Evaluation of cardiac structure, function and tissue characterization with cardiac magnetic resonance imaging (CMR) provides a unique window into the patient with cardiovascular disease. Currently, CMR provides the most accurate assessment of biventricular function, volumes and mass. In addition, CMR visualizes myocardial tissue perfusion, edema and fibrosis, which are vital to identifying areas of myocardial ischemia or infarction.
CMR’s unique tissue characterization ability allows for the evaluation of cardiac masses, infiltrative cardiomyopathies and pericardial diseases. Echocardiography remains the mainstay of diagnosis for valvular heart disease, however, CMR does have a role in the evaluation of stenotic and regurgitant valves. For patients with congenital heart disease, CMR provides excellent visualization of the structural abnormalities as well as information about blood flow and the presence of shunts.
CMR takes advantage of the different electromagnetic spins of hydrogen protons when exposed to a magnetic field. A major advance in CMR stemmed from the development of a magnetic resonance (MR) sequence called steady-state free procession (SSFP) cine imaging, which offers excellent signal-to-noise and contrast-to-noise ratios, as well as fast image acquisition.1 The strength of the magnet influences the imaging quality. Most clinical CMR studies are currently performed at 1.5 Tesla (T). Using a higher field strength of 3T allows for improved signal-to-noise ratios (SNR) for myocardial perfusion, late gadolinium enhancement and angiography. However, using SSFP cine imaging for cardiac function is limited at 3T due to off-resonance artifacts.2 In addition, cardiac gating may be more problematic at higher fields.
Cardiac Anatomy
CMR provides an excellent anatomic assessment of cardiac structures in traditional echocardiographic views, off-axis imaging to best visualize congenital anomalies, complete assessment of the right ventricle and three-dimensional image acquisition approaches.
Using differences in signal intensity with T1- and T2-weighted images, further anatomic differences can be highlighted. On T1-weighted spin echo images, the pericardium appears as a low signal, thin rim (Myocardial Function
Cine CMR sequences obtain a large number of images throughout the cardiac cycle during a breath hold that are played in a movie mode. Measurements of ventricular function and volumes are performed with SSFP sequences. CMR is considered the gold-standard imaging modality for global and regional left ventricular (LV) size and function.3
CMR is uniquely capable of measuring right ventricular volumes, mass, transvalvular flow, as well as myocardial tissue characterization.4 Given the ability to accurately visualize the right ventricle, CMR is the gold standard for imaging of arrhythmogenic right ventricular cardiomyopathy (ARVC) examining ventricular size, focal wall-motion abnormalities and late gadolinium enhancement (LGE) indicating fibro-fatty replacement of the myocardium.5 The presence of intramyocardial fat on T1-weighted CMR images is not part of the diagnostic criteria for ARVC, since it is nonspecific and often found when imaging normal hearts.6
Myocardial tagging uses a grid of saturated areas over a cine image slice, which allows for visualization of the grid deformation over time. Normal myocardium will show uniform grid deformation during the cardiac cycle. Tags quickly fade in the pericardium, unless there is pathologic pericardial fibrosis adherent to the myocardium, which prevents slippage of pericardium along the epicardium. Myocardial tagging is also helpful in visualizing regional wall-motion abnormalities, as well as characterizing the fluid density of a myocardial mass.
Myocardial tagging offers a reproducible method for evaluating regional cardiac function and timing in longitudinal, radial and circumferential directions.7 The ability to characterize myocardial dyssynchrony with tissue tagging is useful for monitoring response to resynchronization therapy. In fact, the assessment of myocardial scar and dyssynchrony with CMR predicts functional class improvement after resynchronization therapy.8 One problem with myocardial tagging has been the time required for quantitative analysis of regional function, although this problem has abated somewhat with the advent of semi-automated analysis techniques.7 A recent study by Markl et al demonstrated superior SSFP tagging at 3T compared to 1.5T, with significantly improved tag persistence and myocardial SNR in the setting of similar overall image quality and artifact level.9
Real-time free-breathing imaging is associated with a lower spatial resolution than traditional breath-hold imaging, however, it is useful in patients with poor functional status or respiratory issues that preclude an adequate breath hold. Real-time free breathing is particularly useful in diagnosing ventricular interdependence seen with constrictive pericarditis. A short-axis cine image of the LV is taken over several cardiac cycles while the patient takes exaggerated respirations. With ventricular interdependence, there is a characteristic motion of the interventricular septum toward the LV during inspiration.
