiographic, imaging, clinical trials, epidemiological, and public policy. It became apparent from the deliberations of the former consensus committee that the term myocardial infarction should not be used without further qualifications, whether in clinical practice, in the description of patient cohorts, or in population studies. Such qualifications should refer to the amount of myocardial cell loss (infarct size), to the circumstances leading to the infarct (e.g. spontaneous or procedure related), and to the timing of the myocardial necrosis relative to the time of the observation (evolving, healing, or healed myocardial infarction).1Following the 1999 ESC/ACC consensus conference, a group of cardiovascular epidemiologists met to address the specific needs of population surveillance. This international meeting, representing several national and international organizations, published recommendations in Circulation 2003.2 These recommendations addressed the needs of researchers engaged in long-term population trend analysis in the context of changing diagnostic tools using retrospective medical record abstraction. Also considered was surveillance in developing countries and out-of-hospital death, both situations with limited and/or missing data. These recommendations continue to form the basis for epidemiological research.Given the considerable advances in the diagnosis and management of myocardial infarction since the original document was published, the leadership of the ESC, the ACC, and the American Heart Association (AHA) convened, together with the World Heart Federation (WHF), a Global Task Force to update the 2000 consensus document.1 As with the previous consensus committee, the Global Task Force was composed of a number of working groups in order to refine the ESC/ACC criteria for the diagnosis of myocardial infarction from various perspectives. With this goal in mind, the working groups were composed of experts within the field of biomarkers, ECG, imaging, interventions, clinical investigations, global perspectives, and implications. During several Task Force meetings, the recommendations of the working groups were coordinated, resulting in the present updated consensus document.The Task Force recognizes that the definition of myocardial infarction will be subject to a variety of changes in the future as a result of scientific advance. Therefore, this document is not the final word on this issue for all time. Further refinement of the present definition will doubtless occur in the future.Clinical Features of IschemiaThe term myocardial infarction reflects cell death of cardiac myocytes caused by ischemia, which is the result of a perfusion imbalance between supply and demand. Ischemia in a clinical setting most often can be identified from the patient’s history and from the ECG. Possible ischemic symptoms include various combinations of chest, upper extremity, jaw, or epigastric discomfort with exertion or at rest. The discomfort associated with acute myocardial infarction usually lasts at least 20 min. Often, the discomfort is diffuse, not localized, not positional, not affected by movement of the region, and it may be accompanied by dyspnea, diaphoresis, nausea, or syncope.These symptoms are not specific to myocardial ischemia and can be misdiagnosed and thus attributed to gastrointestinal, neurological, pulmonary, or musculoskeletal disorders. Myocardial infarction may occur with atypical symptoms, or even without symptoms, being detected only by ECG, biomarker elevations, or cardiac imaging.PathologyMyocardial infarction is defined by pathology as myocardial cell death due to prolonged ischemia. Cell death is categorized pathologically as coagulation and/or contraction band necrosis, which usually evolves through oncosis, but can result to a lesser degree from apoptosis. Careful analysis of histological sections by an experienced observer is essential to distinguish these entities.1After the onset of myocardial ischemia, cell death is not immediate but takes a finite period to develop (as little as 20 min or less in some animal models). It takes several hours before myocardial necrosis can be identified by macroscopic or microscopic post-mortem examination. Complete necrosis of all myocardial cells at risk requires at least 2–4 h or longer depending on the presence of collateral circulation to the ischemic zone, persistent or intermittent coronary arterial occlusion, the sensitivity of the myocytes to ischemia, pre-conditioning, and/or, finally, individual demand for myocardial oxygen and nutrients. Myocardial infarctions are usually classified by size: microscopic (focal necrosis), small [10% of the left ventricular (LV) myocardium], moderate (10–30% of the LV myocardium), and large (.30% of the LV myocardium), and by location. The pathological identification of myocardial necrosis is made without reference to morphological changes in the coronary arterial tree or