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Contrast-enhanced MR Imaging of the Heart: Overview of the Literature¹

¹ From the Department of Radiology, Evanston Northwestern Healthcare, 2650 Ridge Ave, Evanston, IL 60201; and Feinberg School of Medicine, Northwestern University, Chicago, Ill. Received September 29, 2003; revision requested November 11; revision received December 8; accepted January 21, 2004. Supported in part by NIH 5R01HL060708 and 8R01EB002079. Address correspondence to the author (e-mail: redelman@enh.org).

	ABSTRACT

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 
The use of magnetic resonance (MR) imaging for cardiac diagnosis is expanding, aided by the administration of paramagnetic contrast agents for a growing number of clinical applications. This overview of the literature considers the principles and applications of cardiac MR imaging with an emphasis on the use of contrast media. Clinical applications of contrast material–enhanced MR imaging include the detection and characterization of intracardiac masses, thrombi, myocarditis, and sarcoidosis. Suspected myocardial ischemia and infarction, respectively, are diagnosed by using dynamic first-pass and delayed contrast enhancement. Promising new developments include blood pool contrast media, labeling of myocardial precursor cells, and contrast-enhanced imaging at very high fields.

© RSNA, 2004

Index terms: Gadolinium • Iron • Magnetic resonance (MR), contrast media • Manganese • Myocardium, MR, 511.121411, 511.121412, 511.121413, 511.121416, 511.12143 • Reviews

	INTRODUCTION

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 

EDITOR’S NOTE: This review is not intended to provide in-depth coverage of any topic related to contrast-enhanced MR imaging of the heart. Rather, as noted in the title, it is an overview of the literature and is intended to inform our readers of ongoing activity in this area of imaging.

Anthony V. Proto, MD, Editor

Cardiac disease remains the leading cause of death in the United States, with an estimated 1.5 million myocardial infarctions and 500 000 deaths per year attributed to coronary artery disease (CAD) (1). Despite the high prevalence of heart disease and technical limitations of alternative cardiac imaging tests, magnetic resonance (MR) imaging has played only a minor role in the cardiac work-up. There is ongoing growth in the cardiac applications of MR imaging, for instance, to evaluate myocardial viability and cardiac masses and to delineate pulmonary venous anatomy in preparation for radiofrequency (RF) ablation of arrhythmogenic foci. For certain applications, such as the evaluation of myocardial viability, MR imaging is proving to be the most accurate test, whereas in other applications (eg, detection of ventricular thrombi), it can be a helpful adjunct to standard tests such as echocardiography. Contrast agents play a key role in many of these newer applications (2–5).

This overview of the published literature considers the principles and utility of cardiac MR imaging, with an emphasis on the use of contrast media, including contrast agents used experimentally and in humans, methods for contrast agent administration and data acquisition, as well as promising new developments. A literature search covered the period from 1988 to the present with use of multiple databases, including BIOSIS, CAB, DDFU, EMBASE, MEDLINE, and SciSearch. Search terms included "heart," "cardiac," "myocardium," "magnetic resonance," and "contrast media." Only articles and scientific proceedings with at least an abstract in English were included. In addition, several scientific abstracts were included that concerned key topics where no full publications were found. Information about the type of contrast agent, dose, use of a power injector, rate of injection, imaging methods, and clinical applications was compiled.

	GENERAL CONSIDERATIONS FOR CONTRAST-ENHANCED CARDIAC MR IMAGING

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 
Numerous technical challenges limit the ability to acquire contrast material–enhanced images of the heart that possess suitable tissue contrast without degradation from motion artifacts. For cardiac imaging, one needs to overcome both respiratory and heart motion. The need to synchronize the acquisition to the cardiac cycle means that the R-R interval determines the repetition time, which in turn alters the T1-weighting of a spin-echo image and tissue enhancement from contrast agents. Lung tissue surrounds the heart, which results in a distortion of the static magnetic field, making it problematic to use the fast single-shot echo-planar methods that are standard for T2*-weighted contrast-enhanced perfusion imaging of the brain. In addition, the location of the heart toward the center of the chest can make it difficult to obtain images with an adequate signal-to-noise ratio (SNR) in large patients. Fortunately, there has been great technical progress in the field of cardiac MR imaging during the past several years (6,7). On the hardware side, there have been major improvements in the magnetic field gradients and RF coils. New phased-array RF coils developed for cardiac applications have six to 32 or more elements and improved SNRs, compared with SNRs obtained by using earlier coil designs. The newer phased-array coils also permit the use of parallel imaging techniques, which reduce the imaging time by factors of two to four or more (though at the expense of SNR) and thereby improve the temporal resolution of contrast-enhanced MR angiography (8), myocardial perfusion, and cine imaging.

	CATEGORIES OF CONTRAST AGENTS FOR CARDIAC MR IMAGING

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 
Numerous contrast agents have been applied in animal studies, but few have been used to image the myocardium or coronary arteries in humans (9). Contrast agents with potential cardiac utility are summarized in Tables 1 and 2. The agents may be classified as primarily active with use of T1-weighted (eg, gadolinium chelates, manganese chelates) or T2-weighted (eg, iron oxide particles) sequences. Certain contrast agents, such as very small iron particles, can produce enhancement with either T1- or T2-weighted pulse sequences. In addition, contrast agents may be classified as the following according to their distribution in tissue: extracellular, blood pool, mixed blood pool extracellular, intracellular, and receptor targeted (13).

Intravascular blood pool agents include very small coated iron particles (14,15). Examples of iron-based blood pool agents are ultrasmall superparamagnetic iron oxide or monocrystalline iron oxide (16), NC100150 (Clariscan; Amersham Pharmaceuticals, Princeton, NJ) (17), ferumoxtran-10 (Combidex; Advanced Magnetics, Cambridge, Mass) (18), and ferumoxytol (Advanced Magnetics) (19). By virtue of the prolonged enhancement of the blood pool (eg, ferumoxytol has a half-life in the blood of 14 hours), such agents may prove useful for MR angiography and cardiac cine imaging (20). In the heart, they may prove of particular value for non–breath-hold navigator-imaging methods, since the imaging times are lengthy (eg, 10–15 minutes). In addition to their benefits for MR angiography, some particulate blood pool agents can be taken up by macrophages within unstable plaques (21). This property could eventually prove useful for studies in vulnerable patients at risk for coronary plaque rupture.

Among the gadolinium chelates with mixed properties of blood pool and extracellular agents are those bound to albumin or other components of plasma (eg, MS-325; EPIX Medical, Cambridge, Mass), which thereby prolong the residence in the intravascular space. Moreover, such binding slows down the rotation of the molecule and thereby increases T1 relaxivity. One can also improve T1 relaxivity and half-life in the blood by increasing the size of the molecule and the number of gadolinium atoms. For instance, SH L 643A (Gadomer-17; Schering Pharmaceuticals, Berlin, Germany), which consists of a polymer of 24-gadolinium cascades with a molecular weight of 35 kDa, extravasates very slowly out of the intravascular space (22). Blood pool agents enhance the normal myocardium to a lesser degree than do extracellular agents because the fractional distribution volume (only about 5%–10% of the myocardial volume consists of blood) is several times smaller. This might indicate reduced utility for the evaluation of myocardial perfusion. On the other hand, in an animal model of myocardial ischemia, a cascade polymer was found to prolong the temporal window of dynamic contrast-enhanced MR imaging for the differentiation of ischemic and normal myocardium (23). The sensitivity of blood pool agents for myocardial infarction, and therefore, their potential value for evaluation of myocardial viability, is unknown.

Porphyrin derivatives labeled with gadolinium, such as bis-gadolinium mesoporphyrin (Gadophrin-2; Schering, Berlin, Germany), have an affinity for necrotic tissue, including infarcts. Authors of some studies have found that enhancement with bis-gadolinium mesoporphyrin accurately represents the infarct zone as defined with histochemical staining, whereas the area enhanced by gadopentetate dimeglumine is substantially larger. This result suggests that the periinfarct zone, and not just the infarct, enhances with gadolinium chelates (24,25). However, the eventual utility of porphyrin derivatives appears limited because of their toxicity.

Manganese ions differ from other paramagnetic contrast agents since they pass through voltage-dependent calcium channels and localize intracellularly within the myocyte. Manganese is rapidly taken up by normal myocardium, with less uptake and retention by ischemic or infarcted myocardium (26,27). The uptake pattern of manganese is analogous to that of thallium 201 (²⁰¹Tl) used for stress nuclear studies. Unfortunately, free manganese is toxic. To minimize any potential toxicity, the manganese can be chelated (eg, mangafodipir trisodium). Free manganese is slowly released from the chelate and taken up by the myocardium (28). However, this agent must be given at several times the usual clinical dose to produce adequate myocardial contrast enhancement in vivo. Alternatively, manganese can be mixed with calcium ions (EVP-1001; EagleVision Pharmaceuticals, Exton, Pa) to improve tolerance. This agent, which is entering phase II clinical trials, has produced substantial myocardial contrast enhancement and, in an animal model, detection of myocardial ischemia at tolerable doses (29).

With further refinement of molecular imaging methods, there will be still greater specificity for particular anatomic structures, receptors, or cellular processes (30). For instance, ultrasmall iron particles linked to antibodies directed against cardiac myosin help detect infarcted tissue (31). The function of myocardial calcium channels could potentially be studied by using MR contrast agents that change in signal intensity on binding with calcium (32).

	METHODS FOR CONTRAST AGENT ADMINISTRATION

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 
In the articles surveyed, the contrast agents used for cardiac MR imaging included gadopentetate dimeglumine in 82%, gadodiamide in 9%, gadoteridol in 5%, gadobenate dimeglumine in 3%, and gadoversetamide in less than 1% of cases.

The techniques for contrast agent infusion varied widely, depending on the investigator and application. There were few reports about the choice of hand versus power injection, but the ratio was approximately 2:1. In most cases, the contrast agent was administered as a bolus, followed by a saline flush. Among 103 studies in which the dose of contrast agent was reported, less than 0.05 mmol of the contrast agent per kilogram of body weight was used in 10%, 0.05 mmol/kg was used in 18%, 0.1 mmol/kg was used in 42%, 0.15 mmol/kg was used in 2%, and 0.2 mmol/kg was used in 21% of cases. Miscellaneous infusion protocols in the remaining cases included repeated boluses of 0.1 mmol/kg, a bolus of 0.1 mmol/kg followed by a slow infusion of either 0.002 or 0.004 mmol/kg, and non–weight-based boluses of 20–40 mL. The rate of infusion was mentioned in a minority of reports and was mostly in the range of 3–5 mL/sec. A slow prolonged infusion was applied in a few instances to quantify myocardial perfusion.

	ROLE OF CONTRAST AGENTS FOR EVALUATION OF CARDIAC ANATOMY AND FUNCTION

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 
Anatomy
MR imaging is an excellent means to depict cardiac anatomy (33–35), including complex congenital malformations (36,37). In general, contrast agents are not required for morphologic evaluation. On the contrary, they tend to worsen the image quality of dark blood images by shortening the T1 relaxation time of blood. With shorter T1 relaxation time, one must use a reduced inflow time for the dual-inversion magnetization preparation (38) widely used for breath-hold T1-weighted fast spin-echo acquisitions. The shorter inflow time reduces the effectiveness of the method for suppressing intravascular signal intensity. Gadolinium chelates have little effect on T2-weighted acquisitions. However, iron oxides greatly reduce the T2 relaxation time of blood, rendering it dark on fast spin-echo images. The reduced signal intensity of blood eliminates artifact due to slowly flowing or pulsatile blood, with little effect on the signal intensity of myocardium (39). This approach has the potential to improve the quality and robustness of dark blood fast spin-echo imaging of the heart.

Ventricular Function
Cine images shows the motion of the heart and blood over multiple phases of the cardiac cycle (40–42). Cine imaging generally uses some form of a multishot ("segmented") gradient echo. Use of a small number of phase-encoding steps in each breath hold (encompassing a small portion of the cardiac cycle, eg, 20–60 msec) minimizes blurring from cardiac motion. Accumulation of multiple segments over a typical breath-hold period of 10–20 heart beats results in a complete cine examination (43). Balanced steady-state free precession sequences (eg, true FISP [fast imaging with steady-state precession], FIESTA [fast imaging employing steady-state acquisition], or balanced FFE [fast field echo]) give the best image quality, particularly if the repetition and echo times are kept very short and there has been adequate shimming of the static magnetic field to the region of the heart (44). Projection reconstruction techniques that involve radial sampling of k-space also offer great potential for the fast acquisition of cine images with high temporal resolution (45).

