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Revista Española de Cardiología (English Edition) Revista Española de Cardiología (English Edition)
Rev Esp Cardiol. 2014;67:754-64 - Vol. 67 Num.09 DOI: 10.1016/j.rec.2014.04.009

Imaging Techniques in the Evaluation of Post-infarction Function and Scar

Eduardo Pozo a,b, Javier Sanz a,

a The Zena and Michael A. Wiener Cardiovascular Institute and Marie-Josee and Henry R. Kravis Center for Cardiovascular Health; Icahn School of Medicine, New York, United States
b Servicio de Cardiología, Hospital Universitario de La Princesa, Madrid, Spain

Keywords

Myocardial infarction. Imaging techniques. Ventricular function. Scar.

Abstract

Imaging techniques are essential in the clinical evaluation of patients with a myocardial infarction. They are of value for both initial assessment of the ischemic injury and for detection of the subgroup of patients at higher risk of developing cardiovascular events during follow-up. Echocardiography remains the technique of choice for the initial evaluation, owing to its bedside capability to determine strong predictors, such as ventricular volumes, global and regional systolic function, and valvular regurgitation. New techniques for evaluating ventricular mechanics, mainly assessment of ventricular deformation, are revealing important aspects of post-infarction ventricular adaptation. The main alternative to echocardiography is cardiac magnetic resonance imaging. This technique is highly accurate for determining ventricular volumes and ventricular function and has the additional advantage of being able to characterize the myocardium and demonstrate changes associated with the ischemic insult such as necrosis/fibrosis, edema, microvascular obstruction, and intramyocardial hemorrhage. These features not only allow detection and quantification of the infarct size, but also reveal additional characteristics of the scar tissue with prognostic value.

Article

INTRODUCTION

The incidence of acute coronary syndrome in Spain remains high, with around 116 000 new events in 2013, and it is expected to increase in the coming decades.1 Imaging techniques are of great value for establishing a prompt diagnosis in myocardial infarction and for prognostic stratification, enabling identification of patient subgroups at a higher risk of complications during their clinical course. Determination of systolic function and ventricular volumes is the cornerstone for predicting events following a myocardial infarction. To evaluate these parameters, transthoracic echocardiography (TTE) remains the test of choice because of its speed and availability, and cardiac magnetic resonance (CMR) is being increasingly used owing to its excellent reproducibility and accuracy. Alternative modalities, such as nuclear techniques and multidetector computed tomography (MDCT), are also available for this purpose. Another important prognostic factor is the size of the infarct, which can be measured with TTE, nuclear techniques, MDCT or, more accurately, with CMR. In addition, capabilities related to myocardial characterization such as determination of the presence of edema, intramyocardial bleeding, and microvascular obstruction by CMR have emerged over the last few years and have shown prognostic relevance.

The aim of this review is to update evidence on the current use of imaging techniques, particularly CMR, to assess ventricular function and the myocardial scar following infarction (Table). Detailed coverage of residual ischemia detection, another important aspect in post-infarction risk stratification, is beyond the scope of this article.

Role of Imaging Techniques in Assessment Following Myocardial Infarction

  Ventricular function Ventricular mechanics Scar characterization
TTE Technique of choice for the initial assessment because of availability, safety profile, portability, and low cost Most widely used technique Estimation of the scar by myocardial thinning and echogenicity, and regional contractility
 
  Evaluation of global and regional systolic and diastolic function Myocardial velocity by tissue Doppler, with a prognostic impact on calculation of LV filling pressure Quantification of viability using low-dose dobutamine
 
  Additional importance of ventricular remodeling on systolic function Myocardial deformation (strain and strain rate) by tissue Doppler and speckle tracking Possibility to determine microvascular obstruction
Nuclear cardiology Reproducible and non-operator-dependent for assessing systolic function Currently, no techniques are clinical useful Quantification of infarct and viability
 
  Superior to TTE for assessing volumes and RV function   Possibility to determine area at risk
CMR Reference technique for noninvasive assessment of volumes, mass, biventricular function Little clinical application Most accurate quantification of infarct size and transmurality
 
  High reproducibility Determination of deformation through tagging Quantification of viability
      Prognostic impact of scar characteristics: microvascular obstruction, hemorrhage, area at risk
MDCT Accurate Currently, no techniques are clinically useful Feasible to quantify size of the infarct
  Superior to TTE for quantifying volumes and RV function    

CMR, cardiac magnetic resonance; LV, left ventricle; MDCT, multidetector computed tomography; RV, right ventricle; TTE, transthoracic echocardiography.

EVALUATION OF POST-INFARCTION VENTRICULAR FUNCTION AND VENTRICULAR REMODELING Left Ventricular Systolic Function

The left ventricular ejection fraction (LVEF), a powerful predictor of cardiovascular events, is the most widely used parameter in clinical practice to assess the changes occurring in cardiac function after a myocardial infarction.2 However, it is important to keep in mind that both global and regional systolic function can be misleading in the acute phase due to myocardial stunning in noninfarcted segments or compensatory hypercontractility at distant sites. Transthoracic echocardiography is the technique of choice for first-line post-infarction evaluation of ventricular volumes and systolic function.3 Simpson's modified biplanar method is currently recommended, in particular for patients with changes in regional contractility.4 Evaluation of regional contractile function is useful for establishing the diagnosis of an acute coronary syndrome and also has prognostic implications. The wall motion score index, which reflects the extent of contractile dysfunction by estimating the motion index of the 17 left ventricular (LV) segments, has proven to be a predictor of mortality and hospitalization for heart failure following an infarction, regardless of the LVEF.5

Although TTE is widely available, 10% of studies have been estimated to have image quality limitations that hamper interpretation of their findings.6 The use of echocardiographic contrast agents improves visualization of the endocardial border and accuracy in the evaluation of global and regional systolic function.7, 8 In the past, implementation of these agents in acute coronary syndromes was considered contraindicated, but current recommendations allow their use in this context with proper monitoring.9 Another developing echocardiographic technique that has shown increasing clinical utility in daily practice is 3-dimensional echocardiography, particularly in real time. Although a good acoustic window is still required to obtain high-quality studies, this technique enables reformatting of the 3-dimensional data set in any imaging plane and avoids geometric assumptions (Figure 1). In LVEF assessment, 3-dimensional echocardiography has shown excellent correlation and agreement with CMR and better interobserver and intraobserver reproducibility than conventional TTE.10 These findings have been confirmed in infarction patients,11 including in serial follow-up of LV function.12 Nonetheless, it remains controversial whether 3-dimensional echocardiography is also superior to conventional TTE for evaluating regional abnormalities (Figure 1), although administration of contrast agents may improve the diagnostic yield.13

Three-dimensional transthoracic echocardiography of the left ventricle in an experimental infarction model, reformatted in 4-chamber (A), 2-chamber (B), and short-axis (C) views, and analysis of regional contractility (D), which shows apical hypokinesia (in white in the 3-dimensional model). The left ventricular volumes and left-ventricular ejection fraction are shown in the right column. EDV, end-diastolic volume; EF, ejection fraction; ESV, end-systolic volume; SV, stroke volume. Courtesy of Drs. C. Santos-Gallego and J. Badimón.

Figure 1. Three-dimensional transthoracic echocardiography of the left ventricle in an experimental infarction model, reformatted in 4-chamber (A), 2-chamber (B), and short-axis (C) views, and analysis of regional contractility (D), which shows apical hypokinesia (in white in the 3-dimensional model). The left ventricular volumes and left-ventricular ejection fraction are shown in the right column. EDV, end-diastolic volume; EF, ejection fraction; ESV, end-systolic volume; SV, stroke volume. Courtesy of Drs. C. Santos-Gallego and J. Badimón.