Tissue Characterization
Contrast-enhanced tissue perfusion uses the extracellular paramagnetic agent, gadolinium, which easily diffuses from the vasculature to tissues. Gadolinium enhances the T1 signal in tissues with perfusion in a linear relationship at low doses of contrast.10 In 2006, an association was established between gadolinium exposure and the development of nephrogenic systemic fibrosis (NSF) in patients with stage 4 or 5 chronic kidney disease. Based on a recent review, there have been no cases of NSF reported in patients with a glomerular filtration rate > 30 ml/min/1.73 m2.11 As a result, it is recommended that renal function be evaluated prior to giving gadolinium and that it not be administered to patients with severe kidney disease.
One of the current challenges in contrast-enhanced myocardial perfusion imaging is the presence of a subendocardial dark rim artifact that can appear to be a perfusion defect. However, an experienced reader can usually distinguish the dark rim artifact from an actual perfusion defect. The main indications for contrast-enhanced perfusion imaging include evaluation of ischemia and tissue characterization of cardiac masses. First-pass perfusion imaging requires very rapid acquisition of images during the intravenous infusion of gadolinium, due to the rapid distribution of gadolinium in the extracellular space.12
Clinically, one performs qualitative interpretation of contrast-enhanced myocardial perfusion along with the associated functional images and presence of any LGE in order to determine the presence of significant ischemia or infarction.13 Quantitative analysis of myocardial perfusion is used mainly in research settings. The endocardial and epicardial borders of the LV are delineated and myocardial signal intensity upslopes are obtained by taking the myocardial contrast-enhanced signal intensity versus time, normalized to the slope from the LV input. Ultimately the ratio of stress to rest myocardial perfusion slopes is obtained, which is known as the Myocardial Perfusion Reserve Index (MPRI).12 CMR can also detect differences in myocardial blood flow between the subepicardial and subendocardial regions. Methods are being developed for non-contrast-enhanced myocardial perfusion using the techniques of arterial spin labeling and blood-oxygen level-dependent imaging.14
Contrast-enhanced myocardial perfusion is traditionally done on a 1.5T scanner, however, with the increased prevalence of 3T scanners both clinically and for research purposes, there are emerging data about perfusion imaging at 3T. The main advantage of perfusion imaging at 3T is the increased signal-to-noise ratio. In a single-center study of 61 patients referred for diagnostic X-ray coronary angiography, all patients were initially evaluated with adenosine stress CMR at both 1.5T and 3T.15 3T CMR perfusion imaging was superior to 1.5T for detection of significant coronary artery stenosis with a higher diagnostic accuracy (90% vs. 82%), sensitivity (98% vs. 90%), specificity (76% vs. 67%), positive predictive value (89% vs. 84%) and negative predictive value (94% vs. 78%). However, there was no difference for the overall detection of coronary artery disease (CAD) between 3T and 1.5T.
T2-weighted CMR can identify the area at risk in acute myocardial infarction (MI). In the setting of acute ischemia, the T2 relaxation times are increased, leading to areas of higher signal, due in some part to increased water content in the infarcted area.16 In patients with acute infarctions with successful reperfusion, the area at risk seen with T2-weighted imaging is larger than the degree of irreversible injury identified by LGE.17 Differentiating between acute and chronic MI is aided by the presence of increased T2 signal, suggesting more recent injury.18
Late gadolinium enhancement takes advantage of the delayed washout of gadolinium from myocardium and increased interstitial space due to the loss of intact myocytes.19 LGE identifies areas of myocardial fibrosis seen with infarction or infiltrative disorders. LGE can identify subendocardial MI not appreciated by SPECT in 47% of myocardial segments and 13% of patients.20 These small unrecognized infarcts missed by electrocardiography have been demonstrated to portend an adverse cardiac and overall prognosis.21 There are distinct patterns of LGE that aid in the identification of the etiology of certain cardiomyopathies such as ischemic heart disease (Figure 2), myocarditis (Figure 3), cardiac sarcoidosis, amyloidosis and endomyocardial fibrosis.22
Valvular Function
CMR has a unique role in valvular heart disease by examining the valve morphology and function along with ventricular function and evaluation of concurrent cardiac disease.23 CMR has an advantage over echocardiography when evaluating patients with poor acoustic windows due to body habitus or lung disease. In addition, CMR offers the ability to determine the effects of the valvular lesion on ventricular function and volume.24 For example, the evaluation of ischemic mitral regurgitation with CMR allows for accurate assessment of LV volume and function, myocardial viability and regional wall motion.25 The regurgitant fraction for mitral regurgitation with CMR is obtained by subtracting the aortic forward flow from the LV stroke volume.26
Velocity-encoded cine imaging measures blood flow, allowing the flow velocities and volumes across valves to be quantified.27 As part of a comprehensive CMR examination, regurgitant flow through incompetent valves or high velocity jets through stenotic valves can be calculated. Characterizing the degree of aortic stenosis with CMR has been compared to echocardiography28 using direct valvular planimetry with cine imaging at the aortic valve tips and with the continuity equation using velocity-encoded cine images. CMR measurements of the aortic valve area (AVA) by planimetry and continuity equation are equally accurate when compared to echocardiography.