Although contrast agents are not required for cine imaging, image quality generally improves after a contrast agent is administered. Cine gradient-echo acquisitions, which are inherently T1-weighted, show a marked enhancement of the blood pool after administration of a T1-active contrast agent. The enhanced blood pool appears only slightly brighter with a cine steady-state free precession acquisition, where tissue contrast depends primarily on the T2/T1 ratio. The modest amount of T1-weighting is nonetheless sufficient to help detect delayed enhancement of infarcts (46). In addition, iron oxide agents distort the local magnetic field homogeneity, so that image quality with cine imaging techniques that are sensitive to off-resonance effects (spiral imaging and, to a lesser extent, steady-state free precession) may be adversely affected.

Myocardial Tagging
Measurement of myocardial strain previously required invasive placement of markers on the heart. It is now possible to use RF presaturation (eg, spatial modulation of magnetization) (47) and harmonic phase imaging (48) to observe local myocardial motion and measure mechanical properties such as strain. The persistence of the tags is T1-dependent. Because paramagnetic contrast agents shorten the T1 relaxation time of the myocardium and hence reduce the persistence of the tags, tagging measurements should be performed prior to the administration of a contrast agent.

Perfusion MR Imaging
One can assess myocardial perfusion by using a variety of means. For instance, one can use an intrinsic contrast mechanism such as blood oxygen level–dependent, or BOLD, rather than an exogenous contrast agent (49). On the basis of changes in tissue oxygenation manifested on T2*-weighted images, BOLD MR imaging can depict a stenotic coronary artery (50) and, along with measurement of wall thickening, may help differentiate scar from viable myocardium and may help identify patients who would be suitable candidates for revascularization (51). However, these studies are preliminary and have substantial technical limitations, such as low contrast-to-noise ratios that are inherent to the BOLD technique.

Dynamic first-pass imaging.—Dynamic first-pass contrast-enhanced MR imaging is the most practical method for evaluating myocardial perfusion (52–56). From a theoretical point of view, the use of an intravascular contrast agent simplifies the modeling of tissue perfusion since one does not need to model tissue extravasation, but such agents are not yet available for routine clinical use. Nonetheless, accurate measurements are also possible with use of extravascular agents that are widely available, even though 30%–50% of the agent leaks out of the vascular bed during the first pass (57). Close correlation exists between microsphere and MR imaging measures of myocardial perfusion in animal studies with gadopentetate dimeglumine as a contrast agent (58). In patients, there is good correlation between the perfusion reserve with MR imaging and the coronary flow reserve with Doppler ultrasonography (r = 0.80) (59). For quantification of myocardial perfusion, a low dose of contrast agent (eg, 0.025–0.05 mmol/kg) may improve accuracy, whereas a dose of 0.1–0.2 mmol/kg gives better myocardial enhancement and image quality. High infusion rates (eg, 3–5 mL/sec) are typical, followed by a saline flush. Perfusion MR imaging, with use of a pharmacologic agent to induce vasodilatation, is sensitive to flow variations over a wide range of low- and high-flow states (60).

Pulse sequences for dynamic first-pass imaging.—With interleaved gradient-echo echo-planar imaging (61) (essentially a gradient-echo pulse sequence that uses an abbreviated echo-planar read-out of the signal) or an inversion-recovery–prepared fast gradient-echo sequence (snapshot fast low-angle shot or turbo fast low-angle shot) (62,63), one can distinguish perfused tissue in the endocardial and epicardial layers of the myocardium. Recently, the saturation-recovery true fast imaging with steady-state precession sequence proved to give superior image quality, since it makes the most efficient use of the available magnetization (64).

Quantification of perfusion.—The quantification of tissue perfusion derives from the Kety model (65). The procedure is mathematically complex and involves a number of assumptions, including parameters such as water exchange rates, contrast agent distribution, and the relationship between signal intensity and the concentration of contrast agent. Qualitative measures such as the maximum myocardial enhancement, transit time, or upslope of myocardial enhancement (ie, slope of the initial portion of the signal intensity versus time curve after gadolinium administration) (66) are easier to implement in clinical practice. Even simple visual evaluation of the images can be sufficient. For instance, in one study of 104 patients without prior myocardial infarction in which a receiver operating characteristic analysis of myocardial perfusion was used, MR imaging had a 90% sensitivity for depicting at least one coronary artery with significant stenosis and an 85% specificity in identification of patients with significant coronary artery stenoses (67). The authors found that stress enhancement at dynamic MR imaging correlated more closely with quantitative coronary angiography results than did stress enhancement at single photon emission computed tomography (SPECT). Because of the reliance on visual analysis, this study used a relatively large contrast agent dose of 0.075 mmol/kg infused at 4 mL/sec to improve the contrast-to-noise ratio.

Resting perfusion.—Imaging of resting perfusion is only moderately sensitive in CAD. For instance, a study of 12 patients with significant stenoses of major epicardial vessels demonstrated a sensitivity of only 77% (68). Lesser stenoses can prove undetectable at rest. Nonetheless, resting perfusion studies may have some uses. For instance, underperfused regions of myocardium in resting studies correlate with increased amounts of nonviable tissue, as detected with myocardial delayed-enhancement MR imaging (69). Early after acute myocardial infarction, the resting perfusion deficit correlates with the long-term severity of left ventricular functional abnormality, and one finds higher perfusion in segments that have a residual contractile reserve at stress echocardiography (70).

Stress perfusion.—To detect significant stenoses of the epicardial coronary arteries, it is helpful to stress the patient so that a measure of the coronary flow reserve, or similar measures such as the myocardial perfusion reserve index, can be obtained. Though technically possible, it is awkward to perform a physiologic exercise stress test within the confined bore of an MR imager. Instead, a pharmaceutical agent, such as dipyridamole (typical dose, 0.56 mg per kilogram of body weight) or shorter-acting adenosine (typical dose, 140 µg/kg/min), may be administered to induce coronary vasodilatation. Side-effects of dipyridamole may necessitate administration of aminophylline, whereas most side-effects of adenosine are rapidly terminated when the infusion is discontinued. The safety profile and more consistent course of action make adenosine the preferred agent for stress perfusion MR imaging.

An abnormal perfusion reserve at MR imaging helps distinguish patients with CAD from normal subjects (71). In a study of 34 patients with a stenosis of an epicardial coronary artery of at least 75%, a cutoff value of 1.5 for MR imaging perfusion reserve helped differentiate normal from ischemic myocardial segments (72). This cutoff value yielded high sensitivity (90%), specificity (83%), and diagnostic accuracy (87%) for CAD, with excellent inter- and intraobserver agreement. The perfusion reserve was determined by means of a linear fit of the upslope of the signal intensity–time curves in perfusion studies performed at rest and after dipyridamole infusion.

Role in revascularization.—Perfusion MR imaging demonstrates the effectiveness of coronary interventions. In a study of 35 patients with single- and multivessel CAD imaged within 24 hours of coronary revascularization, a myocardial perfusion reserve index (upslope index) was calculated from resting and stress perfusion MR imaging (73). The perfusion reserve index improved but did not normalize after successful revascularization. The improvement was greater in patients receiving stents than in those only undergoing angioplasty.

Comparisons with PET and SPECT.—The coronary flow reserve determined at contrast-enhanced MR imaging correlates well with that at nitrogen 13 ammonia positron emission tomography (PET) (74). Flow reserve values at MR imaging are lower than those at PET, in part, owing to a low extraction fraction for extracellular agents such as gadopentetate dimeglumine.

Findings of several studies have confirmed a sensitivity and specificity of stress perfusion MR imaging equivalent or superior to those of SPECT. In the literature, sensitivity and specificity values of MR imaging range 64%–92% and 71%–100%, respectively (75–80). MR imaging would therefore appear to be a reasonable alternative to SPECT for the evaluation of patients suspected of having CAD, with the additional advantages of better depiction of wall motion, cardiac morphology, and myocardial viability. Nonetheless, MR imaging has yet to make much impact into routine clinical practice, in part because SPECT or dobutamine stress echocardiography can generally provide the needed diagnostic information, and because of a lack of the large-scale multicenter trials that would validate any potential superiority of MR imaging.

Microvascular Integrity
Whereas angiographic methods help evaluate the epicardial coronary arteries, events at the level of the microvasculature (arterioles, capillaries, and venules) are beyond the spatial resolution of standard imaging methods. For instance, one can recanalize an occluded coronary artery, yet within the capillary there may be a persistently diminished blood flow because the microvasculature remains plugged by red blood cell stasis (81). Other possible causes of microvascular obstruction include myocardial edema and endothelial cell damage from free radical formation. The "no-reflow" phenomenon, which indicates lack of reperfusion from microvascular impairment at the core of a reperfused infarct, presents as a subendocardial region of persistent hypoenhancement (82,83). Since flow at the core is very low but not zero, the hypoenhanced regions eventually become hyperenhanced.

In a study of 22 patients with acute myocardial infarction, contrast-enhanced imaging performed a few minutes after contrast agent infusion showed subendocardial hypoenhancement inside hyperenhancing myocardium in nearly half of the patients, which is consistent with no reflow and microvascular obstruction (84). Microvascular obstruction may indicate a worsened prognosis (85) and may predict a larger amount of adverse left ventricular remodeling (86). With respect to the prediction of adverse left ventricular remodeling, the optimal time for assessment of microvascular obstruction was 1 day after coronary angioplasty (87). Microvascular obstruction is also associated with an increased incidence of intramyocardial hemorrhage (88) and is more common after angioplasty than thrombolysis with or without angioplasty (89).

Syndrome X.—Syndrome X refers to a heterogeneous group of patients with anginal symptoms but normal epicardial coronary arteries at angiography and no evidence of coronary artery spasm (90). Although the origin is unknown, one possibility is an ischemic origin related to endothelial dysfunction at the microvascular level. Patients with syndrome X demonstrate a reduced myocardial perfusion reserve at contrast-enhanced MR imaging (91,92). Moreover, a study of 24 patients with syndrome X demonstrated delayed subendocardial gadolinium enhancement in two-thirds of the subjects (93). More interesting, with successful relief of symptoms by using ß-blockers, the delayed contrast enhancement disappeared in most of the patients. The investigators suggested that the enhancement might have been caused by alterations in cell membrane permeability related to the frequent ischemic episodes rather than to the irreversible consequences of infarction.

Myocardial Viability
Infarcts occur when there has been prolonged occlusion (eg, >30–40 minutes) of an epicardial coronary artery without sufficient collateral blood supply to the affected myocardium. The measurement of the amount of scar tissue helps to prognosticate whether patients will functionally improve in response to coronary revascularization therapy. Morphology (eg, wall thickness) alone is inadequate. Standard methods for making this distinction include the use of reinjection ²⁰¹Tl imaging and measurement of wall-motion and systolic thickening with echocardiography.

Dobutamine stress testing.—Viability can be assessed without the need for contrast media by performing cine MR imaging during a low-dose infusion (5–10 µg/kg/min) of dobutamine, which is comparable to dobutamine stress echocardiography. Improved left ventricular wall thickening with stress in a segment that functions poorly at rest indicates viability (94). A comparison among dobutamine stress transesophageal echocardiography, dobutamine cine MR imaging, and fluorine 18 (¹⁸F) fluorodeoxyglucose PET in 43 patients with chronic infarction and wall-motion abnormalities resulted in a respective sensitivity and specificity of 77% and 81% and 94% and 100% for echocardiography and MR imaging (95). Criteria for viability were a resting wall thickness greater than 5.5 mm or wall thickening of at least 1 mm with stress. Dobutamine stress MR imaging can also be used to detect ischemic myocardium (96).

In patients with nondiagnostic echocardiograms, dobutamine stress cardiac MR imaging may have prognostic value (97). The presence of inducible ischemia or left ventricular ejection fraction under 40% was associated with future myocardial infarction or cardiac death, independent of the presence of risk factors for coronary arteriosclerosis.

Delayed enhancement.—Myocardial delayed enhancement, also called "late enhancement," "delayed enhancement MR imaging," "delayed hyperenhancement," and so forth, is the most accurate means to detect myocardial infarction (Fig 1). Delayed uptake of contrast agents within infarcts was first described more than 10 years ago (98), but there have been extensive experimental studies, improved pulse sequences, and recognition of the clinical importance of the method within the past few years (82,99,100). Cellular degradation in the infarcted region results in an increase in the permeability and enlargement of the extravascular space, and hence, an increased distribution volume for the extracellular contrast agent. Moreover, gadolinium chelates wash out of infarcted tissue more slowly than out of healthy myocardium. The net result is that infarcted regions appear bright on delayed contrast-enhanced T1-weighted images. The size and location of the infarcted region, as demonstrated histochemically in animal models, correlate with the size and location of myocardial delayed enhancement.