The most widely used alternative to TTE is CMR, which is currently considered the noninvasive reference technique for measuring the biventricular ejection fraction.14 This noninvasive technique is highly reproducible, a characteristic that is of particular interest in research because it enables reliable study of smaller samples.15 Furthermore, CMR can accurately evaluate regional contractile function abnormalities.16 Other advantages of this technique include an absence of ionizing radiation exposure and the need for contrast agents, although it is less widely available and more costly than TTE. The LVEF and ventricular volumes can be obtained using synchronized single-photon emission computed tomography (SPECT) studies, which have well-characterized prognostic value.17 This technique is not operator-dependent and does not rely on geometric assumptions, but it does use ionizing radiation, and consequently is not commonly used to measure LV function as the only indication. For this same reason, MDCT is rarely used to determine LV volumes and function exclusively, even though it provides highly accurate measurements.18

Left Ventricular Diastolic Function

In conjunction with systolic function, noninvasive assessment of diastolic function by Doppler TTE study of the transmitral flow pattern to estimate LV filling pressure is an important element in the evaluation of an infarction patient. The impact of a restrictive filling pattern on mortality and the incidence of heart failure was soon evident with the use of this technique19 and was subsequently confirmed.20 A recent meta-analysis reported that the presence of a restrictive pattern (defined as an elevated E/A ratio with a deceleration time of E < 140 ms) identifies a more than 2-fold higher risk of death after adjusting for age, sex, and LVEF.21

The development of tissue Doppler has enabled concomitant measurement of myocardial motion velocities and early diastolic mitral annular velocity (e’) to provide noninvasive estimation of LV filling pressure. In this regard, Hillis et al22 demonstrated that an E/e’ value > 15 in the initial evaluation following infarction was associated with a 5-fold greater risk of death during follow-up. This finding was further supported when the E/e’ was shown to identify a subgroup of patients with greater mortality even in the presence of elevated B-type natriuretic protein values.23 These data indicate that in addition to systolic function, myocardial stiffness and relaxation abnormalities play an additional role to systolic function.

The main limitation of Doppler derives from its dependence on hemodynamic conditions; hence, it would be of interest to use a more stable and reproducible parameter. For this reason, the prognostic relevance of left atrial size has been evaluated. An indexed volume > 32 mL/m2 is a powerful predictor of medium-term24 and long-term25 mortality following infarction, regardless of the presence of mitral regurgitation or atrial fibrillation.

Left Ventricular Dilatation and Remodeling

Early experimental studies26 were quick to establish the importance of ventricular remodeling following an ischemic injury. This phenomenon is defined as a change in the ventricular architecture, consisting of a volume increase and changes in the morphology of the cardiac chambers, occurring following ischemic injury. The initial beneficial effect of LV dilatation to maintain the volume pumped is offset in the long-term by a deleterious effect, likely mediated by neuroendocrine stimulation triggered by increased wall stress. In a meta-analysis by Kramer et al27 analyzing interventional studies in patients with systolic dysfunction and heart failure of ischemic and nonischemic origin, a correlation was found between the changes in ventricular remodeling or the LVEF (measured by different techniques) and the effect on mortality. This could indicate that the benefit of these treatments may be mediated, at least in part, by their effect on these ventricular parameters. Several clinical trials28, 29 have shown that the study of ventricular remodeling, represented by the LV end-diastolic and end-systolic volumes, provides further information in addition to LVEF for predicting major events following a myocardial infarction. LV sphericity, another remodeling parameter, has also proven to be a predictor of mortality, even after adjustment for the LVEF and LV end-systolic volume.30 The reference technique for measuring ventricular volumes is, once again, CMR.14 Although 3 -dimensional TTE shows better agreement with CMR than conventional TTE, it can also underestimate ventricular volumes.10

In addition to ventricular dilatation, ventricular hypertrophy also has prognostic relevance. In an echocardiographic substudy of the VALIANT trial,31 the pattern of ventricular remodeling, defined by the indexed LV mass and relative wall thickness, correlated with the incidence of post-infarction major cardiovascular events. Concentric remodeling, eccentric hypertrophy, and concentric hypertrophy were independently associated with a gradual increase in cardiovascular death, reinfarction, heart failure, stroke, and sudden death during follow-up compared with an absence of LV remodeling.

Right Ventricular Function

Right ventricular (RV) infarction is associated with an increased risk of in-hospital complications and death.32 In autopsy studies, up to 50% of myocardial infarctions show RV involvement;33 however, clinical detection of these abnormalities is less frequent, and TTE has considerable limitations for evaluating RV systolic function.34 Three-dimensional echocardiography35 is superior to conventional TTE for assessing RV infarction and provides optimal identification of patients with right systolic dysfunction. A CMR study36 has confirmed that RV involvement is an independent prognostic marker, regardless of LVEF: an RV ejection fraction < 40% is associated with a 27% absolute increase in the risk of major cardiovascular events at 4 years’ follow-up.

Evaluation of Ventricular Mechanics

The last few years have witnessed significant advances in the study of cardiac mechanics by noninvasive techniques, whose clinical applications are under development. The most important of these is tissue Doppler echocardiography, and in particular, speckle tracking. These modalities enable quantitative determination of the regional myocardial velocity, percentage of strain, and strain rate in radial, longitudinal, and circumferential directions.37 In both animal models38, 39 and clinical studies,40, 41 reductions in these parameters have enabled identification of regional contractility abnormalities. Because myocardial thickening greatly depends on the subendocardial myocardial fibers, a pattern showing a loss of regional radial function with relative preservation from longitudinal and, particularly, circumferential deformation has been proposed as a marker of nontransmural infarction.42, 43 Measurement of global myocardial deformation using these techniques has also been proven to have clinical value. In a study of 659 post-infarction patients, preservation of the global longitudinal strain and strain rate was a better predictor of survival than the LVEF or wall motion score index.44

Myocardial deformation can also be determined using CMR. Myocardial tagging is the most extensively used technique, and many authors consider it the reference method for this purpose.40 A straight-line grid of magnetic saturation signal intensity (tags) is applied to the myocardium and maintained during the cardiac cycle to visualize LV deformation, which can then be quantified by specific post-processing software. An experimental animal model45 showed that differences in contractile function between regions adjacent to the infarction and distal regions persisted during the process of ventricular remodeling. These findings were later corroborated in a clinical study.46 In other CMR sequences, the myocardial signal intensity is proportional to the myocardial velocity (phase contrast), displacement (displacement encoding with stimulated echoes, and deformation (strain-encoded imaging); this enables simpler post-processing and has proven useful in patients with myocardial infarction.47, 48, 49 Preliminary studies have also demonstrated the possibility of analyzing myocardial deformation with MDCT50 and SPECT.51

Echocardiographic techniques for the study of myocardial deformation have also been used to evaluate LV torsion,52, 53 which has been correlated with the intraventricular pressure gradient.54 In patients with myocardial infarction, a reduction in subendocardial twist has been observed that is directly related to the extent of the infarction.55 Following anterolateral infarction, CMR has also shown smaller apical rotation, and a delay and prolongation of diastolic untwisting, which are completely lost in ventricular aneurysms.56

Finally, evaluation of intraventricular fluid dynamics during the cardiac cycle and characterization of vortex by contrast-enhanced TTE (Figure 2) has generated considerable recent interest. Nucifora et al57 have reported that abnormal myocardial vortex parameters show a correlation (although weak) with diastolic function in patients with a myocardial infarction. Nonetheless, these parameters are still a long way from being incorporated into clinical practice.