to the clinical history.1Myocardial infarction can be defined pathologically as acute, healing, or healed. Acute myocardial infarction is characterized by the presence of polymorphonuclear leukocytes. If the time interval between the onset of the infarction and death is quite brief, e.g. 6 h, minimal or no polymorphonuclear leukocytes may be seen. The presence of mononuclear cells and fibroblasts, and the absence of polymorphonuclear leukocytes characterize healing infarction. Healed infarction is manifested as scar tissue without cellular infiltration. The entire process leading to a healed infarction usually takes at least 5–6 weeks. Reperfusion may alter the macroscopic and microscopic appearance of the necrotic zone by producing myocytes with contraction bands and large quantities of extravasated erythrocytes. Myocardial infarctions can be classified temporally from clinical and other features, as well as according to the pathological appearance, as evolving (,6 h), acute (6 h–7 days), healing (7–28 days), and healed (29 days and beyond). It should be emphasized that the clinical and electrocardiographic timing of the onset of an acute infarction may not correspond exactly with the pathological timing. For example, the ECG may still demonstrate evolving ST-T changes and cardiac biomarkers may still be elevated (implying a recent infarct) at a time when pathologically the infarction is in the healing phase.1Patients who suffer sudden cardiac death with or without ECG changes suggestive of ischemia represent a challenging diagnostic group. Since these individuals die before pathological changes can develop in the myocardium, it is difficult to say with certainty whether these patients succumbed to a myocardial infarction or to an ischemic event that led to a fatal arrhythmia. The mode of death in these cases is sudden, but the etiology remains uncertain unless the individual reported previous symptoms of ischemic heart disease prior to the cardiac arrest. Some patients with or without a history of coronary disease may develop clinical evidence of ischemia, including prolonged and profound chest pain, diaphoresis and/or shortness of breath, and sudden collapse. These individuals may die before blood samples for biomarkers can be obtained, or these individuals may be in the lag phase before cardiac biomarkers can be identified in the blood. These patients may have suffered an evolving, fatal, acute myocardial infarction. If these patients present with presumably new ECG changes, for example ST elevation, and often with symptoms of ischemia, they should be classified as having had a fatal myocardial infarction even if cardiac biomarker evidence of infarction is lacking. Also, patients with evidence of fresh thrombus by coronary angiography (if performed) and/or at autopsy should be classified as having undergone sudden death as a result of myocardial infarction.Clinical Classification of Myocardial InfarctionClinically the various types of myocardial infarction can be classified as shown in Table 1. Download figureDownload PowerPointOn occasion, patients may manifest more than one type of myocardial infarction simultaneously or sequentially. It should also be noted that the term myocardial infarction does not include myocardial cell death associated with mechanical injury from coronary artery bypass grafting (CABG), for example ventricular venting, or manipulation of the heart; nor does it include myocardial necrosis due to miscellaneous causes, e.g. renal failure, heart failure, cardioversion, electrophysiological ablation, sepsis, myocarditis, cardiac toxins, or infiltrative diseases.Biomarker EvaluationMyocardial cell death can be recognized by the appearance in the blood of different proteins released into the circulation from the damaged myocytes: myoglobin, cardiac troponin T and I, CK, LDH, as well as many others.3 Myocardial infarction is diagnosed when blood levels of sensitive and specific biomarkers such as cardiac troponin or CKMB are increased in the clinical setting of acute myocardial ischemia.1 Although elevations in these biomarkers reflect myocardial necrosis, they do not indicate its mechanism.3,4 Thus, an elevated value of cardiac troponin in the absence of clinical evidence of ischemia should prompt a search for other etiologies of myocardial necrosis, such as myocarditis, aortic dissection, pulmonary embolism, congestive heart failure, renal failure, and other examples indicated in Table 2.5Download figureDownload PowerPointThe preferred biomarker for myocardial necrosis is cardiac troponin (I or T), which has nearly absolute myocardial tissue specificity as well as high clinical sensitivity, thereby reflecting even microscopic zones of myocardial necrosis.3 An increased value for cardiac troponin is defined as a measurement exceeding the 99th percentile of a normal reference population (URL = upper reference limit). Detection of a rise and/or fall of the