View larger version (172K): [in this window] [in a new window] [Download PPT slide]   Figure 1a. (a) Two-chamber inversion-recovery gradient-echo MR image (4.6/1.2/200 [repetition time msec/echo time msec/inversion time msec], 20° flip angle, 192 x 256 matrix gated to every other R wave) and (b) four-chamber view show extensive infarction of enlarged left ventricle with transmural delayed enhancement (arrows).

View larger version (175K): [in this window] [in a new window] [Download PPT slide]   Figure 1b. (a) Two-chamber inversion-recovery gradient-echo MR image (4.6/1.2/200 [repetition time msec/echo time msec/inversion time msec], 20° flip angle, 192 x 256 matrix gated to every other R wave) and (b) four-chamber view show extensive infarction of enlarged left ventricle with transmural delayed enhancement (arrows).

Techniques for contrast-enhanced imaging of myocardial viability.—The current technique involves the rapid infusion of a gadolinium chelate (doses are typically in the range of 0.1–0.2 mmol/kg) followed approximately 5–30 minutes later by a high-resolution cardiac-gated T1-weighted pulse sequence (101). Imaging too early (eg, <5 minutes after contrast agent infusion) may result in an underestimation of the infarcted region, whereas imaging too late (eg, after >30 minutes) may result in excessive washout of the contrast agent and a poor SNR. Animal (102) and human (103) study findings of acute myocardial infarction showed a substantial change in the portion of left ventricle that enhanced depending on the timing of the acquisition with respect to the contrast agent infusion, with overestimation of infarct size if imaging was performed too early. However, there is also evidence that the spatial extent of hyperenhancement does not vary substantially over the 5–30-minute period after contrast agent infusion so long as one selects an appropriate inversion time to minimize the signal intensity of viable myocardium (104).

Although rarely used, an alternative approach involves infusing the contrast agent at a constant rate (105,106). The constant infusion maintains an equilibrium concentration of the contrast agent in the blood and enables quantitative measurement of the tissue-blood partition coefficient, . This parameter increases in infarcts owing to loss of integrity of the cell membrane. The method eliminates the influence of blood flow, regional perfusion, and renal excretion.

The typical pulse sequence for myocardial delayed enhancement is a multishot inversion-recovery–prepared gradient-echo sequence. T1-weighted images are acquired 5–30 minutes after contrast agent infusion (107). Each breath hold yields one or a few sections. Choice of the appropriate inversion time (approximately 200 msec) to null the signal intensity of normal myocardium is critical for accurate delineation of the infarcted region. The healthy myocardium appears dark, whereas the enhancing myocardium appears bright. However, the optimal inversion time will lengthen over time as the concentration of gadolinium in the blood and myocardium gradually diminishes. Phase-sensitive reconstructions render the technique less sensitive to the choice of inversion time and reduce the variation in apparent infarct size (108). One study suggested the use of a very short inversion time (eg, 50–100 msec) to improve contrast between infarct and blood pool (109). Single-shot versions of the pulse sequence appear promising since they do not have motion sensitivity; alternatively, one can image the entire heart in a single breath hold by using a volumetric acquisition (110).

"Bright is dead" hypothesis.—It is widely accepted that delayed enhancement in the proper location and given the appropriate clinical setting represents infarction, but some controversy remains (111). For instance, there is some contrary evidence that myocardial delayed enhancement in the acute postinfarct phase may cause overestimation in the amount of irreversibly damaged tissue. In one study, 18 patients (1015 segments) were studied within 2 weeks and again 3 months after reperfused acute myocardial infarction (112). Of 324 segments with impaired function initially, 180 improved at follow-up. Of the segments with improved function at follow up, 62% showed transmural enhancement involving more than 50% of each segment. The sensitivity and specificity for myocardial delayed enhancement in predicting functional recovery were only 38% and 88%, respectively. Another study of 10 patients suggested that one should combine myocardial delayed enhancement with wall-motion analysis and first-pass enhancement during dobutamine infusion to maximize sensitivity and, to a lesser extent, specificity (113). Nonetheless, the majority of published study findings indicate that myocardial delayed enhancement accurately depicts the extent of nonviable myocardium.

Comparison with other imaging modalities.—Results of myocardial delayed enhancement correlate well with those of dobutamine stress echocardiography (114,115), and there is excellent agreement with PET as well. Delayed enhancement correlates with areas of decreased flow and metabolism at PET (116). However, MR imaging is slightly more sensitive—in one study, 11% of segments called viable with PET showed delayed enhancement with MR imaging. Another study of 26 patients demonstrated a 96% sensitivity and 84% specificity for myocardial delayed enhancement, with ¹⁸F fluorodeoxyglucose PET as the standard (117). In particular, MR imaging is superior in detecting subendocardial infarction (118). There is also good agreement with SPECT (119), but myocardial delayed-enhancement MR imaging has the major advantage of superior spatial resolution by an order of magnitude and the capability to incorporate anatomic and cine imaging in the same imaging session. In a study of 91 patients, SPECT depicted all of the nearly transmural infarctions but missed 47% of subendocardial infarctions that were seen at myocardial delayed-enhancement MR imaging (120). Authors of another study of 20 patients with equivocal stress-rest sestamibi SPECT examination findings found the presence of subendocardial infarction at myocardial delayed-enhancement MR imaging in 40% of the patients (121).

Prognostic implications of myocardial delayed enhancement.—Findings of several studies have shown that the amount of delayed transmural enhancement predicts the degree of functional recovery after acute myocardial infarction (122,123). Extensive transmural myocardial delayed enhancement is highly predictive of a lack of functional improvement after revascularization; conversely, absence of myocardial delayed enhancement correlates with a likelihood of functional recovery (124). In a study of 32 patients with acute myocardial infarction, subjects were imaged within 2 weeks and again after 1 year by using T2-weighted contrast-enhanced first-pass and myocardial delayed-enhancement MR imaging (125). The presence of a high-grade perfusion deficit or delayed enhancement in the early-phase MR imaging study is highly predictive of scar formation and lack of functional recovery at 1 year. Increased signal intensity on T2-weighted images indicates myocardial edema but does not always indicate infarction (126), that distinction requires the additional use of myocardial delayed enhancement. In another study of acute myocardial infarction, the investigators imaged 20 patients within 1 week of the acute event and 7 months later (127). Enhancement patterns correlated with regional circumferential shortening strain (a measure of myocardial function) as determined with the harmonic phase imaging technique. Absence of myocardial delayed enhancement had a positive predictive value of 77% for functional recovery, whereas presence of myocardial delayed enhancement had a negative predictive value of 66%. The authors concluded that, compared with the lack of early hypoenhancement, lack of delayed hyperenhancement is more accurate in predicting functional improvement in dysfunctional segments. The early hypoenhanced regions, corresponding to regions with microvascular obstruction, resulted in substantial underestimation of the amount of irreversibly injured myocardium after acute myocardial ischemia. In the chronic setting, myocardial delayed enhancement correlates inversely with circumferential shortening (128).

History of myocardial infarction greatly increases the mortality rate compared with that of the general population. Although the electrocardiogram is a useful indicator of prior infarction, most infarcts are not associated with the formation of Q waves. MR imaging may therefore be useful in detection of unsuspected myocardial infarcts. In a study of 82 subjects, myocardial delayed enhancement helped predict the presence, location, and transmural extent of healed Q-wave and non–Q-wave myocardial infarction (129).

Myocardial delayed enhancement and myocardial stunning.—Transient hypoperfusion can cause myocardial stunning, which is associated with wall-motion abnormalities in the clinical setting of suspected acute myocardial infarction. Myocardial delayed enhancement in combination with cine MR imaging helps differentiate wall-motion abnormalities of myocardial stunning, which are reversible, from those of myocardial infarction, which are often irreversible depending on the severity of the injury (130). Either condition may cause a wall-motion abnormality, but delayed enhancement occurs only with infarcts. Lack of delayed enhancement indicates stunning rather than infarction and a high likelihood that left ventricular function will fully recover (131). In a study of 30 patients imaged approximately 1 week and 13 weeks after a reperfused myocardial infarction, the likelihood of functional improvement of segments without hyperenhancement was 3, 14, and 20 times higher than that of segments with 26%–50%, 51%–75%, and more than 75% hyperenhancement, respectively. The likelihood of complete functional recovery of segments without hyperenhancement was 3.8, 11.1, and 50.0 times higher than that of segments with 26%–50%, 51%–75%, and more than 75% hyperenhancement, respectively (132). Thus, functional improvement of stunned myocardium is predicted with myocardial delayed-enhancement MR imaging. However, in situations where an intermediate level of myocardial delayed enhancement is present (likely representing a mix of viable and nonviable tissue), the predictive value is less certain.

Triage of patients with chest pain.—Patients who come to the emergency room with chest pain often represent a diagnostic dilemma, since a substantial number of patients with a noncardiac cause of pain can usually be sent home, whereas those with acute coronary syndrome require observation or treatment. One study of 161 patients with more than 30 minutes of chest pain but a nondiagnostic electrocardiogram found that the combination of myocardial delayed enhancement, cine, and perfusion MR imaging was the strongest predictor of CAD and added diagnostic value over clinical parameters (133).

Diagnosis of ventricular aneurysms.—In addition to impairment of left ventricular function and arrhythmias, complications of myocardial infarction include true and false aneurysms. True aneurysms, which are composed of pericardium adherent to underlying epicardium and scar tissue from infarcted myocardium, do not usually rupture. However, false aneurysms, which consist of pericardium that contains a ruptured left ventricle, may enlarge over time and require surgical resection (134). MR imaging can help make this distinction based on morphologic criteria (eg, a wide mouth and anterior location for true aneurysm) (135). A case report demonstrated delayed enhancement of scarred myocardium within the aneurysm wall, which indicated a true aneurysm (136). The wall of a false aneurysm, which does not contain myocardial scar tissue, should not (at least in theory) demonstrate a comparable pattern of enhancement.

Right ventricular infarction.—Right ventricular infarction occurs commonly in patients with ostial right coronary artery occlusion, but the diagnosis is elusive. Delayed enhancement MR imaging is likely the best technique for the noninvasive identification of patients with this syndrome (137).

Cardiomyopathy and Myocarditis
Morphologic features and the presence or absence of contrast enhancement can be helpful in the detection and characterization of various types of cardiomyopathy and myocarditis. Focal myocardial enhancement in conjunction with a wall-motion abnormality correlates strongly with myocarditis (138), which may be of viral or other origin. The contrast-enhancement pattern becomes diffuse over a period of days to weeks (139). One case report described a patient who developed a right ventricular pseudoaneurysm owing to a presumed viral myocarditis. Portions of both the right and left ventricles showed transmural contrast enhancement (140). Contrast-enhanced MR imaging can be helpful for other infectious processes as well (141,142). Another kind of myositis, hypereosinophilic syndrome, is characterized by peripheral eosinophilia and multiorgan dysfunction owing to eosinophilic infiltration. Contrast-enhanced MR imaging depicts myocardial involvement (143) and ventricular thrombi that may occur in this condition (Fig 2).

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 2a. Thrombus (arrows) in left ventricular apex of a patient suspected of having hypereosinophilic syndrome. (a) Transverse contrast-enhanced CT scan. (b) Two-chamber (4.6/1.2/200, 20° flip angle, 192 x 256 matrix gated to every other R wave) and (c) four-chamber myocardial delayed-enhancement MR images delineate and characterize the mass as thrombus by its location, smooth margins, and lack of contrast enhancement.

View larger version (185K): [in this window] [in a new window] [Download PPT slide]   Figure 2b. Thrombus (arrows) in left ventricular apex of a patient suspected of having hypereosinophilic syndrome. (a) Transverse contrast-enhanced CT scan. (b) Two-chamber (4.6/1.2/200, 20° flip angle, 192 x 256 matrix gated to every other R wave) and (c) four-chamber myocardial delayed-enhancement MR images delineate and characterize the mass as thrombus by its location, smooth margins, and lack of contrast enhancement.

View larger version (173K): [in this window] [in a new window] [Download PPT slide]   Figure 2c. Thrombus (arrows) in left ventricular apex of a patient suspected of having hypereosinophilic syndrome. (a) Transverse contrast-enhanced CT scan. (b) Two-chamber (4.6/1.2/200, 20° flip angle, 192 x 256 matrix gated to every other R wave) and (c) four-chamber myocardial delayed-enhancement MR images delineate and characterize the mass as thrombus by its location, smooth margins, and lack of contrast enhancement.