Flow vortices during isovolumetric contraction in a normal individual (A) and a patient with myocardial infarction (B); a loss of flow coherence is seen after infarction, which worsens coupling between the filling and ejection phases. Courtesy of Drs. M. Amaki and P. Sengupta.

Figure 2. Flow vortices during isovolumetric contraction in a normal individual (A) and a patient with myocardial infarction (B); a loss of flow coherence is seen after infarction, which worsens coupling between the filling and ejection phases. Courtesy of Drs. M. Amaki and P. Sengupta.

CARACTERIZATION OF MYOCARDIAL INFARCTION General Considerations

The size of the infarct has been classically assessed using basic clinical tools such as electrocardiography, enzymatic markers of myocardial injury, and global or regional contractile function abnormalities. Additional characterization of the size of the scar and myocardial viability can be carried out with fully validated techniques, such as dobutamine TTE, SPECT, and positron emission tomography. In recent years, however, CMR has emerged as a multipurpose test that not only enables evaluation of contractility, but also provides better-quality tissue characterization than TTE without using ionizing radiation. Preliminary studies have also reported the possibility of characterizing the infarct with MDCT. This section focusses on the role of imaging techniques in the characterization of the infarct scar, with special emphasis on CMR.

Detection and Quantification of the Infarct

If a significant reduction in coronary flow occurring during an acute coronary syndrome lasts for a sufficient amount of time, the cardiomyocytes undergo gradual necrosis, progressing from the subendocardium to the subepicardium, which is later replaced by myocardial fibrosis. Initially, the presence of interstitial edema in the necrotic territory may reach twice the apparent size of the infarct. Thereafter, gradual replacement of necrotic tissue with fibrosis may reduce the volume by 25%.58 Furthermore, compensatory hypertrophy occurring in the distal segments can change the size of the infarct relative to the total LV mass.59 At around week 6, the infarct size is considered relatively stable,60 which should be taken into account when interpreting the results of imaging studies.

These histological changes can be manifested as an absence of radioisotope detection in the infarcted area by nuclear techniques that have been fully validated for quantifying infarct size, in particular, SPECT.61 More recently, infarct size has been visualized with CMR, through a phenomenon known as late gadolinium enhancement (LGE); that is, an accumulation of contrast in the infarcted regions minutes after contrast is administered.5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30 This is due to a buildup of gadolinium chelates (strictly extracellular agents) within the intracellular space during the acute phase, caused by a loss of integrity of the cardiomyocyte membranes, and within the interstitial space during the chronic phase, caused by expansion of the space during the development of fibrosis.62 The same phenomenon occurs with iodinated contrast agents, and preliminary studies have demonstrated the possibility of studying the infarct with MDCT.63

The capability of of this technique to determine the size of the infarct has been extensively validated in animal models.64 The excellent spatial resolution of LGE enables determination of the degree of transmural infarction (Figure 3). This test has proven to be more sensitive than nuclear medicine tests for detecting subendocardial infarction,65, 66 and is able to detect infarcts as small as 1 g67 (Figure 3). For these reasons, LGE-CMR has become the reference clinical technique for evaluating the myocardial scar. It has shown that the prevalence of subclinical infarction is more common than was previously believed and is associated with a poorer prognosis.68, 69 Moreover, LGE enables detection of specific complications, such as RV infarction (also associated with a poorer prognosis),70 papillary muscle involvement,71 and ventricular thrombus72 (Figure 4).

Visualization of the scar by late gadolinium enhancement. A: Septoapical transmural myocardial infarction (arrowheads) with no residual viability. B: Inferolateral subendocardial infarction (arrows) with extensive residual viability. C: Anteroseptal focal infarction (arrow).

Figure 3. Visualization of the scar by late gadolinium enhancement. A: Septoapical transmural myocardial infarction (arrowheads) with no residual viability. B: Inferolateral subendocardial infarction (arrows) with extensive residual viability. C: Anteroseptal focal infarction (arrow).

A: Extension of an inferoseptal infarction (arrowhead) to the inferior wall of the right ventricle (arrow). B: Infarction of the anterolateral papillary muscle (arrow). C: Anterolateral basal aneurysm with extensive wall thrombosis (arrows).

Figure 4. A: Extension of an inferoseptal infarction (arrowhead) to the inferior wall of the right ventricle (arrow). B: Infarction of the anterolateral papillary muscle (arrow). C: Anterolateral basal aneurysm with extensive wall thrombosis (arrows).

Quantification of infarct size using LGE can be carried out by various techniques. The visual method consists of applying a 5-point scale to each of the 17 LV segments, as follows: 0, no hyperenhancement; 1, 1% to 25% of thickness of the segment; 2, 26% to 50%; 3, 51% to 75%, and 4, 76% to 100%. Infarct size as a percentage of LV myocardium can then be calculated by summing the segment scores and dividing by the number of enhancing segments.73 Various semiautomated quantitative methods for segmentation of the infarct are available, based on application of an intensity threshold as related to the viable distal myocardium. The best criterion seems to be full width at half maximum,74 although there is still controversy around this point. Lastly, the absolute or relative mass of the infarct can be delimited manually. This method is considered accurate and of similar prognostic value if the analysis is performed by expert observers.75 Several studies have confirmed the prognostic relevance of infarct size determined by CMR as a better predictor of major cardiovascular events and mortality than systolic function or ventricular volumes when determined in the acute phase,76 and particularly, in the late phase following an ischemic event.77 The degree of transmurality of the scar has also been identified as a prognostic marker in some studies.78

One of the potential applications of characterizing the scar by LGE is to predict malignant ventricular arrhythmias. The importance of the extent of infarction in the development of ventricular arrhythmia has been investigated retrospectively in patients with coronary disease; the size of the area of LGE was found to be an independent predictor of appropriate defibrillator shocks79 and mortality.80 A later prospective study in patients with a primary indication for defibrillator implantation according to the MADIT (Multicenter Automatic Defibrillator Implantation Trial) criteria confirmed that relative infarct transmurality is an independent predictor (odds ratio = 22.1) of appropriate defibrillator shocks and sudden death.81 The heterogeneity of the scar can be determined by mapping the variations in signal intensity. Heterogeneous areas correspond to the presence of conducting channels, which are the substrate of ventricular arrhythmia after an infarction.82 In addition, the preinfarct, or grey area, has been identified, which contains both necrotic and viable tissue. This has been associated with cardiovascular death,83 inducibility of ventricular arrhythmias,84 and appropriate defibrillator therapy in both primary and secondary prevention.85 However, not all the related studies have found an independent value of this parameter with respect to the total size of the infarct.86

Myocardial Viability

Low-dose dobutamine stress echocardiography and SPECT are extensively validated techniques commonly used in daily practice.87 Positron emission tomography, which mainly detects viability as a mismatch between myocardial perfusion and metabolism (Figure 5), is a highly sensitive technique for predicting functional recovery, although it is less widely available in the clinical setting.87 Microcirculation integrity demonstrated with contrast-enhanced TTE has also been associated with residual viability.88 Similarly, preservation of the parameters indicating global and regional myocardial deformation is inversely related to transmurality and the extension of the infarct,89, 90 and has been proposed as a marker of myocardial viability (Figure 6). Improvements in the regional strain and strain rate with low dobutamine doses also predict viability91 and have shown better diagnostic performance than visual evaluation.92 On CMR, viability can be detected by the increase of contractile function with dobutamine or, more often, by the degree of scar transmurality on LGE. The degree of transmurality is inversely related to the probability that contractility will recover following revascularization in the case of myocardial hibernation93 or spontaneously in the case of myocardial stunning.94 In fact, a recent study has questioned the classic concept that myocardial thinning necessarily indicates inviability by demonstrating improvements in thickness and contractility following revascularization when LGE transmurality is < 50%.95 in general, LGE has a higher sensitivity (95%) and negative predictive value (90%) for predicting segmental functional recovery, while low-dose dobutamine stress echocardiography shows greater specificity (91%) and a higher positive predictive value (93%).96

Polar map demonstrating discordance between decreased inferolateral perfusion at rest measured with rubidium-82 (A) and preserved metabolism measured with fluorodeoxyglucose-18 (B; arrows), which indicates viability. Courtesy of Dr. J. Machac.

