From Pictures to Practice Paradigms |
Tissue Characterization of Acute Myocardial Infarction and Myocarditis by Cardiac Magnetic Resonance
Matthias G. Friedrich, MD, FESC*
Departments of Cardiac Sciences and Radiology, Stephenson Cardiovascular MR Centre at the Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada
 |
Abstract
|
|---|
Electrocardiograms, biomarkers, and ventricular function studies are diagnostic tools that are currently used to assess patients with acute myocardial disease. These tools are limited in their diagnostic accuracy and scope. Thus, for informed therapeutic decision making, tissue characterization may serve as a very important source of information in these initially regional diseases. Cardiac magnetic resonance (CMR) is becoming an important tool for phenotyping cardiac patients in vivo. Recent advances of CMR hardware and software as well as protocols have allowed for accurately visualizing tissue changes in patients with acute myocardial diseases. This is of special interest for acute myocardial infarction and acute myocarditis, because these entities may have a very similar clinical presentation and require immediate therapeutic decision making. Several CMR approaches can be combined in a comprehensive CMR examination, which provides information not only on ventricular size, morphology, and function, but also on the stage, degree, and extent of reversible and irreversible myocardial injury. Streamlined protocols allow such a CMR examination to be a time- and cost-efficient diagnostic tool, even in patients with acute disease. Current CMR approaches for visualizing tissue pathology in vivo are reviewed, examples are presented, and the potential role of CMR tissue characterization in patients with acute myocardial disease is discussed. The specific role of imaging the extent and regional distribution of myocardial edema and necrosis is discussed.
Key Words: cardiovascular magnetic resonance • acute myocardial infarction • myocarditis • imaging • tissue characterization
|
Abbreviations and Acronyms
| | CMR = cardiac magnetic resonance | | CT = computed tomography | | NCT = nuclear cardiology techniques |
|
|
Current Diagnostic Tools in Acute Myocardial Disease
|
|---|
Patients with acute heart disease require immediate care. To make informed, timely therapeutic decisions, physicians need fast, accurate, and reliable diagnostic tools. This is especially true for acute myocardial infarction and acute myocarditis, with their often dramatic and sometimes apparently life-threatening clinical presentation.
In patients with a clinical history, symptoms, and physical findings that suggest acute myocardial disease, a combination of ECG and seromarkers such as troponins is used to determine acuity, extent, and location of the injury. Current diagnostic approaches, however, have significant limitations. The diagnostic accuracy of ECGs to detect myocardial ischemia often is inadequately low, which may result in inappropriate treatment (1). Even in controlled trials, more than 4% of patients with acute coronary syndrome may be discharged with missed acute coronary syndrome or acute infarction (2). Echocardiographic studies of left ventricular function are helpful, but also have a moderate diagnostic accuracy (3) and often cannot distinguish between acute and chronic myocardial injury. Troponins accurately identify acute myocardial injury. The sensitivity of any seromarker, however, is limited during the first hours of and late after the onset of the injury. The diagnostic accuracy of these diagnostic tools is even lower when applied to patients with acute myocarditis (4).
Whereas the pathophysiological and pathological features of both acute diseases offer several diagnostic targets (Table 1), each of these routinely used diagnostic tools typically addresses just 1 aspect, providing limited information for clinical decision making. Given the primarily regional nature of the acute injury, tissue abnormalities appear to be the prime candidate for diagnosing acute myocardial disease and estimating its severity. Endomyocardial biopsy, though the gold standard for tissue pathology, does not have a clinical role in acute myocardial infarction and clinical indications in acute myocarditis are limited to patients with otherwise unexplained heart failure (5). Therefore, at least in the acute clinical settings, in vivo imaging appears be the most promising approach to retrieve tissue-related diagnostic information.