Right ventricular dysplasia.—Although most ventricular tachycardias originate from the left side of the heart, the right ventricle may also be a source. The cause can be right ventricular dysplasia (148), which has a poor prognosis, or right ventricular outflow tract tachycardia, which is more benign but can cause sudden death. The diagnosis is made on the basis of major and minor criteria involving family history, genetic factors, arrhythmias, conduction and repolarization abnormalities, biopsy, and right ventricular morphology and function (eg, marked dilatation or dyskinetic areas).

The origin of arrhythmia is commonly determined with an invasive electrophysiologic study. MR imaging can be helpful in problematic cases, sometimes demonstrating abnormal wall motion in the body or outflow tract of the right ventricle and, less commonly, fatty replacement of the myocardium (149). Although contrast enhancement is not commonly used, a recent report suggests that delayed enhancement of the right ventricular myocardium is more common than was previously appreciated and may have diagnostic value (150).

Atrial arrhythmias.—Atrial fibrillation is commonly associated with arrhythmogenic foci located near the pulmonary vein orifices. Contrast agents are helpful in MR angiography of the pulmonary veins, which is used to guide RF ablation procedures and detect complications such as pulmonary vein stenosis (151).

Sarcoidosis.—In advanced sarcoidosis, echocardiography can help detect septal thinning, systolic and diastolic left ventricular dysfunction, and pericardial effusion. Electrocardiographic changes are frequent. However, diagnosis of early sarcoidosis is more challenging. Endomyocardial biopsy can provide the diagnosis but is invasive and has sampling errors. In a study of 16 patients with cardiac sarcoidosis, contrast enhancement was present in half of the cases and diminished after steroid therapy (152). Another study suggested that MR imaging is specific but has low sensitivity for sarcoid involvement of the myocardium (153).

Amyloidosis.—Amyloidosis is a cause of restrictive cardiomyopathy and can be primary or secondary in origin. Infiltration with fibrillar proteins causes a loss of compliance and impairs diastolic function, and systolic function can be reduced as well. Echocardiography may demonstrate a "sparkling" pattern, whereas both echocardiography and MR imaging can show functional impairment and biventricular hypertrophy (154). Inhomogeneous contrast enhancement may occur but is not specific. Some preliminary data suggest that ventricular contrast enhancement may also occur within hypertrophic regions in certain forms of glycogen storage disease, but this pattern is again nonspecific (155).

Dilated cardiomyopathy.—Delayed enhancement MR imaging may help differentiate the underlying origin of dilated cardiomyopathy. In a study of 90 patients with dilated cardiomyopathy, 59% showed no enhancement, whereas myocardial delayed enhancement occurred in 41% of subjects (156). Although in 13%, subendocardial enhancement was indistinguishable from infarction, in 28%, midwall myocardial enhancement (presumably associated with fibrosis) permitted differentiation from an ischemic origin. The authors suggest that use of coronary catheterization, rather than MR imaging, to decide if left ventricular dysfunction was caused by CAD would have led to the incorrect assignment of a diagnosis of dilated cardiomyopathy in 13% of their patients. The degree of enhancement correlates with the severity of functional abnormality (157). In patients undergoing chemotherapy with cardiotoxic agents such as anthracyclines, which can cause dilated cardiomyopathy, an early (day 3) increase in myocardial contrast enhancement was predictive of future worsening in left ventricular function (158).

Cardiac Masses, Thrombi, and Infections
Although echocardiography and CT are often sufficient for the evaluation of cardiac and paracardiac masses, MR imaging can provide useful information in many instances (159). Echocardiography is an excellent method for evaluation of left-sided structures but is less accurate for the right side of the heart, paracardiac region, lungs, and mediastinum. Contrast-enhanced MR imaging can help distinguish tumors (160–165), which generally enhance, from thrombi. Along with cine and T2-weighted images, the standard perfusion and myocardial delayed-enhancement sequences can be very helpful in the evaluation of the contrast enhancement characteristics of cardiac masses.

Preliminary data suggest that myocardial delayed-enhancement MR imaging may be more accurate in detecting left ventricular thrombi than is transthoracic echocardiography (166). In a study of 24 patients, MR imaging was more sensitive than transesophageal echocardiography in detecting intracardiac thrombi (167). Some thrombi showed delayed contrast enhancement, which characterized them as organized clots. However, care must be taken to use thin sections (eg, 5 mm or thinner) for the detection of small thrombi, and the entire region of interest (eg, left atrial appendage or left ventricular apex) must be included in the imaging volume.

Myxomas, the most common benign tumors of the heart, are well evaluated with transthoracic and transesophageal echocardiography (168). However, MR imaging can occasionally provide helpful information about the attachment site and the relationship to key anatomic structures (Fig 3). Myxomas often appear bright on spin-echo images and dark on gradient-echo cine images and may show uniform or inhomogeneous contrast enhancement (169).

View larger version (138K): [in this window] [in a new window] [Download PPT slide]   Figure 3a. Right atrial myxoma (arrows). (a) Dark blood MR image with dual-inversion fast spin-echo pulse sequence (R-R interval/42, echo train length of 24, 192 x 256 matrix gated to every R wave). (b) Myocardial delayed-enhancement MR image (4.6/1.2/200, 20° flip angle, 192 x 256 matrix gated to every other R wave) clearly delineates the margins and attachment of the mass to fossa ovalis.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 3b. Right atrial myxoma (arrows). (a) Dark blood MR image with dual-inversion fast spin-echo pulse sequence (R-R interval/42, echo train length of 24, 192 x 256 matrix gated to every R wave). (b) Myocardial delayed-enhancement MR image (4.6/1.2/200, 20° flip angle, 192 x 256 matrix gated to every other R wave) clearly delineates the margins and attachment of the mass to fossa ovalis.

	CORONARY MR ANGIOGRAPHY

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 
Minimally invasive tests for myocardial ischemia include SPECT (176,177) and PET (178,179). These tests reveal perfusion abnormalities but do not depict the coronary artery stenoses that cause them nor do they provide direct measurements of coronary artery blood flow. The standard of reference for the evaluation of coronary arteries is contrast-enhanced angiography, with more than 500 000 diagnostic cardiac catheterizations performed annually in the United States. Despite the development of multiple noninvasive tests for the detection of myocardial ischemia, up to 20% of these coronary angiograms reveal no substantial CAD (180).

Noninvasive imaging of the coronary arteries, along with quantification of flow (181), would provide obvious benefits. Challenges in coronary artery angiography include inadequate spatial resolution, SNR, and contrast enhancement (182). Findings of a study in which a breath-hold single-section two-dimensional acquisition was used demonstrated good sensitivity and specificity for proximal CAD (183), but subsequent study findings with two-dimensional acquisitions were less sanguine (184). Better results are obtained with volumetric acquisitions that cover a large portion of the coronary artery tree (185).

Navigator-gating methods eliminate the need for breath holding by electronically monitoring the diaphragm location (186,187). Data accumulate only during a specified portion of the respiratory cycle, and the total duration of data acquisition is typically about 5–15 minutes. Navigator-gating methods improve the SNR and in-plane spatial resolution (eg, 0.5 mm). A recent multicenter trial in which navigator techniques without contrast enhancement were used found a moderately high sensitivity and specificity of coronary MR angiography (188). The sensitivity, specificity, and accuracy for patients with disease of the left main coronary artery or with three-vessel disease were 100%, 85%, and 87%, respectively. The negative predictive values for any CAD and for left main artery or three-vessel disease were 81% and 100%, respectively.

Recently, several groups have applied breath-hold three-dimensional acquisitions in combination with bolus administration of a paramagnetic contrast agent (189–191). Potential benefits include improved SNR, less sensitivity to artifacts from slowly flowing blood, and reduced imaging times. Authors of one study found that contrast-enhanced breath-hold three-dimensional MR angiography was more accurate than respiratory-gated three-dimensional MR angiography for the coronary arteries (192). Extracellular contrast agents are less useful for lengthy navigator-gated acquisitions, since the contrast agent concentration in the blood diminishes so rapidly. The concentration of blood pool agents, on the other hand, is nearly constant for minutes to hours after infusion, and therefore, might be beneficial (193–195). For instance, authors of one study in which breath-hold and navigator-gated sequences were used found that the administration of SH L 643A improved contrast-to-noise ratios in the coronary arteries up to 30 minutes after infusion (196).

Coronary MR angiography can demonstrate coronary artery aneurysms in patients with Kawasaki disease. Wall thinning and delayed contrast enhancement occur less consistently, despite clinical evidence of myocardial infarction, than is typically observed in adult patients with infarction (197).

Contrast-enhanced three-dimensional MR angiography, either with or without cardiac gating, demonstrates the patency of coronary artery bypass grafts (198–201), though the accuracy is currently less than that of CT (202–204).

	FUTURE DEVELOPMENTS

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Very High Static Fields
The recent introduction of whole-body MR imaging systems with more powerful static fields (eg, 3.0–9.4 T) has the potential to greatly improve the SNR, and thereby, the quality of cardiac imaging in general and coronary artery images in particular (205). The relaxivity of paramagnetic contrast agents is known to vary with magnetic field strength (206). Early results of contrast-enhanced MR angiography of the pulmonary arteries at 4 T were disappointing (207). On the other hand, contrast-enhanced MR imaging of the brain (208) and contrast-enhanced peripheral MR angiography (209) demonstrated a higher contrast-to-noise ratio at 3 T compared with that at 1.5 T. It is not yet known if comparable benefits for contrast enhancement will be seen in the heart.

Interventional MR Imaging of the Heart
In the future, contrast-enhanced MR imaging may be used to guide interventions. For instance, MR imaging can be used in experimental systems to monitor, in real time, electromagnetic catheter-directed RF ablations (eg, for treatment of atrial fibrillation) within the heart (210). Contrast media are helpful for improving the SNR of volumetric cardiac images upon which the movements of the catheter tip are mapped. The method has the potential to provide more precise positioning of the site of RF ablation and, of course, it eliminates radiation exposure to the operator.

Several new treatments for heart failure are under development that involve the transplantation of primitive cell types (eg, stem cells or myoblasts) into the damaged tissue, where they can trans-differentiate into functional tissue (211). In a study of seven patients with severe heart failure, cardiac MR imaging was used to plan therapy involving direct injection of myoblasts (harvested from leg muscle and expanded in vitro) into segments with a diastolic wall thickness greater than 4 mm and transmural infarction as indicated with myocardial delayed enhancement (212). Stem cell therapy in the heart might further benefit from the combination of molecular imaging methods with interventional MR imaging techniques. In animal models, mesenchymal stem cells have been labeled with iron-based contrast agents to determine myocardial localization after implantation (213,214). This technology may allow in vivo evaluation of stem cell retention, engraftment, and migration. In another animal study, MR imaging was able to accurately localize the targeted catheter-based implantation of iron-loaded myogenic precursor cells into locally infarcted left ventricular myocardium (215).

	CONCLUSION

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Contrast agents expand the range of cardiac applications for MR imaging. Because of its simplicity and high accuracy, myocardial delayed-enhancement MR imaging may be the method of choice for the evaluation of myocardial viability. Dynamic contrast-enhanced MR imaging can be used to quantify myocardial perfusion and detect myocardial ischemia. Contrast agents improve detection of cardiac thrombi and, if properly done, contrast-enhanced MR imaging can rival or exceed the accuracy of echocardiography. Contrast-enhanced MR imaging is complementary to echocardiography and CT in the characterization of intra- and paracardiac masses and can be helpful in the detection of myocarditis, sarcoidosis, as well as other infectious or inflammatory processes of the myocardium.

The utilization of contrast agents for the heart will undoubtedly expand in the coming years. Promising developments include receptor-targeted contrast agents, imaging of MR-guided interventions that include primitive cell transplants for heart failure, and imaging at field strengths higher than 1.5 T.

	ESSENTIALS

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The use of standard gadolinium chelates for cardiac MR imaging improves the detection and characterization of viable myocardium, inflammatory disorders affecting the myocardium and pericardium, thrombi, and other masses.

Unlike the pulse sequences used for contrast-enhanced MR imaging of other organs, a cardiac-gated pulse sequence with an inversion recovery magnetization preparation is used to maximize sensitivity for the T1 effects of contrast agents in the heart.

Contrast-enhanced MR imaging is the most accurate imaging modality for determining myocardial viability; in particular, it is more sensitive for subendocardial infarcts than SPECT, PET, or dobutamine stress echocardiography.

