Introduction
The use of sensitive biomarkers has significantly improved the diagnosis of myocardial infarction (MI), and has been incorporated into the “Universal Definition” of MI (see Chapter 1 ). However, the diagnosis of MI can still be difficult. There is significant overlap with other disorders that result in myocardial injury (see Chapter 6 ). For instance, disorders such as Takotsubo cardiomyopathy and myocarditis are associated with elevation of cardiac biomarkers, and their clinical differentiation from acute MI can be problematic and can often result in invasive diagnostic procedures (see Chapter 7 ). In other instances, patients may present late, after cardiac biomarkers have normalized, resulting in an “unrecognized” MI. Recognizing the value of cardiac imaging in such circumstances, the Universal Definition of MI incorporates imaging findings of a new loss of viable myocardium or new wall motion abnormality in conjunction with other clinical criteria (see Chapter 9 ). Because of its capacity for state-of-the-art imaging of both myocardial structure and wall motion, cardiac magnetic resonance (CMR) has emerged as an important method to confirm the diagnosis in suspected cases, as well as to differentiate MI from other conditions.
Complementing its usefulness in the diagnosis of MI, CMR can provide substantial additional information in the patient with known or suspected MI, including the determination of the infarct-related artery, particularly in non–ST-elevation MI (NSTEMI), the detection of inducible ischemia, and the determination of residual viability (see Chapter 30 ). In addition, CMR can accurately assess various complications of MI such as thrombus formation, or the development of a ventricular aneurysm (see also Chapter 26 ). Lastly, because of its accuracy and precision in determining infarct size, CMR is increasingly used as a research tool in population studies of MI and as a surrogate endpoint in randomized trials of investigational MI therapies. In this chapter, we examine the application of CMR in patients with known or suspected MI, with an emphasis on demonstrating modality-specific aspects and the possible implications for patient care.
Cardiac Magnetic Resonance Technique
CMR has undergone rapid evolution, and technical advances in scanner hardware and coil technology and the development of new pulse sequences have resulted in progressive expansion of clinical applications ( Figure 33-1 ). In particular, new pulse sequences have leveraged the inherently superior soft tissue contrast provided by MR to improve anatomic definition and the delineation of diseased tissue from normal tissue. Overall, these advances have led to the recognition of CMR as the reference standard for the assessment of regional and global systolic function, imaging of MI and viability, and the evaluation of pericardial disease and cardiac masses. In addition, the pattern and distribution of scar as demonstrated by CMR can forewarn of the presence of nonischemic disorders and may be helpful in determining the specific cause of cardiomyopathy. Although previously CMR examinations were lengthy (∼1 hour), and many patients were not capable of completing a standard examination, accelerated imaging techniques are now sufficiently robust such that useful diagnostic information can be provided for patients with arrhythmias and/or limited ability to cooperate in 30 minutes or less. The multiplicity of techniques and the variety of information that can be obtained in a CMR examination can be exhaustive, but increasingly there has been a move toward standardization of imaging protocols tailored to specific indications, an effort spearheaded by the Society of Cardiovascular Magnetic Resonance. Our suggested implementation and a timeline ( Figure 33-2 ) of a CMR protocol for a standard CMR examination is as follows.
Standard Cardiac Magnetic Resonance Examination
Cine Images
Cine images are typically acquired in the short-axis plane from above the mitral valve through the left ventricular (LV) apex, together with standard two-, three-, and four-chamber long-axis views ( Figure 33-e1 ). Typical parameters are shown in Table 33-1 . The cine images have excellent spatial and temporal resolution, and are not limited by acoustic windows. Therefore, they allow comprehensive evaluation of regional and global ventricular function and overall cardiac morphology. Visual evaluation of valvular function and morphology is also performed using these images.