Coronary Imaging
Traditionally, CMR coronary angiography has not used contrast enhancement, but rather takes advantage of the high signal of coronary blood flow to create contrast between the vessels and myocardium.29 CMR coronary angiography uses a free-breathing sequence that acquires a 3-dimensional volume of all the coronary vessels, using both respiratory and ECG gating to minimize motion artifacts.
Evaluation of coronary arteries for stenosis using CMR is limited by lower spatial resolution compared to traditional angiography or multidetector coronary computed tomography angiography. Coronary magnetic resonance angiography (MRA) has a sensitivity of 72% and a specificity of 83% based on a meta-analysis of more than 900 patient studies in whom 83% of the coronary segments were analyzable.30 CMR can accurately visualize the proximal coronary arteries, allowing for identification of anomalous coronaries, as well as coronary artery aneurysms due to their relatively large size.
Recently, Yang et al described their experience with contrast-enhanced whole-heart coronary MRA at 3T. Coronary MRA at 3T showed high sensitivity (91.6%) and moderate specificity (83.1%) for the detection of significant coronary artery stenosis compared to X-ray coronary angiography.31 Further development is needed to decrease the image acquisition time and improve the spatial resolution.
Specific Indications for CMR
Stress CMR. First pass contrast-enhanced myocardial perfusion with pharmacologic stress identifies areas of ischemia and allows for the differentiation of significant coronary stenosis when compared with invasive angiography.32 Pharmacologic stress agents include dobutamine for functional imaging and vasodilators (adenosine, dipyridamole or regadenoson) for perfusion imaging. Both dobutamine and vasodilator stress CMR have excellent negative predictive value over 2–3 years.33 Dobutamine stress CMR imaging uses sequentially higher dobutamine doses with the corresponding acquisition of SSFP cine images,34 similar to dobutamine stress echocardiography. For a vasodilator perfusion stress CMR protocol, usually the stress perfusion images are obtained first, followed by a 10-minute delay before acquiring resting perfusion images (Figure 4). During the interim, LV functional imaging can be performed. The last component of the stress CMR protocol involves obtaining LGE images to identify areas of myocardial fibrosis indicative of prior infarction.
In 2007, Nandalur et al reviewed the diagnostic performance of perfusion-cardiac magnetic resonance (perfusion-CMR) and stress-induced CMR wall-motion abnormalities for the diagnosis of CAD in all stress CMR studies with corresponding X-ray angiography since 1990.35 A high prevalence of CAD was noted; the perfusion CMR studies had a prevalence of 57.4% compared to 70.5% in the stress-induced wall-motion abnormality group. CMR-perfusion imaging had a sensitivity of 0.91 (95% CI 0.88–0.94) and specificity of 0.81 (95% CI 0.77–0.85) compared to angiography. Stress-induced functional imaging had a sensitivity of 0.83 (95% CI 0.79–0.88) and a specificity of 0.86 (95% CI 0.81–0.91) for detecting CAD in patients. A multicenter trial in 2008 examined more than 200 patients with known or suspected CAD who were all evaluated by perfusion-CMR, X-ray coronary angiography and SPECT (single-photon emission computed tomography) myocardial perfusion.36 The difference between perfusion-CMR and gated-SPECT did not reach statistical significance, however, the area under the receiver operating characteristic curve for CMR was larger than for SPECT (0.86 ± 0.06 vs. 0.67 ± 0.5; p 50% transmural LGE is quite low (Figure 5). Adding low-dose dobutamine cine CMR to LGE increases the predictive value for regional functional recovery, particularly in segments with 1–50% transmural LGE in which late enhancement alone is only of intermediate predictive value.40
CMR is also quite useful in determining prognosis after acute MI. Functional recovery is again inversely related to transmurality of late gadolinium enhancement.41 In addition, the presence of areas of low signal at the subendocardial core of larger, more transmural infarcts, regions of microvascular obstruction (Figure 6), portends a lack of functional recovery42 as well as adverse cardiac prognosis after 1–2 years.43,44
Cardiomyopathies. CMR is well suited to differentiate between non-ischemic and ischemic cardiomyopathies based on the presence of regional wall-motion abnormalities, decreased tissue perfusion and the pattern of LGE. In terms of evaluating the etiology of non-ischemic cardiomyopathies, the role of CMR is established in the diagnosis of eosinophilic endocardial disease, hypertrophic cardiomyopathy, transient apical-ballooning syndrome, amyloidosis and sarcoidosis.