Although tissue-specific contrast-agents are not yet approved for cardiac MR imaging, they have the potential to improve the depiction of cardiac morphology, quantify myocardial perfusion, characterize vulnerable plaque, and improve MR angiography of coronary arteries.

	FOOTNOTES

 
The author is a consultant for Advanced Magnetics, Cambridge, Mass, and Eagle Vision Pharmaceuticals, Exton, Pa.

Abbreviations: CAD = coronary artery disease, RF = radiofrequency, SNR = signal-to-noise ratio

	REFERENCES

TOP ABSTRACT INTRODUCTION GENERAL CONSIDERATIONS FOR... CATEGORIES OF CONTRAST AGENTS... METHODS FOR CONTRAST AGENT... ROLE OF CONTRAST AGENTS... CORONARY MR ANGIOGRAPHY FUTURE DEVELOPMENTS CONCLUSION ESSENTIALS REFERENCES

 

1. American Heart Association 2002 heart and stroke statistical update Dallas, Tex: American Heart Association, 2003.
2. Wolf GL. Role of magnetic resonance contrast agents in cardiac imaging. Am J Cardiol 1990; 66:59F-62F.[CrossRef][Medline]
3. Brasch RC. New directions in the development of MR imaging contrast media. Radiology 1992; 183:1-11.[Abstract/Free Full Text]
4. Saeed M, Wendland MF, Higgins CB. The developing role of magnetic resonance contrast media in the detection of ischemic heart disease. Proc Soc Exp Biol Med 1995; 208:238-254.[CrossRef][Medline]
5. Danias PG. Gadolinium-enhanced cardiac magnetic resonance imaging: expanding the spectrum of clinical applications. Am J Med 2001; 110:591-592.[CrossRef][Medline]
6. Castillo E, Bluemke DA. Cardiac MR imaging. Radiol Clin North Am 2003; 41:17-28.[CrossRef][Medline]
7. Doyle M, Biederman RW. Future prospects in cardiac magnetic resonance imaging. Curr Cardiol Rep 2003; 5:83-90.[Medline]
8. Sodickson DK, McKenzie CA, Li W, Wolff S, Manning WJ, Edelman RR. Contrast-enhanced 3D MR angiography with simultaneous acquisition of spatial harmonics: a pilot study. Radiology 2000; 217:284-289.[Abstract/Free Full Text]
9. Saeed M, Wendland MF, Watzinger N, Akbari H, Higgins CB. MR contrast media for myocardial viability, microvascular integrity and perfusion. Eur J Radiol 2000; 34:179-195.[CrossRef][Medline]
10. In: Pettersson H, eds. The encyclopaedia of medical imaging. Vol 1. 2003. Available at: www.medcyclopaedia.com. Accessed August 31.
11. Jung CW, Jacobs P. Physical and chemical properties of superparamagnetic iron oxide MR contrast agents: ferumoxides, ferumoxtran, ferumoxsil. Magn Reson Imaging 1995; 13:661-674.[CrossRef][Medline]
12. Jacobs P, Shenouda M. A phase I pharmacokinetics and safety study of ferumoxytol, a new intravenous iron therapy (abstr). J Am Soc Nephrol 2003; 14:770.
13. Reimer P, Weissleder R, Brady TJ, et al. Experimental hepatocellular carcinoma: MR receptor imaging. Radiology 1991; 180:641-645.[Abstract/Free Full Text]
14. Krombach GA, Wendland MF, Higgins CB, Saeed M. MR imaging of spatial extent of microvascular injury in reperfused ischemically injured rat myocardium: value of blood pool ultrasmall superparamagnetic particles of iron oxide. Radiology 2002; 225:479-486.[Abstract/Free Full Text]
15. Johansson LO, Bjerner T, Bjornerud A, Ahlstrom H, Tarlo KS, Lorenz CH. Utility of NC100150 injection in cardiac MRI. Acad Radiol 2002; 9(suppl 1):S79-S81.
16. Weissleder R, Elizondo G, Wittenberg J, Rabito CA, Bengele HH, Josephson L. Ultrasmall superparamagnetic iron oxide: characterization of a new class of contrast agents for MR imaging. Radiology 1990; 175:489-493.[Abstract/Free Full Text]
17. Taylor AM, Panting JR, Keegan J, et al. Safety and preliminary findings with the intravascular contrast agent NC100150 injection for MR coronary angiography. J Magn Reson Imaging 1999; 9:220-227.[CrossRef][Medline]
18. Harisinghani MG, Barentsz J, Hahn PF, et al. Noninvasive detection of clinically occult lymph-node metastases in prostate cancer. N Engl J Med 2003; 348:2491- 2499.[Abstract/Free Full Text]
19. Prasad PV, Pierchala L, Chen Q, et al. Preliminary evaluation of code 7228 as an iron oxide based blood pool contrast agent for CE-MRA (abstr) In: Proceedings of the 11th Meeting of the International Society for Magnetic Resonance in Medicine. Berkeley, Calif: International Society for Magnetic Resonance in Medicine, 2003; 1338.
20. Amano Y, Herfkens RJ, Shifrin RY, Alley MT, Pelc NJ. Three-dimensional cardiac cine magnetic resonance imaging with an ultrasmall superparamagnetic iron oxide blood pool agent (NC100150). J Magn Reson Imaging 2000; 11:81-86.[CrossRef][Medline]
21. Kooi ME, Cappendijk VC, Cleutjens KB, et al. Accumulation of ultrasmall superparamagnetic particles of iron oxide in human atherosclerotic plaques can be detected by in vivo magnetic resonance imaging. Circulation 2003; 107:2453- 2458.[Abstract/Free Full Text]
22. Tombach B, Schneider J, Reimer P, et al. First pass and blood pool effect of a new Gd-containing blood pool MR contrast agent: phase I clinical trial of Gadomer-17 (abstr) In: Proceedings of the 10th Meeting of the International Society for Magnetic Resonance in Medicine. Berkeley, Calif: International Society for Magnetic Resonance in Medicine, 2002; 2585.
23. Roberts HC, Saeed M, Roberts TP, Mühler A, Brasch RC. MRI of acute myocardial ischemia: comparing a new contrast agent, Gd-DTPA-24-cascade-polymer, with Gd-DTPA. J Magn Reson Imaging 1999; 9:204-208.[CrossRef][Medline]
24. Saeed M, Lund G, Wendland MF, Bremerich J, Weinmann H, Higgins CB. Magnetic resonance characterization of the peri-infarction zone of reperfused myocardial infarction with necrosis-specific and extracellular nonspecific contrast media. Circulation 2001; 103:871-876.[Abstract/Free Full Text]
25. Lee SS, Goo HW, Park SB, et al. MR imaging of reperfused myocardial infarction: comparison of necrosis-specific and intravascular contrast agents in a cat model. Radiology 2003; 226:739-747.[Abstract/Free Full Text]
26. Brady TJ, Goldman MR, Pykett IL, et al. Proton nuclear magnetic resonance imaging of regionally ischemic canine hearts: effect of paramagnetic proton signal enhancement. Radiology 1982; 144:343-347.[Abstract/Free Full Text]
27. Flacke S, Allen JS, Chia JM, et al. Characterization of viable and nonviable myocardium at MR imaging: comparison of gadolinium-based extracellular and blood pool contrast materials versus manganese-based contrast materials in a rat myocardial infarction model. Radiology 2003; 226:731-738.[Abstract/Free Full Text]
28. Bremerich J, Saeed M, Arheden H, Higgins CB, Wendland MF. Normal and infarcted myocardium: differentiation with cellular uptake of manganese at MR imaging in a rat model. Radiology 2000; 216:524-530.[Abstract/Free Full Text]
29. Storey P, Danias PG, Post M, et al. Preliminary evaluation of EVP 1001–1: a new cardiac-specific magnetic resonance contrast agent with kinetics suitable for steady-state imaging of the ischemic heart. Invest Radiol 2003; 38:642-652.[Medline]
30. Weissleder R, Mahmood U. Molecular imaging. Radiology 2001; 219:316-333.[Abstract/Free Full Text]
31. Weissleder R, Lee A, Khaw B, Shen T, Brady T. Detection of myocardial infarction with MION-antimyosin. Radiology 1992; 182:381-385.[Abstract/Free Full Text]
32. Li WH, Parigi G, Fragai M, Luchinat C, Meade TJ. Mechanistic studies of a calcium-dependent MRI contrast agent. Inorg Chem 2002; 41:4018-4024.[CrossRef][Medline]
33. Longmore DB, Klipstein RH, Underwood SR, et al. Dimensional accuracy of magnetic resonance in studies of the heart. Lancet 1985; 1:1360-1362.[Medline]
34. Katz J, Milliken MC, Stray-Gunderson J, et al. Estimation of human myocardial mass with MR imaging. Radiology 1988; 169:495-498.[Abstract/Free Full Text]
35. Ehman RL, Julsrud PR. Magnetic resonance imaging of the heart: current status. Mayo Clin Proc 1989; 64:1134- 1146.[Medline]
36. Boxt LM, Rozenshtein A. MR imaging of congenital heart disease. Magn Reson Imaging Clin N Am 2003; 11:27-48.[CrossRef][Medline]
37. Didier D, Higgins CB, Fisher MR, Osaki L, Silverman NH, Cheitlijn MD. Congenital heart disease: gated MR imaging in 72 patients. Radiology 1986; 158:227-235.[Abstract/Free Full Text]
38. Edelman RR, Chien D, Kim D. Fast selective black blood MR imaging. Radiology 1991; 181:655-660.[Abstract/Free Full Text]
39. Vu T, Li W, Pierchala L, Tutton S, Prasad PV, Edelman RR. Robust multi-slice black blood imaging using a novel blood pool contrast agent (abstr). Radiology 2003; 229(P):311.[Free Full Text]
40. Pettigrew RI. Dynamic cardiac MR imaging: techniques and applications. Radiol Clin North Am 1989; 27:1183-1203.[Medline]
41. Higgins CB, Holt W, Pflugfelder P, Sechtem U. Functional evaluation of the heart with magnetic resonance imaging. Magn Reson Med 1988; 6:121-139.[Medline]
42. Rerkpattanapipat P, Mazur W, Link KM, Hundley WG. Assessment of cardiac function with MR imaging. Magn Reson Imaging Clin N Am 2003; 11:67-80.[CrossRef][Medline]
43. Atkinson DJ, Edelman RR. Cineangiography of the heart in a single breath-hold with a segmented turboFLASH sequence. Radiology 1991; 178:357-360.[Abstract/Free Full Text]
44. Carr JC, Simonetti O, Bundy J, Li D, Pereles S, Finn JP. Cine MR angiography of the heart with segmented true fast imaging with steady-state precession. Radiology 2001; 219:828-823.[Abstract/Free Full Text]
45. Shankaranarayanan A, Simonetti OP, Laub G, Lewin JS, Duerk JL. Segmented k-space and real-time cardiac cine MR imaging with radial trajectories. Radiology 2001; 221:827-836.[Abstract/Free Full Text]
46. Choi B, Chue KO, Kim Y, Chung H, Chung N, Choi D. Contrast-enhanced cine magnetic resonance imaging with balanced turbo field echo in myocardial infarction (abstr). Radiology 2003; 229(P):251.
47. Axel L, Dougherty L. Heart wall motion: improved method of spatial modulation of magnetization for MR imaging. Radiology 1989; 172:349-350.[Abstract/Free Full Text]
48. Kraitchman DL, Sampath S, Castillo E, et al. Quantitative ischemia detection during cardiac magnetic resonance stress testing by use of FastHARP. Circulation 2003; 107:2025-2030.[Abstract/Free Full Text]
49. Li D, Dhawale P, Rubin P, et al. Myocardial signal response to dipyridamole and dobutamine: demonstration of the BOLD effect using double-echo gradient-echo sequence. Magn Reson Med 1996; 36:16-20.[Medline]
50. Wacker CM, Hartlep AW, Pfleger S, et al. Susceptibility-sensitive magnetic resonance imaging detects human myocardium supplied by a stenotic coronary artery without a contrast agent. J Am Coll Cardiol 2003; 41:834-840.[Abstract/Free Full Text]
51. Egred M, Al-Mohammad A, Waiter GD, et al. Detection of scarred and viable myocardium using a new magnetic resonance imaging technique: blood oxygen level dependent (BOLD) MRI. Heart 2003; 89:738-744.[Abstract/Free Full Text]
52. Keijer JT, Bax JJ, van Rossum AC, et al. Myocardial perfusion imaging: clinical experience and recent progress in radionuclide scintigraphy and magnetic resonance imaging. Int J Card Imaging 1997; 13:415-431.[CrossRef][Medline]
53. Nagel E, Al-Saadi N, Fleck E. Cardiovascular magnetic resonance: myocardial perfusion. Herz 2000; 25:409-416.[CrossRef][Medline]
54. Laddis T, Manning WJ, Danias PG. Cardiac MRI for assessment of myocardial perfusion: current status and future perspectives. J Nucl Cardiol 2001; 8:207-214.[CrossRef][Medline]