| Imaging | Sequence Type | Location | Imaging Parameters | Resolution | Notes |
|---|---|---|---|---|---|
| Localizers | Single-shot SSFP images | Axial, sagittal, coronal | 400-mm FOV | Low resolution | Allows scan planning for cardiac imaging |
| Cine SSFP (standard) | Segmented SSFP images obtained with retrospective gating | Short-axis images from base to apex; 2-, 3-, and 4-chamber long-axis views | FOV ≈ 360 × 290 mm Matrix ≈ 256 × 168 pixels; slice thickness, 6–8 mm | Pixel size ≈ 1.7 × 1.4 × 6 mm Temporal res. ≈ 40 ms | 6–10 s breath-hold required |
| DE-CMR (standard) | Segmented gradient echo inversion recovery images with data obtained every other heartbeat | Exactly matched to cines | FOV ≈ 360 × 290 mm Matrix ≈ 256 × 168 pixels; slice thickness, 6–8 mm | Pixel size ≈ 1.7 × 1.4 × 6 mm Temporal res. ≈ 160–200 ms | Inversion time chosen to null signal from myocardium |
| Modifications | |||||
| Cine SSFP (real-time) | Real-time images where each cine frame is obtained in single-shot fashion | Short-axis images from base to apex; 2-, 3-, and 4-chamber images | FOV ≈ 380 × 260 mm Matrix ≈ 192 × 84 pixels; slice thickness, 10 mm | Pixel size ≈ 3.1 × 2.0 × 10 mm Temporal res. ≈ 70 ms | Useful in uncooperative or severely arrhythmic patients |
| DE-CMR (single-shot) | Single-shot SSFP inversion recovery images | Short-axis stack from base to apex; long-axis stack(s) can also be obtained | FOV ≈ 360 × 290 mm Matrix ≈ 208 × 128 pixels; slice thickness, 8 mm | Pixel size ≈ 2.3 × 1.7 × 8 mm Temporal res. ≈ 160–200 ms | Useful in uncooperative or severely arrhythmic patients |
| Optional Sequences | |||||
| Morphologic images | Bright-blood imaging performed with single-shot SSFP; dark-blood imaging performed with HASTE | Stack of images obtained usually in the axial plane; can also obtain sagittal and coronal stacks | FOV ≈ 380 × 315 mm Matrix ≈ 256 × 152 pixels; slice thickness, 8 mm | Pixel size ≈ 2.0 × 1.5 × 8 mm Temporal res. ≈ 60–100 ms | Survey of heart and great vessels; aortic abnormalities, congenital defects |
| T2-weighted images | Gated T2 FSE or STIR images | Matched to short-axis cine and DE-MR images | FOV ≈ 360 × 290 mm Matrix ≈ 256 × 168 pixels; slice thickness, 6–8 mm | Pixel size ≈ 1.7 × 1.4 × 6 mm Temporal res. ≈ 60–80 ms | To evaluate for edema seen with acute disorders (AMI, myocarditis) |
| Flow sensitive images | Velocity-encoded gated images | Typically obtained through stenotic valves or proximal great vessels | FOV ≈ 360 × 240 mm Matrix ≈ 256 × 116 pixels; slice thickness, 6–8 mm | Pixel size ≈ 2.0 × 1.4 × 6 mm Temporal res. ≈ 45 ms | Used to measure peak gradients and flow |
| Perfusion imaging | Saturation recovery (T1-weighted) images to evaluate the transit of contrast through the myocardium | Typically obtained as a stack of 4 short-axis images to cover the LV | FOV ≈ 340 × 255 mm Matrix ≈ 208 × 98 pixels; slice thickness, 8 mm | Pixel size ≈ 2.6 × 1.6 × 8 mm Temporal res. ≈ 120 ms | Can be performed with pharmacologic stress to evaluate for inducible ischemia |
Inter- and intra-observer reproducibility of cine CMR imaging for the quantification of LV volumes and function has been shown in multiple studies to be excellent, predominantly because of its high spatial and temporal resolution and its capacity for complete LV coverage. The improvement in reproducibility relative to echocardiography allows a significant reduction in the sample sizes required for research studies to demonstrate meaningful changes as a result of experimental therapies. This feature has led to increasing use of CMR in research studies that use cardiac morphology and/or function as an efficacy endpoint.