Figure 5. Polar map demonstrating discordance between decreased inferolateral perfusion at rest measured with rubidium-82 (A) and preserved metabolism measured with fluorodeoxyglucose-18 (B; arrows), which indicates viability. Courtesy of Dr. J. Machac.

Radial strain measured by speckle tracking before and after reperfusion in a patient with acute infarction. During the coronary occlusion demonstrated by ST segment elevation (A) there is a progressive decrease of radial systolic strain from the base to the apex (C). Over follow-up, despite the presence of Q waves on electrocardiography (B), regional function has recovered (D), which indicates viability. Courtesy of Drs. M. Amaki and P. Sengupta.

Figure 6. Radial strain measured by speckle tracking before and after reperfusion in a patient with acute infarction. During the coronary occlusion demonstrated by ST segment elevation (A) there is a progressive decrease of radial systolic strain from the base to the apex (C). Over follow-up, despite the presence of Q waves on electrocardiography (B), regional function has recovered (D), which indicates viability. Courtesy of Drs. M. Amaki and P. Sengupta.

A substudy of the prospective, randomized STICH97 trial has recently questioned the clinical significance of myocardial viability for deciding whether revascularization is needed in patients with systolic dysfunction of ischemic etiology. Viability was not identified as an independent predictor of 5-year mortality, nor did it show an interaction with the strategy of revascularization in prognosis. Of note, one of the limitations of this study was that less than half the patients initially recruited were included in this subanalysis and that the indication for a viability study was at the discretion of the attending physician. In addition, the study was performed with SPECT and/or dobutamine TTE. In a prospective study of 144 patients,98 the presence of viability on CMR in the absence of complete revascularization was associated with an almost 5-fold increase in mortality, whereas in the absence of significant viability, revascularization did not improve prognosis. Nonetheless, it is questionable whether the use of CMR (or positron emission tomography) would have led to changes in the STICH results.99

Assessment of the Area at Risk and Myocardial Salvage

Standard, noninvasive techniques for evaluating the myocardial area at risk during coronary occlusion require injection of radioisotopes100 or echocardiographic contrast88 before reperfusion. On another note, CMR has been used to detect myocardial edema in the acute and subacute phases of infarction with specific T2-weighted sequences that enable differentiation between acute and chronic infarction101 and identification of patient subgroups at higher risk during an acute coronary syndrome.102 The edematous areas evaluated days after an ischemic event correspond to the area at risk, as has been validated with radioactive microspheres in animal models,103 and by angiographic scores104 and SPECT,105 considered by many the reference technique, in humans. The area of myocardium at risk defined by T2-weighted sequences is always larger than the size of the infarct determined by LGE, and the myocardial salvage index is calculated as the difference between the 2 values (Figure 7). This parameter has been identified as an independent predictor of mortality and major cardiovascular events at 6 months106 and 18107 months following infarction. Furthermore, determination of the size of the infarct, area at risk, and myocardial salvage is extremely useful in the evaluation of new cardioprotective therapies.108

Calculation of myocardial salvage by demonstration of edema (A and C, arrowheads) and late gadolinium enhancement (B and D, arrows) in an experimental infarction model. The upper row shows an animal in which the areas at risk (edema) and the infarcted areas (late gadolinium enhancement) are similar, indicating little myocardial salvage. The lower row shows another animal, in which the area at risk is much larger than the infarction, which indicates extensive myocardial salvage. Courtesy of Drs. C. Santos-Gallego and J. Badimón.

Figure 7. Calculation of myocardial salvage by demonstration of edema (A and C, arrowheads) and late gadolinium enhancement (B and D, arrows) in an experimental infarction model. The upper row shows an animal in which the areas at risk (edema) and the infarcted areas (late gadolinium enhancement) are similar, indicating little myocardial salvage. The lower row shows another animal, in which the area at risk is much larger than the infarction, which indicates extensive myocardial salvage. Courtesy of Drs. C. Santos-Gallego and J. Badimón.

Microvascular Obstruction and Hemorrhage in Infarction

In addition to infarct size the infarct, other aspects related to characterization of the scar also have a prognostic impact. Injury to the myocardial microcirculation can ensue in relation to severe ischemic injury or the reperfusion carried out. This occurrence, which is known as microvascular obstruction or no-reflow phenomenon, has been classically evaluated with contrast-enhanced TTE, which demonstrates myocardial perfusion abnormalities.88 More recently, this assessment has been done with CMR, in which the microvascular obstruction is visualized as a persistent perfusion defect in first-pass sequences or as an unenhanced area in the center of the scar on LGE109 (Figure 8). Microvascular obstruction is a powerful independent predictor of a permanent inability to recover contractility, adverse remodeling, and subsequent cardiovascular events.110, 111

A: Microvascular obstruction, seen as a hypointense area (arrowheads) in the center of the infarction (arrows). B: Intramyocardial hemorrhage, visualized as a hypointense area (arrowheads) in the center of the edematous area (arrows).

Figure 8. A: Microvascular obstruction, seen as a hypointense area (arrowheads) in the center of the infarction (arrows). B: Intramyocardial hemorrhage, visualized as a hypointense area (arrowheads) in the center of the edematous area (arrows).

In addition, microvascular ischemic injury can cause extravasation of blood and hemorrhage in the infarct, particularly after reperfusion. On CMR this is seen as hypointense areas on T2-weighted sequences,112 or more specifically, on T2*-weighted sequences,113 owing to the presence of products of hemoglobin breakdown (Figure 8). Hemorrhage in the infarct area has also been associated with larger infarct size, adverse ventricular remodeling, and an absence of improvement in contractile function.112, 114

CONFLICT OF INTERESTS

None declared.


☆ Section sponsored by Laboratory AstraZeneca.