55. Arai AE. Magnetic resonance first-pass myocardial perfusion imaging. Top Magn Reson Imaging 2000; 11:383-398.[CrossRef][Medline]
56. Wagner A, Mahrholdt H, Sechtem U, et al. MR imaging of myocardial perfusion and viability. Magn Reson Imaging Clin N Am 2003; 11:49-66.[CrossRef][Medline]
57. Tong CY, Prato FS, Wisenberg G, et al. Techniques for the measurement of the local myocardial extraction efficiency for inert diffusible contrast agents such as gadopentetate dimeglumine. Magn Reson Med 1993; 30:332-336.[Medline]
58. Keijer JT, van Rossum AC, Wilke N, et al. Magnetic resonance imaging of myocardial perfusion in single-vessel coronary artery disease: implications for transmural assessment of myocardial perfusion. J Cardiovasc Magn Reson 2000; 2:189-200.[Medline]
59. Wilke N, Jerosch-Herold M, Wang Y, et al. Myocardial perfusion reserve: assessment with multisection, quantitative, first-pass MR imaging. Radiology 1997; 204:373-384.[Abstract/Free Full Text]
60. Klocke FJ, Simonetti OP, Judd RM. Limits of detection of regional differences in vasodilated flow in viable myocardium by first-pass magnetic resonance perfusion imaging. Circulation 2001; 104:2412-2416.[Abstract/Free Full Text]
61. Ding S, Wolff SD, Epstein FH. Improved coverage in dynamic contrast-enhanced cardiac MRI using interleaved gradient-echo EPI. Magn Reson Med 1998; 39:514-519.[Medline]
62. Haase A. Snapshot FLASH MRI: applications to T1, T2, and chemical-shift imaging. Magn Reson Med 1990; 13:77-89.[Medline]
63. Manning WJ, Atkinson DJ, Grossman W, Paulin S, Edelman RR. First-pass nuclear magnetic resonance imaging studies using gadolinium-DTPA in patients with coronary artery disease. J Am Coll Cardiol 1991; 18:959-965.[Abstract]
64. Schreiber WG, Schmitt M, Kalden P, et al. Dynamic contrast-enhanced myocardial perfusion imaging using saturation-prepared trueFISP. J Magn Reson Imaging 2002; 16:641-652.[CrossRef][Medline]
65. Kety SS. Measurement of local contribution within the brain by means of inert, diffusible tracers: examination of the theory, assumptions, and possible sources of error. Acta Neurol Scand Suppl 1965; 14:20-23.[Medline]
66. Eichenberger AC, Schuiki E, Kochli VD, et al. Ischemic heart disease: assessment with gadolinium-enhanced ultrafast MR imaging and dipyridamole stress. J Magn Reson Imaging 1994; 4:425-31.[Medline]
67. Ishida N, Sakuma H, MD , Motoyasu M, et al. Noninfarcted myocardium: correlation between dynamic first-pass contrast-enhanced myocardial MR imaging and quantitative coronary angiography. Radiology 2003; 229:209-216.[Abstract/Free Full Text]
68. Penzkofer H, Wintersperger BJ, Knez A, et al. Assessment of myocardial perfusion using multi-section first-pass MRI and color-coded parameter maps: a comparison to 99mTc sesta MIBI SPECT and systolic myocardial wall thickening analysis. Magn Reson Imaging 1999; 17:161-170.[CrossRef][Medline]
69. Schvartzman PR, Kasper JM, Weaver JA, Obuchowski NA, White RD. Qualitative analysis of first-pass perfusion, contractility and end-diastolic wall thickness in MRI predicts nonviable myocardium at rest (abstr). Radiology 2000; 217(P):130.
70. Lombardi M, Kvaerness J, Torheim G, et al. Relationship between function and perfusion early after acute myocardial infarction. Int J Cardiovasc Imaging 2001; 17:383-393.[CrossRef][Medline]
71. Cullen JH, Horsfield A, Reek CR, et al. A myocardial perfusion reserve index in humans using first-pass contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol 1999; 33:1386-1394.[Abstract/Free Full Text]
72. Al-Saadi N, Nagel E, Gross M, et al. Noninvasive detection of myocardial ischemia from perfusion reserve based on cardiovascular magnetic resonance. Circulation 2000; 101:1379-1383.[Abstract/Free Full Text]
73. Al-Saadi N, Nagel E, Gross M, et al. Improvement of myocardial perfusion reserve early after coronary intervention: assessment with cardiac magnetic resonance imaging. J Am Coll Cardiol 2000; 36:1557-1564.[Abstract/Free Full Text]
74. Ibrahim T, Nekolla SG, Schreiber K, et al. Assessment of coronary flow reserve: comparison between contrast-enhanced magnetic resonance imaging and positron emission tomography. J Am Coll Cardiol 2002; 39:864-870.[Abstract/Free Full Text]
75. Hartnell G, Cerel A, Kamalesh M, et al. Detection of myocardial ischemia: value of combined myocardial perfusion and cineangiographic MR imaging. AJR Am J Roentgenol 1994; 163:1061-1067.[Abstract/Free Full Text]
76. Lauerma K, Virtanen KS, Sipila LM, et al. Multislice MRI in assessment of myocardial perfusion in patients with single vessel proximal left anterior descending coronary artery disease before and after revascularization. Circulation 1997; 96:2859-2867.[Abstract/Free Full Text]
77. Walsh EG, Doyle M, Lawson MA, et al. Multislice first-pass myocardial perfusion imaging on a conventional clinical scanner. Magn Reson Med 1995; 34:39-47.[Medline]
78. Panting JR, Gatehouse PD, Yang GZ, et al. Echo-planar magnetic resonance myocardial perfusion imaging: parametric map analysis and comparison with thallium SPECT. J Magn Reson Imaging 2001; 13:192-200.[CrossRef][Medline]
79. Keijer JT, van Rossum AC, van Eenige MJ, et al. Magnetic resonance imaging of regional myocardial perfusion in patients with single-vessel coronary artery disease: quantitative comparison with 201Thallium-SPECT and coronary angiography. J Magn Reson Imaging 2000; 11:607-615.[CrossRef][Medline]
80. Wilke NM, Jerosch-Herold M, Zenovich A, Stillman AE. Magnetic resonance first-pass myocardial perfusion imaging: clinical validation and future applications. J Magn Reson Imaging 1999; 10:676-685.[CrossRef][Medline]
81. Ambrosio G, Weisman HF, Mannisi JA, Becker LC. Progressive impairment of regional myocardial perfusion after initial restoration of postischaemic blood flow. Circulation 1989; 80:1846-1861.[Abstract/Free Full Text]
82. Kim RJ, Chen EL, Lima JAC, Judd RM. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation 1996; 94:3318-3326.[Abstract/Free Full Text]
83. Wu KC, Kim RJ, Bluemke DA, 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; 32:1756-1764.[Abstract/Free Full Text]
84. Lima JA, Judd RM, Bazille A, Schulman SP, Atalar E, Zerhouni EA. Regional heterogeneity of human myocardial infarcts demonstrated by contrast-enhanced MRI: potential mechanisms. Circulation 1995; 92:1117-1125.[Abstract/Free Full Text]
85. Wu KC, Zerhouni EA, Judd RM, et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation 1998; 97:765- 772.[Abstract/Free Full Text]
86. Ito H, Maruyama A. Iwakura K, et al. Clinical implications of the ‘no reflow’ phenomenon: a predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation 1996; 93:223-228.
87. Sakuma T, Okada T, Hayashi Y, Otsuka M, Hirai Y. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circ J 2002; 66:685-690.[CrossRef][Medline]
88. Asanuma T, Tanabe K, Ochiai K, et al. Relationship between progressive microvascular damage and intramyocardial hemorrhage in patients with reperfused anterior myocardial infarction. Circulation 1997; 96:448-453.[Abstract/Free Full Text]
89. Motoyama S, Kondo T, Anno H, et al. Relationship between thrombolytic therapy and perfusion defect detected by Gd-DTPA-enhanced fast magnetic resonance imaging in acute myocardial infarction. J Cardiovasc Magn Reson 2001; 3:237- 245.[CrossRef][Medline]
90. Kemp HG. Left ventricular function in patients with the anginal syndrome and normal coronary arteriograms. Am J Cardiol 1973; 32:375-376.[CrossRef][Medline]
91. Jerosch-Herold M, Wilke N, Stillman AE. Magnetic resonance quantification of the myocardial perfusion reserve with a Fermi function model for constrained deconvolution. Med Phys 1998; 25:73-84.[CrossRef][Medline]
92. Panting JR, Gatehouse PD, Yang GZ. Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imaging. N Engl J Med 2002; 346:1948-1953.[Abstract/Free Full Text]
93. Rossetti E, Fragasso G, Mellone R, et al. Magnetic resonance contrast enhancement with gadolinium-DTPA in patients with angina and angiographically normal coronary arteries: effect of chronic beta-blockage. Cardiologia 1999; 44:653- 659.[Medline]
94. Dendale PA, Franken PR, Waldman GJ, et al. Low-dosage dobutamine magnetic resonance imaging as an alternative to echocardiography in the detection of viable myocardium after acute myocardial infarction. Am Heart J 1995; 130:134-140.[CrossRef][Medline]
95. Baer FM, Voth E, LaRosee K, et al. Comparison of dobutamine transesophageal echocardiography and dobutamine magnetic resonance imaging for detection of residual myocardial viability. Am J Cardiol 1996; 78:415-419.[CrossRef][Medline]
96. Nagel E, Lehmkuhl HB, Bocksch W, et al. Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography. Circulation 1999; 99:763-770.[Abstract/Free Full Text]
97. Hundley WG, Morgan TM, Neagle CM, Hamilton CA, Rerkpattanapipat P, Link KM. Magnetic resonance imaging determination of cardiac prognosis. Circulation 2002; 106:2328-2333.[Abstract/Free Full Text]
98. Dulce MC, Duerinckx AJ, Hartiala J, et al. MR imaging of the myocardium using nonionic contrast medium: signal-intensity changes in patients with subacute myocardial infarction. AJR Am J Roentgenol 1993; 160:963-970.[Abstract/Free Full Text]
99. Mahrholdt H, Wagner A, Judd RM, Sechtem U. Assessment of myocardial viability by cardiovascular magnetic resonance imaging. Eur Heart J 2002; 23:602-619.[Free Full Text]
100. Kim RJ, Hillenbrand HB, Judd RM. Evaluation of myocardial viability by MRI. Herz 2000; 25:417-430.[CrossRef][Medline]
101. Kim RJ, Shah DJ, Judd RM. How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 2003; 5:505-514.[CrossRef][Medline]
102. Oshinski JN, Yang Z, Jones JR, Mata JF, French BA. Imaging time after Gd-DTPA injection is critical in using delayed enhancement to determine infarct size accurately with magnetic resonance imaging. Circulation 2001; 104:2838-2842.[Abstract/Free Full Text]
103. Rogers WJ, Rhodes D, Biederman R, et al. "Timing is everything": time course of myocardial delayed enhancement after acute MI (abstr). Circulation 2001; 104(suppl 17):II-639.
104. Kim RJ, Fieno DS, Parrish TB, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 1999; 100:1992-2002.[Abstract/Free Full Text]
105. Pereira RS, Prato FS, Wisenberg G, Sykes J, Yvorchuk KJ. The use of Gd-DTPA as a marker of myocardial viability in reperfused acute myocardial infarction. Int J Cardiovasc Imaging 2001; 17:395-404.[CrossRef][Medline]
106. Flacke SJ, Fischer SE, Lorenz CH. Measurement of the gadopentetate dimeglumine partition coefficient in human myocardium in vivo: normal distribution and elevation in acute and chronic infarction. Radiology 2001; 218:703- 710.[Abstract/Free Full Text]
107. Simonetti OP, Kim RJ, Fieno DS, et al. An improved MR imaging technique for the visualization of myocardial infarction. Radiology 2001; 218:215-223.[Abstract/Free Full Text]
108. Kellman P, Arai AE, McVeigh ER, Aletras AH. Phase-sensitive inversion recovery for detecting myocardial infarction using gadolinium-delayed hyperenhancement. Magn Reson Med 2002; 47:372-383.[CrossRef][Medline]