Delayed-Enhancement Images
These images are obtained 5 to 10 minutes after intravenous (IV) administration of gadolinium-based contrast with 6- to 8-mm slices that are spatially matched to the previously obtained cine images ( Figure 33-e2 ). The delayed-enhancement CMR (DE-CMR) sequence has been shown to be the most sensitive noninvasive imaging test for the detection of MI. It can accurately depict the presence, location, and extent of MI with high spatial resolution irrespective of infarct age. In animal models, DE-CMR has been shown to demonstrate acute and chronic MI with a near-exact spatial match to histopathology specimens ( Figure 33-3 ). In addition, these studies show that DE-CMR can distinguish between reversible and irreversible injury independent of wall motion, infarct age, and reperfusion status. Studies in humans have shown that infarct size measured by DE-CMR and by positron emission tomography (see Chapter 32 ) is associated with peak cardiac biomarker release (see Chapter 7 ). Compared with single-photon emission computed tomography (SPECT) imaging, the DE-CMR technique is significantly more sensitive for the detection of subendocardial infarction, of which more than 40% are missed with SPECT ( Figure 33-4 ). With standard imaging parameters, DE-CMR is capable of demonstrating infarcts involving as little as one one-thousandth of total LV mass, which are undetectable by techniques that assess myocardial perfusion or contractile function. The high spatial resolution of DE-CMR has been used to visualize microinfarctions, involving as little as 1 g of tissue, which may occur during otherwise successful percutaneous coronary intervention.
The technique of DE-CMR has been extensively validated. Its ability to delineate viable from nonviable myocardium is based on the differential distribution of gadolinium contrast in diseased tissue compared with normal tissue. It is important to note that all myocardium—normal, infarcted, or scarred—will demonstrate some contrast enhancement. However, conventional gadolinium contrast agents localize to the extracellular space because they are inert, and intact sarcolemmal membranes prevent them from entering the intracellular space. Normal myocardium, in which the myocytes are densely packed, thus has a limited extracellular volume of distribution (20%) and can be thought of as excluding the contrast agent. With acute necrosis (e.g., acute MI, myocarditis), there is membrane rupture that allows gadolinium to diffuse into myocytes. This diffusion results in increased gadolinium concentration, shortened T1 relaxation, and thus, hyperenhancement. In the chronic setting, scar has replaced necrotic tissue, and the interstitial space is expanded, leading to increased gadolinium concentration and hyperenhancement. In both acute and chronic settings (and all stages in between), viable myocytes are considered as actively excluding gadolinium. Thus, the unifying mechanism of hyperenhancement appears to be the absence of viable myocytes rather than any inherent properties that are specific for acute necrosis, collagenous scar, or other forms of nonviable myocardium ( Figure 33-e3 ).
The standard DE imaging sequence is a heavily T1-weighted segmented gradient echo sequence, in which an inversion pulse has been applied. The inversion pulse serves to flip the magnetization 180 degrees. The recovery of magnetization back to baseline by areas that have a higher gadolinium concentration (e.g., infarcts or scar tissue) will be more rapid (because they have a lower T1 value) than those with a lesser concentration of gadolinium, such as normal myocardium. The time after the inversion pulse at which the magnetization of normal myocardium is at the zero-crossing line will result in maximum suppression of signal from normal myocardium (the myocardium is said to be “nulled”), and will result in maximum conspicuity of the area of infarction ( Figure 33-e4 ). Because the magnetization of infarcted regions, by virtue of their increased contrast content, will recover above the baseline more rapidly (the contrast will accelerate the recovery back to baseline magnetization), infarctions will appear to be bright on these images.
The standard DE sequences are segmented acquisitions, acquired at every other heartbeat to allow recovery of longitudinal magnetization in normal myocardium before the next inversion pulse is applied. They typically take approximately 8 to 12 seconds to acquire. For patients with significant arrhythmia or difficulty with breath-holding, single-shot DE images using a steady-state free-precession (SSFP) inversion recovery readout can provide comparable data in a fraction of the imaging time. These images have slightly worse spatial resolution and contrast-to-noise ratio, but provide a satisfactory alternative in these circumstances.