Received 3 April 2014
Accepted 28 April 2014

Corresponding author: Cardiovascular Institute, Mount Sinai Hospital, One Gustave L. Levy Place, Box 1030, New York, NY 10029, United States. Javier.Sanz@mountsinai.org

Bibliography

1. Dégano IR, Elosua R, Marrugat J. Epidemiología del síndrome coronario agudo en España: estimación del número de casos y la tendencia de 2005 a 2049. Rev Esp Cardiol. 2013;66:472-81.
Medline
2. Candell Riera J. Estratificación pronóstica tras infarto agudo de miocardio. Rev Esp Cardiol. 2003;56:303-13.
Medline
3. Steg PG, James SK, Atar D, Badano LP, Blomstrom-Lundqvist C, Borger MA, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33:2569-619.
Medline
4. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440-63.
Medline
5. Moller JE, Hillis GS, Oh JK, Reeder GS, Gersh BJ, Pellikka PA. Wall motion score index and ejection fraction for risk stratification after acute myocardial infarction. Am Heart J. 2006;151:419-25.
Medline
6. Forteza Albertí JF, Gómez de Diego JJ, Vivancos Delgado R, Candell Riera J, Aguilar Torres R. Situación actual: lo nuevo en técnicas de imagen cardiaca. Rev Esp Cardiol. 2012;65(Supl 1):24-34.
Medline
7. Hoffmann R, Von Bardeleben S, Kasprzak JD, Borges AC, Ten Cate F, Firschke C, et al. Analysis of regional left ventricular function by cineventriculography, cardiac magnetic resonance imaging, and unenhanced and contrast-enhanced echocardiography: a multicenter comparison of methods. J Am Coll Cardiol. 2006;47:121-8.
Medline
8. Hoffmann R, Von Bardeleben S, Ten Cate F, Borges AC, Kasprzak J, Firschke C, et al. Assessment of systolic left ventricular function: a multi-centre comparison of cineventriculography, cardiac magnetic resonance imaging, unenhanced and contrast-enhanced echocardiography. Eur Heart J. 2005;26:607-16.
Medline
9. Mulvagh SL, Rakowski H, Vannan MA, Abdelmoneim SS, Becher H, Bierig SM, et al. American Society of Echocardiography consensus statement on the clinical applications of ultrasonic contrast agents in echocardiography. J Am Soc Echocardiogr. 2008;21:1179-201. quiz, 1281
Medline
10. Dorosz JL, Lezotte DC, Weitzenkamp DA, Allen LA, Salcedo EE. Performance of 3-dimensional echocardiography in measuring left ventricular volumes and ejection fraction: a systematic review and meta-analysis. J Am Coll Cardiol. 2012;59:1799-808.
Medline
11. Jenkins C, Moir S, Chan J, Rakhit D, Haluska B, Marwick TH. Left ventricular volume measurement with echocardiography: a comparison of left ventricular opacification, three-dimensional echocardiography, or both with magnetic resonance imaging. Eur Heart J. 2009;30:98-106.
Medline
12. Jenkins C, Bricknell K, Chan J, Hanekom L, Marwick TH. Comparison of two-and three-dimensional echocardiography with sequential magnetic resonance imaging for evaluating left ventricular volume and ejection fraction over time in patients with healed myocardial infarction. Am J Cardiol. 2007;99:300-6.
Medline
13. Hoffmann R, Von Bardeleben S, Barletta G, Pasques A, Kasprzak J, Greis C, et al. Comparison of two-and three-dimensional unenhanced and contrast-enhanced echocardiographies versus cineventriculography versus cardiac magnetic resonance for determination of left ventricular function. Am J Cardiol. 2014;113:395-401.
Medline
14. Hendel RC, Patel MR, Kramer CM, Poon M, Hendel RC, Carr JC, et al. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging: a report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American College of Radiology, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, American Society of Nuclear Cardiology, North American Society for Cardiac Imaging, Society for Cardiovascular Angiography and Interventions, and Society of Interventional Radiology. J Am Coll Cardiol. 2006;48:1475-97.
Medline
15. Bellenger NG, Marcus NJ, Rajappan K, Yacoub M, Banner NR, Pennell DJ. Comparison of techniques for the measurement of left ventricular function following cardiac transplantation. J Cardiovasc Magn Reson. 2002;4:255-63.
Medline
16. Holman ER, Buller VG, De Roos A, Van der Geest RJ, Baur LH, Van der Laarse A, et al. Detection and quantification of dysfunctional myocardium by magnetic resonance imaging. A new three-dimensional method for quantitative wall-thickening analysis. Circulation. 1997;95:924-31.
Medline
17. Marcassa C, Bax JJ, Bengel F, Hesse B, Petersen CL, Reyes E, et al. Clinical value, cost-effectiveness, and safety of myocardial perfusion scintigraphy: a position statement. Eur Heart J. 2008;29:557-63.
Medline
18. Fuchs A, Kuhl JT, Lonborg J, Engstrom T, Vejlstrup N, Kober L, et al. Automated assessment of heart chamber volumes and function in patients with previous myocardial infarction using multidetector computed tomography. J Cardiovasc Comput Tomogr. 2012;6:325-34.
Medline
19. Oh JK, Ding ZP, Gersh BJ, Bailey KR, Tajik AJ. Restrictive left ventricular diastolic filling identifies patients with heart failure after acute myocardial infarction. J Am Soc Echocardiogr. 1992;5:497-503.
Medline
20. Nijland F, Kamp O, Karreman AJ, Van Eenige MJ, Visser CA. Prognostic implications of restrictive left ventricular filling in acute myocardial infarction: a serial Doppler echocardiographic study. J Am Coll Cardiol. 1997;30:1618-24.
Medline
21. Moller JE, Whalley GA, Dini FL, Doughty RN, Gamble GD, Klein AL, et al. Independent prognostic importance of a restrictive left ventricular filling pattern after myocardial infarction: an individual patient meta-analysis: Meta-Analysis Research Group in Echocardiography acute myocardial infarction. Circulation. 2008;117:2591-8.
Medline
22. Hillis GS, Moller JE, Pellikka PA, Gersh BJ, Wright RS, Ommen SR, et al. Noninvasive estimation of left ventricular filling pressure by E/e’is a powerful predictor of survival after acute myocardial infarction. J Am Coll Cardiol. 2004;43:360-7.
Medline
23. Kruszewski K, Scott AE, Barclay JL, Small GR, Croal BL, Moller JE, et al. Noninvasive assessment of left ventricular filling pressure after acute myocardial infarction: a prospective study of the relative prognostic utility of clinical assessment, echocardiography, and B-type natriuretic peptide. Am Heart J. 2010;159:47-54.
Medline
24. Moller JE, Hillis GS, Oh JK, Seward JB, Reeder GS, Wright RS, et al. Left atrial volume: a powerful predictor of survival after acute myocardial infarction. Circulation. 2003;107:2207-12.
Medline
25. Beinart R, Boyko V, Schwammenthal E, Kuperstein R, Sagie A, Hod H, et al. Long-term prognostic significance of left atrial volume in acute myocardial infarction. J Am Coll Cardiol. 2004;44:327-34.
Medline
26. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990;81:1161-72.
Medline
27. Kramer DG, Trikalinos TA, Kent DM, Antonopoulos GV, Konstam MA, Udelson JE. Quantitative evaluation of drug or device effects on ventricular remodeling as predictors of therapeutic effects on mortality in patients with heart failure and reduced ejection fraction: a meta-analytic approach. J Am Coll Cardiol. 2010;56:392-406.
Medline