109. Schussheim AE, Aletras AH, Kwong RY, Balaban RS, Arai AE. Quantitative MRI analysis of human myocardial infarction suggest benefits of infarct-nulling contrast (abstr). Circulation 2000; 102 (suppl 18):808.
110. Regenfus M, Schlundt C, Ropers D, et al. Validation of a three-dimensional contrast-enhanced magnetic resonance imaging technique for determination of myocardial viability (abstr). Eur Radiol 2001; 11(suppl 2):B-1003.
111. Duerinckx AJ. Myocardial viability using MR imaging: is it ready for clinical use? AJR Am J Roentgenol 2000; 174:1741-1743.[Free Full Text]
112. Beek AM, Kuehl HP, Hofman MB, et al. Delayed contrast-enhanced MRI for the prediction of recovery of function in reperfused acute myocardial infarction: is bright really dead? (abstr). Circulation 2001; 104(suppl 17):II-534.
113. Lauerma K, Niemi P, Hanninen H, et al. Multimodality MR imaging assessment of myocardial viability: combination of first-pass and late contrast enhancement to wall motion dynamics and comparison with FDG PET—initial experience. Radiology 2000; 217:729-736.[Abstract/Free Full Text]
114. Schvartzman PR, Srichai MB, Brunken R, et al. Delayed-enhancement (DE) MR: comparison with dobutamine stress echo (DSE), positron emission tomography (PET), and contraction/perfusion MRI for determination of myocardial viability (abstr). Circulation 2001; 104(suppl 17):II--534.
115. Zamorano J, Delgado J, Almeria C, et al. Reason for discrepancies in identifying myocardial viability by thallium-201 redistribution, magnetic resonance imaging, and dobutamine echocardiography. Am J Cardiol 2002; 90:455-459.[CrossRef][Medline]
116. Klein C, Nekolla SG, Bengel FM, et al. Assessment of myocardial viability with contrast-enhanced magnetic resonance imaging: comparison with positron emission tomography. Circulation 2002; 105:162-167.[Abstract/Free Full Text]
117. Kuhl HP, Beek AM, van der Weerdt AP, et al. Myocardial viability in chronic ischemic heart disease: a comparison of contrast-enhanced magnetic resonance imaging with (18F)-fluorodeoxyglucose positron emission tomography. J Am Coll Cardiol 2003; 41:1341-1348.[Abstract/Free Full Text]
118. Hunold P, Brandt-Mainz K, Knipp S, et al. Cardiac contrast-enhanced MRI and [18F]-FDG-PET in the assessment of myocardial viability: accuracy of the prediction of functional recovery after revascularization (abstr). Radiology 2002; 225(P):298.
119. Gutberlet M, Amthauer HW, Hausmann H, et al. Value of Gd-DTPA "late enhancement" in MRI in comparison with gated SPECT for the assessment of myocardial viability: initial results in patients with impaired LV-function (abstr). Radiology 2001; 221(P):319.
120. Wagner A, Mahrholdt H, Holly TA, 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; 361:374-379.[CrossRef][Medline]
121. Lee VS, Resnick D, Tiu SS, et al. MR imaging evaluation of myocardial viability in the setting of equivocal SPECT results with (99m)Tc sestamibi. Radiology 2004; 230:191-197.[Abstract/Free Full Text]
122. John A, Dill T, Rau M, et al. Transmural late enhancement by contrast-enhanced MRI predicts no functional recovery after acute myocardial infarction (abstr). J Am Coll Cardiol 2001; 37(suppl 2):437A.
123. Bachmann GF, Dill T, Kluge A, et al. Extent of late enhancement in contrast-enhanced MRI after acute myocardial infarction (AMI): correlation with cine and perfusion MRI (abstr). Radiology 2002; 225(P):536.
124. Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 2000; 343:1445-1453.[Abstract/Free Full Text]
125. Miller S, Helber U, Kramer U, et al. Prediction of necrosis and regional viability after myocardial infarction by MR imaging: a 1 year follow-up study (abstr). Eur Radiol 2001; 11(suppl 2):B-1000.
126. De Roos A, van der Wall EE, Bruschke AV, et al. Magnetic resonance imaging in the diagnosis and evaluation of myocardial infarction. Magn Reson Q 1991; 7:191-207.[Medline]
127. Gerber BL, Garot J, Bluemke DA, Wu KC, Lima JA. Accuracy of contrast-enhanced magnetic resonance imaging in predicting improvement of regional myocardial function in patients after acute myocardial infarction. Circulation 2002; 106:1083-1089.[Abstract/Free Full Text]
128. Srichai MB, Schvartzman PR, Sturm B, et al. Hyper-enhancement on non stress cardiac MRI correlates inversely with amount of circumferential shortening (abstr). J Am Coll Cardiol 2001; 37(suppl 2):437A.
129. Wu E, Judd RM, Vargas JD, et al. Visualization of presence, location, and transmural enhancement of healed Q-wave and non-Q-wave myocardial infarction. Lancet 2001; 357:21-28.[CrossRef][Medline]
130. Flamm SD, Wilson JM, Moustapha AI, et al. Delayed-hyperenhancement MRI combined with cine-MRI differentiates myocardial stunning from acute myocardial infarction (abstr). Circulation 2000; 102(suppl 18):709.
131. Weiss CR, Aletras AH, London JF, et al. Stunned, infarcted, and normal myocardium in dogs: simultaneous differentiation by using gadolinium-enhanced Cine MR imaging with magnetization transfer contrast. Radiology 2003; 226:723-730.[Abstract/Free Full Text]
132. Beek AM, Kuhl HP, Bondarenko O, et al. Delayed contrast-enhanced magnetic resonance imaging for the prediction of regional functional improvement after acute myocardial infarction. J Am Coll Cardiol 2003; 42:895-901.[Abstract/Free Full Text]
133. Kwong RY, Schussheim AE, Rekhraj S, et al. Detecting acute coronary syndrome in the emergency department with cardiac magnetic resonance imaging. Circulation 2003; 107:531-537.[Abstract/Free Full Text]
134. Martin RH, Almond CH, Saab S, Watson LE. True and false aneurysms of the left ventricle following myocardial infarction. Am J Med 1977; 62:418-424.[CrossRef][Medline]
135. Harrity P, Patel A, Bianco J, Subramanian R. Improved diagnosis and characterization of postinfarction left ventricular pseudoaneurysm by cardiac magnetic resonance imaging. Clin Cardiol 1991; 14:603-606.[Medline]
136. Kumbasar B, Wu KC, Kamel IR, Lima JA, Bluemke DA. Left ventricular true aneurysm: diagnosis of myocardial viability shown on MR imaging. AJR Am J Roentgenol 2002; 179:472-474.[Free Full Text]
137. Finn AV, Antman EM. Images in clinical medicine: isolated right ventricular infarction. N Engl J Med 2003; 349:1636.[Free Full Text]
138. Roditi GH, Hartnell GG, Cohen MC. MRI changes in myocarditis: evaluation with spin echo, cine MR angiography and contrast enhanced spin echo imaging. Clin Radiol 2000; 55:752-758.[CrossRef][Medline]
139. Laissy JP, Messin B, Varenne O, et al. MRI of acute myocarditis: a comprehensive approach based on various imaging sequences. Chest 2002; 122:1638-1648.[Abstract/Free Full Text]
140. Inoue S, Murakami Y, Shimada T, et al. Right ventricular aneurysm caused by acute myocarditis. Can J Cardiol 2000; 16:1025-1028.[Medline]
141. Odev K, Acikgozoglu S, Gormis N, et al. Pulmonary embolism due to cardiac hydatid disease: imaging findings of unusual complication of hydatid cyst. Eur Radiol 2002; 12:627-633.[Medline]
142. Bocchi EA, Kalil R, Bacal F, et al. Magnetic resonance imaging in chronic Chagas’ disease. Echocardiography 1998; 15:279-287.[Medline]
143. Takahashi N, Murakami Y, Shimada T, et al. Detection of eosinophilic myocarditis using contrast-enhanced magnetic resonance imaging: case report. Can Assoc Radiol J 2001; 52:20-22.[Medline]
144. Bogaert J, Goldstein M, Tannouri F, Golzarian J, Dymarkowski S. Original report: late myocardial enhancement in hypertrophic cardiomyopathy with contrast-enhanced MR imaging. AJR Am J Roentgenol 2003; 180:981-985.[Abstract/Free Full Text]
145. Choudhury L, Mahrholdt H, Wagner A, et al. Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2002; 40:2156-2164.[Abstract/Free Full Text]
146. Moon JC, McKenna WJ, McCrohon JA, Elliott PM, Smith GC, Pennell DJ. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol 2003; 41:1561-1567.[Abstract/Free Full Text]
147. Sievers B, Moon JC, Pennell DJ. Magnetic resonance contrast enhancement of iatrogenic septal myocardial infarction in hypertrophic cardiomyopathy. Circulation 2002; 105:1018.[Free Full Text]
148. Kayser HW, van der Wall EE, Sivananthan MU, Plein S, Bloomer TN, de Roos A. Diagnosis of arrhythmogenic right ventricular dysplasia: a review. RadioGraphics 2002; 22:639-650.[Abstract/Free Full Text]
149. White RD, Trohman RG, Flamm SD, et al. Right ventricular arrhythmia in the absence of arrhythmogenic dysplasia: MR imaging of myocardial abnormalities. Radiology 1998; 207:743-751.[Abstract/Free Full Text]
150. Barkhausen J, Hunold P, Wieneke H, Bruder O, Erbel R, Debatin JF. Late enhancement: a new MR feature of arrhythmogenic right ventricular cardiomyopathy (abstr) In: Radiological Society of North America Scientific Assembly and Annual Meeting Program. Oak Brook, Ill: Radiological Society of North America, 2003; 310.
151. Dill T, Neumann T, Ekinci O, et al. Pulmonary vein diameter reduction after radiofrequency catheter ablation for paroxysmal atrial fibrillation evaluated by contrast- enhanced three-dimensional magnetic resonance imaging. Circulation 2003; 107:845-850.[Abstract/Free Full Text]
152. Shimada T, Shimada K, Sakane T, et al. Diagnosis of cardiac sarcoidosis and evaluation of the effects of steroid therapy by gadolinium-DTPA-enhanced magnetic resonance imaging. Am J Med 2001; 110:520-527.[CrossRef][Medline]
153. Skold CM, Larsen FF, Rasmussen E, Pehrsson SK, Eklund AG. Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiography. J Intern Med 2002; 252:465-471.[CrossRef][Medline]
154. Helber U, Loichat J, Spyridopoulos I, et al. Magnetic resonance imaging in hypertrophied left ventricular myocardium due to amyloidosis. Int J Angiol 1998; 7:169-172.
155. Moon JC, Mundy HR, Lee PJ, Mohiaddin RH, Pennell DJ. Images in cardiovascular medicine: myocardial fibrosis in glycogen storage disease type III. Circulation 2003; 107:e47.[Free Full Text]
156. McCrohon JA, Moon JC, Prasad SK, et al. Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance. Circulation 2003; 108:54-59.[Abstract/Free Full Text]
157. Koito H, Suzuki J, Ohkubo N, et al. Gadolinium-diethylenetriamine pentaacetic acid enhanced magnetic resonance imaging of dilated cardiomyopathy: clinical significance of abnormally high signal intensity of left ventricular myocardium. J Cardiol 1996; 28:41-49.[Medline]
158. Wassmuth R, Erdbruegger U, Leritzsch S, et al. Magnetic resonance imaging for monitoring cardiac function and tissue characterization in anthracyclines therapy (abstr). Circulation 2000; 102(suppl 2):809-810.
159. Gilkeson RC, Chiles C. MR evaluation of cardiac and pericardial malignancy. Magn Reson Imaging Clin N Am 2003; 11:173-186.[CrossRef][Medline]
160. Hoffmann U, Globits S, Frank H. Cardiac and paracardiac masses: current opinion on diagnostic evaluation by magnetic resonance imaging. Eur Heart J 1998; 19:553-563.[Free Full Text]
161. Wintersperger BJ, Becker CR, Gulbins H, et al. Tumors of the cardiac valves: imaging findings in magnetic resonance imaging, electron beam computed tomography, and echocardiography. Eur Radiol 2000; 10:443-449.[CrossRef][Medline]
162. Clarke NR, Mohiaddin RH, Westaby S, Banning AP. Multifocal cardiac leiomyosarcoma: diagnosis and surveillance by transesophageal echocardiography and contrast enhanced cardiovascular magnetic resonance. Postgrad Med J 2002; 78:492-493.[Abstract/Free Full Text]