|
Imaging Tissue Pathology
|
|---|
Current clinical imaging modalities include echocardiography, nuclear cardiology techniques (NCT), computed tomography (CT), and cardiac magnetic resonance (CMR). Each of these modalities is characterized by specific strengths and weaknesses (Fig. 1), with Echocardiography being the most accessible, NCT being the most powerful on a molecular level, and CT providing the most detailed anatomical information. Although CMR appears to be a very versatile modality, its main strength lies in its unique ability to directly visualize tissue characteristics. Unlike all other imaging techniques, CMR uses a signal that is emitted by molecules in the region of interest and that reflects genuine physical (i.e., magnetic) properties. Thus, the contrast-generating mechanism does not depend on reflection (echocardiography), transmission (CT), or radiation of injected radioactive tracers (NCT). Instead, in MR images, molecular properties themselves determine the appearance of the tissue. Furthermore, a large variety of high-frequency pulse sequences ("sequences") allow for specific signal intensity characteristics, which can be used to selectively visualize certain molecular environments. In so-called T1-weighted sequences, for example, water will appear with a very low signal intensity, whereas fat will appear brightly. In contrast, so-called T2-weighted images will show water with high signal intensity. The typical relative signal intensity of any tissue is predictable and any significant abnormality may serve as a diagnostic marker for, often disease-specific, tissue changes.
View larger version (18K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1 Strengths of Currently Used Cardiac Imaging Tools
Diagnostic power of cardiac imaging techniques at different levels of pathophysiology. CMR = cardiac magnetic resonance; CT = computed tomography; Echo = echocardiography; Nuclear = nuclear cardiology techniques.
|
|
Thus, CMR has unique features, making it the imaging tool of choice for in vivo tissue characterization for disease entities such as myocarditis (6). Because CMR also allows the assessment of ventricular morphology, contractile function, and blood flow during the same session, tissue characteristics can be integrated into a comprehensive "all in one" imaging examination.
CMR of the heart is quite different from magnetic resonance imaging of other organs. CMR requires a set of techniques to reduce or eliminate artifacts caused by blood flow, breathing and cardiac motion, and conditions such as arrhythmia (e.g., atrial fibrillation) or breathing during the image acquisition may impair image quality. Significant technical advances, however, allow for a success rate of clinical scans in almost 100% of patients. These advances include hardware components such as high-speed gradient systems, cardiac coils, and improved ECG triggering devices as well as software developments such as parallel data acquisition and ultrafast sequences. Currently, comprehensive scans including assessment of left ventricular function and tissue characterization can be performed in far less than 30 min. This is often faster and cheaper than using other combined approaches to achieve a similarly wide scope of diagnostic information that includes tissue characterization.
|
CMR Techniques to Assess Tissue Pathology
|
|---|
Hypoperfusion (acute myocardial infarction).
In patients, CMR perfusion studies with adenosine accurately identify coronary artery stenosis (7) with an outstanding negative predictive value (8,9). In a protocol combining adenosine with late enhancement, Laissy et al. (10) have shown that CMR discriminates acute myocardial infarction from acute myocarditis. The clinical role of perfusion imaging in acute myocardial disease, however, remains to be defined.
Edema.
In myocardial edema, the predominant magnetic properties of the affected tissue and thus its appearance in applied MR images differ from that of normal myocardium, because protons now are more frequently bound to free water and have a longer transversal relaxation time (T2). So-called T2-weighted sequences, that is, sequences specified to retrieve most of the signal from tissue components with a long T2, will display the edematous area with a higher signal intensity than it displays the remote myocardium (with its still-normal proton binding and hence normal T2). This principle is used in the entire body to visualize water or high tissue water content. This has been shown in acute myocardial infarction (11).
Although T2-weighted CMR has been previously used to assess myocardial infarction, its clinical use has been limited until recently by inconsistent image quality. Because T2-weighted images have relatively low signal-to-noise ratios, they are susceptible to motion artifacts and confounders such as repetition time between repeated data acquisition, motion, and flow. In addition, other tissue components may affect signal intensity, and it is important that hardware and software are optimized for application in the heart. The use of a cardiac coil provides a higher signal-to-noise ratio, but can be problematic, because inferolateral regions may have a lower signal due to the longer distance to the surface coil and thus should only be used if an efficient coil intensity correction algorithm is implemented. Prescription of thicker slices is helpful to increase the signal-to-noise ratio. Sequences should have a repetition time of at least 2 R-R intervals to ensure adequate T2 weighting. Several sequence types are available for T2-weighted imaging of the heart. Whereas most published data have been acquired using a flow- and fat-suppressed spin echocardiography sequence, newer protocols may offer a higher signal-to-noise ratio and a more consistent image quality (12,13).