28. Migrino RQ, Young JB, Ellis SG, White HD, Lundergan CF, Miller DP, et al. End-systolic volume index at 90 to 180 minutes into reperfusion therapy for acute myocardial infarction is a strong predictor of early and late mortality. The Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO)-I Angiographic Investigators. Circulation. 1997;96:116-21.
Medline
29. Solomon SD, Skali H, Anavekar NS, Bourgoun M, Barvik S, Ghali JK, et al. Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction. Circulation. 2005;111:3411-9.
Medline
30. Wong SP, French JK, Lydon AM, Manda SO, Gao W, Ashton NG, et al. Relation of left ventricular sphericity to 10-year survival after acute myocardial infarction. Am J Cardiol. 2004;94:1270-5.
Medline
31. Verma A, Meris A, Skali H, Ghali JK, Arnold JM, Bourgoun M, et al. Prognostic implications of left ventricular mass and geometry following myocardial infarction: the VALIANT (VALsartan In Acute myocardial iNfarcTion) Echocardiographic Study. JACC Cardiovasc Imaging. 2008;1:582-91.
Medline
32. Zehender M, Kasper W, Kauder E, Schonthaler M, Geibel A, Olschewski M, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med. 1993;328:981-8.
Medline
33. Andersen HR, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol. 1987;10:1223-32.
Medline
34. Oldershaw P. Assessment of right ventricular function and its role in clinical practice. Br Heart J. 1992;68:12-5.
Medline
35. Kidawa M, Chizynski K, Zielinska M, Kasprzak JD, Krzeminska-Pakula M. Real-time 3D echocardiography and tissue Doppler echocardiography in the assessment of right ventricle systolic function in patients with right ventricular myocardial infarction. Eur Heart J Cardiovasc Imaging. 2013;14:1002-9.
Medline
36. Miszalski-Jamka T, Klimeczek P, Tomala M, Krupinski M, Zawadowski G, Noelting J, et al. Extent of RV dysfunction and myocardial infarction assessed by CMR are independent outcome predictors early after STEMI treated with primary angioplasty. JACC Cardiovasc Imaging. 2010;3:1237-46.
Medline
37. Mor-Avi V, Lang RM, Badano LP, Belohlavek M, Cardim NM, Derumeaux G, et al. Current and evolving echocardiographic techniques for the quantitative evaluation of cardiac mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of Echocardiography. Eur J Echocardiogr. 2011;12:167-205.
Medline
38. Derumeaux G, Ovize M, Loufoua J, Andre-Fouet X, Minaire Y, Cribier A, et al. Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion. Circulation. 1998;97:1970-7.
Medline
39. Pirat B, Khoury DS, Hartley CJ, Tiller L, Rao L, Schulz DG, et al. A novel feature-tracking echocardiographic method for the quantitation of regional myocardial function: validation in an animal model of ischemia-reperfusion. J Am Coll Cardiol. 2008;51:651-9.
Medline
40. Edvardsen T, Gerber BL, Garot J, Bluemke DA, Lima JA, Smiseth OA. Quantitative assessment of intrinsic regional myocardial deformation by Doppler strain rate echocardiography in humans: validation against three-dimensional tagged magnetic resonance imaging. Circulation. 2002;106:50-6.
Medline
41. Helle-Valle T, Remme EW, Lyseggen E, Pettersen E, Vartdal T, Opdahl A, et al. Clinical assessment of left ventricular rotation and strain: a novel approach for quantification of function in infarcted myocardium and its border zones. Am J Physiol Heart Circ Physiol. 2009;297:H257-67.
Medline
42. Chan J, Hanekom L, Wong C, Leano R, Cho GY, Marwick TH. Differentiation of subendocardial and transmural infarction using two-dimensional strain rate imaging to assess short-axis and long-axis myocardial function. J Am Coll Cardiol. 2006;48:2026-33.
Medline
43. Becker M, Ocklenburg C, Altiok E, Futing A, Balzer J, Krombach G, et al. Impact of infarct transmurality on layer-specific impairment of myocardial function: a myocardial deformation imaging study. Eur Heart J. 2009;30:1467-76.
Medline
44. Antoni ML, Mollema SA, Delgado V, Atary JZ, Borleffs CJ, Boersma E, et al. Prognostic importance of strain and strain rate after acute myocardial infarction. Eur Heart J. 2010;31:1640-7.
Medline
45. Kramer CM, Lima JA, Reichek N, Ferrari VA, Llaneras MR, Palmon LC, et al. Regional differences in function within noninfarcted myocardium during left ventricular remodeling. Circulation. 1993;88:1279-88.
Medline
46. Marcus JT, Gotte MJ, Van Rossum AC, Kuijer JP, Heethaar RM, Axel L, et al. Myocardial function in infarcted and remote regions early after infarction in man: assessment by magnetic resonance tagging and strain analysis. Magn Reson Med. 1997;38:803-10.
Medline
47. Markl M, Schneider B, Hennig J, Peschl S, Winterer J, Krause T, et al. Cardiac phase contrast gradient echo MRI: measurement of myocardial wall motion in healthy volunteers and patients. Int J Card Imaging. 1999;15:441-52.
Medline
48. Le Y, Stein A, Berry C, Kellman P, Bennett EE, Taylor J, et al. Simultaneous myocardial strain and dark-blood perfusion imaging using a displacement-encoded MRI pulse sequence. Magn Reson Med. 2010;64:787-98.
Medline
49. Neizel M, Korosoglou G, Lossnitzer D, Kuhl H, Hoffmann R, Ocklenburg C, et al. Impact of systolic and diastolic deformation indexes assessed by strain-encoded imaging to predict persistent severe myocardial dysfunction in patients after acute myocardial infarction at follow-up. J Am Coll Cardiol. 2010;56:1056-62.
Medline
50. Helle-Valle TM, Yu WC, Fernandes VR, Rosen BD, Lima JA. Usefulness of radial strain mapping by multidetector computer tomography to quantify regional myocardial function in patients with healed myocardial infarction. Am J Cardiol. 2010;106:483-91.
Medline
51. Yamamoto A, Takahashi N, Munakata K, Hosoya T, Shiiba M, Okuyama T, et al. Global and regional evaluation of systolic and diastolic left ventricular temporal parameters using a novel program for ECG-gated myocardial perfusion SPECT—validation by comparison with gated equilibrium radionuclide angiography and speckle-tracking radial strain from echocardiography. Ann Nucl Med. 2007;21:115-21.
Medline
52. Notomi Y, Lysyansky P, Setser RM, Shiota T, Popovic ZB, Martin-Miklovic MG, et al. Measurement of ventricular torsion by two-dimensional ultrasound speckle tracking imaging. J Am Coll Cardiol. 2005;45:2034-41.
Medline
53. Notomi Y, Setser RM, Shiota T, Martin-Miklovic MG, Weaver JA, Popovic ZB, et al. Assessment of left ventricular torsional deformation by Doppler tissue imaging: validation study with tagged magnetic resonance imaging. Circulation. 2005;111:1141-7.
Medline
54. Burns AT, La Gerche A, Prior DL, Macisaac AI. Left ventricular untwisting is an important determinant of early diastolic function. JACC Cardiovasc Imaging. 2009;2:709-16.
Medline
55. Bertini M, Delgado V, Nucifora G, Ajmone Marsan N, Ng AC, Shanks M, et al. Left ventricular rotational mechanics in patients with coronary artery disease: differences in subendocardial and subepicardial layers. Heart. 2010;96:1737-43.
Medline
56. Nagel E, Stuber M, Lakatos M, Scheidegger MB, Boesiger P, Hess OM. Cardiac rotation and relaxation after anterolateral myocardial infarction. Coron Artery Dis. 2000;11:261-7.
Medline
57. Nucifora G, Delgado V, Bertini M, Marsan NA, Van de Veire NR, Ng AC, et al. Left ventricular muscle and fluid mechanics in acute myocardial infarction. Am J Cardiol. 2010;106:1404-9.