163. Bogaert J, Rademakers F, Cappelle L, et al. High-grade immunoblastic sarcoma: an unusual type of a primary cardiac non-Hodgkin lymphoma. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1995; 162:186-188.[Medline]
164. Freedom RM, Lee KJ, MacDonald C, Taylor G. Selected aspects of cardiac tumors in infancy and childhood. Pediatr Cardiol 2000; 21:299-316.[CrossRef][Medline]
165. Kiaffas MG, Powell AJ, Geva T. Magnetic resonance imaging evaluation of cardiac tumor characteristics in infants and children. Am J Cardiol 2002; 89:1229-1233.[CrossRef][Medline]
166. Mollet NR, Dymarkowski S, Volders W, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 2002; 106:2873-2876.[Abstract/Free Full Text]
167. Barkhausen J, Hunold P, Schueler W, et al. Detection and characterization of intracardiac thrombi: comparison of echocardiography and magnetic resonance imaging (abstr). Radiology 2002; 225(P):626.
168. Reynen K. Cardiac myxomas. N Engl J Med 1995; 333:1610-1617.[Free Full Text]
169. Matsuoka H, Hamada M, Honda T, et al. Morphologic and histologic characterization of cardiac myxomas by magnetic resonance imaging. Angiology 1996; 47:693-698.
170. Okuda S, Kikinis R, Geva T, Chung T, Dumanli H, Powell A. 3D-shaded surface rendering of gadolinium-enhanced MR angiography in congenital heart disease. Pediatr Radiol 2000; 30:540-545.[CrossRef][Medline]
171. Rebergen SA, de Roos A. Congenital heart disease: evaluation of anatomy and function by MRI. Herz 2000; 25:365-383.[CrossRef][Medline]
172. Manning WJ, Atkinson DJ, Parker JA, Edelman RR. Assessment of intracardiac shunts with gadolinium-enhanced ultrafast MR imaging. Radiology 1992; 184:357-361.[Abstract/Free Full Text]
173. Taylor AM, Thorne SA, Rubens MB, et al. Coronary artery imaging in grown up congenital heart disease: complementary role of magnetic resonance and x-ray coronary angiography. Circulation 2000; 101:1670-1678.[Abstract/Free Full Text]
174. Muthupillai R, Vick GW, Flamm SD, Chung T. Time-resolved contrast-enhanced magnetic resonance angiography in pediatric patients using sensitivity encoding. J Magn Reson Imaging 2003; 17:559-564.[CrossRef][Medline]
175. Ferrari VA, Sutton SJ, Holland G, et al. Three-dimensional magnetic resonance angiography aids in the definitive diagnosis of abnormal pulmonary venous drainage in adults with congenital heart disease (abstr). J Am Coll Cardiol 1998; 31(suppl 2):381A-382A.
176. Holman BL, Moore SC, Shulkin PM, et al. Quantitation of perfused myocardial mass using Tl-201 and emission computed tomography. Invest Radiol 1983; 18:322-326.[Medline]
177. Caldwell JH, Williams DL, Harp GD, et al. Quantitation of size of relative myocardial perfusion defect by single-photon emission computed tomography. Circulation 1984; 70:1048-1056.[Abstract/Free Full Text]
178. Marshall RC, Tillisch JH, Phelps ME, et al. Identification and differentiation of resting myocardial ischemia and infarction in man with positron computed tomography, F-18 labeled fluorodeoxyglucose and N-13 ammonia. Circulation 1983; 67:766-778.[Abstract/Free Full Text]
179. Brunken R, Tillisch JH, Scwaiger M, et al. Regional perfusion, glucose metabolism and wall motion in patients with chronic electrocardiographic Q-wave infarctions: evidence of persistence of viable tissue in some infarct regions by positron emission tomography. Circulation 1986; 73:951-962.[Abstract/Free Full Text]
180. Johnson LW, Lozner EC, Johnson D, et al. Coronary arteriography 1984–1987: a report of the registry of the Society for Cardiac Angiography and Interventions. I. Results and complications. Cathet Cardiovasc Diagn 1989; 17:5-10.
181. Edelman RR, Manning WJ, Gervino E, Li W. Flow velocity quantification in human coronary arteries with fast, breath-hold MR angiography. J Magn Reson Imaging 1993; 3:699-703.[Medline]
182. Danias PG, Stuber M, Botnar RM, et al. Coronary MR angiography clinical applications and potential for imaging coronary artery disease. Magn Reson Imaging Clin N Am 2003; 11:81-99.[CrossRef][Medline]
183. Manning WJ, Li W, Edelman RR. A preliminary report comparing magnetic resonance coronary angiography with conventional angiography. N Engl J Med 1993; 328:828-832.[Abstract/Free Full Text]
184. Duerinckx AJ, Urman MK. Two-dimensional coronary MR angiography: analysis of initial clinical results. Radiology 1994; 193:731-738.[Abstract/Free Full Text]
185. Li D, Kaushikkar S, Haacke EM, et al. Coronary arteries: three-dimensional MR imaging with retrospective respiratory gating. Radiology 1996; 201:857-863.[Abstract/Free Full Text]
186. Stuber M, Botnar RM, Danias PG, et al. Double-oblique free-breathing high resolution three-dimensinoal coronary magnetic resonance angiography. J Am Coll Cardiol 1999; 34:524-531.[Abstract/Free Full Text]
187. Grimm RC, Rossman PJ, Riederer SJ, Ehman RL. Real-time adaptive motion correction using navigator echoes (abstr) In: Proceedings of the Society of Magnetic Resonance in Medicine and the European Society of Magnetic Resonance in Medicine and Biology. Berkeley, Calif: Society of Magnetic Resonance in Medicine, 1995; 741.
188. Kim WY, Danias PG, Stuber M, et al. Coronary magnetic resonance angiography for the detection of coronary stenoses. N Engl J Med 2001; 345:1863-1869.[Abstract/Free Full Text]
189. Goldfarb JW, Holland AE, Edelman RR. Single breath-hold multi-slab and CINE cardiac-synchronized gadolinium-enhanced three-dimensional angiography. Magn Reson Imaging 2001; 19:1267- 1274.[CrossRef][Medline]
190. Regenfus M, Ropers D, Achenbach S, et al. Noninvasive detection of coronary artery stenosis using contrast-enhanced three-dimensional breath-hold magnetic resonance coronary angiography. J Am Coll Cardiol 2000; 36:44-50.[Abstract/Free Full Text]
191. Deshpande VS, Wielopolski PA, Shea SM, Carr J, Zheng J, Li D. Coronary artery imaging using contrast-enhanced 3D segmented EPI. J Magn Reson Imaging 2001; 13:676-681.[CrossRef][Medline]
192. Regenfus M, Ropers D, Achenbach S, et al. Comparison of contrast-enhanced breath-hold and free-breathing respiratory-gated imaging in three-dimensional magnetic resonance coronary angiography. Am J Cardiol 2002; 90:725-730.[CrossRef][Medline]
193. Bedaux WL, Hofman MB, Wielopolski PA, et al. Three-dimensional magnetic resonance coronary angiography using a new blood pool contrast agent: initial experience. J Cardiovasc Magn Reson 2002; 4:273-282.[CrossRef][Medline]
194. Li D, Zheng J, Weinmann HJ. Contrast-enhanced MR imaging of coronary arteries: comparison of intra- and extravascular contrast agents in swine. Radiology 2001; 218:670-678.[Abstract/Free Full Text]
195. Huber ME, Paetsch I, Schnackenburg B, et al. Performance of a new gadolinium-based intravascular contrast agent in free-breathing inversion recovery 3D coronary MRA. Magn Reson Med 2003; 49:115-121.[CrossRef][Medline]
196. Herborn CU, Barkhausen J, Paetsch I, et al. Coronary arteries: contrast-enhanced MR imaging with SH L 643A—experience in 12 volunteers. Radiology 2003; 229:217-223.[Abstract/Free Full Text]
197. Fujiwara M, Yamada N, Ono Y, et al. Magnetic resonance imaging of old myocardial infarction in young patients with a history of Kawasaki disease. Clin Cardiol 2001; 24:247-252.[Medline]
198. Vrachliotis TG, Bis KG, Aliabadi D, et al. Contrast-enhanced breath-hold MR angiography for evaluating patency of coronary artery bypass grafts. AJR Am J Roentgenol 1997; 168:1073-1080.[Abstract/Free Full Text]
199. Boehm DH, Wintersperger BJ, Reichenspurner H, et al. Contrast-enhanced magnetic resonance angiography for control of minimally invasive coronary artery bypass conduits (MIDCAB/OPCAB). Heart Surg Forum 1999; 2:222-225.[Medline]
200. Bunce NH, Lorenz CH, John AS, Lesser JR, Mohiaddin RH, Pennell DJ. Coronary artery bypass graft patency: assessment with true fast imaging with steady-state precession versus gadolinium-enhanced MR angiography. Radiology 2003; 227:440-446.[Abstract/Free Full Text]
201. Brenner P, Wintersperger B, von Smekal A, et al. Detection of coronary artery bypass graft patency by contrast enhanced magnetic angiography. Eur J Cardiothorac Surg 1999; 15:389-393.
202. Achenbach S, Ropers D, Regenfus M, et al. Noninvasive coronary angiography by magnetic resonance imaging, electron-beam computed tomography, and multislice computed tomography. Am J Cardiol 2001; 88(2A):70E-73E.[CrossRef][Medline]
203. Ropers D, Baum U, Pohle K, et al. Detection of coronary artery stenoses with thin-slice multi-detector row spiral computed tomography and multiplanar reconstruction. Circulation 2003; 107:664- 666.[Abstract/Free Full Text]
204. Ropers D, Regenfus M, Stilianakis N, et al. A direct comparison of noninvasive coronary angiography by electron beam tomography and navigator-echo-based magnetic resonance imaging for the detection of restenosis following coronary angioplasty. Invest Radiol 2002; 37:386-392.[CrossRef][Medline]
205. Stuber M, Botnar RM, Fischer SE, et al. Preliminary report on in vivo coronary MRA at 3 tesla in humans. Magn Reson Med 2002; 48:425-429.[CrossRef][Medline]
206. Lauffer RB. Magnetic resonance contrast media: principles and progress. Magn Reson Q 1990; 6:65-84.[Medline]
207. Uematsu H, Dougherty L, Takahashi M, et al. Pulmonary MR angiography with contrast agent at 4 tesla: a preliminary result. Magn Reson Med 2001; 46:1028-1030.[CrossRef][Medline]
208. Nobauer-Huhmann IM, Ba-Ssalamah A, Mlynarik V, et al. Magnetic resonance imaging contrast enhancement of brain tumors at 3 tesla versus 1.5 tesla. Invest Radiol 2002; 37:114-119.[CrossRef][Medline]
209. Leiner T, de Vries M, Hoogeveen R, Vasbinder GB, Lemaire E, van Engelshoven JM. Contrast-enhanced peripheral MR angiography at 3.0 tesla: initial experience with a whole-body scanner in healthy volunteers. J Magn Reson Imaging 2003; 17:609-614.[CrossRef][Medline]
210. Dickfeld T, Calkins H, Zviman M, et al. Anatomic stereotactic catheter ablation on three-dimensional magnetic resonance images in real time. Circulation 2003; 108:2407-2413.[Abstract/Free Full Text]
211. Orlic D, Hill JM, Arai AE. Stem cells for myocardial regeneration. Circ Res 2002; 91:1092-1102.[Abstract/Free Full Text]
212. Van Geuns RJ, Smits P, De Feyter P, et al. Myocardial viability and function for the selection and follow-up of patients for myoblasts transplantation as a new treatment for heart failure (abstr). Radiology 2002; 225(P):575.[Abstract/Free Full Text]
213. Hill JM, Dick AJ, Raman VK, et al. Serial cardiac magnetic resonance imaging of injected mesenchymal stem cells. Circulation 2003; 108:1009-1014.[Abstract/Free Full Text]
214. Kraitchman DL, Heldman AW, Atalar E, et al. In vivo magnetic resonance imaging of mesenchymal stem cells in myocardial infarction. Circulation 2003; 107:2290-2293.[Abstract/Free Full Text]
215. Garot J, Unterseeh T, Teiger E, et al. Magnetic resonance imaging of targeted catheter-based implantation of myogenic precursor cells into infarcted left ventricular myocardium. J Am Coll Cardiol 2003; 41:1841-1846.[Abstract/Free Full Text]

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