Recently, methods have been developed to reproducibly measure and map myocardial T2 times (14). Clinical data using this promising technique, however, are not yet available. A detailed review of the techniques and clinical role of T2-weighted CMR can be found elsewhere (15).
Hyperemia (myocarditis).
Any tissue inflammation with preserved vasculature is associated with an increased regional blood flow and volume. In acute myocarditis, this has been used as a diagnostic criterion by using contrast-enhanced CMR images obtained early after administration of gadolinium with its initial vascular and brief interstitial steady state (16,17). In these "early enhancement" images, inflamed regions appear with higher signal intensity. Because cardiac output, renal clearance, artifacts, and internal signal post-processing may alter absolute signal intensity, published studies successfully used values normalized to skeletal muscle (16,18). In the case of suspected skeletal muscle involvement, however, the contrast agent-induced relative signal intensity increase was found to be more sensitive without normalization (17).
Necrosis.
Acute, irreversible myocardial injury is best visualized on T1-weighted images acquired late (i.e., at least 5 to 10 min) after the administration of interstitial contrast agents such as gadolinium-diethylenetriaminepentaacetic acid. The delayed washout of these agents is specific to irreversibly injured myocardium (19). Optimized sequence parameter settings allow for selective "nulling" of signal intensity of myocardium without significant gadolinium accumulation and thus for very sensitive detection of necrotic tissue. This method, dubbed "late gadolinium enhancement," is regarded as the noninvasive gold standard for visualizing myocardial infarctions in vivo (20,21). Its sensitivity is outstanding and allows for detecting scars of less than 1 g (22). Late gadolinium enhancement can be used to visualize acute and chronic infarctions; however, it does not allow for discriminating 1 infarction type from the other (20).
No reflow.
Late reperfusion of a large infarction is often associated with a phenomenon called "no reflow," which is currently understood as a complex reperfusion injury that results in an interruption of blood flow to the infarction core despite normalized blood flow in the epicardial portions of the coronary artery system ("microvascular obstruction") (23). Capillary injury, mechanical obstruction of capillaries, and intramyocardial hemorrhage have been observed as pathologic features associated with no reflow.
|
CMR Tissue Characterization in Myocardial Infarction
|
|---|
The acute, typically thrombotic, occlusion of an epicardial coronary artery and the subsequent regional ischemia initiate a cascade of regional events that sequentially affect metabolism, function, and tissue composition. The acute lack of oxygen in the perfusion bed (area at risk) initially leads to a breakdown of membrane integrity, which—within 15 min of no-flow ischemia—begets intracellular sodium accumulation with subsequent intracellular edema (24,25). This is followed by leakage of osmotically relevant components into the interstitial space resulting in extracellular/interstitial edema. A wave of violent cell death (necrosis) spreads from the subendocardial layer of the area at risk through the entire myocardial wall, which—if not revascularized spontaneously or by therapeutic intervention—eventually will be irreversibly injured. Necrosis and accompanying inflammation are followed by the fibrotic mesh of the scar, which remains in place as the long-term sequela of the event.
The T2-weighted CMR visualizes acute reperfused infarctions and allows for discriminating acute from chronic infarctions (26). It can also be used to determine the area at risk in reperfused and nonreperfused infarctions. When T2-weighted CMR is combined with contrast-enhanced imaging of irreversible injury ("late enhancement"), the salvaged area at risk can be quantified and thus the success of revascularization or adjunctive treatment on limiting infarctions size can be assessed (27–29).
Appearance of acute infarctions.
Table 2
summarizes the appearance of acute infarctions in CMR sequences typically used as part of a comprehensive CMR examination.
Whereas necrosis may be almost prevented by early reperfusion, for example, by spontaneous recanalization or immediate revascularization, myocardial edema is an invariable feature of acute infarctions. Although the diagnostic utility of T2-weighted imaging in assessing nonreperfused infarctions has not been tested yet, there are experimental data indicating its clinical potential in this setting (30).
The size of the edematous region reflects the perfusion bed, which represents the area at risk (27). Thus, in a clinical setting of reperfused myocardial infarction, edema as defined by high T2 signal intensity is transmural, even if the acute irreversible injury (i.e., the necrosis) is not (Fig. 2) (26,29).