Traditionally, non-invasive diagnosis of eosinophilic endocardial disease has been difficult, however, the use of cine imaging, first-pass contrast-enhanced perfusion and LGE can identify the presence of endomyocardial fibrosis.45
CMR is very useful in the evaluation of hypertrophic cardiomyopathy (HCM), given the ability to measure LV volume, ejection fraction and determine the extent of hypertrophy, while also characterizing the degree of associated mitral regurgitation and systolic anterior motion of the mitral valve.46 In particular, CMR can accurately diagnosis apical variant HCM (Figures 7 and 8), as well as variants of HCM with hypertrophy in areas that can be difficult to assess by echocardiography such as the anterolateral free wall.47 Smaller patient studies have examined the role of CMR in evaluating patients after alcohol septal ablation therapy, finding an improved LV outflow tract area.48 In patients with symmetric hypertrophic cardiomyopathy, LGE can distinguish those with Fabry’s disease, a genetic lysosomal enzyme deficiency leading to pathologic glycogen tissue deposition, based on a unique pattern of LGE in the inferolateral wall, sparing the subendocardium.49
Transient apical ballooning syndrome, or takotsubo cardiomyopathy, is well characterized by CMR and the abnormal wall motion usually does not have corresponding areas of hypoperfusion or LGE.50
Traditionally, non-invasive diagnosis of cardiac amyloidosis was limited to a “sparkling” appearance of the myocardium and evidence of restrictive physiology on echocardiography in the appropriate clinical scenario. Light chain immunoglobulins infiltrate the cardiac interstitium, resulting in a restrictive cardiomyopathy. The gold standard for establishing cardiac involvement with amyloid has been endomyocardial biopsy. Characteristic CMR findings with amyloidosis include global subendocardial LGE combined with abnormal myocardial gadolinium kinetics with T1-weighted imaging.51 In a recent literature review by Selvanayagam et al, additional patterns of LGE have been found in patients with cardiac amyloid including localized and transmural involvement.52
In patients with pulmonary sarcoidosis, CMR is useful for demonstrating cardiac involvement based on LGE usually involving the basal and lateral walls.53 Making the diagnosis of cardiac sarcoidosis using CMR may allow patients to forgo an endomyocardial biopsy, or if biopsy is still warranted, the location of LGE can guide the procedure.
Constrictive pericarditis. CMR can distinguish between constrictive pericarditis (CP) and restrictive cardiomyopathy.54 The main findings on CMR for CP include: thickened pericardium, atrial enlargement, paradoxical motion of the interventricular septum, enlarged inferior vena cava, myocardial tagging with little change in the tags indicating pericardial adherence to the myocardium and pericardial contrast enhancement. There is evidence of interventricular dependence with CP seen by the motion of the interventricular septum during real-time free-breathing imaging. Interventricular dependence is not seen with restrictive cardiomyopathy and can differentiate CP with a high sensitivity and specificity.55 Velocity-encoded imaging provides graphic information about the early rapid ventricular filling and abrupt truncation of late diastolic filling seen with CP.56
Myocarditis. CMR can monitor reversible and irreversible myocardial injury in the setting of myocarditis as well as provide information about acuity. Late gadolinium enhancement has been validated against LV endomyocardial biopsy in this disorder, demonstrating LGE in areas of acute inflammation.57 Over time, areas of LGE in myocarditis can decrease in size related to normalization of ejection fraction and end-diastolic volume. In a recent study by Zagrosek et al, 36 patients with a clinical diagnosis of myocarditis were studied with CMR during the acute phase and then 18 months later.58 In the acute phase, 86% had increased T2 signal consistent with myocardial edema and 63% had LGE. At the 18-month follow up, the mean ejection fraction increased from 56 ± 8% to 62 ± 7% (p Summary
The clinical indications for CMR studies to evaluate cardiac disease continue to expand. Currently, a comprehensive cardiac evaluation of anatomy, function, blood flow and tissue characterization is integral to the evaluation of CAD, cardiomyopathies, valvular disease, pericarditis/myocarditis and congenital heart anomalies.
From the *Division of Cardiovascular Medicine, and the §Cardiovascular Imaging Center, University of Virginia, Charlottesville, Virginia.
Disclosures: Dr. Kramer is a consultant and receives research support from Siemens Medical Solutions. He has received a research grant from Astellas.
Manuscript submitted May 4, revised and accepted May 19, 2009.
Address for correspondence: Christopher M. Kramer, MD, University of Virginia Health System, Departments of Medicine and Radiology, Lee Street, Box 800170, Charlottesville, VA 22908. E-mail: ckramer@virginia.edu
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