measurements is essential to the diagnosis of acute myocardial infarction.6 The above-mentioned discriminatory percentile is designated as the decision level for the diagnosis of myocardial infarction, and must be determined for each specific assay with appropriate quality control.7–9 Optimal precision [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.10,11 The use of assays that do not have independent validation of optimal precision (CV<10%) is not recommended. The values for the 99th percentile can be found on the International Federation for Clinical Chemistry website http://www.ifcc.org/index.php?option=com_remository&Itemid=120&func=fileinfo&id=7.Blood samples for the measurement of troponin should be drawn on first assessment (often some hours after the onset of symptoms) and 6–9 h later.12 An occasional patient may require an additional sample between 12 and 24 h if the earlier measurements were not elevated and the clinical suspicion of myocardial infarction is high.12 To establish the diagnosis of myocardial infarction, one elevated value above the decision level is required. The demonstration of a rising and/or falling pattern is needed to distinguish background elevated troponin levels, e.g. patients with chronic renal failure (Table 2), from elevations in the same patients which are indicative of myocardial infarction.6 However, this pattern is not absolutely required to make the diagnosis of myocardial infarction if the patient presents >24 h after the onset of symptoms. Troponin values may remain elevated for 7–14 days following the onset of infarction.4If troponin assays are 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 myocardial infarction.9 Gender-specific values should be employed.9 The CKMB measurements should be recorded at the time of the first assessment of the patient and 6–9 h later in order to demonstrate the rise and/or fall exceeding the 99th percentile URL for the diagnosis of myocardial infarction. An occasional patient may require an additional diagnostic sample between 12 and 24 h if the earlier CKMB measurements were not elevated and the clinical suspicion of myocardial infarction is high.Measurement of total CK is not recommended for the diagnosis of myocardial infarction, because of the large skeletal muscle distribution and the lack of specificity of this enzyme.ReinfarctionTraditionally, CKMB has been used to detect reinfarction. However, recent data suggest that troponin values provide similar information.13 In patients where recurrent myocardial infarction is suspected from clinical signs or symptoms following the initial infarction, an immediate measurement of the employed cardiac marker is recommended. A second sample should be obtained 3–6 h later. Recurrent infarction is diagnosed if there is a >20% increase of the value in the second sample. Analytical values are considered to be different if they are different by >3 SDs of the variance of the measures.14 For troponin, this value is 5–7% for most assays at the levels involved with reinfarction. Thus, a 20% change should be considered significant, i.e. over that expected from analytical variability itself. This value should also exceed the 99th percentile URL.Electrocardiographic Detection of Myocardial InfarctionThe ECG is an integral part of the diagnostic work-up of patients with suspected myocardial infarction.1,2,15,16 The acute or evolving changes in the ST-T waveforms and the Q-waves when present potentially allow the clinician to date the event, to suggest the infarct-related artery, and to estimate the amount of myocardium at risk. Coronary artery dominance, size and distribution of arterial segments, collateral vessels, and location, extent, and severity of coronary stenoses can also impact ECG manifestations of myocardial ischemia.17 The ECG by itself is often insufficient to diagnose acute myocardial ischemia or infarction since ST deviation may be observed in other conditions such as acute pericarditis, LV hypertrophy, LBBB, Brugada syndrome, and early repolarization patterns.18 Also Q-waves may occur due to myocardial fibrosis in the absence of coronary artery disease, as in, for example, cardiomyopathy.ECG Abnormalities of Myocardial Ischemia That May Evolve to Myocardial InfarctionECG abnormalities of myocardial ischemia or infarction may be inscribed in the PR segment, the QRS complex, and the ST segment or T-waves. The earliest manifestations of myocardial ischemia are typical T-waves and ST segment changes.19,20 Increased hyper-acute 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. Increased R-wave amplitude and width (giant R-wave with S-wave diminution) are often seen in leads exhibiting ST elevation, and tall T-waves reflecting conduction delay in the ischemic myocardium.21 Transient Q-waves may be observed during an episode of acute ischemia or rarely during acute myocardial infarction with successful reperfusion.22Table 3 lists ECG criteria