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 2 CMR of Acute, Nontransmural Infarction
(Upper panels) Diastolic (left) and systolic (right) frames in a short-axis view. (Lower panels) T2-weighted (left) and post-contrast T1-weighted (late enhancement) (right) images showing infarction-related transmural edema but only subendocardial necrosis (see Online Video 1).
|
|
In contrast to acute infarctions, T2 is abnormally short in fibrotic tissue (31). Therefore, in T2-weighted images, fibrotic scars–in the absence of inflammation or other acute pathology—typically have a lower signal intensity than normal myocardium does (Fig. 3
), and the lack of high signal intensity differentiates acute from chronic myocardial infarction (26).
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 3 CMR of Ischemic Cardiomyopathy With Chronic, Transmural Inferior Infarction
(Upper panels) Diastolic (left) and systolic (right) frames in a short axis view with akinesis of the inferoseptal and inferior segments. (Lower panels) T2-weighted (left) and post-contrast T1-weighted (late enhancement) (right) images showing no edema, but transmural fibrosis (arrows) within the akinetic region (see Online Video 2).
|
|
There is a lack of systematic data on the appearance of no reflow areas in T2-weighted images. In most of the cases, however, this region will appear as an intramural area of low signal intensity, which is embedded in a high signal intensity rim of edema (Fig. 4).
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 4 CMR in a Patient With Acute Myocarditis
(Upper panels) Diastolic (left) and systolic (right) frames of a cine study showing pericardial effusion (bright signal) and largely preserved systolic function. (Lower panels) T2-weighted (left) and post-contrast T1-weighted (late enhancement) (right) images showing lateral edema (arrows) and focal fibrosis typical for the nonischemic injury pattern of myocarditis (arrows) (see Online Video 3).
|
|
Late enhancement images show necrotic myocardium as a region of very bright signal intensity (Figs. 2 to 5). In reperfused infarctions, the subendocardial portion is usually broader than the subepicardial portion. This reflects the termination of the wave front-like expansion of the injury, which spans across the perfusion bed starting in the subendocardium, which is more susceptible to ischemia. In nonreperfusion infarctions, especially those caused by proximal coronary lesions, necrosis most often is transmural (Figs. 3 to 5).
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 5 CMR of Acute, Transmural Infarction
(Upper panels) Diastolic (left) and systolic (right) frames in a short-axis view. (Lower panels) T2-weighted (left) and post-contrast T1-weighted (late enhancement) (right) images showing infarct-related transmural edema with transmural necrosis of the same size (see Online Video 4).
|
|
It is important to emphasize that wall thickness is preserved in acute infarctions. In fact, injury-related edema leads to regional swelling (i.e., an increased wall thickness of the infarcted segments) (Figs. 2 and 5).
Because blood flow is interrupted in areas with no reflow, interstitial compounds such as gadolinium can enter only through inward diffusion from the peripheral border of the no-reflow zone. If this region is sufficiently large and thus a long time is needed for gadolinium to diffuse into its center, the latter will not appear enhanced during the first minutes after administration (Fig. 6). This should not be confused with viable myocardium.
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 6 CMR of Acute, Transmural Infarction With No-Reflow in a Patient With Reperfused Lateral Infarction, Who Presented Late After Onset of Symptoms
(Upper panels) Diastolic (left) and systolic (right) frames in a short-axis view showing preserved wall thickness of the lateral wall but regional akinesis of the anterolateral and inferolateral segments. (Lower panels) T2-weighted (left) and post-contrast T1-weighted (late enhancement) (right) images showing infarction-related transmural edema and matching necrosis in the dysfunctional segments. Both, T2-weighted and late enhancement images show a core with reduced signal intensity reflecting no-reflow (arrowheads) (see Online Video 5).
|
|
|
CMR Tissue Characterization in Myocarditis
|
|---|
Viral agents or other triggers, such as toxins initiating inflammation, will cause cell injury with edema, necrosis, and, if sufficiently large, macroscopic scarring. Although these basic tissue responses show similarities to ischemic injury, its evolution and spatial distribution are substantially different from infarctions. Whereas acute infarctions are characterized by a lack of perfusion, tissue inflammation is usually associated with peripheral vasodilation and thus increased blood volume in the affected region. Furthermore, instead of an outward wave front of reversible and irreversible damage, spreading of myocardial inflammation shows a disseminated, focal or global myocardial involvement. Thus, in contrast to acute infarctions, the injury—with few exceptions—does not show the pattern of infarctions, which again are characterized by predominantly subendocardial or transmural involvement.