The DE single-shot inversion recovery images may also be obtained with a long inversion time (550 to 600 ms at 1.5 T) and are quite useful in the detection of thrombi.
In these images with a long inversion time, thrombi will appear dark in contrast to normal and infarcted myocardium, which will be medium to high in signal intensity. Because these do not require “washout” of contrast from the myocardium, these can be performed shortly after contrast administration, while waiting for the appropriate delay for standard DE-CMR imaging (see Figure 33-2 ).
Optional Sequences
Morphologic Static Images
In many cases, an overview of cardiac and great vessel anatomy is desirable and can be rapidly performed using single-shot dark blood and/or single-shot bright blood techniques such as half-acquisition turbo spin-echo and SSFP sequences, respectively. These result in a stack of still-frame images and are usually acquired in the standard orthogonal imaging planes (axial, sagittal, or coronal). The rapidity of acquisition is such that breath-holding is not required. These produce excellent depiction of the overall myocardial structure and the relationships of the great vessels ( Figure 33-e5 ).
T2-Weighted Images
In cases in which the acuity of an infarction is uncertain, or in cases of suspected acute myocarditis, T2-weighted imaging may be useful in demonstrating the edema characteristically seen in the acute phase of these disorders. These sequences are performed before the administration of IV contrast, because the presence of contrast may complicate image interpretation. These can be obtained via a double or triple inversion fast spin-echo black-blood sequence or with a T2-preparation SSFP bright-blood sequence. The T2-prep bright-blood sequence is far more resistant to artifacts than the black-blood sequence. However, the bright-blood sequence may be less sensitive for detecting regions with more moderate levels of edema, particularly if limited to the subendocardium.
Perfusion Imaging
Increasingly, stress and rest CMR perfusion imaging are being used to detect ischemia in patients with known or suspected coronary disease, and multiple studies have demonstrated excellent sensitivity and specificity, similar to or exceeding those of SPECT imaging. Combined with the superior delineation of infarction provided by DE-CMR relative to SPECT, it is not surprising that some centers are now using stress perfusion CMR as a first-line test, particularly in the United Kingdom, where cardiac imaging is not reimbursed according to a “fee per procedure” structure. A modification of the standard examination to include stress and rest perfusion imaging is shown in Figure 33-e6 . Unlike vasodilator radionuclide imaging in which adenosine is typically infused for 6 minutes (tracer injection at 3 minutes), stress perfusion MR imaging is performed using an abbreviated adenosine protocol (∼3 minutes) because vasodilation needs to be maintained only for the initial first-pass through the myocardium. Although severe reactions to adenosine are rare, a shortened protocol is relevant because moderate reactions that affect patient tolerability are relatively commonplace.
Other Optional Sequences
Velocity-encoded flow studies can be performed as necessary in cases of complicating known or suspected valvular pathology. These sequences can be used to quantify peak gradients through stenotic valves and to measure regurgitant flow.
T1 and T2 mapping techniques are increasingly being investigated in studies of infarction and other myocardial disorders, and can be performed before and/or after the administration of IV contrast. These sequences provide a quantitative assessment of regional myocardial T1 and T2 values and are not subject to surface coil sensitivity profiles that can result in variable image intensity for different regions of the heart. In the absence of gadolinium contrast, T1 and T2 values are increased in the setting of acute necrosis-related edema, and thus, these sequences allow the depiction of edema and provide a metric that may be useful for purposes of quantification and serial assessment. A parametric map of extracellular volume fraction can be made by combining precontrast (“native”) and postcontrast T1 mapping values (see Figure 33-1 ). Extracellular volume fraction will be increased both in the setting of acute necrosis and chronic collagenous scar.
Typical Imaging Findings in Myocardial Infarction
Acute Ischemic Injury
Cine Imaging
Acute ischemic injury of the myocardium usually results in myocardial dysfunction, with reduction of systolic wall thickening evident on cine images. Such dysfunction may occur even in the absence of infarction. Acute infarction may result in transient swelling of the affected segment, with increased signal often apparent on SSFP cine images, reflecting the partial T2 weighting of SSFP sequences and the presence of edema ( Figure 33-5 ).
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