for the diagnosis of acute myocardial ischemia that may lead to infarction. The J-point is used to determine the magnitude of the ST elevation. J-point elevation in men decreases with increasing age; however, that is not observed in women, in whom J-point elevation is less than in men.23Download figureDownload PowerPointContiguous leads means lead groups such as anterior leads (V1-V6), inferior leads (II, III, and aVF), or lateral/apical leads (I and aVL). More accurate spatial contiguity in the frontal plane can be established by the Cabrera display: aVL, I, aVR, II, aVF, and III.24 Supplemental leads such as V3R and V4R reflect the free wall of the right ventricle.Although the criteria in Table 3 require that the ST shift be present in two or more contiguous leads, it should be noted that occasionally acute myocardial ischemia may create sufficient ST segment shift to meet the criteria in one lead but have slightly less than the required ST shift in an adjacent contiguous lead. Lesser degrees of ST displacement or T-wave inversion in leads without prominent R-wave amplitude do not exclude acute myocardial ischemia or evolving myocardial infarction.ST elevation or diagnostic Q-waves in regional lead groups are more specific than ST depression in localizing the site of myocardial ischemia or necrosis.25,26 However, ST depression in leads V1-V3 suggests myocardial ischemia, especially when the terminal T-wave is positive (ST elevation equivalent), and may be confirmed by concomitant ST elevation >0.1 mV recorded in leads V7-V9.27,28 The term ‘posterior’ to reflect the basal part of the LV wall that lies on the diaphragm is no longer recommended. It is preferable to refer to this territory as inferobasal.29 In patients with inferior myocardial infarction it is advisable to record right precordial leads (V3R and V4R) seeking ST elevation in order to identify concomitant right ventricular infarction.30During an acute episode of chest discomfort, pseudo-normalization of previously inverted T-waves may indicate acute myocardial ischemia. Pulmonary embolism, intracranial processes, or peri-/myocarditis may also result in ST-T abnormalities and should be considered (false positives) in the differential diagnosis.The diagnosis of myocardial infarction is difficult in the presence of LBBB even when marked ST-T abnormalities or ST elevation are present that exceed standard criteria.31,32 A previous ECG may be helpful to determine the presence of acute myocardial infarction 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 ischemia in these leads; however, when ST elevation or Q-waves are found, myocardial ischemia or infarction should be considered. Some patients present with ST elevation or new LBBB, and suffer sudden cardiac death before cardiac biomarkers become abnormal or pathological signs of myocardial necrosis become evident at autopsy. These patients should be classified as having had a fatal myocardial infarction.Prior Myocardial InfarctionAs shown in Table 4, Q-waves or QS complexes in the absence of QRS confounders are usually pathognomonic of a prior myocardial infarction.33–35 The specificity of the ECG diagnosis for myocardial infarction is greatest when Q-waves occur in several leads or lead groupings. ST deviations or T-waves alone are non-specific findings for myocardial necrosis. However, when these abnormalities occur in the same leads as the Q-waves, the likelihood of myocardial infarction is increased. For example, minor Q-waves >0.02 and ,0.03 s that are >0.1 mV deep are suggestive of prior infarction if accompanied by inverted T-waves in the same lead group. Download figureDownload PowerPointOther validated myocardial infarction-coding algorithms, such as the Minnesota code, Novacode, and WHO MONICA, define Q-wave depth on the basis of depth, width, and ratio of R-wave amplitude, such as Q-wave depth at least one-third or one-fifth of R-wave amplitude, and have been used extensively in epidemiological studies and clinical trials.36,37Conditions That Confound the ECG Diagnosis of Myocardial InfarctionA QS complex in lead V1 is normal. A Q-wave ,0.03 s and ,1/4 of the R-wave amplitude in lead III is normal if the frontal QRS axis is between 30 and 0°. The 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 s and ,1/4 of the R-wave amplitude in leads I, aVL, aVF, and V4-V6. Pre-excitation, obstructive or dilated cardiomyopathy, LBBB, RBBB, left anterior hemi-block, left and right ventricular hypertrophy, myocarditis, acute cor pulmonale, or hyperkaliemia may be associated with Q/QS complexes in the absence of myocardial infarction. ECG abnormalities that simulate myocardial ischemia or infarction are presented in Table 5. Download figureDownload PowerPointReinfarctionThe ECG diagnosis of reinfarction following the initial infarction may be confounded by the initial evolutionary ECG changes. Reinfarction should be considered when ST elevation >0.1 mV reoccurs in a