The CMR techniques used to visualize tissue pathology of myocarditis are very similar to those for imaging infarctions.
Appearance of acute myocarditis.
The regional distribution of inflammation-induced tissue characteristics is distinct from that of acute myocardial infarction (Table 3). Edema, as defined by high signal intensity in T2-weighted images, may be absent in very early stages of myocarditis (32), but—if present—it is easily identified in subepicardial or intramural layers of the myocardium (Figs. 4 to 8). Global involvement of the heart can be detected by quantifying the signal intensity ratio between the myocardium and skeletal muscles (18,33).
View this table:
[in this window]
[in a new window]
|
Table 3 Appearance of Acute Myocarditis and Sarcoidosis in CMR Sequences Typically Used in a Comprehensive Examination
|
|
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 7 CMR of a Patient With Acute Myocarditis
(Left panel) Diastolic (upper) and systolic (lower) frames of a cine study showing hyperdynamic systolic function. (Middle panel) Non-breath-hold T1-weighted images acquired before (upper) and over the first minutes after gadolinium indicating significant myocardial gadolinium uptake. The uptake ratio (early enhancement) was increased. (Right upper panel) T2-weighted image with high signal intensity of the anterior wall. (Right lower panel) Post-contrast T1-weighted (late enhancement) image showing possible diffuse necrosis but lack of regional injury (see Online Video 6).
|
|
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video
|
Figure 8 CMR of a Patient With Acute Myocarditis and Chronic Scarring
(Left panel) Diastolic (upper) and systolic (lower) frames of a cine study showing grossly systolic function with mild septal hypokinesis. (Middle panel) Non-breath-hold T1-weighted images acquired before (upper) and over the first minutes after gadolinium indicating significant myocardial gadolinium uptake. The uptake ratio (early enhancement) was increased. (Right upper panel) T2-weighted image with high signal intensity of the septum (arrow). (Right lower panel) Post-contrast T1-weighted (late enhancement) image showing a focal scar in the lateral wall but no necrosis in the septal region (see Online Video 7).
|
|
In early enhancement images, the myocardium typically reveals a focal and/or global signal intensity increase (Figs. 7 and 8). The normalized enhancement ratio (compared with that for skeletal muscle) is increased. Early enhancement image quality depends on scanner settings and the patient's breathing pattern.
Late enhancement images in patients with acute myocarditis often show multifocal areas with high signal intensity in predominantly intramural or subepicardial regions (Figs. 4, 8, and 9). Although a recent study linked subendocardial scars to myocarditis-induced coronary spasm induced by parvovirus B-19 (34), the injury pattern found in myocarditis does not predominantly involve the subendocardial layer. Interestingly, the inferolateral wall appears to be affected most often (16,35). There is preliminary evidence that the regional distribution may also depend on the viral species, with parvovirus B-19 predominantly affecting the inferolateral wall and the herpes virus preferring the septum (36). Further studies are needed to confirm these findings and better understand their clinical implications.
View larger version (183K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 9 CMR of a Patient With Remote Myocarditis
This CMR image of a patient with remote myocarditis shows chronic multifocal, partially subendocardial scarring in a T1-weighted (late enhancement) image.
|
|
Combined CMR protocols assessing accompanying pericardial effusion and ventricular function in addition to tissue markers for inflammation and irreversible injury have been found to have the highest diagnostic accuracy in myocarditis (18,33).
|
Clinical Scenarios for Tissue Characterization
|
|---|
Patients with a high clinical suspicion of acute infarction (i.e., high risk profile, diagnostic ECG changes with positive biomarkers) need no further diagnostic workup as this would only delay appropriate revascularization. If, however, the "story does not fit," for example, because the patient is very young or coronary artery stenosis has been ruled out, tissue characterization adds important additional information. Myocarditis is the most frequent diagnosis in patients presenting clinically acute infarctions but with normal coronary arteries on angiograms (37). Myocarditis can be reliably detected in such patients by CMR tissue characterization (38).
