Circulation. 2007;116:2634-2653
Published online before print October 19, 2007,
doi: 10.1161/CIRCULATIONAHA.107.187397
(Circulation. 2007;116:2634-2653.)
© 2007 American Heart Association, Inc.
Expert Consensus Document |
Universal Definition of Myocardial Infarction
Kristian Thygesen;
Joseph S. Alpert;
Harvey D. White, on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction;
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)
 |
Introduction
|
|---|
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.
In 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).1
Following 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 Ischemia
|
|---|
The 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 patients
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.
 |
Pathology
|
|---|
Myocardial 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.
1
After 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.1
Myocardial 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.1
Patients 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 Infarction
|
|---|
Clinically the various types of myocardial infarction can be
classified as shown in
Table 1.
On 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 Evaluation
|
|---|
Myocardial 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.
5
The 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.4
If 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.
 |
Reinfarction
|
|---|
Traditionally, 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 Infarction
|
|---|
The 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 Infarction
|
|---|
ECG 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.
22
Table 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.23
Contiguous 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.30
During 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 Infarction
|
|---|
As 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.
Other 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.36,37
 |
Conditions That Confound the ECG Diagnosis of Myocardial Infarction
|
|---|
A 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 V
4-V
6. 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.
 |
Reinfarction
|
|---|
The 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 patient having a lesser degree of ST elevation or new pathognomonic
Q waves, in at least two contiguous leads, particularly when
associated with ischemic symptoms for 20 min or longer. The
re-elevation of the ST segment can, however, also be seen in
threatening myocardial rupture and should lead to additional
diagnostic work-up. ST depression or LBBB on their own should
not be considered valid criteria for myocardial infarction.
 |
Coronary Revascularization
|
|---|
ECG abnormalities during or after percutaneous coronary intervention
(PCI) are similar to those seen during spontaneous myocardial
infarction. In patients who have undergone CABG, new ST-T abnormalities
are common but not necessarily diagnostic of myocardial ischemia.
38 However, when new pathological Q waves (
Table 4) appear in territories
other than those identified before surgery, myocardial infarction
should be considered, particularly if associated with elevated
biomarkers, new wall motion abnormalities, or hemodynamic instability.
 |
Imaging Techniques
|
|---|
Non-invasive imaging plays many roles in patients with known
or suspected myocardial infarction, but this section concerns
only its role in the diagnosis and characterization of infarction.
The underlying rationale is that regional myocardial hypoperfusion
and ischemia lead to a cascade of events including myocardial
dysfunction, cell death, and healing by fibrosis. Important
imaging parameters are therefore perfusion, myocyte viability,
myocardial thickness, thickening, and motion, and the effects
of fibrosis on the kinetics of radiolabeled and paramagnetic
contrast agents.
Commonly used imaging techniques in acute and chronic infarction are echocardiography, radionuclide ventriculography, myocardial perfusion scintigraphy (MPS), and magnetic resonance imaging (MRI). Positron emission tomography (PET) and X-ray computed tomography (CT) are less common. There is considerable overlap in their capabilities, but only the radionuclide techniques provide a direct assessment of myocardial viability because of the properties of the tracers used. Other techniques provide indirect assessments of myocardial viability, such as myocardial function from echocardiography or myocardial fibrosis from MRI.
 |
Echocardiography
|
|---|