Medline
58. Reimer KA, Jennings RB. The “wavefront phenomenon”of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest. 1979;40:633-44.
Medline
59. Fieno DS, Hillenbrand HB, Rehwald WG, Harris KR, Decker RS, Parker MA, et al. Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size. J Am Coll Cardiol. 2004;43:2124-31.
Medline
60. Kim HW, Farzaneh-Far A, Kim RJ. Cardiovascular magnetic resonance in patients with myocardial infarction: current and emerging applications. J Am Coll Cardiol. 2009;55:1-16.
Medline
61. Gibbons RJ, Valeti US, Araoz PA, Jaffe AS. The quantification of infarct size. J Am Coll Cardiol. 2004;44:1533-42.
Medline
62. Kim RJ, Choi KM, Judd RM. Assessment of myocardial viability by contrast enhancement. En: Higgins C.B., Roos A.D., editors. Cardiovascular MRI and MRA. Philadelphia: Lippincott;2003. 209-37.
63. Gerber BL, Belge B, Legros GJ, Lim P, Poncelet A, Pasquet A, et al. Characterization of acute and chronic myocardial infarcts by multidetector computed tomography: comparison with contrast-enhanced magnetic resonance. Circulation. 2006;113:823-33.
Medline
64. Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation. 1999;100:1992-2002.
Medline
65. Klein C, Nekolla SG, Bengel FM, Momose M, Sammer A, Haas F, et al. Assessment of myocardial viability with contrast-enhanced magnetic resonance imaging: comparison with positron emission tomography. Circulation. 2002;105:162-7.
Medline
66. Wagner A, Mahrholdt H, Holly TA, Elliott MD, Regenfus M, Parker M, et al. Contrast-enhanced MRI and routine single photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study. Lancet. 2003;361:374-9.
Medline
67. Ricciardi MJ, Wu E, Davidson CJ, Choi KM, Klocke FJ, Bonow RO, et al. Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation. Circulation. 2001;103:2780-3.
Medline
68. Kwong RY, Chan AK, Brown KA, Chan CW, Reynolds HG, Tsang S, et al. Impact of unrecognized myocardial scar detected by cardiac magnetic resonance imaging on event-free survival in patients presenting with signs or symptoms of coronary artery disease. Circulation. 2006;113:2733-43.
Medline
69. Schelbert EB, Cao JJ, Sigurdsson S, Aspelund T, Kellman P, Aletras AH, et al. Prevalence and prognosis of unrecognized myocardial infarction determined by cardiac magnetic resonance in older adults. JAMA. 2012;308:890-6.
Medline
70. Grothoff M, Elpert C, Hoffmann J, Zachrau J, Lehmkuhl L, De Waha S, et al. Right ventricular injury in ST-elevation myocardial infarction: risk stratification by visualization of wall motion, edema, and delayed-enhancement cardiac magnetic resonance. Circ Cardiovasc Imaging. 2012;5:60-8.
Medline
71. Tanimoto T, Imanishi T, Kitabata H, Nakamura N, Kimura K, Yamano T, et al. Prevalence and clinical significance of papillary muscle infarction detected by late gadolinium-enhanced magnetic resonance imaging in patients with ST-segment elevation myocardial infarction. Circulation. 2010;122:2281-7.
Medline
72. Mollet NR, Dymarkowski S, Volders W, Wathiong J, Herbots L, Rademakers FE, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation. 2002;106:2873-6.
Medline
73. Kim RJ, Albert TS, Wible JH, Elliott MD, Allen JC, Lee JC, et al. Performance of delayed-enhancement magnetic resonance imaging with gadoversetamide contrast for the detection and assessment of myocardial infarction: an international, multicenter, double-blinded, randomized trial. Circulation. 2008;117:629-37.
Medline
74. Amado LC, Gerber BL, Gupta SN, Rettmann DW, Szarf G, Schock R, et al. Accurate and objective infarct sizing by contrast-enhanced magnetic resonance imaging in a canine myocardial infarction model. J Am Coll Cardiol. 2004;44:2383-9.
Medline
75. Husser O, Bodí V, Sanchis J, Núñez J, Mainar L, Merlos P, et al. Head to head comparison of quantitative versus visual analysis of contrast CMR in the setting of myocardial stunning after STEMI: implications on late systolic function and patient outcome. Int J Cardiovasc Imaging. 2010;26:559-69.
Medline
76. El Aidi H, Adams A, Moons KG, Den Ruijter HM, Mali WP, Doevendans PA, et al. Cardiac magnetic resonance imaging findings and the risk of cardiovascular events in patients with recent myocardial infarction or suspected or known coronary artery disease: a systematic review of prognostic studies. J Am Coll Cardiol. 2014;63:1031-45.
Medline
77. Kwon DH, Halley CM, Carrigan TP, Zysek V, Popovic ZB, Setser R, et al. Extent of left ventricular scar predicts outcomes in ischemic cardiomyopathy patients with significantly reduced systolic function: a delayed hyperenhancement cardiac magnetic resonance study. JACC Cardiovasc Imaging. 2009;2:34-44.
Medline
78. Merlos P, López-Lereu MP, Monmeneu JV, Sanchis J, Núñez J, Bonanad C, et al. Valor pronóstico a largo plazo del análisis completo de los índices de resonancia magnética cardiaca tras un infarto de miocardio con elevación del segmento ST. Rev Esp Cardiol. 2013;66:613-22.
Medline
79. Scott PA, Morgan JM, Carroll N, Murday DC, Roberts PR, Peebles CR, et al. The extent of left ventricular scar quantified by late gadolinium enhancement MRI is associated with spontaneous ventricular arrhythmias in patients with coronary artery disease and implantable cardioverter-defibrillators. Circ Arrhythm Electrophysiol. 2011;4:324-30.
Medline
80. Kwon DH, Hachamovitch R, Adeniyi A, Nutter B, Popovic ZB, Wilkoff BL, et al. Myocardial scar burden predicts survival benefit with implantable cardioverter defibrillator implantation in patients with severe ischaemic cardiomyopathy: influence of gender. Heart. 2014;100:206-13.
Medline
81. Boye P, Abdel-Aty H, Zacharzowsky U, Bohl S, Schwenke C, Van der Geest RJ, et al. Prediction of life-threatening arrhythmic events in patients with chronic myocardial infarction by contrast-enhanced CMR. JACC Cardiovasc Imaging. 2011;4:871-9.
Medline
82. Perez-David E, Arenal A, Rubio-Guivernau JL, Del Castillo R, Atea L, Arbelo E, et al. Noninvasive identification of ventricular tachycardia-related conducting channels using contrast-enhanced magnetic resonance imaging in patients with chronic myocardial infarction: comparison of signal intensity scar mapping and endocardial voltage mapping. J Am Coll Cardiol. 2011;57:184-94.
Medline
83. Yan AT, Shayne AJ, Brown KA, Gupta SN, Chan CW, Luu TM, et al. Characterization of the peri-infarct zone by contrast-enhanced cardiac magnetic resonance imaging is a powerful predictor of post-myocardial infarction mortality. Circulation. 2006;114:32-9.
Medline
84. Schmidt A, Azevedo CF, Cheng A, Gupta SN, Bluemke DA, Foo TK, et al. Infarct tissue heterogeneity by magnetic resonance imaging identifies enhanced cardiac arrhythmia susceptibility in patients with left ventricular dysfunction. Circulation. 2007;115:2006-14.
Medline
85. Roes SD, Borleffs CJ, Van der Geest RJ, Westenberg JJ, Marsan NA, Kaandorp TA, et al. Infarct tissue heterogeneity assessed with contrast-enhanced MRI predicts spontaneous ventricular arrhythmia in patients with ischemic cardiomyopathy and implantable cardioverter-defibrillator. Circ Cardiovasc Imaging. 2009;2:183-90.