An important differential diagnosis in patients presenting with acute chest pain, functional abnormality, ECG changes, and positive seromarkers is stress-induced cardiomyopathy (takotsubo). The CMR tissue characterization has been shown to be very useful for verifying the disease using tissue characterization. Mid and apical dyskinesis in combination with edema and a lack of infarction-like subendocardial necrosis allow for establishing this diagnosis (39,40). Diffuse, spotty regions of high signal intensity, however, may be observed (Fig. 10). Because scars shrink over time, these findings may be reversible through follow-up.
View larger version:
[in this window]
[in a new window]
[Download PPT slide]
Click on image to view video 
Click on image to view video
|
Figure 10 CMR of an Elderly Patient With Acute Anterior Infarction and Invasive Exclusion of Relevant Coronary Artery Stenosis
(A) The CMR images taken at admission of an elderly woman who presented with acute anterior infarction and invasive exclusion of relevant coronary artery stenosis. (Left panel) Diastolic (upper) and systolic (lower) frames of a breath-hold cine study, showing typical extensive mid-ventricular and apical dyskinesia ("ballooning"). (Right upper panel) T2-weighted image showing diffuse intraventricular high signal intensity due to slow flowing blood as well as an increased signal intensity of the mid-ventricular and apical myocardium, presumably reflecting myocardial edema. (Right lower panel) Late gadolinium enhancement study showing no subendocardial high signal intensity but some diffuse late enhancement of the dysfunctional segments. The final diagnosis in this patient was acute stress-induced cardiomyopathy (see Online Video 8). (B) Follow-up study of the same patient after 4 weeks. (Left panel) Diastolic (upper) and systolic (lower) frames of a breath-hold cine study, showing normalization of systolic function. (Right upper panel) T2-weighted image showing homogeneous signal intensity. (Right lower panel) Late gadolinium enhancement study showing persisting diffuse late enhancement of the dysfunctional segments (see Online Video 9).
|
|
Table 4
lists several clinical scenarios of acute heart disease in which CMR tissue characterization can provide important information upon which to base further therapeutic decisions. Tissue characterization using late enhancement is considered highly appropriate for the evaluation of infarction and myocarditis (41) and standard protocols have been recently proposed (42).
|
Limitations of CMR Tissue Characterization
|
|---|
Table 5
lists current limitations of CMR tissue characterization. In clinical settings of acute disease, the most significant limitation may be with logistics of patient transport, setup, and uninterrupted cardiac monitoring during transportation.
|
Conclusions
|
|---|
Myocardial tissue characterization provides very important additional information in many patients with acute myocardial disease. Although further standardization and streamlining of protocols are required, CMR has unique features, making it the diagnostic tool of choice for this purpose, particularly when applied as part of a single, fast and efficient scan of morphology, function, and tissue pathology.
|
Appendix
|
|---|
For an accompanying slide set, and Videos 1 to 9 that correspond to Figures 2 to 10, please see the online version of this article.
* Reprint requests and correspondence: Dr. Matthias G. Friedrich, Suite 700-SSB, Foothills Medical Centre. 1403 29th Street NW, Calgary, Alberta T2N 2T9, Canada (Email: matthias.friedrich{at}ucalgary.ca).
Manuscript received July 17, 2008;
accepted July 21, 2008.
|
REFERENCES
|
|---|
- Masoudi FA, Magid DJ, Vinson DR, et al. Emergency Department Quality in Myocardial Infarction Study Investigators Implications of the failure to identify high-risk electrocardiogram findings for the quality of care of patients with acute myocardial infarction: results of the Emergency Department Quality in Myocardial Infarction (EDQMI) study Circulation 2006;114:1565-1571.[Abstract/Free Full Text]
- Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses of acute cardiac ischemia in the emergency department N Engl J Med 2000;342:1163-1170.[Abstract/Free Full Text]
- Iglesias-Garriz I, Rodríguez MA, García-Porrero E, Ereño F, Garrote C, Suarez G. Emergency nontraumatic chest pain: use of stress echocardiography to detect significant coronary artery stenosis J Am Soc Echocardiogr 2005;18:1181-1186.[CrossRef][Web of Science][Medline]
- Liu PP, Yan AT. Cardiovascular magnetic resonance for the diagnosis of acute myocarditis: prospects for detecting myocardial inflammation J Am Coll Cardiol 2005;45:1823-1825.[Free Full Text]
- Cooper LT, Baughman KL, Feldman AM, et al. American Heart AssociationAmerican College of CardiologyEuropean Society of CardiologyHeart Failure Society of AmericaHeart Failure Association of the European Society of Cardiology The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Endorsed by the Heart Failure Society of America and the Heart Failure Association of the European Society of Cardiology. J Am Coll Cardiol 2007;50:1914-1931.[Free Full Text]
- Skouri HN, Dec GW, Friedrich MG, Cooper LT. Noninvasive imaging in myocarditis J Am Coll Cardiol 2006;48:2085-2093.[Abstract/Free Full Text]
- Schwitter J, Wacker CM, van Rossum AC, et al. MR-IMPACT: comparison of perfusion-cardiac magnetic resonance with single-photon emission computed tomography for the detection of coronary artery disease in a multicentre, multivendor, randomized trial Eur Heart J 2008;29:480-489.[Abstract/Free Full Text]
- Ingkanisorn WP, Kwong RY, Bohme NS, et al. Prognosis of negative adenosine stress magnetic resonance in patients presenting to an emergency department with chest pain J Am Coll Cardiol 2006;47:1427-1432.[Abstract/Free Full Text]
- Jahnke C, Nagel E, Gebker R, et al. Prognostic value of cardiac magnetic resonance stress tests: adenosine stress perfusion and dobutamine stress wall motion imaging Circulation 2007;115:1769-1776.[Abstract/Free Full Text]
- Laissy JP, Hyafil F, Feldman LJ, et al. Differentiating acute myocardial infarction from myocarditis: Diagnostic value of early- and delayed-perfusion cardiac MR imaging Radiology 2005;237:75-82.[Abstract/Free Full Text]
- McNamara MT, Higgins CB, Schechtmann N, et al. Detection and characterization of acute myocardial infarction in man with use of gated magnetic resonance Circulation 1985;71:717-724.[Abstract/Free Full Text]
- Kellman P, Aletras AH, Mancini C, McVeigh ER, Arai AE. T2-prepared SSFP improves diagnostic confidence in edema imaging in acute myocardial infarction compared to turbo spin echo Magn Reson Med 2007;57:891-897.[CrossRef][Web of Science][Medline]
- Aletras AH, Kellman P, Derbyshire JA, Arai AE. ACUT2E TSE-SSFP: a hybrid method for T2-weighted imaging of edema in the heart Magn Reson Med 2008;59:229-235.[CrossRef][Web of Science][Medline]
- Huang TY, Liu YJ, Stemmer A, Poncelet BP. T2 measurement of the human myocardium using a T2-prepared transient-state TrueFISP sequence Magn Reson Med 2007;57:960-966.[CrossRef][Web of Science][Medline]
- Abdel-Aty H, Simonetti O, Friedrich MG. T2-weighted cardiovascular magnetic resonance imaging J Magn Reson Imaging 2007;26:452-459.[CrossRef][Web of Science][Medline]
- Friedrich MG, Strohm O, SchulzMenger J, Marciniak H, Luft FC, Dietz R. Contrast media-enhanced magnetic resonance imaging visualizes myocardial changes in the course of viral myocarditis Circulation 1998;97:1802-1809.[Abstract/Free Full Text]
- 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.[CrossRef][Web of Science][Medline]
- Gutberlet M, Spors B, Thoma T, et al. Suspected chronic myocarditis at cardiac MR: diagnostic accuracy and association with immunohistologically detected inflammation and viral persistence Radiology 2008;246:401-409.[Abstract/Free Full Text]
- Rehwald WG, Fieno DS, Chen EL, Kim RJ, Judd RM. Myocardial magnetic resonance imaging contrast agent concentrations after reversible and irreversible ischemic injury Circulation 2002;105:224-229.[Abstract/Free Full Text]