Medline
86. De Haan S, Meijers TA, Knaapen P, Beek AM, Van Rossum AC, Allaart CP. Scar size and characteristics assessed by CMR predict ventricular arrhythmias in ischaemic cardiomyopathy: comparison of previously validated models. Heart. 2011;97:1951-6.
Medline
87. Schinkel AF, Bax JJ, Poldermans D, Elhendy A, Ferrari R, Rahimtoola SH. Hibernating myocardium: diagnosis and patient outcomes. Curr Probl Cardiol. 2007;32:375-410.
Medline
88. Pérez de Isla L, Rodrigo JL, Almería C, Pérez Ferro M, Serra V, Zamorano JL. Myocardial contrast echocardiography in coronary artery disease. Eur J Echocardiogr. 2004;5(Suppl 2):S11-6.
Medline
89. Roes SD, Mollema SA, Lamb HJ, Van der Wall EE, De Roos A, Bax JJ. Validation of echocardiographic two-dimensional speckle tracking longitudinal strain imaging for viability assessment in patients with chronic ischemic left ventricular dysfunction and comparison with contrast-enhanced magnetic resonance imaging. Am J Cardiol. 2009;104:312-7.
Medline
90. Zhang Y, Chan AK, Yu CM, Yip GW, Fung JW, Lam WW, et al. Strain rate imaging differentiates transmural from non-transmural myocardial infarction: a validation study using delayed-enhancement magnetic resonance imaging. J Am Coll Cardiol. 2005;46:864-71.
Medline
91. Bansal M, Jeffriess L, Leano R, Mundy J, Marwick TH. Assessment of myocardial viability at dobutamine echocardiography by deformation analysis using tissue velocity and speckle-tracking. JACC Cardiovasc Imaging. 2010;3:121-31.
Medline
92. Hanekom L, Jenkins C, Jeffries L, Case C, Mundy J, Hawley C, et al. Incremental value of strain rate analysis as an adjunct to wall-motion scoring for assessment of myocardial viability by dobutamine echocardiography: a follow-up study after revascularization. Circulation. 2005;112:3892-900.
Medline
93. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000;343:1445-53.
Medline
94. Choi KM, Kim RJ, Gubernikoff G, Vargas JD, Parker M, Judd RM. Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function. Circulation. 2001;104:1101-7.
Medline
95. Shah DJ, Kim HW, James O, Parker M, Wu E, Bonow RO, et al. Prevalence of regional myocardial thinning and relationship with myocardial scarring in patients with coronary artery disease. JAMA. 2013;309:909-18.
Medline
96. Romero J, Xue X, Gonzalez W, Garcia MJ. CMR imaging assessing viability in patients with chronic ventricular dysfunction due to coronary artery disease: a meta-analysis of prospective trials. JACC Cardiovasc Imaging. 2012;5:494-508.
Medline
97. Bonow RO, Maurer G, Lee KL, Holly TA, Binkley PF, Desvigne-Nickens P, et al. Myocardial viability and survival in ischemic left ventricular dysfunction. N Engl J Med. 2011;364:1617-25.
Medline
98. Gerber BL, Rousseau MF, Ahn SA, Le Polain de Waroux JB, Pouleur AC, Phlips T, et al, STICH Trial Investigators. Prognostic value of myocardial viability by delayed-enhanced magnetic resonance in patients with coronary artery disease and low ejection fraction: impact of revascularization therapy. J Am Coll Cardiol. 2012;59:825-35.
Medline
99. Asrani NS, Chareonthaitawee P, Pellikka PA. Viability by MRI or PET would not have changed the results of the STICH trial. Prog Cardiovasc Dis. 2013;55:494-7.
Medline
100. Botker HE, Kaltoft AK, Pedersen SF, Kim WY. Measuring myocardial salvage. Cardiovasc Res. 2012;94:266-75.
Medline
101. Abdel-Aty H, Zagrosek A, Schulz-Menger J, Taylor AJ, Messroghli D, Kumar A, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation. 2004;109:2411-6.
Medline
102. Raman SV, Simonetti OP, Winner MW, Dickerson JA, He X, Mazzaferri EL, et al. Cardiac magnetic resonance with edema imaging identifies myocardium at risk and predicts worse outcome in patients with non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2010;55:2480-8.
Medline
103. Aletras AH, Tilak GS, Natanzon A, Hsu LY, Gonzalez FM, Hoyt RF, et al. Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations. Circulation. 2006;113:1865-70.
Medline
104. Fuernau G, Eitel I, Franke V, Hildebrandt L, Meissner J, De Waha S, et al. Myocardium at risk in ST-segment elevation myocardial infarction comparison of T2-weighted edema imaging with the MR-assessed endocardial surface area and validation against angiographic scoring. JACC Cardiovasc Imaging. 2011;4:967-76.
Medline
105. Hadamitzky M, Langhans B, Hausleiter J, Sonne C, Kastrati A, Martinoff S, et al. The assessment of area at risk and myocardial salvage after coronary revascularization in acute myocardial infarction: comparison between CMR and SPECT. JACC Cardiovasc Imaging. 2013;6:358-69.
Medline
106. Eitel I, Desch S, Fuernau G, Hildebrand L, Gutberlet M, Schuler G, et al. Prognostic significance and determinants of myocardial salvage assessed by cardiovascular magnetic resonance in acute reperfused myocardial infarction. J Am Coll Cardiol. 2010;55:2470-9.
Medline
107. Eitel I, Desch S, De Waha S, Fuernau G, Gutberlet M, Schuler G, et al. Long-term prognostic value of myocardial salvage assessed by cardiovascular magnetic resonance in acute reperfused myocardial infarction. Heart. 2011;97:2038-45.
Medline
108. Ibanez B, Prat-Gonzalez S, Speidl WS, Vilahur G, Pinero A, Cimmino G, et al. Early metoprolol administration before coronary reperfusion results in increased myocardial salvage: analysis of ischemic myocardium at risk using cardiac magnetic resonance. Circulation. 2007;115:2909-16.
Medline
109. Wu KC, Kim RJ, Bluemke DA, Rochitte CE, Zerhouni EA, Becker LC, et al. Quantification and time course of microvascular obstruction by contrast-enhanced echocardiography and magnetic resonance imaging following acute myocardial infarction and reperfusion. J Am Coll Cardiol. 1998;32:1756-64.
Medline
110. Nijveldt R, Beek AM, Hirsch A, Stoel MG, Hofman MB, Umans VA, et al. Functional recovery after acute myocardial infarction: comparison between angiography, electrocardiography, and cardiovascular magnetic resonance measures of microvascular injury. J Am Coll Cardiol. 2008;52:181-9.
Medline
111. De Waha S, Desch S, Eitel I, Fuernau G, Zachrau J, Leuschner A, et al. Impact of early vs. late microvascular obstruction assessed by magnetic resonance imaging on long-term outcome after ST-elevation myocardial infarction: a comparison with traditional prognostic markers. Eur Heart J. 2013;31:2660-8.
Medline
112. Ganame J, Messalli G, Dymarkowski S, Rademakers FE, Desmet W, Van de Werf F, et al. Impact of myocardial haemorrhage on left ventricular function and remodelling in patients with reperfused acute myocardial infarction. Eur Heart J. 2009;30:1440-9.
Medline
113. O’Regan DP, Ahmed R, Karunanithy N, Neuwirth C, Tan Y, Durighel G, et al. Reperfusion hemorrhage following acute myocardial infarction: assessment with T2* mapping and effect on measuring the area at risk. Radiology. 2009;250:916-22.
Medline
114. Beek AM, Nijveldt R, Van Rossum AC. Intramyocardial hemorrhage and microvascular obstruction after primary percutaneous coronary intervention. Int J Cardiovasc Imaging. 2010;26:49-55.
Medline

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