- 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]
- 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][Web of Science][Medline]
- Ricciardi MJ, Wu E, Davidson CJ, et al. Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation Circulation 2001;103:2780-2783.[Abstract/Free Full Text]
- Rezkalla SH, Kloner RA. No-reflow phenomenon Circulation 2002;105:656-662.[Free Full Text]
- Kloner RA, Jennings RB. Consequences of brief ischemia: stunning, preconditioning, and their clinical implications: part 1 Circulation 2001;104:2981-2989.[Abstract/Free Full Text]
- Kloner RA, Jennings RB. Consequences of brief ischemia: stunning, preconditioning, and their clinical implications: part 2 Circulation 2001;104:3158-3167.[Abstract/Free Full Text]
- Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction Circulation 2004;109:2411-2416.[Abstract/Free Full Text]
- Aletras AH, Tilak GS, Natanzon A, et al. Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations Circulation 2006;113:1865-1870.[Abstract/Free Full Text]
- Ibanez B, Prat-González S, Speidl WS, et al. Early metoprolol administration before coronary reperfusion results in increased myocardial salvage: analysis of ischemic myocardium at risk using cardiac magnetic resonance Circulation 2007;115:2909-2916.[Abstract/Free Full Text]
- Friedrich MG, Abdel-Aty H, Taylor A, Schulz-Menger J, Messroghli D, Dietz R. The salvaged area at risk in reperfused acute myocardial infarction as visualized by cardiovascular magnetic resonance J Am Coll Cardiol 2008;51:1581-1587.[Abstract/Free Full Text]
- Tilak GS, Hsu LY, Hoyt RF, Arai AE, Aletras AH. In vivo T2-weighted magnetic resonance imaging can accurately determine the ischemic area at risk for 2-day-old nonreperfused myocardial infarction Invest Radiol 2008;43:7-15.[CrossRef][Web of Science][Medline]
- McNamara MT, Higgins CB. Magnetic resonance imaging of chronic myocardial infarcts in man AJR Am J Roentgenol 1986;146:315-320.[Abstract/Free Full Text]
- Friedrich MG, Strohm O, Schulz-Menger J, Marciniak H, Luft FC, Dietz R. Noninvasive diagnosis of acute myocarditis by contrast-enhanced magnetic resonance imaging—response to the author Circulation 1999;99:459-460.[Web of Science][Medline]
- Abdel-Aty H, Boye P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches J Am Coll Cardiol 2005;45:1815-1822.[Abstract/Free Full Text]
- Yilmaz A, Mahrholdt H, Athanasiadis A, et al. Coronary vasospasm as the underlying cause for chest pain in patients with PVB19-myocarditis Heart 2008 Jan 29[E-pub ahead of print].
- Mahrholdt H, Goedecke C, Wagner A, et al. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology Circulation 2004;109:1250-1258.[Abstract/Free Full Text]
- Mahrholdt H, Wagner A, Deluigi CC, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis Circulation 2006;114:1581-1590.[Abstract/Free Full Text]
- Sarda L, Colin P, Boccara F, et al. Myocarditis in patients with clinical presentation of myocardial infarction and normal coronary angiograms J Am Coll Cardiol 2001;37:786-792.[Abstract/Free Full Text]
- Assomull RG, Lyne JC, Keenan N, et al. The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries Eur Heart J 2007;28:1242-1249.[Abstract/Free Full Text]
- Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States Circulation 2005;111:472-479.[Abstract/Free Full Text]
- Abdel-Aty H, Cocker M, Friedrich MG. Myocardial edema is a feature of Tako-Tsubo cardiomyopathy and is related to the severity of systolic dysfunction: insights from T2-weighted cardiovascular magnetic resonance Int J Cardiol 2007 Dec 15[E-pub ahead of print].
- Hendel RC, Patel MR, Kramer CM, et al. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging: a report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American College of Radiology, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, American Society of Nuclear Cardiology, North American Society for Cardiac Imaging, Society for Cardiovascular Angiography and Interventions, and Society of Interventional Radiology J Am Coll Cardiol 2006;48:1475-1497.[Free Full Text]
- Kramer CM, Barkhausen J, Flamm SD, Kim RJ, Nagel E. Standardized cardiovascular magnetic resonance imaging (CMR) protocols J Cardiovasc Magn Reson 2008;10:35.[Medline]
|
Top
Abstract
Current Diagnostic Tools in...